tag:blogger.com,1999:blog-64049500199843500272023-11-15T09:09:55.490-08:00PORCINE SPONGIFORM ENCEPHALOPATHY PSETerry S. Singeltary Sr.http://www.blogger.com/profile/06986622967539963260noreply@blogger.comBlogger14125tag:blogger.com,1999:blog-6404950019984350027.post-6646404908859692602021-10-06T13:16:00.001-07:002021-10-06T13:16:07.888-07:00Classical BSE prions emerge from asymptomatic pigs challenged with atypical/Nor98 scrapie<p>Published: 31 August 2021</p><div><div><span style="font-size: 13.3333px;">Classical BSE prions emerge from asymptomatic pigs challenged with atypical/Nor98 scrapie</span></div><div><span style="font-size: 13.3333px;"><br /></span></div><div><span style="font-size: 13.3333px;">Belén Marín, Alicia Otero, Séverine Lugan, Juan Carlos Espinosa, Alba Marín-Moreno, Enric Vidal, Carlos Hedman, Antonio Romero, Martí Pumarola, Juan J. Badiola, Juan María Torres, Olivier Andréoletti & Rosa Bolea </span></div><div><span style="font-size: 13.3333px;"><br /></span></div><div><span style="font-size: 13.3333px;">Scientific Reports volume 11, Article number: 17428 (2021) Cite this article</span></div><div><span style="font-size: 13.3333px;"><br /></span></div><div><span style="font-size: 13.3333px;">Abstract</span></div><div><span style="font-size: 13.3333px;"><br /></span></div><div><span style="font-size: 13.3333px;">Pigs are susceptible to infection with the classical bovine spongiform encephalopathy (C-BSE) agent following experimental inoculation, and PrPSc accumulation was detected in porcine tissues after the inoculation of certain scrapie and chronic wasting disease isolates. However, a robust transmission barrier has been described in this species and, although they were exposed to C-BSE agent in many European countries, no cases of natural transmissible spongiform encephalopathies (TSE) infections have been reported in pigs. Transmission of atypical scrapie to bovinized mice resulted in the emergence of C-BSE prions. Here, we conducted a study to determine if pigs are susceptible to atypical scrapie. To this end, 12, 8–9-month-old minipigs were intracerebrally inoculated with two atypical scrapie sources. Animals were euthanized between 22- and 72-months post inoculation without clinical signs of TSE. All pigs tested negative for PrPSc accumulation by enzyme immunoassay, immunohistochemistry, western blotting and bioassay in porcine PrP mice. Surprisingly, in vitro protein misfolding cyclic amplification demonstrated the presence of C-BSE prions in different brain areas from seven pigs inoculated with both atypical scrapie isolates. Our results suggest that pigs exposed to atypical scrapie prions could become a reservoir for C-BSE and corroborate that C-BSE prions emerge during interspecies passage of atypical scrapie.</span></div><div><span style="font-size: 13.3333px;"><br /></span></div><div><span style="font-size: 13.3333px;">snip...</span></div><div><span style="font-size: 13.3333px;"><br /></span></div><div><span style="font-size: 13.3333px;">Discussion The outbreak of C-BSE was followed by the appearance of TSE in species that had never been diagnosed with prion diseases and the emergence in humans of vCJD16,17,18. However, no natural prion disease has been described in pigs, even though they were exposed to C-BSE contaminated feed12. Posterior experimental challenges in pigs and mice expressing porcine PrP have demonstrated that, although they are not completely resistant, pigs present a robust transmission barrier for C-BSE prions4,14,19.</span></div><div><span style="font-size: 13.3333px;"><br /></span></div><div><span style="font-size: 13.3333px;">However, the possible transmission of a TSE to swine is a public health concern due to the wide use of pork as a source of human food, and the increasing use of pigs as tissue donors, being reported a case of vCJD in a human patient receiving a swine dura mater graft20. Although pigs are apparently non-susceptible to C-BSE after oral challenge4,5,21, infectivity has been detected in tissues from pigs orally inoculated with classical scrapie or CWD10,11. In addition, these positive orally inoculated pigs are often subclinical, what could represent a public health concern, considering that these animals could reach the slaughterhouse without showing signs suggestive of prion disease.</span></div><div><span style="font-size: 13.3333px;"><br /></span></div><div><span style="font-size: 13.3333px;">In the present study, we evaluated the transmissibility of atypical scrapie to pigs. Pigs were euthanized between 22- and 72-months post inoculation (mpi), and their tissues tested for PrPSc accumulation and infectivity. We did not find evidence of transmission of atypical scrapie to any of the animals by EIA (Table 2), western blotting, or mouse bioassay (Table 3). PrPSc accumulation can be detected in BSE-challenged pigs at 34 mpi4, and at 22 mpi when inoculated with SBSE7. Although scrapie or CWD-inoculated pigs do not show clinical signs, PrPSc presence can be found in scrapie-challenged animals at 51 mpi11 and as early as 6 mpi in the case of CWD10.</span></div><div><span style="font-size: 13.3333px;"><br /></span></div><div><span style="font-size: 13.3333px;">Our main goal was to test the ability of atypical scrapie/Nor98 strain to propagate in swine, given that mice expressing porcine PrP (PoPrP-Tg001/tgPo mice) showed to be susceptible to atypical scrapie inoculation. One atypical scrapie isolate adapted to this transgenic line, reaching a 100% attack rate and rapid incubation periods in serial passages13, a similar adaptation to that observed with the C-BSE agent19. However, when this atypical scrapie isolate was tested for propagation in tgPo mice again, together with other atypical scrapie isolates, no positive results were obtained, in vitro nor in vivo14. These results, together with the negative transmissions showed in the present study, reinforce the conclusion that porcine species is highly resistant to atypical scrapie. However, we only performed one passage in tgPo mice, and further passages in this line and/or PMCA analysis of tgPo brains to detect any possible prion replication would be of interest.</span></div><div><span style="font-size: 13.3333px;"><br /></span></div><div><span style="font-size: 13.3333px;">However, it was demonstrated that C-BSE prions can be present as a minor variant in ovine atypical scrapie isolates and that C-BSE can emerge during the passage of these isolates to bovine PrP mice15. Considering that the aforementioned atypical scrapie isolate also acquired BSE-like properties when transmitted to tgPo mice13, and that C-BSE is the only prion that efficiently propagates in swine PrP4,7,14, we decided to investigate whether C-BSE prions could emerge from atypical scrapie during the ovine-porcine interspecies transmission.</span></div><div><span style="font-size: 13.3333px;"><br /></span></div><div><span style="font-size: 13.3333px;">Interestingly, PMCA reactions seeded with brain material from 7 pigs propagated in tgBov substrate showing PrPres with identical biochemical characteristics to those of C-BSE (Fig. 1). Positive C-BSE amplification was detected in the brain of pigs inoculated with either the PS152 or TOA3 atypical scrapie isolates, at minimum incubation periods of 28- and 35-months post inoculation, respectively. From each animal, positive reactions were not obtained from all brain areas tested (Supplementary table 1). Although PrPres amplified from the pigs showed C-BSE biochemical characteristics, further bioassays in tgBov mice are required to know whether these prions replicate the neuropathological features of C-BSE.</span></div><div><span style="font-size: 13.3333px;"><br /></span></div><div><span style="font-size: 13.3333px;">Altogether, our results and data obtained from transmission studies of prions to pigs, tgPo mice and in vitro studies using porcine substrate have shown that pig PrP has a very limited ability to sustain prion replication. No significant polymorphisms have been described for pig PRNP22, and it has been suggested that the conformational flexibility of pig PrP sequence is very low, limiting the number of PrPSc conformations able to produce misfolding14. No differences have been found between pig and minipig PrP sequences either23, suggesting that the conclusions obtained here could be extrapolated to domestic, non-experimental pigs. However, using tgBov substrate, we have demonstrated in vitro the presence of C-BSE seeding activity in some pig brain areas, suggesting that C-BSE prions emerged during the transmission of ovine atypical scrapie prions to pigs. Interestingly, C-BSE prions did not emerge from brain material of all the pigs, and, of those from which it did emerge, it was not detected in all brarsain areas tested. No correlation between time after inoculation and BSE emergence was found either. When the emergence of C-BSE from atypical scrapie in PMCA was described, it was associated to low levels of C-BSE prions that were present in the original atypical scrapie isolates15. It is possible that this result is related to the great resistance that pigs present to prion diseases, making the penetrance of the BSE prions that could be present in the original inoculum incomplete. In addition, considering that the amount of C-BSE conformers in the atypical scrapie inocula is probably very reduced and perhaps not homogeneously distributed throughout the isolate, it is also possible that not all the pigs received a sufficient amount of C-BSE conformers capable of being detected by PMCA. Finally, we should consider that PMCA amplification of prions is sometimes a stochastic phenomenon, which could explain why no C-BSE propagation was obtained from some of the pigs. It could be also discussed that C-BSE emergence from the pig brains could be related to persistence of the original atypical scrapie inoculum. However, C-BSE amplification was not obtained from all of the pigs and, in some of them (i.e. P-1217 and P-1231) C-BSE propagation was detected in caudal regions of the brain (cerebellum or occipital cortex) but not in more rostral areas (such as parietal cortex). If C-BSE amplification from pig brain samples were associated to inoculum persistence and not bona fide propagation of C-BSE prions it would be expected that such amplification would be detected mainly in the most rostral areas of the brain. Finally, even though the titer generated was not enough to produce disease in the pigs, these results evidence again the issue that pigs could act as subclinical reservoirs for prion diseases as observed with scrapie and CWD, and that the presence of prions can be detected in pigs short after exposure to prions7,10,11.</span></div><div><span style="font-size: 13.3333px;"><br /></span></div><div><span style="font-size: 13.3333px;">In conclusion, our findings suggest that, although pigs present a strong transmission barrier against the propagation of atypical scrapie, they can propagate low levels of C-BSE prions. The prevalence of atypical scrapie and the presence of infectivity in tissues from atypical scrapie infected sheep are underestimated24,25. Given that pigs have demonstrated being susceptible to other prion diseases, and to propagate prions without showing signs of disease, the measures implemented to ban the inclusion of ruminant proteins in livestock feed must not be interrupted.</span></div><div><br /></div></div><div><a href="https://www.nature.com/articles/s41598-021-96818-2" style="color: #0096ef; cursor: pointer; text-decoration-line: none;">https://www.nature.com/articles/s41598-021-96818-2</a><br /></div><div><br /></div><div>>>> The prevalence of atypical scrapie and the presence of infectivity in tissues from atypical scrapie infected sheep are underestimated24,25. </div><div><br /></div><div>>>> Given that pigs have demonstrated being susceptible to other prion diseases, and to propagate prions without showing signs of disease, the measures implemented to ban the inclusion of ruminant proteins in livestock feed must not be interrupted.<br /></div><div><br /></div><div><br /></div><div><div><a href="https://www.hjortevilt.no/bekrefter-atypisk-skrantesjuke-pa-hjort-i-etne/?fbclid=IwAR3MGseZb7apE5WXo34vyLRzaElC1OGPn95J-7Q_WQbD93pe-yuWK40N5YM" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://www.hjortevilt.no/bekrefter-atypisk-skrantesjuke-pa-hjort-i-etne/?fbclid=IwAR3MGseZb7apE5WXo34vyLRzaElC1OGPn95J-7Q_WQbD93pe-yuWK40N5YM</a></div><div><br /></div><div><span style="font-size: 10pt;">***> This is a variant of scrapie that we consider non-contagious. </span><br /></div><div><br /></div><div><span style="font-size: 10pt;">***> Atypical/Nor98 scrapie occurs in sheep that tend to be resistant to classical scrapie and it is thought to occur spontaneously.</span><br /></div><div><div><div><br /></div><div> ***> Unlike classical scrapie (CS), AS is thought to be a spontaneously occurring disease [1–3].</div><div><br /></div><div>***> It typically affects a single older sheep within a flock, and cases of AS are sporadic and isolated suggesting that natural transmission is unlikely.</div><div><br /></div><div>***> Several experiments have demonstrated the ability of the AS agent to transmit within the natural host after intracranial inoculation [14–16]. </div><div><br /></div><div>***> One study found that the AS agent could transmit after a high oral dose of AS brain homogenate [17]. </div><div><br /></div><div>***> Nonetheless, AS is still considered unlikely to transmit under field conditions; therefore, eradication and surveillance programs for CS have allowed exceptions for AS. </div></div><div><br /></div><div>I disagree, and this is a foolish move taking this stance, because Science has shown us that the atypical scrapie IS TRANSMISSIBLE!</div><div><br /></div><div>EFSA SAYS <span style="font-size: 10pt;">ATYPICAL SCRAPIE ROUGHLY HAS 50 50 CHANCE ATYPICAL SCRAPIE IS CONTAGIOUS, AS NON-CONTAGIOUS!</span></div><div><br /></div><div>TO CONTINUE THIS CHARADE, THAT ''<span style="font-size: 10pt;">variant of scrapie that we consider non-contagious'' and </span><span style="font-size: 10pt;">''</span><span style="font-size: 10pt;">AS is thought to be a spontaneously occurring disease'', </span><span style="font-size: 10pt;">WILL ONLY CONTINUE TO SPREAD CWD TSE PRION, INCLUDING ATYPICAL SCRAPIE...TERRY</span></div><div><br /></div><div><div>***Moreover, sporadic disease has never been observed in breeding colonies or primate research laboratories, most notably among hundreds of animals over several decades of study at the National Institutes of Health25, and in nearly twenty older animals continuously housed in our own facility.***</div><div><br /></div><div>Even if the prevailing view is that sporadic CJD is due to the spontaneous formation of CJD prions, it remains possible that its apparent sporadic nature may, at least in part, result from our limited capacity to identify an environmental origin.</div><div><br /></div><div><a href="https://www.nature.com/articles/srep11573" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://www.nature.com/articles/srep11573</a> </div></div></div><div><br /></div><div><div>THURSDAY, JULY 8, 2021</div><div><br /></div><div>EFSA Scientific report on the analysis of the 2‐year compulsory intensified monitoring of atypical scrapie</div></div><div><br /></div><div><span style="font-size: 10pt;">***> AS is considered more likely (subjective probability range 50–66%) that AS is a non-contagious, rather than a contagious, disease.</span><br /></div><div><div style="font-size: 10pt;"><br /></div><div style="font-size: 10pt;">ATYPICAL SCRAPIE ROUGHLY HAS 50 50 CHANCE ATYPICAL SCRAPIE IS CONTAGIOUS, AS NON-CONTAGIOUS, TAKE YOUR PICK, BUT I SAID IT LONG AGO WHEN USDA OIE ET AL MADE ATYPICAL SCRAPIE A LEGAL TRADING COMODITY, I SAID YOUR PUTTING THE CART BEFORE THE HORSE, AND THAT'S EXACTLY WHAT THEY DID, and it's called in Texas, TEXAS TSE PRION HOLDEM POKER, WHO'S ALL IN $$$<br /></div><div style="font-size: 10pt;"><br /></div><div><div>THURSDAY, JULY 8, 2021</div><div><br /></div><div>EFSA Scientific report on the analysis of the 2‐year compulsory intensified monitoring of atypical scrapie</div></div></div><div><br /></div><div><a href="https://efsa.onlinelibrary.wiley.com/doi/10.2903/j.efsa.2021.6686" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://efsa.onlinelibrary.wiley.com/doi/10.2903/j.efsa.2021.6686</a><br /></div><div><br /></div><div><div>ACCEPTED MANUSCRIPT</div><div><br /></div><div>North American and Norwegian Chronic Wasting Disease prions exhibit different potential for interspecies transmission and zoonotic risk</div><div><br /></div><div>Sandra Pritzkow, Damian Gorski, Frank Ramirez, Glenn C Telling, Sylvie L Benestad, Claudio Soto</div><div><br /></div><div>The Journal of Infectious Diseases, jiab385, <a href="https://doi.org/10.1093/infdis/jiab385" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://doi.org/10.1093/infdis/jiab385</a></div><div><br /></div><div>Published: 24 July 2021 Article history Abstract</div><div><br /></div><div>Chronic wasting disease (CWD) is a rapidly spreading prion disorder affecting various species of wild and captive cervids. The risk that CWD poses to co-habiting animals or more importantly to humans is largely unknown. </div><div><br /></div><div>In this study we investigated differences in the capacity of CWD isolates obtained from six different cervid species to induce prion conversion in vitro by PMCA. We define and quantify spillover and zoonotic potential indices as the efficiency by which CWD prions sustain prion generation in vitro at expenses of normal prion proteins from various mammals and human, respectively. </div><div><br /></div><div>Our data suggest that reindeer and red deer from Norway could be the most transmissible CWD prions to other mammals, whereas North American CWD prions were more prone to generate human prions in vitro. </div><div><br /></div><div>Our results suggest that Norway and North American CWD prions correspond to different strains with distinct spillover and zoonotic potentials.</div><div><br /></div><div>prions, prion disease, chronic wasting disease, CWD, prion strains, PMCA, spillover potential, zoonotic potential, moose, reindeer, red deer, elk, white-tailed deer, mule deer</div><div><br /></div><div>Topic: prion diseases prions reindeer wasting disease, chronic norwegian peritoneal mucinous carcinomatosis</div><div><br /></div><div>Issue Section: Major Article</div><div><br /></div></div><div><a href="https://academic.oup.com/jid/advance-article-abstract/doi/10.1093/infdis/jiab385/6327572?redirectedFrom=fulltext" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://academic.oup.com/jid/advance-article-abstract/doi/10.1093/infdis/jiab385/6327572?redirectedFrom=fulltext</a><br /></div><div><br /></div><div><div>Chronic wasting disease: a cervid prion infection looming to spillover</div><div><br /></div><div>Alicia Otero 1 2 3, Camilo Duque Velásquez 1 2, Judd Aiken 2 4, Debbie McKenzie 5 6</div><div><br /></div><div>Affiliations expand</div><div><br /></div><div>PMID: 34488900 DOI: 10.1186/s13567-021-00986-y</div><div><br /></div><div><a href="https://veterinaryresearch.biomedcentral.com/articles/10.1186/s13567-021-00986-y" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://veterinaryresearch.biomedcentral.com/articles/10.1186/s13567-021-00986-y</a><br /></div><div><br /></div><div><a href="https://link.springer.com/content/pdf/10.1186/s13567-021-00986-y.pdf" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://link.springer.com/content/pdf/10.1186/s13567-021-00986-y.pdf</a></div></div><div><br /></div><div><span style="font-size: 10pt;">Transmission of the atypical/Nor98 scrapie agent to Suffolk sheep with VRQ/ARQ, ARQ/ARQ, and ARQ/ARR genotypes</span><br /></div><div><div><br /></div><div>Eric D. Cassmann,Najiba Mammadova,S. Jo Moore,Sylvie Benestad,Justin J. Greenlee </div><div><br /></div><div>Published: February 11, 2021https:<a href="https://doi.org/10.1371/journal.pone.0246503" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">//doi.org/10.1371/journal.pone.0246503</a></div><div><br /></div><div>Citation: Cassmann ED, Mammadova N, Moore SJ, Benestad S, Greenlee JJ (2021) Transmission of the atypical/Nor98 scrapie agent to Suffolk sheep with VRQ/ARQ, ARQ/ARQ, and ARQ/ARR genotypes. PLoS ONE 16(2): e0246503. <a href="https://doi.org/10.1371/journal.pone.0246503" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://doi.org/10.1371/journal.pone.0246503</a></div><div><br /></div><div>Editor: Gianluigi Zanusso, University of Verona, ITALY</div><div><br /></div><div>Received: November 24, 2020; Accepted: January 21, 2021; Published: February 11, 2021</div><div><br /></div><div>Abstract</div><div><br /></div><div>Scrapie is a transmissible spongiform encephalopathy that occurs in sheep. Atypical/Nor98 scrapie occurs in sheep that tend to be resistant to classical scrapie and it is thought to occur spontaneously. The purpose of this study was to test the transmission of the Atypical/Nor98 scrapie agent in three genotypes of Suffolk sheep and characterize the distribution of misfolded prion protein (PrPSc). Ten sheep were intracranially inoculated with brain homogenate from a sheep with Atypical/Nor98 scrapie. All sheep with the ARQ/ARQ and ARQ/ARR genotypes developed Atypical/Nor98 scrapie confirmed by immunohistochemistry, and one sheep with the VRQ/ARQ genotype had detectable PrPSc consistent with Atypical/Nor98 scrapie at the experimental endpoint of 8 years. Sheep with mild early accumulations of PrPSc in the cerebellum had concomitant retinal PrPSc. Accordingly, large amounts of retinal PrPSc were identified in clinically affected sheep and sheep with dense accumulations of PrPSc in the cerebellum.</div><div><br /></div><div>snip...</div><div><br /></div><div>Results and discussion</div><div><br /></div><div>All three genotypes of sheep, VRQ/ARQ, ARQ/ARQ, and ARQ/ARR, were susceptible to the AS agent after intracranial inoculation of donor brain homogenate. The diagnosis of AS was confirmed by enzyme immunoassay (EIA) and immunohistochemistry (IHC) with the latter being confirmative. Previous studies have demonstrated experimental transmission of AS to AHQ/AHQ [14, 15] and ARQ/ARQ [16] genotype sheep after intracerebral transmission. Another study showed a phenotypic shift from AS to CH1641-like classical scrapie in a sheep with the AHQ/AHQ genotype [18]. In this study, sheep with the ARQ/ARR genotype had the shortest incubation period ranging from 4.9 years to the experimental endpoint of 8 years (Table 1), and the attack rate was 100% (5/5). Clinical signs were observed in all ARQ/ARR sheep except for a single wether that was culled early to help establish experimental endpoints. Three ARQ/ARR genotype sheep were euthanized due to clinical neurologic disease 4.9–6.7 years post-inoculation. Out of the three genotypes examined, only the ARQ/ARR genotype sheep developed clinical neurologic disease within the eight-year incubation period. In clinically neurologic sheep, we observed stiff legged and hypermetric ataxia (dysmetria), abnormal rear stance, generalized tremors, tremors of the lips, weight loss, and generalized malaise. The spectrum of clinical signs was comparable to other reports of experimental AS in sheep [14, 15]. Three ARQ/ARR genotype sheep (804, 927 and 948) with the most severe dysmetria also had the greatest amount of cerebellar PrPSc. Since dysmetria is typical of animals with cerebellar disease [20], the tendency to observe this as the most consistent and severe neurologic sign is likely related to the characteristic cerebellar accumulation of PrPSc in sheep with AS. The ARQ/ARQ genotype had a long incubation period and remained clinically asymptomatic, as also reported by Okada et al. [16].</div><div><br /></div><div>snip...</div><div><br /></div><div>This experiment demonstrated the transmission of atypical scrapie to three genotypes of sheep after intracranially inoculation, and it is the first study demonstrating experimental transmission to sheep with a VRQ/ARQ PRNP genotype. Additionally, atypical scrapie is further characterized by demonstrating early accumulation of PrPSc in the retina of experimentally inoculated sheep.</div><div><br /></div><div><a href="https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0246503" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0246503</a><br /></div><div><br /></div><div><div>Published: 31 August 2021</div><div><br /></div><div>Classical BSE prions emerge from asymptomatic pigs challenged with atypical/Nor98 scrapie</div><div><br /></div><div>Belén Marín, Alicia Otero, Séverine Lugan, Juan Carlos Espinosa, Alba Marín-Moreno, Enric Vidal, Carlos Hedman, Antonio Romero, Martí Pumarola, Juan J. Badiola, Juan María Torres, Olivier Andréoletti & Rosa Bolea </div><div><br /></div><div>Scientific Reports volume 11, Article number: 17428 (2021) Cite this article</div><div><br /></div><div>Abstract</div><div><br /></div><div>Pigs are susceptible to infection with the classical bovine spongiform encephalopathy (C-BSE) agent following experimental inoculation, and PrPSc accumulation was detected in porcine tissues after the inoculation of certain scrapie and chronic wasting disease isolates. However, a robust transmission barrier has been described in this species and, although they were exposed to C-BSE agent in many European countries, no cases of natural transmissible spongiform encephalopathies (TSE) infections have been reported in pigs. Transmission of atypical scrapie to bovinized mice resulted in the emergence of C-BSE prions. Here, we conducted a study to determine if pigs are susceptible to atypical scrapie. To this end, 12, 8–9-month-old minipigs were intracerebrally inoculated with two atypical scrapie sources. Animals were euthanized between 22- and 72-months post inoculation without clinical signs of TSE. All pigs tested negative for PrPSc accumulation by enzyme immunoassay, immunohistochemistry, western blotting and bioassay in porcine PrP mice. Surprisingly, in vitro protein misfolding cyclic amplification demonstrated the presence of C-BSE prions in different brain areas from seven pigs inoculated with both atypical scrapie isolates. Our results suggest that pigs exposed to atypical scrapie prions could become a reservoir for C-BSE and corroborate that C-BSE prions emerge during interspecies passage of atypical scrapie.</div><div><br /></div><div>snip...</div><div><br /></div><div>In conclusion, our findings suggest that, although pigs present a strong transmission barrier against the propagation of atypical scrapie, they can propagate low levels of C-BSE prions. The prevalence of atypical scrapie and the presence of infectivity in tissues from atypical scrapie infected sheep are underestimated24,25. Given that pigs have demonstrated being susceptible to other prion diseases, and to propagate prions without showing signs of disease, the measures implemented to ban the inclusion of ruminant proteins in livestock feed must not be interrupted.</div><div><br /></div><div><a href="https://www.nature.com/articles/s41598-021-96818-2" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://www.nature.com/articles/s41598-021-96818-2</a><br /></div><div><br /></div><div><div>Update on chronic wasting disease (CWD) III</div><div><br /></div><div>EFSA Panel on Biological Hazards (BIOHAZ),Kostas Koutsoumanis,Ana Allende,Avelino Alvarez-Ordoňez,Declan Bolton,Sara Bover-Cid,Marianne Chemaly,Robert Davies,Alessandra De Cesare,Lieve Herman,Friederike Hilbert,Roland Lindqvist,Maarten Nauta,Luisa Peixe,Giuseppe Ru,Panagiotis Skandamis,Elisabetta Suffredini,Olivier Andreoletti,Sylvie L Benestad,Emmanuel Comoy,Romolo Nonno,Teresa da Silva Felicio,Angel Ortiz-Pelaez,Marion M Simmons, … </div><div><br /></div><div>First published: 11 November 2019 <a href="https://doi.org/10.2903/j.efsa.2019.5863" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://doi.org/10.2903/j.efsa.2019.5863</a></div></div><div><br /></div><div><div>3.2.1.2 Non‐cervid domestic species</div><div><br /></div><div>The remarkably high rate of natural CWD transmission in the ongoing NA epidemics raises the question of the risk to livestock grazing on CWD‐contaminated shared rangeland and subsequently developing a novel CWD‐related prion disease. This issue has been investigated by transmitting CWD via experimental challenge to cattle, sheep and pigs and to tg mouse lines expressing the relevant species PrP.</div><div><br /></div><div>For cattle challenged with CWD, PrPSc was detected in approximately 40% of intracerebrally inoculated animals (Hamir et al., 2005, 2006a, 2007). Tg mice expressing bovine PrP have also been challenged with CWD and while published studies have negative outcomes (Tamguney et al., 2009b), unpublished data provided for the purposes of this Opinion indicate that some transmission of individual isolates to bovinised mice is possible (Table 1).</div><div><br /></div><div>In small ruminant recipients, a low rate of transmission was reported between 35 and 72 months post‐infection (mpi) in ARQ/ARQ and ARQ/VRQ sheep intracerebrally challenged with mule deer CWD (Hamir et al., 2006b), while two out of two ARQ/ARQ sheep intracerebrally inoculated with elk CWD developed clinical disease after 28 mpi (Madsen‐Bouterse et al., 2016). However, tg mice expressing ARQ sheep PrP were resistant (Tamguney et al., 2006) and tg mice expressing the VRQ PrP allele were poorly susceptible to clinical disease (Beringue et al., 2012; Madsen‐Bouterse et al., 2016). In contrast, tg mice expressing VRQ sheep PrP challenged with CWD have resulted in highly efficient, life‐long asymptomatic replication of these prions in the spleen tissue (Beringue et al., 2012).</div><div><br /></div><div>A recent study investigated the potential for swine to serve as hosts of the CWD agent(s) by intracerebral or oral challenge of crossbred piglets (Moore et al., 2016b, 2017). Pigs sacrificed at 6 mpi, approximately the age at which pigs reach market weight, were clinically healthy and negative by diagnostic tests, although low‐level CWD agent replication could be detected in the CNS by bioassay in tg cervinised mice. Among pigs that were incubated for up to 73 mpi, some gave diagnostic evidence of CWD replication in the brain between 42 and 72 mpi. Importantly, this was observed also in one orally challenged pig at 64 mpi and the presence of low‐level CWD replication was confirmed by mouse bioassay. The authors of this study argued that pigs can support low‐level amplification of CWD prions, although the species barrier to CWD infection is relatively high and that the detection of infectivity in orally inoculated pigs with a mouse bioassay raises the possibility that naturally exposed pigs could act as a reservoir of CWD infectivity.</div></div><div><div class="yiv0273681782p1" style="font-family: Arial, Helvetica, sans-serif; font-size: 12px;"><br /></div><div class="yiv0273681782p1" style="font-family: Arial, Helvetica, sans-serif; font-size: 12px;"><a href="https://efsa.onlinelibrary.wiley.com/doi/10.2903/j.efsa.2019.5863" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://efsa.onlinelibrary.wiley.com/doi/10.2903/j.efsa.2019.5863</a><br /></div></div><div><br /></div><div><div style="font-size: 10pt;"><div><div>Research Project: Pathobiology, Genetics, and Detection of Transmissible Spongiform Encephalopathies Location: Virus and Prion Research</div><div><br /></div><div>Title: Experimental transmission of the chronic wasting disease agent to swine after oral or intracranial inoculation</div><div><br /></div><div>Author item MOORE, SARAH - Orise Fellow item WEST GREENLEE, M - Iowa State University item KONDRU, NAVEEN - Iowa State University item MANNE, SIREESHA - Iowa State University item Smith, Jodi item Kunkle, Robert item KANTHASAMY, ANUMANTHA - Iowa State University item Greenlee, Justin Submitted to: Journal of Virology Publication Type: Peer Reviewed Journal Publication Acceptance Date: 7/6/2017 Publication Date: 9/12/2017</div><div><br /></div><div>Citation: Moore, S.J., West Greenlee, M.H., Kondru, N., Manne, S., Smith, J.D., Kunkle, R.A., Kanthasamy, A., Greenlee, J.J. 2017. Experimental transmission of the chronic wasting disease agent to swine after oral or intracranial inoculation. Journal of Virology. 91(19):e00926-17. <a href="https://doi.org/10.1128/JVI.00926-17" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://doi.org/10.1128/JVI.00926-17</a>.</div><div><br /></div><div>Interpretive Summary: Chronic wasting disease (CWD) is a fatal disease of wild and captive deer and elk that causes damaging changes in the brain. The infectious agent is an abnormal protein called a prion that has misfolded from its normal state. Whether CWD can transmit to swine is unknown. This study evaluated the potential of pigs to develop CWD after either intracranial or oral inoculation. Our data indicates that swine do accumulate the abnormal prion protein associated with CWD after intracranial or oral inoculation. Further, there was evidence of abnormal prion protein accumulation in lymph nodes. Currently, swine rations in the U.S. could contain animal derived components including materials from deer or elk. In addition, feral swine could be exposed to infected carcasses in areas where CWD is present in wildlife populations. This information is useful to wildlife managers and individuals in the swine and captive cervid industries. These findings could impact future regulations for the disposal of offal from deer and elk slaughtered in commercial operations. U.S. regulators should carefully consider the new information from this study before relaxing feed ban standards designed to control potentially feed borne prion diseases.</div><div><br /></div><div>Technical Abstract: Chronic wasting disease (CWD) is a naturally occurring, fatal neurodegenerative disease of cervids. The potential for swine to serve as a host for the agent of chronic wasting disease is unknown. The purpose of this study was to investigate the susceptibility of swine to the CWD agent following oral or intracranial experimental inoculation. Crossbred piglets were assigned to one of three groups: intracranially inoculated (n=20), orally inoculated (n=19), or non-inoculated (n=9). At approximately the age at which commercial pigs reach market weight, half of the pigs in each group were culled ('market weight' groups). The remaining pigs ('aged' groups) were allowed to incubate for up to 73 months post inoculation (MPI). Tissues collected at necropsy were examined for disease-associated prion protein (PrPSc) by western blotting (WB), antigen-capture immunoassay (EIA), immunohistochemistry (IHC) and in vitro real-time quaking induced conversion (RT-QuIC). Brain samples from selected pigs were also bioassayed in mice expressing porcine prion protein. Four intracranially inoculated aged pigs and one orally inoculated aged pig were positive by EIA, IHC and/or WB. Using RT-QuIC, PrPSc was detected in lymphoid and/or brain tissue from pigs in all inoculated groups. Bioassay was positive in 4 out of 5 pigs assayed. This study demonstrates that pigs can serve as hosts for CWD, though with scant PrPSc accumulation requiring sensitive detection methods. Detection of infectivity in orally inoculated pigs using mouse bioassay raises the possibility that naturally exposed pigs could act as a reservoir of CWD infectivity.</div><div><br /></div><div><a href="https://www.ars.usda.gov/research/publications/publication/?seqNo115=339093" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://www.ars.usda.gov/research/publications/publication/?seqNo115=339093</a><br /></div><div><br /></div><div>12 September 2017</div><div><br /></div><div>Experimental Transmission of the Chronic Wasting Disease Agent to Swine after Oral or Intracranial Inoculation</div><div><br /></div><div>Authors: S. Jo Moore, M. Heather West Greenlee, Naveen Kondru, Sireesha Manne, Jodi D. Smith, Robert A. Kunkle, Anumantha Kanthasamy, and Justin J. Greenlee </div><div><br /></div><div><a href="https://orcid.org/0000-0003-2202-3054" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://orcid.org/0000-0003-2202-3054</a></div><div><br /></div><div>AUTHORS INFO & AFFILIATIONS</div><div><br /></div><div>DOI: <a href="https://doi.org/10.1128/JVI.00926-17" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://doi.org/10.1128/JVI.00926-17</a></div><div><br /></div><div>Volume 91, Number 19</div><div><br /></div><div>1 October 2017</div><div><br /></div><div>ABSTRACT</div><div><br /></div><div>ABSTRACT</div><div><br /></div><div>Chronic wasting disease (CWD) is a naturally occurring, fatal neurodegenerative disease of cervids. The potential for swine to serve as hosts for the agent of CWD is unknown. The purpose of this study was to investigate the susceptibility of swine to the CWD agent following experimental oral or intracranial inoculation. Crossbred piglets were assigned to three groups, intracranially inoculated (n = 20), orally inoculated (n = 19), and noninoculated (n = 9). At approximately the age at which commercial pigs reach market weight, half of the pigs in each group were culled (“market weight” groups). The remaining pigs (“aged” groups) were allowed to incubate for up to 73 months postinoculation (mpi). Tissues collected at necropsy were examined for disease-associated prion protein (PrPSc) by Western blotting (WB), antigen capture enzyme immunoassay (EIA), immunohistochemistry (IHC), and in vitro real-time quaking-induced conversion (RT-QuIC). Brain samples from selected pigs were also bioassayed in mice expressing porcine prion protein. Four intracranially inoculated aged pigs and one orally inoculated aged pig were positive by EIA, IHC, and/or WB. By RT-QuIC, PrPSc was detected in lymphoid and/or brain tissue from one or more pigs in each inoculated group. The bioassay was positive in four out of five pigs assayed. This study demonstrates that pigs can support low-level amplification of CWD prions, although the species barrier to CWD infection is relatively high. However, detection of infectivity in orally inoculated pigs with a mouse bioassay raises the possibility that naturally exposed pigs could act as a reservoir of CWD infectivity. IMPORTANCE We challenged domestic swine with the chronic wasting disease agent by inoculation directly into the brain (intracranially) or by oral gavage (orally). Disease-associated prion protein (PrPSc) was detected in brain and lymphoid tissues from intracranially and orally inoculated pigs as early as 8 months of age (6 months postinoculation). Only one pig developed clinical neurologic signs suggestive of prion disease. The amount of PrPSc in the brains and lymphoid tissues of positive pigs was small, especially in orally inoculated pigs. Regardless, positive results obtained with orally inoculated pigs suggest that it may be possible for swine to serve as a reservoir for prion disease under natural conditions.</div><div><br /></div><div><a href="https://journals.asm.org/doi/10.1128/JVI.00926-17" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://journals.asm.org/doi/10.1128/JVI.00926-17</a></div></div><div style="font-size: 10pt;"><br /></div><div style="font-size: 10pt;"><div style="font-size: 10pt;">Research Project: TRANSMISSION, DIFFERENTIATION, AND PATHOBIOLOGY OF TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES Location: Virus and Prion Research</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">Title: Disease-associated prion protein detected in lymphoid tissues from pigs challenged with the agent of chronic wasting disease </div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">Conclusions: This study demonstrates that PrPSc accumulates in lymphoid tissues from pigs challenged intracranially or orally with the CWD agent, and can be detected as early as 4 months after challenge. CWD-infected pigs rarely develop clinical disease and if they do, they do so after a long incubation period. This raises the possibility that CWD-infected pigs could shed prions into their environment long before they develop clinical disease. Furthermore, lymphoid tissues from CWD-infected pigs could present a potential source of CWD infectivity in the animal and human food chains.</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;"><a href="https://www.ars.usda.gov/research/publications/publication/?seqNo115=337105" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://www.ars.usda.gov/research/publications/publication/?seqNo115=337105</a></div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;"><a href="https://www.ars.usda.gov/research/publications/publication/?seqNo115=326166" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://www.ars.usda.gov/research/publications/publication/?seqNo115=326166</a></div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">Research Project: Pathobiology, Genetics, and Detection of Transmissible Spongiform Encephalopathies Location: Virus and Prion Research</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">Title: The agent of chronic wasting disease from pigs is infectious in transgenic mice expressing human PRNP </div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">Author item MOORE, S - Orise Fellow item Kokemuller, Robyn item WEST-GREENLEE, M - Iowa State University item BALKEMA-BUSCHMANN, ANNE - Friedrich-Loeffler-institut item GROSCHUP, MARTIN - Friedrich-Loeffler-institut item Greenlee, Justin Submitted to: Prion Publication Type: Abstract Only Publication Acceptance Date: 5/10/2018 Publication Date: 5/22/2018 Citation: Moore, S.J., Kokemuller, R.D., West-Greenlee, M.H., Balkema-Buschmann, A., Groschup, M.H., Greenlee, J.J. 2018. The agent of chronic wasting disease from pigs is infectious in transgenic mice expressing human PRNP. Prion 2018, Santiago de Compostela, Spain, May 22-25, 2018. Paper No. WA15, page 44.</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">Interpretive Summary:</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;"> The successful transmission of pig-passaged CWD to Tg40 mice reported here suggests that passage of the CWD agent through pigs results in a change of the transmission characteristics which reduces the transmission barrier of Tg40 mice to the CWD agent. If this biological behavior is recapitulated in the original host species, passage of the CWD agent through pigs could potentially lead to increased pathogenicity of the CWD agent in humans.</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;"><a href="https://www.ars.usda.gov/research/publications/publication/?seqNo115=353091" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://www.ars.usda.gov/research/publications/publication/?seqNo115=353091</a></div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">cwd scrapie pigs oral routes </div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">***> However, at 51 months of incubation or greater, 5 animals were positive by one or more diagnostic methods. Furthermore, positive bioassay results were obtained from all inoculated groups (oral and intracranial; market weight and end of study) suggesting that swine are potential hosts for the agent of scrapie. <*** </div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">>*** Although the current U.S. feed ban is based on keeping tissues from TSE infected cattle from contaminating animal feed, swine rations in the U.S. could contain animal derived components including materials from scrapie infected sheep and goats. These results indicating the susceptibility of pigs to sheep scrapie, coupled with the limitations of the current feed ban, indicates that a revision of the feed ban may be necessary to protect swine production and potentially human health. <*** </div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">***> Results: PrPSc was not detected by EIA and IHC in any RPLNs. All tonsils and MLNs were negative by IHC, though the MLN from one pig in the oral <6 month group was positive by EIA. PrPSc was detected by QuIC in at least one of the lymphoid tissues examined in 5/6 pigs in the intracranial <6 months group, 6/7 intracranial >6 months group, 5/6 pigs in the oral <6 months group, and 4/6 oral >6 months group. Overall, the MLN was positive in 14/19 (74%) of samples examined, the RPLN in 8/18 (44%), and the tonsil in 10/25 (40%). </div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">***> Conclusions: This study demonstrates that PrPSc accumulates in lymphoid tissues from pigs challenged intracranially or orally with the CWD agent, and can be detected as early as 4 months after challenge. CWD-infected pigs rarely develop clinical disease and if they do, they do so after a long incubation period. This raises the possibility that CWD-infected pigs could shed prions into their environment long before they develop clinical disease. Furthermore, lymphoid tissues from CWD-infected pigs could present a potential source of CWD infectivity in the animal and human food chains. </div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;"><a href="https://www.ars.usda.gov/research/publications/publication/?seqNo115=353091" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://www.ars.usda.gov/research/publications/publication/?seqNo115=353091</a></div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;"><a href="https://www.ars.usda.gov/research/project/?accnNo=432011&fy=2017" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://www.ars.usda.gov/research/project/?accnNo=432011&fy=2017</a></div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;"><a href="https://www.ars.usda.gov/research/publications/publication/?seqNo115=337105" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://www.ars.usda.gov/research/publications/publication/?seqNo115=337105</a></div><div style="font-size: 10pt;"><div style="font-size: small;"><br /></div><div style="font-size: small;">CONFIDENTIAL</div><div style="font-size: small;"><br /></div><div style="font-size: small;"><span style="font-size: 10pt;">EXPERIMENTAL PORCINE SPONGIFORM ENCEPHALOPATHY</span></div><div style="font-size: small;"><span style="font-size: 10pt;"><br /></span></div><div style="font-size: small;"><div style="font-size: 13.3333px;"><div>LINE TO TAKE</div><div><br /></div><div>3. If questions on pharmaceuticals are raised at the Press conference, the suggested line to take is as follows:- </div><div><br /></div><div> "There are no medicinal products licensed for use on the market which make use of UK-derived porcine tissues with which any hypothetical “high risk" ‘might be associated. The results of the recent experimental work at the CSM will be carefully examined by the CSM‘s Working Group on spongiform encephalopathy at its next meeting.</div><div><br /></div><div>DO Hagger RM 1533 MT Ext 3201</div></div><div style="font-size: 10pt;"><br /></div><div style="font-size: 10pt;"><a href="http://web.archive.org/web/20030822054419/www.bseinquiry.gov.uk/files/yb/1990/09/21009001.pdf" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://web.archive.org/web/20030822054419/www.bseinquiry.gov.uk/files/yb/1990/09/21009001.pdf</a></div></div><div style="font-size: small;"><br /></div><div style="font-size: small;"><span style="font-size: 10pt;">While this clearly is a cause for concern we should not jump to the conclusion that this means that pigs will necessarily be infected by bone and meat meal fed by the oral route as is the case with cattle. ...</span></div><div style="font-size: small;"><br /></div><div style="font-size: small;"><span style="font-size: 10pt;"><a href="http://web.archive.org/web/20031026000118/www.bseinquiry.gov.uk/files/yb/1990/08/23004001.pdf" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://web.archive.org/web/20031026000118/www.bseinquiry.gov.uk/files/yb/1990/08/23004001.pdf</a></span></div><div style="font-size: small;"><br /></div><div style="font-size: small;"><span style="font-size: 10pt;">we cannot rule out the possibility that unrecognised subclinical spongiform encephalopathy could be present in British pigs though there is no evidence for this: only with parenteral/implantable pharmaceuticals/devices is the theoretical risk to humans of sufficient concern to consider any action.</span></div><div style="font-size: small;"><br /></div><div style="font-size: small;"><span style="font-size: 10pt;"><a href="http://web.archive.org/web/20030822031154/www.bseinquiry.gov.uk/files/yb/1990/09/10007001.pdf" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://web.archive.org/web/20030822031154/www.bseinquiry.gov.uk/files/yb/1990/09/10007001.pdf</a></span></div><div style="font-size: small;"><br /></div><div style="font-size: small;"><span style="font-size: 10pt;">May I, at the outset, reiterate that we should avoid dissemination of papers relating to this experimental finding to prevent premature release of the information. ...</span></div><div style="font-size: small;"><br /></div><div style="font-size: small;"><span style="font-size: 10pt;"><a href="http://web.archive.org/web/20030822052332/www.bseinquiry.gov.uk/files/yb/1990/09/11005001.pdf" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://web.archive.org/web/20030822052332/www.bseinquiry.gov.uk/files/yb/1990/09/11005001.pdf</a></span></div><div style="font-size: small;"><br /></div><div style="font-size: small;"><span style="font-size: 10pt;">3. It is particularly important that this information is not passed outside the Department, until Ministers have decided how they wish it to be handled. ...</span></div><div style="font-size: small;"><br /></div><div style="font-size: small;"><span style="font-size: 10pt;"><a href="http://web.archive.org/web/20030822052438/www.bseinquiry.gov.uk/files/yb/1990/09/12002001.pdf" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://web.archive.org/web/20030822052438/www.bseinquiry.gov.uk/files/yb/1990/09/12002001.pdf</a></span></div><div style="font-size: small;"><br /></div><div style="font-size: small;"><span style="font-size: 10pt;">But it would be easier for us if pharmaceuticals/devices are not directly mentioned at all. ...</span></div><div style="font-size: small;"><br /></div><div style="font-size: small;"><span style="font-size: 10pt;"><a href="http://web.archive.org/web/20030518170213/www.bseinquiry.gov.uk/files/yb/1990/09/13004001.pdf" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://web.archive.org/web/20030518170213/www.bseinquiry.gov.uk/files/yb/1990/09/13004001.pdf</a></span></div><div style="font-size: small;"><br /></div><div style="font-size: small;"><span style="font-size: 10pt;">Our records show that while some use is made of porcine materials in medicinal products, the only products which would appear to be in a hypothetically ''higher risk'' area are the adrenocorticotrophic hormone for which the source material comes from outside the United Kingdom, namely America China Sweden France and Germany. The products are manufactured by Ferring and Armour. A further product, ''Zenoderm Corium implant'' manufactured by Ethicon, makes use of porcine skin - which is not considered to be a ''high risk'' tissue, but one of its uses is described in the data sheet as ''in dural replacement''. This product is sourced from the United Kingdom.....</span></div><div style="font-size: small;"><br /></div><div style="font-size: small;"><span style="font-size: 10pt;"><a href="http://web.archive.org/web/20030822054419/www.bseinquiry.gov.uk/files/yb/1990/09/21009001.pdf" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://web.archive.org/web/20030822054419/www.bseinquiry.gov.uk/files/yb/1990/09/21009001.pdf</a></span></div></div></div></div></div></div><div><br /></div></div><div><div><div dir="ltr" style="font-size: 10pt;"><span style="font-family: arial, helvetica;">Friday, December 14, 2012 </span></div><div dir="ltr" style="font-size: 10pt;"><span style="font-family: arial, helvetica;"><br /></span></div><div dir="ltr" style="font-size: 10pt;"><span style="font-family: arial, helvetica;">DEFRA U.K. What is the risk of Chronic Wasting Disease CWD being introduced into Great Britain? A Qualitative Risk Assessment October 2012 </span></div><div dir="ltr" style="font-size: 10pt;"><span style="font-family: arial, helvetica;"><br /></span></div><div dir="ltr" style="font-size: 10pt;"><span style="font-family: arial, helvetica;">snip..... </span></div><div dir="ltr" style="font-size: 10pt;"><span style="font-family: arial, helvetica;"><br /></span></div><div dir="ltr" style="font-size: 10pt;"><span style="font-family: arial, helvetica;">In the USA, under the Food and Drug Administration's BSE Feed Regulation (21 CFR 589.2000) most material (exceptions include milk, tallow, and gelatin) from deer and elk is prohibited for use in feed for ruminant animals. With regards to feed for non-ruminant animals, under FDA law, CWD positive deer may not be used for any animal feed or feed ingredients. For elk and deer considered at high risk for CWD, the FDA recommends that these animals do not enter the animal feed system. However, this recommendation is guidance and not a requirement by law. Animals considered at high risk for CWD include: </span></div><div dir="ltr" style="font-size: 10pt;"><span style="font-family: arial, helvetica;"><br /></span></div><div dir="ltr" style="font-size: 10pt;"><span style="font-family: arial, helvetica;">1) animals from areas declared to be endemic for CWD and/or to be CWD eradication zones and </span></div><div dir="ltr" style="font-size: 10pt;"><span style="font-family: arial, helvetica;"><br /></span></div><div dir="ltr" style="font-size: 10pt;"><span style="font-family: arial, helvetica;">2) deer and elk that at some time during the 60-month period prior to slaughter were in a captive herd that contained a CWD-positive animal. </span></div><div dir="ltr" style="font-size: 10pt;"><span style="font-family: arial, helvetica;"><br /></span></div><div dir="ltr" style="font-size: 10pt;"><span style="font-family: arial, helvetica;">Therefore, in the USA, materials from cervids other than CWD positive animals may be used in animal feed and feed ingredients for non-ruminants. </span></div><div dir="ltr" style="font-size: 10pt;"><span style="font-family: arial, helvetica;"><br /></span></div><div dir="ltr" style="font-size: 10pt;"><span style="font-family: arial, helvetica;">The amount of animal PAP that is of deer and/or elk origin imported from the USA to GB can not be determined, however, as it is not specified in TRACES. </span></div><div dir="ltr" style="font-size: 10pt;"><span style="font-family: arial, helvetica;"><br /></span></div><div dir="ltr" style="font-size: 10pt;"><span style="font-family: arial, helvetica;">It may constitute a small percentage of the 8412 kilos of non-fish origin processed animal proteins that were imported from US into GB in 2011. </span></div><div dir="ltr" style="font-size: 10pt;"><span style="font-family: arial, helvetica;"><br /></span></div><div dir="ltr" style="font-size: 10pt;"><span style="font-family: arial, helvetica;">Overall, therefore, it is considered there is a __greater than negligible risk___ that (nonruminant) animal feed and pet food containing deer and/or elk protein is imported into GB. </span></div><div dir="ltr" style="font-size: 10pt;"><span style="font-family: arial, helvetica;"><br /></span></div><div dir="ltr" style="font-size: 10pt;"><span style="font-family: arial, helvetica;">There is uncertainty associated with this estimate given the lack of data on the amount of deer and/or elk protein possibly being imported in these products. </span></div><div dir="ltr" style="font-size: 10pt;"><span style="font-family: arial, helvetica;"><br /></span></div><div dir="ltr" style="font-size: 10pt;"><span style="font-family: arial, helvetica;">snip..... </span></div><div dir="ltr" style="font-size: 10pt;"><span style="font-family: arial, helvetica;"><br /></span></div><div dir="ltr" style="font-size: 10pt;"><span style="font-family: arial, helvetica;">36% in 2007 (Almberg et al., 2011). In such areas, population declines of deer of up to 30 to 50% have been observed (Almberg et al., 2011). In areas of Colorado, the prevalence can be as high as 30% (EFSA, 2011). The clinical signs of CWD in affected adults are weight loss and behavioural changes that can span weeks or months (Williams, 2005). In addition, signs might include excessive salivation, behavioural alterations including a fixed stare and changes in interaction with other animals in the herd, and an altered stance (Williams, 2005). These signs are indistinguishable from cervids experimentally infected with bovine spongiform encephalopathy (BSE). Given this, if CWD was to be introduced into countries with BSE such as GB, for example, infected deer populations would need to be tested to differentiate if they were infected with CWD or BSE to minimise the risk of BSE entering the human food-chain via affected venison. snip..... The rate of transmission of CWD has been reported to be as high as 30% and can approach 100% among captive animals in endemic areas (Safar et al., 2008). </span></div><div dir="ltr" style="font-size: 10pt;"><span style="font-family: arial, helvetica;"><br /></span></div><div dir="ltr" style="font-size: 10pt;"><span style="font-family: arial, helvetica;">snip..... </span></div><div dir="ltr" style="font-size: 10pt;"><span style="font-family: arial, helvetica;"><br /></span></div><div dir="ltr" style="font-size: 10pt;"><span style="font-family: arial, helvetica;">In summary, in endemic areas, there is a medium probability that the soil and surrounding environment is contaminated with CWD prions and in a bioavailable form. In rural areas where CWD has not been reported and deer are present, there is a greater than negligible risk the soil is contaminated with CWD prion. snip..... In summary, given the volume of tourists, hunters and servicemen moving between GB and North America, the probability of at least one person travelling to/from a CWD affected area and, in doing so, contaminating their clothing, footwear and/or equipment prior to arriving in GB is greater than negligible... For deer hunters, specifically, the risk is likely to be greater given the increased contact with deer and their environment. However, there is significant uncertainty associated with these estimates. </span></div><div dir="ltr" style="font-size: 10pt;"><span style="font-family: arial, helvetica;"><br /></span></div><div dir="ltr" style="font-size: 10pt;"><span style="font-family: arial, helvetica;">snip..... </span></div><div dir="ltr" style="font-size: 10pt;"><span style="font-family: arial, helvetica;"><br /></span></div><div dir="ltr" style="font-size: 10pt;"><span style="font-family: arial, helvetica;">Therefore, it is considered that farmed and park deer may have a higher probability of exposure to CWD transferred to the environment than wild deer given the restricted habitat range and higher frequency of contact with tourists and returning GB residents. </span></div><div dir="ltr" style="font-size: 10pt;"><span style="font-family: arial, helvetica;"><br /></span></div><div dir="ltr" style="font-size: 10pt;"><span style="font-family: arial, helvetica;">snip..... </span></div><div dir="ltr" style="font-size: 10pt;"><span style="font-family: arial, helvetica;"><br /></span></div><div dir="ltr" style="font-size: 10pt;"><a href="https://web.archive.org/web/20170404125557/http://webarchive.nationalarchives.gov.uk/20130822084033/http://www.defra.gov.uk/animal-diseases/files/qra_chronic-wasting-disease-121029.pdf" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://web.archive.org/web/20170404125557/http://webarchive.nationalarchives.gov.uk/20130822084033/http://www.defra.gov.uk/animal-diseases/files/qra_chronic-wasting-disease-121029.pdf</a><br /></div><div dir="ltr" style="font-size: 10pt;"><span style="font-family: arial, helvetica;"><br /></span></div><div dir="ltr" style="font-size: 10pt;"><span style="font-family: arial, helvetica;">***> READ THIS VERY, VERY, CAREFULLY, AUGUST 1997 MAD COW FEED BAN WAS A SHAM, AS I HAVE STATED SINCE 1997! 3 FAILSAFES THE FDA ET AL PREACHED AS IF IT WERE THE GOSPEL, IN TERMS OF MAD COW BSE DISEASE IN USA, AND WHY IT IS/WAS/NOT A PROBLEM FOR THE USA, and those are; </span></div><div dir="ltr" style="font-size: 10pt;"><span style="font-family: arial, helvetica;"><br /></span></div><div dir="ltr" style="font-size: 10pt;"><span style="font-family: arial, helvetica;">BSE TESTING (failed terribly and proven to be a sham) </span></div><div dir="ltr" style="font-size: 10pt;"><span style="font-family: arial, helvetica;"><br /></span></div><div dir="ltr" style="font-size: 10pt;"><span style="font-family: arial, helvetica;">BSE SURVEILLANCE (failed terribly and proven to be a sham) </span></div><div dir="ltr" style="font-size: 10pt;"><span style="font-family: arial, helvetica;"><br /></span></div><div dir="ltr" style="font-size: 10pt;"><span style="font-family: arial, helvetica;">BSE 589.2001 FEED REGULATIONS (another colossal failure, and proven to be a sham) </span></div><div dir="ltr" style="font-size: 10pt;"><span style="font-family: arial, helvetica;"><br /></span></div><div dir="ltr" style="font-size: 10pt;"><span style="font-family: arial, helvetica;">these are facts folks. trump et al just admitted it with the feed ban. </span></div><div dir="ltr" style="font-size: 10pt;"><span style="font-family: arial, helvetica;"><br /></span></div><div dir="ltr" style="font-size: 10pt;"><span style="font-family: arial, helvetica;">see; </span></div><div dir="ltr" style="font-size: 10pt;"><span style="font-family: arial, helvetica;"><br /></span></div><div dir="ltr" style="font-size: 10pt;"><span style="font-family: arial, helvetica;">FDA Reports on VFD Compliance </span></div><div dir="ltr" style="font-size: 10pt;"><span style="font-family: arial, helvetica;"><br /></span></div><div dir="ltr" style="font-size: 10pt;"><span style="font-family: arial, helvetica;">John Maday </span></div><div dir="ltr" style="font-size: 10pt;"><span style="font-family: arial, helvetica;"><br /></span></div><div dir="ltr" style="font-size: 10pt;"><span style="font-family: arial, helvetica;">August 30, 2019 09:46 AM VFD-Form 007 (640x427) </span></div><div dir="ltr" style="font-size: 10pt;"><span style="font-family: arial, helvetica;"><br /></span></div><div dir="ltr" style="font-size: 10pt;"><span style="font-family: arial, helvetica;">Before and after the current Veterinary Feed Directive rules took full effect in January, 2017, the FDA focused primarily on education and outreach. ( John Maday ) Before and after the current Veterinary Feed Directive (VFD) rules took full effect in January, 2017, the FDA focused primarily on education and outreach to help feed mills, veterinarians and producers understand and comply with the requirements. Since then, FDA has gradually increased the number of VFD inspections and initiated enforcement actions when necessary. On August 29, FDA released its first report on inspection and compliance activities. The report, titled “Summary Assessment of Veterinary Feed Directive Compliance Activities Conducted in Fiscal Years 2016 – 2018,” is available online.</span></div><div dir="ltr" style="font-size: 10pt;"><span style="font-family: arial, helvetica;"><br /></span></div><div dir="ltr" style="font-size: 10pt;"><a href="https://www.fda.gov/media/130382/download" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://www.fda.gov/media/130382/download</a><br /></div><div dir="ltr" style="font-size: 10pt;"><span style="font-family: arial, helvetica;"><br /></span></div><div dir="ltr" style="font-size: 10pt;"><span style="font-family: arial, helvetica;">SUNDAY, SEPTEMBER 1, 2019 </span></div><div dir="ltr" style="font-size: 10pt;"><span style="font-family: arial, helvetica;"><br /></span></div><div dir="ltr" style="font-size: 10pt;"><span style="font-family: arial, helvetica;">***> FDA Reports on VFD Compliance </span></div><div dir="ltr" style="font-size: 10pt;"><span style="font-family: arial, helvetica;"><br /></span></div><div dir="ltr" style="font-size: 10pt;"><a href="https://bovineprp.blogspot.com/2019/09/fda-reports-on-vfd-compliance.html" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://bovineprp.blogspot.com/2019/09/fda-reports-on-vfd-compliance.html</a><br /></div><div dir="ltr" style="font-size: 10pt;"><span style="font-family: arial, helvetica;"><br /></span></div><div dir="ltr" style="font-size: 10pt;"><span style="font-family: arial, helvetica;">TUESDAY, APRIL 18, 2017 </span></div><div dir="ltr" style="font-size: 10pt;"><span style="font-family: arial, helvetica;"><br /></span></div><div dir="ltr" style="font-size: 10pt;"><span style="font-family: arial, helvetica;">*** EXTREME USA FDA PART 589 TSE PRION FEED LOOP HOLE STILL EXIST, AND PRICE OF POKER GOES UP *** </span></div><div dir="ltr" style="font-size: 10pt;"><span style="font-family: arial, helvetica;"><br /></span></div><div dir="ltr" style="font-size: 10pt;"><a href="http://usdameatexport.blogspot.com/2017/04/extreme-usa-fda-part-589-tse-prion-feed.html" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://usdameatexport.blogspot.com/2017/04/extreme-usa-fda-part-589-tse-prion-feed.html</a><br /></div><div dir="ltr" style="font-size: 10pt;"><span style="font-family: arial, helvetica;"><br /></span></div><div dir="ltr" style="font-size: 10pt;"><a href="http://camelusprp.blogspot.com/2018/04/dromedary-camels-algeria-prion-mad.html" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://camelusprp.blogspot.com/2018/04/dromedary-camels-algeria-prion-mad.html</a></div></div><div dir="ltr" style="font-size: 10pt;"><br /></div><div dir="ltr" style="font-size: 10pt;"><div style="color: #29303b; font-family: arial, helvetica; font-size: 10pt;">2020</div><div style="color: #29303b; font-family: arial, helvetica; font-size: 10pt;"><br clear="none" /></div><div style="color: #29303b;"><div><span style="font-family: arial, helvetica;">Monday, November 30, 2020 </span></div><div><span style="font-family: arial, helvetica;"><br clear="none" /></span></div><div><span style="font-family: arial, helvetica;">Tunisia has become the second country after Algeria to detect a case of CPD Camel Prion Disease within a year </span></div><div><span style="font-family: arial, helvetica;"><br clear="none" /></span></div><div><span style="font-family: arial, helvetica;">REPORT OF THE MEETING OF THE OIE SCIENTIFIC COMMISSION FOR ANIMAL DISEASES Paris, 9–13 September 2019</span></div><div><span style="font-family: arial, helvetica;"><br clear="none" /></span></div><div><span style="font-family: arial, helvetica;">Scientific Commission/September 2019</span></div><div><span style="font-family: arial, helvetica;"><br clear="none" /></span></div><div><span style="font-family: arial, helvetica;">Tunisia has become the second country after Algeria to detect a case of CPD within a year</span></div><div><span style="font-family: arial, helvetica;"><br clear="none" /></span></div><div><span style="font-family: arial, helvetica;">10.2. Prion disease in dromedary camels </span></div><div><span style="font-family: arial, helvetica;"><br clear="none" /></span></div><div><span style="font-family: arial, helvetica;"><a href="https://camelusprp.blogspot.com/2020/11/" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://camelusprp.blogspot.com/2020/11/</a></span></div></div></div><div dir="ltr" style="font-size: 10pt;"><br /></div><div dir="ltr" style="font-size: 10pt;"><div><span style="font-family: arial, helvetica;">TUESDAY, SEPTEMBER 07, 2021 </span></div><div><span style="font-family: arial, helvetica;"><br clear="none" /></span></div><div><span style="font-family: arial, helvetica;">Atypical Bovine Spongiform Encephalopathy BSE OIE, FDA 589.2001 FEED REGULATIONS, and Ingestion Therefrom<br clear="none" /></span></div><div><span style="font-family: arial, helvetica;"><br clear="none" /></span></div><div><span style="font-family: arial, helvetica;"><a href="https://bse-atypical.blogspot.com/2021/09/atypical-bovine-spongiform.html" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://bse-atypical.blogspot.com/2021/09/atypical-bovine-spongiform.html</a></span></div></div><div><br /></div><div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;">ZOONOSIS OF SCRAPIE TSE PRION<br clear="none" style="line-height: 1.22em;" /></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;">O.05: Transmission of prions to primates after extended silent incubation periods: Implications for BSE and scrapie risk assessment in human populations <br clear="none" style="line-height: 1.22em;" /></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">Emmanuel Comoy, Jacqueline Mikol, Valerie Durand, Sophie Luccantoni, Evelyne Correia, Nathalie Lescoutra, Capucine Dehen, and Jean-Philippe Deslys Atomic Energy Commission; Fontenay-aux-Roses, France </span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">Prion diseases (PD) are the unique neurodegenerative proteinopathies reputed to be transmissible under field conditions since decades. The transmission of Bovine Spongiform Encephalopathy (BSE) to humans evidenced that an animal PD might be zoonotic under appropriate conditions. Contrarily, in the absence of obvious (epidemiological or experimental) elements supporting a transmission or genetic predispositions, PD, like the other proteinopathies, are reputed to occur spontaneously (atpical animal prion strains, sporadic CJD summing 80% of human prion cases). </span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">Non-human primate models provided the first evidences supporting the transmissibiity of human prion strains and the zoonotic potential of BSE. Among them, cynomolgus macaques brought major information for BSE risk assessment for human health (Chen, 2014), according to their phylogenetic proximity to humans and extended lifetime. We used this model to assess the zoonotic potential of other animal PD from bovine, ovine and cervid origins even after very long silent incubation periods. </span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">*** We recently observed the direct transmission of a natural classical scrapie isolate to macaque after a 10-year silent incubation period, </span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">***with features similar to some reported for human cases of sporadic CJD, albeit requiring fourfold long incubation than BSE. Scrapie, as recently evoked in humanized mice (Cassard, 2014), </span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">***is the third potentially zoonotic PD (with BSE and L-type BSE), </span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">***thus questioning the origin of human sporadic cases. </span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">We will present an updated panorama of our different transmission studies and discuss the implications of such extended incubation periods on risk assessment of animal PD for human health. </span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">=============== </span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">***thus questioning the origin of human sporadic cases*** </span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">=============== </span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">***our findings suggest that possible transmission risk of H-type BSE to sheep and human. Bioassay will be required to determine whether the PMCA products are infectious to these animals. </span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">============== </span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><a href="https://prion2015.files.wordpress.com/2015/05/prion2015abstracts.pdf" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">https://prion2015.files.wordpress.com/2015/05/prion2015abstracts.pdf</a> </span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;">***Transmission data also revealed that several scrapie prions propagate in HuPrP-Tg mice with efficiency comparable to that of cattle BSE. While the efficiency of transmission at primary passage was low, subsequent passages resulted in a highly virulent prion disease in both Met129 and Val129 mice. <br clear="none" style="line-height: 1.22em;" /></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">***Transmission of the different scrapie isolates in these mice leads to the emergence of prion strain phenotypes that showed similar characteristics to those displayed by MM1 or VV2 sCJD prion. </span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">***These results demonstrate that scrapie prions have a zoonotic potential and raise new questions about the possible link between animal and human prions. </span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><a href="http://www.tandfonline.com/doi/abs/10.1080/19336896.2016.1163048?journalCode=kprn20" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">http://www.tandfonline.com/doi/abs/10.1080/19336896.2016.1163048?journalCode=kprn20</a></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"> </span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;">PRION 2016 TOKYO<br clear="none" style="line-height: 1.22em;" /></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">Saturday, April 23, 2016</span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">SCRAPIE WS-01: Prion diseases in animals and zoonotic potential 2016</span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">Prion. 10:S15-S21. 2016 ISSN: 1933-6896 printl 1933-690X online</span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">Taylor & Francis</span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">Prion 2016 Animal Prion Disease Workshop Abstracts</span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">WS-01: Prion diseases in animals and zoonotic potential</span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">Juan Maria Torres a, Olivier Andreoletti b, J uan-Carlos Espinosa a. Vincent Beringue c. Patricia Aguilar a,</span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">Natalia Fernandez-Borges a. and Alba Marin-Moreno a</span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">"Centro de Investigacion en Sanidad Animal ( CISA-INIA ). Valdeolmos, Madrid. Spain; b UMR INRA -ENVT 1225 Interactions Holes Agents Pathogenes. ENVT. Toulouse. France: "UR892. Virologie lmmunologie MolécuIaires, Jouy-en-Josas. France</span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">Dietary exposure to bovine spongiform encephalopathy (BSE) contaminated bovine tissues is considered as the origin of variant Creutzfeldt Jakob (vCJD) disease in human. To date, BSE agent is the only recognized zoonotic prion... Despite the variety of Transmissible Spongiform Encephalopathy (TSE) agents that have been circulating for centuries in farmed ruminants there is no apparent epidemiological link between exposure to ruminant products and the occurrence of other form of TSE in human like sporadic Creutzfeldt Jakob Disease (sCJD). However, the zoonotic potential of the diversity of circulating TSE agents has never been systematically assessed. The major issue in experimental assessment of TSEs zoonotic potential lies in the modeling of the ‘species barrier‘, the biological phenomenon that limits TSE agents’ propagation from a species to another. In the last decade, mice genetically engineered to express normal forms of the human prion protein has proved essential in studying human prions pathogenesis and modeling the capacity of TSEs to cross the human species barrier.</span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">To assess the zoonotic potential of prions circulating in farmed ruminants, we study their transmission ability in transgenic mice expressing human PrPC (HuPrP-Tg). Two lines of mice expressing different forms of the human PrPC (129Met or 129Val) are used to determine the role of the Met129Val dimorphism in susceptibility/resistance to the different agents.</span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">These transmission experiments confirm the ability of BSE prions to propagate in 129M- HuPrP-Tg mice and demonstrate that Met129 homozygotes may be susceptible to BSE in sheep or goat to a greater degree than the BSE agent in cattle and that these agents can convey molecular properties and neuropathological indistinguishable from vCJD. However homozygous 129V mice are resistant to all tested BSE derived prions independently of the originating species suggesting a higher transmission barrier for 129V-PrP variant.</span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">Transmission data also revealed that several scrapie prions propagate in HuPrP-Tg mice with efficiency comparable to that of cattle BSE. While the efficiency of transmission at primary passage was low, subsequent passages resulted in a highly virulent prion disease in both Met129 and Val129 mice. </span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">Transmission of the different scrapie isolates in these mice leads to the emergence of prion strain phenotypes that showed similar characteristics to those displayed by MM1 or VV2 sCJD prion. </span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">These results demonstrate that scrapie prions have a zoonotic potential and raise new questions about the possible link between animal and human prions. </span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><a href="http://www.tandfonline.com/doi/abs/10.1080/19336896.2016.1163048?journalCode=kprn20" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">http://www.tandfonline.com/doi/abs/10.1080/19336896.2016.1163048?journalCode=kprn20</a></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"> </span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;">***> why do we not want to do TSE transmission studies on chimpanzees $<br clear="none" style="line-height: 1.22em;" /></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">5. A positive result from a chimpanzee challenged severly would likely create alarm in some circles even if the result could not be interpreted for man. </span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">***> I have a view that all these agents could be transmitted provided a large enough dose by appropriate routes was given and the animals kept long enough. </span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">***> Until the mechanisms of the species barrier are more clearly understood it might be best to retain that hypothesis.</span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">snip...</span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">R. BRADLEY</span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><a href="https://web.archive.org/web/20170126051158/http://collections.europarchive.org/tna/20080102222950/http://www.bseinquiry.gov.uk/files/yb/1990/09/23001001.pdf" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">https://web.archive.org/web/20170126051158/http://collections.europarchive.org/tna/20080102222950/http://www.bseinquiry.gov.uk/files/yb/1990/09/23001001.pdf</a></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">Title: Transmission of scrapie prions to primate after an extended silent incubation period) </span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">*** In complement to the recent demonstration that humanized mice are susceptible to scrapie, we report here the first observation of direct transmission of a natural classical scrapie isolate to a macaque after a 10-year incubation period. Neuropathologic examination revealed all of the features of a prion disease: spongiform change, neuronal loss, and accumulation of PrPres throughout the CNS. </span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">*** This observation strengthens the questioning of the harmlessness of scrapie to humans, at a time when protective measures for human and animal health are being dismantled and reduced as c-BSE is considered controlled and being eradicated. </span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">*** Our results underscore the importance of precautionary and protective measures and the necessity for long-term experimental transmission studies to assess the zoonotic potential of other animal prion strains. </span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><a href="http://www.ars.usda.gov/research/publications/publications.htm?SEQ_NO_115=313160" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">http://www.ars.usda.gov/research/publications/publications.htm?SEQ_NO_115=313160</a> </span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;">***> Moreover, sporadic disease has never been observed in breeding colonies or primate research laboratories, most notably among hundreds of animals over several decades of study at the National Institutes of Health25, and in nearly twenty older animals continuously housed in our own facility. <***<br clear="none" style="line-height: 1.22em;" /></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">Transmission of scrapie prions to primate after an extended silent incubation period </span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">Emmanuel E. Comoy, Jacqueline Mikol, Sophie Luccantoni-Freire, Evelyne Correia, Nathalie Lescoutra-Etchegaray, Valérie Durand, Capucine Dehen, Olivier Andreoletti, Cristina Casalone, Juergen A. Richt, Justin J. Greenlee, Thierry Baron, Sylvie L. Benestad, Paul Brown & Jean-Philippe Deslys Scientific Reports volume 5, Article number: 11573 (2015) | Download Citation</span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">Abstract </span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">Classical bovine spongiform encephalopathy (c-BSE) is the only animal prion disease reputed to be zoonotic, causing variant Creutzfeldt-Jakob disease (vCJD) in humans and having guided protective measures for animal and human health against animal prion diseases. Recently, partial transmissions to humanized mice showed that the zoonotic potential of scrapie might be similar to c-BSE. We here report the direct transmission of a natural classical scrapie isolate to cynomolgus macaque, a highly relevant model for human prion diseases, after a 10-year silent incubation period, with features similar to those reported for human cases of sporadic CJD. Scrapie is thus actually transmissible to primates with incubation periods compatible with their life expectancy, although fourfold longer than BSE. Long-term experimental transmission studies are necessary to better assess the zoonotic potential of other prion diseases with high prevalence, notably Chronic Wasting Disease of deer and elk and atypical/Nor98 scrapie.</span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">SNIP...</span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">Discussion We describe the transmission of spongiform encephalopathy in a non-human primate inoculated 10 years earlier with a strain of sheep c-scrapie. Because of this extended incubation period in a facility in which other prion diseases are under study, we are obliged to consider two alternative possibilities that might explain its occurrence. We first considered the possibility of a sporadic origin (like CJD in humans). Such an event is extremely improbable because the inoculated animal was 14 years old when the clinical signs appeared, i.e. about 40% through the expected natural lifetime of this species, compared to a peak age incidence of 60–65 years in human sporadic CJD, or about 80% through their expected lifetimes. Moreover, sporadic disease has never been observed in breeding colonies or primate research laboratories, most notably among hundreds of animals over several decades of study at the National Institutes of Health25, and in nearly twenty older animals continuously housed in our own facility.</span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">The second possibility is a laboratory cross-contamination. Three facts make this possibility equally unlikely. First, handling of specimens in our laboratory is performed with fastidious attention to the avoidance of any such cross-contamination. Second, no laboratory cross-contamination has ever been documented in other primate laboratories, including the NIH, even between infected and uninfected animals housed in the same or adjacent cages with daily intimate contact (P. Brown, personal communication). Third, the cerebral lesion profile is different from all the other prion diseases we have studied in this model19, with a correlation between cerebellar lesions (massive spongiform change of Purkinje cells, intense PrPres staining and reactive gliosis26) and ataxia. The iron deposits present in the globus pallidus are a non specific finding that have been reported previously in neurodegenerative diseases and aging27. Conversely, the thalamic lesion was reminiscent of a metabolic disease due to thiamine deficiency28 but blood thiamine levels were within normal limits (data not shown). The preferential distribution of spongiform change in cortex associated with a limited distribution in the brainstem is reminiscent of the lesion profile in MM2c and VV1 sCJD patients29, but interspecies comparison of lesion profiles should be interpreted with caution. It is of note that the same classical scrapie isolate induced TSE in C57Bl/6 mice with similar incubation periods and lesional profiles as a sample derived from a MM1 sCJD patient30.</span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">We are therefore confident that the illness in this cynomolgus macaque represents a true transmission of a sheep c-scrapie isolate directly to an old-world monkey, which taxonomically resides in the primate subdivision (parvorder of catarrhini) that includes humans. With an homology of its PrP protein with humans of 96.4%31, cynomolgus macaque constitutes a highly relevant model for assessing zoonotic risk of prion diseases. Since our initial aim was to show the absence of transmission of scrapie to macaques in the worst-case scenario, we obtained materials from a flock of naturally-infected sheep, affecting animals with different genotypes32. This c-scrapie isolate exhibited complete transmission in ARQ/ARQ sheep (332 ± 56 days) and Tg338 transgenic mice expressing ovine VRQ/VRQ prion protein (220 ± 5 days) (O. Andreoletti, personal communication). From the standpoint of zoonotic risk, it is important to note that sheep with c-scrapie (including the isolate used in our study) have demonstrable infectivity throughout their lymphoreticular system early in the incubation period of the disease (3 months-old for all the lymphoid organs, and as early as 2 months-old in gut-associated lymph nodes)33. In addition, scrapie infectivity has been identified in blood34, milk35 and skeletal muscle36 from asymptomatic but scrapie infected small ruminants which implies a potential dietary exposure for consumers.</span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">Two earlier studies have reported the occurrence of clinical TSE in cynomolgus macaques after exposures to scrapie isolates. In the first study, the “Compton” scrapie isolate (derived from an English sheep) and serially propagated for 9 passages in goats did not transmit TSE in cynomolgus macaque, rhesus macaque or chimpanzee within 7 years following intracerebral challenge1; conversely, after 8 supplementary passages in conventional mice, this “Compton” isolate induced TSE in a cynomolgus macaque 5 years after intracerebral challenge, but rhesus macaques and chimpanzee remained asymptomatic 8.5 years post-exposure8. However, multiple successive passages that are classically used to select laboratory-adapted prion strains can significantly modify the initial properties of a scrapie isolate, thus questioning the relevance of zoonotic potential for the initial sheep-derived isolate. The same isolate had also induced disease into squirrel monkeys (new-world monkey)9. A second historical observation reported that a cynomolgus macaque developed TSE 6 years post-inoculation with brain homogenate from a scrapie-infected Suffolk ewe (derived from USA), whereas a rhesus macaque and a chimpanzee exposed to the same inoculum remained healthy 9 years post-exposure1. This inoculum also induced TSE in squirrel monkeys after 4 passages in mice. Other scrapie transmission attempts in macaque failed but had more shorter periods of observation in comparison to the current study. Further, it is possible that there are differences in the zoonotic potential of different scrapie strains.</span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">The most striking observation in our study is the extended incubation period of scrapie in the macaque model, which has several implications. Firstly, our observations constitute experimental evidence in favor of the zoonotic potential of c-scrapie, at least for this isolate that has been extensively studied32,33,34,35,36. The cross-species zoonotic ability of this isolate should be confirmed by performing duplicate intracerebral exposures and assessing the transmissibility by the oral route (a successful transmission of prion strains through the intracerebral route may not necessarily indicate the potential for oral transmission37). However, such confirmatory experiments may require more than one decade, which is hardly compatible with current general management and support of scientific projects; thus this study should be rather considered as a case report.</span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">Secondly, transmission of c-BSE to primates occurred within 8 years post exposure for the lowest doses able to transmit the disease (the survival period after inoculation is inversely proportional to the initial amount of infectious inoculum). The occurrence of scrapie 10 years after exposure to a high dose (25 mg) of scrapie-infected sheep brain suggests that the macaque has a higher species barrier for sheep c-scrapie than c-BSE, although it is notable that previous studies based on in vitro conversion of PrP suggested that BSE and scrapie prions would have a similar conversion potential for human PrP38.</span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">Thirdly, prion diseases typically have longer incubation periods after oral exposure than after intracerebral inoculations: since humans can develop Kuru 47 years after oral exposure39, an incubation time of several decades after oral exposure to scrapie would therefore be expected, leading the disease to occur in older adults, i.e. the peak age for cases considered to be sporadic disease, and making a distinction between scrapie-associated and truly sporadic disease extremely difficult to appreciate.</span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">Fourthly, epidemiologic evidence is necessary to confirm the zoonotic potential of an animal disease suggested by experimental studies. A relatively short incubation period and a peculiar epidemiological situation (e.g., all the first vCJD cases occurring in the country with the most important ongoing c-BSE epizootic) led to a high degree of suspicion that c-BSE was the cause of vCJD. Sporadic CJD are considered spontaneous diseases with an almost stable and constant worldwide prevalence (0.5–2 cases per million inhabitants per year), and previous epidemiological studies were unable to draw a link between sCJD and classical scrapie6,7,40,41, even though external causes were hypothesized to explain the occurrence of some sCJD clusters42,43,44. However, extended incubation periods exceeding several decades would impair the predictive values of epidemiological surveillance for prion diseases, already weakened by a limited prevalence of prion diseases and the multiplicity of isolates gathered under the phenotypes of “scrapie” and “sporadic CJD”.</span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">Fifthly, considering this 10 year-long incubation period, together with both laboratory and epidemiological evidence of decade or longer intervals between infection and clinical onset of disease, no premature conclusions should be drawn from negative transmission studies in cynomolgus macaques with less than a decade of observation, as in the aforementioned historical transmission studies of scrapie to primates1,8,9. Our observations and those of others45,46 to date are unable to provide definitive evidence regarding the zoonotic potential of CWD, atypical/Nor98 scrapie or H-type BSE. The extended incubation period of the scrapie-affected macaque in the current study also underscores the limitations of rodent models expressing human PrP for assessing the zoonotic potential of some prion diseases since their lifespan remains limited to approximately two years21,47,48. This point is illustrated by the fact that the recently reported transmission of scrapie to humanized mice was not associated with clinical signs for up to 750 days and occurred in an extreme minority of mice with only a marginal increase in attack rate upon second passage13. The low attack rate in these studies is certainly linked to the limited lifespan of mice compared to the very long periods of observation necessary to demonstrate the development of scrapie. Alternatively, one could estimate that a successful second passage is the result of strain adaptation to the species barrier, thus poorly relevant of the real zoonotic potential of the original scrapie isolate of sheep origin49. The development of scrapie in this primate after an incubation period compatible with its lifespan complements the study conducted in transgenic (humanized) mice; taken together these studies suggest that some isolates of sheep scrapie can promote misfolding of the human prion protein and that scrapie can develop within the lifespan of some primate species.</span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">In addition to previous studies on scrapie transmission to primate1,8,9 and the recently published study on transgenic humanized mice13, our results constitute new evidence for recommending that the potential risk of scrapie for human health should not be dismissed. Indeed, human PrP transgenic mice and primates are the most relevant models for investigating the human transmission barrier. To what extent such models are informative for measuring the zoonotic potential of an animal TSE under field exposure conditions is unknown. During the past decades, many protective measures have been successfully implemented to protect cattle from the spread of c-BSE, and some of these measures have been extended to sheep and goats to protect from scrapie according to the principle of precaution. Since cases of c-BSE have greatly reduced in number, those protective measures are currently being challenged and relaxed in the absence of other known zoonotic animal prion disease. We recommend that risk managers should be aware of the long term potential risk to human health of at least certain scrapie isolates, notably for lymphotropic strains like the classical scrapie strain used in the current study. Relatively high amounts of infectivity in peripheral lymphoid organs in animals infected with these strains could lead to contamination of food products produced for human consumption. Efforts should also be maintained to further assess the zoonotic potential of other animal prion strains in long-term studies, notably lymphotropic strains with high prevalence like CWD, which is spreading across North America, and atypical/Nor98 scrapie (Nor98)50 that was first detected in the past two decades and now represents approximately half of all reported cases of prion diseases in small ruminants worldwide, including territories previously considered as scrapie free... Even if the prevailing view is that sporadic CJD is due to the spontaneous formation of CJD prions, it remains possible that its apparent sporadic nature may, at least in part, result from our limited capacity to identify an environmental origin.</span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><a href="https://www.nature.com/articles/srep11573" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">https://www.nature.com/articles/srep11573</a></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><br /></div><div style="line-height: 1.22em;"><div style="font-size: small;"><span style="font-size: x-small;">1: J Infect Dis 1980 Aug;142(2):205-8</span></div><div style="font-size: small;"><span style="font-size: x-small;"><br clear="none" /></span></div><div style="font-size: small;"><span style="font-size: x-small;">Oral transmission of kuru, Creutzfeldt-Jakob disease, and scrapie to nonhuman primates.</span></div><div style="font-size: small;"><span style="font-size: x-small;"><br clear="none" /></span></div><div style="font-size: small;"><span style="font-size: x-small;">Gibbs CJ Jr, Amyx HL, Bacote A, Masters CL, Gajdusek DC.</span></div><div style="font-size: small;"><span style="font-size: x-small;"><br clear="none" /></span></div><div style="font-size: small;"><span style="font-size: x-small;">Kuru and Creutzfeldt-Jakob disease of humans and scrapie disease of sheep and goats were transmitted to squirrel monkeys (Saimiri sciureus) that were exposed to the infectious agents only by their nonforced consumption of known infectious tissues. The asymptomatic incubation period in the one monkey exposed to the virus of kuru was 36 months; that in the two monkeys exposed to the virus of Creutzfeldt-Jakob disease was 23 and 27 months, respectively; and that in the two monkeys exposed to the virus of scrapie was 25 and 32 months, respectively. Careful physical examination of the buccal cavities of all of the monkeys failed to reveal signs or oral lesions. One additional monkey similarly exposed to kuru has remained asymptomatic during the 39 months that it has been under observation.</span></div><div style="font-size: small;"><span style="font-size: x-small;"><br clear="none" /></span></div><div style="font-size: small;"><span style="font-size: x-small;">snip...</span></div><div style="font-size: small;"><span style="font-size: x-small;"><br clear="none" /></span></div><div style="font-size: small;"><span style="font-size: x-small;">The successful transmission of kuru, Creutzfeldt-Jakob disease, and scrapie by natural feeding to squirrel monkeys that we have reported provides further grounds for concern that scrapie-infected meat may occasionally give rise in humans to Creutzfeldt-Jakob disease.</span></div><div style="font-size: small;"><span style="font-size: x-small;"><br clear="none" /></span></div><div style="font-size: small;"><span style="font-size: x-small;">PMID: 6997404</span></div><div style="font-size: small;"><span style="font-size: x-small;"><br clear="none" /></span></div><div style="font-size: small;"><a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=6997404&dopt=Abstract" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=6997404&dopt=Abstract</a><br clear="none" /></div><div style="font-size: small;"><span style="font-size: x-small;"><br clear="none" /></span></div><div style="font-size: small;"><span style="font-size: x-small;">Recently the question has again been brought up as to whether scrapie is transmissible to man. This has followed reports that the disease has been transmitted to primates. One particularly lurid speculation (Gajdusek 1977) conjectures that the agents of scrapie, kuru, Creutzfeldt-Jakob disease and transmissible encephalopathy of mink are varieties of a single "virus". The U.S. Department of Agriculture concluded that it could "no longer justify or permit scrapie-blood line and scrapie-exposed sheep and goats to be processed for human or animal food at slaughter or rendering plants" (ARC 84/77)" The problem is emphasised by the finding that some strains of scrapie produce lesions identical to the once which characterise the human dementias"</span></div><div style="font-size: small;"><span style="font-size: x-small;"><br clear="none" /></span></div><div style="font-size: small;"><span style="font-size: x-small;">Whether true or not. the hypothesis that these agents might be transmissible to man raises two considerations. First, the safety of laboratory personnel requires prompt attention. Second, action such as the "scorched meat" policy of USDA makes the solution of the acrapie problem urgent if the sheep industry is not to suffer grievously.</span></div><div style="font-size: small;"><span style="font-size: x-small;"><br clear="none" /></span></div><div style="font-size: small;"><span style="font-size: x-small;">snip...</span></div><div style="font-size: small;"><span style="font-size: x-small;"><br clear="none" /></span></div><div style="font-size: small;"><span style="font-size: x-small;">76/10.12/4.6</span></div><div style="font-size: small;"><span style="font-size: x-small;"><br clear="none" /></span></div><div style="font-size: small;"><a href="http://web.archive.org/web/20010305223125/www.bseinquiry.gov.uk/files/yb/1976/10/12004001.pdf" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">http://web.archive.org/web/20010305223125/www.bseinquiry.gov.uk/files/yb/1976/10/12004001.pdf</a><br clear="none" /></div><div style="font-size: small;"><br clear="none" /></div><div style="font-size: small;"><span style="font-size: x-small;">Nature. 1972 Mar 10;236(5341):73-4.</span></div><div style="font-size: small;"><span style="font-size: x-small;"><br clear="none" /></span></div><div style="font-size: small;"><span style="font-size: x-small;">Transmission of scrapie to the cynomolgus monkey (Macaca fascicularis).</span></div><div style="font-size: small;"><span style="font-size: x-small;"><br clear="none" /></span></div><div style="font-size: small;"><span style="font-size: x-small;">Gibbs CJ Jr, Gajdusek DC.</span></div><div style="font-size: small;"><span style="font-size: x-small;"><br clear="none" /></span></div><div style="font-size: small;"><span style="font-size: x-small;">Nature 236, 73 - 74 (10 March 1972); doi:10.1038/236073a0</span></div><div style="font-size: small;"><span style="font-size: x-small;"><br clear="none" /></span></div><div style="font-size: small;"><span style="font-size: x-small;">Transmission of Scrapie to the Cynomolgus Monkey (Macaca fascicularis)</span></div><div style="font-size: small;"><span style="font-size: x-small;"><br clear="none" /></span></div><div style="font-size: small;"><span style="font-size: x-small;">C. J. GIBBS jun. & D. C. GAJDUSEK</span></div><div style="font-size: small;"><span style="font-size: x-small;"><br clear="none" /></span></div><div style="font-size: small;"><span style="font-size: x-small;">National Institute of Neurological Diseases and Stroke, National Institutes of Health, Bethesda, Maryland</span></div><div style="font-size: small;"><span style="font-size: x-small;"><br clear="none" /></span></div><div style="font-size: small;"><span style="font-size: x-small;">SCRAPIE has been transmitted to the cynomolgus, or crab-eating, monkey (Macaca fascicularis) with an incubation period of more than 5 yr from the time of intracerebral inoculation of scrapie-infected mouse brain. The animal developed a chronic central nervous system degeneration, with ataxia, tremor and myoclonus with associated severe scrapie-like pathology of intensive astroglial hypertrophy and proliferation, neuronal vacuolation and status spongiosus of grey matter. The strain of scrapie virus used was the eighth passage in Swiss mice (NIH) of a Compton strain of scrapie obtained as ninth intracerebral passage of the agent in goat brain, from Dr R. L. Chandler (ARC, Compton, Berkshire).</span></div><div style="font-size: small;"><span style="font-size: x-small;"><br clear="none" /></span></div><div style="font-size: small;"><a href="http://www.nature.com/nature/journal/v236/n5341/abs/236073a0.html" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">http://www.nature.com/nature/journal/v236/n5341/abs/236073a0.html</a></div><div style="font-size: small;"><br /></div><div style="font-size: small;"><div style="font-size: 13.3333px; line-height: 1.22em;">WEDNESDAY, FEBRUARY 03, 2021 <div><br /></div><div>Scrapie TSE Prion United States of America a Review February 2021 Singeltary et al</div><div><br /></div><div><a href="https://scrapie-usa.blogspot.com/2021/02/scrapie-tse-prion-united-states-of.html" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://scrapie-usa.blogspot.com/2021/02/scrapie-tse-prion-united-states-of.html</a></div></div><div style="font-size: 13.3333px; line-height: 1.22em;"><br /></div><div style="font-size: 13.3333px; line-height: 1.22em;"><div><span style="font-size: small;">THURSDAY, JANUARY 7, 2021 </span></div><div><span style="font-size: small;"><br /></span></div><div><span style="font-size: small;">Atypical Nor-98 Scrapie TSE Prion USA State by State Update January 2021</span><br /></div><div><span style="font-size: small;"><br /></span></div><div><span style="font-size: small;"><a href="https://nor-98.blogspot.com/2021/01/atypical-nor-98-scrapie-tse-prion-usa.html" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://nor-98.blogspot.com/2021/01/atypical-nor-98-scrapie-tse-prion-usa.html</a></span></div><div><br /></div><div><div style="line-height: 1.22em;">WEDNESDAY, MAY 29, 2019 </div><div style="line-height: 1.22em;"><br /></div><div style="line-height: 1.22em;">***> Incomplete inactivation of atypical scrapie following recommended autoclave decontamination procedures </div><div style="line-height: 1.22em;"><br /></div><div style="line-height: 1.22em;"><a href="https://nor-98.blogspot.com/2019/05/incomplete-inactivation-of-atypical.html" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://nor-98.blogspot.com/2019/05/incomplete-inactivation-of-atypical.html</a><br /></div><div style="line-height: 1.22em;"><br /></div><div style="line-height: 1.22em;"><div style="line-height: 1.22em;">THURSDAY, DECEMBER 31, 2020 </div><div style="line-height: 1.22em;"><br /></div><div style="line-height: 1.22em;">Autoclave treatment of the classical scrapie agent US No. 13-7 and experimental inoculation to susceptible VRQ/ARQ sheep via the oral route results in decreased transmission efficiency<br /></div><div style="line-height: 1.22em;"><br /></div><div style="line-height: 1.22em;"><a href="https://scrapie-usa.blogspot.com/2020/12/autoclave-treatment-of-classical.html" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://scrapie-usa.blogspot.com/2020/12/autoclave-treatment-of-classical.html</a></div><div style="line-height: 1.22em;"><div style="font-size: 10pt; line-height: 1.22em;"><div style="line-height: 1.22em;"><br /></div><div style="line-height: 1.22em;"><div style="line-height: 1.22em;">TUESDAY, SEPTEMBER 22, 2020 </div><div style="line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="line-height: 1.22em;">APHIS USDA MORE SCRAPIE ATYPICAL Nor-98 Confirmed USA September 15 2020<br clear="none" style="line-height: 1.22em;" /></div><div style="line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="line-height: 1.22em;"><a href="https://scrapie-usa.blogspot.com/2020/09/aphis-usda-more-scrapie-atypical-nor-98.html" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">https://scrapie-usa.blogspot.com/2020/09/aphis-usda-more-scrapie-atypical-nor-98.html</a></div><div style="line-height: 1.22em;"><br /></div><div style="line-height: 1.22em;"><div style="line-height: 1.22em;">MONDAY, JULY 27, 2020 </div><div style="line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="line-height: 1.22em;">APHIS USDA Nor98-like scrapie was confirmed in a sheep sampled at slaughter in May 2020<br clear="none" style="line-height: 1.22em;" /></div><div style="line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="line-height: 1.22em;"><a href="https://nor-98.blogspot.com/2020/07/aphis-usda-nor98-like-scrapie-was.html" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">https://nor-98.blogspot.com/2020/07/aphis-usda-nor98-like-scrapie-was.html</a></div><div style="line-height: 1.22em;"><br /></div><div style="line-height: 1.22em;"><div><span style="color: #29303b;">TUESDAY, JANUARY 26, 2021 </span></div><div><span style="color: #29303b;"><br /></span></div><div><span style="color: #29303b;">Pennsylvania Scrapie Update Outbreak August 2018 and 3 Nor-98 atypical Cases Detected</span><br /></div><div><span style="color: #29303b;"><br /></span></div><div><span style="color: #29303b;"><a href="https://scrapie-usa.blogspot.com/2021/01/pennsylvania-scrapie-update-outbreak.html" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://scrapie-usa.blogspot.com/2021/01/pennsylvania-scrapie-update-outbreak.html</a></span></div></div><div style="line-height: 1.22em;"><br /></div><div style="line-height: 1.22em;"><div style="line-height: 1.22em;"><span style="font-family: Arial, Helvetica, sans-serif; font-size: 12px; line-height: 1.22em;">MONDAY, JULY 13, 2020 </span></div><div style="line-height: 1.22em;"><span style="font-family: Arial, Helvetica, sans-serif; font-size: 12px; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="line-height: 1.22em;"><span style="font-family: Arial, Helvetica, sans-serif; font-size: 12px; line-height: 1.22em;">Efficient transmission of classical scrapie agent x124 by intralingual route to genetically susceptible sheep with a low dose inoculum</span><br clear="none" style="line-height: 1.22em;" /></div><div style="line-height: 1.22em;"><span style="font-family: Arial, Helvetica, sans-serif; font-size: 12px; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="line-height: 1.22em;"><span style="font-family: Arial, Helvetica, sans-serif; font-size: 12px; line-height: 1.22em;"><a href="https://scrapie-usa.blogspot.com/2020/07/efficient-transmission-of-classical.html" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">https://scrapie-usa.blogspot.com/2020/07/efficient-transmission-of-classical.html</a></span></div></div></div></div></div><div style="color: #29303b; font-size: 10pt;"><br /></div><div style="color: #29303b; font-size: 10pt;"><div style="color: black;">*** Singeltary reply ; Molecular, Biochemical and Genetic Characteristics of BSE in Canada Singeltary reply ;</div><div style="color: black;"><br /></div><div style="color: black;"><a href="https://journals.plos.org/plosone/article/comment?id=10.1371/annotation/4f9be886-69fe-4c7c-922b-85b0ecbe6d53" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://journals.plos.org/plosone/article/comment?id=10.1371/annotation/4f9be886-69fe-4c7c-922b-85b0ecbe6d53</a></div><div style="color: black;"><br /></div><div style="color: black;"><div>Epidemiology of Scrapie in the United States 1977 </div><div><br /></div><div>snip... </div><div><br /></div><div>Scrapie Field Trial Experiments Mission, Texas A Scrapie Field Trial was developed at Mission, Texas, to provide additional information for the eradication program on the epidemiology of natural scrapie. The Mission Field Trial Station is located on 450 acres of pastureland, part of the former Moore Air Force Base, near Mission, Texas. </div><div><br /></div><div>It was designed to bring previously exposed, and later also unexposed, sheep or goats to the Station and maintain and breed them under close observation for extended periods to determine which animals would develop scrapie and define more closely the natural spread and other epidemiological aspects of the disease. </div><div><br /></div><div>The 547 previously exposed sheep brought to the Mission Station beginning in 1964 were of the Cheviot, Hampshire, Montadale, or Suffolk breeds. </div><div><br /></div><div>They were purchased as field outbreaks occurred, and represented 21 bloodlines in which scrapie had been diagnosed. </div><div><br /></div><div>Upon arrival at the Station, the sheep were maintained on pasture, with supplemental feeding as necessary. </div><div><br /></div><div>The station was divided into 2 areas: </div><div><br /></div><div>(1) a series of pastures and-pens occupied by male animals only, and </div><div><br /></div><div>(2) a series of pastures and pens occupied by females and young progeny of both sexes. </div><div><br /></div><div>... snip...</div><div><br /></div><div>see full text ; </div><div><br /></div><div><a href="http://web.archive.org/web/20030513212324/http://www.bseinquiry.gov.uk/files/mb/m08b/tab64.pdf" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://web.archive.org/web/20030513212324/http://www.bseinquiry.gov.uk/files/mb/m08b/tab64.pdf</a></div><div><div id="yiv1173273489"><div style="font-stretch: normal; line-height: normal;"><div style="font-size: 10pt;"><br /></div><div style="font-size: 10pt;">COLORADO THE ORIGIN OF CHRONIC WASTING DISEASE CWD TSE PRION?</div><div style="font-size: 10pt;"><br /></div><div style="font-size: 10pt;">*** Spraker suggested an interesting explanation for the occurrence of CWD. The deer pens at the Foot Hills Campus were built some 30-40 years ago by a Dr. Bob Davis. At or abut that time, allegedly, some scrapie work was conducted at this site. When deer were introduced to the pens they occupied ground that had previously been occupied by sheep.</div><div style="font-size: 10pt;"><br /></div><div style="font-size: 10pt;"><a href="http://webarchive.nationalarchives.gov.uk/20080102193705/http://www.bseinquiry.gov.uk/files/mb/m11b/tab01.pdf" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://webarchive.nationalarchives.gov.uk/20080102193705/http://www.bseinquiry.gov.uk/files/mb/m11b/tab01.pdf</a></div><div style="font-size: 10pt;"><br /></div><div style="font-size: 10pt;">Title: Scrapie transmits to white-tailed deer by the oral route and has a molecular profile similar to chronic wasting disease</div><div style="font-size: 10pt;"><br /></div><div style="font-size: 10pt;"><a href="https://www.ars.usda.gov/research/publications/publication/?seqNo115=317901" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://www.ars.usda.gov/research/publications/publication/?seqNo115=317901</a></div><div style="font-size: 10pt;"><br /></div><div style="font-size: 10pt;">''Given the results of this study, current diagnostic techniques would be unlikely to distinguish CWD in sheep from scrapie in sheep if cross-species transmission occurred naturally.''</div><div style="font-size: 10pt;"><br /></div><div style="font-size: 10pt;">2021 May 28</div><div style="font-size: 10pt;"><br /></div><div style="font-size: 10pt;">Second passage of chronic wasting disease of mule deer to sheep by intracranial inoculation compared to classical scrapie</div><div style="font-size: 10pt;"><br /></div><div style="font-size: 10pt;"><a href="https://journals.sagepub.com/doi/full/10.1177/10406387211017615" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://journals.sagepub.com/doi/full/10.1177/10406387211017615</a></div><div style="font-size: 10pt;"><br /></div><div style="font-size: 10pt;">Title: Second passage of chronic wasting disease of mule deer in sheep compared to classical scrapie after intracranial inoculation</div><div style="font-size: 10pt;"><br /></div><div style="font-size: 10pt;"><a href="https://www.ars.usda.gov/research/publications/publication/?seqNo115=376956" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://www.ars.usda.gov/research/publications/publication/?seqNo115=376956</a></div><div style="font-size: 10pt;"><br /></div><div style="font-size: 10pt;">''We inoculated WTD by a natural route of exposure (concurrent oral and intranasal (IN); n=5) with a US scrapie isolate. All scrapie-inoculated deer had evidence of PrPSc accumulation.''</div><div style="font-size: 10pt;"><br /></div><div style="font-size: 10pt;">Title: Passage of scrapie to deer results in a new phenotype upon return passage to sheep</div><div style="font-size: 10pt;"><br /></div><div style="font-size: 10pt;"><a href="https://www.ars.usda.gov/research/publications/publication/?seqNo115=337278" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://www.ars.usda.gov/research/publications/publication/?seqNo115=337278</a></div><div style="font-size: 10pt;"><br /></div><div style="font-size: 10pt;">Title: Transmission of the agent of sheep scrapie to deer results in PrPSc with two distinct molecular profiles </div><div style="font-size: 10pt;"><br /></div><div style="font-size: 10pt;">In summary, this work demonstrates that WTD are susceptible to the agent of scrapie, two distinct molecular profiles of PrPSc are present in the tissues of affected deer, and inoculum of either profile type readily passes to deer. </div><div style="font-size: 10pt;"><br /></div><div style="font-size: 10pt;"><a href="http://www.ars.usda.gov/research/publications/publications.htm?SEQ_NO_115=314097" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://www.ars.usda.gov/research/publications/publications.htm?SEQ_NO_115=314097</a></div><div><br /></div><div><div>FRIDAY, OCTOBER 1, 2021 </div><div><br /></div><div>Bovine Spongiform Encephalopathy BSE TSE Prion Origin, USA, what if?<br /></div><div><br /></div><div><a href="https://bovineprp.blogspot.com/2021/10/bovine-spongiform-encephalopathy-bse.html" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://bovineprp.blogspot.com/2021/10/bovine-spongiform-encephalopathy-bse.html</a></div></div><div><br /></div><div><div style="font-size: 10pt;">Scrapie Agent (Strain 263K) Can Transmit Disease via the Oral Route after Persistence in Soil over Years</div><div style="font-size: 10pt;"><br /></div><div style="font-size: 10pt;">Published: May 9, 2007</div><div style="font-size: 10pt;"><br /></div><div style="font-size: 10pt;"><a href="https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0000435" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0000435</a></div><div style="font-size: 10pt;"><br /></div><div style="font-size: 10pt;">WEDNESDAY, DECEMBER 04, 2013 </div><div style="font-size: 10pt;"><br /></div><div style="font-size: 10pt;">Chronic Wasting Disease CWD and Land Value concerns? </div><div style="font-size: 10pt;"><br /></div><div style="font-size: 10pt;">***> This is very likely to have parallels with control efforts for CWD in cervids. <***</div><div style="font-size: 10pt;"><br /></div><div style="font-size: 10pt;">Paper</div><div style="font-size: 10pt;"><br /></div><div style="font-size: 10pt;">Rapid recontamination of a farm building occurs after attempted prion removal</div><div style="font-size: 10pt;"><br /></div><div style="font-size: 10pt;">First published: 19 January 2019 <a href="https://doi.org/10.1136/vr.105054" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://doi.org/10.1136/vr.105054</a></div><div style="font-size: 10pt;"><br /></div><div style="font-size: 10pt;">This study clearly demonstrates the difficulty in removing scrapie infectivity from the farm environment. Practical and effective prion decontamination methods are still urgently required for decontamination of scrapie infectivity from farms that have had cases of scrapie and this is particularly relevant for scrapiepositive goatherds, which currently have limited genetic resistance to scrapie within commercial breeds.24 This is very likely to have parallels with control efforts for CWD in cervids.</div><div style="font-size: 10pt;"><br /></div><div style="font-size: 10pt;"><a href="https://bvajournals.onlinelibrary.wiley.com/doi/abs/10.1136/vr.105054" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://bvajournals.onlinelibrary.wiley.com/doi/abs/10.1136/vr.105054</a></div><div style="font-size: 10pt;"><br /></div><div style="font-size: 10pt;">***>This is very likely to have parallels with control efforts for CWD in cervids.</div><div style="font-size: 10pt;"><br /></div><div style="font-size: 10pt;">***> Infectious agent of sheep scrapie may persist in the environment for at least 16 years</div><div style="font-size: 10pt;"><br /></div><div style="font-size: 10pt;">***> Nine of these recurrences occurred 14–21 years after culling, apparently as the result of environmental contamination, but outside entry could not always be absolutely excluded. </div><div style="font-size: 10pt;"><br /></div><div style="font-size: 10pt;">JOURNAL OF GENERAL VIROLOGY Volume 87, Issue 12</div><div style="font-size: 10pt;"><br /></div><div style="font-size: 10pt;">Infectious agent of sheep scrapie may persist in the environment for at least 16 years Free</div><div style="font-size: 10pt;"><br /></div><div style="font-size: 10pt;">Gudmundur Georgsson1, Sigurdur Sigurdarson2, Paul Brown3</div><div style="font-size: 10pt;"><br /></div><div style="font-size: 10pt;"><a href="http://www.microbiologyresearch.org/docserver/fulltext/jgv/87/12/3737.pdf?expires=1540908280&id=id&accname=guest&checksum=ED0572E1E5B272C100A32212A3E3761A" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://www.microbiologyresearch.org/docserver/fulltext/jgv/87/12/3737.pdf?expires=1540908280&id=id&accname=guest&checksum=ED0572E1E5B272C100A32212A3E3761A</a></div><div style="font-size: 10pt;"><br /></div><div style="font-size: 10pt;"><div style="font-size: 10pt;"><div>5 or 6 years quarantine is NOT LONG ENOUGH FOR CWD TSE PRION !!!</div><div><br clear="none" /></div><div>QUARANTINE NEEDS TO BE 21 YEARS FOR CWD TSE PRION !</div></div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;"><div style="font-size: 10pt;"><div style="line-height: 1.22em;"><div>FRIDAY, APRIL 30, 2021 </div><div><br clear="none" /></div><div>Should Property Evaluations Contain Scrapie, CWD, TSE PRION Environmental Contamination of the land?<br clear="none" /></div><div><br clear="none" /></div><div><div class="yiv1173273489aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;"><span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;">***> Confidential!!!!</span></span></div><div class="yiv1173273489aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;"><span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;"><br clear="none" /></span></span></div><div class="yiv1173273489aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;"><span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;">***> As early as 1992-3 there had been long studies conducted on small pastures containing scrapie infected sheep at the sheep research station associated with the Neuropathogenesis Unit in Edinburgh, Scotland. Whether these are documented...I don't know. But personal recounts both heard and recorded in a daily journal indicate that leaving the pastures free and replacing the topsoil completely at least 2 feet of thickness each year for SEVEN years....and then when very clean (proven scrapie free) sheep were placed on these small pastures.... the new sheep also broke out with scrapie and passed it to offspring. I am not sure that TSE contaminated ground could ever be free of the agent!! A very frightening revelation!!!</span></span></div><div class="yiv1173273489aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;"><span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;"><br clear="none" /></span></span></div><div class="yiv1173273489aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;"><span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;">---end personal email---end...tss</span></span></div></div><div><br clear="none" /></div><div><a href="https://transmissiblespongiformencephalopathy.blogspot.com/2021/04/should-property-evaluations-contain.html" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://transmissiblespongiformencephalopathy.blogspot.com/2021/04/should-property-evaluations-contain.html</a></div></div><div style="line-height: 1.22em;"><br clear="none" /></div><div style="line-height: 1.22em;">WEDNESDAY, DECEMBER 04, 2013 </div><div style="line-height: 1.22em;"><br clear="none" /></div><div style="line-height: 1.22em;">Chronic Wasting Disease CWD and Land Value concerns? </div></div></div></div><div style="font-size: 10pt;"><br /></div><div><div style="font-size: 10pt;">FRIDAY, OCTOBER 01, 2021 </div><div style="font-size: 10pt;"><br /></div><div style="font-size: 10pt;">TEXAS CWD TSE PRION recent discoveries of new cases bring the total number of positive deer to 261 in 14 counties </div><div style="font-size: 10pt;"><br /></div><div>To date, 168 of those positives are associated with captive breeding facilities, </div><div><br /></div><div>25 from release sites associated with those positive captive breeding facilities, </div><div><br /></div><div>and 68 in free-ranging deer populations. Fifty-seven of the free-range positives are in the Trans Pecos and Texas panhandle, with the remaining 11 in Medina and Val Verde counties.<br /></div><div><br /></div><div><a href="http://%20https//tpwd.texas.gov/newsmedia/releases/?req=20211001a&utm_campaign=govdelivery-email&utm_medium=email&utm_source=govdelivery" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http:// https://tpwd.texas.gov/newsmedia/releases/?req=20211001a&utm_campaign=govdelivery-email&utm_medium=email&utm_source=govdelivery</a></div><div style="font-size: 10pt;"><br /></div><div style="font-size: 10pt;"><div style="font-family: Helvetica; font-size: 12px; font-stretch: normal; line-height: normal; margin: 0px;"><span style="font-size: 12pt;">Control of Chronic Wasting Disease OMB Control Number: 0579-0189 APHIS-2021-0004 Singeltary Submission</span></div><div style="font-family: Helvetica; font-size: 12px; font-stretch: normal; line-height: normal; margin: 0px; min-height: 13.8px;"><span style="font-size: 12pt;"></span><br clear="none" /></div><div style="font-family: Helvetica; font-size: 12px; font-stretch: normal; line-height: normal; margin: 0px;"><span style="font-size: 12pt;"><a href="https://www.regulations.gov/comment/APHIS-2021-0004-0002" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://www.regulations.gov/comment/APHIS-2021-0004-0002</a></span></div><div style="font-family: Helvetica; font-size: 12px; font-stretch: normal; line-height: normal; margin: 0px; min-height: 13.8px;"><span style="font-size: 12pt;"></span><br clear="none" /></div><div style="font-family: Helvetica; font-size: 12px; font-stretch: normal; line-height: normal; margin: 0px;"><span style="font-size: 12pt;"><a href="https://downloads.regulations.gov/APHIS-2021-0004-0002/attachment_1.pdf" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://downloads.regulations.gov/APHIS-2021-0004-0002/attachment_1.pdf</a></span></div><div style="font-family: Helvetica; font-size: 12px; font-stretch: normal; line-height: normal; margin: 0px; min-height: 13.8px;"><span style="font-size: 12pt;"></span><br clear="none" /></div><div style="font-family: Helvetica; font-size: 12px; font-stretch: normal; line-height: normal; margin: 0px;"><span style="font-size: 12pt;">Docket No. APHIS-2018-0011 Chronic Wasting Disease Herd Certification</span></div><div style="font-family: Helvetica; font-size: 12px; font-stretch: normal; line-height: normal; margin: 0px; min-height: 13.8px;"><span style="font-size: 12pt;"></span><br clear="none" /></div><div style="font-family: Helvetica; font-size: 12px; font-stretch: normal; line-height: normal; margin: 0px;"><span style="font-size: 12pt;"><a href="https://www.regulations.gov/document/APHIS-2018-0011-0003" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://www.regulations.gov/document/APHIS-2018-0011-0003</a></span></div><div style="font-family: Helvetica; font-size: 12px; font-stretch: normal; line-height: normal; margin: 0px; min-height: 13.8px;"><span style="font-size: 12pt;"></span><br clear="none" /></div><div style="font-family: Helvetica; font-size: 12px; font-stretch: normal; line-height: normal; margin: 0px;"><span style="font-size: 12pt;"><a href="https://downloads.regulations.gov/APHIS-2018-0011-0003/attachment_1.pdf" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://downloads.regulations.gov/APHIS-2018-0011-0003/attachment_1.pdf</a></span></div><div style="font-family: Helvetica; font-size: 12px; font-stretch: normal; line-height: normal; margin: 0px;"><br /></div><div style="font-family: Helvetica; font-size: 12px; font-stretch: normal; line-height: normal; margin: 0px;"><div style="color: #29303b; font-family: arial; font-size: 13.3333px;"><div style="font-size: 10pt; margin-bottom: 2em; margin-top: 0.5em;"><span style="font-size: 10pt;">Sunday, January 10, 2021 </span></div><div style="font-size: 10pt; margin-bottom: 2em; margin-top: 0.5em;"><div dir="ltr" style="font-family: Helvetica, Arial, sans-serif; font-size: 10pt;"><div style="font-family: arial;">APHIS Concurrence With OIE Risk Designation for Bovine Spongiform Encephalopathy [Docket No. APHIS-2018-0087] Singeltary Submission June 17, 2019</div><div style="font-family: arial;"><br clear="none" /></div><div style="font-family: arial;">APHIS Concurrence With OIE Risk Designation for Bovine Spongiform Encephalopathy [Docket No. APHIS-2018-0087] Singeltary Submission</div><div style="font-family: arial;"><br clear="none" /></div><div style="font-family: arial;">Greetings APHIS et al, </div><div style="font-family: arial;"><br clear="none" /></div><div style="font-family: arial;">I would kindly like to comment on APHIS Concurrence With OIE Risk Designation for Bovine Spongiform Encephalopathy [Docket No. APHIS-2018-0087], and my comments are as follows, with the latest peer review and transmission studies as references of evidence.</div><div style="font-family: arial;"><br clear="none" /></div><div style="font-family: arial;">THE OIE/USDA BSE Minimal Risk Region MRR is nothing more than free pass to import and export the Transmissible Spongiform Encephalopathy TSE Prion disease. December 2003, when the USDA et al lost it's supposedly 'GOLD CARD' ie BSE FREE STATUS (that was based on nothing more than not looking and not finding BSE), once the USA lost it's gold card BSE Free status, the USDA OIE et al worked hard and fast to change the BSE Geographical Risk Statuses i.e. the BSE GBR's, and replaced it with the BSE MRR policy, the legal tool to trade mad cow type disease TSE Prion Globally. The USA is doing just what the UK did, when they shipped mad cow disease around the world, except with the BSE MRR policy, it's now legal. </div><div style="font-family: arial;"><br clear="none" /></div><div style="font-family: arial;">Also, the whole concept of the BSE MRR policy is based on a false pretense, that atypical BSE is not transmissible, and that only typical c-BSE is transmissible via feed. This notion that atypical BSE TSE Prion is an old age cow disease that is not infectious is absolutely false, there is NO science to show this, and on the contrary, we now know that atypical BSE will transmit by ORAL ROUTES, but even much more concerning now, recent science has shown that Chronic Wasting Disease CWD TSE Prion in deer and elk which is rampant with no stopping is sight in the USA, and Scrapie TSE Prion in sheep and goat, will transmit to PIGS by oral routes, this is our worst nightmare, showing even more risk factors for the USA FDA PART 589 TSE PRION FEED ban. </div><div style="font-family: arial;"><br clear="none" /></div><div style="font-family: arial;">The FDA PART 589 TSE PRION FEED ban has failed terribly bad, and is still failing, since August 1997. there is tonnage and tonnage of banned potential mad cow feed that went into commerce, and still is, with one decade, 10 YEARS, post August 1997 FDA PART 589 TSE PRION FEED ban, 2007, with 10,000,000 POUNDS, with REASON, Products manufactured from bulk feed containing blood meal that was cross contaminated with prohibited meat and bone meal and the labeling did not bear cautionary BSE statement. you can see all these feed ban warning letters and tonnage of mad cow feed in commerce, year after year, that is not accessible on the internet anymore like it use to be, you can see history of the FDA failure August 1997 FDA PART 589 TSE PRION FEED ban here, but remember this, we have a new outbreak of TSE Prion disease in a new livestock species, the camel, and this too is very worrisome.</div><div style="font-family: arial;"><br clear="none" /></div><div style="font-family: arial;">WITH the OIE and the USDA et al weakening the global TSE prion surveillance, by not classifying the atypical Scrapie as TSE Prion disease, and the notion that they want to do the same thing with typical scrapie and atypical BSE, it's just not scientific.</div><div style="font-family: arial;"><br clear="none" /></div><div style="font-family: arial;">WE MUST abolish the BSE MRR policy, go back to the BSE GBR risk assessments by country, and enhance them to include all strains of TSE Prion disease in all species. With Chronic Wasting CWD TSE Prion disease spreading in Europe, now including, Norway, Finland, Sweden, also in Korea, Canada and the USA, and the TSE Prion in Camels, the fact the the USA is feeding potentially CWD, Scrapie, BSE, typical and atypical, to other animals, and shipping both this feed and or live animals or even grains around the globe, potentially exposed or infected with the TSE Prion. this APHIS Concurrence With OIE Risk Designation for Bovine Spongiform Encephalopathy [Docket No. APHIS-2018-0087], under it's present definition, does NOT show the true risk of the TSE Prion in any country. as i said, it's nothing more than a legal tool to trade the TSE Prion around the globe, nothing but ink on paper.</div><div style="font-family: arial;"><br clear="none" /></div><div style="font-family: arial;">AS long as the BSE MRR policy stays in effect, TSE Prion disease will continued to be bought and sold as food for both humans and animals around the globe, and the future ramifications from friendly fire there from, i.e. iatrogenic exposure and transmission there from from all of the above, should not be underestimated. ... </div><div style="font-family: arial;"><br clear="none" /></div><div style="font-family: arial;"><a href="https://beta.regulations.gov/document/APHIS-2018-0087-0002" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://beta.regulations.gov/document/APHIS-2018-0087-0002</a></div><div style="font-family: arial;"><br clear="none" /></div><div style="font-family: arial;"><a href="https://downloads.regulations.gov/APHIS-2018-0087-0002/attachment_1.pdf" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://downloads.regulations.gov/APHIS-2018-0087-0002/attachment_1.pdf</a></div></div></div></div><div style="color: #29303b; font-family: arial; font-size: 13.3333px;"><div><span style="font-family: arial, helvetica;">TUESDAY, SEPTEMBER 07, 2021 </span></div><div><span style="font-family: arial, helvetica;"><br clear="none" /></span></div><div><span style="font-family: arial, helvetica;">Atypical Bovine Spongiform Encephalopathy BSE OIE, FDA 589.2001 FEED REGULATIONS, and Ingestion Therefrom<br clear="none" /></span></div><div><span style="font-family: arial, helvetica;"><br clear="none" /></span></div><div><span style="font-family: arial, helvetica;"><a href="https://bse-atypical.blogspot.com/2021/09/atypical-bovine-spongiform.html" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://bse-atypical.blogspot.com/2021/09/atypical-bovine-spongiform.html</a></span></div></div><div class="yiv9925787285yqt2153808545" id="yiv9925787285yqtfd27948" style="color: #29303b; font-family: arial; font-size: 13.3333px;"><div><br clear="none" /></div><div>MONDAY, JULY 27, 2020 </div><div><br clear="none" /></div><div>BSE Inquiry DFA's a review</div><div><br clear="none" /></div></div><div style="color: #29303b; font-family: arial; font-size: 13.3333px;"><div class="yiv9925787285yqt2153808545" id="yiv9925787285yqtfd75551"><a href="https://bseinquiry.blogspot.com/2020/07/bse-inquiry-dfas-review.html" rel="nofollow noopener noreferrer" shape="rect" style="color: #0096ef; cursor: pointer; text-decoration-line: none;" target="_blank">https://bseinquiry.blogspot.com/2020/07/bse-inquiry-dfas-review.html</a></div> </div><div style="color: #29303b; font-family: arial; font-size: 13.3333px;">Terry S. Singeltary Sr.</div></div></div></div></div></div></div></div></div></div></div></div></div></div></div></div></div></div></div>Terry S. Singeltary Sr.http://www.blogger.com/profile/06986622967539963260noreply@blogger.com0tag:blogger.com,1999:blog-6404950019984350027.post-43226246078212903642021-08-27T08:54:00.005-07:002021-08-27T09:00:31.000-07:00 The agent of chronic wasting disease from pigs is infectious in transgenic mice expressing human PRNP<p><span style="background-color: white; font-family: arial, helvetica; font-size: 10pt;">Subject: The agent of chronic wasting disease from pigs is infectious in transgenic mice expressing human PRNP</span></p><div id="yiv3138727584" style="background-color: white; font-family: arial; font-size: 13.3333px;"><div style="font-stretch: normal; font-variant-east-asian: normal; font-variant-numeric: normal; line-height: normal;"><div style="font-size: 10pt;">Research Project: Pathobiology, Genetics, and Detection of Transmissible Spongiform Encephalopathies Location: Virus and Prion Research</div><div style="font-size: 10pt;"><br /></div><div style="font-size: 10pt;">Title: The agent of chronic wasting disease from pigs is infectious in transgenic mice expressing human PRNP</div><div style="font-size: 10pt;"><br /></div><div style="font-size: 10pt;">Author item MOORE, S - Orise Fellow item Kokemuller, Robyn item WEST-GREENLEE, M - Iowa State University item BALKEMA-BUSCHMANN, ANNE - Friedrich-Loeffler-institut item GROSCHUP, MARTIN - Friedrich-Loeffler-institut item Greenlee, Justin Submitted to: Prion Publication Type: Abstract Only Publication Acceptance Date: 5/10/2018 Publication Date: 5/22/2018</div><div style="font-size: 10pt;"><br /></div><div style="font-size: 10pt;">Citation: Moore, S.J., Kokemuller, R.D., West-Greenlee, M.H., Balkema-Buschmann, A., Groschup, M.H., Greenlee, J.J. 2018. The agent of chronic wasting disease from pigs is infectious in transgenic mice expressing human PRNP. Prion 2018, Santiago de Compostela, Spain, May 22-25, 2018. Paper No. WA15, page 44. Interpretive Summary:</div><div style="font-size: 10pt;"><br /></div><div style="font-size: 10pt;">Technical Abstract: We have previously shown that the chronic wasting disease (CWD) agent from white-tailed deer can be transmitted to domestic pigs via intracranial or oral inoculation although with low attack rates and restricted PrPSc accumulation. The objective of this study was to assess the potential for cross-species transmission of pig-passaged CWD using bioassay in transgenic mice. Transgenic mice expressing human (Tg40), bovine (TgBovXV) or porcine (Tg002) PRNP were inoculated intracranially with 1% brain homogenate from a pig that had been intracranially inoculated with a pool of CWD from white-tailed deer. This pig developed neurological clinical signs, was euthanized at 64 months post-inoculation, and PrPSc was detected in the brain. Mice were monitored daily for clinical signs of disease until the end of the study. Mice were considered positive if PrPSc was detected in the brain using an enzyme immunoassay (EIA). In transgenic mice expressing porcine prion protein the average incubation period was 167 days post-inoculation (dpi) and 3/27 mice were EIA positive (attack rate = 11%). All 3 mice were found dead and clinical signs were not noted prior to death. One transgenic mouse expressing bovine prion protein was euthanized due to excessive scratching at 617 dpi and 2 mice culled at the end of the study at 700 dpi were EIA positive resulting in an overall attack rate of 3/16 (19%). None of the transgenic mice expressing human prion protein that died or were euthanized up to 769 dpi were EIA positive and at study end point at 800 dpi 2 mice had positive EIA results (overall attack rate = 2/20 = 10%). The EIA optical density (OD) readings for all positive mice were at the lower end of the reference range (positive mice range, OD = 0.266-0.438; test positive reference range, OD = 0.250-4.000). To the authors’ knowledge, cervid-derived CWD isolates have not been successfully transmitted to transgenic mice expressing human prion protein. The successful transmission of pig-passaged CWD to Tg40 mice reported here suggests that passage of the CWD agent through pigs results in a change of the transmission characteristics which reduces the transmission barrier of Tg40 mice to the CWD agent. If this biological behavior is recapitulated in the original host species, passage of the CWD agent through pigs could potentially lead to increased pathogenicity of the CWD agent in humans.</div><div style="font-size: 10pt;"><br /></div><div style="font-size: 10pt;"><a href="https://www.ars.usda.gov/research/publications/publication/?seqNo115=353091" rel="nofollow noopener noreferrer" style="color: #0096ef; cursor: pointer; text-decoration-line: none;" target="_blank">https://www.ars.usda.gov/research/publications/publication/?seqNo115=353091</a><br /></div><div style="font-size: 10pt;"><br /></div><div style="font-size: 10pt;"><div>Research Project: Pathobiology, Genetics, and Detection of Transmissible Spongiform Encephalopathies Location: Virus and Prion Research</div><div><br /></div><div>Title: Experimental transmission of the chronic wasting disease agent to swine after oral or intracranial inoculation</div><div><br /></div><div>Author item MOORE, SARAH - Orise Fellow item WEST GREENLEE, M - Iowa State University item KONDRU, NAVEEN - Iowa State University item MANNE, SIREESHA - Iowa State University item Smith, Jodi item Kunkle, Robert item KANTHASAMY, ANUMANTHA - Iowa State University item Greenlee, Justin Submitted to: Journal of Virology Publication Type: Peer Reviewed Journal Publication Acceptance Date: 7/6/2017 Publication Date: 9/12/2017</div><div><br /></div><div>Citation: Moore, S.J., West Greenlee, M.H., Kondru, N., Manne, S., Smith, J.D., Kunkle, R.A., Kanthasamy, A., Greenlee, J.J. 2017. Experimental transmission of the chronic wasting disease agent to swine after oral or intracranial inoculation. Journal of Virology. 91(19):e00926-17. <a href="https://doi.org/10.1128/JVI.00926-17" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://doi.org/10.1128/JVI.00926-17</a>.</div><div><br /></div><div>Interpretive Summary: Chronic wasting disease (CWD) is a fatal disease of wild and captive deer and elk that causes damaging changes in the brain. The infectious agent is an abnormal protein called a prion that has misfolded from its normal state. Whether CWD can transmit to swine is unknown. This study evaluated the potential of pigs to develop CWD after either intracranial or oral inoculation. Our data indicates that swine do accumulate the abnormal prion protein associated with CWD after intracranial or oral inoculation. Further, there was evidence of abnormal prion protein accumulation in lymph nodes. Currently, swine rations in the U.S. could contain animal derived components including materials from deer or elk. In addition, feral swine could be exposed to infected carcasses in areas where CWD is present in wildlife populations. This information is useful to wildlife managers and individuals in the swine and captive cervid industries. These findings could impact future regulations for the disposal of offal from deer and elk slaughtered in commercial operations. U.S. regulators should carefully consider the new information from this study before relaxing feed ban standards designed to control potentially feed borne prion diseases.</div><div><br /></div><div>Technical Abstract: Chronic wasting disease (CWD) is a naturally occurring, fatal neurodegenerative disease of cervids. The potential for swine to serve as a host for the agent of chronic wasting disease is unknown. The purpose of this study was to investigate the susceptibility of swine to the CWD agent following oral or intracranial experimental inoculation. Crossbred piglets were assigned to one of three groups: intracranially inoculated (n=20), orally inoculated (n=19), or non-inoculated (n=9). At approximately the age at which commercial pigs reach market weight, half of the pigs in each group were culled ('market weight' groups). The remaining pigs ('aged' groups) were allowed to incubate for up to 73 months post inoculation (MPI). Tissues collected at necropsy were examined for disease-associated prion protein (PrPSc) by western blotting (WB), antigen-capture immunoassay (EIA), immunohistochemistry (IHC) and in vitro real-time quaking induced conversion (RT-QuIC). Brain samples from selected pigs were also bioassayed in mice expressing porcine prion protein. Four intracranially inoculated aged pigs and one orally inoculated aged pig were positive by EIA, IHC and/or WB. Using RT-QuIC, PrPSc was detected in lymphoid and/or brain tissue from pigs in all inoculated groups. Bioassay was positive in 4 out of 5 pigs assayed. This study demonstrates that pigs can serve as hosts for CWD, though with scant PrPSc accumulation requiring sensitive detection methods. Detection of infectivity in orally inoculated pigs using mouse bioassay raises the possibility that naturally exposed pigs could act as a reservoir of CWD infectivity.</div><div><br /></div><div><a href="https://www.ars.usda.gov/research/publications/publication/?seqNo115=339093" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://www.ars.usda.gov/research/publications/publication/?seqNo115=339093</a><br /></div><div><br /></div><div>12 September 2017</div><div><br /></div><div>Experimental Transmission of the Chronic Wasting Disease Agent to Swine after Oral or Intracranial Inoculation</div><div><br /></div><div>Authors: S. Jo Moore, M. Heather West Greenlee, Naveen Kondru, Sireesha Manne, Jodi D. Smith, Robert A. Kunkle, Anumantha Kanthasamy, and Justin J. Greenlee </div><div><br /></div><div><a href="https://orcid.org/0000-0003-2202-3054" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://orcid.org/0000-0003-2202-3054</a></div><div><br /></div><div>AUTHORS INFO & AFFILIATIONS</div><div><br /></div><div>DOI: <a href="https://doi.org/10.1128/JVI.00926-17" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://doi.org/10.1128/JVI.00926-17</a></div><div><br /></div><div>Volume 91, Number 19</div><div><br /></div><div>1 October 2017</div><div><br /></div><div>ABSTRACT</div><div><br /></div><div>ABSTRACT</div><div><br /></div><div>Chronic wasting disease (CWD) is a naturally occurring, fatal neurodegenerative disease of cervids. The potential for swine to serve as hosts for the agent of CWD is unknown. The purpose of this study was to investigate the susceptibility of swine to the CWD agent following experimental oral or intracranial inoculation. Crossbred piglets were assigned to three groups, intracranially inoculated (n = 20), orally inoculated (n = 19), and noninoculated (n = 9). At approximately the age at which commercial pigs reach market weight, half of the pigs in each group were culled (“market weight” groups). The remaining pigs (“aged” groups) were allowed to incubate for up to 73 months postinoculation (mpi). Tissues collected at necropsy were examined for disease-associated prion protein (PrPSc) by Western blotting (WB), antigen capture enzyme immunoassay (EIA), immunohistochemistry (IHC), and in vitro real-time quaking-induced conversion (RT-QuIC). Brain samples from selected pigs were also bioassayed in mice expressing porcine prion protein. Four intracranially inoculated aged pigs and one orally inoculated aged pig were positive by EIA, IHC, and/or WB. By RT-QuIC, PrPSc was detected in lymphoid and/or brain tissue from one or more pigs in each inoculated group. The bioassay was positive in four out of five pigs assayed. This study demonstrates that pigs can support low-level amplification of CWD prions, although the species barrier to CWD infection is relatively high. However, detection of infectivity in orally inoculated pigs with a mouse bioassay raises the possibility that naturally exposed pigs could act as a reservoir of CWD infectivity. IMPORTANCE We challenged domestic swine with the chronic wasting disease agent by inoculation directly into the brain (intracranially) or by oral gavage (orally). Disease-associated prion protein (PrPSc) was detected in brain and lymphoid tissues from intracranially and orally inoculated pigs as early as 8 months of age (6 months postinoculation). Only one pig developed clinical neurologic signs suggestive of prion disease. The amount of PrPSc in the brains and lymphoid tissues of positive pigs was small, especially in orally inoculated pigs. Regardless, positive results obtained with orally inoculated pigs suggest that it may be possible for swine to serve as a reservoir for prion disease under natural conditions.</div><div><br /></div><div><a href="https://journals.asm.org/doi/10.1128/JVI.00926-17" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://journals.asm.org/doi/10.1128/JVI.00926-17</a><br /></div></div><div style="font-size: 10pt;"><br /></div><div><div style="font-size: 10pt;"><span style="background-color: transparent; font-size: 10pt;">2021 Transmissible Spongiform Encephalopathy TSE Prion End of Year Report 2020</span><br /></div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">CJD FOUNDATION VIRTUAL CONFERENCE CJD Foundation Research Grant Recipient Reports Panel 2 Nov 3, 2020</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">zoonotic potential of PMCA-adapted CWD PrP 96SS inoculum</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;"><a href="https://youtu.be/VfazuR7cjMc?t=1992" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://youtu.be/VfazuR7cjMc?t=1992</a></div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">4 different CWD strains, and these 4 strains have different potential to induce any folding of the human prion protein. </div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;"><a href="https://youtu.be/VfazuR7cjMc?t=2019" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://youtu.be/VfazuR7cjMc?t=2019</a></div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">***> PIGS, WILD BOAR, CWD <***</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">***> POPULATIONS OF WILD BOARS IN THE UNITED STATES INCREASING SUPSTANTUALLY AND IN MANY AREAS WE CAN SEE A HIGH DENSITY OF WILD BOARS AND HIGH INCIDENT OF CHRONIC WASTING DISEASE</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">HYPOTHOSIS AND SPECIFIC AIMS</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">HYPOTHOSIS </div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">BSE, SCRAPIE, AND CWD, EXPOSED DOMESTIC PIGS ACCUMULATE DIFFERENT QUANTITIES AND STRAINS OF PRIONS IN PERIPHERAL TISSUES, EACH ONE OF THEM WITH PARTICULAR ZOONOTIC POTENTIALS</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;"><a href="https://youtu.be/VfazuR7cjMc" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://youtu.be/VfazuR7cjMc</a></div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">Final Report – CJD Foundation Grant Program A. </div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">Project Title: Systematic evaluation of the zoonotic potential of different CWD isolates. Principal Investigator: Rodrigo Morales, PhD.</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;"><a href="https://cjdfoundation.org/sites/default/files/grant-downloads/Final%20Report%20-%20CJD%20Foundation%20-%20Morales.pdf" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://cjdfoundation.org/sites/default/files/grant-downloads/Final%20Report%20-%20CJD%20Foundation%20-%20Morales.pdf</a></div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">Systematic evaluation of the zoonotic potential of different CWD isolates. Rodrigo Morales, PhD Assistant Professor Protein Misfolding Disorders lab Mitchell Center for Alzheimer’s disease and Related Brain Disorders Department of Neurology University of Texas Health Science Center at Houston Washington DC. July 14th, 2018</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">Conclusions and Future Directions • We have developed a highly sensitive and specific CWD-PMCA platform to be used as a diagnostic tool. • Current PMCA set up allow us to mimic relevant prion inter-species transmission events. • Polymorphic changes at position 96 of the prion protein apparently alter strain properties and, consequently, the zoonotic potential of CWD isolates. • Inter-species and inter-polymorphic PrPC → PrPSc conversions further increase the spectrum of CWD isolates possibly present in nature. • CWD prions generated in 96SS PrPC substrate apparently have greater inter-species transmission potentials. • Future experiments will explore the zoonotic potential of CWD prions along different adaptation scenarios, including inter-species and inter-polymorphic.</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;"><a href="https://cjdfoundation.org/files/Conf2018/Rodrigo%20Morales%202018.pdf" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://cjdfoundation.org/files/Conf2018/Rodrigo%20Morales%202018.pdf</a></div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;"><a href="https://www.youtube.com/watch?v=CzQKemJRBlE&list=PLGXRDfDPg57yTYvn6tifH13NrSiLjv1d7&index=7&t=0s" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://www.youtube.com/watch?v=CzQKemJRBlE&list=PLGXRDfDPg57yTYvn6tifH13NrSiLjv1d7&index=7&t=0s</a></div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">Research Project: TRANSMISSION, DIFFERENTIATION, AND PATHOBIOLOGY OF TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES Location: Virus and Prion Research</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">Title: Disease-associated prion protein detected in lymphoid tissues from pigs challenged with the agent of chronic wasting disease </div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">Conclusions: This study demonstrates that PrPSc accumulates in lymphoid tissues from pigs challenged intracranially or orally with the CWD agent, and can be detected as early as 4 months after challenge. CWD-infected pigs rarely develop clinical disease and if they do, they do so after a long incubation period. This raises the possibility that CWD-infected pigs could shed prions into their environment long before they develop clinical disease. Furthermore, lymphoid tissues from CWD-infected pigs could present a potential source of CWD infectivity in the animal and human food chains.</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;"><a href="https://www.ars.usda.gov/research/publications/publication/?seqNo115=337105" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://www.ars.usda.gov/research/publications/publication/?seqNo115=337105</a></div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;"><a href="https://www.ars.usda.gov/research/publications/publication/?seqNo115=326166" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://www.ars.usda.gov/research/publications/publication/?seqNo115=326166</a></div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">Research Project: Pathobiology, Genetics, and Detection of Transmissible Spongiform Encephalopathies Location: Virus and Prion Research</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">Title: The agent of chronic wasting disease from pigs is infectious in transgenic mice expressing human PRNP </div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">Author item MOORE, S - Orise Fellow item Kokemuller, Robyn item WEST-GREENLEE, M - Iowa State University item BALKEMA-BUSCHMANN, ANNE - Friedrich-Loeffler-institut item GROSCHUP, MARTIN - Friedrich-Loeffler-institut item Greenlee, Justin Submitted to: Prion Publication Type: Abstract Only Publication Acceptance Date: 5/10/2018 Publication Date: 5/22/2018 Citation: Moore, S.J., Kokemuller, R.D., West-Greenlee, M.H., Balkema-Buschmann, A., Groschup, M.H., Greenlee, J.J. 2018. The agent of chronic wasting disease from pigs is infectious in transgenic mice expressing human PRNP. Prion 2018, Santiago de Compostela, Spain, May 22-25, 2018. Paper No. WA15, page 44.</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">Interpretive Summary:</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;"> The successful transmission of pig-passaged CWD to Tg40 mice reported here suggests that passage of the CWD agent through pigs results in a change of the transmission characteristics which reduces the transmission barrier of Tg40 mice to the CWD agent. If this biological behavior is recapitulated in the original host species, passage of the CWD agent through pigs could potentially lead to increased pathogenicity of the CWD agent in humans.</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;"><a href="https://www.ars.usda.gov/research/publications/publication/?seqNo115=353091" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://www.ars.usda.gov/research/publications/publication/?seqNo115=353091</a></div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">cwd scrapie pigs oral routes </div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">***> However, at 51 months of incubation or greater, 5 animals were positive by one or more diagnostic methods. Furthermore, positive bioassay results were obtained from all inoculated groups (oral and intracranial; market weight and end of study) suggesting that swine are potential hosts for the agent of scrapie. <*** </div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">>*** Although the current U.S. feed ban is based on keeping tissues from TSE infected cattle from contaminating animal feed, swine rations in the U.S. could contain animal derived components including materials from scrapie infected sheep and goats. These results indicating the susceptibility of pigs to sheep scrapie, coupled with the limitations of the current feed ban, indicates that a revision of the feed ban may be necessary to protect swine production and potentially human health. <*** </div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">***> Results: PrPSc was not detected by EIA and IHC in any RPLNs. All tonsils and MLNs were negative by IHC, though the MLN from one pig in the oral <6 month group was positive by EIA. PrPSc was detected by QuIC in at least one of the lymphoid tissues examined in 5/6 pigs in the intracranial <6 months group, 6/7 intracranial >6 months group, 5/6 pigs in the oral <6 months group, and 4/6 oral >6 months group. Overall, the MLN was positive in 14/19 (74%) of samples examined, the RPLN in 8/18 (44%), and the tonsil in 10/25 (40%). </div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">***> Conclusions: This study demonstrates that PrPSc accumulates in lymphoid tissues from pigs challenged intracranially or orally with the CWD agent, and can be detected as early as 4 months after challenge. CWD-infected pigs rarely develop clinical disease and if they do, they do so after a long incubation period. This raises the possibility that CWD-infected pigs could shed prions into their environment long before they develop clinical disease. Furthermore, lymphoid tissues from CWD-infected pigs could present a potential source of CWD infectivity in the animal and human food chains. </div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;"><a href="https://www.ars.usda.gov/research/publications/publication/?seqNo115=353091" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://www.ars.usda.gov/research/publications/publication/?seqNo115=353091</a></div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;"><a href="https://www.ars.usda.gov/research/project/?accnNo=432011&fy=2017" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://www.ars.usda.gov/research/project/?accnNo=432011&fy=2017</a></div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;"><a href="https://www.ars.usda.gov/research/publications/publication/?seqNo115=337105" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://www.ars.usda.gov/research/publications/publication/?seqNo115=337105</a></div><div><div style="font-size: small;"><br /></div><div style="font-size: small;">Conclusions: This study demonstrates that PrPSc accumulates in lymphoid tissues from pigs challenged intracranially or orally with the CWD agent, and can be detected as early as 4 months after challenge. CWD-infected pigs rarely develop clinical disease and if they do, they do so after a long incubation period. This raises the possibility that CWD-infected pigs could shed prions into their environment long before they develop clinical disease. Furthermore, lymphoid tissues from CWD-infected pigs could present a potential source of CWD infectivity in the animal and human food chains.</div><div style="font-size: small;"><br /></div><div style="font-size: small;"><a href="https://www.ars.usda.gov/research/publications/publication/?seqNo115=337105" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://www.ars.usda.gov/research/publications/publication/?seqNo115=337105</a><br /></div><div style="font-size: small;"><br /></div><div style="font-size: small;">CONFIDENTIAL</div><div style="font-size: small;"><br /></div><div style="font-size: small;"><span style="font-size: 10pt;">EXPERIMENTAL PORCINE SPONGIFORM ENCEPHALOPATHY</span></div><div style="font-size: small;"><span style="font-size: 10pt;"><br /></span></div><div style="font-size: small;"><div style="font-size: 13.3333px;"><div>LINE TO TAKE</div><div><br /></div><div>3. If questions on pharmaceuticals are raised at the Press conference, the suggested line to take is as follows:- </div><div><br /></div><div> "There are no medicinal products licensed for use on the market which make use of UK-derived porcine tissues with which any hypothetical “high risk" ‘might be associated. The results of the recent experimental work at the CSM will be carefully examined by the CSM‘s Working Group on spongiform encephalopathy at its next meeting.</div><div><br /></div><div>DO Hagger RM 1533 MT Ext 3201</div></div><div style="font-size: 10pt;"><br /></div><div style="font-size: 10pt;"><a href="http://web.archive.org/web/20030822054419/www.bseinquiry.gov.uk/files/yb/1990/09/21009001.pdf" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://web.archive.org/web/20030822054419/www.bseinquiry.gov.uk/files/yb/1990/09/21009001.pdf</a></div></div><div style="font-size: small;"><br /></div><div style="font-size: small;"><span style="font-size: 10pt;">While this clearly is a cause for concern we should not jump to the conclusion that this means that pigs will necessarily be infected by bone and meat meal fed by the oral route as is the case with cattle. ...</span></div><div style="font-size: small;"><br /></div><div style="font-size: small;"><span style="font-size: 10pt;"><a href="http://web.archive.org/web/20031026000118/www.bseinquiry.gov.uk/files/yb/1990/08/23004001.pdf" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://web.archive.org/web/20031026000118/www.bseinquiry.gov.uk/files/yb/1990/08/23004001.pdf</a></span></div><div style="font-size: small;"><br /></div><div style="font-size: small;"><span style="font-size: 10pt;">we cannot rule out the possibility that unrecognised subclinical spongiform encephalopathy could be present in British pigs though there is no evidence for this: only with parenteral/implantable pharmaceuticals/devices is the theoretical risk to humans of sufficient concern to consider any action.</span></div><div style="font-size: small;"><br /></div><div style="font-size: small;"><span style="font-size: 10pt;"><a href="http://web.archive.org/web/20030822031154/www.bseinquiry.gov.uk/files/yb/1990/09/10007001.pdf" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://web.archive.org/web/20030822031154/www.bseinquiry.gov.uk/files/yb/1990/09/10007001.pdf</a></span></div><div style="font-size: small;"><br /></div><div style="font-size: small;"><span style="font-size: 10pt;">May I, at the outset, reiterate that we should avoid dissemination of papers relating to this experimental finding to prevent premature release of the information. ...</span></div><div style="font-size: small;"><br /></div><div style="font-size: small;"><span style="font-size: 10pt;"><a href="http://web.archive.org/web/20030822052332/www.bseinquiry.gov.uk/files/yb/1990/09/11005001.pdf" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://web.archive.org/web/20030822052332/www.bseinquiry.gov.uk/files/yb/1990/09/11005001.pdf</a></span></div><div style="font-size: small;"><br /></div><div style="font-size: small;"><span style="font-size: 10pt;">3. It is particularly important that this information is not passed outside the Department, until Ministers have decided how they wish it to be handled. ...</span></div><div style="font-size: small;"><br /></div><div style="font-size: small;"><span style="font-size: 10pt;"><a href="http://web.archive.org/web/20030822052438/www.bseinquiry.gov.uk/files/yb/1990/09/12002001.pdf" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://web.archive.org/web/20030822052438/www.bseinquiry.gov.uk/files/yb/1990/09/12002001.pdf</a></span></div><div style="font-size: small;"><br /></div><div style="font-size: small;"><span style="font-size: 10pt;">But it would be easier for us if pharmaceuticals/devices are not directly mentioned at all. ...</span></div><div style="font-size: small;"><br /></div><div style="font-size: small;"><span style="font-size: 10pt;"><a href="http://web.archive.org/web/20030518170213/www.bseinquiry.gov.uk/files/yb/1990/09/13004001.pdf" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://web.archive.org/web/20030518170213/www.bseinquiry.gov.uk/files/yb/1990/09/13004001.pdf</a></span></div><div style="font-size: small;"><br /></div><div style="font-size: small;"><span style="font-size: 10pt;">Our records show that while some use is made of porcine materials in medicinal products, the only products which would appear to be in a hypothetically ''higher risk'' area are the adrenocorticotrophic hormone for which the source material comes from outside the United Kingdom, namely America China Sweden France and Germany. The products are manufactured by Ferring and Armour. A further product, ''Zenoderm Corium implant'' manufactured by Ethicon, makes use of porcine skin - which is not considered to be a ''high risk'' tissue, but one of its uses is described in the data sheet as ''in dural replacement''. This product is sourced from the United Kingdom.....</span></div><div style="font-size: small;"><br /></div><div style="font-size: small;"><span style="font-size: 10pt;"><a href="http://web.archive.org/web/20030822054419/www.bseinquiry.gov.uk/files/yb/1990/09/21009001.pdf" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://web.archive.org/web/20030822054419/www.bseinquiry.gov.uk/files/yb/1990/09/21009001.pdf</a></span></div><div style="font-size: small;"><br /></div><div style="font-size: small;"><div style="font-size: 13.3333px;"><div>***> cattle, pigs, sheep, cwd, tse, prion, oh my! </div><div><br clear="none" /></div><div>***> In contrast, cattle are highly susceptible to white-tailed deer CWD and mule deer CWD in experimental conditions but no natural CWD infections in cattle have been reported (Sigurdson, 2008; Hamir et al., 2006). </div><div><br clear="none" /></div><div>Sheep and cattle may be exposed to CWD via common grazing areas with affected deer but so far, appear to be poorly susceptible to mule deer CWD (Sigurdson, 2008). In contrast, cattle are highly susceptible to white-tailed deer CWD and mule deer CWD in experimental conditions but no natural CWD infections in cattle have been reported (Sigurdson, 2008; Hamir et al., 2006). It is not known how susceptible humans are to CWD but given that the prion can be present in muscle, it is likely that humans have been exposed to the agent via consumption of venison (Sigurdson, 2008). Initial experimental research suggests that human susceptibility to CWD is low and there may be a robust species barrier for CWD transmission to humans (Sigurdson, 2008), however the risk appetite for a public health threat may still find this level unacceptable. </div><div><br clear="none" /></div><div><a href="https://assets.publishing.service.gov.uk/government/uploads/system/uploads/attachment_data/file/733407/DEFRA_QRA_TSE_in_cervids_June2018_v1.pdf" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://assets.publishing.service.gov.uk/government/uploads/system/uploads/attachment_data/file/733407/DEFRA_QRA_TSE_in_cervids_June2018_v1.pdf</a> </div><div><br clear="none" /></div><div><a href="http://chronic-wasting-disease.blogspot.com/2012/08/susceptibility-of-cattle-to-agent-of.html" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">http://chronic-wasting-disease.blogspot.com/2012/08/susceptibility-of-cattle-to-agent-of.html</a> </div></div><div style="font-size: 13.3333px;"><div style="font-size: 10pt;"><div style="line-height: 1.22em;"><div style="line-height: 1.22em; margin: 0in 0in 0.0001pt;"><div style="background-color: whitesmoke; margin-bottom: 24px;"><div style="margin-bottom: 24px;"><div style="margin-bottom: 24px;"><div style="line-height: 1.22em;"><div style="line-height: 1.22em;"><div style="line-height: 1.22em;"><div dir="ltr" style="background-color: white;"><div style="font-family: Arial, Helvetica, sans-serif; font-size: 12px; letter-spacing: 0px; line-height: 1.6em; margin: 0px 0px 0.75em;"><div style="font-family: arial; font-size: 10pt;"><div style="font-size: small;"><div style="margin: 0px;"><div style="color: #29303b; font-size: 13.3333px;"><div style="font-family: arial, helvetica; font-size: 12px;"><div style="color: black; font-family: arial; font-size: 10pt;"><br clear="none" /></div><div style="color: black; font-family: arial; font-size: 10pt;"><div><span style="font-size: 10pt;">Friday, December 14, 2012 </span></div><div><span style="font-size: 10pt;"><br clear="none" /></span></div><div><span style="font-size: 10pt;">DEFRA U.K. What is the risk of Chronic Wasting Disease CWD being introduced into Great Britain? A Qualitative Risk Assessment October 2012 </span></div><div><span style="font-size: 10pt;"><br clear="none" /></span></div><div><span style="font-size: 10pt;">snip..... </span></div><div><span style="font-size: 10pt;"><br clear="none" /></span></div><div><span style="font-size: 10pt;">In the USA, under the Food and Drug Administration's BSE Feed Regulation (21 CFR 589.2000) most material (exceptions include milk, tallow, and gelatin) from deer and elk is prohibited for use in feed for ruminant animals. With regards to feed for non-ruminant animals, under FDA law, CWD positive deer may not be used for any animal feed or feed ingredients. For elk and deer considered at high risk for CWD, the FDA recommends that these animals do not enter the animal feed system. However, this recommendation is guidance and not a requirement by law. Animals considered at high risk for CWD include: </span></div><div><span style="font-size: 10pt;"><br clear="none" /></span></div><div><span style="font-size: 10pt;">1) animals from areas declared to be endemic for CWD and/or to be CWD eradication zones and </span></div><div><span style="font-size: 10pt;"><br clear="none" /></span></div><div><span style="font-size: 10pt;">2) deer and elk that at some time during the 60-month period prior to slaughter were in a captive herd that contained a CWD-positive animal. </span></div><div><span style="font-size: 10pt;"><br clear="none" /></span></div><div><span style="font-size: 10pt;">Therefore, in the USA, materials from cervids other than CWD positive animals may be used in animal feed and feed ingredients for non-ruminants. </span></div><div><span style="font-size: 10pt;"><br clear="none" /></span></div><div><span style="font-size: 10pt;">The amount of animal PAP that is of deer and/or elk origin imported from the USA to GB can not be determined, however, as it is not specified in TRACES. </span></div><div><span style="font-size: 10pt;"><br clear="none" /></span></div><div><span style="font-size: 10pt;">It may constitute a small percentage of the 8412 kilos of non-fish origin processed animal proteins that were imported from US into GB in 2011. </span></div><div><span style="font-size: 10pt;"><br clear="none" /></span></div><div><span style="font-size: 10pt;">Overall, therefore, it is considered there is a __greater than negligible risk___ that (nonruminant) animal feed and pet food containing deer and/or elk protein is imported into GB. </span></div><div><span style="font-size: 10pt;"><br clear="none" /></span></div><div><span style="font-size: 10pt;">There is uncertainty associated with this estimate given the lack of data on the amount of deer and/or elk protein possibly being imported in these products.</span><span style="font-size: 10pt;"> </span></div><div><span style="font-size: 10pt;"><br clear="none" /></span></div><div><span style="font-size: 10pt;">snip..... </span><br clear="none" /></div><div><span style="font-size: 10pt;"><br clear="none" /></span></div><div><span style="font-size: 10pt;">36% in 2007 (Almberg et al., 2011). In such areas, population declines of deer of up to 30 to 50% have been observed (Almberg et al., 2011). In areas of Colorado, the prevalence can be as high as 30% (EFSA, 2011). The clinical signs of CWD in affected adults are weight loss and behavioural changes that can span weeks or months (Williams, 2005). In addition, signs might include excessive salivation, behavioural alterations including a fixed stare and changes in interaction with other animals in the herd, and an altered stance (Williams, 2005). These signs are indistinguishable from cervids experimentally infected with bovine spongiform encephalopathy (BSE). Given this, if CWD was to be introduced into countries with BSE such as GB, for example, infected deer populations would need to be tested to differentiate if they were infected with CWD or BSE to minimise the risk of BSE entering the human food-chain via affected venison. snip..... The rate of transmission of CWD has been reported to be as high as 30% and can approach 100% among captive animals in endemic areas (Safar et al., 2008). </span></div><div><span style="font-size: 10pt;"><br clear="none" /></span></div><div><span style="font-size: 10pt;">snip..... </span></div><div><span style="font-size: 10pt;"><br clear="none" /></span></div><div><span style="font-size: 10pt;">In summary, in endemic areas, there is a medium probability that the soil and surrounding environment is contaminated with CWD prions and in a bioavailable form. In rural areas where CWD has not been reported and deer are present, there is a greater than negligible risk the soil is contaminated with CWD prion. snip..... In summary, given the volume of tourists, hunters and servicemen moving between GB and North America, the probability of at least one person travelling to/from a CWD affected area and, in doing so, contaminating their clothing, footwear and/or equipment prior to arriving in GB is greater than negligible... For deer hunters, specifically, the risk is likely to be greater given the increased contact with deer and their environment. However, there is significant uncertainty associated with these estimates. </span></div><div><span style="font-size: 10pt;"><br clear="none" /></span></div><div><span style="font-size: 10pt;">snip..... </span></div><div><span style="font-size: 10pt;"><br clear="none" /></span></div><div><span style="font-size: 10pt;">Therefore, it is considered that farmed and park deer may have a higher probability of exposure to CWD transferred to the environment than wild deer given the restricted habitat range and higher frequency of contact with tourists and returning GB residents. </span></div><div><span style="font-size: 10pt;"><br clear="none" /></span></div><div><span style="font-size: 10pt;">s</span><span style="font-size: 10pt;">nip..... </span></div><div><span style="font-size: 10pt;"><br clear="none" /></span></div><div><a href="https://web.archive.org/web/20170404125557/http://webarchive.nationalarchives.gov.uk/20130822084033/http://www.defra.gov.uk/animal-diseases/files/qra_chronic-wasting-disease-121029.pdf" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://web.archive.org/web/20170404125557/http://webarchive.nationalarchives.gov.uk/20130822084033/http://www.defra.gov.uk/animal-diseases/files/qra_chronic-wasting-disease-121029.pdf</a></div><div><br /></div></div></div></div></div></div></div></div></div></div></div></div></div></div></div></div></div></div></div></div><div><div style="font-size: 10pt; line-height: 1.22em;">BSE 589.2001 FEED REGULATIONS ???</div><div style="font-size: 10pt; line-height: 1.22em;"><br /></div><div style="font-size: 10pt; line-height: 1.22em;"><div style="line-height: 1.22em;">10,000,000+ LBS. of PROHIBITED BANNED MAD COW FEED I.E. BLOOD LACED MBM IN COMMERCE USA 2007</div><div style="line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="line-height: 1.22em;">Date: March 21, 2007 at 2:27 pm PST</div><div style="line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="line-height: 1.22em;">RECALLS AND FIELD CORRECTIONS: VETERINARY MEDICINES -- CLASS II</div><div style="line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="line-height: 1.22em;">___________________________________</div><div style="line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="line-height: 1.22em;">PRODUCT</div><div style="line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="line-height: 1.22em;">Bulk cattle feed made with recalled Darling's 85% Blood Meal, Flash Dried, Recall # V-024-2007</div><div style="line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="line-height: 1.22em;">CODE</div><div style="line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="line-height: 1.22em;">Cattle feed delivered between 01/12/2007 and 01/26/2007</div><div style="line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="line-height: 1.22em;">RECALLING FIRM/MANUFACTURER</div><div style="line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="line-height: 1.22em;">Pfeiffer, Arno, Inc, Greenbush, WI. by conversation on February 5, 2007.</div><div style="line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="line-height: 1.22em;">Firm initiated recall is ongoing.</div><div style="line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="line-height: 1.22em;">REASON</div><div style="line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="line-height: 1.22em;">Blood meal used to make cattle feed was recalled because it was cross- contaminated with prohibited bovine meat and bone meal that had been manufactured on common equipment and labeling did not bear cautionary BSE statement.</div><div style="line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="line-height: 1.22em;">VOLUME OF PRODUCT IN COMMERCE</div><div style="line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="line-height: 1.22em;">42,090 lbs.</div><div style="line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="line-height: 1.22em;">DISTRIBUTION</div><div style="line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="line-height: 1.22em;">WI</div><div style="line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="line-height: 1.22em;">___________________________________</div><div style="line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="line-height: 1.22em;">PRODUCT</div><div style="line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="line-height: 1.22em;">Custom dairy premix products: MNM ALL PURPOSE Pellet, HILLSIDE/CDL Prot- Buffer Meal, LEE, M.-CLOSE UP PX Pellet, HIGH DESERT/ GHC LACT Meal, TATARKA, M CUST PROT Meal, SUNRIDGE/CDL PROTEIN Blend, LOURENZO, K PVM DAIRY Meal, DOUBLE B DAIRY/GHC LAC Mineral, WEST PIONT/GHC CLOSEUP Mineral, WEST POINT/GHC LACT Meal, JENKS, J/COMPASS PROTEIN Meal, COPPINI - 8# SPECIAL DAIRY Mix, GULICK, L-LACT Meal (Bulk), TRIPLE J - PROTEIN/LACTATION, ROCK CREEK/GHC MILK Mineral, BETTENCOURT/GHC S.SIDE MK-MN, BETTENCOURT #1/GHC MILK MINR, V&C DAIRY/GHC LACT Meal, VEENSTRA, F/GHC LACT Meal, SMUTNY, A- BYPASS ML W/SMARTA, Recall # V-025-2007</div><div style="line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="line-height: 1.22em;">CODE</div><div style="line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="line-height: 1.22em;">The firm does not utilize a code - only shipping documentation with commodity and weights identified.</div><div style="line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="line-height: 1.22em;">RECALLING FIRM/MANUFACTURER</div><div style="line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="line-height: 1.22em;">Rangen, Inc, Buhl, ID, by letters on February 13 and 14, 2007. Firm initiated recall is complete.</div><div style="line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="line-height: 1.22em;">REASON</div><div style="line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="line-height: 1.22em;">Products manufactured from bulk feed containing blood meal that was cross contaminated with prohibited meat and bone meal and the labeling did not bear cautionary BSE statement.</div><div style="line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="line-height: 1.22em;">VOLUME OF PRODUCT IN COMMERCE</div><div style="line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="line-height: 1.22em;">9,997,976 lbs.</div><div style="line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="line-height: 1.22em;">DISTRIBUTION</div><div style="line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="line-height: 1.22em;">ID and NV</div><div style="line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="line-height: 1.22em;">END OF ENFORCEMENT REPORT FOR MARCH 21, 2007</div><div style="line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="line-height: 1.22em;"><a href="http://www.fda.gov/Safety/Recalls/EnforcementReports/2007/ucm120446.htm" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">http://www.fda.gov/Safety/Recalls/EnforcementReports/2007/ucm120446.htm</a></div></div><div style="font-size: 10pt; line-height: 1.22em;"><span style="color: #29303b; font-size: x-small; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-size: 10pt; line-height: 1.22em;"><span style="color: #29303b; font-size: x-small; line-height: 1.22em;"></span><div style="line-height: 1.22em;">BANNED MAD COW FEED IN COMMERCE IN ALABAMA </div><div style="line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="line-height: 1.22em;"> Date: September 6, 2006 at 7:58 am PST PRODUCT</div><div style="line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="line-height: 1.22em;">a) EVSRC Custom dairy feed, Recall # V-130-6;</div><div style="line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="line-height: 1.22em;">b) Performance Chick Starter, Recall # V-131-6;</div><div style="line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="line-height: 1.22em;">c) Performance Quail Grower, Recall # V-132-6;</div><div style="line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="line-height: 1.22em;">d) Performance Pheasant Finisher, Recall # V-133-6.</div><div style="line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="line-height: 1.22em;">CODE None RECALLING FIRM/MANUFACTURER Donaldson & Hasenbein/dba J&R Feed Service, Inc., Cullman, AL, by telephone on June 23, 2006 and by letter dated July 19, 2006. Firm initiated recall is complete.</div><div style="line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="line-height: 1.22em;">REASON</div><div style="line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="line-height: 1.22em;">Dairy and poultry feeds were possibly contaminated with ruminant based protein.</div><div style="line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="line-height: 1.22em;">VOLUME OF PRODUCT IN COMMERCE 477.72 tons</div><div style="line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="line-height: 1.22em;">DISTRIBUTION AL</div><div style="line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="line-height: 1.22em;">______________________________</div><div style="line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="line-height: 1.22em;"><a href="http://www.fda.gov/bbs/topics/enforce/2006/ENF00968.html" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">http://www.fda.gov/bbs/topics/enforce/2006/ENF00968.html</a> </div><div style="line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="line-height: 1.22em;">PRODUCT Bulk custom dairy pre-mixes,</div><div style="line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="line-height: 1.22em;">Recall # V-120-6 CODE None RECALLING FIRM/MANUFACTURER Ware Milling Inc., Houston, MS, by telephone on June 23, 2006. Firm initiated recall is complete. REASON Possible contamination of dairy animal feeds with ruminant derived meat and bone meal.</div><div style="line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="line-height: 1.22em;">VOLUME OF PRODUCT IN COMMERCE 350 tons</div><div style="line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="line-height: 1.22em;">DISTRIBUTION AL and MS</div><div style="line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="line-height: 1.22em;">______________________________</div><div style="line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="line-height: 1.22em;">PRODUCT</div><div style="line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="line-height: 1.22em;">a) Tucker Milling, LLC Tm 32% Sinking Fish Grower, #2680-Pellet, 50 lb.. bags, Recall # V-121-6;</div><div style="line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="line-height: 1.22em;">b) Tucker Milling, LLC #31120, Game Bird Breeder Pellet, 50 lb. bags, Recall # V-122-6;</div><div style="line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="line-height: 1.22em;">c) Tucker Milling, LLC #31232 Game Bird Grower, 50 lb. bags, Recall # V-123-6;</div><div style="line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="line-height: 1.22em;">d) Tucker Milling, LLC 31227-Crumble, Game Bird Starter, BMD Medicated, 50 lb bags, Recall # V-124-6;</div><div style="line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="line-height: 1.22em;">e) Tucker Milling, LLC #31120, Game Bird Breeder, 50 lb bags, Recall # V-125-6;</div><div style="line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="line-height: 1.22em;">f) Tucker Milling, LLC #30230, 30 % Turkey Starter, 50 lb bags, Recall # V-126-6;</div><div style="line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="line-height: 1.22em;">g) Tucker Milling, LLC #30116, TM Broiler Finisher, 50 lb bags, Recall # V-127-6</div><div style="line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="line-height: 1.22em;">CODE All products manufactured from 02/01/2005 until 06/20/2006 RECALLING FIRM/MANUFACTURER Recalling Firm: Tucker Milling LLC, Guntersville, AL, by telephone and visit on June 20, 2006, and by letter on June 23, 2006. Manufacturer: H. J. Baker and Brothers Inc., Stamford, CT. Firm initiated recall is ongoing.</div><div style="line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="line-height: 1.22em;">REASON Poultry and fish feeds which were possibly contaminated with ruminant based protein were not labeled as "Do not feed to ruminants".</div><div style="line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="line-height: 1.22em;">VOLUME OF PRODUCT IN COMMERCE 7,541-50 lb bags</div><div style="line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="line-height: 1.22em;">DISTRIBUTION AL, GA, MS, and TN</div><div style="line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="line-height: 1.22em;">END OF ENFORCEMENT REPORT FOR AUGUST 9, 2006</div><div style="line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="line-height: 1.22em;">###</div><div style="line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="line-height: 1.22em;"><a href="http://www.fda.gov/bbs/topics/ENFORCE/2006/ENF00964.html" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">http://www.fda.gov/bbs/topics/ENFORCE/2006/ENF00964.html</a> </div><div style="line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="line-height: 1.22em;">Subject: MAD COW FEED RECALL AL AND FL VOLUME OF PRODUCT IN COMMERCE 125 TONS Products manufactured from 02/01/2005 until 06/06/2006</div><div style="line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="line-height: 1.22em;">Date: August 6, 2006 at 6:16 pm PST PRODUCT</div><div style="line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="line-height: 1.22em;">a) CO-OP 32% Sinking Catfish, Recall # V-100-6;</div><div style="line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="line-height: 1.22em;">b) Performance Sheep Pell W/Decox/A/N, medicated, net wt. 50 lbs, Recall # V-101-6;</div><div style="line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="line-height: 1.22em;">c) Pro 40% Swine Conc Meal -- 50 lb, Recall # V-102-6;</div><div style="line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="line-height: 1.22em;">d) CO-OP 32% Sinking Catfish Food Medicated, Recall # V-103-6;</div><div style="line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="line-height: 1.22em;">e) "Big Jim's" BBB Deer Ration, Big Buck Blend, Recall # V-104-6;</div><div style="line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="line-height: 1.22em;">f) CO-OP 40% Hog Supplement Medicated Pelleted, Tylosin 100 grams/ton, 50 lb. bag, Recall # V-105-6;</div><div style="line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="line-height: 1.22em;">g) Pig Starter Pell II, 18% W/MCDX Medicated 282020, Carbadox -- 0.0055%, Recall # V-106-6;</div><div style="line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="line-height: 1.22em;">h) CO-OP STARTER-GROWER CRUMBLES, Complete Feed for Chickens from Hatch to 20 Weeks, Medicated, Bacitracin Methylene Disalicylate, 25 and 50 Lbs, Recall # V-107-6;</div><div style="line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="line-height: 1.22em;">i) CO-OP LAYING PELLETS, Complete Feed for Laying Chickens, Recall # 108-6;</div><div style="line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="line-height: 1.22em;">j) CO-OP LAYING CRUMBLES, Recall # V-109-6;</div><div style="line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="line-height: 1.22em;">k) CO-OP QUAIL FLIGHT CONDITIONER MEDICATED, net wt 50 Lbs, Recall # V-110-6;</div><div style="line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="line-height: 1.22em;">l) CO-OP QUAIL STARTER MEDICATED, Net Wt. 50 Lbs, Recall # V-111-6;</div><div style="line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="line-height: 1.22em;">m) CO-OP QUAIL GROWER MEDICATED, 50 Lbs, Recall # V-112-6 CODE</div><div style="line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="line-height: 1.22em;">Product manufactured from 02/01/2005 until 06/06/2006</div><div style="line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="line-height: 1.22em;">RECALLING FIRM/MANUFACTURER Alabama Farmers Cooperative, Inc., Decatur, AL, by telephone, fax, email and visit on June 9, 2006. FDA initiated recall is complete.</div><div style="line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="line-height: 1.22em;">REASON Animal and fish feeds which were possibly contaminated with ruminant based protein not labeled as "Do not feed to ruminants".</div><div style="line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="line-height: 1.22em;">VOLUME OF PRODUCT IN COMMERCE 125 tons</div><div style="line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="line-height: 1.22em;">DISTRIBUTION AL and FL</div><div style="line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="line-height: 1.22em;">END OF ENFORCEMENT REPORT FOR AUGUST 2, 2006</div><div style="line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="line-height: 1.22em;">###</div><div style="line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="line-height: 1.22em;"><a href="http://www.fda.gov/bbs/topics/enforce/2006/ENF00963.html" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">http://www.fda.gov/bbs/topics/enforce/2006/ENF00963.html</a> </div><div style="line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="line-height: 1.22em;">MAD COW FEED RECALL USA EQUALS 10,878.06 TONS NATIONWIDE Sun Jul 16, 2006 09:22 71.248.128.67</div><div style="line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="line-height: 1.22em;">RECALLS AND FIELD CORRECTIONS: VETERINARY MEDICINE -- CLASS II</div><div style="line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="line-height: 1.22em;">______________________________</div><div style="line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="line-height: 1.22em;">PRODUCT</div><div style="line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="line-height: 1.22em;">a) PRO-LAK, bulk weight, Protein Concentrate for Lactating Dairy Animals, Recall # V-079-6;</div><div style="line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="line-height: 1.22em;">b) ProAmino II, FOR PREFRESH AND LACTATING COWS, net weight 50lb (22.6 kg), Recall # V-080-6;</div><div style="line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="line-height: 1.22em;">c) PRO-PAK, MARINE & ANIMAL PROTEIN CONCENTRATE FOR USE IN ANIMAL FEED, Recall # V-081-6;</div><div style="line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="line-height: 1.22em;">d) Feather Meal, Recall # V-082-6 CODE</div><div style="line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="line-height: 1.22em;">a) Bulk</div><div style="line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="line-height: 1.22em;">b) None</div><div style="line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="line-height: 1.22em;">c) Bulk</div><div style="line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="line-height: 1.22em;">d) Bulk</div><div style="line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="line-height: 1.22em;">RECALLING FIRM/MANUFACTURER H. J. Baker & Bro., Inc., Albertville, AL, by telephone on June 15, 2006 and by press release on June 16, 2006. Firm initiated recall is ongoing.</div><div style="line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="line-height: 1.22em;">REASON</div><div style="line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="line-height: 1.22em;">Possible contamination of animal feeds with ruminent derived meat and bone meal.</div><div style="line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="line-height: 1.22em;">VOLUME OF PRODUCT IN COMMERCE 10,878.06 tons</div><div style="line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="line-height: 1.22em;">DISTRIBUTION Nationwide</div><div style="line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="line-height: 1.22em;">END OF ENFORCEMENT REPORT FOR July 12, 2006</div><div style="line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="line-height: 1.22em;">###</div><div style="line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="line-height: 1.22em;"><a href="http://www.fda.gov/bbs/topics/enforce/2006/ENF00960.html" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">http://www.fda.gov/bbs/topics/enforce/2006/ENF00960.html</a> </div><div style="line-height: 1.22em;"><br /></div><div style="line-height: 1.22em;"><div><span style="font-size: x-small;">TUESDAY, AUGUST 17, 2021 </span></div><div><span style="font-size: x-small;"><br /></span></div><div><span style="font-size: x-small;">EU Feed ban Commission authorises use of certain animal proteins, risk another mad cow type outbreak</span><br /></div><div><span style="font-size: x-small;"><br /></span></div><div><span style="font-size: x-small;"><a href="https://efsaopinionbseanimalprotein.blogspot.com/2021/08/eu-feed-ban-commission-authorises-use.html" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://efsaopinionbseanimalprotein.blogspot.com/2021/08/eu-feed-ban-commission-authorises-use.html</a></span></div></div></div><div style="font-size: 10pt; line-height: 1.22em;"><span style="color: #29303b; font-size: x-small; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-size: 10pt; line-height: 1.22em;"><span style="color: #29303b; font-size: x-small; line-height: 1.22em;">Saturday, August 14, 2010</span></div><div style="font-size: 10pt; line-height: 1.22em;"><span style="color: #29303b; font-size: x-small; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-size: 10pt; line-height: 1.22em;"><span style="color: #29303b; font-size: x-small; line-height: 1.22em;">BSE Case Associated with Prion Protein Gene Mutation (g-h-BSEalabama) and VPSPr PRIONPATHY</span></div><div style="font-size: 10pt; line-height: 1.22em;"><span style="color: #29303b; font-size: x-small; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-size: 10pt; line-height: 1.22em;"><span style="color: #29303b; font-size: x-small; line-height: 1.22em;">(see mad cow feed in COMMERCE IN ALABAMA...TSS)</span></div><div style="font-size: 10pt; line-height: 1.22em;"><span style="color: #29303b; font-size: x-small; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-size: 10pt; line-height: 1.22em;"><a href="http://prionpathy.blogspot.com/2010/08/bse-case-associated-with-prion-protein.html" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">http://prionpathy.blogspot.com/2010/08/bse-case-associated-with-prion-protein.html</a><br clear="none" style="line-height: 1.22em;" /></div><div style="font-size: 10pt; line-height: 1.22em;"><span style="color: #29303b; font-size: x-small; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-size: 10pt; line-height: 1.22em;"><span style="color: #29303b; font-size: x-small; line-height: 1.22em;">2009 UPDATE ON ALABAMA AND TEXAS MAD COWS 2005 and 2006</span></div><div style="font-size: 10pt; line-height: 1.22em;"><span style="color: #29303b; font-size: x-small; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-size: 10pt; line-height: 1.22em;"><a href="http://bse-atypical.blogspot.com/2006/08/bse-atypical-texas-and-alabama-update.html" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">http://bse-atypical.blogspot.com/2006/08/bse-atypical-texas-and-alabama-update.html</a><br clear="none" style="line-height: 1.22em;" /></div><div style="font-size: 10pt; line-height: 1.22em;"><br /></div><div style="font-size: 10pt; line-height: 1.22em;"><div style="font-family: Helvetica, Arial, sans-serif;"><h2 class="yiv9562913344date-header" style="font-weight: normal; margin: 0px; padding: 0px;"><span style="font-size: small;"><span style="background-color: rgba(255, 255, 255, 0);">WEDNESDAY, DECEMBER 23, 2020</span></span></h2><div><span style="font-size: small;"><span style="background-color: rgba(255, 255, 255, 0);"><br /></span></span></div><div class="yiv9562913344date-posts"><div class="yiv9562913344post-outer"><div class="yiv9562913344post yiv9562913344hentry yiv9562913344uncustomized-post-template" style="margin: 8px 0px 24px;"><span style="color: black;"><span style="background-color: rgba(255, 255, 255, 0);"><a name="3781343997501907466" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer; text-decoration-line: underline;"></a></span></span><h3 class="yiv9562913344post-title yiv9562913344entry-title" itemprop="name" style="font-weight: normal; margin: 0px; padding: 0px;"><span style="font-size: small;"><span style="background-color: rgba(255, 255, 255, 0);">BSE research project final report 2005 to 2008 SE1796 SID5</span></span></h3></div></div></div></div><div style="font-family: Helvetica, Arial, sans-serif;"><div style="font-stretch: normal; line-height: normal;"><span lang="EN-GB" style="background-color: rgba(255, 255, 255, 0);">***>As a result, using more sensitive diagnostic assays, we were able to diagnose BSE positive cattle from the years 1997-1999 inclusive that were originally negative by vacuolation. From these data we have estimated that approximately 3% of the total suspect cases submitted up until the year 1999 were mis-diagnosed. <br /></span></div><div style="font-stretch: normal; line-height: normal;"><span lang="EN-GB" style="background-color: rgba(255, 255, 255, 0);"><br /></span></div><div style="font-stretch: normal; line-height: normal;"><span lang="EN-GB" style="background-color: rgba(255, 255, 255, 0);">YOU know, Confucius is confused again LOL, i seem to have remembered something in line with this here in the USA...</span></div></div><div style="font-family: Helvetica, Arial, sans-serif; font-stretch: normal; line-height: normal;"><span lang="EN-GB" style="background-color: rgba(255, 255, 255, 0);"><br /></span></div><a href="http://bovineprp.blogspot.com/2020/12/bse-research-project-final-report-2005.html" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer; font-family: Helvetica, Arial, sans-serif;" target="_blank">http://bovineprp.blogspot.com/2020/12/bse-research-project-final-report-2005.html</a><br /></div><div style="font-size: 10pt; line-height: 1.22em;"><span style="color: #29303b; font-size: x-small; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="line-height: 1.22em;"><div style="font-size: 10pt; line-height: 1.22em;">***> Wednesday, January 23, 2019 </div><div style="font-size: 10pt; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="font-size: 10pt; line-height: 1.22em;">***> CFIA SFCR Guidance on Specified risk material (SRM) came into force on January 15, 2019 <***</div><div style="font-size: 10pt; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="font-size: 10pt; line-height: 1.22em;"><a href="https://specifiedriskmaterial.blogspot.com/2019/01/cfia-sfcr-guidance-on-specified-risk.html" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">https://specifiedriskmaterial.blogspot.com/2019/01/cfia-sfcr-guidance-on-specified-risk.html</a></div><div style="font-size: 10pt; line-height: 1.22em;"><br /></div><div style="line-height: 1.22em;"><div style="font-size: 10pt;">TUESDAY, JANUARY 5, 2021 </div><div style="font-size: 10pt;"><br /></div><div style="font-size: 10pt;">Exploration of genetic factors resulting in abnormal disease in cattle experimentally challenged with bovine spongiform encephalopathy<br /></div><div style="font-size: 10pt;"><br /></div><div style="font-size: 10pt;"><a href="https://bovineprp.blogspot.com/2021/01/exploration-of-genetic-factors.html" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://bovineprp.blogspot.com/2021/01/exploration-of-genetic-factors.html</a></div><div style="font-size: 10pt;"><br /></div><div><div style="font-size: 10pt;">*** Singeltary reply ; Molecular, Biochemical and Genetic Characteristics of BSE in Canada Singeltary reply ;</div><div style="font-size: 10pt;"><br /></div><div style="font-size: 10pt;"><a href="https://journals.plos.org/plosone/article/comment?id=10.1371/annotation/4f9be886-69fe-4c7c-922b-85b0ecbe6d53" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://journals.plos.org/plosone/article/comment?id=10.1371/annotation/4f9be886-69fe-4c7c-922b-85b0ecbe6d53</a><br /></div><div style="font-size: 10pt;"><br /></div><div style="font-size: 10pt;">IBNC Tauopathy or TSE Prion disease, it appears, no one is sure </div><div style="font-size: 10pt;"><br /></div><div style="font-size: 10pt;">Terry S. Singeltary Sr., 03 Jul 2015 at 16:53 GMT</div><div style="font-size: 10pt;"><br /></div><div style="font-size: 10pt;"><div style="color: #29303b; font-family: arial, helvetica; font-size: small; line-height: 1.22em;"><div style="line-height: 1.22em;"><div style="font-size: 10pt; line-height: 1.22em;"><div style="font-size: 10pt; line-height: 1.22em;"><div style="font-family: arial; font-size: small; line-height: 1.22em;"><div style="font-family: arial, helvetica; font-size: 10pt; line-height: 1.22em;"><div style="line-height: 1.22em;"><em style="color: #333333; font-family: arial; font-size: 13px; line-height: 1.22em;">PLOS ONE Journal </em></div></div></div></div></div></div></div><div style="line-height: 1.22em;"><div id="yiv2254009208aolmail_aolmail_AOLMsgPart_2_231efb16-bece-4be2-9555-8828489cb794" style="line-height: 1.22em;"><div class="yiv2254009208aolmail_aolmail_aolReplacedBody" style="line-height: 1.22em;"><div id="yiv2254009208aolmail_aolmail_aolmail_AOLMsgPart_2_076c3e68-3f1c-492a-b84c-fa586eb49e44" style="line-height: 1.22em;"><div class="yiv2254009208aolmail_aolmail_aolmail_aolReplacedBody" style="line-height: 1.22em;"><div id="yiv2254009208aolmail_aolmail_aolmail_aolmail_AOLMsgPart_2_314a32af-6aac-473d-8dc2-78ba9131e347" style="line-height: 1.22em;"><div class="yiv2254009208aolmail_aolmail_aolmail_aolmail_aolReplacedBody" style="line-height: 1.22em;"><div id="yiv2254009208aolmail_aolmail_aolmail_aolmail_aolmail_AOLMsgPart_2_162e08c0-024f-424d-bebb-66f89d627450" style="line-height: 1.22em;"><div class="yiv2254009208aolmail_aolmail_aolmail_aolmail_aolmail_aolReplacedBody" style="line-height: 1.22em;"><div id="yiv2254009208aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_AOLMsgPart_2_55d0d5c6-e95d-4ef2-81fc-d72be9f7a63c" style="line-height: 1.22em;"><div class="yiv2254009208aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolReplacedBody" style="line-height: 1.22em;"><div id="yiv2254009208aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_AOLMsgPart_2_268b3d40-d03f-4bd8-817c-0b0a21454b9b" style="line-height: 1.22em;"><div class="yiv2254009208aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolReplacedBody" style="line-height: 1.22em;"><div style="line-height: 1.22em;"><div style="line-height: 1.22em;"><div style="color: #29303b; font-family: arial, helvetica; font-size: x-small; line-height: 1.22em;"><span style="font-family: Georgia; line-height: 1.22em;"><span style="font-size: 13px; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></span></div><div style="color: #29303b; font-family: arial, helvetica; font-size: x-small; line-height: 1.22em;"><span style="font-family: Georgia; line-height: 1.22em;"><span style="font-size: 13px; line-height: 1.22em;">IBNC Tauopathy or TSE Prion disease, it appears, no one is sure </span></span></div><div style="color: #29303b; font-family: arial, helvetica; font-size: x-small; line-height: 1.22em;"><span style="font-family: Georgia; line-height: 1.22em;"><span style="font-size: 13px; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></span></div><div style="color: #29303b; font-family: arial, helvetica; font-size: x-small; line-height: 1.22em;"><span style="font-family: Georgia; line-height: 1.22em;"><span style="font-size: 13px; line-height: 1.22em;">Terry S. Singeltary Sr., 03 Jul 2015 at 16:53 GMT</span></span></div><div style="color: #29303b; font-family: Georgia; font-size: 13px; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="color: #29303b; font-family: Georgia; font-size: 13px; line-height: 1.22em;">***however in 1 C-type challenged animal, Prion 2015 Poster Abstracts S67 PrPsc was not detected using rapid tests for BSE.<br clear="none" style="line-height: 1.22em;" /><br clear="none" style="line-height: 1.22em;" />***Subsequent testing resulted in the detection of pathologic lesion in unusual brain location and PrPsc detection by PMCA only.<br clear="none" style="line-height: 1.22em;" /><br clear="none" style="line-height: 1.22em;" />*** IBNC Tauopathy or TSE Prion disease, it appears, no one is sure ***<br /></div></div></div></div></div></div></div></div></div></div></div></div></div></div></div></div></div><div style="font-size: 10pt;"><br /></div><div style="font-size: 10pt;"><a href="https://journals.plos.org/plosone/article/comment?id=10.1371/annotation/5adef4ac-a7e4-46a4-8806-c8533d5c862c" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://journals.plos.org/plosone/article/comment?id=10.1371/annotation/5adef4ac-a7e4-46a4-8806-c8533d5c862c</a><br /></div><div style="font-size: 10pt;"><br /></div><div style="font-size: 10pt;"><div style="font-size: 10pt;"><span style="background-color: transparent; font-size: 10pt;">***> CHRONIC WASTING DISEASE TSE PRP HUMANS ZOONOSIS ZOONOTIC <***</span><br clear="none" /></div><div style="font-size: 10pt;"><div style="font-family: Helvetica; font-size: 12px; font-stretch: normal; line-height: normal; margin: 0px;"><br clear="none" /></div><div>WHAT WE HAVE HERE, IS A LACK OF COMMUNICATION!</div><div><br clear="none" /></div><div>seems to me we might have another zoonotic tse prion disease, OR multiple new tse prion zoonotic diseases, that no one wants to talk about, and that's bad...terry</div><div><br clear="none" /></div><div>i thought i might share some news about cwd zoonosis that i got, that i cannot share or post to the public yet, i promised for various reasons, one that it will cause a shit storm for sure, but it was something i really already knew from previous studies, but, i was told that ;<div><br clear="none" /></div><div>==================<br clear="none" /><div><br clear="none" /></div><div><span face="Arial, Helvetica, sans-serif" style="font-size: 12px;">''As you can imagine, 2 and 5 (especially 5) may raise alarms. The evidence we have for 4 are not as strong or tight as I would like to have. At this point, please do not post any of the points publicly yet, but you can refer to points 1-3 in private discussions and all 5 points when discussing with relevant public officials to highlight the long-term risks of CWD zoonosis.''</span><br clear="none" /></div><div><span face="Arial, Helvetica, sans-serif" style="font-size: 12px;"><br clear="none" /></span></div><div><span face="Arial, Helvetica, sans-serif" style="font-size: 12px;">====================</span></div><div><span face="Arial, Helvetica, sans-serif" style="font-size: 12px;"><br clear="none" /></span></div><div><span face="Arial, Helvetica, sans-serif"><span style="font-size: 12px;">so, i figure your as about as official as it gets, and i think this science is extremely important for you to know and to converse about with your officials. it's about to burn a whole in my pocket. this is about as close as it will ever get for cwd zoonosis to be proven in my time, this and what Canada Czub et al found with the Macaques, plus an old study from cjd surveillance unit back that showed cjd and a 9% increase in risk from folks that eat venison, i will post all this below for your files Sir. i remember back in the BSE nvCJD days, from when the first BSE case in bovine was confirmed around 1984 maybe 83, i forget the good vets named that screwed it up first, Carol something, but from 83ish to 95 96 when nvCJD was linked to humans from BSE in cattle, so that took 10 to 15 years. hell, at that rate, especially with Texas and cwd zoonsis, hell, i'll be dead before it's official, if ever, so here ya go Sir. there was a grant study on cwd zoonosis that had been going on for some time, i followed it over the years, then the grant date for said study had expired, so, i thought i would write the good Professor about said study i.e. Professor Kong, CWRU et al. i will post the grant study abstract first, and then after that, what reply i got back, about said study that i was told not to post/publish...</span></span></div><div><span face="Arial, Helvetica, sans-serif"><span style="font-size: 12px;"><br clear="none" /></span></span></div><div><span face="Arial, Helvetica, sans-serif"><span style="font-size: 12px;">CWD ZOONOSIS GRANT FIRST;</span></span></div><div><span face="Arial, Helvetica, sans-serif"><span style="font-size: 12px;"><br clear="none" /></span></span></div><div><span face="Arial, Helvetica, sans-serif"><span style="font-size: 12px;">===============</span></span></div><div><span face="Arial, Helvetica, sans-serif"><span style="font-size: 12px;"><br clear="none" /></span></span></div><div><span face="Arial, Helvetica, sans-serif"><span style="font-size: 12px;"></span></span><div>Cervid to human prion transmission</div><div><br clear="none" /></div><div>Kong, Qingzhong </div><div><br clear="none" /></div><div>Case Western Reserve University, Cleveland, OH, United States</div><div><br clear="none" /></div><div> Abstract Prion disease is transmissible and invariably fatal. Chronic wasting disease (CWD) is the prion disease affecting deer, elk and moose, and it is a widespread and expanding epidemic affecting 22 US States and 2 Canadian provinces so far. CWD poses the most serious zoonotic prion transmission risks in North America because of huge venison consumption (>6 million deer/elk hunted and consumed annually in the USA alone), significant prion infectivity in muscles and other tissues/fluids from CWD-affected cervids, and usually high levels of individual exposure to CWD resulting from consumption of the affected animal among often just family and friends. However, we still do not know whether CWD prions can infect humans in the brain or peripheral tissues or whether clinical/asymptomatic CWD zoonosis has already occurred, and we have no essays to reliably detect CWD infection in humans. We hypothesize that: (1) The classic CWD prion strain can infect humans at low levels in the brain and peripheral lymphoid tissues; (2) The cervid-to-human transmission barrier is dependent on the cervid prion strain and influenced by the host (human) prion protein (PrP) primary sequence; (3) Reliable essays can be established to detect CWD infection in humans; and (4) CWD transmission to humans has already occurred. We will test these hypotheses in 4 Aims using transgenic (Tg) mouse models and complementary in vitro approaches. </div><div><br clear="none" /></div><div>Aim 1 will prove that the classical CWD strain may infect humans in brain or peripheral lymphoid tissues at low levels by conducting systemic bioassays in a set of humanized Tg mouse lines expressing common human PrP variants using a number of CWD isolates at varying doses and routes. Experimental human CWD samples will also be generated for Aim 3. </div><div><br clear="none" /></div><div>Aim 2 will test the hypothesis that the cervid-to-human prion transmission barrier is dependent on prion strain and influenced by the host (human) PrP sequence by examining and comparing the transmission efficiency and phenotypes of several atypical/unusual CWD isolates/strains as well as a few prion strains from other species that have adapted to cervid PrP sequence, utilizing the same panel of humanized Tg mouse lines as in Aim 1. </div><div><br clear="none" /></div><div>Aim 3 will establish reliable essays for detection and surveillance of CWD infection in humans by examining in details the clinical, pathological, biochemical and in vitro seeding properties of existing and future experimental human CWD samples generated from Aims 1-2 and compare them with those of common sporadic human Creutzfeldt-Jakob disease (sCJD) prions. </div><div><br clear="none" /></div><div>Aim 4 will attempt to detect clinical CWD-affected human cases by examining a significant number of brain samples from prion-affected human subjects in the USA and Canada who have consumed venison from CWD-endemic areas utilizing the criteria and essays established in Aim 3. The findings from this proposal will greatly advance our understandings on the potential and characteristics of cervid prion transmission in humans, establish reliable essays for CWD zoonosis and potentially discover the first case(s) of CWD infection in humans.</div><div><br clear="none" /></div><div>Public Health Relevance There are significant and increasing human exposure to cervid prions because chronic wasting disease (CWD, a widespread and highly infectious prion disease among deer and elk in North America) continues spreading and consumption of venison remains popular, but our understanding on cervid-to-human prion transmission is still very limited, raising public health concerns. This proposal aims to define the zoonotic risks of cervid prions and set up and apply essays to detect CWD zoonosis using mouse models and in vitro methods. The findings will greatly expand our knowledge on the potentials and characteristics of cervid prion transmission in humans, establish reliable essays for such infections and may discover the first case(s) of CWD infection in humans.</div><div><br clear="none" /></div><div> Funding Agency Agency National Institute of Health (NIH) Institute National Institute of Neurological Disorders and Stroke (NINDS) Type Research Project (R01) Project # 1R01NS088604-01A1 Application # 9037884 Study Section Cellular and Molecular Biology of Neurodegeneration Study Section (CMND) Program Officer Wong, May Project Start 2015-09-30 Project End 2019-07-31 Budget Start 2015-09-30 Budget End 2016-07-31 Support Year 1 Fiscal Year 2015 Total Cost $337,507 Indirect Cost $118,756</div><div><br clear="none" /></div><div>snip... </div><div><br clear="none" /></div><div><a href="https://grantome.com/grant/NIH/R01-NS088604-01A1#panel-abstract" rel="nofollow noopener noreferrer" shape="rect" style="color: #0563c1; cursor: pointer;" target="_blank">https://grantome.com/grant/NIH/R01-NS088604-01A1#panel-abstract</a><br clear="none" /></div><div><br clear="none" /></div><div>Professor Kongs reply to me just this month about above grant study that has NOT been published in peer reveiw yet...</div><div><br clear="none" /></div><div>=================================</div><div><br clear="none" /></div><div><div dir="ltr"><div dir="ltr"><div>Here is a brief summary of our findings:</div><div><br clear="none" /></div><div>snip...can't post, made a promise...tss</div></div><br clear="none" /></div><div class="yiv1670726472yqt0436007372" id="yiv1670726472yqt66981"><div class="yiv1670726472gmail_quote"><div class="yiv1670726472gmail_attr" dir="ltr">On Sat, Apr 3, 2021 at 12:19 PM Terry Singeltary <<a href="mailto:flounder9@verizon.net" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank" ymailto="mailto:flounder9@verizon.net">flounder9@verizon.net</a>> wrote:</div><div class="yiv1670726472gmail_attr" dir="ltr"><br clear="none" /></div><div class="yiv1670726472gmail_attr" dir="ltr">snip...</div><div class="yiv1670726472gmail_attr" dir="ltr"><br clear="none" /></div><div class="yiv1670726472gmail_attr" dir="ltr">end...tss</div><div class="yiv1670726472gmail_attr" dir="ltr"><br clear="none" /></div><div class="yiv1670726472gmail_attr" dir="ltr">==============</div></div></div></div><div><br clear="none" /></div></div><div>CWD ZOONOSIS THE FULL MONTY TO DATE</div><div><div><br clear="none" /></div><div><div style="font-size: 10pt;"><div style="font-size: 10pt;">International Conference on Emerging Diseases, Outbreaks & Case Studies & 16th Annual Meeting on Influenza March 28-29, 2018 | Orlando, USA</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">Qingzhong Kong</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">Case Western Reserve University School of Medicine, USA</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">Zoonotic potential of chronic wasting disease prions from cervids</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">Chronic wasting disease (CWD) is the prion disease in cervids (mule deer, white-tailed deer, American elk, moose, and reindeer). It has become an epidemic in North America, and it has been detected in the Europe (Norway) since 2016. The widespread CWD and popular hunting and consumption of cervid meat and other products raise serious public health concerns, but questions remain on human susceptibility to CWD prions, especially on the potential difference in zoonotic potential among the various CWD prion strains. We have been working to address this critical question for well over a decade. We used CWD samples from various cervid species to inoculate transgenic mice expressing human or elk prion protein (PrP). We found infectious prions in the spleen or brain in a small fraction of CWD-inoculated transgenic mice expressing human PrP, indicating that humans are not completely resistant to CWD prions; this finding has significant ramifications on the public health impact of CWD prions. The influence of cervid PrP polymorphisms, the prion strain dependence of CWD-to-human transmission barrier, and the characterization of experimental human CWD prions will be discussed.</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">Speaker Biography Qingzhong Kong has completed his PhD from the University of Massachusetts at Amherst and Post-doctoral studies at Yale University. He is currently an Associate Professor of Pathology, Neurology and Regenerative Medicine. He has published over 50 original research papers in reputable journals (including Science Translational Medicine, JCI, PNAS and Cell Reports) and has been serving as an Editorial Board Member on seven scientific journals. He has multiple research interests, including public health risks of animal prions (CWD of cervids and atypical BSE of cattle), animal modeling of human prion diseases, mechanisms of prion replication and pathogenesis, etiology of sporadic Creutzfeldt-Jacob disease (CJD) in humans, normal cellular PrP in the biology and pathology of multiple brain and peripheral diseases, proteins responsible for the α-cleavage of cellular PrP, as well as gene therapy and DNA vaccination.</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;"><a href="mailto:qxk2@case.edu" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank" ymailto="mailto:qxk2@case.edu">qxk2@case.edu</a> </div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;"><a href="https://www.alliedacademies.org/conference-abstracts-files/zoonotic-potential-of-chronic-wasting-disease-prions-from.pdf" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://www.alliedacademies.org/conference-abstracts-files/zoonotic-potential-of-chronic-wasting-disease-prions-from.pdf</a><br clear="none" /></div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;"><a href="https://prionconference.blogspot.com/2018/02/prion-round-table-conference-2018-may.html" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://prionconference.blogspot.com/2018/02/prion-round-table-conference-2018-may.html</a><br clear="none" /></div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;"><a href="http://prionconference.blogspot.com/2018/02/prion-round-table-conference-2018-may.html" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">http://prionconference.blogspot.com/2018/02/prion-round-table-conference-2018-may.html</a><br clear="none" /></div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;"><a href="http://prionconference.blogspot.com/" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">http://prionconference.blogspot.com/</a></div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;"><div>SUNDAY, JULY 25, 2021 </div><div><br clear="none" /></div><div>North American and Norwegian Chronic Wasting Disease prions exhibit different potential for interspecies transmission and zoonotic risk </div><div><br clear="none" /></div><div>''Our data suggest that reindeer and red deer from Norway could be the most transmissible CWD prions to other mammals, whereas North American CWD prions were more prone to generate human prions in vitro.''</div><div><br clear="none" /></div><div><a href="https://chronic-wasting-disease.blogspot.com/2021/07/north-american-and-norwegian-chronic.html" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://chronic-wasting-disease.blogspot.com/2021/07/north-american-and-norwegian-chronic.html</a></div></div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;"><div dir="ltr" style="font-family: Helvetica, Arial, sans-serif;">MONDAY, JULY 19, 2021 <br clear="none" /></div><div dir="ltr" style="font-family: Helvetica, Arial, sans-serif;"><br clear="none" /></div><div dir="ltr" style="font-family: Helvetica, Arial, sans-serif;">***> U Calgary researchers at work on a vaccine against a fatal infectious disease affecting deer and potentially people<br clear="none" /></div><div dir="ltr" style="font-family: Helvetica, Arial, sans-serif;"><br clear="none" /></div><div dir="ltr" style="font-family: Helvetica, Arial, sans-serif;"><a href="https://chronic-wasting-disease.blogspot.com/2021/07/u-calgary-researchers-at-work-on.html" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://chronic-wasting-disease.blogspot.com/2021/07/u-calgary-researchers-at-work-on.html</a></div></div></div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">Prion Conference 2018 Abstracts</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">BSE aka MAD COW DISEASE, was first discovered in 1984, and it took until 1995 to finally admit that BSE was causing nvCJD, the rest there is history, but that science is still evolving i.e. science now shows that indeed atypical L-type BSE, atypical Nor-98 Scrapie, and typical Scrapie are all zoonosis, zoonotic for humans, there from. </div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">HOW long are we going to wait for Chronic Wasting Disease, CWD TSE Prion of Cervid, and zoonosis, zoonotic tranmission to humans there from?</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">Studies have shown since 1994 that humans are susceptible to CWD TSE Prion, so, what's the hold up with making CWD a zoonotic zoonosis disease, the iatrogenic transmissions there from is not waiting for someone to make a decision.</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">Prion Conference 2018 Abstracts</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">P190 Human prion disease mortality rates by occurrence of chronic wasting disease in freeranging cervids, United States</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">Abrams JY (1), Maddox RA (1), Schonberger LB (1), Person MK (1), Appleby BS (2), Belay ED (1)</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">(1) Centers for Disease Control and Prevention (CDC), National Center for Emerging and Zoonotic Infectious Diseases, Atlanta, GA, USA (2) Case Western Reserve University, National Prion Disease Pathology Surveillance Center (NPDPSC), Cleveland, OH, USA.</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">Background</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">Chronic wasting disease (CWD) is a prion disease of deer and elk that has been identified in freeranging cervids in 23 US states. While there is currently no epidemiological evidence for zoonotic transmission through the consumption of contaminated venison, studies suggest the CWD agent can cross the species barrier in experimental models designed to closely mimic humans. We compared rates of human prion disease in states with and without CWD to examine the possibility of undetermined zoonotic transmission.</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">Methods</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">Death records from the National Center for Health Statistics, case records from the National Prion Disease Pathology Surveillance Center, and additional state case reports were combined to create a database of human prion disease cases from 2003-2015. Identification of CWD in each state was determined through reports of positive CWD tests by state wildlife agencies. Age- and race-adjusted mortality rates for human prion disease, excluding cases with known etiology, were determined for four categories of states based on CWD occurrence: highly endemic (>16 counties with CWD identified in free-ranging cervids); moderately endemic (3-10 counties with CWD); low endemic (1-2 counties with CWD); and no CWD states. States were counted as having no CWD until the year CWD was first identified. Analyses stratified by age, sex, and time period were also conducted to focus on subgroups for which zoonotic transmission would be more likely to be detected: cases <55 years old, male sex, and the latter half of the study (2010-2015).</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">Results</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">Highly endemic states had a higher rate of prion disease mortality compared to non-CWD states (rate ratio [RR]: 1.12, 95% confidence interval [CI] = 1.01 - 1.23), as did low endemic states (RR: 1.15, 95% CI = 1.04 - 1.27). Moderately endemic states did not have an elevated mortality rate (RR: 1.05, 95% CI = 0.93 - 1.17). In age-stratified analyses, prion disease mortality rates among the <55 year old population were elevated for moderately endemic states (RR: 1.57, 95% CI = 1.10 – 2.24) while mortality rates were elevated among those ≥55 for highly endemic states (RR: 1.13, 95% CI = 1.02 - 1.26) and low endemic states (RR: 1.16, 95% CI = 1.04 - 1.29). In other stratified analyses, prion disease mortality rates for males were only elevated for low endemic states (RR: 1.27, 95% CI = 1.10 - 1.48), and none of the categories of CWD-endemic states had elevated mortality rates for the latter time period (2010-2015).</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">Conclusions</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">While higher prion disease mortality rates in certain categories of states with CWD in free-ranging cervids were noted, additional stratified analyses did not reveal markedly elevated rates for potentially sensitive subgroups that would be suggestive of zoonotic transmission. Unknown confounding factors or other biases may explain state-by-state differences in prion disease mortality.</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">=====</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">P172 Peripheral Neuropathy in Patients with Prion Disease</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">Wang H(1), Cohen M(1), Appleby BS(1,2)</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">(1) University Hospitals Cleveland Medical Center, Cleveland, Ohio (2) National Prion Disease Pathology Surveillance Center, Cleveland, Ohio.</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">Prion disease is a fatal progressive neurodegenerative disease due to deposition of an abnormal protease-resistant isoform of prion protein. Typical symptoms include rapidly progressive dementia, myoclonus, visual disturbance and hallucinations. Interestingly, in patients with prion disease, the abnormal protein canould also be found in the peripheral nervous system. Case reports of prion deposition in peripheral nerves have been reported. Peripheral nerve involvement is thought to be uncommon; however, little is known about the exact prevalence and features of peripheral neuropathy in patients with prion disease.</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">We reviewed autopsy-proven prion cases from the National Prion Disease Pathology Surveillance Center that were diagnosed between September 2016 to March 2017. We collected information regarding prion protein diagnosis, demographics, comorbidities, clinical symptoms, physical exam, neuropathology, molecular subtype, genetics lab, brain MRI, image and EMG reports. Our study included 104 patients. Thirteen (12.5%) patients had either subjective symptoms or objective signs of peripheral neuropathy. Among these 13 patients, 3 had other known potential etiologies of peripheral neuropathy such as vitamin B12 deficiency or prior chemotherapy. Among 10 patients that had no other clear etiology, 3 (30%) had familial CJD. The most common sCJD subtype was MV1-2 (30%), followed by MM1-2 (20%). The Majority of cases wasere male (60%). Half of them had exposure to wild game. The most common subjective symptoms were tingling and/or numbness of distal extremities. The most common objective finding was diminished vibratory sensation in the feet. Half of them had an EMG with the findings ranging from fasciculations to axonal polyneuropathy or demyelinating polyneuropathy.</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">Our study provides an overview of the pattern of peripheral neuropathy in patients with prion disease. Among patients with peripheral neuropathy symptoms or signs, majority has polyneuropathy. It is important to document the baseline frequency of peripheral neuropathy in prion diseases as these symptoms may become important when conducting surveillance for potential novel zoonotic prion diseases.</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">=====</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">P177 PrP plaques in methionine homozygous Creutzfeldt-Jakob disease patients as a potential marker of iatrogenic transmission</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">Abrams JY (1), Schonberger LB (1), Cali I (2), Cohen Y (2), Blevins JE (2), Maddox RA (1), Belay ED (1), Appleby BS (2), Cohen ML (2)</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">(1) Centers for Disease Control and Prevention (CDC), National Center for Emerging and Zoonotic Infectious Diseases, Atlanta, GA, USA (2) Case Western Reserve University, National Prion Disease Pathology Surveillance Center (NPDPSC), Cleveland, OH, USA.</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">Background</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">Sporadic Creutzfeldt-Jakob disease (CJD) is widely believed to originate from de novo spontaneous conversion of normal prion protein (PrP) to its pathogenic form, but concern remains that some reported sporadic CJD cases may actually be caused by disease transmission via iatrogenic processes. For cases with methionine homozygosity (CJD-MM) at codon 129 of the PRNP gene, recent research has pointed to plaque-like PrP deposition as a potential marker of iatrogenic transmission for a subset of cases. This phenotype is theorized to originate from specific iatrogenic source CJD types that comprise roughly a quarter of known CJD cases.</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">Methods</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">We reviewed scientific literature for studies which described PrP plaques among CJD patients with known epidemiological links to iatrogenic transmission (receipt of cadaveric human grown hormone or dura mater), as well as in cases of reported sporadic CJD. The presence and description of plaques, along with CJD classification type and other contextual factors, were used to summarize the current evidence regarding plaques as a potential marker of iatrogenic transmission. In addition, 523 cases of reported sporadic CJD cases in the US from January 2013 through September 2017 were assessed for presence of PrP plaques.</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">Results</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">We identified four studies describing 52 total cases of CJD-MM among either dura mater recipients or growth hormone recipients, of which 30 were identified as having PrP plaques. While sporadic cases were not generally described as having plaques, we did identify case reports which described plaques among sporadic MM2 cases as well as case reports of plaques exclusively in white matter among sporadic MM1 cases. Among the 523 reported sporadic CJD cases, 0 of 366 MM1 cases had plaques, 2 of 48 MM2 cases had kuru plaques, and 4 of 109 MM1+2 cases had either kuru plaques or both kuru and florid plaques. Medical chart review of the six reported sporadic CJD cases with plaques did not reveal clinical histories suggestive of potential iatrogenic transmission.</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">Conclusions</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">PrP plaques occur much more frequently for iatrogenic CJD-MM cases compared to sporadic CJDMM cases. Plaques may indicate iatrogenic transmission for CJD-MM cases without a type 2 Western blot fragment. The study results suggest the absence of significant misclassifications of iatrogenic CJD as sporadic. To our knowledge, this study is the first to describe grey matter kuru plaques in apparently sporadic CJD-MM patients with a type 2 Western blot fragment.</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">=====</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">P180 Clinico-pathological analysis of human prion diseases in a brain bank series</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">Ximelis T (1), Aldecoa I (1,2), Molina-Porcel L (1,3), Grau-Rivera O (4), Ferrer I (5), Nos C (6), Gelpi E (1,7), Sánchez-Valle R (1,4)</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">(1) Neurological Tissue Bank of the Biobanc-Hospital ClÃnic-IDIBAPS, Barcelona, Spain (2) Pathological Service of Hospital ClÃnic de Barcelona, Barcelona, Spain (3) EAIA Trastorns Cognitius, Centre Emili Mira, Parc de Salut Mar, Barcelona, Spain (4) Department of Neurology of Hospital ClÃnic de Barcelona, Barcelona, Spain (5) Institute of Neuropathology, Hospital Universitari de Bellvitge, Hospitalet de Llobregat, Barcelona (6) General subdirectorate of Surveillance and Response to Emergencies in Public Health, Department of Public Health in Catalonia, Barcelona, Spain (7) Institute of Neurology, Medical University of Vienna, Vienna, Austria.</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">Background and objective:</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">The Neurological Tissue Bank (NTB) of the Hospital Clínic-Institut d‘Investigacions Biomèdiques August Pi i Sunyer, Barcelona, Spain is the reference center in Catalonia for the neuropathological study of prion diseases in the region since 2001. The aim of this study is to analyse the characteristics of the confirmed prion diseases registered at the NTB during the last 15 years.</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">Methods:</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">We reviewed retrospectively all neuropathologically confirmed cases registered during the period January 2001 to December 2016.</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">Results:</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">176 cases (54,3% female, mean age: 67,5 years and age range: 25-86 years) of neuropathological confirmed prion diseases have been studied at the NTB. 152 cases corresponded to sporadic Creutzfeldt-Jakob disease (sCJD), 10 to genetic CJD, 10 to Fatal Familial Insomnia, 2 to GerstmannSträussler-Scheinker disease, and 2 cases to variably protease-sensitive prionopathy (VPSPr). Within sCJD subtypes the MM1 subtype was the most frequent, followed by the VV2 histotype.</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">Clinical and neuropathological diagnoses agreed in 166 cases (94%). The clinical diagnosis was not accurate in 10 patients with definite prion disease: 1 had a clinical diagnosis of Fronto-temporal dementia (FTD), 1 Niemann-Pick‘s disease, 1 Lewy Body‘s Disease, 2 Alzheimer‘s disease, 1 Cortico-basal syndrome and 2 undetermined dementia. Among patients with VPSPr, 1 had a clinical diagnosis of Amyotrophic lateral sclerosis (ALS) and the other one with FTD.</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">Concomitant pathologies are frequent in older age groups, mainly AD neuropathological changes were observed in these subjects.</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">Discussion:</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">A wide spectrum of human prion diseases have been identified in the NTB being the relative frequencies and main characteristics like other published series. There is a high rate of agreement between clinical and neuropathological diagnoses with prion diseases. These findings show the importance that public health has given to prion diseases during the past 15 years. Continuous surveillance of human prion disease allows identification of new emerging phenotypes. Brain tissue samples from these donors are available to the scientific community. For more information please visit:</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;"><a href="http://www.clinicbiobanc.org/banc-teixits-neurologics/mostres/en_index.html" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">http://www.clinicbiobanc.org/banc-teixits-neurologics/mostres/en_index.html</a><br clear="none" /></div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">=====</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">P192 Prion amplification techniques for the rapid evaluation of surface decontamination procedures</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">Bruyere-Ostells L (1), Mayran C (1), Belondrade M (1), Boublik Y (2), Haïk S (3), Fournier-Wirth C (1), Nicot S (1), Bougard D (1)</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">(1) Pathogenesis and control of chronic infections, Etablissement Français du Sang, Inserm, Université de Montpellier, Montpellier, France. (2) Centre de Recherche en Biologie cellulaire de Montpellier, CNRS, Université de Montpellier, Montpellier, France. (3) Inserm U 1127, CNRS UMR 7225, Sorbonne Universités, UPMC Université Paris 06 UMR S 1127, Institut du Cerveau et de la Moelle épinière, ICM, Paris, France.</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">Aims:</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">Transmissible Spongiform Encephalopathies (TSE) or prion diseases are a group of incurable and always fatal neurodegenerative disorders including Creutzfeldt-Jakob diseases (CJD) in humans. These pathologies include sporadic (sCJD), genetic and acquired (variant CJD) forms. By the past, sCJD and vCJD were transmitted by different prion contaminated biological materials to patients resulting in more than 400 iatrogenic cases (iCJD). The atypical nature and the biochemical properties of the infectious agent, formed by abnormal prion protein or PrPTSE, make it particularly resistant to conventional decontamination procedures. In addition, PrPTSE is widely distributed throughout the organism before clinical onset in vCJD and can also be detected in some peripheral tissues in sporadic CJD. Risk of iatrogenic transmission of CJD by contaminated medical device remains thus a concern for healthcare facilities. Bioassay is the gold standard method to evaluate the efficacy of prion decontamination procedures but is time-consuming and expensive. Here, we propose to compare in vitro prion amplification techniques: Protein Misfolding Cyclic Amplification (PMCA) and Real-Time Quaking Induced Conversion (RT-QuIC) for the detection of residual prions on surface after decontamination.</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">Methods:</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">Stainless steel wires, by mimicking the surface of surgical instruments, were proposed as a carrier model of prions for inactivation studies. To determine the sensitivity of the two amplification techniques on wires (Surf-PMCA and Surf-QuIC), steel wires were therefore contaminated with serial dilutions of brain homogenates (BH) from a 263k infected hamster and from a patient with sCJD (MM1 subtype). We then compared the different standard decontamination procedures including partially and fully efficient treatments by detecting the residual seeding activity on 263K and sCJD contaminated wires. We completed our study by the evaluation of marketed reagents endorsed for prion decontamination.</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">Results:</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">The two amplification techniques can detect minute quantities of PrPTSE adsorbed onto a single wire. 8/8 wires contaminated with a 10-6 dilution of 263k BH and 1/6 with the 10-8 dilution are positive with Surf-PMCA. Similar performances were obtained with Surf-QuIC on 263K: 10/16 wires contaminated with 10-6 dilution and 1/8 wires contaminated with 10-8 dilution are positive. Regarding the human sCJD-MM1 prion, Surf-QuIC allows us to detect 16/16 wires contaminated with 10-6 dilutions and 14/16 with 10-7 . Results obtained after decontamination treatments are very similar between 263K and sCJD prions. Efficiency of marketed treatments to remove prions is lower than expected.</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">Conclusions:</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">Surf-PMCA and Surf-QuIC are very sensitive methods for the detection of prions on wires and could be applied to prion decontamination studies for rapid evaluation of new treatments. Sodium hypochlorite is the only product to efficiently remove seeding activity of both 263K and sCJD prions.</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">=====</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;"><div>WA2 Oral transmission of CWD into Cynomolgus macaques: signs of atypical disease, prion conversion and infectivity in macaques and bio-assayed transgenic mice</div><div><br clear="none" /></div><div>Schatzl HM (1, 2), Hannaoui S (1, 2), Cheng Y-C (1, 2), Gilch S (1, 2), Beekes M (3), SchulzSchaeffer W (4), Stahl-Hennig C (5) and Czub S (2, 6)</div><div><br clear="none" /></div><div>(1) University of Calgary, Calgary Prion Research Unit, Calgary, Canada (2) University of Calgary, Faculty of Veterinary Medicine, Calgary, Canada, (3) Robert Koch Institute, Berlin, Germany, (4) University of Homburg/Saar, Homburg, Germany, (5) German Primate Center, Goettingen, Germany, (6) Canadian Food Inspection Agency (CFIA), Lethbridge, Canada.</div><div><br clear="none" /></div><div>To date, BSE is the only example of interspecies transmission of an animal prion disease into humans. The potential zoonotic transmission of CWD is an alarming issue and was addressed by many groups using a variety of in vitro and in vivo experimental systems. Evidence from these studies indicated a substantial, if not absolute, species barrier, aligning with the absence of epidemiological evidence suggesting transmission into humans. Studies in non-human primates were not conclusive so far, with oral transmission into new-world monkeys and no transmission into old-world monkeys. Our consortium has challenged 18 Cynomolgus macaques with characterized CWD material, focusing on oral transmission with muscle tissue. Some macaques have orally received a total of 5 kg of muscle material over a period of 2 years. After 5-7 years of incubation time some animals showed clinical symptoms indicative of prion disease, and prion neuropathology and PrPSc deposition were found in spinal cord and brain of euthanized animals. PrPSc in immunoblot was weakly detected in some spinal cord materials and various tissues tested positive in RT-QuIC, including lymph node and spleen homogenates. To prove prion infectivity in the macaque tissues, we have intracerebrally inoculated 2 lines of transgenic mice, expressing either elk or human PrP. At least 3 TgElk mice, receiving tissues from 2 different macaques, showed clinical signs of a progressive prion disease and brains were positive in immunoblot and RT-QuIC. Tissues (brain, spinal cord and spleen) from these and preclinical mice are currently tested using various read-outs and by second passage in mice. Transgenic mice expressing human PrP were so far negative for clear clinical prion disease (some mice >300 days p.i.). In parallel, the same macaque materials are inoculated into bank voles. Taken together, there is strong evidence of transmissibility of CWD orally into macaques and from macaque tissues into transgenic mouse models, although with an incomplete attack rate. The clinical and pathological presentation in macaques was mostly atypical, with a strong emphasis on spinal cord pathology. Our ongoing studies will show whether the transmission of CWD into macaques and passage in transgenic mice represents a form of non-adaptive prion amplification, and whether macaque-adapted prions have the potential to infect mice expressing human PrP. The notion that CWD can be transmitted orally into both new-world and old-world non-human primates asks for a careful reevaluation of the zoonotic risk of CWD.</div><div><br clear="none" /></div><div>See also poster P103</div><div><br clear="none" /></div><div>***> The notion that CWD can be transmitted orally into both new-world and old-world non-human primates asks for a careful reevaluation of the zoonotic risk of CWD.<br clear="none" /></div><div><br clear="none" /></div><div>=====</div><div><br clear="none" /></div><div>WA16 Monitoring Potential CWD Transmission to Humans</div><div><br clear="none" /></div><div>Belay ED</div><div><br clear="none" /></div><div>Centers for Disease Control and Prevention (CDC), National Center for Emerging and Zoonotic Infectious Diseases, Atlanta, GA, USA.</div><div><br clear="none" /></div><div>The spread of chronic wasting disease (CWD) in animals has raised concerns about increasing human exposure to the CWD agent via hunting and venison consumption, potentially facilitating CWD transmission to humans. Several studies have explored this possibility, including limited epidemiologic studies, in vitro experiments, and laboratory studies using various types of animal models. Most human exposures to the CWD agent in the United States would be expected to occur in association with deer and elk hunting in CWD-endemic areas. The Centers for Disease Control and Prevention (CDC) collaborated with state health departments in Colorado, Wisconsin, and Wyoming to identify persons at risk of CWD exposure and to monitor their vital status over time. Databases were established of persons who hunted in Colorado and Wyoming and those who reported consumption of venison from deer that later tested positive in Wisconsin. Information from the databases is periodically cross-checked with mortality data to determine the vital status and causes of death for deceased persons. Long-term follow-up of these hunters is needed to assess their risk of development of a prion disease linked to CWD exposure.</div><div><br clear="none" /></div><div>=====</div><div><br clear="none" /></div><div>P166 Characterization of CJD strain profiles in venison consumers and non-consumers from Alberta and Saskatchewan</div><div><br clear="none" /></div><div>Stephanie Booth (1,2), Lise Lamoureux (1), Debra Sorensen (1), Jennifer L. Myskiw (1,2), Megan Klassen (1,2), Michael Coulthart (3), Valerie Sim (4)</div><div><br clear="none" /></div><div>(1) Zoonotic Diseases and Special Pathogens, National Microbiology Laboratory, Public Health Agency of Canada, Winnipeg (2) Department of Medical Microbiology and Infectious Diseases, University of Manitoba, Winnipeg (3) Canadian CJD Surveillance System, Public Health Agency of Canada, Ottawa (4) Division of Neurology, Department of Medicine Centre for Prions and Protein Folding Diseases, University of Alberta, Edmonton.</div><div><br clear="none" /></div><div>Chronic wasting disease (CWD) is spreading rapidly through wild cervid populations in the Canadian provinces of Alberta and Saskatchewan. While this has implications for tourism and hunting, there is also concern over possible zoonotic transmission to humans who eat venison from infected deer. Whilst there is no evidence of any human cases of CWD to date, the Canadian CJD Surveillance System (CJDSS) in Canada is staying vigilant. When variant CJD occurred following exposure to BSE, the unique biochemical fingerprint of the pathologic PrP enabled a causal link to be confirmed. However, we cannot be sure what phenotype human CWD prions would present with, or indeed, whether this would be distinct from that see in sporadic CJD. Therefore we are undertaking a systematic analysis of the molecular diversity of CJD cases of individuals who resided in Alberta and Saskatchewan at their time of death comparing venison consumers and non-consumers, using a variety of clinical, imaging, pathological and biochemical markers. Our initial objective is to develop novel biochemical methodologies that will extend the baseline glycoform and genetic polymorphism typing that is already completed by the CJDSS. Firstly, we are reviewing MRI, EEG and pathology information from over 40 cases of CJD to select clinically affected areas for further investigation. Biochemical analysis will include assessment of the levels of protease sensitive and resistant prion protein, glycoform typing using 2D gel electrophoresis, testing seeding capabilities and kinetics of aggregation by quaking-induced conversion, and determining prion oligomer size distributions with asymmetric flow field fractionation with in-line light scattering. Progress and preliminary data will be presented. Ultimately, we intend to further define the relationship between PrP structure and disease phenotype and establish a baseline for the identification of future atypical CJD cases that may arise as a result of exposure to CWD.</div><div><br clear="none" /></div><div>=====</div></div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">Source Prion Conference 2018 Abstracts</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;"><a href="http://transmissiblespongiformencephalopathy.blogspot.com/2018/05/prion-2018-may-22-25-2018-santiago-de.html" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">http://transmissiblespongiformencephalopathy.blogspot.com/2018/05/prion-2018-may-22-25-2018-santiago-de.html</a><br clear="none" /></div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;"><a href="http://chronic-wasting-disease.blogspot.com/2018/07/oral-transmission-of-cwd-into.html" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">http://chronic-wasting-disease.blogspot.com/2018/07/oral-transmission-of-cwd-into.html</a><br clear="none" /></div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;"><a href="http://prionconference.blogspot.com/2018/" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">http://prionconference.blogspot.com/2018/</a></div><div style="font-size: 10pt;"><br clear="none" /></div><div><div>Volume 24, Number 8—August 2018 Research Susceptibility of Human Prion Protein to Conversion by Chronic Wasting Disease Prions</div><div><br clear="none" /></div><div>Marcelo A. BarriaComments to Author , Adriana Libori, Gordon Mitchell, and Mark W. Head Author affiliations: National CJD Research and Surveillance Unit, University of Edinburgh, Edinburgh, Scotland, UK (M.A. Barria, A. Libori, M.W. Head); National and OIE Reference Laboratory for Scrapie and CWD, Canadian Food Inspection Agency, Ottawa, Ontario, Canada (G. Mitchell)</div><div><br clear="none" /></div><div>Abstract Chronic wasting disease (CWD) is a contagious and fatal neurodegenerative disease and a serious animal health issue for deer and elk in North America. The identification of the first cases of CWD among free-ranging reindeer and moose in Europe brings back into focus the unresolved issue of whether CWD can be zoonotic like bovine spongiform encephalopathy. We used a cell-free seeded protein misfolding assay to determine whether CWD prions from elk, white-tailed deer, and reindeer in North America can convert the human prion protein to the disease-associated form. We found that prions can convert, but the efficiency of conversion is affected by polymorphic variation in the cervid and human prion protein genes. In view of the similarity of reindeer, elk, and white-tailed deer in North America to reindeer, red deer, and roe deer, respectively, in Europe, a more comprehensive and thorough assessment of the zoonotic potential of CWD might be warranted.</div><div><br clear="none" /></div><div>snip...</div><div><br clear="none" /></div><div>Discussion Characterization of the transmission properties of CWD and evaluation of their zoonotic potential are important for public health purposes. Given that CWD affects several members of the family Cervidae, it seems reasonable to consider whether the zoonotic potential of CWD prions could be affected by factors such as CWD strain, cervid species, geographic location, and Prnp–PRNP polymorphic variation. We have previously used an in vitro conversion assay (PMCA) to investigate the susceptibility of the human PrP to conversion to its disease-associated form by several animal prion diseases, including CWD (15,16,22). The sensitivity of our molecular model for the detection of zoonotic conversion depends on the combination of 1) the action of proteinase K to degrade the abundant human PrPC that constitutes the substrate while only N terminally truncating any human PrPres produced and 2) the presence of the 3F4 epitope on human but not cervid PrP. In effect, this degree of sensitivity means that any human PrPres formed during the PMCA reaction can be detected down to the limit of Western blot sensitivity. In contrast, if other antibodies that detect both cervid and human PrP are used, such as 6H4, then newly formed human PrPres must be detected as a measurable increase in PrPres over the amount remaining in the reaction product from the cervid seed. Although best known for the efficient amplification of prions in research and diagnostic contexts, the variation of the PMCA method employed in our study is optimized for the definitive detection of zoonotic reaction products of inherently inefficient conversion reactions conducted across species barriers. By using this system, we previously made and reported the novel observation that elk CWD prions could convert human PrPC from human brain and could also convert recombinant human PrPC expressed in transgenic mice and eukaryotic cell cultures (15).</div><div><br clear="none" /></div><div>A previous publication suggested that mule deer PrPSc was unable to convert humanized transgenic substrate in PMCA assays (23) and required a further step of in vitro conditioning in deer substrate PMCA before it was able to cross the deer–human molecular barrier (24). However, prions from other species, such as elk (15) and reindeer affected by CWD, appear to be compatible with the human protein in a single round of amplification (as shown in our study). These observations suggest that different deer species affected by CWD could present differing degrees of the olecular compatibility with the normal form of human PrP.</div><div><br clear="none" /></div><div>The contribution of the polymorphism at codon 129 of the human PrP gene has been extensively studied and is recognized as a risk factor for Creutzfeldt-Jakob disease (4). In cervids, the equivalent codon corresponds to the position 132 encoding methionine or leucine. This polymorphism in the elk gene has been shown to play an important role in CWD susceptibility (25,26). We have investigated the effect of this cervid Prnp polymorphism on the conversion of the humanized transgenic substrate according to the variation in the equivalent PRNP codon 129 polymorphism. Interestingly, only the homologs methionine homozygous seed–substrate reactions could readily convert the human PrP, whereas the heterozygous elk PrPSc was unable to do so, even though comparable amounts of PrPres were used to seed the reaction. In addition, we observed only low levels of human PrPres formation in the reactions seeded with the homozygous methionine (132 MM) and the heterozygous (132 ML) seeds incubated with the other 2 human polymorphic substrates (129 MV and 129 VV). The presence of the amino acid leucine at position 132 of the elk Prnp gene has been attributed to a lower degree of prion conversion compared with methionine on the basis of experiments in mice made transgenic for these polymorphic variants (26). Considering the differences observed for the amplification of the homozygous human methionine substrate by the 2 polymorphic elk seeds (MM and ML), reappraisal of the susceptibility of human PrPC by the full range of cervid polymorphic variants affected by CWD would be warranted.</div><div><br clear="none" /></div><div>In light of the recent identification of the first cases of CWD in Europe in a free-ranging reindeer (R. tarandus) in Norway (2), we also decided to evaluate the in vitro conversion potential of CWD in 2 experimentally infected reindeer (18). Formation of human PrPres was readily detectable after a single round of PMCA, and in all 3 humanized polymorphic substrates (MM, MV, and VV). This finding suggests that CWD prions from reindeer could be more compatible with human PrPC generally and might therefore present a greater risk for zoonosis than, for example, CWD prions from white-tailed deer. A more comprehensive comparison of CWD in the affected species, coupled with the polymorphic variations in the human and deer PRNP–Prnp genes, in vivo and in vitro, will be required before firm conclusions can be drawn. Analysis of the Prnp sequence of the CWD reindeer in Norway was reported to be identical to the specimens used in our study (2). This finding raises the possibility of a direct comparison of zoonotic potential between CWD acquired in the wild and that produced in a controlled laboratory setting. (Table).</div><div><br clear="none" /></div><div>The prion hypothesis proposes that direct molecular interaction between PrPSc and PrPC is necessary for conversion and prion replication. Accordingly, polymorphic variants of the PrP of host and agent might play a role in determining compatibility and potential zoonotic risk. In this study, we have examined the capacity of the human PrPC to support in vitro conversion by elk, white-tailed deer, and reindeer CWD PrPSc. Our data confirm that elk CWD prions can convert the human PrPC, at least in vitro, and show that the homologous PRNP polymorphisms at codon 129 and 132 in humans and cervids affect conversion efficiency. Other species affected by CWD, particularly caribou or reindeer, also seem able to convert the human PrP. It will be important to determine whether other polymorphic variants found in other CWD-affected Cervidae or perhaps other factors (17) exert similar effects on the ability to convert human PrP and thus affect their zoonotic potential.</div><div><br clear="none" /></div><div>Dr. Barria is a research scientist working at the National CJD Research and Surveillance Unit, University of Edinburgh. His research has focused on understanding the molecular basis of a group of fatal neurologic disorders called prion diseases.</div><div><br clear="none" /></div><div>Acknowledgments We thank Aru Balachandran for originally providing cervid brain tissues, Abigail Diack and Jean Manson for providing mouse brain tissue, and James Ironside for his critical reading of the manuscript at an early stage.</div><div><br clear="none" /></div><div>This report is independent research commissioned and funded by the United Kingdom’s Department of Health Policy Research Programme and the Government of Scotland. The views expressed in this publication are those of the authors and not necessarily those of the Department of Health or the Government of Scotland.</div><div><br clear="none" /></div><div>Author contributions: The study was conceived and designed by M.A.B. and M.W.H. The experiments were conducted by M.A.B. and A.L. Chronic wasting disease brain specimens were provided by G.M. The manuscript was written by M.A.B. and M.W.H. All authors contributed to the editing and revision of the manuscript.</div><div><br clear="none" /></div><div><a href="https://wwwnc.cdc.gov/eid/article/24/8/16-1888_article" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://wwwnc.cdc.gov/eid/article/24/8/16-1888_article</a><br clear="none" /></div><div><br clear="none" /></div><div><a href="https://www.ed.ac.uk/clinical-brain-sciences/news/news-jul-dec-2018/cwd-prions-human-conversion" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://www.ed.ac.uk/clinical-brain-sciences/news/news-jul-dec-2018/cwd-prions-human-conversion</a><br clear="none" /></div></div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;"><div style="background-color: whitesmoke; color: #222222; font-family: arial, helvetica; font-size: 16px; margin-bottom: 24px;"><span face="Arial, Helvetica, sans-serif">Prion 2017 Conference Abstracts</span></div><div style="background-color: whitesmoke; font-family: arial, helvetica; font-size: 12px; margin-bottom: 24px;"><div style="margin-bottom: 24px;"><span style="color: #222222; font-size: 16px;">First evidence of intracranial and peroral transmission of Chronic Wasting Disease (CWD) into Cynomolgus macaques: a work in progress Stefanie Czub1, Walter Schulz-Schaeffer2, Christiane Stahl-Hennig3, Michael Beekes4, Hermann Schaetzl5 and Dirk Motzkus6 1 </span></div><div style="margin-bottom: 24px;"><span style="color: #222222; font-size: 16px;">University of Calgary Faculty of Veterinary Medicine/Canadian Food Inspection Agency; 2Universitatsklinikum des Saarlandes und Medizinische Fakultat der Universitat des Saarlandes; 3 Deutsches Primaten Zentrum/Goettingen; 4 Robert-Koch-Institut Berlin; 5 University of Calgary Faculty of Veterinary Medicine; 6 presently: Boehringer Ingelheim Veterinary Research Center; previously: Deutsches Primaten Zentrum/Goettingen </span><br clear="none" /></div><div style="margin-bottom: 24px;"><span style="color: #222222; font-size: 16px;">This is a progress report of a project which started in 2009. </span></div><div style="margin-bottom: 24px;"><span style="color: #222222; font-size: 16px;">21 cynomolgus macaques were challenged with characterized CWD material from white-tailed deer (WTD) or elk by intracerebral (ic), oral, and skin exposure routes. Additional blood transfusion experiments are supposed to assess the CWD contamination risk of human blood product. Challenge materials originated from symptomatic cervids for ic, skin scarification and partially per oral routes (WTD brain). Challenge material for feeding of muscle derived from preclinical WTD and from preclinical macaques for blood transfusion experiments. We have confirmed that the CWD challenge material contained at least two different CWD agents (brain material) as well as CWD prions in muscle-associated nerves. </span><br clear="none" /></div><div style="margin-bottom: 24px;"><span style="color: #222222; font-size: 16px;">Here we present first data on a group of animals either challenged ic with steel wires or per orally and sacrificed with incubation times ranging from 4.5 to 6.9 years at postmortem. Three animals displayed signs of mild clinical disease, including anxiety, apathy, ataxia and/or tremor. In four animals wasting was observed, two of those had confirmed diabetes. All animals have variable signs of prion neuropathology in spinal cords and brains and by supersensitive IHC, reaction was detected in spinal cord segments of all animals. Protein misfolding cyclic amplification (PMCA), real-time quaking-induced conversion (RT-QuiC) and PET-blot assays to further substantiate these findings are on the way, as well as bioassays in bank voles and transgenic mice. </span><br clear="none" /></div><div style="margin-bottom: 24px;"><span style="color: #222222; font-size: 16px;">At present, a total of 10 animals are sacrificed and read-outs are ongoing. Preclinical incubation of the remaining macaques covers a range from 6.4 to 7.10 years. Based on the species barrier and an incubation time of > 5 years for BSE in macaques and about 10 years for scrapie in macaques, we expected an onset of clinical disease beyond 6 years post inoculation. </span><br clear="none" /></div><div style="margin-bottom: 24px;"><span style="color: #222222; font-size: 16px;">PRION 2017 DECIPHERING NEURODEGENERATIVE DISORDERS ABSTRACTS REFERENCE</span></div></div></div><div style="font-size: 10pt;">8. Even though human TSE‐exposure risk through consumption of game from European cervids can be assumed to be minor, if at all existing, no final conclusion can be drawn due to the overall lack of scientific data. In particular the US data do not clearly exclude the possibility of human (sporadic or familial) TSE development due to consumption of venison. The Working Group thus recognizes a potential risk to consumers if a TSE would be present in European cervids. It might be prudent considering appropriate measures to reduce such a risk, e.g. excluding tissues such as CNS and lymphoid tissues from the human food chain, which would greatly reduce any potential risk for consumers. However, it is stressed that currently, no data regarding a risk of TSE infections from cervid products are available.</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;"><a href="https://efsa.onlinelibrary.wiley.com/doi/full/10.2903/j.efsa.2018.5132" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://efsa.onlinelibrary.wiley.com/doi/full/10.2903/j.efsa.2018.5132</a></div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;"><div style="background-color: whitesmoke; color: #222222; font-family: Roboto, sans-serif; font-size: small; line-height: 1.22em;">SATURDAY, FEBRUARY 23, 2019 </div><div style="background-color: whitesmoke; color: #222222; font-family: Roboto, sans-serif; font-size: small; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="background-color: whitesmoke; color: #222222; font-family: Roboto, sans-serif; font-size: small; line-height: 1.22em;">Chronic Wasting Disease CWD TSE Prion and THE FEAST 2003 CDC an updated review of the science 2019</div><div style="background-color: whitesmoke; color: #222222; font-family: Roboto, sans-serif; font-size: small; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="background-color: whitesmoke; color: #222222; font-family: Roboto, sans-serif; font-size: small; line-height: 1.22em;"><a href="https://chronic-wasting-disease.blogspot.com/2019/02/chronic-wasting-disease-cwd-tse-prion.html" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">https://chronic-wasting-disease.blogspot.com/2019/02/chronic-wasting-disease-cwd-tse-prion.html</a><br clear="none" style="line-height: 1.22em;" /></div><div style="background-color: whitesmoke; color: #222222; font-family: Roboto, sans-serif; font-size: small; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="background-color: whitesmoke; color: #222222; font-family: Roboto, sans-serif; font-size: small; line-height: 1.22em;">TUESDAY, NOVEMBER 04, 2014 </div><div style="background-color: whitesmoke; color: #222222; font-family: Roboto, sans-serif; font-size: small; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="background-color: whitesmoke; color: #222222; font-family: Roboto, sans-serif; font-size: small; line-height: 1.22em;">Six-year follow-up of a point-source exposure to CWD contaminated venison in an Upstate New York community: risk behaviours and health outcomes 2005–2011</div><div style="background-color: whitesmoke; color: #222222; font-family: Roboto, sans-serif; font-size: small; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="background-color: whitesmoke; color: #222222; font-family: Roboto, sans-serif; font-size: small; line-height: 1.22em;">Authors, though, acknowledged the study was limited in geography and sample size and so it couldn't draw a conclusion about the risk to humans. They recommended more study. Dr. Ermias Belay was the report's principal author but he said New York and Oneida County officials are following the proper course by not launching a study. "There's really nothing to monitor presently. No one's sick," Belay said, noting the disease's incubation period in deer and elk is measured in years. "</div><div style="background-color: whitesmoke; color: #222222; font-family: Roboto, sans-serif; font-size: small; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="background-color: whitesmoke; color: #222222; font-family: Roboto, sans-serif; font-size: small; line-height: 1.22em;"><a href="http://chronic-wasting-disease.blogspot.com/2014/11/six-year-follow-up-of-point-source.html" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">http://chronic-wasting-disease.blogspot.com/2014/11/six-year-follow-up-of-point-source.html</a> </div><div style="background-color: whitesmoke; color: #222222; font-family: Roboto, sans-serif; font-size: small; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="background-color: whitesmoke; color: #222222; font-size: small; line-height: 1.22em;"><div style="font-family: Roboto, sans-serif; font-size: 12px; line-height: 1.22em;">Transmission Studies</div><div style="font-family: Roboto, sans-serif; font-size: 12px; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="font-family: Roboto, sans-serif; font-size: 12px; line-height: 1.22em;">Mule deer transmissions of CWD were by intracerebral inoculation and compared with natural cases {the following was written but with a single line marked through it ''first passage (by this route)}....TSS</div><div style="font-family: Roboto, sans-serif; font-size: 12px; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="font-family: Roboto, sans-serif; font-size: 12px; line-height: 1.22em;">resulted in a more rapidly progressive clinical disease with repeated episodes of synocopy ending in coma. One control animal became affected, it is believed through contamination of inoculum (?saline). Further CWD transmissions were carried out by Dick Marsh into ferret, mink and squirrel monkey. Transmission occurred in ALL of these species with the shortest incubation period in the ferret.</div><div style="font-family: Roboto, sans-serif; font-size: 12px; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="font-family: Roboto, sans-serif; font-size: 12px; line-height: 1.22em;">snip.... </div><div style="font-family: Roboto, sans-serif; font-size: 12px; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="font-family: Roboto, sans-serif; font-size: 12px; line-height: 1.22em;"><a href="https://web.archive.org/web/20090506002237/http://www.bseinquiry.gov.uk/files/mb/m11b/tab01.pdf" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">https://web.archive.org/web/20090506002237/http://www..bseinquiry.gov.uk/files/mb/m11b/tab01.pdf</a></div><div style="font-family: Roboto, sans-serif; font-size: 12px; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="font-family: Roboto, sans-serif; font-size: 12px; line-height: 1.22em;">Prion Infectivity in Fat of Deer with Chronic Wasting Disease▿ </div><div style="font-family: Roboto, sans-serif; font-size: 12px; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="font-family: Roboto, sans-serif; font-size: 12px; line-height: 1.22em;">Brent Race#, Kimberly Meade-White#, Richard Race and Bruce Chesebro* + Author Affiliations</div><div style="font-family: Roboto, sans-serif; font-size: 12px; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="font-family: Roboto, sans-serif; font-size: 12px; line-height: 1.22em;">In mice, prion infectivity was recently detected in fat. Since ruminant fat is consumed by humans and fed to animals, we determined infectivity titers in fat from two CWD-infected deer. Deer fat devoid of muscle contained low levels of CWD infectivity and might be a risk factor for prion infection of other species. </div><div style="font-family: Roboto, sans-serif; font-size: 12px; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="font-family: Roboto, sans-serif; font-size: 12px; line-height: 1.22em;"><a href="http://jvi.asm.org/content/83/18/9608.full" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">http://jvi.asm.org/content/83/18/9608.full</a> </div><div style="font-family: Roboto, sans-serif; font-size: 12px; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="font-family: Roboto, sans-serif; font-size: 12px; line-height: 1.22em;">Prions in Skeletal Muscles of Deer with Chronic Wasting Disease </div><div style="font-family: Roboto, sans-serif; font-size: 12px; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="font-family: Roboto, sans-serif; font-size: 12px; line-height: 1.22em;">Here bioassays in transgenic mice expressing cervid prion protein revealed the presence of infectious prions in skeletal muscles of CWD-infected deer, demonstrating that humans consuming or handling meat from CWD-infected deer are at risk to prion exposure. </div><div style="font-family: Roboto, sans-serif; font-size: 12px; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="font-family: Roboto, sans-serif; font-size: 12px; line-height: 1.22em;"><a href="http://science.sciencemag.org/content/311/5764/1117..long" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">http://science.sciencemag.org/content/311/5764/1117..long</a> </div><div style="font-family: Roboto, sans-serif; font-size: 12px; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="font-family: Roboto, sans-serif; font-size: 12px; line-height: 1.22em;">*** now, let’s see what the authors said about this casual link, personal communications years ago, and then the latest on the zoonotic potential from CWD to humans from the TOKYO PRION 2016 CONFERENCE.</div><div style="font-family: Roboto, sans-serif; font-size: 12px; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="font-family: Roboto, sans-serif; font-size: 12px; line-height: 1.22em;">see where it is stated NO STRONG evidence. so, does this mean there IS casual evidence ???? “Our conclusion stating that we found no strong evidence of CWD transmission to humans”</div><div style="font-family: Roboto, sans-serif; font-size: 12px; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="font-family: Roboto, sans-serif; font-size: 12px; line-height: 1.22em;">From: TSS </div><div style="font-family: Roboto, sans-serif; font-size: 12px; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="font-family: Roboto, sans-serif; font-size: 12px; line-height: 1.22em;">Subject: CWD aka MAD DEER/ELK TO HUMANS ???</div><div style="font-family: Roboto, sans-serif; font-size: 12px; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="font-family: Roboto, sans-serif; font-size: 12px; line-height: 1.22em;">Date: September 30, 2002 at 7:06 am PST</div><div style="font-family: Roboto, sans-serif; font-size: 12px; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="font-family: Roboto, sans-serif; font-size: 12px; line-height: 1.22em;">From: "Belay, Ermias"</div><div style="font-family: Roboto, sans-serif; font-size: 12px; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="font-family: Roboto, sans-serif; font-size: 12px; line-height: 1.22em;">To: Cc: "Race, Richard (NIH)" ; ; "Belay, Ermias"</div><div style="font-family: Roboto, sans-serif; font-size: 12px; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="font-family: Roboto, sans-serif; font-size: 12px; line-height: 1.22em;">Sent: Monday, September 30, 2002 9:22 AM</div><div style="font-family: Roboto, sans-serif; font-size: 12px; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="font-family: Roboto, sans-serif; font-size: 12px; line-height: 1.22em;">Subject: RE: TO CDC AND NIH - PUB MED- 3 MORE DEATHS - CWD - YOUNG HUNTERS</div><div style="font-family: Roboto, sans-serif; font-size: 12px; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="font-family: Roboto, sans-serif; font-size: 12px; line-height: 1.22em;">Dear Sir/Madam,</div><div style="font-family: Roboto, sans-serif; font-size: 12px; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="font-family: Roboto, sans-serif; font-size: 12px; line-height: 1.22em;">In the Archives of Neurology you quoted (the abstract of which was attached to your email), we did not say CWD in humans will present like variant CJD.. That assumption would be wrong. I encourage you to read the whole article and call me if you have questions or need more clarification (phone: 404-639-3091). Also, we do not claim that "no-one has ever been infected with prion disease from eating venison." Our conclusion stating that we found no strong evidence of CWD transmission to humans in the article you quoted or in any other forum is limited to the patients we investigated.</div><div style="font-family: Roboto, sans-serif; font-size: 12px; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="font-family: Roboto, sans-serif; font-size: 12px; line-height: 1.22em;">Ermias Belay, M.D. Centers for Disease Control and Prevention</div><div style="font-family: Roboto, sans-serif; font-size: 12px; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="font-family: Roboto, sans-serif; font-size: 12px; line-height: 1.22em;">-----Original Message-----</div><div style="font-family: Roboto, sans-serif; font-size: 12px; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="font-family: Roboto, sans-serif; font-size: 12px; line-height: 1.22em;">From: Sent: Sunday, September 29, 2002 10:15 AM</div><div style="font-family: Roboto, sans-serif; font-size: 12px; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="font-family: Roboto, sans-serif; font-size: 12px; line-height: 1.22em;">To: <a href="mailto:rr26k@nih.gov" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank" ymailto="mailto:rr26k@nih.gov">rr26k@nih.gov</a>; <a href="mailto:rrace@niaid.nih.gov" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank" ymailto="mailto:rrace@niaid.nih.gov">rrace@niaid.nih.gov</a>; <a href="mailto:ebb8@CDC.GOV" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank" ymailto="mailto:ebb8@CDC.GOV">ebb8@CDC.GOV</a></div><div style="font-family: Roboto, sans-serif; font-size: 12px; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="font-family: Roboto, sans-serif; font-size: 12px; line-height: 1.22em;">Subject: TO CDC AND NIH - PUB MED- 3 MORE DEATHS - CWD - YOUNG HUNTERS</div><div style="font-family: Roboto, sans-serif; font-size: 12px; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="font-family: Roboto, sans-serif; font-size: 12px; line-height: 1.22em;">Sunday, November 10, 2002 6:26 PM .......snip........end..............TSS</div><div style="font-family: Roboto, sans-serif; font-size: 12px; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="font-family: Roboto, sans-serif; font-size: 12px; line-height: 1.22em;">Thursday, April 03, 2008</div><div style="font-family: Roboto, sans-serif; font-size: 12px; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="font-family: Roboto, sans-serif; font-size: 12px; line-height: 1.22em;">A prion disease of cervids: Chronic wasting disease 2008 1: Vet Res. 2008 Apr 3;39(4):41 A prion disease of cervids: Chronic wasting disease Sigurdson CJ.</div><div style="font-family: Roboto, sans-serif; font-size: 12px; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="font-family: Roboto, sans-serif; font-size: 12px; line-height: 1.22em;">snip...</div><div style="font-family: Roboto, sans-serif; font-size: 12px; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="font-family: Roboto, sans-serif; font-size: 12px; line-height: 1.22em;">*** twenty-seven CJD patients who regularly consumed venison were reported to the Surveillance Center***,</div><div style="font-family: Roboto, sans-serif; font-size: 12px; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="font-family: Roboto, sans-serif; font-size: 12px; line-height: 1.22em;">snip... full text ; </div><div style="font-family: Roboto, sans-serif; font-size: 12px; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="font-family: Roboto, sans-serif; font-size: 12px; line-height: 1.22em;"><a href="http://chronic-wasting-disease.blogspot.com/2008/04/prion-disease-of-cervids-chronic.html" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">http://chronic-wasting-disease.blogspot.com/2008/04/prion-disease-of-cervids-chronic.html</a> </div><div style="font-family: Roboto, sans-serif; font-size: 12px; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="font-family: Roboto, sans-serif; font-size: 12px; line-height: 1.22em;">> However, to date, no CWD infections have been reported in people. </div><div style="font-family: Roboto, sans-serif; font-size: 12px; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="font-size: 12px; line-height: 1.22em;"><span face="Roboto, sans-serif">sporadic, spontaneous CJD, 85%+ of all human TSE, </span><span face="Arial, Helvetica, sans-serif">did</span><span face="Roboto, sans-serif"> not just happen. never in scientific literature has this been proven.</span></div><div style="font-family: Roboto, sans-serif; font-size: 12px; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="font-family: Roboto, sans-serif; font-size: 12px; line-height: 1.22em;">if one looks up the word sporadic or spontaneous at pubmed, you will get a laundry list of disease that are classified in such a way;</div><div style="font-family: Roboto, sans-serif; font-size: 12px; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="font-family: Roboto, sans-serif; font-size: 12px; line-height: 1.22em;">sporadic = 54,983 hits <a href="https://www.ncbi.nlm.nih.gov/pubmed/?term=sporadic" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">https://www.ncbi.nlm.nih.gov/pubmed/?term=sporadic</a></div><div style="font-family: Roboto, sans-serif; font-size: 12px; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="font-family: Roboto, sans-serif; font-size: 12px; line-height: 1.22em;">spontaneous = 325,650 hits <a href="https://www.ncbi.nlm.nih.gov/pubmed/?term=spontaneous" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">https://www.ncbi.nlm.nih.gov/pubmed/?term=spontaneous</a></div><div style="font-family: Roboto, sans-serif; font-size: 12px; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="font-family: Roboto, sans-serif; font-size: 12px; line-height: 1.22em;">key word here is 'reported'. science has shown that CWD in humans will look like sporadic CJD. SO, how can one assume that CWD has not already transmitted to humans? they can't, and it's as simple as that. from all recorded science to date, CWD has already transmitted to humans, and it's being misdiagnosed as sporadic CJD. ...terry </div><div style="font-family: Roboto, sans-serif; font-size: 12px; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="font-family: Roboto, sans-serif; font-size: 12px; line-height: 1.22em;">*** LOOKING FOR CWD IN HUMANS AS nvCJD or as an ATYPICAL CJD, LOOKING IN ALL THE WRONG PLACES $$$ ***</div></div></div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;"><div style="background-color: whitesmoke; color: #222222; font-family: Roboto, sans-serif; font-size: 16px; margin-bottom: 24px;">> However, to date, no CWD infections have been reported in people.<br clear="none" /></div><div style="background-color: whitesmoke; color: #222222; font-family: Roboto, sans-serif; font-size: 16px; margin-bottom: 24px;">key word here is ‘reported’. science has shown that CWD in humans will look like sporadic CJD. SO, how can one assume that CWD has not already transmitted to humans? they can’t, and it’s as simple as that. from all recorded science to date, CWD has already transmitted to humans, and it’s being misdiagnosed as sporadic CJD. …terry</div><div style="background-color: whitesmoke; color: #222222; font-family: Roboto, sans-serif; font-size: 16px; margin-bottom: 24px;">*** LOOKING FOR CWD IN HUMANS AS nvCJD or as an ATYPICAL CJD, LOOKING IN ALL THE WRONG PLACES $$$ ***</div><div style="background-color: whitesmoke; color: #222222; font-family: Roboto, sans-serif; font-size: 16px; margin-bottom: 24px;">*** These results would seem to suggest that CWD does indeed have zoonotic potential, at least as judged by the compatibility of CWD prions and their human PrPC target. Furthermore, extrapolation from this simple in vitro assay suggests that if zoonotic CWD occurred, it would most likely effect those of the PRNP codon 129-MM genotype and that the PrPres type would be similar to that found in the most common subtype of sCJD (MM1).***</div><div style="background-color: whitesmoke; color: #222222; font-family: Roboto, sans-serif; font-size: 16px; margin-bottom: 24px;"><a href="http://www.tandfonline.com/doi/full/10.4161/pri.28124?src=recsys" rel="nofollow noopener noreferrer" shape="rect" style="background-color: inherit; color: #222222; cursor: pointer; transition: all 0s ease-in-out 0s;" target="_blank">http://www.tandfonline.com/doi/full/10.4161/pri.28124?src=recsys</a></div><div style="background-color: whitesmoke; color: #222222; font-family: Roboto, sans-serif; font-size: 16px; margin-bottom: 24px;"><a href="http://www.tandfonline.com/doi/pdf/10.4161/pri.28124?needAccess=true" rel="nofollow noopener noreferrer" shape="rect" style="background-color: inherit; color: #222222; cursor: pointer; transition: all 0s ease-in-out 0s;" target="_blank">http://www.tandfonline.com/doi/pdf/10.4161/pri.28124?needAccess=true</a></div><div style="background-color: whitesmoke; color: #222222; font-family: Roboto, sans-serif; font-size: 16px; margin-bottom: 24px;"><a href="https://wwwnc.cdc.gov/eid/article/20/1/13-0858_article" rel="nofollow noopener noreferrer" shape="rect" style="background-color: inherit; color: #222222; cursor: pointer; transition: all 0s ease-in-out 0s;" target="_blank">https://wwwnc.cdc.gov/eid/article/20/1/13-0858_article</a></div></div><div style="background-color: whitesmoke; margin-bottom: 24px;"><div style="background-color: white; font-size: 10pt;"><div style="font-size: 10pt; letter-spacing: 0px;">CWD TSE PRION AND ZOONOTIC, ZOONOSIS, POTENTIAL</div><div style="font-size: 10pt; letter-spacing: 0px;"><br clear="none" /></div><div><div style="line-height: 1.22em;"><div style="color: #29303b; font-size: small; letter-spacing: 0px; line-height: 1.22em; margin-bottom: 6px; margin-top: 6px;"><span face="helvetica, arial, sans-serif" style="color: #1d2129; line-height: 1.22em;"><span style="font-size: 14px; line-height: 1.22em;">Subject: Re: DEER SPONGIFORM ENCEPHALOPATHY SURVEY & HOUND STUDY </span></span></div><div style="color: #29303b; font-size: small; letter-spacing: 0px; line-height: 1.22em; margin-bottom: 6px; margin-top: 6px;"><span face="helvetica, arial, sans-serif" style="color: #1d2129; line-height: 1.22em;"><span style="font-size: 14px; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></span></div><div style="color: #29303b; font-size: small; letter-spacing: 0px; line-height: 1.22em; margin-bottom: 6px; margin-top: 6px;"><span face="helvetica, arial, sans-serif" style="color: #1d2129; line-height: 1.22em;"><span style="font-size: 14px; line-height: 1.22em;">Date: Fri, 18 Oct 2002 23:12:22 +0100 </span></span></div><div style="color: #29303b; font-size: small; letter-spacing: 0px; line-height: 1.22em; margin-bottom: 6px; margin-top: 6px;"><span face="helvetica, arial, sans-serif" style="color: #1d2129; line-height: 1.22em;"><span style="font-size: 14px; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></span></div><div style="color: #29303b; font-size: small; letter-spacing: 0px; line-height: 1.22em; margin-bottom: 6px; margin-top: 6px;"><span face="helvetica, arial, sans-serif" style="color: #1d2129; line-height: 1.22em;"><span style="font-size: 14px; line-height: 1.22em;">From: Steve Dealler </span></span></div><div style="color: #29303b; font-size: small; letter-spacing: 0px; line-height: 1.22em; margin-bottom: 6px; margin-top: 6px;"><span face="helvetica, arial, sans-serif" style="color: #1d2129; line-height: 1.22em;"><span style="font-size: 14px; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></span></div><div style="color: #29303b; font-size: small; letter-spacing: 0px; line-height: 1.22em; margin-bottom: 6px; margin-top: 6px;"><span face="helvetica, arial, sans-serif" style="color: #1d2129; line-height: 1.22em;"><span style="font-size: 14px; line-height: 1.22em;">Reply-To: Bovine Spongiform Encephalopathy Organization: Netscape Online member </span></span></div><div style="color: #29303b; font-size: small; letter-spacing: 0px; line-height: 1.22em; margin-bottom: 6px; margin-top: 6px;"><span face="helvetica, arial, sans-serif" style="color: #1d2129; line-height: 1.22em;"><span style="font-size: 14px; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></span></div><div style="color: #29303b; font-size: small; letter-spacing: 0px; line-height: 1.22em; margin-bottom: 6px; margin-top: 6px;"><span face="helvetica, arial, sans-serif" style="color: #1d2129; line-height: 1.22em;"><span style="font-size: 14px; line-height: 1.22em;">To: BSE-L@ References: <3daf5023 .4080804="" <a href="http://wt.net/" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">wt.net</a>=""></span></span></div><div style="color: #29303b; font-size: small; letter-spacing: 0px; line-height: 1.22em; margin-bottom: 6px; margin-top: 6px;"><span face="helvetica, arial, sans-serif" style="color: #1d2129; line-height: 1.22em;"><span style="font-size: 14px; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></span></div><div style="color: #29303b; font-size: small; letter-spacing: 0px; line-height: 1.22em; margin-bottom: 6px; margin-top: 6px;"><span face="helvetica, arial, sans-serif" style="color: #1d2129; line-height: 1.22em;"><span style="font-size: 14px; line-height: 1.22em;">Dear Terry,</span></span></div><div style="color: #29303b; font-size: small; letter-spacing: 0px; line-height: 1.22em; margin-bottom: 6px; margin-top: 6px;"><span face="helvetica, arial, sans-serif" style="color: #1d2129; line-height: 1.22em;"><span style="font-size: 14px; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></span></div><div style="color: #29303b; font-size: small; letter-spacing: 0px; line-height: 1.22em; margin-bottom: 6px; margin-top: 6px;"><span face="helvetica, arial, sans-serif" style="color: #1d2129; line-height: 1.22em;"><span style="font-size: 14px; line-height: 1.22em;">An excellent piece of review as this literature is desparately difficult to get back from Government sites.</span></span></div><div style="color: #29303b; font-size: small; letter-spacing: 0px; line-height: 1.22em; margin-bottom: 6px; margin-top: 6px;"><span face="helvetica, arial, sans-serif" style="color: #1d2129; line-height: 1.22em;"><span style="font-size: 14px; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></span></div><div style="color: #29303b; font-size: small; letter-spacing: 0px; line-height: 1.22em; margin-bottom: 6px; margin-top: 6px;"><span face="helvetica, arial, sans-serif" style="color: #1d2129; line-height: 1.22em;"><span style="font-size: 14px; line-height: 1.22em;">What happened with the deer was that an association between deer meat eating and sporadic CJD was found in about 1993. The evidence was not great but did not disappear after several years of asking CJD cases what they had eaten. I think that the work into deer disease largely stopped because it was not helpful to the UK industry...and no specific cases were reported. Well, if you dont look adequately like they are in USA currenly then you wont find any!</span></span></div><div style="color: #29303b; font-size: small; letter-spacing: 0px; line-height: 1.22em; margin-bottom: 6px; margin-top: 6px;"><span face="helvetica, arial, sans-serif" style="color: #1d2129; line-height: 1.22em;"><span style="font-size: 14px; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></span></div><div style="color: #29303b; font-size: small; letter-spacing: 0px; line-height: 1.22em; margin-bottom: 6px; margin-top: 6px;"><span face="helvetica, arial, sans-serif" style="color: #1d2129; line-height: 1.22em;"><span style="font-size: 14px; line-height: 1.22em;">Steve Dealler =============== </span></span></div><div style="color: #1d2129; font-family: inherit; font-size: 14px; letter-spacing: 0px; line-height: 1.22em; margin-bottom: 6px; margin-top: 6px;"><br clear="none" style="line-height: 1.22em;" /></div><div style="color: #1d2129; font-family: inherit; font-size: 14px; letter-spacing: 0px; line-height: 1.22em; margin-bottom: 6px; margin-top: 6px;"><a href="https://caninespongiformencephalopathy.blogspot.com/2010/03/canine-spongiform-encephalopathy-aka.html" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">https://caninespongiformencephalopathy.blogspot.com/2010/03/canine-spongiform-encephalopathy-aka.html</a></div><div style="color: #1d2129; font-family: inherit; font-size: 14px; letter-spacing: 0px; line-height: 1.22em; margin-bottom: 6px; margin-top: 6px;"><br clear="none" /></div><div style="color: #1d2129; font-family: inherit; font-size: 14px; letter-spacing: 0px; line-height: 1.22em; margin-bottom: 6px; margin-top: 6px;">''The association between venison eating and risk of CJD shows similar pattern, with regular venison eating associated with a 9 FOLD INCREASE IN RISK OF CJD (p = 0.04).''<br clear="none" /></div><div style="color: #1d2129; font-family: inherit; font-size: 14px; letter-spacing: 0px; line-height: 1.22em; margin-bottom: 6px; margin-top: 6px;"><br clear="none" /></div><div style="line-height: 1.22em; margin-bottom: 6px; margin-top: 6px;"><div style="line-height: 1.22em; margin-bottom: 6px; margin-top: 6px;"><span style="color: #1d2129; font-size: 14px;">CREUTZFELDT JAKOB DISEASE SURVEILLANCE IN THE UNITED KINGDOM THIRD ANNUAL REPORT AUGUST 1994</span></div><div style="line-height: 1.22em; margin-bottom: 6px; margin-top: 6px;"><span style="color: #1d2129; font-size: 14px;"><br clear="none" /></span></div><div style="line-height: 1.22em; margin-bottom: 6px; margin-top: 6px;"><span style="color: #1d2129; font-size: 14px;">Consumption of venison and veal was much less widespread among both cases and controls. For both of these meats there was evidence of a trend with increasing frequency of consumption being associated with increasing risk of CJD. (not nvCJD, but sporadic CJD...tss) These associations were largely unchanged when attention was restricted to pairs with data obtained from relatives. ...</span></div><div style="line-height: 1.22em; margin-bottom: 6px; margin-top: 6px;"><span style="color: #1d2129; font-size: 14px;"><br clear="none" /></span></div><div style="line-height: 1.22em; margin-bottom: 6px; margin-top: 6px;"><span style="color: #1d2129; font-size: 14px;">Table 9 presents the results of an analysis of these data.</span></div><div style="line-height: 1.22em; margin-bottom: 6px; margin-top: 6px;"><span style="color: #1d2129; font-size: 14px;"><br clear="none" /></span></div><div style="line-height: 1.22em; margin-bottom: 6px; margin-top: 6px;"><span style="color: #1d2129; font-size: 14px;">There is STRONG evidence of an association between ‘’regular’’ veal eating and risk of CJD (p = .0.01).</span></div><div style="line-height: 1.22em; margin-bottom: 6px; margin-top: 6px;"><span style="color: #1d2129; font-size: 14px;"><br clear="none" /></span></div><div style="line-height: 1.22em; margin-bottom: 6px; margin-top: 6px;"><span style="color: #1d2129; font-size: 14px;">Individuals reported to eat veal on average at least once a year appear to be at 13 TIMES THE RISK of individuals who have never eaten veal.</span></div><div style="line-height: 1.22em; margin-bottom: 6px; margin-top: 6px;"><span style="color: #1d2129; font-size: 14px;"><br clear="none" /></span></div><div style="line-height: 1.22em; margin-bottom: 6px; margin-top: 6px;"><span style="color: #1d2129; font-size: 14px;">There is, however, a very wide confidence interval around this estimate. There is no strong evidence that eating veal less than once per year is associated with increased risk of CJD (p = 0.51).</span></div><div style="line-height: 1.22em; margin-bottom: 6px; margin-top: 6px;"><span style="color: #1d2129; font-size: 14px;"><br clear="none" /></span></div><div style="line-height: 1.22em; margin-bottom: 6px; margin-top: 6px;"><span style="color: #1d2129; font-size: 14px;">The association between venison eating and risk of CJD shows similar pattern, with regular venison eating associated with a 9 FOLD INCREASE IN RISK OF CJD (p = 0.04).</span></div><div style="line-height: 1.22em; margin-bottom: 6px; margin-top: 6px;"><span style="color: #1d2129; font-size: 14px;"><br clear="none" /></span></div><div style="line-height: 1.22em; margin-bottom: 6px; margin-top: 6px;"><span style="color: #1d2129; font-size: 14px;">There is some evidence that risk of CJD INCREASES WITH INCREASING FREQUENCY OF LAMB EATING (p = 0.02).</span></div><div style="line-height: 1.22em; margin-bottom: 6px; margin-top: 6px;"><span style="color: #1d2129; font-size: 14px;"><br clear="none" /></span></div><div style="line-height: 1.22em; margin-bottom: 6px; margin-top: 6px;"><span style="color: #1d2129; font-size: 14px;">The evidence for such an association between beef eating and CJD is weaker (p = 0.14). When only controls for whom a relative was interviewed are included, this evidence becomes a little STRONGER (p = 0.08).</span></div><div style="line-height: 1.22em; margin-bottom: 6px; margin-top: 6px;"><span style="color: #1d2129; font-size: 14px;"><br clear="none" /></span></div><div style="line-height: 1.22em; margin-bottom: 6px; margin-top: 6px;"><span style="color: #1d2129; font-size: 14px;">snip...</span></div><div style="line-height: 1.22em; margin-bottom: 6px; margin-top: 6px;"><span style="color: #1d2129; font-size: 14px;"><br clear="none" /></span></div><div style="line-height: 1.22em; margin-bottom: 6px; margin-top: 6px;"><span style="color: #1d2129; font-size: 14px;">It was found that when veal was included in the model with another exposure, the association between veal and CJD remained statistically significant (p = < 0.05 for all exposures), while the other exposures ceased to be statistically significant (p = > 0.05).</span></div><div style="line-height: 1.22em; margin-bottom: 6px; margin-top: 6px;"><span style="color: #1d2129; font-size: 14px;"><br clear="none" /></span></div><div style="line-height: 1.22em; margin-bottom: 6px; margin-top: 6px;"><span style="color: #1d2129; font-size: 14px;">snip...</span></div><div style="line-height: 1.22em; margin-bottom: 6px; margin-top: 6px;"><span style="color: #1d2129; font-size: 14px;"><br clear="none" /></span></div><div style="line-height: 1.22em; margin-bottom: 6px; margin-top: 6px;"><span style="color: #1d2129; font-size: 14px;">In conclusion, an analysis of dietary histories revealed statistical associations between various meats/animal products and INCREASED RISK OF CJD. When some account was taken of possible confounding, the association between VEAL EATING AND RISK OF CJD EMERGED AS THE STRONGEST OF THESE ASSOCIATIONS STATISTICALLY. ...</span></div><div style="line-height: 1.22em; margin-bottom: 6px; margin-top: 6px;"><span style="color: #1d2129; font-size: 14px;"><br clear="none" /></span></div><div style="line-height: 1.22em; margin-bottom: 6px; margin-top: 6px;"><span style="color: #1d2129; font-size: 14px;">snip...</span></div><div style="line-height: 1.22em; margin-bottom: 6px; margin-top: 6px;"><span style="color: #1d2129; font-size: 14px;"><br clear="none" /></span></div><div style="line-height: 1.22em; margin-bottom: 6px; margin-top: 6px;"><span style="color: #1d2129; font-size: 14px;">In the study in the USA, a range of foodstuffs were associated with an increased risk of CJD, including liver consumption which was associated with an apparent SIX-FOLD INCREASE IN THE RISK OF CJD. By comparing the data from 3 studies in relation to this particular dietary factor, the risk of liver consumption became non-significant with an odds ratio of 1.2 (PERSONAL COMMUNICATION, PROFESSOR A. HOFMAN. ERASMUS UNIVERSITY, ROTTERDAM). (???...TSS)</span></div><div style="line-height: 1.22em; margin-bottom: 6px; margin-top: 6px;"><span style="color: #1d2129; font-size: 14px;"><br clear="none" /></span></div><div style="line-height: 1.22em; margin-bottom: 6px; margin-top: 6px;"><span style="color: #1d2129; font-size: 14px;">snip...see full report ;</span></div><div style="line-height: 1.22em; margin-bottom: 6px; margin-top: 6px;"><span style="color: #1d2129; font-size: 14px;"><br clear="none" /></span></div><div style="line-height: 1.22em; margin-bottom: 6px; margin-top: 6px;"><a href="http://web.archive.org/web/20090506050043/http://www.bseinquiry.gov.uk/files/yb/1994/08/00004001.pdf" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer; font-size: 14px;" target="_blank">http://web.archive.org/web/20090506050043/http://www.bseinquiry.gov.uk/files/yb/1994/08/00004001.pdf</a><br clear="none" /></div><div style="line-height: 1.22em; margin-bottom: 6px; margin-top: 6px;"><span style="color: #1d2129; font-size: 14px;"><br clear="none" /></span></div><div style="line-height: 1.22em; margin-bottom: 6px; margin-top: 6px;"><span style="color: #1d2129; font-size: 14px;"> </span><a href="http://web.archive.org/web/20090506050007/http://www.bseinquiry.gov.uk/files/yb/1994/10/00003001.pdf" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer; font-family: inherit; font-size: 14px; letter-spacing: 0px;" target="_blank">http://web.archive.org/web/20090506050007/http://www.bseinquiry.gov.uk/files/yb/1994/10/00003001.pdf</a></div></div><div style="color: #1d2129; font-family: inherit; font-size: 14px; letter-spacing: 0px; line-height: 1.22em; margin-bottom: 6px; margin-top: 6px;"><br clear="none" /></div><div style="color: #1d2129; font-family: inherit; font-size: 14px; letter-spacing: 0px; line-height: 1.22em; margin-bottom: 6px; margin-top: 6px;"><a href="http://web.archive.org/web/20090506050244/http://www.bseinquiry.gov.uk/files/yb/1994/07/00001001.pdf" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">http://web.archive.org/web/20090506050244/http://www.bseinquiry.gov.uk/files/yb/1994/07/00001001.pdf</a><br clear="none" /></div><div style="color: #1d2129; font-family: inherit; font-size: 14px; letter-spacing: 0px; line-height: 1.22em; margin-bottom: 6px; margin-top: 6px;"><br clear="none" /></div><div style="color: #29303b; font-size: 10pt; letter-spacing: 0px; line-height: 1.22em; margin-bottom: 6px; margin-top: 6px;"><span style="background-color: #fef9f5; color: #121212; font-size: 17px; line-height: 1.22em;">Stephen Dealler is a consultant medical microbiologist</span><span style="background-color: #fef9f5; color: #121212; font-size: 17px; line-height: 1.22em;"><span face="arial, helvetica, sans-serif" style="line-height: 1.22em;"> </span></span><span face="arial, helvetica, sans-serif" style="color: #121212; line-height: 1.22em;"><span style="font-size: 17px; line-height: 1.22em;"> <a href="mailto:deal@airtime.co.uk" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank" ymailto="mailto:deal@airtime.co.uk">deal@airtime.co.uk</a> </span></span></div><div style="color: #29303b; font-size: 10pt; letter-spacing: 0px; line-height: 1.22em; margin-bottom: 6px; margin-top: 6px;"><span face="arial, helvetica, sans-serif" style="color: #121212; line-height: 1.22em;"><span style="font-size: 17px; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></span></div><div style="color: #1d2129; font-family: inherit; font-size: 14px; letter-spacing: 0px; line-height: 1.22em; margin-bottom: 6px; margin-top: 6px;">BSE Inquiry Steve Dealler</div><div style="color: #1d2129; font-family: inherit; font-size: 14px; letter-spacing: 0px; line-height: 1.22em; margin-bottom: 6px; margin-top: 6px;"><br clear="none" style="line-height: 1.22em;" /></div><div style="color: #1d2129; font-family: inherit; font-size: 14px; letter-spacing: 0px; line-height: 1.22em; margin-bottom: 6px; margin-top: 6px;">Management In Confidence</div><div style="color: #1d2129; font-family: inherit; font-size: 14px; letter-spacing: 0px; line-height: 1.22em; margin-bottom: 6px; margin-top: 6px;"><br clear="none" style="line-height: 1.22em;" /></div><div style="color: #1d2129; font-family: inherit; font-size: 14px; letter-spacing: 0px; line-height: 1.22em; margin-bottom: 6px; margin-top: 6px;">BSE: Private Submission of Bovine Brain Dealler</div><div style="color: #1d2129; font-family: inherit; font-size: 14px; letter-spacing: 0px; line-height: 1.22em; margin-bottom: 6px; margin-top: 6px;"><br clear="none" style="line-height: 1.22em;" /></div><div style="color: #1d2129; font-family: inherit; font-size: 14px; letter-spacing: 0px; line-height: 1.22em; margin-bottom: 6px; margin-top: 6px;">snip...see full text;</div></div><div style="font-size: 10pt; letter-spacing: 0px; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="font-size: 10pt; letter-spacing: 0px; line-height: 1.22em;">MONDAY, FEBRUARY 25, 2019</div><div style="font-size: 10pt; letter-spacing: 0px; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="font-size: 10pt; letter-spacing: 0px; line-height: 1.22em;">***> MAD DOGS AND ENGLISHMEN BSE, SCRAPIE, CWD, CJD, TSE PRION A REVIEW 2019</div><div style="font-size: 10pt; letter-spacing: 0px; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="font-size: 10pt; letter-spacing: 0px; line-height: 1.22em;"><a href="https://bseinquiry..blogspot.com/2019/02/mad-dogs-and-englishmen-bse-scrapie-cwd.html" rel="nofollow noopener noreferrer" shape="rect" style="color: purple; cursor: pointer; line-height: 1.22em;" target="_blank">https://bseinquiry.blogspot.com/2019/02/mad-dogs-and-englishmen-bse-scrapie-cwd.html</a></div><div style="font-size: 10pt; letter-spacing: 0px; line-height: 1.22em;"><br clear="none" /></div><div style="font-size: 10pt; letter-spacing: 0px; line-height: 1.22em;">***> ''<span style="color: #1d2129; font-size: 14px;">The association between venison eating and risk of CJD shows similar pattern, with regular venison eating associated with a 9 FOLD INCREASE IN RISK OF CJD (p = 0.04).''</span></div></div></div><div style="background-color: white; color: #222222; font-family: Roboto, sans-serif; font-size: 10pt; letter-spacing: 0px;"><br clear="none" /></div><div style="background-color: white;"><div style="background-color: whitesmoke; margin-bottom: 24px;"><div style="background-color: white;"><div style="line-height: 1.22em;"><div class="yiv1670726472aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;"><div style="color: #222222; font-family: Roboto, sans-serif; font-size: 10pt; letter-spacing: 0px;"><span style="font-family: arial, helvetica;">***> In conclusion, sensory symptoms and loss of reflexes in Gerstmann-Sträussler-Scheinker syndrome can be explained by neuropathological changes in the spinal cord. We conclude that the sensory symptoms and loss of lower limb reflexes in Gerstmann-Sträussler-Scheinker syndrome is due to pathology in the caudal spinal cord. <***</span></div><div style="color: #222222; font-family: Roboto, sans-serif; font-size: 10pt; letter-spacing: 0px;"><span style="font-family: arial, helvetica;"><br clear="none" /></span></div><div style="color: #222222; font-family: Roboto, sans-serif; font-size: 10pt; letter-spacing: 0px;"><div style="font-family: arial, helvetica; font-size: small;"><span style="font-size: 13.3333px;">***> The clinical and pathological presentation in macaques was mostly atypical, with a strong emphasis on spinal cord pathology.<*** </span></div><div style="font-family: arial, helvetica; font-size: small;"><span style="font-size: 13.3333px;"><br clear="none" /></span></div><div style="font-family: arial, helvetica; font-size: small;"><span style="font-size: 13.3333px;">***> The notion that CWD can be transmitted orally into both new-world and old-world non-human primates asks for a careful reevaluation of the zoonotic risk of CWD. <***</span></div></div><div style="color: #222222; font-family: Roboto, sans-serif; font-size: small; letter-spacing: 0px;"><span style="font-size: 13.3333px;"><br clear="none" /></span></div><div style="color: #222222; font-family: Roboto, sans-serif; font-size: small; letter-spacing: 0px;"><span style="font-size: 13.3333px;">***> All animals have variable signs of prion neuropathology in spinal cords and brains and by supersensitive IHC, reaction was detected in spinal cord segments of all animals.<*** </span></div><div style="color: #222222; font-family: Roboto, sans-serif; font-size: 10pt; letter-spacing: 0px;"><span style="font-family: arial, helvetica;"><br clear="none" /></span></div><div style="color: #222222; font-family: Roboto, sans-serif; font-size: 10pt; letter-spacing: 0px;"><span style="font-family: arial, helvetica;">***> In particular the US data do not clearly exclude the possibility of human (sporadic or familial) TSE development due to consumption of venison. The Working Group thus recognizes a potential risk to consumers if a TSE would be present in European cervids.'' Scientific opinion on chronic wasting disease (II) <***</span></div><div style="color: #222222; font-family: Roboto, sans-serif; font-size: 10pt; letter-spacing: 0px;"><span style="font-family: arial, helvetica;"><br clear="none" /></span></div><div style="color: #222222; font-family: Roboto, sans-serif; font-size: 10pt; letter-spacing: 0px;"><span style="font-family: arial, helvetica;"><a href="https://familialcjdtseprion.blogspot.com/2019/02/cwd-gss-tse-prion-spinal-cord-confucius.html" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://familialcjdtseprion.blogspot.com/2019/02/cwd-gss-tse-prion-spinal-cord-confucius.html</a></span></div><div style="color: #222222; font-family: Roboto, sans-serif; font-size: 10pt; letter-spacing: 0px;"><br clear="none" /></div><div style="color: #222222; font-family: Roboto, sans-serif; font-size: 10pt; letter-spacing: 0px;"><div style="color: black; font-family: arial;"><div><div>North American and Norwegian Chronic Wasting Disease prions exhibit different potential for interspecies transmission and zoonotic risk</div><div><br clear="none" /></div><div>Sandra Pritzkow1,*, Damian Gorski1,*, Frank Ramirez1 , Glenn C. Telling2 , Sylvie L. Benestad3 and Claudio Soto1,#</div><div><br clear="none" /></div><div>1 Mitchell Center for Alzheimer's disease and related Brain disorders, Department of Neurology, University of Texas McGovern Medical School at Houston, Texas, USA 2 Prion Research Center, Department of Microbiology, Immunology and Pathology, Colorado State University, Fort Collins, Colorado, USA 3 Norwegian Veterinary Institute, OIE Reference Laboratory for CWD, Oslo, Norway.</div><div><br clear="none" /></div><div>Summary: We investigated the in vitro spillover and zoonotic potential of CWD from various cervid species. Our results suggest that Norway CWD prions have a higher potential to infect other animals, but NorthAmerican CWD appear more prone to generate human prions.</div></div><div><br clear="none" /></div><div>The current evidence for CWD transmission to humans is controversial; indeed, while transgenic mice expressing human PrP did not develop disease when challenged with CWD prions in various laboratories [6-8, 41], experimental inoculation of CWD into squirrel monkeys produced disease [9, 10]. Studies in macaques, which are phylogenetically closer to humans than squirrel monkeys [45] have shown mixed results. A study from Czub and colleagues found that CWD prions can induce disease and pathologic abnormalities typical of prion disease in macaques exposed to CWD prions, even by oral inoculation of muscle tissue from cervids affected by CWD [46]. However, a different study found no evidence for prion disease in macaques inoculated with CWD [47]. To assess the cervid/human species barrier, we previously used PMCA to determine prion replication in vitro. We found that, after stabilization by successive passages in deer PrPC, PrPSc from CWD infected deer can convert human PrPC into a novel form of PrPSc [13]. Our current study to evaluate in vitro zoonotic potential of various CWD prions showed that although the cervid/human barrier is large, we were able to observe generation of human PrPSc with some specific CWD strains in a second round of PMCA (Fig. 5). The three North American CWD isolates were capable to sustain generation of human PrPSc, with white-tailed deer showing the highest efficiency. Conversely, none of the three Norway CWD isolates generated any detectable PrPSc signal up to the second round of PMCA. This data suggest that North American CWD prions might be of a greater risk to humans than the infected animals in Northern Europe. We speculate that these differences might be due to Norwegian CWD being less stable prion strains as compared to North American CWD, which have had longer time to replicate in cervids and become stabilized through many rounds of natural infection. Our findings may provide important information to understand the diversity of natural CWD prion strains in different animals across distinct geographical areas and their consequences for the spillover into other animal species, including humans.<br clear="none" /></div><div><br clear="none" /></div><div><a href="https://academic.oup.com/jid/advance-article-abstract/doi/10.1093/infdis/jiab385/6327572?redirectedFrom=fulltext" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://academic.oup.com/jid/advance-article-abstract/doi/10.1093/infdis/jiab385/6327572?redirectedFrom=fulltext</a></div></div><div dir="ltr" style="font-family: arial, helvetica; font-size: 10pt; letter-spacing: 0px;"><br clear="none" /></div><div style="color: black; font-family: arial;"><div>MONDAY, JULY 19, 2021 </div><div><br clear="none" /></div><div>U Calgary researchers at work on a vaccine against a fatal infectious disease affecting deer and potentially people<br clear="none" /></div><div><br clear="none" /></div><div><a href="https://chronic-wasting-disease.blogspot.com/2021/07/u-calgary-researchers-at-work-on.html" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://chronic-wasting-disease.blogspot.com/2021/07/u-calgary-researchers-at-work-on.html</a></div></div><div style="color: black; font-family: arial;"><br clear="none" /></div><div style="color: black; font-family: arial;"><div>TUESDAY, JULY 13, 2021</div><div><br clear="none" /></div><div>Chronic Wasting Disease and the Canadian Agriculture and Agri-food Sectors Current Knowledge Risks and Policy Options</div><div><br clear="none" /></div><div>''The science is progressing on the possibility of transmission of CWD to humans through oral transmission, but the complete assessment of this possibility remains to be done.''</div><div><br clear="none" /></div><div><a href="https://chronic-wasting-disease.blogspot.com/2021/07/chronic-wasting-disease-and-canadian.html" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://chronic-wasting-disease.blogspot.com/2021/07/chronic-wasting-disease-and-canadian.html</a></div></div><div style="color: black; font-family: arial;"><br clear="none" /></div><div style="color: black; font-family: arial;"><div dir="ltr" style="color: #222222; font-family: arial, helvetica; font-size: 10pt; letter-spacing: 0px;">MONDAY, DECEMBER 16, 2019 <br clear="none" /></div><div dir="ltr" style="color: #222222; font-family: arial, helvetica; font-size: 10pt; letter-spacing: 0px;"><br clear="none" /></div><div dir="ltr" style="color: #222222; font-family: arial, helvetica; font-size: 10pt; letter-spacing: 0px;">Chronic Wasting Disease CWD TSE Prion aka mad cow type disease in cervid Zoonosis Update<br clear="none" /></div><div dir="ltr" style="color: #222222; font-family: arial, helvetica; font-size: 10pt; letter-spacing: 0px;"><br clear="none" /></div><div dir="ltr" style="color: #222222; font-family: arial, helvetica; font-size: 10pt; letter-spacing: 0px;">***> ''In particular the US data do not clearly exclude the possibility of human (sporadic or familial) TSE development due to consumption of venison. The Working Group thus recognizes a potential risk to consumers if a TSE would be present in European cervids.'' Scientific opinion on chronic wasting disease (II) <***<br clear="none" /></div><div dir="ltr" style="color: #222222; font-family: arial, helvetica; font-size: 10pt; letter-spacing: 0px;"><br clear="none" /></div><div dir="ltr" style="color: #222222; font-family: arial, helvetica; font-size: 10pt; letter-spacing: 0px;">What if?<br clear="none" /></div><div dir="ltr" style="color: #222222; font-family: arial, helvetica; font-size: 10pt; letter-spacing: 0px;"><br clear="none" /></div><div dir="ltr" style="color: #222222; font-family: arial, helvetica; font-size: 10pt; letter-spacing: 0px;"><a href="https://chronic-wasting-disease.blogspot.com/2019/12/chronic-wasting-disease-cwd-tse-prion.html" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://chronic-wasting-disease.blogspot.com/2019/12/chronic-wasting-disease-cwd-tse-prion.html</a></div></div><div dir="ltr" style="font-family: arial, helvetica; font-size: 10pt; letter-spacing: 0px;"><br clear="none" /></div><div dir="ltr" style="font-family: arial, helvetica; font-size: 10pt; letter-spacing: 0px;"><div style="color: black; font-family: arial; font-size: 10pt;"><div style="font-size: 10pt;"><div class="yiv1670726472yqt3924989209" id="yiv1670726472yqt29531" style="font-family: Arial, Helvetica, sans-serif; font-size: 12px;"><div class="yiv1670726472WordSection1"><div id="yiv1670726472"><div style="margin-bottom: 24pt; margin-top: 6pt;"><div><div class="yiv1670726472MsoNormal" style="font-size: 12pt; line-height: 14.65pt; margin: 0cm 0cm 0.0001pt;"><span face="sans-serif" style="font-size: 10pt;">TUESDAY, MAY 11, 2021 </span></div></div><div><div class="yiv1670726472MsoNormal" style="font-size: 12pt; line-height: 14.65pt; margin: 0cm 0cm 0.0001pt;"><span face="sans-serif" style="font-size: 10pt;"> </span></div></div><div><div class="yiv1670726472MsoNormal" style="font-size: 12pt; line-height: 14.65pt; margin: 0cm 0cm 0.0001pt;"><span face="sans-serif" style="font-size: 10pt;">A Unique Presentation of Creutzfeldt-Jakob Disease in a Patient Consuming Deer Antler Velvet</span></div></div><div><div class="yiv1670726472MsoNormal" style="font-size: 12pt; line-height: 14.65pt; margin: 0cm 0cm 0.0001pt;"><span face="sans-serif" style="font-size: 10pt;"> </span></div></div><div><div class="yiv1670726472MsoNormal" style="font-size: 12pt; line-height: 14.65pt; margin: 0cm 0cm 0.0001pt;"><span face="sans-serif" style="font-size: 10pt;"><a href="https://creutzfeldt-jakob-disease.blogspot.com/2021/05/a-unique-presentation-of-creutzfeldt.html" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://creutzfeldt-jakob-disease.blogspot.com/2021/05/a-unique-presentation-of-creutzfeldt.html</a></span></div><div class="yiv1670726472MsoNormal" style="font-size: 12pt; line-height: 14.65pt; margin: 0cm 0cm 0.0001pt;"><span style="background-color: transparent; font-family: arial; font-size: 13.3333px;"><br clear="none" /></span></div><div class="yiv1670726472MsoNormal" style="font-size: 12pt; line-height: 14.65pt; margin: 0cm 0cm 0.0001pt;"><span style="background-color: transparent; font-family: arial; font-size: 13.3333px;">Saturday, May 1, 2021 </span></div><div class="yiv1670726472MsoNormal" style="font-size: 12pt; line-height: 14.65pt; margin: 0cm 0cm 0.0001pt;"><span style="background-color: transparent; font-family: arial; font-size: 13.3333px;"><br clear="none" /></span></div><div class="yiv1670726472MsoNormal" style="font-size: 12pt; line-height: 14.65pt; margin: 0cm 0cm 0.0001pt;"><span style="background-color: transparent; font-family: arial; font-size: 13.3333px;">Clinical Use of Improved Diagnostic Testing for Detection of Prion Disease</span></div><div class="yiv1670726472MsoNormal" style="font-size: 12pt; line-height: 14.65pt; margin: 0cm 0cm 0.0001pt;"><br clear="none" /></div><div class="yiv1670726472MsoNormal" style="font-size: 12pt; line-height: 14.65pt; margin: 0cm 0cm 0.0001pt;"><a href="https://prionprp.blogspot.com/2021/05/clinical-use-of-improved-diagnostic.html" rel="nofollow noopener noreferrer" shape="rect" style="background-color: transparent; color: blue; cursor: pointer; font-family: arial; font-size: 13.3333px;" target="_blank">https://prionprp.blogspot.com/2021/05/clinical-use-of-improved-diagnostic.html</a></div></div></div></div></div></div></div></div></div></div><div><div style="color: #222222; font-family: arial, helvetica; font-size: 12px; letter-spacing: 0px;"><span style="font-family: arial, helvetica;"> </span><span style="font-family: Georgia, serif; font-size: 10pt;">***Moreover, sporadic disease has never been observed in breeding colonies or primate research laboratories, most notably among hundreds of animals over several decades of study at the National Institutes of Health25, and in nearly twenty older animals continuously housed in our own facility.***</span></div><div style="color: #222222; font-family: Roboto, sans-serif; font-size: 12px; letter-spacing: 0px;"><span style="font-size: 10pt; line-height: 1.22em;"><span style="font-family: Georgia, serif;"><br clear="none" /></span></span></div><div style="color: #222222; font-family: Roboto, sans-serif; font-size: 12px; letter-spacing: 0px;"><span style="font-size: 10pt; line-height: 1.22em;"></span><div style="font-family: arial, helvetica; line-height: 1.22em;"><div style="line-height: 1.22em;">Even if the prevailing view is that sporadic CJD is due to the spontaneous formation of CJD prions, it remains possible that its apparent sporadic nature may, at least in part, result from our limited capacity to identify an environmental origin.</div></div><br clear="none" style="line-height: 1.22em;" /><span face="Arial, sans-serif" style="font-size: 10pt; line-height: 1.22em;"><a href="https://www..nature.com/articles/srep11573" rel="nofollow noopener noreferrer" shape="rect" style="color: purple; cursor: pointer; line-height: 1.22em;" target="_blank"><span face="Verdana, sans-serif" style="line-height: 1.22em;"></span></a><a href="https://www.nature.com/articles/srep11573" rel="nofollow noopener noreferrer" shape="rect" style="color: purple; cursor: pointer; line-height: 1.22em;" target="_blank">https://www.nature.com/articles/srep11573</a></span><span style="font-family: Georgia, serif; font-size: 10pt; line-height: 1.22em;"> </span><span style="font-family: arial, helvetica;"><br clear="none" /></span></div><div style="color: #222222; font-family: Roboto, sans-serif; font-size: 12px; letter-spacing: 0px;"><span style="font-family: Georgia, serif; font-size: 10pt; line-height: 1.22em;"><br clear="none" /></span></div><div><span style="color: #222222; font-family: Georgia, serif; font-size: 10pt; letter-spacing: 0px; line-height: 1.22em;"></span><div style="color: #222222; font-family: Roboto, sans-serif; font-size: 12px; letter-spacing: 0px; line-height: 1.22em;"><span style="font-size: 10pt; line-height: 1.22em;">O.05: Transmission of prions to primates after extended silent incubation periods: Implications for BSE and scrapie risk assessment in human populations </span></div><span style="color: #222222; font-family: monospace; font-size: small; letter-spacing: 0px; line-height: 1.22em; white-space: pre;">
</span><div style="line-height: 1.22em;"><div class="yiv1670726472aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="color: #222222; font-family: arial, helvetica; font-size: 10pt; letter-spacing: 0px; line-height: 1.22em;"><span style="font-family: Georgia, serif; font-size: 10pt; line-height: 1.22em;"><span style="line-height: 1.22em;">Emmanuel Comoy, Jacqueline Mikol, Valerie Durand, Sophie Luccantoni, Evelyne Correia, Nathalie Lescoutra, Capucine Dehen, and Jean-Philippe Deslys Atomic Energy Commission; Fontenay-aux-Roses, France </span><br clear="none" style="line-height: 1.22em;" /><br clear="none" style="line-height: 1.22em;" /><span style="line-height: 1.22em;">Prion diseases (PD) are the unique neurodegenerative proteinopathies reputed to be transmissible under field conditions since decades. The transmission of Bovine Spongiform Encephalopathy (BSE) to humans evidenced that an animal PD might be zoonotic under appropriate conditions. Contrarily, in the absence of obvious (epidemiological or experimental) elements supporting a transmission or genetic predispositions, PD, like the other proteinopathies, are reputed to occur spontaneously (atpical animal prion strains, sporadic CJD summing 80% of human prion cases). </span><br clear="none" style="line-height: 1.22em;" /><br clear="none" style="line-height: 1.22em;" /><span style="line-height: 1.22em;">Non-human primate models provided the first evidences supporting the transmissibiity of human prion strains and the zoonotic potential of BSE. Among them, cynomolgus macaques brought major information for BSE risk assessment for human health (Chen, 2014), according to their phylogenetic proximity to humans and extended lifetime. We used this model to assess the zoonotic potential of other animal PD from bovine, ovine and cervid origins even after very long silent incubation periods. </span><br clear="none" style="line-height: 1.22em;" /><br clear="none" style="line-height: 1.22em;" /><span style="line-height: 1.22em;">*** We recently observed the direct transmission of a natural classical scrapie isolate to macaque after a 10-year silent incubation period, </span><br clear="none" style="line-height: 1.22em;" /><br clear="none" style="line-height: 1.22em;" /><span style="line-height: 1.22em;">***with features similar to some reported for human cases of sporadic CJD, albeit requiring fourfold long incubation than BSE. Scrapie, as recently evoked in humanized mice (Cassard, 2014), </span><br clear="none" style="line-height: 1.22em;" /><br clear="none" style="line-height: 1.22em;" /><span style="line-height: 1.22em;">***is the third potentially zoonotic PD (with BSE and L-type BSE), </span><br clear="none" style="line-height: 1.22em;" /><br clear="none" style="line-height: 1.22em;" /><span style="line-height: 1.22em;">***thus questioning the origin of human sporadic cases. </span><br clear="none" style="line-height: 1.22em;" /><br clear="none" style="line-height: 1.22em;" /><span style="line-height: 1.22em;">We will present an updated panorama of our different transmission studies and discuss the implications of such extended incubation periods on risk assessment of animal PD for human health. </span><br clear="none" style="line-height: 1.22em;" /><br clear="none" style="line-height: 1.22em;" /><span style="line-height: 1.22em;">=============== </span><br clear="none" style="line-height: 1.22em;" /><br clear="none" style="line-height: 1.22em;" /><span style="line-height: 1.22em;">***thus questioning the origin of human sporadic cases*** </span><br clear="none" style="line-height: 1.22em;" /><br clear="none" style="line-height: 1.22em;" /><span style="line-height: 1.22em;">=============== </span><br clear="none" style="line-height: 1.22em;" /><br clear="none" style="line-height: 1.22em;" /><span style="line-height: 1.22em;">***our findings suggest that possible transmission risk of H-type BSE to sheep and human. Bioassay will be required to determine whether the PMCA products are infectious to these animals. </span><br clear="none" style="line-height: 1.22em;" /><br clear="none" style="line-height: 1.22em;" /><span style="line-height: 1.22em;">============== </span><br clear="none" style="line-height: 1.22em;" /><br clear="none" style="line-height: 1.22em;" /></span><span face="Arial, sans-serif" style="font-size: 10pt; line-height: 1.22em;"><a href="https://prion2015.files.wordpress.com/2015/05/prion2015abstracts.pdf" rel="nofollow noopener noreferrer" shape="rect" style="color: purple; cursor: pointer; line-height: 1.22em;" target="_blank"><span face="Verdana, sans-serif" style="line-height: 1.22em;"></span></a><a href="https://prion2015.files.wordpress.com/2015/05/prion2015abstracts.pdf" rel="nofollow noopener noreferrer" shape="rect" style="color: purple; cursor: pointer; line-height: 1.22em;" target="_blank">https://prion2015.files.wordpress.com/2015/05/prion2015abstracts.pdf</a></span><span style="font-family: Georgia, serif; font-size: 10pt; line-height: 1.22em;"> </span><span style="font-family: Georgia, serif; font-size: 10pt; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /><br clear="none" style="line-height: 1.22em;" /><span style="line-height: 1.22em;">***Transmission data also revealed that several scrapie prions propagate in HuPrP-Tg mice with efficiency comparable to that of cattle BSE. While the efficiency of transmission at primary passage was low, subsequent passages resulted in a highly virulent prion disease in both Met129 and Val129 mice. </span><br clear="none" style="line-height: 1.22em;" /><br clear="none" style="line-height: 1.22em;" /><span style="line-height: 1.22em;">***Transmission of the different scrapie isolates in these mice leads to the emergence of prion strain phenotypes that showed similar characteristics to those displayed by MM1 or VV2 sCJD prion. </span><br clear="none" style="line-height: 1.22em;" /><br clear="none" style="line-height: 1.22em;" /><span style="line-height: 1.22em;">***These results demonstrate that scrapie prions have a zoonotic potential and raise new questions about the possible link between animal and human prions. </span><br clear="none" style="line-height: 1.22em;" /><br clear="none" style="line-height: 1.22em;" /></span><span face="Arial, sans-serif" style="font-size: 10pt; line-height: 1.22em;"><a href="http://www.tandfonline..com/doi/abs/10.1080/19336896.2016.1163048?journalCode=kprn20" rel="nofollow noopener noreferrer" shape="rect" style="color: purple; cursor: pointer; line-height: 1.22em;" target="_blank"><span face="Verdana, sans-serif" style="line-height: 1.22em;"></span></a><a href="http://www.tandfonline.com/doi/abs/10.1080/19336896.2016.1163048?journalCode=kprn20" rel="nofollow noopener noreferrer" shape="rect" style="color: purple; cursor: pointer; line-height: 1.22em;" target="_blank">http://www.tandfonline.com/doi/abs/10.1080/19336896.2016.1163048?journalCode=kprn20</a></span><span style="font-family: Georgia, serif; font-size: 10pt; line-height: 1.22em;"> </span></div><div class="yiv1670726472aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="color: #222222; font-family: arial, helvetica; font-size: 10pt; letter-spacing: 0px; line-height: 1.22em;"><span style="font-family: Georgia, serif; font-size: 10pt; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /><span style="line-height: 1.22em;">PRION 2016 TOKYO</span><br clear="none" style="line-height: 1.22em;" /><br clear="none" style="line-height: 1.22em;" /><span style="line-height: 1.22em;">Saturday, April 23, 2016</span><br clear="none" style="line-height: 1.22em;" /><br clear="none" style="line-height: 1.22em;" /><span style="line-height: 1.22em;">SCRAPIE WS-01: Prion diseases in animals and zoonotic potential 2016</span><br clear="none" style="line-height: 1.22em;" /><br clear="none" style="line-height: 1.22em;" /><span style="line-height: 1.22em;">Prion. 10:S15-S21. 2016 ISSN: 1933-6896 printl 1933-690X online</span><br clear="none" style="line-height: 1.22em;" /><br clear="none" style="line-height: 1.22em;" /><span style="line-height: 1.22em;">Taylor & Francis</span><br clear="none" style="line-height: 1.22em;" /><br clear="none" style="line-height: 1.22em;" /><span style="line-height: 1.22em;">Prion 2016 Animal Prion Disease Workshop Abstracts</span><br clear="none" style="line-height: 1.22em;" /><br clear="none" style="line-height: 1.22em;" /><span style="line-height: 1.22em;">WS-01: Prion diseases in animals and zoonotic potential</span><br clear="none" style="line-height: 1.22em;" /><br clear="none" style="line-height: 1.22em;" /><span style="line-height: 1.22em;">Transmission of the different scrapie isolates in these mice leads to the emergence of prion strain phenotypes that showed similar characteristics to those displayed by MM1 or VV2 sCJD prion. </span><br clear="none" style="line-height: 1.22em;" /><br clear="none" style="line-height: 1.22em;" /><span style="line-height: 1.22em;">These results demonstrate that scrapie prions have a zoonotic potential and raise new questions about the possible link between animal and human prions. </span><br clear="none" style="line-height: 1.22em;" /><br clear="none" style="line-height: 1.22em;" /></span><span face="Arial, sans-serif" style="font-size: 10pt; line-height: 1.22em;"><a href="http://www.tandfonline..com/doi/abs/10.1080/19336896.2016.1163048?journalCode=kprn20" rel="nofollow noopener noreferrer" shape="rect" style="color: purple; cursor: pointer; line-height: 1.22em;" target="_blank"><span face="Verdana, sans-serif" style="line-height: 1.22em;"></span></a><a href="http://www.tandfonline.com/doi/abs/10.1080/19336896.2016.1163048?journalCode=kprn20" rel="nofollow noopener noreferrer" shape="rect" style="color: purple; cursor: pointer; line-height: 1.22em;" target="_blank">http://www.tandfonline.com/doi/abs/10.1080/19336896.2016.1163048?journalCode=kprn20</a></span></div><div class="yiv1670726472aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="color: #222222; font-family: arial, helvetica; font-size: 12pt; letter-spacing: 0px; line-height: 1.22em; margin: 0in 0in 0.0001pt;"><span style="font-size: 10pt; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /><span style="font-family: Georgia, serif; line-height: 1.22em;">Title: Transmission of scrapie prions to primate after an extended silent incubation period) </span><br clear="none" style="line-height: 1.22em;" /><br clear="none" style="line-height: 1.22em;" /><span style="font-family: Georgia, serif; line-height: 1.22em;">*** In complement to the recent demonstration that humanized mice are susceptible to scrapie, we report here the first observation of direct transmission of a natural classical scrapie isolate to a macaque after a 10-year incubation period. Neuropathologic examination revealed all of the features of a prion disease: spongiform change, neuronal loss, and accumulation of PrPres throughout the CNS. </span><br clear="none" style="line-height: 1.22em;" /><br clear="none" style="line-height: 1.22em;" /><span style="font-family: Georgia, serif; line-height: 1.22em;">*** This observation strengthens the questioning of the harmlessness of scrapie to humans, at a time when protective measures for human and animal health are being dismantled and reduced as c-BSE is considered controlled and being eradicated. </span><br clear="none" style="line-height: 1.22em;" /><br clear="none" style="line-height: 1.22em;" /><span style="font-family: Georgia, serif; line-height: 1.22em;">*** Our results underscore the importance of precautionary and protective measures and the necessity for long-term experimental transmission studies to assess the zoonotic potential of other animal prion strains. </span><br clear="none" style="line-height: 1.22em;" /><br clear="none" style="line-height: 1.22em;" /></span><span face="Arial, sans-serif" style="font-size: 10pt; line-height: 1.22em;"><a href="http://www.ars.usda.gov/research/publications/publications.htm?SEQ_NO_115=313160" rel="nofollow noopener noreferrer" shape="rect" style="color: purple; cursor: pointer; line-height: 1.22em;" target="_blank"><span face="Verdana, sans-serif" style="line-height: 1.22em;"></span></a><a href="http://www.ars.usda.gov/research/publications/publications.htm?SEQ_NO_115=313160" rel="nofollow noopener noreferrer" shape="rect" style="color: purple; cursor: pointer; line-height: 1.22em;" target="_blank">http://www.ars.usda.gov/research/publications/publications.htm?SEQ_NO_115=313160</a></span></div><div class="yiv1670726472aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="color: #222222; font-family: arial, helvetica; font-size: 12pt; letter-spacing: 0px; line-height: 1.22em; margin: 0in 0in 0.0001pt;"><br clear="none" /></div><div class="yiv1670726472aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;"><div style="color: #222222; font-family: Roboto, sans-serif; font-size: small; letter-spacing: 0px;"><span style="font-size: x-small;">1: J Infect Dis 1980 Aug;142(2):205-8</span></div><div style="color: #222222; font-family: Roboto, sans-serif; font-size: small; letter-spacing: 0px;"><span style="font-size: x-small;"><br clear="none" /></span></div><div style="color: #222222; font-family: Roboto, sans-serif; font-size: small; letter-spacing: 0px;"><span style="font-size: x-small;">Oral transmission of kuru, Creutzfeldt-Jakob disease, and scrapie to nonhuman primates.</span></div><div style="color: #222222; font-family: Roboto, sans-serif; font-size: small; letter-spacing: 0px;"><span style="font-size: x-small;"><br clear="none" /></span></div><div style="color: #222222; font-family: Roboto, sans-serif; font-size: small; letter-spacing: 0px;"><span style="font-size: x-small;">Gibbs CJ Jr, Amyx HL, Bacote A, Masters CL, Gajdusek DC.</span></div><div style="color: #222222; font-family: Roboto, sans-serif; font-size: small; letter-spacing: 0px;"><span style="font-size: x-small;"><br clear="none" /></span></div><div style="color: #222222; font-family: Roboto, sans-serif; font-size: small; letter-spacing: 0px;"><span style="font-size: x-small;">Kuru and Creutzfeldt-Jakob disease of humans and scrapie disease of sheep and goats were transmitted to squirrel monkeys (Saimiri sciureus) that were exposed to the infectious agents only by their nonforced consumption of known infectious tissues. The asymptomatic incubation period in the one monkey exposed to the virus of kuru was 36 months; that in the two monkeys exposed to the virus of Creutzfeldt-Jakob disease was 23 and 27 months, respectively; and that in the two monkeys exposed to the virus of scrapie was 25 and 32 months, respectively. Careful physical examination of the buccal cavities of all of the monkeys failed to reveal signs or oral lesions. One additional monkey similarly exposed to kuru has remained asymptomatic during the 39 months that it has been under observation.</span></div><div style="color: #222222; font-family: Roboto, sans-serif; font-size: small; letter-spacing: 0px;"><span style="font-size: x-small;"><br clear="none" /></span></div><div style="color: #222222; font-family: Roboto, sans-serif; font-size: small; letter-spacing: 0px;"><span style="font-size: x-small;">snip...</span></div><div style="color: #222222; font-family: Roboto, sans-serif; font-size: small; letter-spacing: 0px;"><span style="font-size: x-small;"><br clear="none" /></span></div><div style="color: #222222; font-family: Roboto, sans-serif; font-size: small; letter-spacing: 0px;"><span style="font-size: x-small;">The successful transmission of kuru, Creutzfeldt-Jakob disease, and scrapie by natural feeding to squirrel monkeys that we have reported provides further grounds for concern that scrapie-infected meat may occasionally give rise in humans to Creutzfeldt-Jakob disease.</span></div><div style="color: #222222; font-family: Roboto, sans-serif; font-size: small; letter-spacing: 0px;"><span style="font-size: x-small;"><br clear="none" /></span></div><div style="color: #222222; font-family: Roboto, sans-serif; font-size: small; letter-spacing: 0px;"><span style="font-size: x-small;">PMID: 6997404</span></div><div style="color: #222222; font-family: Roboto, sans-serif; font-size: small; letter-spacing: 0px;"><span style="font-size: x-small;"><br clear="none" /></span></div><div style="color: #222222; font-family: Roboto, sans-serif; font-size: small; letter-spacing: 0px;"><a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=6997404&dopt=Abstract" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=6997404&dopt=Abstract</a><br clear="none" /></div><div style="color: #222222; font-family: Roboto, sans-serif; font-size: small; letter-spacing: 0px;"><span style="font-size: x-small;"><br clear="none" /></span></div><div style="color: #222222; font-family: Roboto, sans-serif; font-size: small; letter-spacing: 0px;"><span style="font-size: x-small;">Recently the question has again been brought up as to whether scrapie is transmissible to man. This has followed reports that the disease has been transmitted to primates. One particularly lurid speculation (Gajdusek 1977) conjectures that the agents of scrapie, kuru, Creutzfeldt-Jakob disease and transmissible encephalopathy of mink are varieties of a single "virus". The U.S. Department of Agriculture concluded that it could "no longer justify or permit scrapie-blood line and scrapie-exposed sheep and goats to be processed for human or animal food at slaughter or rendering plants" (ARC 84/77)" The problem is emphasised by the finding that some strains of scrapie produce lesions identical to the once which characterise the human dementias"</span></div><div style="color: #222222; font-family: Roboto, sans-serif; font-size: small; letter-spacing: 0px;"><span style="font-size: x-small;"><br clear="none" /></span></div><div style="color: #222222; font-family: Roboto, sans-serif; font-size: small; letter-spacing: 0px;"><span style="font-size: x-small;">Whether true or not. the hypothesis that these agents might be transmissible to man raises two considerations. First, the safety of laboratory personnel requires prompt attention. Second, action such as the "scorched meat" policy of USDA makes the solution of the scrapie problem urgent if the sheep industry is not to suffer grievously.</span></div><div style="color: #222222; font-family: Roboto, sans-serif; font-size: small; letter-spacing: 0px;"><span style="font-size: x-small;"><br clear="none" /></span></div><div style="color: #222222; font-family: Roboto, sans-serif; font-size: small; letter-spacing: 0px;"><span style="font-size: x-small;">snip...</span></div><div style="color: #222222; font-family: Roboto, sans-serif; font-size: small; letter-spacing: 0px;"><span style="font-size: x-small;"><br clear="none" /></span></div><div style="color: #222222; font-family: Roboto, sans-serif; font-size: small; letter-spacing: 0px;"><span style="font-size: x-small;">76/10.12/4.6</span></div><div style="color: #222222; font-family: Roboto, sans-serif; font-size: small; letter-spacing: 0px;"><span style="font-size: x-small;"><br clear="none" /></span></div><div style="color: #222222; font-family: Roboto, sans-serif; font-size: small; letter-spacing: 0px;"><a href="http://web.archive.org/web/20010305223125/www.bseinquiry.gov.uk/files/yb/1976/10/12004001.pdf" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">http://web.archive.org/web/20010305223125/www.bseinquiry.gov.uk/files/yb/1976/10/12004001.pdf</a><br clear="none" /></div><div style="color: #222222; font-family: Roboto, sans-serif; font-size: small; letter-spacing: 0px;"><br clear="none" /></div><div style="color: #222222; font-family: Roboto, sans-serif; font-size: small; letter-spacing: 0px;"><span style="font-size: x-small;">Nature. 1972 Mar 10;236(5341):73-4.</span></div><div style="color: #222222; font-family: Roboto, sans-serif; font-size: small; letter-spacing: 0px;"><span style="font-size: x-small;"><br clear="none" /></span></div><div style="color: #222222; font-family: Roboto, sans-serif; font-size: small; letter-spacing: 0px;"><span style="font-size: x-small;">Transmission of scrapie to the cynomolgus monkey (Macaca fascicularis).</span></div><div style="color: #222222; font-family: Roboto, sans-serif; font-size: small; letter-spacing: 0px;"><span style="font-size: x-small;"><br clear="none" /></span></div><div style="color: #222222; font-family: Roboto, sans-serif; font-size: small; letter-spacing: 0px;"><span style="font-size: x-small;">Gibbs CJ Jr, Gajdusek DC.</span></div><div style="color: #222222; font-family: Roboto, sans-serif; font-size: small; letter-spacing: 0px;"><span style="font-size: x-small;"><br clear="none" /></span></div><div style="color: #222222; font-family: Roboto, sans-serif; font-size: small; letter-spacing: 0px;"><span style="font-size: x-small;">Nature 236, 73 - 74 (10 March 1972); doi:10.1038/236073a0</span></div><div style="color: #222222; font-family: Roboto, sans-serif; font-size: small; letter-spacing: 0px;"><span style="font-size: x-small;"><br clear="none" /></span></div><div style="color: #222222; font-family: Roboto, sans-serif; font-size: small; letter-spacing: 0px;"><span style="font-size: x-small;">Transmission of Scrapie to the Cynomolgus Monkey (Macaca fascicularis)</span></div><div style="color: #222222; font-family: Roboto, sans-serif; font-size: small; letter-spacing: 0px;"><span style="font-size: x-small;"><br clear="none" /></span></div><div style="color: #222222; font-family: Roboto, sans-serif; font-size: small; letter-spacing: 0px;"><span style="font-size: x-small;">C. J. GIBBS jun. & D. C. GAJDUSEK</span></div><div style="color: #222222; font-family: Roboto, sans-serif; font-size: small; letter-spacing: 0px;"><span style="font-size: x-small;"><br clear="none" /></span></div><div style="color: #222222; font-family: Roboto, sans-serif; font-size: small; letter-spacing: 0px;"><span style="font-size: x-small;">National Institute of Neurological Diseases and Stroke, National Institutes of Health, Bethesda, Maryland</span></div><div style="color: #222222; font-family: Roboto, sans-serif; font-size: small; letter-spacing: 0px;"><span style="font-size: x-small;"><br clear="none" /></span></div><div style="color: #222222; font-family: Roboto, sans-serif; font-size: small; letter-spacing: 0px;"><span style="font-size: x-small;">SCRAPIE has been transmitted to the cynomolgus, or crab-eating, monkey (Macaca fascicularis) with an incubation period of more than 5 yr from the time of intracerebral inoculation of scrapie-infected mouse brain. The animal developed a chronic central nervous system degeneration, with ataxia, tremor and myoclonus with associated severe scrapie-like pathology of intensive astroglial hypertrophy and proliferation, neuronal vacuolation and status spongiosus of grey matter. The strain of scrapie virus used was the eighth passage in Swiss mice (NIH) of a Compton strain of scrapie obtained as ninth intracerebral passage of the agent in goat brain, from Dr R. L. Chandler (ARC, Compton, Berkshire).</span></div><div style="color: #222222; font-family: Roboto, sans-serif; font-size: small; letter-spacing: 0px;"><span style="font-size: x-small;"><br clear="none" /></span></div><div style="color: #222222; font-family: Roboto, sans-serif; font-size: small; letter-spacing: 0px;"><a href="http://www.nature.com/nature/journal/v236/n5341/abs/236073a0.html" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">http://www.nature.com/nature/journal/v236/n5341/abs/236073a0.html</a><br clear="none" /></div><div style="color: #222222; font-family: Roboto, sans-serif; font-size: small; letter-spacing: 0px;"><br clear="none" /></div><div style="color: #222222; font-family: Roboto, sans-serif; font-size: small; letter-spacing: 0px;"><a href="http://scrapie-usa.blogspot.com/2010/04/scrapie-and-atypical-scrapie.html" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">http://scrapie-usa.blogspot.com/2010/04/scrapie-and-atypical-scrapie.html</a><br clear="none" /></div><div style="color: #222222; font-family: Roboto, sans-serif; font-size: small; letter-spacing: 0px;"><br clear="none" /></div><div style="color: #222222; font-family: Roboto, sans-serif; font-size: small; letter-spacing: 0px;"><span style="font-size: x-small;">Wednesday, February 16, 2011</span></div><div style="color: #222222; font-family: Roboto, sans-serif; font-size: small; letter-spacing: 0px;"><span style="font-size: x-small;"><br clear="none" /></span></div><div style="color: #222222; font-family: Roboto, sans-serif; font-size: small; letter-spacing: 0px;"><span style="font-size: x-small;">IN CONFIDENCE</span></div><div style="color: #222222; font-family: Roboto, sans-serif; font-size: small; letter-spacing: 0px;"><span style="font-size: x-small;"><br clear="none" /></span></div><div style="color: #222222; font-family: Roboto, sans-serif; font-size: small; letter-spacing: 0px;"><span style="font-size: x-small;">SCRAPIE TRANSMISSION TO CHIMPANZEES</span></div><div style="color: #222222; font-family: Roboto, sans-serif; font-size: small; letter-spacing: 0px;"><span style="font-size: x-small;"><br clear="none" /></span></div><div style="color: #222222; font-family: Roboto, sans-serif; font-size: small; letter-spacing: 0px;"><span style="font-size: x-small;">IN CONFIDENCE</span></div><div style="color: #222222; font-family: Roboto, sans-serif; font-size: small; letter-spacing: 0px;"><span style="font-size: x-small;"><br clear="none" /></span></div><div style="font-size: 10pt;"><span face="Arial, Helvetica, sans-serif" style="color: #222222; font-size: small;"></span><div>reference...</div><div><br clear="none" /></div><div>RB3.20</div><div><br clear="none" /></div><div>TRANSMISSION TO CHIMPANZEES</div><div><br clear="none" /></div><div>1. Kuru and CJD have been successfully transmitted to chimpanzees but scrapie and TME have not.</div><div><br clear="none" /></div><div>2. We cannot say that scrapie will not transmit to chimpanzees. There are several scrapie strains and I am not aware that all have been tried (that would have to be from mouse passaged material). Nor has a wide enough range of field isolates subsequently strain typed in mice been inoculated by the appropriate routes (i/c, ilp and i/v) :</div><div><br clear="none" /></div><div>3. I believe the proposed experiment to determine transmissibility, if conducted, would only show the susceptibility or resistance of the chimpanzee to infection/disease by the routes used and the result could not be interpreted for the predictability of the susceptibility for man. Proposals for prolonged oral exposure of chimpanzees to milk from cattle were suggested a long while ago and rejected.</div><div><br clear="none" /></div><div>4. In view of Dr Gibbs' probable use of chimpazees Mr Wells' comments (enclosed) are pertinent. I have yet to receive a direct communication from Dr Schellekers but before any collaboration or provision of material we should identify the Gibbs' proposals and objectives.</div><div><br clear="none" /></div><div>5. A positive result from a chimpanzee challenged severely would likely create alarm in some circles even if the result could not be interpreted for man. I have a view that all these agents could be transmitted provided a large enough dose by appropriate routes was given and the animals kept long enough. Until the mechanisms of the species barrier are more clearly understood it might be best to retain that hypothesis.</div><div><br clear="none" /></div><div>6. A negative result would take a lifetime to determine but that would be a shorter period than might be available for human exposure and it would still not answer the question regarding mans' susceptibility. In the meantime no doubt the negativity would be used defensively. It would however be counterproductive if the experiment finally became positive. We may learn more about public reactions following next Monday' s meeting.</div><div><br clear="none" /></div><div>R. Bradley</div><div><br clear="none" /></div><div>23 September 1990</div><div><br clear="none" /></div><div>CVO (+Mr Wells' comments)</div><div><br clear="none" /></div><div>Dr T W A Little</div><div><br clear="none" /></div><div>Dr B J Shreeve</div><div><br clear="none" /></div><div>90/9.23/1.1.</div></div><div style="color: #222222; font-family: Roboto, sans-serif; font-size: small; letter-spacing: 0px;"><span style="font-size: x-small;"><br clear="none" /></span></div><div style="font-size: 10pt;"><a href="http://web.archive.org/web/20090506041740/http://www.bseinquiry.gov.uk/files/yb/1990/09/23001001.pdf" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">http://web.archive.org/web/20090506041740/http://www.bseinquiry.gov.uk/files/yb/1990/09/23001001.pdf</a><br clear="none" /></div><div style="font-size: 10pt;"><br clear="none" /></div><div><div style="font-size: 10pt;">IN CONFIDENCE CHIMPANZEES</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">CODE 18-77 Reference RB3.46</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">Some further information that may assist in decision making has been gained by discussion with Dr Rosalind Ridley.</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">She says that careful study of Gajdusek's work shows no increased susceptibility of chimpanzees over New World Monkeys such as Squirrel Monkeys. She does not think it would tell you anything about the susceptibility to man. Also Gajdusek did not, she believes, challenge chimpanzees with scrapie as severely as we did pigs and we know little of that source of scrapie. Comparisons would be difficult. She also would not expect the Home Office to sanction such experiments here unless there was a very clear and important objective that would be important for human health protection. She doubted such a case could be made. If this is the case she thought it would be unethical to do an experiment abroad because we could not do it in our own country.</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">Retrospectively she feels they should have put up more marmosets than they did. They all remain healthy. They would normally regard the transmission as negative if no disease resulted in five years.</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">We are not being asked for a decision but I think that before we made one we should gain as much knowledge as we can. If we decided to proceed we would have to bear any criticisms for many years if there was an adverse view by scientists ormedia. This should not be undertaken lightly. There is already some adverse comment here, I gather, on the pig experiment though that will subside.</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">The Gibbs' (as' distinct from Schellekers') study is somewhat different. We are merely supplying material for comparative studies in a laboratory with the greatest experience of human SEs in the world and it has been sanctioned by USDA (though we do not know for certain yet if chimpanzees specifically will be used). This would keep it at a lower profile than if we conducted such an experiment in the UK or Europe.</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">I consider we must have very powerful and defendable objectives to go beyond Gibbs' proposed experiments and should not initiate others just because an offer has been made.</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">Scientists have a responsibility to seek other methods of investigative research other than animal experimentation. At present no objective has convinced me we need to do research using Chimpanzees - a species in need of protection. Resisting such proposals would enable us to communicate that information to the scientist and the public should the need arise. A line would have been drawn.</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">CVO cc Dr T Dr B W A Little Dr B J Shreeve</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">R Bradley</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">26 September 1990</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">90/9.26/3.2</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;"><a href="http://web.archive.org/web/20090506041605/http://www.bseinquiry.gov.uk/files/yb/1990/09/26003001.pdf" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">http://web.archive.org/web/20090506041605/http://www.bseinquiry.gov.uk/files/yb/1990/09/26003001.pdf</a><br clear="none" /></div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">this is tse prion political theater here, i.e. what i call TSE PRION POKER...tss</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;"><a href="http://web.archive.org/web/20031028205208/www.bseinquiry.gov.uk/files/yb/1990/08/28002001.pdf" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">http://web.archive.org/web/20031028205208/www.bseinquiry.gov.uk/files/yb/1990/08/28002001.pdf</a><br clear="none" /></div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;"><a href="http://web.archive.org/web/20030822170317/www.bseinquiry.gov.uk/files/yb/1990/11/01005001.pdf" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">http://web.archive.org/web/20030822170317/www.bseinquiry.gov.uk/files/yb/1990/11/01005001.pdf</a><br clear="none" /></div><div style="font-size: 10pt;"><br clear="none" /></div><div>3. Prof. A. Robertson gave a brief account of BSE. The US approach was to accord it a very low profile indeed. Dr. A Thiermann showed the picture in the ''Independent'' with cattle being incinerated and thought this was a fanatical incident to be avoided in the US at all costs.<br clear="none" /></div><div><br clear="none" /></div><div>snip...</div><div style="font-size: 10pt;"><br clear="none" /></div><div><div>PAGE 26</div><div><br clear="none" /></div><div>Transmission Studies</div><div><br clear="none" /></div><div>Mule deer transmissions of CWD were by intracerebral inoculation and compared with natural cases {the following was written but with a single line marked through it ''first passage (by this route)}....TSS</div><div><br clear="none" /></div><div>resulted in a more rapidly progressive clinical disease with repeated episodes of synocopy ending in coma. One control animal became affected, it is believed through contamination of inoculum (?saline). Further CWD transmissions were carried out by Dick Marsh into ferret, mink and squirrel monkey. Transmission occurred in ALL of these species with the shortest incubation period in the ferret.</div><div><br clear="none" /></div><div>The occurrence of CWD must be viewed against the contest of the locations in which it occurred. It was an incidental and unwelcome complication of the respective wildlife research programmes. Despite its subsequent recognition as a new disease of cervids, therefore justifying direct investigation, no specific research funding was forthcoming. The USDA veiwed it as a wildlife problem and consequently not their province! ...page 26. <br clear="none" /></div><div><br clear="none" /></div><div>snip...see;</div><div><br clear="none" /></div><div>IN CONFIDENCE</div><div><br clear="none" /></div><div>PERCEPTIONS OF UNCONVENTIONAL SLOW VIRUS DISEASE OF ANIMALS IN THE USA</div><div><br clear="none" /></div><div>GAH WELLS</div><div><br clear="none" /></div><div>REPORT OF A VISIT TO THE USA</div><div><br clear="none" /></div><div>APRIL-MAY 1989</div><div><br clear="none" /></div><div><a href="http://web.archive.org/web/20090506002237/http://www.bseinquiry.gov.uk/files/mb/m11b/tab01.pdf" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">http://web.archive.org/web/20090506002237/http://www.bseinquiry.gov.uk/files/mb/m11b/tab01.pdf</a></div><div><br clear="none" /></div><div><div dir="ltr" style="font-family: Arial, Helvetica, sans-serif; font-size: 12px;">Thursday, July 29, 2021 <br clear="none" /></div><div dir="ltr" style="font-family: Arial, Helvetica, sans-serif; font-size: 12px;"><br clear="none" /></div><div dir="ltr" style="font-family: Arial, Helvetica, sans-serif; font-size: 12px;">TSE PRION OCCUPATIONAL EXPOSURE VIA ANIMAL OR HUMAN, iatrogenic transmission, nvCJD or sCJD, what if? <br clear="none" /></div><div dir="ltr" style="font-family: Arial, Helvetica, sans-serif; font-size: 12px;"><br clear="none" /></div><div dir="ltr" style="font-family: Arial, Helvetica, sans-serif; font-size: 12px;"><a href="https://itseprion.blogspot.com/2021/07/tse-prion-occupational-exposure-via.html" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://itseprion.blogspot.com/2021/07/tse-prion-occupational-exposure-via.html</a></div></div></div></div></div></div></div></div></div></div></div></div></div></div></div></div></div></div></div><div style="font-size: 10pt;">Terry S. Singeltary Sr., Bacliff, Texas USA, Galveston Bay <<a href="mailto:flounder9@verizon.net" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank" ymailto="mailto:flounder9@verizon.net">flounder9@verizon.net</a>></div></div></div></div></div></div></div></div></div></div>Terry S. Singeltary Sr.http://www.blogger.com/profile/06986622967539963260noreply@blogger.com0tag:blogger.com,1999:blog-6404950019984350027.post-86861409428545739352021-06-03T13:08:00.000-07:002021-06-03T13:08:06.848-07:00Porcine Spongiform Encephalopathy PSE TSE Prion disease <div style="font-size: 10pt;">Spongiform Encephalopathy In Pigs</div><div style="font-size: 10pt;"><br /></div><div><div><span style="font-size: 13.3333px;">MF580391/1 0187</span></div><div><span style="font-size: 13.3333px;"><br /></span></div><div><span style="font-size: 13.3333px;">TO Dr J Metters IPCS FROM DO Hagger MCA/B</span></div><div><span style="font-size: 13.3333px;"><br /></span></div><div><span style="font-size: 13.3333px;">DATE 21 September 1990</span></div><div><span style="font-size: 13.3333px;"><br /></span></div><div><span style="font-size: 13.3333px;">cc Dr Jones (OR)</span></div><div><span style="font-size: 13.3333px;"><br /></span></div><div><span style="font-size: 13.3333px;">Dr Jefferys (OR}</span></div><div><span style="font-size: 13.3333px;"><br /></span></div><div><span style="font-size: 13.3333px;">Dr Rotblat (OR)</span></div><div><span style="font-size: 13.3333px;"><br /></span></div><div><span style="font-size: 13.3333px;">Dr Raine</span></div><div><span style="font-size: 13.3333px;"><br /></span></div><div><span style="font-size: 13.3333px;">Dr Purves</span></div><div><span style="font-size: 13.3333px;"><br /></span></div><div><span style="font-size: 13.3333px;">Dr Pickles</span></div><div><span style="font-size: 13.3333px;"><br /></span></div><div><span style="font-size: 13.3333px;">Dr Richardson HDD</span></div><div><span style="font-size: 13.3333px;"><br /></span></div><div><span style="font-size: 13.3333px;">SPONGTFORM ENCEPHALOPATHY IN PIGS</span></div><div><span style="font-size: 13.3333px;"><br /></span></div><div><span style="font-size: 13.3333px;">1. With reference to Dr Pickles’ minute to Dr Richardson and me of 20 September, I formally acknowledge that attention has been drawn to paragraph 7 of the internal minutes of the Tyrrell committee following its meeting on 19 September. The MCA are preparing papers for the next meeting of the CSM's Working Group which is scheduled for 31 October.</span></div><div><span style="font-size: 13.3333px;"><br /></span></div><div><span style="font-size: 13.3333px;">2. The questionnaires issued in 1989 by the MCA following Southwood sought information from the manufacturers of medicinal products on the use of tissue from all animal species, not just of bovine. Our records show that while some use is made of porcine materials in medicinal products, the only products which would appear to be in a hypothetically “higher risk" area are the adrenocorticotrophic hormone for which the source material comes from outside the United Kingdom, namely America China Sweden France and Germany. The products are manufactured by Ferring and Armour. A further product, "Zenoderm Corium implant" manufactured by Ethicon, an) makes use of porcine skin - which is not considered to be a “high See risk" tissue, - but one of its uses is described in the data sheet as ''in dural replacement' This product is sourced: from the” United Kingdom. Papers on both these products are being prepared by the MCA for consideration by the CSM Working Party at its next meeting.</span></div><div><span style="font-size: 13.3333px;"><br /></span></div><div><span style="font-size: 13.3333px;">LINE TO TAKE</span></div><div><span style="font-size: 13.3333px;"><br /></span></div><div><span style="font-size: 13.3333px;">3. If questions on pharmaceuticals are raised at the Press conference, the suggested line to take is as follows:- </span></div><div><span style="font-size: 13.3333px;"><br /></span></div><div><span style="font-size: 13.3333px;"> "There are no medicinal products licensed for use on the market which make use of UK-derived porcine tissues with which any hypothetical “high risk" ‘might be associated. The results of the recent experimental work at the CSM will be carefully examined by the CSM‘s Working Group on spongiform encephalopathy at its next meeting.</span></div><div><span style="font-size: 13.3333px;"><br /></span></div><div><span style="font-size: 13.3333px;">DO Hagger RM 1533 MT Ext 3201</span></div></div><div style="font-size: 10pt;"><br /></div><div style="font-size: 10pt;"><a href="http://web.archive.org/web/20030822054419/www.bseinquiry.gov.uk/files/yb/1990/09/21009001.pdf" style="color: #0096ef; cursor: pointer; text-decoration-line: none;">http://web.archive.org/web/20030822054419/www.bseinquiry.gov.uk/files/yb/1990/09/21009001.pdf</a><br /></div><div style="font-size: 10pt;"><br /></div><div style="font-size: 10pt;">2021 Transmissible Spongiform Encephalopathy TSE Prion End of Year Report 2020</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">CJD FOUNDATION VIRTUAL CONFERENCE CJD Foundation Research Grant Recipient Reports Panel 2 Nov 3, 2020</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">zoonotic potential of PMCA-adapted CWD PrP 96SS inoculum</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;"><a href="https://youtu.be/VfazuR7cjMc?t=1992" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://youtu.be/VfazuR7cjMc?t=1992</a></div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">4 different CWD strains, and these 4 strains have different potential to induce any folding of the human prion protein. </div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;"><a href="https://youtu.be/VfazuR7cjMc?t=2019" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://youtu.be/VfazuR7cjMc?t=2019</a></div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">***> PIGS, WILD BOAR, CWD <***</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">***> POPULATIONS OF WILD BOARS IN THE UNITED STATES INCREASING SUPSTANTUALLY AND IN MANY AREAS WE CAN SEE A HIGH DENSITY OF WILD BOARS AND HIGH INCIDENT OF CHRONIC WASTING DISEASE</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">HYPOTHOSIS AND SPECIFIC AIMS</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">HYPOTHOSIS </div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">BSE, SCRAPIE, AND CWD, EXPOSED DOMESTIC PIGS ACCUMULATE DIFFERENT QUANTITIES AND STRAINS OF PRIONS IN PERIPHERAL TISSUES, EACH ONE OF THEM WITH PARTICULAR ZOONOTIC POTENTIALS</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;"><a href="https://youtu.be/VfazuR7cjMc" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://youtu.be/VfazuR7cjMc</a></div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">Final Report – CJD Foundation Grant Program A. </div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">Project Title: Systematic evaluation of the zoonotic potential of different CWD isolates. Principal Investigator: Rodrigo Morales, PhD.</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;"><a href="https://cjdfoundation.org/sites/default/files/grant-downloads/Final%20Report%20-%20CJD%20Foundation%20-%20Morales.pdf" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://cjdfoundation.org/sites/default/files/grant-downloads/Final%20Report%20-%20CJD%20Foundation%20-%20Morales.pdf</a></div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">Systematic evaluation of the zoonotic potential of different CWD isolates. Rodrigo Morales, PhD Assistant Professor Protein Misfolding Disorders lab Mitchell Center for Alzheimer’s disease and Related Brain Disorders Department of Neurology University of Texas Health Science Center at Houston Washington DC. July 14th, 2018</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">Conclusions and Future Directions • We have developed a highly sensitive and specific CWD-PMCA platform to be used as a diagnostic tool. • Current PMCA set up allow us to mimic relevant prion inter-species transmission events. • Polymorphic changes at position 96 of the prion protein apparently alter strain properties and, consequently, the zoonotic potential of CWD isolates. • Inter-species and inter-polymorphic PrPC → PrPSc conversions further increase the spectrum of CWD isolates possibly present in nature. • CWD prions generated in 96SS PrPC substrate apparently have greater inter-species transmission potentials. • Future experiments will explore the zoonotic potential of CWD prions along different adaptation scenarios, including inter-species and inter-polymorphic.</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;"><a href="https://cjdfoundation.org/files/Conf2018/Rodrigo%20Morales%202018.pdf" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://cjdfoundation.org/files/Conf2018/Rodrigo%20Morales%202018.pdf</a></div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;"><a href="https://www.youtube.com/watch?v=CzQKemJRBlE&list=PLGXRDfDPg57yTYvn6tifH13NrSiLjv1d7&index=7&t=0s" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://www.youtube.com/watch?v=CzQKemJRBlE&list=PLGXRDfDPg57yTYvn6tifH13NrSiLjv1d7&index=7&t=0s</a></div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">Research Project: TRANSMISSION, DIFFERENTIATION, AND PATHOBIOLOGY OF TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES Location: Virus and Prion Research</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">Title: Disease-associated prion protein detected in lymphoid tissues from pigs challenged with the agent of chronic wasting disease </div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">Author item MOORE, SARAH - Orise Fellow item Kunkle, Robert item KONDRU, NAVEEN - Iowa State University item MANNE, SIREESHA - Iowa State University item SMITH, JODI - Iowa State University item KANTHASAMY, ANUMANTHA - Iowa State University item WEST GREENLEE, M - Iowa State University item Greenlee, Justin Submitted to: Prion Publication Type: Abstract Only Publication Acceptance Date: 3/15/2017 Publication Date: N/A Citation: N/A Interpretive Summary:</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">Technical Abstract: Aims: Chronic wasting disease (CWD) is a naturally-occurring, fatal neurodegenerative disease of cervids. We previously demonstrated that disease-associated prion protein (PrPSc) can be detected in the brain and retina from pigs challenged intracranially or orally with the CWD agent. In that study, neurological signs consistent with prion disease were observed only in one pig: an intracranially challenged pig that was euthanized at 64 months post-challenge. The purpose of this study was to use an antigen-capture immunoassay (EIA) and real-time quaking-induced conversion (QuIC) to determine whether PrPSc is present in lymphoid tissues from pigs challenged with the CWD agent. </div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">Methods: At two months of age, crossbred pigs were challenged by the intracranial route (n=20), oral route (n=19), or were left unchallenged (n=9). At approximately 6 months of age, the time at which commercial pigs reach market weight, half of the pigs in each group were culled (<6 month challenge groups). The remaining pigs (>6 month challenge groups) were allowed to incubate for up to 73 months post challenge (mpc). The retropharyngeal lymph node (RPLN) was screened for the presence of PrPSc by EIA and immunohistochemistry (IHC). The RPLN, palatine tonsil, and mesenteric lymph node (MLN) from 6-7 pigs per challenge group were also tested using EIA and QuIC. </div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">Results: PrPSc was not detected by EIA and IHC in any RPLNs. All tonsils and MLNs were negative by IHC, though the MLN from one pig in the oral <6 month group was positive by EIA. PrPSc was detected by QuIC in at least one of the lymphoid tissues examined in 5/6 pigs in the intracranial <6 months group, 6/7 intracranial >6 months group, 5/6 pigs in the oral <6 months group, and 4/6 oral >6 months group. Overall, the MLN was positive in 14/19 (74%) of samples examined, the RPLN in 8/18 (44%), and the tonsil in 10/25 (40%). </div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">Conclusions: This study demonstrates that PrPSc accumulates in lymphoid tissues from pigs challenged intracranially or orally with the CWD agent, and can be detected as early as 4 months after challenge. CWD-infected pigs rarely develop clinical disease and if they do, they do so after a long incubation period. This raises the possibility that CWD-infected pigs could shed prions into their environment long before they develop clinical disease. Furthermore, lymphoid tissues from CWD-infected pigs could present a potential source of CWD infectivity in the animal and human food chains.</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;"><a href="https://www.ars.usda.gov/research/publications/publication/?seqNo115=337105" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://www.ars.usda.gov/research/publications/publication/?seqNo115=337105</a></div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;"><a href="https://www.ars.usda.gov/research/publications/publication/?seqNo115=326166" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://www.ars.usda.gov/research/publications/publication/?seqNo115=326166</a></div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">Research Project: Pathobiology, Genetics, and Detection of Transmissible Spongiform Encephalopathies Location: Virus and Prion Research</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">Title: The agent of chronic wasting disease from pigs is infectious in transgenic mice expressing human PRNP </div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">Author item MOORE, S - Orise Fellow item Kokemuller, Robyn item WEST-GREENLEE, M - Iowa State University item BALKEMA-BUSCHMANN, ANNE - Friedrich-Loeffler-institut item GROSCHUP, MARTIN - Friedrich-Loeffler-institut item Greenlee, Justin Submitted to: Prion Publication Type: Abstract Only Publication Acceptance Date: 5/10/2018 Publication Date: 5/22/2018 Citation: Moore, S.J., Kokemuller, R.D., West-Greenlee, M.H., Balkema-Buschmann, A., Groschup, M.H., Greenlee, J.J. 2018. The agent of chronic wasting disease from pigs is infectious in transgenic mice expressing human PRNP. Prion 2018, Santiago de Compostela, Spain, May 22-25, 2018. Paper No. WA15, page 44.</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">Interpretive Summary:</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">Technical Abstract: We have previously shown that the chronic wasting disease (CWD) agent from white-tailed deer can be transmitted to domestic pigs via intracranial or oral inoculation although with low attack rates and restricted PrPSc accumulation. The objective of this study was to assess the potential for cross-species transmission of pig-passaged CWD using bioassay in transgenic mice. Transgenic mice expressing human (Tg40), bovine (TgBovXV) or porcine (Tg002) PRNP were inoculated intracranially with 1% brain homogenate from a pig that had been intracranially inoculated with a pool of CWD from white-tailed deer. This pig developed neurological clinical signs, was euthanized at 64 months post-inoculation, and PrPSc was detected in the brain. Mice were monitored daily for clinical signs of disease until the end of the study. Mice were considered positive if PrPSc was detected in the brain using an enzyme immunoassay (EIA). In transgenic mice expressing porcine prion protein the average incubation period was 167 days post-inoculation (dpi) and 3/27 mice were EIA positive (attack rate = 11%). All 3 mice were found dead and clinical signs were not noted prior to death. One transgenic mouse expressing bovine prion protein was euthanized due to excessive scratching at 617 dpi and 2 mice culled at the end of the study at 700 dpi were EIA positive resulting in an overall attack rate of 3/16 (19%). None of the transgenic mice expressing human prion protein that died or were euthanized up to 769 dpi were EIA positive and at study end point at 800 dpi 2 mice had positive EIA results (overall attack rate = 2/20 = 10%). The EIA optical density (OD) readings for all positive mice were at the lower end of the reference range (positive mice range, OD = 0.266-0.438; test positive reference range, OD = 0.250-4.000). To the authors’ knowledge, cervid-derived CWD isolates have not been successfully transmitted to transgenic mice expressing human prion protein. The successful transmission of pig-passaged CWD to Tg40 mice reported here suggests that passage of the CWD agent through pigs results in a change of the transmission characteristics which reduces the transmission barrier of Tg40 mice to the CWD agent. If this biological behavior is recapitulated in the original host species, passage of the CWD agent through pigs could potentially lead to increased pathogenicity of the CWD agent in humans.</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;"><a href="https://www.ars.usda.gov/research/publications/publication/?seqNo115=353091" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://www.ars.usda.gov/research/publications/publication/?seqNo115=353091</a></div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">cwd scrapie pigs oral routes </div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">***> However, at 51 months of incubation or greater, 5 animals were positive by one or more diagnostic methods. Furthermore, positive bioassay results were obtained from all inoculated groups (oral and intracranial; market weight and end of study) suggesting that swine are potential hosts for the agent of scrapie. <*** </div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">>*** Although the current U.S. feed ban is based on keeping tissues from TSE infected cattle from contaminating animal feed, swine rations in the U.S. could contain animal derived components including materials from scrapie infected sheep and goats. These results indicating the susceptibility of pigs to sheep scrapie, coupled with the limitations of the current feed ban, indicates that a revision of the feed ban may be necessary to protect swine production and potentially human health. <*** </div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">***> Results: PrPSc was not detected by EIA and IHC in any RPLNs. All tonsils and MLNs were negative by IHC, though the MLN from one pig in the oral <6 month group was positive by EIA. PrPSc was detected by QuIC in at least one of the lymphoid tissues examined in 5/6 pigs in the intracranial <6 months group, 6/7 intracranial >6 months group, 5/6 pigs in the oral <6 months group, and 4/6 oral >6 months group. Overall, the MLN was positive in 14/19 (74%) of samples examined, the RPLN in 8/18 (44%), and the tonsil in 10/25 (40%). </div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">***> Conclusions: This study demonstrates that PrPSc accumulates in lymphoid tissues from pigs challenged intracranially or orally with the CWD agent, and can be detected as early as 4 months after challenge. CWD-infected pigs rarely develop clinical disease and if they do, they do so after a long incubation period. This raises the possibility that CWD-infected pigs could shed prions into their environment long before they develop clinical disease. Furthermore, lymphoid tissues from CWD-infected pigs could present a potential source of CWD infectivity in the animal and human food chains. </div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;"><a href="https://www.ars.usda.gov/research/publications/publication/?seqNo115=353091" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://www.ars.usda.gov/research/publications/publication/?seqNo115=353091</a></div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;"><a href="https://www.ars.usda.gov/research/project/?accnNo=432011&fy=2017" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://www.ars.usda.gov/research/project/?accnNo=432011&fy=2017</a></div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;"><a href="https://www.ars.usda.gov/research/publications/publication/?seqNo115=337105" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://www.ars.usda.gov/research/publications/publication/?seqNo115=337105</a></div><div style="font-size: 10pt;"><br /></div><div style="font-size: 10pt;"><div style="font-size: small;">Research Project: TRANSMISSION, DIFFERENTIATION, AND PATHOBIOLOGY OF TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES</div><div style="font-size: small;"><br /></div><div style="font-size: small;">Location: Virus and Prion Research</div><div style="font-size: small;"><br /></div><div style="font-size: small;">Title: Disease-associated prion protein detected in lymphoid tissues from pigs challenged with the agent of chronic wasting disease)</div><div style="font-size: small;"><br /></div><div style="font-size: small;">Author item Moore, Sarah item Kunkle, Robert item Kondru, Naveen item Manne, Sireesha item Smith, Jodi item Kanthasamy, Anumantha item West Greenlee, M item Greenlee, Justin</div><div style="font-size: small;"><br /></div><div style="font-size: small;">Submitted to: Prion Publication Type: Abstract Only Publication Acceptance Date: 3/15/2017 Publication Date: N/A Citation: N/A Interpretive Summary:</div><div style="font-size: small;"><br /></div><div style="font-size: small;">Technical Abstract: Aims: Chronic wasting disease (CWD) is a naturally-occurring, fatal neurodegenerative disease of cervids. We previously demonstrated that disease-associated prion protein (PrPSc) can be detected in the brain and retina from pigs challenged intracranially or orally with the CWD agent. In that study, neurological signs consistent with prion disease were observed only in one pig: an intracranially challenged pig that was euthanized at 64 months post-challenge. The purpose of this study was to use an antigen-capture immunoassay (EIA) and real-time quaking-induced conversion (QuIC) to determine whether PrPSc is present in lymphoid tissues from pigs challenged with the CWD agent. Methods: At two months of age, crossbred pigs were challenged by the intracranial route (n=20), oral route (n=19), or were left unchallenged (n=9). At approximately 6 months of age, the time at which commercial pigs reach market weight, half of the pigs in each group were culled (<6 month challenge groups). The remaining pigs (>6 month challenge groups) were allowed to incubate for up to 73 months post challenge (mpc). The retropharyngeal lymph node (RPLN) was screened for the presence of PrPSc by EIA and immunohistochemistry (IHC). The RPLN, palatine tonsil, and mesenteric lymph node (MLN) from 6-7 pigs per challenge group were also tested using EIA and QuIC. Results: PrPSc was not detected by EIA and IHC in any RPLNs. All tonsils and MLNs were negative by IHC, though the MLN from one pig in the oral <6 month group was positive by EIA. PrPSc was detected by QuIC in at least one of the lymphoid tissues examined in 5/6 pigs in the intracranial <6 months group, 6/7 intracranial >6 months group, 5/6 pigs in the oral <6 months group, and 4/6 oral >6 months group. Overall, the MLN was positive in 14/19 (74%) of samples examined, the RPLN in 8/18 (44%), and the tonsil in 10/25 (40%). </div><div style="font-size: small;"><br /></div><div style="font-size: small;">Conclusions: This study demonstrates that PrPSc accumulates in lymphoid tissues from pigs challenged intracranially or orally with the CWD agent, and can be detected as early as 4 months after challenge. CWD-infected pigs rarely develop clinical disease and if they do, they do so after a long incubation period. This raises the possibility that CWD-infected pigs could shed prions into their environment long before they develop clinical disease. Furthermore, lymphoid tissues from CWD-infected pigs could present a potential source of CWD infectivity in the animal and human food chains.</div><div style="font-size: small;"><br /></div><div style="font-size: small;"><a href="https://www.ars.usda.gov/research/publications/publication/?seqNo115=337105%C2%A0" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://www.ars.usda.gov/research/publications/publication/?seqNo115=337105 </a>;</div><div style="font-size: small;"><br /></div><div style="font-size: small;">CONFIDENTIAL</div><div style="font-size: small;"><br /></div><div style="font-size: small;"><span style="font-size: 10pt;">EXPERIMENTAL PORCINE SPONGIFORM ENCEPHALOPATHY</span></div><div style="font-size: small;"><br /></div><div style="font-size: small;"><span style="font-size: 10pt;">While this clearly is a cause for concern we should not jump to the conclusion that this means that pigs will necessarily be infected by bone and meat meal fed by the oral route as is the case with cattle. ...</span></div><div style="font-size: small;"><br /></div><div style="font-size: small;"><span style="font-size: 10pt;"><a href="http://web.archive.org/web/20031026000118/www.bseinquiry.gov.uk/files/yb/1990/08/23004001.pdf" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://web.archive.org/web/20031026000118/www.bseinquiry.gov.uk/files/yb/1990/08/23004001.pdf</a></span></div><div style="font-size: small;"><br /></div><div style="font-size: small;"><span style="font-size: 10pt;">we cannot rule out the possibility that unrecognised subclinical spongiform encephalopathy could be present in British pigs though there is no evidence for this: only with parenteral/implantable pharmaceuticals/devices is the theoretical risk to humans of sufficient concern to consider any action.</span></div><div style="font-size: small;"><br /></div><div style="font-size: small;"><span style="font-size: 10pt;"><a href="http://web.archive.org/web/20030822031154/www.bseinquiry.gov.uk/files/yb/1990/09/10007001.pdf" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://web.archive.org/web/20030822031154/www.bseinquiry.gov.uk/files/yb/1990/09/10007001.pdf</a></span></div><div style="font-size: small;"><br /></div><div style="font-size: small;"><span style="font-size: 10pt;">May I, at the outset, reiterate that we should avoid dissemination of papers relating to this experimental finding to prevent premature release of the information. ...</span></div><div style="font-size: small;"><br /></div><div style="font-size: small;"><span style="font-size: 10pt;"><a href="http://web.archive.org/web/20030822052332/www.bseinquiry.gov.uk/files/yb/1990/09/11005001.pdf" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://web.archive.org/web/20030822052332/www.bseinquiry.gov.uk/files/yb/1990/09/11005001.pdf</a></span></div><div style="font-size: small;"><br /></div><div style="font-size: small;"><span style="font-size: 10pt;">3. It is particularly important that this information is not passed outside the Department, until Ministers have decided how they wish it to be handled. ...</span></div><div style="font-size: small;"><br /></div><div style="font-size: small;"><span style="font-size: 10pt;"><a href="http://web.archive.org/web/20030822052438/www.bseinquiry.gov.uk/files/yb/1990/09/12002001.pdf" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://web.archive.org/web/20030822052438/www.bseinquiry.gov.uk/files/yb/1990/09/12002001.pdf</a></span></div><div style="font-size: small;"><br /></div><div style="font-size: small;"><span style="font-size: 10pt;">But it would be easier for us if pharmaceuticals/devices are not directly mentioned at all. ...</span></div><div style="font-size: small;"><br /></div><div style="font-size: small;"><span style="font-size: 10pt;"><a href="http://web.archive.org/web/20030518170213/www.bseinquiry.gov.uk/files/yb/1990/09/13004001.pdf" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://web.archive.org/web/20030518170213/www.bseinquiry.gov.uk/files/yb/1990/09/13004001.pdf</a></span></div><div style="font-size: small;"><br /></div><div style="font-size: small;"><span style="font-size: 10pt;">Our records show that while some use is made of porcine materials in medicinal products, the only products which would appear to be in a hypothetically ''higher risk'' area are the adrenocorticotrophic hormone for which the source material comes from outside the United Kingdom, namely America China Sweden France and Germany. The products are manufactured by Ferring and Armour. A further product, ''Zenoderm Corium implant'' manufactured by Ethicon, makes use of porcine skin - which is not considered to be a ''high risk'' tissue, but one of its uses is described in the data sheet as ''in dural replacement''. This product is sourced from the United Kingdom.....</span></div><div style="font-size: small;"><br /></div><div style="font-size: small;"><span style="font-size: 10pt;"><a href="http://web.archive.org/web/20030822054419/www.bseinquiry.gov.uk/files/yb/1990/09/21009001.pdf" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://web.archive.org/web/20030822054419/www.bseinquiry.gov.uk/files/yb/1990/09/21009001.pdf</a></span></div><div style="font-size: small;"><br /></div><div style="font-size: small;"><span style="font-size: 10pt;">snip...</span></div><div style="font-size: small;"><br /></div><div style="font-size: small;"><span style="font-size: 10pt;">It was not until . . . August 1990, that the result from the pig persuaded both SEAC and us to change our view and to take out of pig rations any residual infectivity that might have arisen from the SBOs.</span></div><div style="font-size: small;"><br /></div><div style="font-size: small;"><span style="font-size: 10pt;"><a href="http://web.archive.org/web/20071014143511/http://www.bseinquiry.gov.uk/files/tr/tab69.pdf" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://web.archive.org/web/20071014143511/http://www.bseinquiry.gov.uk/files/tr/tab69.pdf</a></span></div><div style="font-size: small;"><br /></div><div style="font-size: small;"><span style="font-size: 10pt;">4.303 The minutes of the meeting record that:</span></div><div style="font-size: small;"><br /></div><div style="font-size: small;"><span style="font-size: 10pt;">It was very difficult to draw conclusions from one experimental result for what may happen in the field. However it would be prudent to exclude specified bovine offals from the pig diet. Although any relationship between BSE and the finding of a spongiform encephalopathy in cats had yet to be demonstrated, the fact that this had occurred suggested that a cautious view should be taken of those species which might be susceptible. The 'specified offals' of bovines should therefore be excluded from the feed of all species. 17</span></div><div style="font-size: small;"><br /></div><div style="font-size: small;"><span style="font-size: 10pt;"><a href="http://web.archive.org/web/20031026084516/http://www.bseinquiry.gov.uk/files/yb/1990/09/07001001.pdf" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://web.archive.org/web/20031026084516/http://www.bseinquiry.gov.uk/files/yb/1990/09/07001001.pdf</a></span></div><div style="font-size: small;"><br /></div><div style="font-size: small;"><span style="font-size: 10pt;">IN CONFIENCE</span></div><div style="font-size: small;"><br /></div><div style="font-size: small;"><span style="font-size: 10pt;">EXPERIMENTAL PORCINE SPONGIFORM ENCEPHALOPATHY</span></div><div style="font-size: small;"><br /></div><div style="font-size: small;"><span style="font-size: 10pt;">1. CMO should be aware that a pig inoculated experimentally (ic, iv, and ip) with BSE brain suspension has after 15 months developed an illness, now confirmed as a spongiform encephalopathy. This is the first ever description of such a disease in a pig, although it seems there ar no previous attempts at experimental inoculation with animal material. The Southwood group had thought igs would not be susceptible. Most pigs are slaughtered when a few weeks old but there have been no reports of relevant neurological illness in breeding sows or other elderly pigs. ...see full text ;</span></div><div style="font-size: small;"><br /></div><div style="font-size: small;"><span style="font-size: 10pt;"><a href="http://web.archive.org/web/20040302031004/www.bseinquiry.gov.uk/files/yb/1990/08/23001001.pdf" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://web.archive.org/web/20040302031004/www.bseinquiry.gov.uk/files/yb/1990/08/23001001.pdf</a></span></div><div style="font-size: small;"><br /></div><div style="font-size: small;"><span style="font-size: 10pt;">IN CONFIDENCE</span></div><div style="font-size: small;"><br /></div><div style="font-size: small;"><span style="font-size: 10pt;">So it is plausible pigs could be preclinically affected with BSE but since so few are allowed to reach adulthood this has not been recognised through clinical disease. ...</span></div><div style="font-size: small;"><br /></div><div style="font-size: small;"><span style="font-size: 10pt;"><a href="http://web.archive.org/web/20040904150118/www.bseinquiry.gov.uk/files/yb/1990/08/23002001.pdf" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://web.archive.org/web/20040904150118/www.bseinquiry.gov.uk/files/yb/1990/08/23002001.pdf</a></span></div><div style="font-size: small;"><br /></div><div style="font-size: small;"><span style="font-size: 10pt;">CONFIDENTIAL</span></div><div style="font-size: small;"><br /></div><div style="font-size: small;"><span style="font-size: 10pt;">EXPERIMENTAL PORCINE SPONGIFORM ENCEPHALOPATHY</span></div><div style="font-size: small;"><br /></div><div style="font-size: small;"><span style="font-size: 10pt;">While this clearly is a cause for concern we should not jump to the conclusion that this means that pigs will necessarily be infected by bone and meat meal fed by the oral route as is the case with cattle. ...</span></div><div style="font-size: small;"><br /></div><div style="font-size: small;"><span style="font-size: 10pt;"><a href="http://web.archive.org/web/20031026000118/www.bseinquiry.gov.uk/files/yb/1990/08/23004001.pdf" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://web.archive.org/web/20031026000118/www.bseinquiry.gov.uk/files/yb/1990/08/23004001.pdf</a></span></div><div style="font-size: small;"><br /></div><div style="font-size: small;"><span style="font-size: 10pt;">we cannot rule out the possibility that unrecognised subclinical spongiform encephalopathy could be present in British pigs though there is no evidence for this: only with parenteral/implantable pharmaceuticals/devices is the theoretical risk to humans of sufficient concern to consider any action.</span></div><div style="font-size: small;"><br /></div><div style="font-size: small;"><span style="font-size: 10pt;"><a href="http://web.archive.org/web/20030822031154/www.bseinquiry.gov.uk/files/yb/1990/09/10007001.pdf" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://web.archive.org/web/20030822031154/www.bseinquiry.gov.uk/files/yb/1990/09/10007001.pdf</a></span></div><div style="font-size: small;"><br /></div><div style="font-size: small;"><span style="font-size: 10pt;">May I, at the outset, reiterate that we should avoid dissemination of papers relating to this experimental finding to prevent premature release of the information. ...</span></div><div style="font-size: small;"><br /></div><div style="font-size: small;"><span style="font-size: 10pt;"><a href="http://web.archive.org/web/20030822052332/www.bseinquiry.gov.uk/files/yb/1990/09/11005001.pdf" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://web.archive.org/web/20030822052332/www.bseinquiry.gov.uk/files/yb/1990/09/11005001.pdf</a></span></div><div style="font-size: small;"><br /></div><div style="font-size: small;"><span style="font-size: 10pt;">3. It is particularly important that this information is not passed outside the Department, until Ministers have decided how they wish it to be handled. ...</span></div><div style="font-size: small;"><br /></div><div style="font-size: small;"><span style="font-size: 10pt;"><a href="http://web.archive.org/web/20030822052438/www.bseinquiry.gov.uk/files/yb/1990/09/12002001.pdf" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://web.archive.org/web/20030822052438/www.bseinquiry.gov.uk/files/yb/1990/09/12002001.pdf</a></span></div><div style="font-size: small;"><br /></div><div style="font-size: small;"><span style="font-size: 10pt;">But it would be easier for us if pharmaceuticals/devices are not directly mentioned at all. ...</span></div><div style="font-size: small;"><br /></div><div style="font-size: small;"><span style="font-size: 10pt;"><a href="http://web.archive.org/web/20030518170213/www.bseinquiry.gov.uk/files/yb/1990/09/13004001.pdf" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://web.archive.org/web/20030518170213/www.bseinquiry.gov.uk/files/yb/1990/09/13004001.pdf</a></span></div><div style="font-size: small;"><br /></div><div style="font-size: small;"><span style="font-size: 10pt;">Our records show that while some use is made of porcine materials in medicinal products, the only products which would appear to be in a hypothetically ''higher risk'' area are the adrenocorticotrophic hormone for which the source material comes from outside the United Kingdom, namely America China Sweden France and Germany. The products are manufactured by Ferring and Armour. A further product, ''Zenoderm Corium implant'' manufactured by Ethicon, makes use of porcine skin - which is not considered to be a ''high risk'' tissue, but one of its uses is described in the data sheet as ''in dural replacement''. This product is sourced from the United Kingdom.....</span></div><div style="font-size: small;"><br /></div><div style="font-size: small;"><span style="font-size: 10pt;"><a href="http://web.archive.org/web/20030822054419/www.bseinquiry.gov.uk/files/yb/1990/09/21009001.pdf" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://web.archive.org/web/20030822054419/www.bseinquiry.gov.uk/files/yb/1990/09/21009001.pdf</a></span></div><div style="font-size: small;"><br /></div><div style="font-size: small;"><span style="font-size: 10pt;">BSE TO PIGS NEWS RELEASE</span></div><div style="font-size: small;"><br /></div><div style="font-size: small;"><span style="font-size: 10pt;"><a href="http://web.archive.org/web/20030822162313/www.bseinquiry.gov.uk/files/yb/1990/09/24001001.pdf" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://web.archive.org/web/20030822162313/www.bseinquiry.gov.uk/files/yb/1990/09/24001001.pdf</a></span></div><div style="font-size: small;"><br /></div><div style="font-size: small;"><span style="font-size: 10pt;">CONFIDENTIAL</span></div><div style="font-size: small;"><br /></div><div style="font-size: small;"><span style="font-size: 10pt;">BSE: PRESS PRESENTATION</span></div><div style="font-size: small;"><br /></div><div style="font-size: small;"><span style="font-size: 10pt;"><a href="http://web.archive.org/web/20030822160958/www.bseinquiry.gov.uk/files/yb/1990/09/20003001.pdf" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://web.archive.org/web/20030822160958/www.bseinquiry.gov.uk/files/yb/1990/09/20003001.pdf</a></span></div><div style="font-size: small;"><br /></div><div style="font-size: small;"><span style="font-size: 10pt;"><a href="http://web.archive.org/web/20040623191707/www.bseinquiry.gov.uk/files/yb/1990/09/24013001.pdf" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://web.archive.org/web/20040623191707/www.bseinquiry.gov.uk/files/yb/1990/09/24013001.pdf</a></span></div><div style="font-size: small;"><br /></div><div style="font-size: small;"><span style="font-size: 10pt;"><a href="http://web.archive.org/web/20030820195733/http://www.bseinquiry.gov.uk/files/yb/1990/09/20010001.pdf" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://web.archive.org/web/20030820195733/http://www.bseinquiry.gov.uk/files/yb/1990/09/20010001.pdf</a></span></div><div style="font-size: small;"><br /></div><div style="font-size: small;"><span style="font-size: 10pt;"><a href="http://web.archive.org/web/20030820195733/http://www.bseinquiry.gov.uk/files/yb/1990/09/25013001.pdf" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://web.archive.org/web/20030820195733/http://www.bseinquiry.gov.uk/files/yb/1990/09/25013001.pdf</a></span></div><div style="font-size: small;"><br /></div><div style="font-size: small;"><span style="font-size: 10pt;"><a href="http://web.archive.org/web/20030820195733/http://www.bseinquiry.gov.uk/files/yb/1990/09/25015001.pdf" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://web.archive.org/web/20030820195733/http://www.bseinquiry.gov.uk/files/yb/1990/09/25015001.pdf</a></span></div><div style="font-size: small;"><br /></div><div style="font-size: small;"><span style="font-size: 10pt;">INDUSTRY RESPONSE TYPICAL</span></div><div style="font-size: small;"><br /></div><div style="font-size: small;"><span style="font-size: 10pt;"><a href="http://web.archive.org/web/20030822055917/www.bseinquiry.gov.uk/files/yb/1990/09/25007001.pdf" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://web.archive.org/web/20030822055917/www.bseinquiry.gov.uk/files/yb/1990/09/25007001.pdf</a></span></div><div style="font-size: small;"><br /></div><div style="font-size: small;"><span style="font-size: 10pt;">DEFENSIVE BRIEFING</span></div><div style="font-size: small;"><br /></div><div style="font-size: small;"><span style="font-size: 10pt;"><a href="http://web.archive.org/web/20030820195733/http://www.bseinquiry.gov.uk/files/yb/1990/09/25016001.pdf" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://web.archive.org/web/20030820195733/http://www.bseinquiry.gov.uk/files/yb/1990/09/25016001.pdf</a></span></div><div style="font-size: small;"><br /></div><div style="font-size: small;"><span style="font-size: 10pt;">CONFIDENTIAL</span></div><div style="font-size: small;"><br /></div><div style="font-size: small;"><span style="font-size: 10pt;">pigs & pharmaceuticals</span></div><div style="font-size: small;"><br /></div><div style="font-size: small;"><span style="font-size: 10pt;"><a href="http://web.archive.org/web/20010305223234/www.bseinquiry.gov.uk/files/yb/1990/09/10007001.pdf" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://web.archive.org/web/20010305223234/www.bseinquiry.gov.uk/files/yb/1990/09/10007001.pdf</a></span></div><div style="font-size: small;"><br /></div><div style="font-size: small;"><span style="font-size: 10pt;"><a href="http://web.archive.org/web/20010305223234/www.bseinquiry.gov.uk/files/yb/1990/08/23002001.pdf" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://web.archive.org/web/20010305223234/www.bseinquiry.gov.uk/files/yb/1990/08/23002001.pdf</a></span></div><div style="font-size: small;"><br /></div><div style="font-size: small;"><span style="font-size: 10pt;"><a href="http://web.archive.org/web/20010305223234/www.bseinquiry.gov.uk/files/yb/1990/08/23004001.pdf" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://web.archive.org/web/20010305223234/www.bseinquiry.gov.uk/files/yb/1990/08/23004001.pdf</a></span></div><div style="font-size: small;"><br /></div><div style="font-size: small;"><span style="font-size: 10pt;"><a href="http://web.archive.org/web/20010305223234/www.bseinquiry.gov.uk/files/yb/1990/08/29003001.pdf" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://web.archive.org/web/20010305223234/www.bseinquiry.gov.uk/files/yb/1990/08/29003001.pdf</a></span></div><div style="font-size: small;"><br /></div><div style="font-size: small;"><span style="font-size: 10pt;">COMMERCIAL IN CONFIDENCE COMMITTEE ON SAFETY OF MEDICINE NOT FOR PUBLICATION BOVINE SPONGIFORM ENCEPHALOPATHY WORKING GROUP</span></div><div style="font-size: small;"><br /></div><div style="font-size: small;"><span style="font-size: 10pt;">There are only two products using porcine brain and these use corticotrophin BP, made from porcine pituitary, source from outside the UK.............</span></div><div style="font-size: small;"><br /></div><div style="font-size: small;"><span style="font-size: 10pt;"><a href="http://web.archive.org/web/20040622220349/www.bseinquiry.gov.uk/files/yb/1990/10/31003001.pdf" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://web.archive.org/web/20040622220349/www.bseinquiry.gov.uk/files/yb/1990/10/31003001.pdf</a></span></div><div style="font-size: small;"><br /></div><div style="font-size: small;"><span style="font-size: 10pt;">snip...</span></div><div style="font-size: small;"><br /></div><div style="font-size: small;">7 OF 10 LITTLE PIGGIES WENT ON TO DEVELOP BSE;</div><div style="font-size: small;"><br /></div><div style="font-size: small;">1: J Comp Pathol. 2000 Feb-Apr; 122(2-3): 131-43. Related Articles,</div><div style="font-size: small;"><br /></div><div style="font-size: small;">The neuropathology of experimental bovine spongiform encephalopathy in the pig.</div><div style="font-size: small;"><br /></div><div style="font-size: small;">Ryder SJ, Hawkins SA, Dawson M, Wells GA.</div><div style="font-size: small;"><br /></div><div style="font-size: small;">Veterinary Laboratories Agency Weybridge, Woodham Lane, New Haw, Addlestone, Surrey, KT15 3NB, UK.</div><div style="font-size: small;"><br /></div><div style="font-size: small;">In an experimental study of the transmissibility of BSE to the pig, seven of 10 pigs, infected at 1-2 weeks of age by multiple-route parenteral inoculation with a homogenate of bovine brain from natural BSE cases developed lesions typical of spongiform encephalopathy. The lesions consisted principally of severe neuropil vacuolation affecting most areas of the brain, but mainly the forebrain. In addition, some vacuolar change was identified in the rostral colliculi and hypothalamic areas of normal control pigs. PrP accumulations were detected immunocytochemically in the brains of BSE-infected animals. PrP accumulation was sparse in many areas and its density was not obviously related to the degree of vacuolation. The patterns of PrP immunolabelling in control pigs differed strikingly from those in the infected animals.</div><div style="font-size: small;"><br /></div><div style="font-size: small;">PMID: 10684682 [PubMed - indexed for MEDLINE]</div><div style="font-size: small;"><br /></div><div style="font-size: small;"><a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?holding=npg&cmd=Retrieve&db=PubMed&list_uids=10684682&dopt=Abstract" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?holding=npg&cmd=Retrieve&db=PubMed&list_uids=10684682&dopt=Abstract</a></div><div style="font-size: small;"><br /></div><div style="font-size: small;">snip...</div><div style="font-size: small;"><br /></div><div style="font-size: small;">In the United States, feeding of ruminant by-products to ruminants is prohibited, but feeding of ruminant materials to swine and poultry still occurs. The potential for swine to have access to scrapie-contaminated feedstuffs exists, but the potential for swine to serve as a host for replication/accumulation of the agent of scrapie is unknown. The purpose of this study was to perform oral and intracerebral inoculation of the U.S. scrapie agent to determine the potential of swine as a host for the scrapie agent and their clinical susceptibility.</div><div style="font-size: small;"><br /></div><div style="font-size: small;">see full text and more transmission studies here ;</div><div style="font-size: small;"><br /></div><div style="font-size: small;"><a href="http://chronic-wasting-disease.blogspot.com/2011/07/swine-are-susceptible-to-chronic.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://chronic-wasting-disease.blogspot.com/2011/07/swine-are-susceptible-to-chronic.html</a></div></div><div style="font-size: 10pt;"><br clear="none" /></div><div><div>America BSE 589.2001 FEED REGULATIONS, BSE SURVEILLANCE, BSE TESTING, and CJD TSE Prion</div><div><br clear="none" /></div><div>so far, we have been lucky. to date, with the science at hand, no cwd transmitted to cattle, that has been documented, TO DATE, WITH THE SCIENCE AT HAND, it's not to say it has not already happened, just like with zoonosis of cwd i.e. molecular transmission studies have shown that cwd transmission to humans would look like sporadic cjd, NOT nvCJD or what they call now vCJD. the other thing is virulence and or horizontal transmission. this is very concerning with the recent fact of what seems to be a large outbreak of a new tse prion disease in camels in Africa. there is much concern now with hay, straw, grains, and such, with the cwd tse prion endemic countries USA, Canada. what is of greatest concern is the different strains of cwd, and the virulence there from? this thing (cwd) keeps mutating to different strains, and to different species, the bigger the chance of one of these strains that WILL TRANSMIT TO CATTLE OR HUMANS, and that it is documented (i believe both has already occured imo with scienct to date). with that said, a few things to ponder, and i am still very concerned with, the animal feed. we now know from transmission studies that cwd and scrapie will transmit to pigs by oral routes. the atypical bse strains will transmit by oral routes. i don't mean to keep kicking a mad cow, just look at the science; </div><div><br clear="none" /></div><div>***> cattle, pigs, sheep, cwd, tse, prion, oh my! </div><div><br clear="none" /></div><div>***> In contrast, cattle are highly susceptible to white-tailed deer CWD and mule deer CWD in experimental conditions but no natural CWD infections in cattle have been reported (Sigurdson, 2008; Hamir et al., 2006). </div><div><br clear="none" /></div><div>Sheep and cattle may be exposed to CWD via common grazing areas with affected deer but so far, appear to be poorly susceptible to mule deer CWD (Sigurdson, 2008). In contrast, cattle are highly susceptible to white-tailed deer CWD and mule deer CWD in experimental conditions but no natural CWD infections in cattle have been reported (Sigurdson, 2008; Hamir et al., 2006). It is not known how susceptible humans are to CWD but given that the prion can be present in muscle, it is likely that humans have been exposed to the agent via consumption of venison (Sigurdson, 2008). Initial experimental research suggests that human susceptibility to CWD is low and there may be a robust species barrier for CWD transmission to humans (Sigurdson, 2008), however the risk appetite for a public health threat may still find this level unacceptable. </div><div><br clear="none" /></div><div><a href="https://assets.publishing.service.gov.uk/government/uploads/system/uploads/attachment_data/file/733407/DEFRA_QRA_TSE_in_cervids_June2018_v1.pdf" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://assets.publishing.service.gov.uk/government/uploads/system/uploads/attachment_data/file/733407/DEFRA_QRA_TSE_in_cervids_June2018_v1.pdf</a> </div><div><br clear="none" /></div><div><a href="http://chronic-wasting-disease.blogspot.com/2012/08/susceptibility-of-cattle-to-agent-of.html" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">http://chronic-wasting-disease.blogspot.com/2012/08/susceptibility-of-cattle-to-agent-of.html</a> </div></div><div><div style="font-size: 10pt;"><div style="line-height: 1.22em;"><div style="line-height: 1.22em; margin: 0in 0in 0.0001pt;"><div style="background-color: whitesmoke; margin-bottom: 24px;"><div style="margin-bottom: 24px;"><div style="margin-bottom: 24px;"><div style="line-height: 1.22em;"><div style="line-height: 1.22em;"><div style="line-height: 1.22em;"><div dir="ltr" style="background-color: white;"><div style="font-family: Arial, Helvetica, sans-serif; font-size: 12px; letter-spacing: 0px; line-height: 1.6em; margin: 0px 0px 0.75em;"><div style="font-family: arial; font-size: 10pt;"><div style="font-size: small;"><div style="margin: 0px;"><div style="color: #29303b; font-size: 13.3333px;"><div style="font-family: arial, helvetica; font-size: 12px;"><div style="color: black; font-family: arial; font-size: 10pt;"><br clear="none" /></div><div style="color: black; font-family: arial; font-size: 10pt;"><div><span style="font-size: 10pt;">Friday, December 14, 2012 </span></div><div><span style="font-size: 10pt;"><br clear="none" /></span></div><div><span style="font-size: 10pt;">DEFRA U.K. What is the risk of Chronic Wasting Disease CWD being introduced into Great Britain? A Qualitative Risk Assessment October 2012 </span></div><div><span style="font-size: 10pt;"><br clear="none" /></span></div><div><span style="font-size: 10pt;">snip..... </span></div><div><span style="font-size: 10pt;"><br clear="none" /></span></div><div><span style="font-size: 10pt;">In the USA, under the Food and Drug Administration's BSE Feed Regulation (21 CFR 589.2000) most material (exceptions include milk, tallow, and gelatin) from deer and elk is prohibited for use in feed for ruminant animals. With regards to feed for non-ruminant animals, under FDA law, CWD positive deer may not be used for any animal feed or feed ingredients. For elk and deer considered at high risk for CWD, the FDA recommends that these animals do not enter the animal feed system. However, this recommendation is guidance and not a requirement by law. Animals considered at high risk for CWD include: </span></div><div><span style="font-size: 10pt;"><br clear="none" /></span></div><div><span style="font-size: 10pt;">1) animals from areas declared to be endemic for CWD and/or to be CWD eradication zones and </span></div><div><span style="font-size: 10pt;"><br clear="none" /></span></div><div><span style="font-size: 10pt;">2) deer and elk that at some time during the 60-month period prior to slaughter were in a captive herd that contained a CWD-positive animal. </span></div><div><span style="font-size: 10pt;"><br clear="none" /></span></div><div><span style="font-size: 10pt;">Therefore, in the USA, materials from cervids other than CWD positive animals may be used in animal feed and feed ingredients for non-ruminants. </span></div><div><span style="font-size: 10pt;"><br clear="none" /></span></div><div><span style="font-size: 10pt;">The amount of animal PAP that is of deer and/or elk origin imported from the USA to GB can not be determined, however, as it is not specified in TRACES. </span></div><div><span style="font-size: 10pt;"><br clear="none" /></span></div><div><span style="font-size: 10pt;">It may constitute a small percentage of the 8412 kilos of non-fish origin processed animal proteins that were imported from US into GB in 2011. </span></div><div><span style="font-size: 10pt;"><br clear="none" /></span></div><div><span style="font-size: 10pt;">Overall, therefore, it is considered there is a __greater than negligible risk___ that (nonruminant) animal feed and pet food containing deer and/or elk protein is imported into GB. </span></div><div><span style="font-size: 10pt;"><br clear="none" /></span></div><div><span style="font-size: 10pt;">There is uncertainty associated with this estimate given the lack of data on the amount of deer and/or elk protein possibly being imported in these products.</span><span style="font-size: 10pt;"> </span></div><div><span style="font-size: 10pt;"><br clear="none" /></span></div><div><span style="font-size: 10pt;">snip..... </span><br clear="none" /></div><div><span style="font-size: 10pt;"><br clear="none" /></span></div><div><span style="font-size: 10pt;">36% in 2007 (Almberg et al., 2011). In such areas, population declines of deer of up to 30 to 50% have been observed (Almberg et al., 2011). In areas of Colorado, the prevalence can be as high as 30% (EFSA, 2011). The clinical signs of CWD in affected adults are weight loss and behavioural changes that can span weeks or months (Williams, 2005). In addition, signs might include excessive salivation, behavioural alterations including a fixed stare and changes in interaction with other animals in the herd, and an altered stance (Williams, 2005). These signs are indistinguishable from cervids experimentally infected with bovine spongiform encephalopathy (BSE). Given this, if CWD was to be introduced into countries with BSE such as GB, for example, infected deer populations would need to be tested to differentiate if they were infected with CWD or BSE to minimise the risk of BSE entering the human food-chain via affected venison. snip..... The rate of transmission of CWD has been reported to be as high as 30% and can approach 100% among captive animals in endemic areas (Safar et al., 2008). </span></div><div><span style="font-size: 10pt;"><br clear="none" /></span></div><div><span style="font-size: 10pt;">snip..... </span></div><div><span style="font-size: 10pt;"><br clear="none" /></span></div><div><span style="font-size: 10pt;">In summary, in endemic areas, there is a medium probability that the soil and surrounding environment is contaminated with CWD prions and in a bioavailable form. In rural areas where CWD has not been reported and deer are present, there is a greater than negligible risk the soil is contaminated with CWD prion. snip..... In summary, given the volume of tourists, hunters and servicemen moving between GB and North America, the probability of at least one person travelling to/from a CWD affected area and, in doing so, contaminating their clothing, footwear and/or equipment prior to arriving in GB is greater than negligible... For deer hunters, specifically, the risk is likely to be greater given the increased contact with deer and their environment. However, there is significant uncertainty associated with these estimates. </span></div><div><span style="font-size: 10pt;"><br clear="none" /></span></div><div><span style="font-size: 10pt;">snip..... </span></div><div><span style="font-size: 10pt;"><br clear="none" /></span></div><div><span style="font-size: 10pt;">Therefore, it is considered that farmed and park deer may have a higher probability of exposure to CWD transferred to the environment than wild deer given the restricted habitat range and higher frequency of contact with tourists and returning GB residents. </span></div><div><span style="font-size: 10pt;"><br clear="none" /></span></div><div><span style="font-size: 10pt;">s</span><span style="font-size: 10pt;">nip..... </span></div><div><span style="font-size: 10pt;"><br clear="none" /></span></div><div><a href="https://web.archive.org/web/20170404125557/http://webarchive.nationalarchives.gov.uk/20130822084033/http://www.defra.gov.uk/animal-diseases/files/qra_chronic-wasting-disease-121029.pdf" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://web.archive.org/web/20170404125557/http://webarchive.nationalarchives.gov.uk/20130822084033/http://www.defra.gov.uk/animal-diseases/files/qra_chronic-wasting-disease-121029.pdf</a><br clear="none" /></div><div><span style="font-size: 10pt;"><br clear="none" /></span></div><div><span style="font-size: 10pt;">***> READ THIS VERY, VERY, CAREFULLY, AUGUST 1997 MAD COW FEED BAN WAS A SHAM, AS I HAVE STATED SINCE 1997! 3 FAILSAFES THE FDA ET AL PREACHED AS IF IT WERE THE GOSPEL, IN TERMS OF MAD COW BSE DISEASE IN USA, AND WHY IT IS/WAS/NOT A PROBLEM FOR THE USA, and those are; </span></div><div><span style="font-size: 10pt;"><br clear="none" /></span></div><div><span style="font-size: 10pt;">BSE TESTING (failed terribly and proven to be a sham) </span></div><div><span style="font-size: 10pt;"><br clear="none" /></span></div><div><span style="font-size: 10pt;">BSE SURVEILLANCE (failed terribly and proven to be a sham) </span></div><div><span style="font-size: 10pt;"><br clear="none" /></span></div><div><span style="font-size: 10pt;">BSE 589.2001 FEED REGULATIONS (another colossal failure, and proven to be a sham) </span></div><div><span style="font-size: 10pt;"><br clear="none" /></span></div><div><span style="font-size: 10pt;">these are facts folks. trump et al just admitted it with the feed ban. </span></div><div><span style="font-size: 10pt;"><br clear="none" /></span></div><div><span style="font-size: 10pt;">see; </span></div><div><span style="font-size: 10pt;"><br clear="none" /></span></div><div><span style="font-size: 10pt;">FDA Reports on VFD Compliance </span></div><div><span style="font-size: 10pt;"><br clear="none" /></span></div><div><span style="font-size: 10pt;">John Maday </span></div><div><span style="font-size: 10pt;"><br clear="none" /></span></div><div><span style="font-size: 10pt;">August 30, 2019 09:46 AM VFD-Form 007 (640x427) </span></div><div><span style="font-size: 10pt;"><br clear="none" /></span></div><div><span style="font-size: 10pt;">Before and after the current Veterinary Feed Directive rules took full effect in January, 2017, the FDA focused primarily on education and outreach. ( John Maday ) Before and after the current Veterinary Feed Directive (VFD) rules took full effect in January, 2017, the FDA focused primarily on education and outreach to help feed mills, veterinarians and producers understand and comply with the requirements. Since then, FDA has gradually increased the number of VFD inspections and initiated enforcement actions when necessary. On August 29, FDA released its first report on inspection and compliance activities. The report, titled “Summary Assessment of Veterinary Feed Directive Compliance Activities Conducted in Fiscal Years 2016 – 2018,” is available online.</span></div><div><span style="font-size: 10pt;"><br clear="none" /></span></div><div><a href="https://www.fda.gov/media/130382/download" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://www.fda.gov/media/130382/download</a><br clear="none" /></div><div><span style="font-size: 10pt;"><br clear="none" /></span></div><div><span style="font-size: 10pt;">SUNDAY, SEPTEMBER 1, 2019 </span></div><div><span style="font-size: 10pt;"><br clear="none" /></span></div><div><span style="font-size: 10pt;">***> FDA Reports on VFD Compliance </span></div><div><span style="font-size: 10pt;"><br clear="none" /></span></div><div><a href="https://bovineprp.blogspot.com/2019/09/fda-reports-on-vfd-compliance.html" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://bovineprp.blogspot.com/2019/09/fda-reports-on-vfd-compliance.html</a><br clear="none" /></div><div><span style="font-size: 10pt;"><br clear="none" /></span></div><div><span style="font-size: 10pt;">TUESDAY, APRIL 18, 2017 </span></div><div><span style="font-size: 10pt;"><br clear="none" /></span></div><div><span style="font-size: 10pt;">*** EXTREME USA FDA PART 589 TSE PRION FEED LOOP HOLE STILL EXIST, AND PRICE OF POKER GOES UP *** </span></div><div><span style="font-size: 10pt;"><br clear="none" /></span></div><div><a href="http://usdameatexport.blogspot.com/2017/04/extreme-usa-fda-part-589-tse-prion-feed.html" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">http://usdameatexport.blogspot.com/2017/04/extreme-usa-fda-part-589-tse-prion-feed.html</a></div></div></div></div></div></div></div></div></div></div></div></div></div></div></div></div></div></div><div><div style="font-stretch: normal; line-height: normal;"><div dir="ltr" style="line-height: 1.22em;"><div style="line-height: 1.22em;"><div style="line-height: 1.22em;">THURSDAY, SEPTEMBER 26, 2019 </div><div style="line-height: 1.22em;"><br clear="none" /></div><div style="line-height: 1.22em;">Veterinary Biologics Guideline 3.32E: Guideline for minimising the risk of introducing transmissible spongiform encephalopathy prions and other infectious agents through veterinary biologics<br clear="none" /></div><div style="line-height: 1.22em;"><br clear="none" /></div><div style="line-height: 1.22em;"><a href="https://bovineprp.blogspot.com/2019/09/veterinary-biologics-guideline-332e.html" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://bovineprp.blogspot.com/2019/09/veterinary-biologics-guideline-332e.html</a></div><div style="line-height: 1.22em;"><br clear="none" /></div><div style="line-height: 1.22em;"><div style="color: #29303b; font-size: 10pt;">U.S.A. 50 STATE BSE MAD COW CONFERENCE CALL Jan. 9, 2001</div><div style="color: #29303b; font-size: 10pt;"><br clear="none" /></div><div style="color: #29303b; font-size: 10pt;">Subject: BSE--U.S. 50 STATE CONFERENCE CALL Jan. 9, 2001</div><div style="color: #29303b; font-size: 10pt;"><br clear="none" /></div><div style="color: #29303b; font-size: 10pt;">Date: Tue, 9 Jan 2001 16:49:00 -0800</div><div style="color: #29303b; font-size: 10pt;"><br clear="none" /></div><div style="color: #29303b; font-size: 10pt;">From: "Terry S. Singeltary Sr."</div><div style="color: #29303b; font-size: 10pt;"><br clear="none" /></div><div style="color: #29303b; font-size: 10pt;">Reply-To: Bovine Spongiform Encephalopathy</div><div style="color: #29303b; font-size: 10pt;"><br clear="none" /></div><div style="color: #29303b; font-size: 10pt;">To: <a href="mailto:BSE-L@uni-karlsruhe.de" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank" ymailto="mailto:BSE-L@uni-karlsruhe.de">BSE-L@uni-karlsruhe.de</a></div><div style="color: #29303b; font-size: 10pt;"><br clear="none" /></div><div style="color: #29303b; font-size: 10pt;">snip...</div><div style="color: #29303b; font-size: 10pt;"><br clear="none" /></div><div style="color: #29303b; font-size: 10pt;">[host Richard Barns] and now a question from Terry S. Singeltary of CJD Watch.</div><div style="color: #29303b; font-size: 10pt;"><br clear="none" /></div><div style="color: #29303b; font-size: 10pt;">[TSS] yes, thank you, U.S. cattle, what kind of guarantee can you give for serum or tissue donor herds?</div><div style="color: #29303b; font-size: 10pt;"><br clear="none" /></div><div style="color: #29303b; font-size: 10pt;">[no answer, you could hear in the back ground, mumbling and 'we can't. have him ask the question again.]</div><div style="color: #29303b; font-size: 10pt;"><br clear="none" /></div><div style="color: #29303b; font-size: 10pt;">[host Richard] could you repeat the question?</div><div style="color: #29303b; font-size: 10pt;"><br clear="none" /></div><div style="color: #29303b; font-size: 10pt;">[TSS] U.S. cattle, what kind of guarantee can you give for serum or tissue donor herds?</div><div style="color: #29303b; font-size: 10pt;"><br clear="none" /></div><div style="color: #29303b; font-size: 10pt;">[not sure whom ask this] what group are you with?</div><div style="color: #29303b; font-size: 10pt;"><br clear="none" /></div><div style="color: #29303b; font-size: 10pt;">[TSS] CJD Watch, my Mom died from hvCJD and we are tracking CJD world-wide.</div><div style="color: #29303b; font-size: 10pt;"><br clear="none" /></div><div style="color: #29303b; font-size: 10pt;">[not sure who is speaking] could you please disconnect Mr. Singeltary</div><div style="color: #29303b; font-size: 10pt;"><br clear="none" /></div><div style="color: #29303b; font-size: 10pt;">[TSS] you are not going to answer my question?</div><div style="color: #29303b; font-size: 10pt;"><br clear="none" /></div><div style="color: #29303b; font-size: 10pt;">[not sure whom speaking] NO</div><div style="color: #29303b; font-size: 10pt;"><br clear="none" /></div><div style="color: #29303b; font-size: 10pt;">snip...see full archive and more of this;</div><div style="color: #29303b; font-size: 10pt;"><br clear="none" /></div><div style="color: #29303b; font-size: 10pt;"><a href="https://protect2.fireeye.com/v1/url?k=56309245-0a71f6f2-56325e8f-002590f4ce32-f388444e395b325d&q=1&e=eaae77dc-9ea7-4996-b8cd-e6a0b004c974&u=https%3A%2F%2Furldefense.proofpoint.com%2Fv2%2Furl%3Fu%3Dhttp-3A__tseac.blogspot.com_2011_02_usa-2D50-2Dstate-2Dbse-2Dmad-2Dcow-2Dconference.html%26d%3DDwMFaQ%26c%3DGSntNbUav5AC0JJIyPOufmfQT3u3zI7UKdoVzPd-7og%26r%3DWUkrqFfyTINKdEKan1fw3ykVVZIC_CPt4oXXzPtT-cw%26m%3DPZ-nUcomhuQHG7d2Ik9AWSDfvzWvkaGQjLOa4gBnbo4%26s%3Dx2cnB1oAu0wlCoSkJw2E9RyLDr40LMuYR6jLH3CFP7M%26e%3D" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">http://tseac.blogspot.com/2011/02/usa-50-state-bse-mad-cow-conference.html</a></div><div style="color: #29303b; font-size: 10pt;"><br clear="none" /></div><div><div><span style="color: #29303b;">3.2.1.2 Non‐cervid domestic species</span></div><div><span style="color: #29303b;"><br clear="none" /></span></div><div><span style="color: #29303b;">The remarkably high rate of natural CWD transmission in the ongoing NA epidemics raises the question of the risk to livestock grazing on CWD‐contaminated shared rangeland and subsequently developing a novel CWD‐related prion disease. This issue has been investigated by transmitting CWD via experimental challenge to cattle, sheep and pigs and to tg mouse lines expressing the relevant species PrP.</span></div><div><span style="color: #29303b;"><br clear="none" /></span></div><div><span style="color: #29303b;">For cattle challenged with CWD, PrPSc was detected in approximately 40% of intracerebrally inoculated animals (Hamir et al., 2005, 2006a, 2007). Tg mice expressing bovine PrP have also been challenged with CWD and while published studies have negative outcomes (Tamguney et al., 2009b), unpublished data provided for the purposes of this Opinion indicate that some transmission of individual isolates to bovinised mice is possible (Table 1).</span></div><div><span style="color: #29303b;"><br clear="none" /></span></div><div><span style="color: #29303b;">In small ruminant recipients, a low rate of transmission was reported between 35 and 72 months post‐infection (mpi) in ARQ/ARQ and ARQ/VRQ sheep intracerebrally challenged with mule deer CWD (Hamir et al., 2006b), while two out of two ARQ/ARQ sheep intracerebrally inoculated with elk CWD developed clinical disease after 28 mpi (Madsen‐Bouterse et al., 2016). However, tg mice expressing ARQ sheep PrP were resistant (Tamguney et al., 2006) and tg mice expressing the VRQ PrP allele were poorly susceptible to clinical disease (Beringue et al., 2012; Madsen‐Bouterse et al., 2016). In contrast, tg mice expressing VRQ sheep PrP challenged with CWD have resulted in highly efficient, life‐long asymptomatic replication of these prions in the spleen tissue (Beringue et al., 2012).</span></div><div><span style="color: #29303b;"><br clear="none" /></span></div><div><span style="color: #29303b;">A recent study investigated the potential for swine to serve as hosts of the CWD agent(s) by intracerebral or oral challenge of crossbred piglets (Moore et al., 2016b, 2017). Pigs sacrificed at 6 mpi, approximately the age at which pigs reach market weight, were clinically healthy and negative by diagnostic tests, although low‐level CWD agent replication could be detected in the CNS by bioassay in tg cervinised mice. Among pigs that were incubated for up to 73 mpi, some gave diagnostic evidence of CWD replication in the brain between 42 and 72 mpi. Importantly, this was observed also in one orally challenged pig at 64 mpi and the presence of low‐level CWD replication was confirmed by mouse bioassay. The authors of this study argued that pigs can support low‐level amplification of CWD prions, although the species barrier to CWD infection is relatively high and that the detection of infectivity in orally inoculated pigs with a mouse bioassay raises the possibility that naturally exposed pigs could act as a reservoir of CWD infectivity.</span></div><div><span style="color: #29303b;"><br clear="none" /></span></div><div><a href="https://efsa.onlinelibrary.wiley.com/doi/10.2903/j.efsa.2019.5863" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://efsa.onlinelibrary.wiley.com/doi/10.2903/j.efsa.2019.5863</a><br clear="none" /></div><div><span style="color: #29303b;"><br clear="none" /></span></div><div><a href="http://chronic-wasting-disease.blogspot.com/2012/08/susceptibility-of-cattle-to-agent-of.html" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">http://chronic-wasting-disease.blogspot.com/2012/08/susceptibility-of-cattle-to-agent-of.html</a><br clear="none" /></div><div><span style="color: #29303b;"><br clear="none" /></span></div><div><a href="http://bovineprp.blogspot.com/2020/06/first-report-of-potential-bovine.html" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">http://bovineprp.blogspot.com/2020/06/first-report-of-potential-bovine.html</a><br clear="none" /></div></div><div><br /></div><div><div style="line-height: 1.22em;"><span style="font-family: Arial, Helvetica, sans-serif;"><span style="font-size: 12px;">MONDAY, JULY 27, 2020 </span></span></div><div style="line-height: 1.22em;"><span style="font-family: Arial, Helvetica, sans-serif;"><span style="font-size: 12px;"><br /></span></span></div><div style="line-height: 1.22em;"><span style="font-family: Arial, Helvetica, sans-serif;"><span style="font-size: 12px;">BSE Inquiry DFA's a review</span></span><br /></div><div style="line-height: 1.22em;"><span style="font-family: Arial, Helvetica, sans-serif;"><span style="font-size: 12px;"><br /></span></span></div><div style="line-height: 1.22em;"><span style="font-family: Arial, Helvetica, sans-serif;"><span style="font-size: 12px;"><a href="https://bseinquiry.blogspot.com/2020/07/bse-inquiry-dfas-review.html" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://bseinquiry.blogspot.com/2020/07/bse-inquiry-dfas-review.html</a></span></span></div></div><div><span style="font-family: Arial, Helvetica, sans-serif;"><br /></span></div><div><span style="font-family: Arial, Helvetica, sans-serif;"><a href="https://bseinquiry.blogspot.com/" style="color: #0096ef; cursor: pointer; text-decoration-line: none;">https://bseinquiry.blogspot.com/</a><br /></span></div><div><br /></div><div>Terry S. Singeltary Sr.</div></div></div></div></div></div></div><div style="font-size: 10pt;"><br clear="none" style="background-color: white; font-family: arial;" /></div>Terry S. Singeltary Sr.http://www.blogger.com/profile/06986622967539963260noreply@blogger.com0tag:blogger.com,1999:blog-6404950019984350027.post-68378826080825830752020-02-08T08:31:00.001-08:002020-02-08T08:40:04.930-08:00Downed pigs are turned into pork products A new lawsuit seeks to stop that<div style="background-color: white; font-family: arial; font-size: 13.3333px;">
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<span style="font-size: 10pt;">Downed pigs are turned into pork products. A new lawsuit seeks to stop that</span></div>
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Congress ordered the U.S. Department of Agriculture nearly 20 years ago to investigate how often pork plants slaughter hogs that arrive too sick or exhausted to stand. The goal of the mandate was to develop ways to humanely handle the animals — and to determine whether they should be keep out of the food supply. That never happened. Now, as dozens of U.S. pork plants are poised to begin a new safety inspection system, animal welfare groups and some members of Congress are trying to stop lame and fatigued animals from being turned into food for humans. The new program makes plant workers — not USDA inspectors — responsible for evaluating the health of pigs as they arrive at the facilities. On Thursday, Farm Sanctuary and six other animal protection groups filed a federal lawsuit that seeks to make it illegal for pork plants to slaughter the animals, typically referred to as “downers” or “downed” pigs because they are unable to stand or walk when they arrive at the plants.</div>
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Rep. Earl Blumenauer (D-Ore.) said he supports the groups’ efforts and is working with other lawmakers on a plan that will include a public education campaign and renewed efforts to pressure the USDA to take action.</div>
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“It’s shameful that this is where we are at. These are sick, damaged animals,” Blumenauer, a member of Congress’s Animal Protection Caucus, said in an interview. “It’s ludicrous that this is still an issue and that the industry is now in charge of [evaluating] the animals. We will ultimately win like we did with downer cows.”</div>
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The USDA made it illegal in 2007 to slaughter downed cattle for beef products, and in 2016 outlawed the slaughter of downed calves for veal. Agriculture officials cited safety concerns because the lame animals are more likely to harbor and transmit food-borne diseases in beef. The USDA also said that allowing their slaughter “may have created an incentive for establishments to inhumanely attempt to force these animals to rise.”</div>
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The agency’s inspection records show plant workers in recent years have kicked, shocked and dragged downed pigs in an effort to get them to stand upright. Mobilizing pigs, even for a few minutes, means the animal can be rendered fit for slaughter and be turned into pork products shipped to grocery stores and restaurants.</div>
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The USDA declined an interview request and did not answer written questions, saying the agency could not comment because there is pending litigation on the matter.</div>
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The industry estimates that about 500,000 pigs unable to walk or stand arrive at pork plants each year. The animal welfare groups cite industry-sponsored research that places the number closer to 1 million. It’s unclear how many of those downed pigs are removed by inspectors and not slaughtered.</div>
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The number of downed pigs represents a tiny fraction of the 124 million market hogs that are slaughtered annually, but there is no way for consumers to know whether the pork they eat came from a downed pig.</div>
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When it comes to livestock, no other animal in the United States is slaughtered for food more often than pigs. Market hogs — 5 to 6 months old and uniform in size — represent about 75 percent of all slaughtered livestock, well behind cattle, which represents 39 percent, and goats and sheep that round out the remainder, industry records show. About one-quarter of U.S. pork is exported. (USDA does not consider chickens and turkeys to be livestock.)</div>
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The National Pork Producers Council contends that most of the downed pigs are not sick and simply need time to rest. They suffer from stress, often during the journey from farms to pork plants, which can cause some to develop a condition known as fatigued hog syndrome. A similar malady does not exist for cattle.</div>
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“It’s a metabolic state. Recovery typically takes place within two hours, but they will fully recover,” said Daniel Kovich, the council’s assistant director of science and technology. Kovich said he could not say what percentage of downed pigs have the syndrome, but believes it is “the vast majority.”</div>
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Farm Sanctuary has previously attempted to get the USDA to adopt a slaughter ban for downed pigs. In 2014, it filed a petition with the agency, asking it to follow the course it had already taken with cattle.</div>
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Five months ago, USDA denied the petition, saying existing federal regulations are sufficient to keep diseased pigs out of the food supply. They also said USDA inspectors are well-positioned in plants to prevent immobilized pigs from being mistreated or tortured.</div>
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The next day, USDA said it had finalized the new inspection system that gives plant workers the responsibility for evaluating the health of pigs as they arrive at the facilities.</div>
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The Centers for Disease Control and Prevention estimates that pork containing pathogens leads to about 525,000 infections, 2,900 hospitalizations and 82 deaths annually. The USDA’s Office of Inspector General has issued numerous reports over the past decade criticizing the agency for its failure to stop the inhumane treatment of pigs in pork plants.</div>
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Efforts to prevent the slaughter of downed livestock dates to 1986, after Farm Sanctuary founder Gene Baur rescued a sheep at a Pennsylvania stockyard that had been left for dead.</div>
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Baur used the story of the downed sheep — which he nursed back to health and named Hilda — to persuade stockyards to euthanize downed livestock instead of selling them for slaughter. But the voluntary “no-downer policy” didn’t hold.</div>
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“Culturally, the agriculture industry is very resistant to hearing from animal protection organizations that are challenging their practices. There is a tendency to dig in,” said Baur, who has a master’s degree in agricultural economics from Cornell University.</div>
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In 1998, Bauer filed a petition with the USDA asking the agency to make it illegal for downed cattle to be slaughtered.</div>
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At the same time, members of Congress were alarmed by the rising number of downed livestock. In 2002, Congress amended the Humane Methods of Slaughter Act, ordering the USDA to investigate and submit a report to Congress that would determine the causes and scope of downed livestock. Congress said the USDA should consider proposing new rules to prevent downed animals from being treated inhumanely.</div>
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The USDA said it completed the report but would not release a copy to The Washington Post, saying that the documents are now “Congress’ records, therefore we are unable to share them.” Agricultural committees in Congress said they were unable to locate the report.</div>
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The agency did not take any action on Baur’s cattle petition until 2007 — after mad cow disease threatened herds. The disease affects the central nervous system of adult cattle, making it difficult for them to walk or stand. Keeping potentially infected cattle out of the food supply became imperative, because humans can develop a fatal brain disease if they eat beef from infected cattle.</div>
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Former congressman Gary L. Ackerman (D-N.Y.) remembers taking the fight to the House floor in the early 2000s, when he held up a picture of a crippled cow and said, “This does not a good steak make.”</div>
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Ackerman said he worries the USDA is about to repeat itself by not acting until a threatening disease strikes pigs. “We are not smart until a disaster happens, and then people become crazy concerned and take every precaution they should have taken in the first place,” he said.</div>
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Animal welfare and food safety groups share Ackerman’s concern, especially because some of the largest pork plants in the nation are expected to adopt the USDA’s new swine inspection system this year. Under the new system, plant workers will identify, isolate and sometimes remove diseased and downed hogs that arrive at the plants.</div>
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Kovich said the quality of these evaluations will remain the same.</div>
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However, animal welfare and food safety groups have expressed concern, because the USDA is not requiring any specific training for employees. The length and rigor of the training will be determined by plant owners.</div>
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The job of evaluating the health of pigs as they arrive at slaughterhouses has traditionally been conducted by USDA inspectors and veterinarians who are trained to spot signs of disease that could cause food-borne illnesses. They are also skilled at spotting contagious diseases such as African swine fever, which has recently decimated the pig population in Asia and has the USDA planning its own contingency plans should the disease strike in the United States.</div>
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Pat Basu, former USDA chief veterinarian, said the change is risky.</div>
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“This is like Russian roulette,” Basu said. “You might not get it, but you might. One disease condition can spread and ruin the entire country’s economy. It doesn’t matter if you eat pork or you don’t eat pork. It’s risky for everyone.”</div>
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<a fg_scanned="1" href="https://www.washingtonpost.com/national/downed-pigs-are-turned-into-pork-products-a-new-lawsuit-seeks-to-stop-that/2020/02/06/3f8302ea-46c8-11ea-bc78-8a18f7afcee7_story.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://www.washingtonpost.com/national/downed-pigs-are-turned-into-pork-products-a-new-lawsuit-seeks-to-stop-that/2020/02/06/3f8302ea-46c8-11ea-bc78-8a18f7afcee7_story.html</a></div>
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<span style="font-family: arial;"><span style="font-size: 13.3333px;">USDA NSLP et al thought that it would be alright, to feed our children all across the USA, via the NSLP, DEAD STOCK DOWNER COWS, the most high risk cattle for mad cow type disease, and other dangerous pathogens, and they did this for 4 years, that was documented, then hid what they did by having a recall, one of the largest recalls ever, and they made this recall and masked the reason for the recall due to animal abuse (I do not condone animal abuse), not for the reason of the potential for these animals to have mad cow BSE type disease (or other dangerous and deadly pathogens). these TSE prion disease can lay dormant for 5, 10, 20 years, or longer, WHO WILL WATCH OUR CHILDREN FOR THE NEXT 5 DECADES FOR CJD ??? </span></span><br />
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<span style="font-family: arial;"><span style="font-size: 13.3333px;">> > > Ackerman says downed cattle are 50 times more likely to have mad cow disease (also known as Bovine Spongiform Encephalopathy, or BSE) than ambulatory cattle that are suspected of having BSE. Of the 20 confirmed cases of mad cow disease in North America since 1993, at least 16 have involved downer cattle, he said. < < <</span></span><br />
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<a href="http://cattlebusinessweekly.com/PrintArticle.aspx?aid=4138&uid=d9004be1-7d90-405c-b34f-dfd619de3df7">http://cattlebusinessweekly.com/PrintArticle.aspx?aid=4138&uid=d9004be1-7d90-405c-b34f-dfd619de3df7</a><br />
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<span style="font-family: arial;"><span style="font-size: 13.3333px;">Surveillance is more than a numbers game, Detwiler says: "It depends on the population you're testing and how good your rate of return is." The U.S. focuses on the highest-risk animals: neurologically ill and nonambulatory ("downer") cows, in which most BSE cases occur. The U.S. has about 200,000 downer cows every year, "and if you test 12,500 out of that population, you should be able to detect it at that rate of one per million," Detwiler states. Moreover, Europe has a different reason for testing. Whereas the U.S. simply wants to see if BSE has arrived, European nations know they have it and test "to pull more animals out of the food chain," she explains.</span></span><br />
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<a href="http://www.sciam.com/article.cfm?articleID=000A2927-B9DC-1D07-8E49809EC588EEDF&catID=2">http://www.sciam.com/article.cfm?articleID=000A2927-B9DC-1D07-8E49809EC588EEDF&catID=2</a><br />
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<span style="background-color: rgba(255, 255, 255, 0);">USDA NSLP SCHOOL LUNCH PROGRAM FROM DOWNER CATTLE</span></div>
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<span style="color: black;"><span style="background-color: rgba(255, 255, 255, 0);"><a fg_scanned="1" href="http://downercattle.blogspot.com/2009/05/who-will-watch-children.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://downercattle.blogspot.com/2009/05/who-will-watch-children.html</a></span></span></div>
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<span style="color: black;"><span style="background-color: rgba(255, 255, 255, 0);"><a fg_scanned="1" href="http://downercattle.blogspot.com/" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://downercattle.blogspot.com/</a></span></span></div>
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<span style="background-color: rgba(255, 255, 255, 0);">DID YOUR CHILD CONSUME SOME OF THESE DEAD STOCK DOWNER COWS, THE MOST HIGH RISK FOR MAD COW DISEASE ???</span></div>
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<span style="background-color: rgba(255, 255, 255, 0);">you can check and see here ;</span></div>
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<span style="color: black;"><span style="background-color: rgba(255, 255, 255, 0);"><a href="http://www.fns.usda.gov/fns/safety/pdf/Hallmark-Westland_byState.pdf" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://www.fns.usda.gov/fns/safety/pdf/Hallmark-Westland_byState.pdf</a></span></span></div>
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<span style="background-color: rgba(255, 255, 255, 0);">Hallmark - Westland SFA Report by State 3-24-2008 Page 1 of 226</span></div>
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<a fg_scanned="1" href="http://downercattle.blogspot.com/2013/09/school-food-authorities-affected-by.html" rel="noopener noreferrer" style="background-color: rgba(255, 255, 255, 0); color: blue; cursor: pointer;" target="_blank"><span style="color: black;">http://downercattle.blogspot.com/2013/09/school-food-authorities-affected-by.html</span></a></div>
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***> cattle, pigs, sheep, cwd, tse, prion, oh my! </div>
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***> In contrast, cattle are highly susceptible to white-tailed deer CWD and mule deer CWD in experimental conditions but no natural CWD infections in cattle have been reported (Sigurdson, 2008; Hamir et al., 2006). </div>
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Sheep and cattle may be exposed to CWD via common grazing areas with affected deer but so far, appear to be poorly susceptible to mule deer CWD (Sigurdson, 2008). In contrast, cattle are highly susceptible to white-tailed deer CWD and mule deer CWD in experimental conditions but no natural CWD infections in cattle have been reported (Sigurdson, 2008; Hamir et al., 2006). It is not known how susceptible humans are to CWD but given that the prion can be present in muscle, it is likely that humans have been exposed to the agent via consumption of venison (Sigurdson, 2008). Initial experimental research suggests that human susceptibility to CWD is low and there may be a robust species barrier for CWD transmission to humans (Sigurdson, 2008), however the risk appetite for a public health threat may still find this level unacceptable.<span style="font-size: 10pt;"> </span></div>
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<span style="font-size: 10pt;"><a href="https://assets.publishing.service.gov.uk/government/uploads/system/uploads/attachment_data/file/733407/DEFRA_QRA_TSE_in_cervids_June2018_v1.pdf" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://assets.publishing.service.gov.uk/government/uploads/system/uploads/attachment_data/file/733407/DEFRA_QRA_TSE_in_cervids_June2018_v1.pdf</a></span><span style="font-size: 10pt;"> </span></div>
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<span style="font-size: 10pt;"><a fg_scanned="1" href="http://chronic-wasting-disease.blogspot.com/2012/08/susceptibility-of-cattle-to-agent-of.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://chronic-wasting-disease.blogspot.com/2012/08/susceptibility-of-cattle-to-agent-of.html</a></span><span style="font-size: 10pt;"> </span></div>
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<span style="font-size: 10pt;">cwd scrapie pigs oral routes </span></div>
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<span style="font-size: 10pt;">***> However, at 51 months of incubation or greater, 5 animals were positive by one or more diagnostic methods. Furthermore, positive bioassay results were obtained from all inoculated groups (oral and intracranial; market weight and end of study) suggesting that swine are potential hosts for the agent of scrapie. <*** </span></div>
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<span style="font-size: 10pt;">>*** Although the current U.S. feed ban is based on keeping tissues from TSE infected cattle from contaminating animal feed, swine rations in the U.S. could contain animal derived components including materials from scrapie infected sheep and goats. These results indicating the susceptibility of pigs to sheep scrapie, coupled with the limitations of the current feed ban, indicates that a revision of the feed ban may be necessary to protect swine production and potentially human health. <*** </span></div>
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<span style="font-size: 10pt;">***> Results: PrPSc was not detected by EIA and IHC in any RPLNs. All tonsils and MLNs were negative by IHC, though the MLN from one pig in the oral <6 5="" 6="" at="" by="" detected="" eia.="" examined="" group="" in="" intracranial="" least="" lymphoid="" month="" months="" of="" one="" pigs="" positive="" prpsc="" quic="" the="" tissues="" was="">6 months group, 5/6 pigs in the oral <6 4="" and="" group="" months="" oral="">6 months group. Overall, the MLN was positive in 14/19 (74%) of samples examined, the RPLN in 8/18 (44%), and the tonsil in 10/25 (40%). </6></6></span></div>
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<span style="font-size: 10pt;">***> Conclusions: This study demonstrates that PrPSc accumulates in lymphoid tissues from pigs challenged intracranially or orally with the CWD agent, and can be detected as early as 4 months after challenge. CWD-infected pigs rarely develop clinical disease and if they do, they do so after a long incubation period. This raises the possibility that CWD-infected pigs could shed prions into their environment long before they develop clinical disease. Furthermore, lymphoid tissues from CWD-infected pigs could present a potential source of CWD infectivity in the animal and human food chains. </span></div>
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<a fg_scanned="1" href="https://www.ars.usda.gov/research/publications/publication/?seqNo115=353091" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://www.ars.usda.gov/research/publications/publication/?seqNo115=353091</a></div>
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<a fg_scanned="1" href="https://www.ars.usda.gov/research/project/?accnNo=432011&fy=2017" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://www.ars.usda.gov/research/project/?accnNo=432011&fy=2017</a></div>
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<a fg_scanned="1" href="https://www.ars.usda.gov/research/publications/publication/?seqNo115=337105" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://www.ars.usda.gov/research/publications/publication/?seqNo115=337105</a></div>
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<span style="font-family: "arial" , "helvetica"; line-height: 1.22em;">Friday, December 14, 2012</span></div>
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<span style="font-family: "arial" , "helvetica"; line-height: 1.22em;">DEFRA U.K. What is the risk of Chronic Wasting Disease CWD being introduced into Great Britain? A Qualitative Risk Assessment October 2012</span></div>
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<span style="font-family: "arial" , "helvetica"; line-height: 1.22em;">In the USA, under the Food and Drug Administration's BSE Feed Regulation (21 CFR 589.2000) most material (exceptions include milk, tallow, and gelatin) from deer and elk is prohibited for use in feed for ruminant animals. With regards to feed for non-ruminant animals, under FDA law, CWD positive deer may not be used for any animal feed or feed ingredients. For elk and deer considered at high risk for CWD, the FDA recommends that these animals do not enter the animal feed system. However, this recommendation is guidance and not a requirement by law.</span></div>
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<span style="font-family: "arial" , "helvetica"; line-height: 1.22em;">Animals considered at high risk for CWD include:</span></div>
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<span style="font-family: "arial" , "helvetica"; line-height: 1.22em;">1) animals from areas declared to be endemic for CWD and/or to be CWD eradication zones and</span></div>
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<span style="font-family: "arial" , "helvetica"; line-height: 1.22em;">2) deer and elk that at some time during the 60-month period prior to slaughter were in a captive herd that contained a CWD-positive animal.</span></div>
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<span style="font-family: "arial" , "helvetica"; line-height: 1.22em;">Therefore, in the USA, materials from cervids other than CWD positive animals may be used in animal feed and feed ingredients for non-ruminants.</span></div>
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<span style="font-family: "arial" , "helvetica"; line-height: 1.22em;">The amount of animal PAP that is of deer and/or elk origin imported from the USA to GB can not be determined, however, as it is not specified in TRACES. It may constitute a small percentage of the 8412 kilos of non-fish origin processed animal proteins that were imported from US into GB in 2011.</span></div>
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<span style="font-family: "arial" , "helvetica"; line-height: 1.22em;">Overall, therefore, it is considered there is a __greater than negligible risk___ that (nonruminant) animal feed and pet food containing deer and/or elk protein is imported into GB.</span></div>
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<span style="font-family: "arial" , "helvetica"; line-height: 1.22em;">There is uncertainty associated with this estimate given the lack of data on the amount of deer and/or elk protein possibly being imported in these products.</span></div>
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<span style="font-family: "arial" , "helvetica"; line-height: 1.22em;">36% in 2007 (Almberg et al., 2011). In such areas, population declines of deer of up to 30 to 50% have been observed (Almberg et al., 2011). In areas of Colorado, the prevalence can be as high as 30% (EFSA, 2011).</span></div>
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<span style="font-family: "arial" , "helvetica"; line-height: 1.22em;">The clinical signs of CWD in affected adults are weight loss and behavioural changes that can span weeks or months (Williams, 2005). In addition, signs might include excessive salivation, behavioural alterations including a fixed stare and changes in interaction with other animals in the herd, and an altered stance (Williams, 2005). These signs are indistinguishable from cervids experimentally infected with bovine spongiform encephalopathy (BSE).</span></div>
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<span style="font-family: "arial" , "helvetica"; line-height: 1.22em;">Given this, if CWD was to be introduced into countries with BSE such as GB, for example, infected deer populations would need to be tested to differentiate if they were infected with CWD or BSE to minimise the risk of BSE entering the human food-chain via affected venison.</span></div>
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<span style="font-family: "arial" , "helvetica"; line-height: 1.22em;">The rate of transmission of CWD has been reported to be as high as 30% and can approach 100% among captive animals in endemic areas (Safar et al., 2008).</span></div>
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<span style="font-family: "arial" , "helvetica"; line-height: 1.22em;">In summary, in endemic areas, there is a medium probability that the soil and surrounding environment is contaminated with CWD prions and in a bioavailable form. In rural areas where CWD has not been reported and deer are present, there is a greater than negligible risk the soil is contaminated with CWD prion.</span></div>
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<span style="font-family: "arial" , "helvetica"; line-height: 1.22em;">In summary, given the volume of tourists, hunters and servicemen moving between GB and North America, the probability of at least one person travelling to/from a CWD affected area and, in doing so, contaminating their clothing, footwear and/or equipment prior to arriving in GB is greater than negligible... For deer hunters, specifically, the risk is likely to be greater given the increased contact with deer and their environment. However, there is significant uncertainty associated with these estimates.</span></div>
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<span style="font-family: "arial" , "helvetica"; line-height: 1.22em;">Therefore, it is considered that farmed and park deer may have a higher probability of exposure to CWD transferred to the environment than wild deer given the restricted habitat range and higher frequency of contact with tourists and returning GB residents.</span></div>
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<a href="https://web.archive.org/web/20170404125557/http://webarchive.nationalarchives.gov.uk/20130822084033/http://www.defra.gov.uk/animal-diseases/files/qra_chronic-wasting-disease-121029.pdf" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">https://web.archive.org/web/20170404125557/http://webarchive.nationalarchives.gov.uk/20130822084033/http://www.defra.gov.uk/animal-diseases/files/qra_chronic-wasting-disease-121029.pdf</a></div>
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<span style="font-family: "arial" , "helvetica"; line-height: 1.22em;">TUESDAY, APRIL 18, 2017 </span></div>
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<span style="font-family: "arial" , "helvetica"; line-height: 1.22em;">*** EXTREME USA FDA PART 589 TSE PRION FEED LOOP HOLE STILL EXIST, AND PRICE OF POKER GOES UP ***</span></div>
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<a fg_scanned="1" href="http://usdameatexport.blogspot.com/2017/04/extreme-usa-fda-part-589-tse-prion-feed.html" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">http://usdameatexport.blogspot.com/2017/04/extreme-usa-fda-part-589-tse-prion-feed.html</a></div>
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***> Wednesday, January 23, 2019 </div>
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***> CFIA SFCR Guidance on Specified risk material (SRM) came into force on January 15, 2019 <***</div>
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<a fg_scanned="1" href="https://specifiedriskmaterial.blogspot.com/2019/01/cfia-sfcr-guidance-on-specified-risk.html" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">https://specifiedriskmaterial.blogspot.com/2019/01/cfia-sfcr-guidance-on-specified-risk.html</a></div>
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Prion Conference 2018</div>
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O5 Prion Disease in Dromedary Camels </div>
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Babelhadj B (1), Di Bari MA (2), Pirisinu L (2), Chiappini B (2), Gaouar SB (3), Riccardi G (2), Marcon S (2), Agrimi U (2), Nonno R (2), Vaccari G (2) (1) École Normale Supérieure Ouargla. Laboratoire de protection des écosystèmes en zones arides et semi arides University Kasdi Merbah Ouargla, Ouargla, Algeria; (2) Istituto Superiore di Sanità, Department of Food Safety, Nutrition and Veterinary Public Health, Rome, Italy (3) University Abou Bekr Bélkaid, Tlemcen, Algeria. </div>
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Prions are responsible for fatal and transmissible neurodegenerative diseases including CreutzfeldtJakob disease in humans, scrapie in small ruminants and bovine spongiform encephalopathy (BSE). Following the BSE epidemic and the demonstration of its zoonotic potential, general concerns have been raised on animal prions. </div>
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Here we report the identification of a prion disease in dromedary camels (Camelus dromedarius) in Algeria and designate it as Camel Prion Disease (CPD). In the last years, neurological symptoms have been observed in adult male and female dromedaries presented for slaughter at the Ouargla abattoir. The symptoms include weight loss, behavioral abnormalities and neurological symptoms such as tremors, aggressiveness, hyper-reactivity, typical down and upwards movements of the head, hesitant and uncertain gait, ataxia of the hind limbs, occasional falls and difficult getting up. During 2015 and 2016, symptoms suggestive of prion disease were observed in 3.1% of 2259 dromedaries presented at ante-mortem examination. Laboratory diagnosis was obtained in three symptomatic dromedaries, sampled in 2016 and 2017, by the detection of typical neurodegeneration and disease-specific prion protein (PrPSc) in brain tissues. </div>
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Histopathological examination revealed spongiform change, gliosis and neuronal loss preferentially in grey matter of subcortical brain areas. Abundant PrPSc deposition was detected in the same brain areas by immunohistochemistry and PET-blot. Western blot analysis confirmed the presence of PK-resistant PrPSc, whose N-terminal cleaved PK-resistant core was characterized by a mono-glycosylated dominant form and by a distinctive N-terminal cleavage, different from that observed in BSE and scrapie. </div>
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PrPSc was also detected, by immunohistochemistry, in all sampled lymph nodes (cervical, prescapular and lumbar aortic) of the only animal from which they were collected. </div>
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The PRNP sequence of the two animals for which frozen material was available, showed 100% nucleotide identity with the PRNP sequence already reported for dromedary camel. </div>
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Overall, these data demonstrate the presence of a prion disease in dromedary camelswhose nature, origin and spread need further investigations. However, our preliminary observations on the rather high prevalence of symptomatic dromedaries and the involvement of lymphoid tissues, are consistent with CPD being an infectious disease. In conclusion, the emergence of a new prion disease in a livestock species of crucial importance for millions of people around the world, makes urgent to assess the risk for humans and to develop policies able to control the spread of the disease in animals and to minimize human exposure. </div>
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<span style="font-family: "arial" , "helvetica"; line-height: 1.22em;">Volume 24, Number 6—June 2018 Research </span></div>
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Prions cause fatal and transmissible neurodegenerative diseases, including Creutzfeldt-Jakob disease in humans, scrapie in small ruminants, and bovine spongiform encephalopathy (BSE). After the BSE epidemic, and the associated human infections, began in 1996 in the United Kingdom, general concerns have been raised about animal prions. We detected a prion disease in dromedary camels (Camelus dromedarius) in Algeria. Symptoms suggesting prion disease occurred in 3.1% of dromedaries brought for slaughter to the Ouargla abattoir in 2015–2016. We confirmed diagnosis by detecting pathognomonic neurodegeneration and disease-specific prion protein (PrPSc) in brain tissues from 3 symptomatic animals. Prion detection in lymphoid tissues is suggestive of the infectious nature of the disease. PrPSc biochemical characterization showed differences with BSE and scrapie. Our identification of this prion disease in a geographically widespread livestock species requires urgent enforcement of surveillance and assessment of the potential risks to human and animal health.</div>
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The possibility that dromedaries acquired the disease from eating prion-contaminated waste needs to be considered.</div>
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Tracing the origin of prion diseases is challenging. In the case of CPD, the traditional extensive and nomadic herding practices of dromedaries represent a formidable factor for accelerating the spread of the disease at long distances, making the path of its diffusion difficult to determine. Finally, the major import flows of live animals to Algeria from Niger, Mali, and Mauritania (<a class="yiv1437632715aolmail_aolmail_aolmail_tp-link-policy" fg_scanned="1" href="https://wwwnc.cdc.gov/eid/article/24/6/17-2007_article#r27" rel="noopener noreferrer" shape="rect" style="color: #075290; cursor: pointer; line-height: 1.22em;" target="_blank" title="27"><em style="line-height: 1.22em;">27</em></a>) should be investigated to trace the possible origin of CPD from other countries.</div>
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Camels are a vital animal species for millions of persons globally. The world camel population has a yearly growth rate of 2.1% (<a class="yiv1437632715aolmail_aolmail_aolmail_tp-link-policy" fg_scanned="1" href="https://wwwnc.cdc.gov/eid/article/24/6/17-2007_article#r28" rel="noopener noreferrer" shape="rect" style="color: #075290; cursor: pointer; line-height: 1.22em;" target="_blank" title="28"><em style="line-height: 1.22em;">28</em></a>). In 2014, the population was estimated at ≈28 million animals, but this number is probably underestimated.. Approximately 88% of camels are found in Africa, especially eastern Africa, and 12% are found in Asia. Official data reported 350,000 dromedaries in Algeria in 2014 (<a class="yiv1437632715aolmail_aolmail_aolmail_tp-link-policy" fg_scanned="1" href="https://wwwnc..cdc.gov/eid/article/24/6/17-2007_article#r28" rel="noopener noreferrer" shape="rect" style="color: #075290; cursor: pointer; line-height: 1.22em;" target="_blank" title="28"><em style="line-height: 1.22em;">28</em></a>).</div>
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On the basis of phenotypic traits and sociogeographic criteria, several dromedary populations have been suggested to exist in Algeria (<a class="yiv1437632715aolmail_aolmail_aolmail_tp-link-policy" fg_scanned="1" href="https://wwwnc.cdc.gov/eid/article/24/6/17-2007_article#r29" rel="noopener noreferrer" shape="rect" style="color: #075290; cursor: pointer; line-height: 1.22em;" target="_blank" title="29"><em style="line-height: 1.22em;">29</em></a>). However, recent genetic studies in Algeria and Egypt point to a weak differentiation of the dromedary population as a consequence of historical use as a cross-continental beast of burden along trans-Saharan caravan routes, coupled with traditional extensive/nomadic herding practices (<a class="yiv1437632715aolmail_aolmail_aolmail_tp-link-policy" fg_scanned="1" href="https://wwwnc.cdc.gov/eid/article/24/6/17-2007_article#r30" rel="noopener noreferrer" shape="rect" style="color: #075290; cursor: pointer; line-height: 1.22em;" target="_blank" title="30"><em style="line-height: 1.22em;">30</em></a>).</div>
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Such genetic homogeneity also might be reflected in <em style="line-height: 1.22em;">PRNP</em>. Studies on <em style="line-height: 1.22em;">PRNP</em> variability in camels are therefore warranted to explore the existence of genotypes resistant to CPD, which could represent an important tool for CPD management as it was for breeding programs for scrapie eradication in sheep.</div>
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In the past 10 years, the camel farming system has changed rapidly, with increasing setup of periurban dairy farms and dairy plants and diversification of camel products and market penetration (<a class="yiv1437632715aolmail_aolmail_aolmail_tp-link-policy" fg_scanned="1" href="https://wwwnc.cdc.gov/eid/article/24/6/17-2007_article#r13" rel="noopener noreferrer" shape="rect" style="color: #075290; cursor: pointer; line-height: 1.22em;" target="_blank" title="13"><em style="line-height: 1.22em;">13</em></a>). This evolution requires improved health standards for infectious diseases and, in light of CPD, for prion diseases.</div>
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The emergence of another prion disease in an animal species of crucial importance for millions of persons worldwide makes it necessary to assess the risk for humans and develop evidence-based policies to control and limit the spread of the disease in animals and minimize human exposure. The implementation of a surveillance system for prion diseases would be a first step to enable disease control and minimize human and animal exposure. Finally, the diagnostic capacity of prion diseases needs to be improved in all countries in Africa where dromedaries are part of the domestic livestock.</div>
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<span style="font-size: 13.3333px; line-height: 1.22em;">***SEE MASSIVE AMOUNTS OF BANNED ANIMAL PROTEIN AKA MAD COW FEED IN COMMERCE USA DECADES AFTER POST BAN ***</span></div>
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<a fg_scanned="1" href="http://camelusprp.blogspot.com/2018/04/dromedary-camels-algeria-prion-mad.html" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">http://camelusprp.blogspot.com/2018/04/dromedary-camels-algeria-prion-mad.html</a></div>
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<span style="font-size: x-small;">***> Traceability of animal protein byproducts in ruminants by multivariate analysis of isotope ratio mass spectrometry to prevent transmission of prion diseases</span></div>
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<span style="font-size: x-small;"><a fg_scanned="1" href="https://bovineprp.blogspot.com/2019/06/traceability-of-animal-protein.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://bovineprp.blogspot.com/2019/06/traceability-of-animal-protein.html</a></span></div>
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ponder this; ***> Adriano Aguzzi...''We even showed that a prion AEROSOL will infect 100% of mice within 10 seconds of exposure''</div>
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SUNDAY, SEPTEMBER 1, 2019 </div>
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FDA Reports on VFD Compliance</div>
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Before and after the current Veterinary Feed Directive (VFD) rules took full effect in January, 2017, the FDA focused primarily on education and outreach to help feed mills, veterinarians and producers understand and comply with the requirements. Since then, FDA has gradually increased the number of VFD inspections and initiated enforcement actions when necessary.</div>
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<a fg_scanned="1" href="https://bovineprp.blogspot.com/2019/09/fda-reports-on-vfd-compliance.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://bovineprp.blogspot.com/2019/09/fda-reports-on-vfd-compliance.html</a> </div>
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ZOONOSIS OF SCRAPIE TSE PRION</div>
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O.05: Transmission of prions to primates after extended silent incubation periods: Implications for BSE and scrapie risk assessment in human populations </div>
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<span style="font-family: "arial" , "helvetica"; line-height: 1.22em;">Emmanuel Comoy, Jacqueline Mikol, Valerie Durand, Sophie Luccantoni, Evelyne Correia, Nathalie Lescoutra, Capucine Dehen, and Jean-Philippe Deslys Atomic Energy Commission; Fontenay-aux-Roses, France </span></div>
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<span style="font-family: "arial" , "helvetica"; line-height: 1.22em;">Prion diseases (PD) are the unique neurodegenerative proteinopathies reputed to be transmissible under field conditions since decades. The transmission of Bovine Spongiform Encephalopathy (BSE) to humans evidenced that an animal PD might be zoonotic under appropriate conditions. Contrarily, in the absence of obvious (epidemiological or experimental) elements supporting a transmission or genetic predispositions, PD, like the other proteinopathies, are reputed to occur spontaneously (atpical animal prion strains, sporadic CJD summing 80% of human prion cases). </span></div>
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<span style="font-family: "arial" , "helvetica"; line-height: 1.22em;">Non-human primate models provided the first evidences supporting the transmissibiity of human prion strains and the zoonotic potential of BSE. Among them, cynomolgus macaques brought major information for BSE risk assessment for human health (Chen, 2014), according to their phylogenetic proximity to humans and extended lifetime. We used this model to assess the zoonotic potential of other animal PD from bovine, ovine and cervid origins even after very long silent incubation periods. </span></div>
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<span style="font-family: "arial" , "helvetica"; line-height: 1.22em;">*** We recently observed the direct transmission of a natural classical scrapie isolate to macaque after a 10-year silent incubation period, </span></div>
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<span style="font-family: "arial" , "helvetica"; line-height: 1.22em;">***with features similar to some reported for human cases of sporadic CJD, albeit requiring fourfold long incubation than BSE. Scrapie, as recently evoked in humanized mice (Cassard, 2014), </span></div>
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<span style="font-family: "arial" , "helvetica"; line-height: 1.22em;">***is the third potentially zoonotic PD (with BSE and L-type BSE), </span></div>
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<span style="font-family: "arial" , "helvetica"; line-height: 1.22em;">***thus questioning the origin of human sporadic cases. </span></div>
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<span style="font-family: "arial" , "helvetica"; line-height: 1.22em;">We will present an updated panorama of our different transmission studies and discuss the implications of such extended incubation periods on risk assessment of animal PD for human health. </span></div>
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<span style="font-family: "arial" , "helvetica"; line-height: 1.22em;">=============== </span></div>
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<span style="font-family: "arial" , "helvetica"; line-height: 1.22em;">***thus questioning the origin of human sporadic cases*** </span></div>
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<span style="font-family: "arial" , "helvetica"; line-height: 1.22em;">=============== </span></div>
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<span style="font-family: "arial" , "helvetica"; line-height: 1.22em;">***our findings suggest that possible transmission risk of H-type BSE to sheep and human. Bioassay will be required to determine whether the PMCA products are infectious to these animals. </span></div>
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<span style="font-family: "arial" , "helvetica"; line-height: 1.22em;">============== </span></div>
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<span style="font-family: "arial" , "helvetica"; line-height: 1.22em;"><a href="https://prion2015.files.wordpress.com/2015/05/prion2015abstracts.pdf" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">https://prion2015.files.wordpress.com/2015/05/prion2015abstracts.pdf</a> </span></div>
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***Transmission data also revealed that several scrapie prions propagate in HuPrP-Tg mice with efficiency comparable to that of cattle BSE. While the efficiency of transmission at primary passage was low, subsequent passages resulted in a highly virulent prion disease in both Met129 and Val129 mice. </div>
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<span style="font-family: "arial" , "helvetica"; line-height: 1.22em;">***Transmission of the different scrapie isolates in these mice leads to the emergence of prion strain phenotypes that showed similar characteristics to those displayed by MM1 or VV2 sCJD prion. </span></div>
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<span style="font-family: "arial" , "helvetica"; line-height: 1.22em;">***These results demonstrate that scrapie prions have a zoonotic potential and raise new questions about the possible link between animal and human prions. </span></div>
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<span style="font-family: "arial" , "helvetica"; line-height: 1.22em;"><a fg_scanned="1" href="http://www.tandfonline.com/doi/abs/10.1080/19336896.2016.1163048?journalCode=kprn20" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">http://www.tandfonline.com/doi/abs/10.1080/19336896.2016.1163048?journalCode=kprn20</a></span></div>
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PRION 2016 TOKYO</div>
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<span style="font-family: "arial" , "helvetica"; line-height: 1.22em;">Saturday, April 23, 2016</span></div>
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<span style="font-family: "arial" , "helvetica"; line-height: 1.22em;">SCRAPIE WS-01: Prion diseases in animals and zoonotic potential 2016</span></div>
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<span style="font-family: "arial" , "helvetica"; line-height: 1.22em;">Prion. 10:S15-S21. 2016 ISSN: 1933-6896 printl 1933-690X online</span></div>
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<span style="font-family: "arial" , "helvetica"; line-height: 1.22em;">Taylor & Francis</span></div>
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<span style="font-family: "arial" , "helvetica"; line-height: 1.22em;">Prion 2016 Animal Prion Disease Workshop Abstracts</span></div>
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<span style="font-family: "arial" , "helvetica"; line-height: 1.22em;">WS-01: Prion diseases in animals and zoonotic potential</span></div>
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<span style="font-family: "arial" , "helvetica"; line-height: 1.22em;">Juan Maria Torres a, Olivier Andreoletti b, J uan-Carlos Espinosa a. Vincent Beringue c. Patricia Aguilar a,</span></div>
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<span style="font-family: "arial" , "helvetica"; line-height: 1.22em;">Natalia Fernandez-Borges a. and Alba Marin-Moreno a</span></div>
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<span style="font-family: "arial" , "helvetica"; line-height: 1.22em;">"Centro de Investigacion en Sanidad Animal ( CISA-INIA ). Valdeolmos, Madrid. Spain; b UMR INRA -ENVT 1225 Interactions Holes Agents Pathogenes. ENVT. Toulouse. France: "UR892. Virologie lmmunologie MolécuIaires, Jouy-en-Josas. France</span></div>
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<span style="font-family: "arial" , "helvetica"; line-height: 1.22em;">Dietary exposure to bovine spongiform encephalopathy (BSE) contaminated bovine tissues is considered as the origin of variant Creutzfeldt Jakob (vCJD) disease in human. To date, BSE agent is the only recognized zoonotic prion... Despite the variety of Transmissible Spongiform Encephalopathy (TSE) agents that have been circulating for centuries in farmed ruminants there is no apparent epidemiological link between exposure to ruminant products and the occurrence of other form of TSE in human like sporadic Creutzfeldt Jakob Disease (sCJD). However, the zoonotic potential of the diversity of circulating TSE agents has never been systematically assessed. The major issue in experimental assessment of TSEs zoonotic potential lies in the modeling of the ‘species barrier‘, the biological phenomenon that limits TSE agents’ propagation from a species to another. In the last decade, mice genetically engineered to express normal forms of the human prion protein has proved essential in studying human prions pathogenesis and modeling the capacity of TSEs to cross the human species barrier.</span></div>
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<span style="font-family: "arial" , "helvetica"; line-height: 1.22em;">To assess the zoonotic potential of prions circulating in farmed ruminants, we study their transmission ability in transgenic mice expressing human PrPC (HuPrP-Tg). Two lines of mice expressing different forms of the human PrPC (129Met or 129Val) are used to determine the role of the Met129Val dimorphism in susceptibility/resistance to the different agents.</span></div>
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<span style="font-family: "arial" , "helvetica"; line-height: 1.22em;">These transmission experiments confirm the ability of BSE prions to propagate in 129M- HuPrP-Tg mice and demonstrate that Met129 homozygotes may be susceptible to BSE in sheep or goat to a greater degree than the BSE agent in cattle and that these agents can convey molecular properties and neuropathological indistinguishable from vCJD. However homozygous 129V mice are resistant to all tested BSE derived prions independently of the originating species suggesting a higher transmission barrier for 129V-PrP variant.</span></div>
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<span style="font-family: "arial" , "helvetica"; line-height: 1.22em;">Transmission data also revealed that several scrapie prions propagate in HuPrP-Tg mice with efficiency comparable to that of cattle BSE. While the efficiency of transmission at primary passage was low, subsequent passages resulted in a highly virulent prion disease in both Met129 and Val129 mice. </span></div>
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<span style="font-family: "arial" , "helvetica"; line-height: 1.22em;">Transmission of the different scrapie isolates in these mice leads to the emergence of prion strain phenotypes that showed similar characteristics to those displayed by MM1 or VV2 sCJD prion. </span></div>
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<span style="font-family: "arial" , "helvetica"; line-height: 1.22em;">These results demonstrate that scrapie prions have a zoonotic potential and raise new questions about the possible link between animal and human prions. </span></div>
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<span style="font-family: "arial" , "helvetica"; line-height: 1.22em;"><a fg_scanned="1" href="http://www.tandfonline.com/doi/abs/10.1080/19336896.2016.1163048?journalCode=kprn20" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">http://www.tandfonline.com/doi/abs/10.1080/19336896.2016.1163048?journalCode=kprn20</a></span></div>
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***> why do we not want to do TSE transmission studies on chimpanzees $</div>
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<span style="font-family: "arial" , "helvetica"; line-height: 1.22em;">5. A positive result from a chimpanzee challenged severly would likely create alarm in some circles even if the result could not be interpreted for man. </span></div>
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<span style="font-family: "arial" , "helvetica"; line-height: 1.22em;">***> I have a view that all these agents could be transmitted provided a large enough dose by appropriate routes was given and the animals kept long enough. </span></div>
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<span style="font-family: "arial" , "helvetica"; line-height: 1.22em;">***> Until the mechanisms of the species barrier are more clearly understood it might be best to retain that hypothesis.</span></div>
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<span style="font-family: "arial" , "helvetica"; line-height: 1.22em;">R. BRADLEY</span></div>
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<a href="https://web.archive.org/web/20170126051158/http://collections.europarchive.org/tna/20080102222950/http://www.bseinquiry.gov.uk/files/yb/1990/09/23001001.pdf" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">https://web.archive.org/web/20170126051158/http://collections.europarchive.org/tna/20080102222950/http://www.bseinquiry.gov.uk/files/yb/1990/09/23001001.pdf</a></div>
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<span style="font-family: "arial" , "helvetica"; line-height: 1.22em;">Title: Transmission of scrapie prions to primate after an extended silent incubation period) </span></div>
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<span style="font-family: "arial" , "helvetica"; line-height: 1.22em;">*** In complement to the recent demonstration that humanized mice are susceptible to scrapie, we report here the first observation of direct transmission of a natural classical scrapie isolate to a macaque after a 10-year incubation period. Neuropathologic examination revealed all of the features of a prion disease: spongiform change, neuronal loss, and accumulation of PrPres throughout the CNS. </span></div>
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<span style="font-family: "arial" , "helvetica"; line-height: 1.22em;">*** This observation strengthens the questioning of the harmlessness of scrapie to humans, at a time when protective measures for human and animal health are being dismantled and reduced as c-BSE is considered controlled and being eradicated. </span></div>
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<span style="font-family: "arial" , "helvetica"; line-height: 1.22em;">*** Our results underscore the importance of precautionary and protective measures and the necessity for long-term experimental transmission studies to assess the zoonotic potential of other animal prion strains. </span></div>
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***> Moreover, sporadic disease has never been observed in breeding colonies or primate research laboratories, most notably among hundreds of animals over several decades of study at the National Institutes of Health25, and in nearly twenty older animals continuously housed in our own facility. <***</div>
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<span style="font-family: "arial" , "helvetica"; line-height: 1.22em;">Transmission of scrapie prions to primate after an extended silent incubation period </span></div>
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<span style="font-family: "arial" , "helvetica"; line-height: 1.22em;">Emmanuel E. Comoy, Jacqueline Mikol, Sophie Luccantoni-Freire, Evelyne Correia, Nathalie Lescoutra-Etchegaray, Valérie Durand, Capucine Dehen, Olivier Andreoletti, Cristina Casalone, Juergen A. Richt, Justin J. Greenlee, Thierry Baron, Sylvie L. Benestad, Paul Brown & Jean-Philippe Deslys Scientific Reports volume 5, Article number: 11573 (2015) | Download Citation</span></div>
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<span style="font-family: "arial" , "helvetica"; line-height: 1.22em;">Abstract </span></div>
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<span style="font-family: "arial" , "helvetica"; line-height: 1.22em;">Classical bovine spongiform encephalopathy (c-BSE) is the only animal prion disease reputed to be zoonotic, causing variant Creutzfeldt-Jakob disease (vCJD) in humans and having guided protective measures for animal and human health against animal prion diseases. Recently, partial transmissions to humanized mice showed that the zoonotic potential of scrapie might be similar to c-BSE. We here report the direct transmission of a natural classical scrapie isolate to cynomolgus macaque, a highly relevant model for human prion diseases, after a 10-year silent incubation period, with features similar to those reported for human cases of sporadic CJD. Scrapie is thus actually transmissible to primates with incubation periods compatible with their life expectancy, although fourfold longer than BSE. Long-term experimental transmission studies are necessary to better assess the zoonotic potential of other prion diseases with high prevalence, notably Chronic Wasting Disease of deer and elk and atypical/Nor98 scrapie.</span></div>
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<span style="font-family: "arial" , "helvetica"; line-height: 1.22em;">SNIP...</span></div>
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<span style="font-family: "arial" , "helvetica"; line-height: 1.22em;">Discussion We describe the transmission of spongiform encephalopathy in a non-human primate inoculated 10 years earlier with a strain of sheep c-scrapie. Because of this extended incubation period in a facility in which other prion diseases are under study, we are obliged to consider two alternative possibilities that might explain its occurrence. We first considered the possibility of a sporadic origin (like CJD in humans). Such an event is extremely improbable because the inoculated animal was 14 years old when the clinical signs appeared, i.e. about 40% through the expected natural lifetime of this species, compared to a peak age incidence of 60–65 years in human sporadic CJD, or about 80% through their expected lifetimes. Moreover, sporadic disease has never been observed in breeding colonies or primate research laboratories, most notably among hundreds of animals over several decades of study at the National Institutes of Health25, and in nearly twenty older animals continuously housed in our own facility.</span></div>
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<span style="font-family: "arial" , "helvetica"; line-height: 1.22em;">The second possibility is a laboratory cross-contamination. Three facts make this possibility equally unlikely. First, handling of specimens in our laboratory is performed with fastidious attention to the avoidance of any such cross-contamination. Second, no laboratory cross-contamination has ever been documented in other primate laboratories, including the NIH, even between infected and uninfected animals housed in the same or adjacent cages with daily intimate contact (P. Brown, personal communication). Third, the cerebral lesion profile is different from all the other prion diseases we have studied in this model19, with a correlation between cerebellar lesions (massive spongiform change of Purkinje cells, intense PrPres staining and reactive gliosis26) and ataxia. The iron deposits present in the globus pallidus are a non specific finding that have been reported previously in neurodegenerative diseases and aging27. Conversely, the thalamic lesion was reminiscent of a metabolic disease due to thiamine deficiency28 but blood thiamine levels were within normal limits (data not shown). The preferential distribution of spongiform change in cortex associated with a limited distribution in the brainstem is reminiscent of the lesion profile in MM2c and VV1 sCJD patients29, but interspecies comparison of lesion profiles should be interpreted with caution. It is of note that the same classical scrapie isolate induced TSE in C57Bl/6 mice with similar incubation periods and lesional profiles as a sample derived from a MM1 sCJD patient30.</span></div>
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<span style="font-family: "arial" , "helvetica"; line-height: 1.22em;">We are therefore confident that the illness in this cynomolgus macaque represents a true transmission of a sheep c-scrapie isolate directly to an old-world monkey, which taxonomically resides in the primate subdivision (parvorder of catarrhini) that includes humans. With an homology of its PrP protein with humans of 96.4%31, cynomolgus macaque constitutes a highly relevant model for assessing zoonotic risk of prion diseases. Since our initial aim was to show the absence of transmission of scrapie to macaques in the worst-case scenario, we obtained materials from a flock of naturally-infected sheep, affecting animals with different genotypes32. This c-scrapie isolate exhibited complete transmission in ARQ/ARQ sheep (332 ± 56 days) and Tg338 transgenic mice expressing ovine VRQ/VRQ prion protein (220 ± 5 days) (O. Andreoletti, personal communication). From the standpoint of zoonotic risk, it is important to note that sheep with c-scrapie (including the isolate used in our study) have demonstrable infectivity throughout their lymphoreticular system early in the incubation period of the disease (3 months-old for all the lymphoid organs, and as early as 2 months-old in gut-associated lymph nodes)33. In addition, scrapie infectivity has been identified in blood34, milk35 and skeletal muscle36 from asymptomatic but scrapie infected small ruminants which implies a potential dietary exposure for consumers.</span></div>
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<span style="font-family: "arial" , "helvetica"; line-height: 1.22em;">Two earlier studies have reported the occurrence of clinical TSE in cynomolgus macaques after exposures to scrapie isolates. In the first study, the “Compton” scrapie isolate (derived from an English sheep) and serially propagated for 9 passages in goats did not transmit TSE in cynomolgus macaque, rhesus macaque or chimpanzee within 7 years following intracerebral challenge1; conversely, after 8 supplementary passages in conventional mice, this “Compton” isolate induced TSE in a cynomolgus macaque 5 years after intracerebral challenge, but rhesus macaques and chimpanzee remained asymptomatic 8.5 years post-exposure8. However, multiple successive passages that are classically used to select laboratory-adapted prion strains can significantly modify the initial properties of a scrapie isolate, thus questioning the relevance of zoonotic potential for the initial sheep-derived isolate. The same isolate had also induced disease into squirrel monkeys (new-world monkey)9. A second historical observation reported that a cynomolgus macaque developed TSE 6 years post-inoculation with brain homogenate from a scrapie-infected Suffolk ewe (derived from USA), whereas a rhesus macaque and a chimpanzee exposed to the same inoculum remained healthy 9 years post-exposure1. This inoculum also induced TSE in squirrel monkeys after 4 passages in mice. Other scrapie transmission attempts in macaque failed but had more shorter periods of observation in comparison to the current study. Further, it is possible that there are differences in the zoonotic potential of different scrapie strains.</span></div>
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<span style="font-family: "arial" , "helvetica"; line-height: 1.22em;">The most striking observation in our study is the extended incubation period of scrapie in the macaque model, which has several implications. Firstly, our observations constitute experimental evidence in favor of the zoonotic potential of c-scrapie, at least for this isolate that has been extensively studied32,33,34,35,36. The cross-species zoonotic ability of this isolate should be confirmed by performing duplicate intracerebral exposures and assessing the transmissibility by the oral route (a successful transmission of prion strains through the intracerebral route may not necessarily indicate the potential for oral transmission37). However, such confirmatory experiments may require more than one decade, which is hardly compatible with current general management and support of scientific projects; thus this study should be rather considered as a case report.</span></div>
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<span style="font-family: "arial" , "helvetica"; line-height: 1.22em;">Secondly, transmission of c-BSE to primates occurred within 8 years post exposure for the lowest doses able to transmit the disease (the survival period after inoculation is inversely proportional to the initial amount of infectious inoculum). The occurrence of scrapie 10 years after exposure to a high dose (25 mg) of scrapie-infected sheep brain suggests that the macaque has a higher species barrier for sheep c-scrapie than c-BSE, although it is notable that previous studies based on in vitro conversion of PrP suggested that BSE and scrapie prions would have a similar conversion potential for human PrP38.</span></div>
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<span style="font-family: "arial" , "helvetica"; line-height: 1.22em;">Thirdly, prion diseases typically have longer incubation periods after oral exposure than after intracerebral inoculations: since humans can develop Kuru 47 years after oral exposure39, an incubation time of several decades after oral exposure to scrapie would therefore be expected, leading the disease to occur in older adults, i.e. the peak age for cases considered to be sporadic disease, and making a distinction between scrapie-associated and truly sporadic disease extremely difficult to appreciate.</span></div>
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<span style="font-family: "arial" , "helvetica"; line-height: 1.22em;">Fourthly, epidemiologic evidence is necessary to confirm the zoonotic potential of an animal disease suggested by experimental studies. A relatively short incubation period and a peculiar epidemiological situation (e.g., all the first vCJD cases occurring in the country with the most important ongoing c-BSE epizootic) led to a high degree of suspicion that c-BSE was the cause of vCJD. Sporadic CJD are considered spontaneous diseases with an almost stable and constant worldwide prevalence (0.5–2 cases per million inhabitants per year), and previous epidemiological studies were unable to draw a link between sCJD and classical scrapie6,7,40,41, even though external causes were hypothesized to explain the occurrence of some sCJD clusters42,43,44. However, extended incubation periods exceeding several decades would impair the predictive values of epidemiological surveillance for prion diseases, already weakened by a limited prevalence of prion diseases and the multiplicity of isolates gathered under the phenotypes of “scrapie” and “sporadic CJD”.</span></div>
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<span style="font-family: "arial" , "helvetica"; line-height: 1.22em;">Fifthly, considering this 10 year-long incubation period, together with both laboratory and epidemiological evidence of decade or longer intervals between infection and clinical onset of disease, no premature conclusions should be drawn from negative transmission studies in cynomolgus macaques with less than a decade of observation, as in the aforementioned historical transmission studies of scrapie to primates1,8,9. Our observations and those of others45,46 to date are unable to provide definitive evidence regarding the zoonotic potential of CWD, atypical/Nor98 scrapie or H-type BSE. The extended incubation period of the scrapie-affected macaque in the current study also underscores the limitations of rodent models expressing human PrP for assessing the zoonotic potential of some prion diseases since their lifespan remains limited to approximately two years21,47,48. This point is illustrated by the fact that the recently reported transmission of scrapie to humanized mice was not associated with clinical signs for up to 750 days and occurred in an extreme minority of mice with only a marginal increase in attack rate upon second passage13. The low attack rate in these studies is certainly linked to the limited lifespan of mice compared to the very long periods of observation necessary to demonstrate the development of scrapie. Alternatively, one could estimate that a successful second passage is the result of strain adaptation to the species barrier, thus poorly relevant of the real zoonotic potential of the original scrapie isolate of sheep origin49. The development of scrapie in this primate after an incubation period compatible with its lifespan complements the study conducted in transgenic (humanized) mice; taken together these studies suggest that some isolates of sheep scrapie can promote misfolding of the human prion protein and that scrapie can develop within the lifespan of some primate species.</span></div>
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<span style="font-family: "arial" , "helvetica"; line-height: 1.22em;">In addition to previous studies on scrapie transmission to primate1,8,9 and the recently published study on transgenic humanized mice13, our results constitute new evidence for recommending that the potential risk of scrapie for human health should not be dismissed. Indeed, human PrP transgenic mice and primates are the most relevant models for investigating the human transmission barrier. To what extent such models are informative for measuring the zoonotic potential of an animal TSE under field exposure conditions is unknown. During the past decades, many protective measures have been successfully implemented to protect cattle from the spread of c-BSE, and some of these measures have been extended to sheep and goats to protect from scrapie according to the principle of precaution. Since cases of c-BSE have greatly reduced in number, those protective measures are currently being challenged and relaxed in the absence of other known zoonotic animal prion disease. We recommend that risk managers should be aware of the long term potential risk to human health of at least certain scrapie isolates, notably for lymphotropic strains like the classical scrapie strain used in the current study. Relatively high amounts of infectivity in peripheral lymphoid organs in animals infected with these strains could lead to contamination of food products produced for human consumption. Efforts should also be maintained to further assess the zoonotic potential of other animal prion strains in long-term studies, notably lymphotropic strains with high prevalence like CWD, which is spreading across North America, and atypical/Nor98 scrapie (Nor98)50 that was first detected in the past two decades and now represents approximately half of all reported cases of prion diseases in small ruminants worldwide, including territories previously considered as scrapie free... Even if the prevailing view is that sporadic CJD is due to the spontaneous formation of CJD prions, it remains possible that its apparent sporadic nature may, at least in part, result from our limited capacity to identify an environmental origin.</span></div>
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<a fg_scanned="1" href="https://www.nature.com/articles/srep11573" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">https://www.nature.com/articles/srep11573</a></div>
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THURSDAY, JANUARY 30, 2020 </div>
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Docket Number: FDA-2012-D-0307 Recommendations to Reduce the Possible Risk of Transmission of Creutzfeldt-Jakob Disease and Variant Creutzfeldt-Jakob Disease by Blood and Blood Components; Draft Guidance for Industry Draft Guidance for Industry Singeltary Submission</div>
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Part 2 Singeltary submission</div>
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FRIDAY, JANUARY 31, 2020</div>
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CJD TSE Prion Blood Products, iatrogenic transmission, Confucius is confused again, WHAT IF? Docket Number: FDA-2012-D-0307</div>
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<a fg_scanned="1" href="https://creutzfeldt-jakob-disease.blogspot.com/2020/01/cjd-tse-prion-blood-products-iatrogenic.html" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">https://creutzfeldt-jakob-disease.blogspot.com/2020/01/cjd-tse-prion-blood-products-iatrogenic.html</a></div>
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<span style="color: #222222;">THURSDAY, JANUARY 23, 2020 </span></div>
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<span style="color: #222222;">USDA Consolidates Regulations for NAHLN Laboratory Testing USDA Animal and Plant Health Inspection Service sent this bulletin at 01/23/2020 02:15 PM EST</span></div>
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<span style="color: #222222;"><a fg_scanned="1" href="https://madcowusda.blogspot.com/2020/01/usda-consolidates-regulations-for-nahln.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://madcowusda.blogspot.com/2020/01/usda-consolidates-regulations-for-nahln.html</a></span></div>
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snip...</div>
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<span style="font-family: "arial" , "helvetica";">ONE DECADE POST MAD COW FEED BAN OF AUGUST 1997...2007</span></div>
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<span style="font-size: xx-small;">2007</span></div>
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<span style="font-size: xx-small;">10,000,000 POUNDS REASON Products manufactured from bulk feed containing blood meal that was cross contaminated with prohibited meat and bone meal and the labeling did not bear cautionary BSE statement.</span></div>
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<span style="font-size: xx-small;">2007</span></div>
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<span style="font-size: xx-small;">Date: March 21, 2007 at 2:27 pm PST</span></div>
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<span style="font-size: xx-small;">RECALLS AND FIELD CORRECTIONS: VETERINARY MEDICINES -- CLASS II PRODUCT</span></div>
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<span style="font-size: xx-small;">Bulk cattle feed made with recalled Darling's 85% Blood Meal, Flash Dried, Recall # V-024-2007 CODE Cattle feed delivered between 01/12/2007 and 01/26/2007 RECALLING FIRM/MANUFACTURER Pfeiffer, Arno, Inc, Greenbush,</span></div>
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<span style="font-size: xx-small;">WI. by conversation on February 5, 2007.</span></div>
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<span style="font-size: xx-small;">Firm initiated recall is ongoing.</span></div>
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<span style="font-size: xx-small;">REASON Blood meal used to make cattle feed was recalled because it was cross- contaminated with prohibited bovine meat and bone meal that had been manufactured on common equipment and labeling did not bear cautionary BSE statement.</span></div>
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<span style="font-size: xx-small;">VOLUME OF PRODUCT IN COMMERCE 42,090 lbs. DISTRIBUTION WI</span></div>
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<span style="font-size: xx-small;">___________________________________</span></div>
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<span style="font-size: xx-small;">PRODUCT Custom dairy premix products: MNM ALL PURPOSE Pellet, HILLSIDE/CDL Prot- Buffer Meal, LEE, M.-CLOSE UP PX Pellet, HIGH DESERT/ GHC LACT Meal, TATARKA, M CUST PROT Meal, SUNRIDGE/CDL PROTEIN Blend, LOURENZO, K PVM DAIRY Meal, DOUBLE B DAIRY/GHC LAC Mineral, WEST PIONT/GHC CLOSEUP Mineral, WEST POINT/GHC LACT Meal, JENKS, J/COMPASS PROTEIN Meal, COPPINI - 8# SPECIAL DAIRY Mix, GULICK, L-LACT Meal (Bulk), TRIPLE J - PROTEIN/LACTATION, ROCK CREEK/GHC MILK Mineral, BETTENCOURT/GHC S.SIDE MK-MN, BETTENCOURT #1/GHC MILK MINR, V&C DAIRY/GHC LACT Meal, VEENSTRA, F/GHC LACT Meal, SMUTNY, A- BYPASS ML W/SMARTA, Recall # V-025-2007</span></div>
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<span style="font-size: xx-small;">CODE The firm does not utilize a code - only shipping documentation with commodity and weights identified.</span></div>
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<span style="font-size: xx-small;">RECALLING FIRM/MANUFACTURER Rangen, Inc, Buhl, ID, by letters on February 13 and 14, 2007.</span></div>
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<span style="font-size: xx-small;">Firm initiated recall is complete.</span></div>
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<span style="font-size: xx-small;">REASON Products manufactured from bulk feed containing blood meal that was cross contaminated with prohibited meat and bone meal and the labeling did not bear cautionary BSE statement.</span></div>
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<span style="font-size: xx-small;">VOLUME OF PRODUCT IN COMMERCE 9,997,976 lbs. DISTRIBUTION ID and NV</span></div>
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<span style="font-size: xx-small;">END OF ENFORCEMENT REPORT FOR MARCH 21, 2007</span></div>
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<span style="font-size: xx-small;">PAGE NOT FOUND</span></div>
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<a fg_scanned="1" href="http://www.fda.gov/Safety/Recalls/EnforcementReports/2007/ucm120446.htm" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://www.fda.gov/Safety/Recalls/EnforcementReports/2007/ucm120446.htm</a></div>
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ALABAMA MAD COW FEED IN COMMERCE 2006</div>
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RECALLS AND FIELD CORRECTIONS: VETERINARY MEDICINE -- CLASS II</div>
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______________________________ </div>
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PRODUCT</div>
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a) CO-OP 32% Sinking Catfish, Recall # V-100-6;</div>
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b) Performance Sheep Pell W/Decox/A/N, medicated, net wt. 50 lbs, Recall # V-101-6;</div>
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c) Pro 40% Swine Conc Meal -- 50 lb, Recall # V-102-6;</div>
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d) CO-OP 32% Sinking Catfish Food Medicated, Recall # V-103-6;</div>
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e) "Big Jim’s" BBB Deer Ration, Big Buck Blend, Recall # V-104-6;</div>
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f) CO-OP 40% Hog Supplement Medicated Pelleted, Tylosin 100 grams/ton, 50 lb. bag, Recall # V-105-6;</div>
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g) Pig Starter Pell II, 18% W/MCDX Medicated 282020, Carbadox -- 0.0055%, Recall # V-106-6;</div>
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h) CO-OP STARTER-GROWER CRUMBLES, Complete Feed for Chickens from Hatch to 20 Weeks, Medicated, Bacitracin Methylene Disalicylate, 25 and 50 Lbs, Recall # V-107-6;</div>
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i) CO-OP LAYING PELLETS, Complete Feed for Laying Chickens, Recall # 108-6;</div>
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j) CO-OP LAYING CRUMBLES, Recall # V-109-6;</div>
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k) CO-OP QUAIL FLIGHT CONDITIONER MEDICATED, net wt 50 Lbs, Recall # V-110-6;</div>
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l) CO-OP QUAIL STARTER MEDICATED, Net Wt. 50 Lbs, Recall # V-111-6;</div>
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m) CO-OP QUAIL GROWER MEDICATED, 50 Lbs, Recall # V-112-6</div>
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CODE</div>
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Product manufactured from 02/01/2005 until 06/06/2006</div>
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RECALLING FIRM/MANUFACTURER</div>
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Alabama Farmers Cooperative, Inc., Decatur, AL, by telephone, fax, email and visit on June 9, 2006. FDA initiated recall is complete.</div>
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REASON</div>
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Animal and fish feeds which were possibly contaminated with ruminant based protein not labeled as "Do not feed to ruminants".</div>
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VOLUME OF PRODUCT IN COMMERCE</div>
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125 tons</div>
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DISTRIBUTION</div>
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AL and FL </div>
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______________________________</div>
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PRODUCT</div>
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Bulk custom dairy feds manufactured from concentrates, Recall # V-113-6</div>
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CODE</div>
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All dairy feeds produced between 2/1/05 and 6/16/06 and containing H. J. Baker recalled feed products.</div>
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RECALLING FIRM/MANUFACTURER</div>
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Vita Plus Corp., Gagetown, MI, by visit beginning on June 21, 2006. Firm initiated recall is complete.</div>
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REASON</div>
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The feed was manufactured from materials that may have been contaminated with mammalian protein.</div>
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VOLUME OF PRODUCT IN COMMERCE</div>
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27,694,240 lbs</div>
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DISTRIBUTION</div>
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MI </div>
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______________________________</div>
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PRODUCT</div>
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Bulk custom made dairy feed, Recall # V-114-6</div>
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CODE</div>
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None</div>
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RECALLING FIRM/MANUFACTURER</div>
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Burkmann Feeds LLC, Glasgow, KY, by letter on July 14, 2006. Firm initiated recall is ongoing.</div>
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REASON</div>
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Custom made feeds contain ingredient called Pro-Lak, which may contain ruminant derived meat and bone meal.</div>
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VOLUME OF PRODUCT IN COMMERCE</div>
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?????</div>
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DISTRIBUTION</div>
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KY</div>
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END OF ENFORCEMENT REPORT FOR AUGUST 2, 2006</div>
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###</div>
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<a fg_scanned="1" href="http://data.nber.org/fda/enforcement-report/2006/ucm120413.htm" rel="noopener noreferrer" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">http://data.nber.org/fda/enforcement-report/2006/ucm120413.htm</a></div>
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=====</div>
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PRODUCT </div>
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Bulk Whole Barley, Recall # V-256-2009</div>
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CODE</div>
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No code or lot number.</div>
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RECALLING FIRM/MANUFACTURER</div>
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<br style="line-height: 1.22em;" /></div>
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Mars Petcare US, Clinton, OK, by telephone on May 21, 2009. Firm initiated recall is complete.</div>
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REASON</div>
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<br style="line-height: 1.22em;" /></div>
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Product may have contained prohibited materials without cautionary statement on the label.</div>
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VOLUME OF PRODUCT IN COMMERCE</div>
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<br style="line-height: 1.22em;" /></div>
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208,820 pounds</div>
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DISTRIBUTION</div>
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TX</div>
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END OF ENFORCEMENT REPORT FOR AUGUST 26, 2009</div>
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###</div>
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<a fg_scanned="1" href="https://www.fda.gov/Safety/Recalls/EnforcementReports/ucm180348.htm" rel="noopener noreferrer" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">https://www.fda.gov/Safety/Recalls/EnforcementReports/ucm180348.htm</a></div>
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Subject: MAD COW FEED RECALL KY VOLUME OF PRODUCT IN COMMERCE ????? </div>
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Date: August 6, 2006 at 6:19 pm PST </div>
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PRODUCT Bulk custom made dairy feed, Recall # V-114-6 </div>
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CODE None </div>
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RECALLING FIRM/MANUFACTURER Burkmann Feeds LLC, Glasgow, KY, by letter on July 14, 2006. </div>
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<div style="font-family: Georgia; line-height: 1.22em;">
Firm initiated recall is ongoing. REASON Custom made feeds contain ingredient called Pro-Lak, which may contain ruminant derived meat and bone meal. </div>
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VOLUME OF PRODUCT IN COMMERCE ????? </div>
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DISTRIBUTION KY </div>
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END OF ENFORCEMENT REPORT FOR AUGUST 2, 2006</div>
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### </div>
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<br style="line-height: 1.22em;" /></div>
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<a fg_scanned="1" href="http://www.fda.gov/bbs/topics/enforce/2006/ENF00963.html" rel="noopener noreferrer" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">http://www.fda.gov/bbs/topics/enforce/2006/ENF00963.html</a></div>
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<br style="line-height: 1.22em;" /></div>
<div style="font-family: Georgia; line-height: 1.22em;">
MAD COW FEED RECALL USA EQUALS 10,878.06 TONS NATIONWIDE Sun Jul 16, 2006 09:22 71.248.128.67 </div>
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RECALLS AND FIELD CORRECTIONS: VETERINARY MEDICINE -- CLASS II </div>
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<span style="line-height: 1.22em;"><br style="line-height: 1.22em;" /></span></div>
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<span style="line-height: 1.22em;">______________________________ </span></div>
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<div style="font-family: Georgia; line-height: 1.22em;">
PRODUCT a) PRO-LAK, bulk weight, Protein Concentrate for Lactating Dairy Animals, Recall # V-079-6; </div>
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<br style="line-height: 1.22em;" /></div>
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b) ProAmino II, FOR PREFRESH AND LACTATING COWS, net weight 50lb (22.6 kg), Recall # V-080-6; </div>
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c) PRO-PAK, MARINE & ANIMAL PROTEIN CONCENTRATE FOR USE IN ANIMAL FEED, Recall # V-081-6; </div>
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<br style="line-height: 1.22em;" /></div>
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d) Feather Meal, Recall # V-082-6 </div>
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CODE a) Bulk b) None c) Bulk d) Bulk </div>
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RECALLING FIRM/MANUFACTURER H. J. Baker & Bro., Inc., Albertville, AL, by telephone on June 15, 2006 and by press release on June 16, 2006. </div>
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Firm initiated recall is ongoing.</div>
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REASON Possible contamination of animal feeds with ruminent derived meat and bone meal.. </div>
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VOLUME OF PRODUCT IN COMMERCE 10,878.06 tons </div>
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DISTRIBUTION Nationwide</div>
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END OF ENFORCEMENT REPORT FOR July 12, 2006</div>
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###</div>
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<br style="line-height: 1.22em;" /></div>
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<a fg_scanned="1" href="http://www.fda.gov/bbs/topics/enforce/2006/ENF00960.html" rel="noopener noreferrer" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">http://www.fda.gov/bbs/topics/enforce/2006/ENF00960.html</a></div>
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<br style="line-height: 1.22em;" /></div>
<div style="font-family: Georgia; line-height: 1.22em;">
Subject: MAD COW FEED BAN WARNING LETTER ISSUED MAY 17, 2006 </div>
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<div style="font-family: Georgia; line-height: 1.22em;">
Date: June 27, 2006 at 7:42 am PST Public Health Service Food and Drug Administration</div>
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<br style="line-height: 1.22em;" /></div>
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New Orleans District 297 Plus Park Blvd. Nashville, TN 37217</div>
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Telephone: 615-781-5380 Fax: 615-781-5391</div>
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May 17, 2006</div>
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WARNING LETTER NO.. 2006-NOL-06</div>
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FEDERAL EXPRESS OVERNIGHT DELIVERY</div>
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Mr. William Shirley, Jr., Owner Louisiana.DBA Riegel By-Products 2621 State Street Dallas, Texas 75204</div>
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Dear Mr. Shirley:</div>
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<br style="line-height: 1.22em;" /></div>
<div style="font-family: Georgia; line-height: 1.22em;">
On February 12, 17, 21, and 22, 2006, a U.S. Food & Drug Administration (FDA) investigator inspected your rendering plant, located at 509 Fortson Street, Shreveport, Louisiana. The inspection revealed significant deviations from the requirements set forth in Title 21, Code of Federal Regulations, Part 589.2000 [21 CFR 589.2000], Animal Proteins Prohibited in Ruminant Feed. This regulation is intended to prevent the establishment and amplification of Bovine Spongiform Encephalopathy (BSE). You failed to follow the requirements of this regulation; products being manufactured and distributed by your facility are misbranded within the meaning of Section 403(a)(1) [21 USC 343(a)(1)] of the Federal Food, Drug, and Cosmetic Act (the Act).</div>
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Our investigation found you failed to provide measures, including sufficient written procedures, to prevent commingling or cross-contamination and to maintain sufficient written procedures [21 CFR 589.2000(e)] because:</div>
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You failed to use clean-out procedures or other means adequate to prevent carryover of protein derived from mammalian tissues into animal protein or feeds which may be used for ruminants. For example, your facility uses the same equipment to process mammalian and poultry tissues. However, you use only hot water to clean the cookers between processing tissues from each species. You do not clean the auger, hammer mill, grinder, and spouts after processing mammalian tissues.</div>
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You failed to maintain written procedures specifying the clean-out procedures or other means to prevent carryover of protein derived from mammalian tissues into feeds which may be used for ruminants.</div>
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As a result . the poultry meal you manufacture may contain protein derived from mammalian tissues prohibited in ruminant feed. Pursuant to 21 CFR 589.2000(e)(1)(i), any products containing or may contain protein derived from mammalian tissues must be labeled, "Do not feed to cattle or other ruminants." Since you failed to label a product which may contain protein derived from mammalian tissues with the required cautionary statement. the poultry meal is misbranded under Section 403(a)(1) [21 USC 343(a)(1)] of the Act.</div>
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This letter is not intended as an all-inclusive list of violations at your facility. As a manufacturer of materials intended for animal feed use, you are responsible for ensuring your overall operation and the products you manufacture and distribute are in compliance with the law. You should take prompt action to correct these violations, and you should establish a system whereby violations do not recur. Failure to promptly correct these violations may result in regulatory action, such as seizure and/or injunction, without further notice.</div>
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You should notify this office in writing within 15 working days of receiving this letter, outlining the specific steps you have taken to bring your firm into compliance with the law. Your response should include an explanation of each step taken to correct the violations and prevent their recurrence. If corrective action cannot be completed within 15 working days, state the reason for the delay and the date by which the corrections will be completed. Include copies of any available documentation demonstrating corrections have been made.</div>
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Your reply should be directed to Mark W. Rivero, Compliance Officer, U.S. Food and Drug Administration, 2424 Edenborn Avenue, Suite 410, Metairie, Louisiana 70001. If you have questions regarding any issue in this letter, please contact Mr. Rivero at (504) 219-8818, extension 103.</div>
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Sincerely,</div>
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<br style="line-height: 1.22em;" /></div>
<div style="font-family: Georgia; line-height: 1.22em;">
/S</div>
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<div style="font-family: Georgia; line-height: 1.22em;">
Carol S. Sanchez Acting District Director New Orleans District </div>
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<a fg_scanned="1" href="http://www.fda.gov/foi/warning_letters/g5883d.htm" rel="noopener noreferrer" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">http://www.fda.gov/foi/warning_letters/g5883d.htm</a></div>
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PLEASE NOTE, THE FDA URLS FOR OLD WARNING LETTERS ARE OBSOLETE AND DO NOT WORK IN MOST CASES.. I LOOKED UP THE OLD ONE ABOVE AND FOUND IT, BUT HAVE NOT DONE THAT FOR THE OTHERS TO FOLLOW. THE DATA IS VALID THOUGH! </div>
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<div style="font-family: Georgia; line-height: 1.22em;">
Subject: MAD COW PROTEIN IN COMMERCE USA 2006 RECALL UPDATE </div>
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<div style="font-family: Georgia; line-height: 1.22em;">
From: "Terry S. Singeltary Sr." <[log in to unmask]> </div>
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<div style="font-family: Georgia; line-height: 1.22em;">
Reply-To: SAFETY <[log in to unmask]> </div>
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<br style="line-height: 1.22em;" /></div>
<div style="font-family: Georgia; line-height: 1.22em;">
Date: Mon, 9 Oct 2006 14:10:37 -0500 </div>
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<br style="line-height: 1.22em;" /></div>
<div style="font-family: Georgia; line-height: 1.22em;">
Subject: MAD COW FEED RECALL USA SEPT 6, 2006 1961.72 TONS </div>
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<br style="line-height: 1.22em;" /></div>
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IN COMMERCE AL, TN, AND WV </div>
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<br style="line-height: 1.22em;" /></div>
<div style="font-family: Georgia; line-height: 1.22em;">
Date: September 6, 2006 at 7:58 am PST</div>
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<br style="line-height: 1.22em;" /></div>
<div style="font-family: Georgia; line-height: 1.22em;">
PRODUCT a) EVSRC Custom dairy feed, Recall # V-130-6; b) Performance Chick Starter, Recall # V-131-6; c) Performance Quail Grower, Recall # V-132-6; d) Performance Pheasant Finisher, Recall # V-133-6. CODE None RECALLING FIRM/MANUFACTURER Donaldson & Hasenbein/dba J&R Feed Service, Inc., Cullman, AL, by telephone on June 23, 2006 and by letter dated July 19, 2006. </div>
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<br style="line-height: 1.22em;" /></div>
<div style="font-family: Georgia; line-height: 1.22em;">
Firm initiated recall is complete.</div>
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<br style="line-height: 1.22em;" /></div>
<div style="font-family: Georgia; line-height: 1.22em;">
REASON Dairy and poultry feeds were possibly contaminated with ruminant based protein.</div>
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<br style="line-height: 1.22em;" /></div>
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VOLUME OF PRODUCT IN COMMERCE 477.72 tons </div>
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<br style="line-height: 1.22em;" /></div>
<div style="font-family: Georgia; line-height: 1.22em;">
DISTRIBUTION AL</div>
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______________________________</div>
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<br style="line-height: 1.22em;" /></div>
<div style="font-family: Georgia; line-height: 1.22em;">
snip...</div>
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<br style="line-height: 1.22em;" /></div>
<div style="font-family: Georgia; line-height: 1.22em;">
<a fg_scanned="1" href="http://www.fda.gov/bbs/topics/enforce/2006/ENF00968.html" rel="noopener noreferrer" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">http://www.fda.gov/bbs/topics/enforce/2006/ENF00968.html</a></div>
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<br style="line-height: 1.22em;" /></div>
<div style="font-family: Georgia; line-height: 1.22em;">
Subject: MAD COW FEED RECALLS ENFORCEMENT REPORT FOR AUGUST 9, 2006 KY, LA, MS, AL, GA, AND TN 11,000+ TONS </div>
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<br style="line-height: 1.22em;" /></div>
<div style="font-family: Georgia; line-height: 1.22em;">
Date: August 16, 2006 at 9:19 am PST RECALLS AND FIELD CORRECTIONS: VETERINARY MEDICINE - CLASS II</div>
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______________________________</div>
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snip...</div>
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______________________________</div>
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<br style="line-height: 1.22em;" /></div>
<div style="font-family: Georgia; line-height: 1.22em;">
PRODUCT Bulk custom dairy pre-mixes, Recall # V-120-6 </div>
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<br style="line-height: 1.22em;" /></div>
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CODE None </div>
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<br style="line-height: 1.22em;" /></div>
<div style="font-family: Georgia; line-height: 1.22em;">
RECALLING FIRM/MANUFACTURER Ware Milling Inc., Houston, MS, by telephone on June 23, 2006. Firm initiated recall is complete.</div>
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<br style="line-height: 1.22em;" /></div>
<div style="font-family: Georgia; line-height: 1.22em;">
REASON Possible contamination of dairy animal feeds with ruminant derived meat and bone meal..</div>
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<br style="line-height: 1.22em;" /></div>
<div style="font-family: Georgia; line-height: 1.22em;">
VOLUME OF PRODUCT IN COMMERCE 350 tons DISTRIBUTION AL and MS</div>
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______________________________</div>
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PRODUCT </div>
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a) Tucker Milling, LLC Tm 32% Sinking Fish Grower, #2680-Pellet, 50 lb. bags, Recall # V-121-6; </div>
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b) Tucker Milling, LLC #31120, Game Bird Breeder Pellet, 50 lb. bags, Recall # V-122-6; </div>
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c) Tucker Milling, LLC #31232 Game Bird Grower, 50 lb. bags, Recall # V-123-6; </div>
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d) Tucker Milling, LLC 31227-Crumble, Game Bird Starter, BMD Medicated, 50 lb bags, Recall # V-124-6; </div>
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e) Tucker Milling, LLC #31120, Game Bird Breeder, 50 lb bags, Recall # V-125-6; </div>
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f) Tucker Milling, LLC #30230, 30 % Turkey Starter, 50 lb bags, Recall # V-126-6; </div>
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g) Tucker Milling, LLC #30116, TM Broiler Finisher, 50 lb bags, Recall # V-127-6 </div>
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CODE All products manufactured from 02/01/2005 until 06/20/2006 </div>
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RECALLING FIRM/MANUFACTURER Recalling Firm: Tucker Milling LLC, Guntersville, AL, by telephone and visit on June 20, 2006, and by letter on June 23, 2006. Manufacturer: H. J. Baker and Brothers Inc., Stamford, CT. Firm initiated recall is ongoing.</div>
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REASON Poultry and fish feeds which were possibly contaminated with ruminant based protein were not labeled as "Do not feed to ruminants".</div>
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VOLUME OF PRODUCT IN COMMERCE 7,541-50 lb bags</div>
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DISTRIBUTION AL, GA, MS, and TN</div>
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END OF ENFORCEMENT REPORT FOR AUGUST 9, 2006</div>
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###</div>
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<a fg_scanned="1" href="http://www.fda.gov/bbs/topics/ENFORCE/2006/ENF00964.html" rel="noopener noreferrer" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">http://www.fda.gov/bbs/topics/ENFORCE/2006/ENF00964.html</a></div>
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Subject: MAD COW FEED RECALL AL AND FL VOLUME OF PRODUCT IN COMMERCE 125 TONS</div>
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Products manufactured from 02/01/2005 until 06/06/2006 </div>
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Date: August 6, 2006 at 6:16 pm PST </div>
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PRODUCT </div>
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a) CO-OP 32% Sinking Catfish, Recall # V-100-6; </div>
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b) Performance Sheep Pell W/Decox/A/N, medicated, net wt. 50 lbs, Recall # V-101-6; </div>
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c) Pro 40% Swine Conc Meal -- 50 lb, Recall # V-102-6; d) CO-OP 32% Sinking Catfish Food Medicated, Recall # V-103-6; </div>
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e) "Big Jim's" BBB Deer Ration, Big Buck Blend, Recall # V-104-6; </div>
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f) CO-OP 40% Hog Supplement Medicated Pelleted, Tylosin 100 grams/ton, 50 lb. bag, Recall # V-105-6; </div>
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g) Pig Starter Pell II, 18% W/MCDX Medicated 282020, Carbadox -- 0.0055%, Recall # V-106-6; </div>
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h) CO-OP STARTER-GROWER CRUMBLES, Complete Feed for Chickens from Hatch to 20 Weeks, Medicated, Bacitracin Methylene Disalicylate, 25 and 50 Lbs, Recall # V-107-6; </div>
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i) CO-OP LAYING PELLETS, Complete Feed for Laying Chickens, Recall # 108-6; </div>
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j) CO-OP LAYING CRUMBLES, Recall # V-109-6; </div>
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k) CO-OP QUAIL FLIGHT CONDITIONER MEDICATED, net wt 50 Lbs, Recall # V-110-6; </div>
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l) CO-OP QUAIL STARTER MEDICATED, Net Wt. 50 Lbs, Recall # V-111-6; </div>
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m) CO-OP QUAIL GROWER MEDICATED, 50 Lbs, Recall # V-112-6 </div>
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CODE </div>
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Product manufactured from 02/01/2005 until 06/06/2006 RECALLING FIRM/MANUFACTURER Alabama Farmers Cooperative, Inc., Decatur, AL, by telephone, fax, email and visit on June 9, 2006. FDA initiated recall is complete.</div>
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REASON Animal and fish feeds which were possibly contaminated with ruminant based protein not labeled as "Do not feed to ruminants".</div>
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VOLUME OF PRODUCT IN COMMERCE 125 tons DISTRIBUTION AL and FL</div>
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END OF ENFORCEMENT REPORT FOR AUGUST 2, 2006</div>
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###</div>
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<a fg_scanned="1" href="http://www.fda.gov/bbs/topics/enforce/2006/ENF00963.html" rel="noopener noreferrer" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">http://www.fda.gov/bbs/topics/enforce/2006/ENF00963.html</a></div>
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MAD COW FEED RECALL USA EQUALS 10,878.06 TONS NATIONWIDE Sun Jul 16, 2006 09:22 71.248..128.67</div>
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RECALLS AND FIELD CORRECTIONS: VETERINARY MEDICINE -- CLASS II</div>
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______________________________</div>
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PRODUCT </div>
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<div style="font-family: Georgia; line-height: 1.22em;">
a) PRO-LAK, bulk weight, Protein Concentrate for Lactating Dairy Animals, Recall # V-079-6; </div>
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b) ProAmino II, FOR PREFRESH AND LACTATING COWS, net weight 50lb (22.6 kg), Recall # V-080-6; </div>
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c) PRO-PAK, MARINE & ANIMAL PROTEIN CONCENTRATE FOR USE IN ANIMAL FEED, Recall # V-081-6; </div>
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d) Feather Meal, Recall # V-082-6 </div>
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CODE a) Bulk b) None c) Bulk d) Bulk </div>
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RECALLING FIRM/MANUFACTURER H. J. Baker & Bro., Inc., Albertville, AL, by telephone on June 15, 2006 and by press release on June 16, 2006. </div>
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Firm initiated recall is ongoing.</div>
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REASON Possible contamination of animal feeds with ruminent derived meat and bone meal.</div>
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VOLUME OF PRODUCT IN COMMERCE 10,878.06 tons</div>
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DISTRIBUTION Nationwide</div>
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END OF ENFORCEMENT REPORT FOR July 12, 2006</div>
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###</div>
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<a fg_scanned="1" href="http://www.fda.gov/bbs/topics/enforce/2006/ENF00960.html" rel="noopener noreferrer" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">http://www.fda.gov/bbs/topics/enforce/2006/ENF00960.html</a></div>
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<span style="font-family: "georgia";">Product Details</span></div>
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<span style="font-family: "georgia";">Product Description:</span></div>
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<span style="font-family: "georgia";"><br /></span></div>
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<span style="font-family: "georgia";">CalDensity Black Label, CalDensity White Label with HA, packaged in white plastic 5, 15, 25, 40, 60 lb pails with plastic liner and white plastic lid. Reason for Recall:</span></div>
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<span style="font-family: "georgia";"><br /></span></div>
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<span style="font-family: "georgia";">During an FDA inspection it was found that the CalDensity Black label and CalDensity White Label with HA product containers did not include the precautionary statement DO NOT FEED TO CATTLE OR OTHER RUMINANTS</span></div>
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<span style="font-family: "georgia";"><br /></span></div>
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<span style="font-family: "georgia";">Product Quantity: 50,935 lbs</span></div>
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<span style="font-family: "georgia";">Recall Number: V-209-2012</span></div>
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<span style="font-family: "georgia";"><br /></span></div>
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<span style="font-family: "georgia";">Code Information: 042009, 051009, 061209, 071509, 091009, 011510, 030310, 031610, 052610, 092410, 120110, 011211, 020111, 030911, 050111, 071111 & 090111. Classification: Class II Event Details</span></div>
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<span style="font-family: "georgia";">Event ID: 61880</span></div>
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<span style="font-family: "georgia";">Voluntary / Mandated:</span></div>
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<span style="font-family: "georgia";"><br /></span></div>
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<span style="font-family: "georgia";">Voluntary: Firm Initiated</span></div>
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<span style="font-family: "georgia";"><br /></span></div>
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<span style="font-family: "georgia";">Product Type:</span></div>
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<span style="font-family: "georgia";"><br /></span></div>
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<span style="font-family: "georgia";">Veterinary</span></div>
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<span style="font-family: "georgia";"><br /></span></div>
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<span style="font-family: "georgia";">Initial Firm Notification of Consignee or Public:</span></div>
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<span style="font-family: "georgia";"><br /></span></div>
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<span style="font-family: "georgia";">E-Mail</span></div>
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<span style="font-family: "georgia";"><br /></span></div>
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<span style="font-family: "georgia";">Status:</span></div>
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<span style="font-family: "georgia";"><br /></span></div>
<div style="line-height: 1.22em;">
<span style="font-family: "georgia";">Terminated</span></div>
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<span style="font-family: "georgia";"><br /></span></div>
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<span style="font-family: "georgia";">Distribution Pattern:</span></div>
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<span style="font-family: "georgia";"><br /></span></div>
<div style="line-height: 1.22em;">
<span style="font-family: "georgia";">Nationwide distribution: AL, AR, AZ, CA, CO, FL, GA, IA, ID, IL, KY, LA, MD, MI, MN, MO, MS, NC, NE, NJ, NM, NY, OH, OK, PA, SC, TX, UT, VA, WA & WV. No shipments were made to foreign countries including Canada.</span></div>
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<span style="font-family: "georgia";"><br /></span></div>
<div style="line-height: 1.22em;">
<span style="font-family: "georgia";">Recalling Firm:</span></div>
<div style="line-height: 1.22em;">
<span style="font-family: "georgia";"><br /></span></div>
<div style="line-height: 1.22em;">
<span style="font-family: "georgia";">Process Managers LLC</span></div>
<div style="line-height: 1.22em;">
<span style="font-family: "georgia";"><br /></span></div>
<div style="line-height: 1.22em;">
<span style="font-family: "georgia";">485 Gawthrope Dr </span></div>
<div style="line-height: 1.22em;">
<span style="font-family: "georgia";"><br /></span></div>
<div style="line-height: 1.22em;">
<span style="font-family: "georgia";">Winchester, KY 40391-8910</span></div>
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<span style="font-family: "georgia";"><br /></span></div>
<div style="line-height: 1.22em;">
<span style="font-family: "georgia";">United States</span></div>
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<span style="font-family: "georgia";"><br /></span></div>
<div style="line-height: 1.22em;">
<span style="font-family: "georgia";">Recall Initiation Date:</span></div>
<div style="line-height: 1.22em;">
<span style="font-family: "georgia";"><br /></span></div>
<div style="line-height: 1.22em;">
<span style="font-family: "georgia";">1/6/2012</span></div>
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<span style="font-family: "georgia";"><br /></span></div>
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<span style="font-family: "georgia";">Center Classification Date:</span></div>
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<span style="font-family: "georgia";"><br /></span></div>
<div style="line-height: 1.22em;">
<span style="font-family: "georgia";">9/7/2012</span></div>
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<span style="font-family: "georgia";"><br /></span></div>
<div style="line-height: 1.22em;">
<span style="font-family: "georgia";">Date Terminated:</span></div>
<div style="line-height: 1.22em;">
<span style="font-family: "georgia";"><br /></span></div>
<div style="line-height: 1.22em;">
<span style="font-family: "georgia";">1/24/2014</span></div>
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<span style="font-family: "georgia";"><br /></span></div>
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<a fg_scanned="1" href="https://www.accessdata.fda.gov/scripts/ires/index.cfm#tabNav_advancedSearch" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://www.accessdata.fda.gov/scripts/ires/index.cfm#tabNav_advancedSearch </a></div>
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<div style="font-family: Georgia; line-height: 1.22em;">
<br /></div>
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<div style="line-height: 1.22em;">
<span style="font-family: "georgia";">Product Details</span></div>
<div style="line-height: 1.22em;">
<span style="font-family: "georgia";"><br /></span></div>
<div style="line-height: 1.22em;">
<span style="font-family: "georgia";">Product Description:</span></div>
<div style="line-height: 1.22em;">
<span style="font-family: "georgia";"><br /></span></div>
<div style="line-height: 1.22em;">
<span style="font-family: "georgia";">Regular Chicken 50# Ingredients: Corn, Wheat, Oats, Oyster shells, Medium Grit, CCC, ADS, Plant Protein Products, Animal Protein Products, Processed Grain By-Products, Roughage Products, Animal Fat procession with DHA, etc</span></div>
<div style="line-height: 1.22em;">
<span style="font-family: "georgia";"><br /></span></div>
<div style="line-height: 1.22em;">
<span style="font-family: "georgia";">Reason for Recall:</span></div>
<div style="line-height: 1.22em;">
<span style="font-family: "georgia";"><br /></span></div>
<div style="line-height: 1.22em;">
<span style="font-family: "georgia";">During an FDA sample collection, the firms 50# Regular Chicken Feed was found to contain mammalian protein. The label does not contain the warning statement.</span></div>
<div style="line-height: 1.22em;">
<span style="font-family: "georgia";"><br /></span></div>
<div style="line-height: 1.22em;">
<span style="font-family: "georgia";">Product Quantity:</span></div>
<div style="line-height: 1.22em;">
<span style="font-family: "georgia";"><br /></span></div>
<div style="line-height: 1.22em;">
<span style="font-family: "georgia";">5400lbs (50lb bags)</span></div>
<div style="line-height: 1.22em;">
<span style="font-family: "georgia";"><br /></span></div>
<div style="line-height: 1.22em;">
<span style="font-family: "georgia";">Recall Number:</span></div>
<div style="line-height: 1.22em;">
<span style="font-family: "georgia";"><br /></span></div>
<div style="line-height: 1.22em;">
<span style="font-family: "georgia";">V-137-2013</span></div>
<div style="line-height: 1.22em;">
<span style="font-family: "georgia";"><br /></span></div>
<div style="line-height: 1.22em;">
<span style="font-family: "georgia";">Code Information:</span></div>
<div style="line-height: 1.22em;">
<span style="font-family: "georgia";"><br /></span></div>
<div style="line-height: 1.22em;">
<span style="font-family: "georgia";">8/6/2012</span></div>
<div style="line-height: 1.22em;">
<span style="font-family: "georgia";"><br /></span></div>
<div style="line-height: 1.22em;">
<span style="font-family: "georgia";">Classification:</span></div>
<div style="line-height: 1.22em;">
<span style="font-family: "georgia";"><br /></span></div>
<div style="line-height: 1.22em;">
<span style="font-family: "georgia";">Class III</span></div>
<div style="line-height: 1.22em;">
<span style="font-family: "georgia";"><br /></span></div>
<div style="line-height: 1.22em;">
<span style="font-family: "georgia";">Event Details</span></div>
<div style="line-height: 1.22em;">
<span style="font-family: "georgia";"><br /></span></div>
<div style="line-height: 1.22em;">
<span style="font-family: "georgia";">Event ID:</span></div>
<div style="line-height: 1.22em;">
<span style="font-family: "georgia";"><br /></span></div>
<div style="line-height: 1.22em;">
<span style="font-family: "georgia";">63743</span></div>
<div style="line-height: 1.22em;">
<span style="font-family: "georgia";"><br /></span></div>
<div style="line-height: 1.22em;">
<span style="font-family: "georgia";">Voluntary / Mandated:</span></div>
<div style="line-height: 1.22em;">
<span style="font-family: "georgia";"><br /></span></div>
<div style="line-height: 1.22em;">
<span style="font-family: "georgia";">Voluntary: Firm Initiated</span></div>
<div style="line-height: 1.22em;">
<span style="font-family: "georgia";"><br /></span></div>
<div style="line-height: 1.22em;">
<span style="font-family: "georgia";">Product Type:</span></div>
<div style="line-height: 1.22em;">
<span style="font-family: "georgia";"><br /></span></div>
<div style="line-height: 1.22em;">
<span style="font-family: "georgia";">Veterinary</span></div>
<div style="line-height: 1.22em;">
<span style="font-family: "georgia";"><br /></span></div>
<div style="line-height: 1.22em;">
<span style="font-family: "georgia";">Initial Firm Notification of Consignee or Public:</span></div>
<div style="line-height: 1.22em;">
<span style="font-family: "georgia";"><br /></span></div>
<div style="line-height: 1.22em;">
<span style="font-family: "georgia";">Other</span></div>
<div style="line-height: 1.22em;">
<span style="font-family: "georgia";"><br /></span></div>
<div style="line-height: 1.22em;">
<span style="font-family: "georgia";">Status:</span></div>
<div style="line-height: 1.22em;">
<span style="font-family: "georgia";"><br /></span></div>
<div style="line-height: 1.22em;">
<span style="font-family: "georgia";">Terminated</span></div>
<div style="line-height: 1.22em;">
<span style="font-family: "georgia";"><br /></span></div>
<div style="line-height: 1.22em;">
<span style="font-family: "georgia";">Distribution Pattern:</span></div>
<div style="line-height: 1.22em;">
<span style="font-family: "georgia";"><br /></span></div>
<div style="line-height: 1.22em;">
<span style="font-family: "georgia";">Midland MI area only.</span></div>
<div style="line-height: 1.22em;">
<span style="font-family: "georgia";"><br /></span></div>
<div style="line-height: 1.22em;">
<span style="font-family: "georgia";">Recalling Firm:</span></div>
<div style="line-height: 1.22em;">
<span style="font-family: "georgia";"><br /></span></div>
<div style="line-height: 1.22em;">
<span style="font-family: "georgia";">Cohoons Elevator Inc.</span></div>
<div style="line-height: 1.22em;">
<span style="font-family: "georgia";"><br /></span></div>
<div style="line-height: 1.22em;">
<span style="font-family: "georgia";">802 Townsend St </span></div>
<div style="line-height: 1.22em;">
<span style="font-family: "georgia";"><br /></span></div>
<div style="line-height: 1.22em;">
<span style="font-family: "georgia";">Midland, MI 48640-5362</span></div>
<div style="line-height: 1.22em;">
<span style="font-family: "georgia";"><br /></span></div>
<div style="line-height: 1.22em;">
<span style="font-family: "georgia";">United States</span></div>
<div style="line-height: 1.22em;">
<span style="font-family: "georgia";"><br /></span></div>
<div style="line-height: 1.22em;">
<span style="font-family: "georgia";">Recall Initiation Date:</span></div>
<div style="line-height: 1.22em;">
<span style="font-family: "georgia";"><br /></span></div>
<div style="line-height: 1.22em;">
<span style="font-family: "georgia";">11/21/2012</span></div>
<div style="line-height: 1.22em;">
<span style="font-family: "georgia";"><br /></span></div>
<div style="line-height: 1.22em;">
<span style="font-family: "georgia";">Center Classification Date:</span></div>
<div style="line-height: 1.22em;">
<span style="font-family: "georgia";"><br /></span></div>
<div style="line-height: 1.22em;">
<span style="font-family: "georgia";">2/8/2013</span></div>
<div style="line-height: 1.22em;">
<span style="font-family: "georgia";"><br /></span></div>
<div style="line-height: 1.22em;">
<span style="font-family: "georgia";">Date Terminated:</span></div>
<div style="line-height: 1.22em;">
<span style="font-family: "georgia";"><br /></span></div>
<div style="line-height: 1.22em;">
<span style="font-family: "georgia";">2/12/2013</span></div>
<div style="line-height: 1.22em;">
<span style="font-family: "georgia";"><br /></span></div>
<div style="line-height: 1.22em;">
<span style="font-family: "georgia";"><a fg_scanned="1" href="https://www.accessdata.fda.gov/scripts/ires/index.cfm#tabNav_advancedSearch" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://www.accessdata.fda.gov/scripts/ires/index.cfm#tabNav_advancedSearch</a></span></div>
<div style="line-height: 1.22em;">
<span style="font-family: "georgia";"><br /></span></div>
<div style="line-height: 1.22em;">
<div style="font-family: Arial, sans-serif; font-size: 12px;">
V. Use in animal feed of material from deer and elk NOT considered at high risk for CWD </div>
<div style="font-family: Arial, sans-serif; font-size: 12px;">
<br /></div>
<div style="font-family: Arial, sans-serif; font-size: 12px;">
FDA continues to consider materials from deer and elk NOT considered at high risk for CWD to be acceptable for use in NON-RUMINANT animal feeds in accordance with current agency regulations, 21 CFR 589.2000. </div>
<div style="font-family: Arial, sans-serif; font-size: 12px;">
<br /></div>
<div style="font-family: Arial, sans-serif; font-size: 12px;">
Deer and elk not considered at high risk include: </div>
<div style="font-family: Arial, sans-serif; font-size: 12px;">
<br /></div>
<div style="font-family: Arial, sans-serif; font-size: 12px;">
(1) deer and elk from areas not declared by State officials to be endemic for CWD and/or to be CWD eradication zones; and </div>
<div style="font-family: Arial, sans-serif; font-size: 12px;">
<br /></div>
<div style="font-family: Arial, sans-serif; font-size: 12px;">
(2) deer and elk that were not at some time during the 60-month period immediately before the time of slaughter in a captive herd that contained a CWD-positive animal.</div>
<div style="font-family: Arial, sans-serif; font-size: 12px;">
<br /></div>
<div style="font-family: Arial, sans-serif; font-size: 12px;">
<a href="https://www.fda.gov/downloads/animalveterinary/guidancecomplianceenforcement/guidanceforindustry/ucm052506.pdf" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://www.fda.gov/downloads/animalveterinary/guidancecomplianceenforcement/guidanceforindustry/ucm052506.pdf</a></div>
<div style="font-family: Arial, sans-serif; font-size: 12px;">
<br /></div>
<div style="font-family: Arial, sans-serif; font-size: 12px;">
<br /></div>
<div style="font-family: Arial, sans-serif; font-size: 12px;">
<div style="font-family: arial; font-size: 13.3333px;">
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<div class="yiv1437632715aolmail_aolmail_aolmail_center" style="background-image: none; border-style: none; height: auto; margin-bottom: 6px; margin-top: 6px;">
<span style="font-family: "arial" , sans-serif;">2017 Section 21 C.F.R. 589.2000, Animal Proteins Prohibited in Ruminant Feed</span></div>
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snip...</div>
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<br /></div>
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<div style="color: #29303b; font-family: arial; font-size: 13.3333px;">
<span style="font-size: 10pt;">WEDNESDAY, JULY 31, 2019 </span></div>
<div style="color: #29303b; font-family: arial; font-size: 13.3333px; line-height: 1.22em;">
<br /></div>
<div style="color: #29303b; font-family: arial; font-size: 13.3333px; line-height: 1.22em;">
The agent of transmissible mink encephalopathy passaged in sheep is similar to BSE-L</div>
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<br /></div>
<div style="color: #29303b; font-family: arial; font-size: 13.3333px; line-height: 1.22em;">
<a fg_scanned="1" href="https://transmissible-mink-encephalopathy.blogspot.com/2019/07/the-agent-of-transmissible-mink.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://transmissible-mink-encephalopathy.blogspot.com/2019/07/the-agent-of-transmissible-mink.html</a></div>
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<br /></div>
<div style="color: #29303b; font-family: arial; font-size: 13.3333px;">
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<span style="color: #191919; font-family: "verdana" , "arial" , sans-serif; font-size: 15px;"><br /></span></div>
<div style="margin: 0px; padding: 0px;">
<span style="color: #191919; font-family: "verdana" , "arial" , sans-serif; font-size: 15px;">Tuesday, September 10, 2019 </span></div>
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<span style="color: #191919; font-family: "verdana" , "arial" , sans-serif; font-size: 15px;"><br /></span></div>
<div style="margin: 0px; padding: 0px;">
<span style="color: #191919; font-family: "verdana" , "arial" , sans-serif; font-size: 15px;">FSIS [Docket No. FSIS–2019–0021] Notice of Request To Renew an Approved Information Collection: Specified Risk Materials Singeltary Submission</span></div>
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<span style="color: #191919; font-family: "verdana" , "arial" , sans-serif; font-size: 15px;"><a fg_scanned="1" href="https://specifiedriskmaterial.blogspot.com/2019/09/fsis-docket-no-fsis20190021-notice-of.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://specifiedriskmaterial.blogspot.com/2019/09/fsis-docket-no-fsis20190021-notice-of.html</a></span></div>
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<div style="color: #29303b; font-family: Georgia, "New sans-serif"; font-size: 13px; margin: 0px; padding: 0px;">
<div style="font-family: Helvetica; font-size: 12px; font-stretch: normal; line-height: normal;">
<span style="font-size: 12pt;"><br /></span></div>
<div style="font-family: Helvetica; font-size: 12px; font-stretch: normal; line-height: normal;">
<span style="font-size: 12pt;">MONDAY, FEBRUARY 25, 2019</span></div>
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<span style="font-size: 12pt;"></span><br /></div>
<div style="font-family: Helvetica; font-size: 12px; font-stretch: normal; line-height: normal;">
<span style="font-size: 12pt;">MAD DOGS AND ENGLISHMEN BSE, SCRAPIE, CWD, CJD, TSE PRION A REVIEW 2019</span></div>
<div style="font-family: Helvetica; font-size: 12px; font-stretch: normal; line-height: normal; min-height: 13.8px;">
<span style="font-size: 12pt;"></span><br /></div>
<div style="font-family: Helvetica; font-size: 12px; font-stretch: normal; line-height: normal;">
<span style="font-size: 12pt;"><a fg_scanned="1" href="https://bseinquiry.blogspot.com/2019/02/mad-dogs-and-englishmen-bse-scrapie-cwd.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://bseinquiry.blogspot.com/2019/02/mad-dogs-and-englishmen-bse-scrapie-cwd.html</a></span></div>
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<br /></div>
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<span style="font-family: "helvetica";"><span style="font-size: 12px;"><br /></span></span></div>
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<span style="font-family: "helvetica";"><span style="font-size: 12px;">TUESDAY, JULY 10, 2018 </span></span></div>
<div style="font-stretch: normal; line-height: normal;">
<span style="font-family: "helvetica";"><span style="font-size: 12px;"><br /></span></span></div>
<div style="font-stretch: normal; line-height: normal;">
<span style="font-family: "helvetica";"><span style="font-size: 12px;">CONFIDENTIAL </span></span></div>
<div style="font-stretch: normal; line-height: normal;">
<span style="font-family: "helvetica";"><span style="font-size: 12px;"><br /></span></span></div>
<div style="font-stretch: normal; line-height: normal;">
<span style="font-family: "helvetica";"><span style="font-size: 12px;">IN CONFIDENCE </span></span></div>
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<span style="font-family: "helvetica";"><span style="font-size: 12px;"><br /></span></span></div>
<div style="font-stretch: normal; line-height: normal;">
<span style="font-family: "helvetica";"><span style="font-size: 12px;">SPONGIFORM ENCEPHALOPATHY OF PIGS </span></span></div>
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<span style="font-family: "helvetica";"><span style="font-size: 12px;"><br /></span></span></div>
<div style="font-stretch: normal; line-height: normal;">
<span style="font-family: "helvetica";"><span style="font-size: 12px;">*** ''but feeding of other ruminant protein, including scrapie-infected sheep, can continue to pigs.''</span></span></div>
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<span style="font-family: "helvetica";"><span style="font-size: 12px;"><br /></span></span></div>
<div style="font-stretch: normal; line-height: normal;">
<span style="font-family: "helvetica";"><span style="font-size: 12px;">CONFIDENTIAL SPONGIFORM ENCEPHALOPATHY OF PIGS</span></span></div>
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<span style="font-family: "helvetica";"><span style="font-size: 12px;"><br /></span></span></div>
<div style="font-stretch: normal; line-height: normal;">
<span style="font-family: "helvetica";"><span style="font-size: 12px;">CONFIDENTIAL</span></span></div>
<div style="font-stretch: normal; line-height: normal;">
<span style="font-family: "helvetica";"><span style="font-size: 12px;"><br /></span></span></div>
<div style="font-stretch: normal; line-height: normal;">
<span style="font-family: "helvetica";"><span style="font-size: 12px;">Ref: Pigs10i</span></span></div>
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<span style="font-family: "helvetica";"><span style="font-size: 12px;"><br /></span></span></div>
<div style="font-stretch: normal; line-height: normal;">
<span style="font-family: "helvetica";"><span style="font-size: 12px;">IN CONFIDENCE</span></span></div>
</div>
<div style="font-family: Helvetica; font-size: 12px; font-stretch: normal; line-height: normal;">
<br /></div>
<div style="font-family: Helvetica; font-size: 12px; font-stretch: normal; line-height: normal;">
<a fg_scanned="1" href="https://madporcinedisease.blogspot.com/2018/07/confidential-in-confidence-spongiform.html" rel="noopener noreferrer" style="color: #956839; cursor: pointer;" target="_blank">https://madporcinedisease.blogspot.com/2018/07/confidential-in-confidence-spongiform.html</a></div>
</div>
</div>
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<br /></div>
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snip...see full text;</div>
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<a fg_scanned="1" href="https://madporcinedisease.blogspot.com/2019/09/usda-modernizes-swine-slaughter.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://madporcinedisease.blogspot.com/2019/09/usda-modernizes-swine-slaughter.html</a></div>
</span></div>
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<div>
<br /></div>
<div>
WEDNESDAY, SEPTEMBER 18, 2019 </div>
<div>
<br /></div>
<div>
USDA Modernizes Swine Slaughter Inspection for the First Time in Over 50 Years and TSE Prion Risk Factors</div>
<div>
<br /></div>
<div>
<a fg_scanned="1" href="https://madporcinedisease.blogspot.com/2019/09/usda-modernizes-swine-slaughter.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://madporcinedisease.blogspot.com/2019/09/usda-modernizes-swine-slaughter.html</a></div>
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<br /></div>
<div>
<div>
FRIDAY, FEBRUARY 07, 2020 </div>
<div>
<br /></div>
<div>
Montana 142 animals tested positive for CWD thus far during 2019/20 sampling</div>
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<br /></div>
<div>
<a fg_scanned="1" href="https://chronic-wasting-disease.blogspot.com/2020/02/montana-142-animals-tested-positive-for.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://chronic-wasting-disease.blogspot.com/2020/02/montana-142-animals-tested-positive-for.html</a></div>
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<div>
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<div>
<div style="font-family: Helvetica; font-size: 12px; font-stretch: normal; line-height: normal;">
<span style="font-size: 12pt;">Colorado Chronic Wasting Disease Response Plan December 2018</span></div>
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<span style="font-size: 12pt;">I. Executive Summary Mule deer, white-tailed deer, elk and moose are highly valued species in North America. Some of Colorado’s herds of these species are increasingly becoming infected with chronic wasting disease (CWD). As of July 2018, at least 31 of Colorado's 54 deer herds (57%), 16 of 43 elk herds (37%), and 2 of 9 moose herds (22%) are known to be infected with CWD. Four of Colorado's 5 largest deer herds and 2 of the state’s 5 largest elk herds are infected. Deer herds tend to be more heavily infected than elk and moose herds living in the same geographic area. Not only are the number of infected herds increasing, the past 15 years of disease trends generally show an increase in the proportion of infected animals within herds as well. Of most concern, greater than a 10-fold increase in CWD prevalence has been estimated in some mule deer herds since the early 2000s; CWD is now adversely affecting the performance of these herds.</span></div>
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<span style="font-size: 12pt;">(the map on page 71, cwd marked in red, is shocking...tss)</span></div>
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<a href="https://cpw.state.co.us/Documents/RulesRegs/Brochure/BigGame/biggame.pdf" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://cpw.state.co.us/Documents/RulesRegs/Brochure/BigGame/biggame.pdf</a></div>
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<span style="font-family: "arial" , "helvetica" , sans-serif; font-size: 12px;">CWD Advisory Group</span></div>
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<a fg_scanned="1" href="https://cpw.state.co.us/learn/Pages/CWD-Advisory-Council.aspx" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://cpw.state.co.us/learn/Pages/CWD-Advisory-Council.aspx</a></div>
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<span style="font-family: "arial" , "helvetica" , sans-serif; font-size: 12px;">A Colorado alternative livestock producer who has had no CWD positive tests in the previous 60 months and who has had at least 60 months of CWD surveillance status may apply for a waiver from the mandatory surveillance requirements. Application to Waive CWD Sample Submission for Imported Elk</span></div>
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<span style="font-family: "arial" , "helvetica" , sans-serif; font-size: 12px;"><a fg_scanned="1" href="https://www.colorado.gov/pacific/aganimals/chronic-wasting-disease" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://www.colorado.gov/pacific/aganimals/chronic-wasting-disease</a></span></div>
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<a fg_scanned="1" href="https://www.colorado.gov/pacific/aganimals/elk" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://www.colorado.gov/pacific/aganimals/elk</a></div>
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<span style="font-family: "arial" , "helvetica" , sans-serif; font-size: 12px;">COLORADO THE ORIGIN OF CHRONIC WASTING DISEASE CWD TSE PRION?</span></div>
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<span style="font-family: "arial" , "helvetica" , sans-serif; font-size: 12px;">*** Spraker suggested an interesting explanation for the occurrence of CWD. The deer pens at the Foot Hills Campus were built some 30-40 years ago by a Dr. Bob Davis. At or abut that time, allegedly, some scrapie work was conducted at this site. When deer were introduced to the pens they occupied ground that had previously been occupied by sheep. </span></div>
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<span style="font-family: "arial" , "helvetica" , sans-serif; font-size: 12px;">IN CONFIDENCE, REPORT OF AN UNCONVENTIONAL SLOW VIRUS DISEASE IN ANIMALS IN THE USA 1989</span></div>
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<a href="http://webarchive.nationalarchives.gov.uk/20080102193705/http://www.bseinquiry.gov.uk/files/mb/m11b/tab01.pdf" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">http://webarchive.nationalarchives.gov.uk/20080102193705/http://www.bseinquiry.gov.uk/files/mb/m11b/tab01.pdf</a></div>
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<span style="font-family: "arial" , "helvetica" , sans-serif; font-size: 12px;">ALSO, one of the most, if not the most top TSE Prion God in Science today is Professor Adriano Aguzzi, and he recently commented on just this, on a cwd post on my facebook page August 20 at 1:44pm, quote;</span></div>
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<span style="font-family: "arial" , "helvetica" , sans-serif; font-size: 12px;">''it pains me to no end to even contemplate the possibility, but it seems entirely plausible that CWD originated from scientist-made spread of scrapie from sheep to deer in the colorado research facility. If true, a terrible burden for those involved.'' August 20 at 1:44pm ...end</span></div>
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<span style="font-family: "arial" , "helvetica" , sans-serif; font-size: 12px;">”The occurrence of CWD must be viewed against the contest of the locations in which it occurred. It was an incidental and unwelcome complication of the respective wildlife research programmes. Despite it’s subsequent recognition as a new disease of cervids, therefore justifying direct investigation, no specific research funding was forthcoming. The USDA viewed it as a wildlife problem and consequently not their province!” page 26.</span></div>
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<span style="font-family: "arial" , "helvetica" , sans-serif; font-size: 12px;"><a href="https://web.archive.org/web/20060307063531/http://www.bseinquiry.gov.uk/files/mb/m11b/tab01.pdf" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://web.archive.org/web/20060307063531/http://www.bseinquiry.gov.uk/files/mb/m11b/tab01.pdf</a></span></div>
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SATURDAY, FEBRUARY 01, 2020 </div>
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Colorado confirmed CWD TSE Prion in 24 game management units in the state where it previously hadn’t been found</div>
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<a fg_scanned="1" href="https://chronic-wasting-disease.blogspot.com/2020/02/colorado-confirmed-cwd-tse-prion-in-24.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://chronic-wasting-disease.blogspot.com/2020/02/colorado-confirmed-cwd-tse-prion-in-24.html</a></div>
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MONDAY, MAY 21, 2018 </div>
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Colorado Chronic Wasting disease CWD TSE Prion hits 16 percent of male deer, elk, moose tested in some parts of state</div>
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<a fg_scanned="1" href="http://chronic-wasting-disease.blogspot.com/2018/05/colorado-chronic-wasting-disease-cwd.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://chronic-wasting-disease.blogspot.com/2018/05/colorado-chronic-wasting-disease-cwd.html</a></div>
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I STRENUOUSLY URGE TEXAS FDA MODIFY THESE FEED BANS ASAP!</div>
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SEE;</div>
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Docket No. APHIS-2018-0011 Chronic Wasting Disease Herd Certification Program Standards Singeltary</div>
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<a fg_scanned="1" href="http://chronic-wasting-disease.blogspot.com/2018/03/docket-no-aphis-2018-0011-chronic.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://chronic-wasting-disease.blogspot.com/2018/03/docket-no-aphis-2018-0011-chronic.html</a></div>
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SATURDAY, JANUARY 18, 2020 </div>
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United States wildlife and wildlife product imports from 2000–2014 and TSE PRION aka Mad Cow Type Disease </div>
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***> HUMAN TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHY TSE PRION DISEASE 1 IN 5,000 NOT ONE IN A MILLION! </div>
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***> I urge every Country around the Globe to Declare an Extraordinary Emergency Due To A Foreign Animal Disease Chronic Wasting Disease CWD TSE Prion from the USA, Canada, and Mexico (they have no clue), all of North America should have this Declaration of Emergency against them, just like the one called way back when the shoe was on the other foot with the mad sheep of mad river valley, except this time, it's not a wag the dog false flag, this is for real...terry</div>
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<a fg_scanned="1" href="https://usdameatexport.blogspot.com/2020/01/united-states-wildlife-and-wildlife.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://usdameatexport.blogspot.com/2020/01/united-states-wildlife-and-wildlife.html</a> </div>
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<span style="font-family: "arial"; font-size: 10pt;">THE TSE Prion aka mad cow type disease is not your normal pathogen.</span></div>
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The TSE prion disease survives ashing to 600 degrees celsius, that’s around 1112 degrees farenheit.</div>
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you cannot cook the TSE prion disease out of meat.</div>
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you can take the ash and mix it with saline and inject that ash into a mouse, and the mouse will go down with TSE.</div>
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Prion Infected Meat-and-Bone Meal Is Still Infectious after Biodiesel Production as well.</div>
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the TSE prion agent also survives Simulated Wastewater Treatment Processes.</div>
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IN fact, you should also know that the TSE Prion agent will survive in the environment for years, if not decades.</div>
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you can bury it and it will not go away.</div>
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The TSE agent is capable of infected your water table i.e. Detection of protease-resistant cervid prion protein in water from a CWD-endemic area.</div>
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it’s not your ordinary pathogen you can just cook it out and be done with. that’s what’s so worrisome about Iatrogenic mode of transmission, a simple autoclave will not kill this TSE prion agent.</div>
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snip...see full text submission;</div>
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FRIDAY, DECEMBER 20, 2019</div>
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Texas TAHC, Administrative Code, Title 4, Part 2, Chapter 40, Chronic Wasting Disease Amendments Open For Comment beginning December 20, 2019 thru January 20, 2020 Terry Singeltary Comments Submission</div>
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<a fg_scanned="1" href="https://chronic-wasting-disease.blogspot.com/2019/12/texas-tahc-administrative-code-title-4.html" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://chronic-wasting-disease.blogspot.com/2019/12/texas-tahc-administrative-code-title-4.html</a></div>
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2020 Transmissible Spongiform Encephalopathy TSE Prion</div>
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***> 2020 CWD TSE PRION UPDATE GLOBAL MAP 2020</div>
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CWD TSE PRION UPDATE GLOBAL MAP 2020</div>
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SATURDAY, JANUARY 18, 2020 </div>
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United States wildlife and wildlife product imports from 2000–2014 and TSE PRION aka Mad Cow Type Disease </div>
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***> HUMAN TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHY TSE PRION DISEASE 1 IN 5,000 NOT ONE IN A MILLION! </div>
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***> I urge every Country around the Globe to Declare an Extraordinary Emergency Due To A Foreign Animal Disease Chronic Wasting Disease CWD TSE Prion from the USA, Canada, and Mexico (they have no clue), all of North America should have this Declaration of Emergency against them, just like the one called way back when the shoe was on the other foot with the mad sheep of mad river valley, except this time, it's not a wag the dog false flag, this is for real...terry</div>
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<a fg_scanned="1" href="https://usdameatexport.blogspot.com/2020/01/united-states-wildlife-and-wildlife.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://usdameatexport.blogspot.com/2020/01/united-states-wildlife-and-wildlife.html</a></div>
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<a fg_scanned="1" href="https://chronic-wasting-disease.blogspot.com/2020/01/tennessee-2019-20-deer-season-462-cwd.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://chronic-wasting-disease.blogspot.com/2020/01/tennessee-2019-20-deer-season-462-cwd.html</a></div>
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<a fg_scanned="1" href="https://chronic-wasting-disease.blogspot.com/2020/01/canadian-food-inspection-agency-cfia.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://chronic-wasting-disease.blogspot.com/2020/01/canadian-food-inspection-agency-cfia.html</a></div>
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<a fg_scanned="1" href="https://chronic-wasting-disease.blogspot.com/2020/01/2004-european-commission-chronic.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://chronic-wasting-disease.blogspot.com/2020/01/2004-european-commission-chronic.html</a></div>
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<a fg_scanned="1" href="https://madcowusda.blogspot.com/2020/01/usda-consolidates-regulations-for-nahln.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://madcowusda.blogspot.com/2020/01/usda-consolidates-regulations-for-nahln.html</a></div>
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TUESDAY, JANUARY 07, 2020 </div>
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Oklahoma Farmed Elk Lincoln County CWD Depopulation 3 Positive Elk with 1 Additional Dead Trace Out Confirmed Positive</div>
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<a fg_scanned="1" href="https://chronic-wasting-disease.blogspot.com/2020/01/oklahoma-farmed-elk-lincoln-county-cwd.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://chronic-wasting-disease.blogspot.com/2020/01/oklahoma-farmed-elk-lincoln-county-cwd.html</a></div>
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WEDNESDAY, JANUARY 29, 2020 </div>
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Pennsylvania CWD TSE Prion 2019-20 hunting seasons as of January 14, 148 of the samples had tested positive for CWD in Wild Deer</div>
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SUNDAY, DECEMBER 22, 2019<br />
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Pennsylvania Steady Climb of CWD TSE Prion Confirms 250 Positive To Date In Wild Cervid As At September 12, 2019 </div>
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Pennsylvania Captive Cervid Industry Total CWD TSE Prion ??? anyone's guess...</div>
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<a fg_scanned="1" href="https://chronic-wasting-disease.blogspot.com/2019/12/pennsylvania-steady-climb-of-cwd-tse.html" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">https://chronic-wasting-disease.blogspot.com/2019/12/pennsylvania-steady-climb-of-cwd-tse.html</a></div>
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MONDAY, JANUARY 27, 2020 </div>
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Michigan CWD TSE Prion MDARD 3 positive white-tailed deer from a Newaygo County deer farm depopulation and quarantine efforts update?</div>
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<a fg_scanned="1" href="https://chronic-wasting-disease.blogspot.com/2020/01/michigan-cwd-tse-prion-mdard-3-positive.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://chronic-wasting-disease.blogspot.com/2020/01/michigan-cwd-tse-prion-mdard-3-positive.html</a></div>
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TUESDAY, JANUARY 07, 2020 </div>
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Michigan Total CWD TSE Prion Positive Suspect-Positive Deer Jump To 174 confirmed to date</div>
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TUESDAY, JANUARY 14, 2020 </div>
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Michigan MDARD has confirmed chronic wasting disease (CWD) in 3 white-tailed deer from a Newaygo County deer farm</div>
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<a fg_scanned="1" href="https://chronic-wasting-disease.blogspot.com/2020/01/michigan-mdard-has-confirmed-chronic.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://chronic-wasting-disease.blogspot.com/2020/01/michigan-mdard-has-confirmed-chronic.html</a></div>
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<span style="font-family: "arial" , "helvetica" , sans-serif; font-size: 12px;">Tennessee 2019-20 deer season 462 CWD TSE Prion Confirmed To Date</span></div>
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<span style="font-family: "arial" , "helvetica" , sans-serif; font-size: 12px;"><a fg_scanned="1" href="https://chronic-wasting-disease.blogspot.com/2020/01/tennessee-2019-20-deer-season-462-cwd.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://chronic-wasting-disease.blogspot.com/2020/01/tennessee-2019-20-deer-season-462-cwd.html</a></span></div>
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FRIDAY, JANUARY 24, 2020</div>
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<span style="font-family: "arial" , "helvetica";">Wyoming Game & Fish Discovers CWD-Positive Mule Deer in Pinedale, Discourages Feeding of Wildlife</span></div>
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<span style="font-family: "arial" , "helvetica";">''As of September 2019, CWD has been identified in 31 of 37 (84%) Wyoming mule deer herds, nine of 36 (25%) elk herds, and generally wherever white-tailed deer occur. Increasing prevalence and distribution of CWD has the potential to cause widespread and long-term negative impacts to Wyoming’s cervid populations. Prevalence of this disease in chronically infected Wyoming deer herds has exceeded 40%, with one elk herd exhibiting nearly 15% prevalence.''</span></div>
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<span style="font-family: "arial" , "helvetica";">''for the first time, there is clear evidence that CWD is adversely affecting the overall health and viability of some herds.''</span></div>
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<span style="font-family: "arial" , "helvetica";"><a fg_scanned="1" href="https://chronic-wasting-disease.blogspot.com/2020/01/wyoming-game-fish-discovers-cwd.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://chronic-wasting-disease.blogspot.com/2020/01/wyoming-game-fish-discovers-cwd.html</a></span></div>
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<span style="color: #222222;">FRIDAY, JANUARY 24, 2020 </span></div>
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<span style="color: #222222;">A</span><span style="color: #222222;">rkansas Chronic Wasting Disease CWD TSE Prion FY2020 211 Positive Cases as of January 17, 2020</span></div>
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<span style="color: #222222;"><a fg_scanned="1" href="https://chronic-wasting-disease.blogspot.com/2020/01/arkansas-chronic-wasting-disease-cwd_24.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://chronic-wasting-disease.blogspot.com/2020/01/arkansas-chronic-wasting-disease-cwd_24.html</a></span></div>
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SUNDAY, JANUARY 05, 2020 </div>
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<span style="font-family: "arial" , "helvetica" , sans-serif;"><span style="font-size: 12px;">Arkansas Chronic Wasting Disease CWD TSE Prion 2019 to 2020 Totals As Of December 3, 2019 399 Confirmed with more pending results</span></span></div>
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<span style="font-family: "arial" , "helvetica" , sans-serif;"><span style="font-size: 12px;"><a fg_scanned="1" href="https://chronic-wasting-disease.blogspot.com/2020/01/arkansas-chronic-wasting-disease-cwd.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://chronic-wasting-disease.blogspot.com/2020/01/arkansas-chronic-wasting-disease-cwd.html</a></span></span></div>
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WEDNESDAY, JANUARY 29, 2020 </div>
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Utah CWD TSE Prion Since July 1, 2019, the DWR confirmed 16 positive deer statewide Six of those, including Coal, were in the La Sal Unit, 59 test pending</div>
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<a fg_scanned="1" href="https://chronic-wasting-disease.blogspot.com/2020/01/utah-cwd-tse-prion-since-july-1-2019.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://chronic-wasting-disease.blogspot.com/2020/01/utah-cwd-tse-prion-since-july-1-2019.html</a></div>
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FRIDAY, JANUARY 17, 2020 </div>
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North Dakota 11 Positive Chronic Wasting Disease CWD TSE Prion detected since Sept 1, 2019</div>
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<a fg_scanned="1" href="https://chronic-wasting-disease.blogspot.com/2020/01/north-dakota-11-positive-chronic.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://chronic-wasting-disease.blogspot.com/2020/01/north-dakota-11-positive-chronic.html</a></div>
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TUESDAY, JANUARY 21, 2020 </div>
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Minnesota CWD update test results from deer harvested in the 2019 hunting season and the special hunts have returned 27 wild deer tested positive for CWD all from the southeast DMZ</div>
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<a fg_scanned="1" href="https://chronic-wasting-disease.blogspot.com/2020/01/minnesota-cwd-update-test-results-from.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://chronic-wasting-disease.blogspot.com/2020/01/minnesota-cwd-update-test-results-from.html</a></div>
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<span style="font-family: "arial" , "helvetica"; font-size: x-small;">FRIDAY, JANUARY 10, 2020 </span></div>
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<span style="font-family: "arial" , "helvetica"; font-size: x-small;">Minnesota Investigation leads to additional CWD positive deer on Pine County farm</span></div>
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<span style="font-family: "arial" , "helvetica"; font-size: x-small;"><a fg_scanned="1" href="https://chronic-wasting-disease.blogspot.com/2020/01/minnesota-investigation-leads-to.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://chronic-wasting-disease.blogspot.com/2020/01/minnesota-investigation-leads-to.html</a></span></div>
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<span style="color: #222222;">THURSDAY, JANUARY 23, 2020 </span></div>
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<span style="color: #222222;">Wisconsin Confirms CWD Detected In Marquette and Marathon County</span></div>
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<span style="color: #222222;"><a fg_scanned="1" href="https://chronic-wasting-disease.blogspot.com/2020/01/wisconsin-confirms-cwd-detected-in.html" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://chronic-wasting-disease.blogspot.com/2020/01/wisconsin-confirms-cwd-detected-in.html</a></span></div>
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WEDNESDAY, JANUARY 08, 2020 </div>
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Wisconsin Chronic Wasting Disease CWD TSE Prion Positives in Farm-raised Deer in 2019 </div>
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The majority of the positives have come after 2013 when DATCP began letting some deer farms and hunting ranches continue operating after CWD was detected on their property.</div>
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<a fg_scanned="1" href="https://chronic-wasting-disease.blogspot.com/2020/01/wisconsin-chronic-wasting-disease-cwd_8.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://chronic-wasting-disease.blogspot.com/2020/01/wisconsin-chronic-wasting-disease-cwd_8.html</a></div>
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TUESDAY, JANUARY 07, 2020 </div>
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Oklahoma Farmed Elk Lincoln County CWD Depopulation 3 Positive Elk with 1 Additional Dead Trace Out Confirmed Positive</div>
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<a fg_scanned="1" href="https://chronic-wasting-disease.blogspot.com/2020/01/oklahoma-farmed-elk-lincoln-county-cwd.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://chronic-wasting-disease.blogspot.com/2020/01/oklahoma-farmed-elk-lincoln-county-cwd.html</a></div>
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<span style="font-family: "arial" , "helvetica";">WEDNESDAY, FEBRUARY 05, 2020 </span></div>
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<span style="font-family: "arial" , "helvetica";">Wisconsin CWD TSE Prion 2019 to date wild deer 1317 positive and Captive Farmed Livestock Cervid CWD update</span></div>
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<span style="font-family: "arial" , "helvetica";"><a fg_scanned="1" href="https://chronic-wasting-disease.blogspot.com/2020/02/wisconsin-cwd-tse-prion-2019-to-date.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://chronic-wasting-disease.blogspot.com/2020/02/wisconsin-cwd-tse-prion-2019-to-date.html</a></span></div>
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<span style="background-color: transparent;"><span style="font-family: "arial" , "helvetica";">TUESDAY, FEBRUARY 04, 2020 </span></span></div>
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<span style="background-color: transparent;"><span style="font-family: "arial" , "helvetica";">TEXAS REPORTS 20 NEW CWD TSE PRION CASES 3 WILD 17 BREEDER 166 POSITIVE TO DATE</span></span></div>
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<span style="background-color: transparent;"><span style="font-family: "arial" , "helvetica";"><a fg_scanned="1" href="https://chronic-wasting-disease.blogspot.com/2020/02/texas-reports-20-new-cwd-tse-prion.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://chronic-wasting-disease.blogspot.com/2020/02/texas-reports-20-new-cwd-tse-prion.html</a></span></span></div>
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THURSDAY, DECEMBER 19, 2019</div>
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TEXAS Val Verde County White-tailed Deer Tests Positive for Chronic Wasting Disease CWD TSE Prion State Positive NOW at 147 Confirmed</div>
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<a fg_scanned="1" href="https://chronic-wasting-disease.blogspot.com/2019/12/texas-val-verde-county-white-tailed.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://chronic-wasting-disease.blogspot.com/2019/12/texas-val-verde-county-white-tailed.html</a></div>
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FRIDAY, DECEMBER 20, 2019</div>
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Texas TAHC, Administrative Code, Title 4, Part 2, Chapter 40, Chronic Wasting Disease Amendments Open For Comment beginning December 20, 2019 thru January 20, 2020 Terry Singeltary Comments Submission</div>
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FRIDAY, DECEMBER 20, 2019</div>
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TEXAS ANIMAL HEALTH COMMISSION EXECUTIVE DIRECTOR ORDER DECLARING A CHRONIC WASTING DISEASE HIGH RISK AREA CONTAINMENT ZONE FOR PORTIONS OF VAL VERDE COUNTY</div>
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TUESDAY, DECEMBER 31, 2019 <span style="font-size: 10pt; line-height: 1.22em;">In Vitro detection of Chronic Wasting Disease (CWD) prions in semen and reproductive tissues of white tailed deer bucks (Odocoileus virginianus </span></div>
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<span style="font-size: 10pt; line-height: 1.22em;">SUNDAY, AUGUST 02, 2015 </span>TEXAS CWD, Have you been ThunderStruck, deer semen, straw bred bucks, super ovulation, and the potential TSE Prion connection, what if? </div>
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TUESDAY, JANUARY 28, 2020 </div>
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Mississippi MDWFP North MS CWD Management Zone Since October 2019, 25 CWD-positive deer have been detected from this zone</div>
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SATURDAY, JANUARY 04, 2020 </div>
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Mississippi CWD TOTALS JUST ABOUT DOUBLE Since October 1, 2019 To Date Statewide Total is 37 Confirmed</div>
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SUNDAY, JANUARY 19, 2020 </div>
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Missouri CWD TSE Prion 2019-2020 SAMPLING RESULTS TO DATE 25 Positive</div>
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THURSDAY, JANUARY 02, 2020 </div>
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Missouri MDC officially reports more than 20 new cases of Chronic Wasting Disease CWD TSE Prion</div>
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<span style="font-family: "arial" , "helvetica";">FRIDAY, JANUARY 17, 2020</span></div>
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<span style="font-family: "arial" , "helvetica";">Montana Moose Tests Positive for Chronic Wasting Disease CWD TSE PRION in Libby Area</span></div>
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<span style="font-family: "arial" , "helvetica";">Montana Fish, Wildlife & Parks 2019 CWD Surveillance Hunter Test Results CWD TSE PRION LOOKS LIKE 136 POSITIVE SO FAR, count them up...</span></div>
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WEDNESDAY, DECEMBER 25, 2019 </div>
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Montana 16 more deer positive for CWD first time positive hunting district 705 in southeast</div>
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SUNDAY, DECEMBER 22, 2019 </div>
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Illinois CWD TSE Prion 90 CWD-positive deer with 826 confirmed positive Total positives through June 30, 2019</div>
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<span style="color: #222222;">THURSDAY, JANUARY 23, 2020 </span></div>
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<span style="color: #222222;">Canadian Food Inspection Agency (CFIA) has updated the following chapter of the Accredited Veterinarian's Manual: Chapter 13 Chronic Wasting Disease Herd Certification Programs</span></div>
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TUESDAY, JANUARY 21, 2020 </div>
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2004 European Commission Chronic wasting disease AND TISSUES THAT MIGHT CARRY A RISK FOR HUMAN FOOD AND ANIMAL FEED CHAINS REPORT UPDATED 2020</div>
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MONDAY, JANUARY 27, 2020 </div>
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Michigan CWD TSE Prion MDARD 3 positive white-tailed deer from a Newaygo County deer farm depopulation and quarantine efforts update?</div>
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THURSDAY, JANUARY 30, 2020 </div>
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Michigan CWD TSE Prion Total Suspect Positive Deer Jumps To 181 to date</div>
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TSE surveillance statistics exotic species and domestic cats Update December 2019</div>
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<a fg_scanned="1" href="https://transmissiblespongiformencephalopathy.blogspot.com/2019/12/tse-surveillance-statistics-exotic.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://transmissiblespongiformencephalopathy.blogspot.com/2019/12/tse-surveillance-statistics-exotic.html</a></div>
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THURSDAY, DECEMBER 19, 2019 </div>
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The emergence of classical BSE from atypical/Nor98 scrapie</div>
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FRIDAY, DECEMBER 06, 2019 </div>
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Estimating relative CWD susceptibility and disease progression in farmed white-tailed deer with rare PRNP alleles</div>
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WEDNESDAY, NOVEMBER 20, 2019 </div>
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Review: Update on Classical and Atypical Scrapie in Sheep and Goats</div>
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WEDNESDAY, NOVEMBER 20, 2019 </div>
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Sheep Are Susceptible to the Bovine Adapted Transmissible Mink Encephalopathy agent by Intracranial Inoculation and Have Evidence of Infectivity in Lymphoid Tissues</div>
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<span style="color: #3e3d40; font-family: "georgia" , serif; font-size: 20px;">***> ''indicating that sheep inoculated with the bovine TME agent harbor infectivity in their lymph nodes despite a lack of detection with conventional immunoassays.''</span></div>
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FRIDAY, NOVEMBER 15, 2019 </div>
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Southwest Wisconsin CWD, Deer and Predator Study</div>
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FRIDAY, NOVEMBER 08, 2019 </div>
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EFSA Panel on Biological Hazards (BIOHAZ) Update on chronic wasting disease (CWD) III</div>
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WEDNESDAY, OCTOBER 16, 2019 </div>
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Australia Assessment of bulk wheat from Canada Part B: Animal biosecurity risk advice, CWD TSE Prion concerns are mounting </div>
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<span style="font-size: x-small;">FRIDAY, MAY 24, 2019 </span></div>
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<span style="font-size: x-small;">Assessing chronic wasting disease strain differences in free-ranging cervids across the United States</span></div>
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TUESDAY, FEBRUARY 04, 2020 </div>
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Predicting the spread-risk potential of chronic wasting disease to sympatric ungulate species</div>
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New Outbreak of TSE Prion in NEW LIVESTOCK SPECIES</div>
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Prion Disease in Dromedary Camels, Algeria Abstract</div>
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Prions cause fatal and transmissible neurodegenerative diseases, including Creutzfeldt-Jakob disease in humans, scrapie in small ruminants, and bovine spongiform encephalopathy (BSE). After the BSE epidemic, and the associated human infections, began in 1996 in the United Kingdom, general concerns have been raised about animal prions. We detected a prion disease in dromedary camels (Camelus dromedarius) in Algeria. Symptoms suggesting prion disease occurred in 3.1% of dromedaries brought for slaughter to the Ouargla abattoir in 2015–2016. We confirmed diagnosis by detecting pathognomonic neurodegeneration and disease-specific prion protein (PrPSc) in brain tissues from 3 symptomatic animals. Prion detection in lymphoid tissues is suggestive of the infectious nature of the disease. PrPSc biochemical characterization showed differences with BSE and scrapie. Our identification of this prion disease in a geographically widespread livestock species requires urgent enforcement of surveillance and assessment of the potential risks to human and animal health.</div>
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The possibility that dromedaries acquired the disease from eating prion-contaminated waste needs to be considered.</div>
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Tracing the origin of prion diseases is challenging. In the case of CPD, the traditional extensive and nomadic herding practices of dromedaries represent a formidable factor for accelerating the spread of the disease at long distances, making the path of its diffusion difficult to determine. Finally, the major import flows of live animals to Algeria from Niger, Mali, and Mauritania (27) should be investigated to trace the possible origin of CPD from other countries. Camels are a vital animal species for millions of persons globally. The world camel population has a yearly growth rate of 2.1% (28). In 2014, the population was estimated at ≈28 million animals, but this number is probably underestimated.. Approximately 88% of camels are found in Africa, especially eastern Africa, and 12% are found in Asia. Official data reported 350,000 dromedaries in Algeria in 2014 (28).</div>
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On the basis of phenotypic traits and sociogeographic criteria, several dromedary populations have been suggested to exist in Algeria (29). However, recent genetic studies in Algeria and Egypt point to a weak differentiation of the dromedary population as a consequence of historical use as a cross-continental beast of burden along trans-Saharan caravan routes, coupled with traditional extensive/nomadic herding practices (30).</div>
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Such genetic homogeneity also might be reflected in PRNP. Studies on PRNP variability in camels are therefore warranted to explore the existence of genotypes resistant to CPD, which could represent an important tool for CPD management as it was for breeding programs for scrapie eradication in sheep. In the past 10 years, the camel farming system has changed rapidly, with increasing setup of periurban dairy farms and dairy plants and diversification of camel products and market penetration (13). This evolution requires improved health standards for infectious diseases and, in light of CPD, for prion diseases.</div>
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The emergence of another prion disease in an animal species of crucial importance for millions of persons worldwide makes it necessary to assess the risk for humans and develop evidence-based policies to control and limit the spread of the disease in animals and minimize human exposure. The implementation of a surveillance system for prion diseases would be a first step to enable disease control and minimize human and animal exposure. Finally, the diagnostic capacity of prion diseases needs to be improved in all countries in Africa where dromedaries are part of the domestic livestock. <a fg_scanned="1" href="https://wwwnc.cdc.gov/eid/article/24/6/17-2007_article%C2%A0" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://wwwnc.cdc.gov/eid/article/24/6/17-2007_article </a>;</div>
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***> IMPORTS AND EXPORTS <***</div>
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***SEE MASSIVE AMOUNTS OF BANNED ANIMAL PROTEIN AKA MAD COW FEED IN COMMERCE USA DECADES AFTER POST BAN ***</div>
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<a fg_scanned="1" href="http://camelusprp.blogspot.com/2018/04/dromedary-camels-algeria-prion-mad.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://camelusprp.blogspot.com/2018/04/dromedary-camels-algeria-prion-mad.html</a></div>
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<span style="font-family: "arial" , "helvetica"; font-size: x-small;">USAHA-AAVLD Annual Meeting October 24-30, 2019 Transmissible Spongiform Encephalopathy TSE Prion CWD, Scrapie UPDATE</span></div>
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MONDAY, OCTOBER 07, 2019 </div>
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Chronic Wasting Disease (CWD) and Government Response Congressional Research Service May 17, 2019</div>
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WEDNESDAY, OCTOBER 02, 2019 </div>
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Chronic Wasting Disease In Cervids: Prevalence, Impact And Management Strategies</div>
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WEDNESDAY, JUNE 26, 2019 </div>
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Subcommittee Hearing: Chronic Wasting Disease: The Threats to Wildlife, Public Lands, Hunting, and Health</div>
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CHRONIC WASTING DISEASE CONGRESS Serial No. 107-117 May 16, 2002</div>
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CHRONIC WASTING DISEASE</div>
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JOINT OVERSIGHT HEARING BEFORE THE SUBCOMMITTEE ON FORESTS AND FOREST HEALTH JOINT WITH THE SUBCOMMITTEE ON FISHERIES CONSERVATION, WILDLIFE AND OCEANS OF THE COMMITTEE ON RESOURCES U.S. HOUSE OF REPRESENTATIVES ONE HUNDRED SEVENTH CONGRESS SECOND SESSION</div>
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Serial No. 107-117</div>
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Mr. MCINNIS. Today, this joint Subcommittee hearing will explore an issue of immeasurable importance to the growing number of communities in wide-ranging parts of this country, the growing incidence of Chronic Wasting Disease in North America’s wild and captive deer and elk populations. In a matter of just a few months, this once parochial concern has grown into something much larger and much more insidious than anyone could have imagined or predicted.</div>
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As each day passes, this problem grows in its size, scope, and consequence. One thing becomes clear. Chronic Wasting Disease is not a Colorado problem. It is a Wisconsin problem or a Nebraska or Wyoming problem. It is a national problem and anything short of a fully integrated, systematic national assault on this simply will not do, which is precisely why we brought our group together here today.</div>
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So this is a disease that is spreading throughout the continent and it is going to require a national response as well as the efforts that are currently taking place in States like Wisconsin, Colorado, Nebraska, Wyoming, the interest they now have down in Texas and some of the neighboring States that have large white-tailed deer population and also elk.</div>
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This is a huge issue for us, Mr. Chairman, in the State of Wisconsin. I want to commend Governor McCallum and your staff and the various agencies for the rapid response that you have shown, given the early detection of CWD after the last deer hunting season. The problem that we have, though, is just a lack of information, good science in regards to what is the best response, how dangerous is this disease. We cannot close the door, quite frankly, with the paucity of scientific research that is out there right now in regards to how the disease spreads, the exposure of other livestock herds—given the importance of our dairy industry in the State, that is a big issue—and also the human health effects.</div>
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<a href="https://www.govinfo.gov/content/pkg/CHRG-107hhrg79658/pdf/CHRG-107hhrg79658.pdf?fbclid=IwAR1-dMPpYLher4m8SyMICwoGXNyQcVjcinPvAw8CvIys1lEG7hxgzWplJlk" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer; font-weight: bold;" target="_blank">https://www.govinfo.gov/content/pkg/CHRG-107hhrg79658/pdf/CHRG-107hhrg79658.pdf?fbclid=IwAR1-dMPpYLher4m8SyMICwoGXNyQcVjcinPvAw8CvIys1lEG7hxgzWplJlk</a></div>
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Inactivation of chronic wasting disease prions using sodium hypochlorite</div>
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<span style="background-color: #fcfce5; color: #141414; font-family: "georgia" , serif; font-size: 14.6667px;">i think some hunters that don't read this carefully are going to think this is a cure all for cwd tse contamination. IT'S NOT!</span><br />
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<span style="background-color: #fcfce5; color: #141414; font-family: "georgia" , serif; font-size: 14.6667px;">first off, it would take a strong bleach type sodium hypochlorite, that is NOT your moms bleach she uses in her clothes, and store bought stuff.</span><br />
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<span style="background-color: #fcfce5; color: #141414; font-family: "georgia" , serif; font-size: 14.6667px;">Concentrated </span><b style="background-color: #fcfce5; color: #141414; font-size: 14.6667px;">bleach</b><span style="background-color: #fcfce5; color: #141414; font-family: "georgia" , serif; font-size: 14.6667px;"> is an 8.25 </span><b style="background-color: #fcfce5; color: #141414; font-size: 14.6667px;">percent</b><span style="background-color: #fcfce5; color: #141414; font-family: "georgia" , serif; font-size: 14.6667px;"> solution of sodium hypochlorite, up from the “regular </span><b style="background-color: #fcfce5; color: #141414; font-size: 14.6667px;">bleach</b><span style="background-color: #fcfce5; color: #141414; font-family: "georgia" , serif; font-size: 14.6667px;">” </span><b style="background-color: #fcfce5; color: #141414; font-size: 14.6667px;">concentration</b><span style="background-color: #fcfce5; color: #141414; font-family: "georgia" , serif; font-size: 14.6667px;"> of 5.25 </span><b style="background-color: #fcfce5; color: #141414; font-size: 14.6667px;">percent</b><span style="background-color: #fcfce5; color: #141414; font-family: "georgia" , serif; font-size: 14.6667px;">.Nov 1, 2013 </span><a class="yiv1437632715externalLink" fg_scanned="1" href="https://waterandhealth.org/disinfect/high-strength-bleach-2/" rel="noopener noreferrer" shape="rect" style="background-color: #fcfce5; border-radius: 5px; color: #0429e4; cursor: pointer; font-size: 14.6667px; font-weight: bold; margin: 0px -3px; padding: 0px 3px;" target="_blank">https://waterandhealth.org/disinfect/high-strength-bleach-2/</a><br />
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<span style="background-color: #fcfce5; color: #141414; font-family: "georgia" , serif; font-size: 14.6667px;">second off, the study states plainly;</span><br />
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<span style="background-color: #fcfce5; color: #141414; font-family: "georgia" , serif; font-size: 14.6667px;">''We found that a five-minute treatment with a 40% dilution of household bleach was effective at inactivating CWD seeding activity from stainless-steel wires and CWD-infected brain homogenates. However, bleach was not able to inactivate CWD seeding activity from solid tissues in our studies.''</span><br />
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<span style="background-color: #fcfce5; color: #141414; font-family: "georgia" , serif; font-size: 14.6667px;">''We initially tested brains from two CWD-infected mice and one uninfected mouse using 40% bleach for 5 minutes. The results from these experiments showed almost no elimination of prion seeding activity (</span><a class="yiv1437632715externalLink" fg_scanned="1" href="https://journals.plos.org/plosone/article?id=10.1371%2Fjournal.pone.0223659&fbclid=IwAR3riclZfVRwL6SZC-oWk1xDFqCXHj9DEzVZPcBG52UK2rjzYuGEOXhxZ48#pone-0223659-t004" rel="noopener noreferrer" shape="rect" style="background-color: #fcfce5; border-radius: 5px; color: #0429e4; cursor: pointer; font-size: 14.6667px; font-weight: bold; margin: 0px -3px; padding: 0px 3px;" target="_blank">Table 4</a><span style="background-color: #fcfce5; color: #141414; font-family: "georgia" , serif; font-size: 14.6667px;">). We then increased the treatment time to 30 minutes and tested 40% and 100% bleach treatments. Again, the results were disappointing and showed less than a 10-fold decrease in CWD-seeding activity (</span><a class="yiv1437632715externalLink" fg_scanned="1" href="https://journals.plos.org/plosone/article?id=10.1371%2Fjournal.pone.0223659&fbclid=IwAR3riclZfVRwL6SZC-oWk1xDFqCXHj9DEzVZPcBG52UK2rjzYuGEOXhxZ48#pone-0223659-t004" rel="noopener noreferrer" shape="rect" style="background-color: #fcfce5; border-radius: 5px; color: #0429e4; cursor: pointer; font-size: 14.6667px; font-weight: bold; margin: 0px -3px; padding: 0px 3px;" target="_blank">Table 4</a><span style="background-color: #fcfce5; color: #141414; font-family: "georgia" , serif; font-size: 14.6667px;">). Clearly, bleach is not able to inactivate prions effectively from small brain pieces under the conditions tested here.''</span><br />
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<span style="background-color: #fcfce5; color: #141414; font-family: "georgia" , serif; font-size: 14.6667px;">''We found that both the concentration of bleach and the time of treatment are critical for inactivation of CWD prions. A 40% bleach treatment for 5 minutes successfully eliminated detectable prion seeding activity from both CWD-positive brain homogenate and stainless-steel wires bound with CWD. However, even small solid pieces of CWD-infected brain were not successfully decontaminated with the use of bleach.''</span><br />
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<a class="yiv1437632715externalLink" fg_scanned="1" href="https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0223659" rel="noopener noreferrer" shape="rect" style="background-color: #fcfce5; border-radius: 5px; color: #0429e4; cursor: pointer; font-size: 14.6667px; font-weight: bold; margin: 0px -3px; padding: 0px 3px;" target="_blank">https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0223659</a><br />
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<a class="yiv1437632715externalLink" fg_scanned="1" href="https://chronic-wasting-disease.blogspot.com/2019/10/inactivation-of-chronic-wasting-disease.html" rel="noopener noreferrer" shape="rect" style="background-color: #fcfce5; border-radius: 5px; color: #0429e4; cursor: pointer; font-size: 14.6667px; font-weight: bold; margin: 0px -3px; padding: 0px 3px;" target="_blank">https://chronic-wasting-disease.blogspot.com/2019/10/inactivation-of-chronic-wasting-disease.html</a><br />
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<span style="background-color: #fcfce5; color: #141414; font-family: "georgia" , serif; font-size: 14.6667px;">i think with all the fear from recent studies, and there are many, of potential, or likelihood of zoonosis, if it has not already happened as scjd, i think this study came out to help out on some of that fear, that maybe something will help, but the study plainly states it's for sure not a cure all for exposure and contamination of the cwd tse prion on surface materials. imo...terry</span></div>
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HUNTERS, CWD TSE PRION, THIS SHOULD A WAKE UP CALL TO ALL OF YOU GUTTING AND BONING OUT YOUR KILL IN THE FIELD, AND YOUR TOOLS YOU USE...</div>
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<em style="border: 0px; margin: 0px; padding: 0px; vertical-align: baseline;">*</em> 1: J Neurol Neurosurg Psychiatry 1994 Jun;57(6):757-8</div>
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Transmission of Creutzfeldt-Jakob disease to a chimpanzee by electrodes contaminated during neurosurgery.</div>
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Gibbs CJ Jr, Asher DM, Kobrine A, Amyx HL, Sulima MP, Gajdusek DC.</div>
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Laboratory of Central Nervous System Studies, National Institute of</div>
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Neurological Disorders and Stroke, National Institutes of Health,</div>
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Bethesda, MD 20892.</div>
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Stereotactic multicontact electrodes used to probe the cerebral cortex of a middle aged woman with progressive dementia were previously implicated in the accidental transmission of Creutzfeldt-Jakob disease (CJD) to two younger patients. The diagnoses of CJD have been confirmed for all three cases. More than two years after their last use in humans, after three cleanings and repeated sterilisation in ethanol and formaldehyde vapour, the electrodes were implanted in the cortex of a chimpanzee. Eighteen months later the animal became ill with CJD. This finding serves to re-emphasise the potential danger posed by reuse of instruments contaminated with the agents of spongiform encephalopathies, even after scrupulous attempts to clean them.</div>
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PMID: 8006664 [PubMed - indexed for MEDLINE]</div>
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<a fg_scanned="1" href="http://jnnp.bmj.com/content/57/6/757.long" rel="noopener noreferrer" shape="rect" style="border: 0px; color: #162a3a; cursor: pointer; font-weight: bold; margin: 0px; padding: 0px; vertical-align: baseline;" target="_blank">http://jnnp.bmj.com/content/57/6/757.long</a></div>
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Wednesday, September 11, 2019 </div>
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Is the re-use of sterilized implant abutments safe enough? (Implant abutment safety) iatrogenic TSE Prion</div>
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<a fg_scanned="1" href="https://prionprp.blogspot.com/2019/09/is-re-use-of-sterilized-implant.html" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer; font-weight: bold; line-height: 1.22em;" target="_blank">https://prionprp.blogspot.com/2019/09/is-re-use-of-sterilized-implant.html</a></div>
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<a fg_scanned="1" href="https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0223659" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0223659</a></div>
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172. Establishment of PrP<span style="font-size: 15.6px; line-height: 0; position: relative; vertical-align: baseline;">CWD</span> extraction and detection methods in the farm soil</h3>
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Kyung Je Park, Hoo Chang Park, In Soon Roh, Hyo Jin Kim, Hae-Eun Kang and Hyun Joo Sohn</div>
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Foreign Animal Disease Division, Animal and Plant Quarantine Agency, Gimcheon, Gyeongsangbuk-do, Korea</div>
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<b>ABSTRACT</b></div>
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<b>Introduction</b>: Transmissible spongiform encephalopathy (TSE) is a fatal neurodegenerative disorder, which is so-called as prion diseases due to the causative agents (PrP<span style="font-size: 13.2px; line-height: 0; position: relative; vertical-align: baseline;">Sc</span>). TSEs are believed to be due to the template-directed accumulation of disease-associated prion protein, generally designated PrP<span style="font-size: 13.2px; line-height: 0; position: relative; vertical-align: baseline;">Sc</span>. Chronic wasting disease (CWD) is the prion disease that is known spread horizontally. CWD has confirmed last in Republic of Korea in 2016 since first outbreak of CWD in 2001. The environmental reservoirs mediate the transmission of this disease. The significant levels of infectivity have been detected in the saliva, urine, and faeces of TSE-infected animals. Soil can serve as a stable reservoir for infectious prion proteins. We found that PrP<span style="font-size: 13.2px; line-height: 0; position: relative; vertical-align: baseline;">CWD</span> can be extracted and detected in CWD contaminated soil which has kept at room temperature until 4 years after 0.001 ~ 1% CWD exposure and natural CWD-affected farm soil through PBS washing and sPMCAb.</div>
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<b>Materials and Methods: Procedure of serial PMCAb</b>. CWD contaminated soil which has kept at room temperature (RT) for 1 ~ 4 year after 0.001%~1% CWD brain homogenates exposure for 4 months collected 0.14 g. The soil was collected by the same method once of year until 4 year after stop CWD exposure. We had conducted the two steps. There are two kinds of 10 times washing step and one amplification step. The washing step was detached PrP<span style="font-size: 13.2px; line-height: 0; position: relative; vertical-align: baseline;">Sc</span> from contaminated soil by strong vortex with maximum rpm. We harvest supernatant every time by 10 times. As the other washing step, the Washed soil was made by washing 10 times soil using slow rotator and then harvest resuspended PBS for removing large impurity material. Last step was prion amplification step for detection of PrP<span style="font-size: 13.2px; line-height: 0; position: relative; vertical-align: baseline;">CWD</span> in soil supernatant and the washed soil by sPMCAb. Normal brain homogenate (NBH) was prepared by homogenization of brains with glass dounce in 9 volumes of cold PBS with TritonX-100, 5 mM EDTA, 150 mM NaCl and 0.05% Digitonin (sigma) plus Complete mini protease inhibitors (Roche) to a final concentration of 5%(w/v) NBHs were centrifuged at 2000 g for 1 min, and supernatant removed and frozen at −70 C for use. CWD consisted of brain from natural case in Korea and was prepared as 10%(w/v) homogenate. Positive sample was diluted to a final dilution 1:1000 in NBH, with serial 3:7 dilutions in NBH. Sonication was performed with a Misonix 4000 sonicator with amplitude set to level 70, generating an average output of 160W with two teflon beads during each cycle. One round consisted of 56 cycles of 30 s of sonication followed 9 min 30 s of 37°C incubation. <b>Western Blotting (WB) for PrP<span style="font-size: 13.2px; line-height: 0; position: relative; vertical-align: baseline;">Sc</span> detection</b>. The samples (20 µL) after each round of amplification were mixed with proteinase K (2 mg/ml) and incubated 37°C for 1 h. Samples were separated by SDS-PAGE and transferred onto PVDF membrane. After blocking, the membrane was incubated for 1 h with 1st antibody S1 anti rabbit serum (APQA, 1:3000) and developed with enhanced chemiluminescence detection system.</div>
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<b>Results</b>: We excluded from first to third supernatant in view of sample contamination. It was confirmed abnormal PrP amplification in all soil supernatants from fourth to tenth. From 0.01% to 1% contaminated washed soils were identified as abnormal prions. 0.001% contaminated washed soil did not show PrP specific band (Fig 1). The soil was collected by the same method once of year until 4 year after stop CWD exposure. After sPMCAb, there were no PrP<span style="font-size: 13.2px; line-height: 0; position: relative; vertical-align: baseline;">CWD</span> band in from second to fourth year 0.001% washed soil. but It was confirmed that the abnormal prion was amplified in the washing supernatant which was not amplified in the washed soil. we have decided to use soil supernatant for soil testing (Fig. 2). After third rounds of amplification, PrP<span style="font-size: 13.2px; line-height: 0; position: relative; vertical-align: baseline;">Sc</span> signals observed in three out of four sites from CWD positive farm playground. No signals were observed in all soil samples from four CWD negative farm (Fig. 3).</div>
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<b>Conclusions</b>: Our studies showed that PrP<span style="font-size: 13.2px; line-height: 0; position: relative; vertical-align: baseline;">CWD</span> persist in 0.001% CWD contaminated soil for at least 4 year and natural CWD-affected farm soil. When cervid reintroduced into CWD outbreak farm, the strict decontamination procedures of the infectious agent should be performed in the environment of CWD-affected cervid habitat.</div>
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186. Serial detection of hematogenous prions in CWD-infected deer</h3>
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Amy V. Nalls, Erin E. McNulty, Nathaniel D. Denkers, Edward A. Hoover and Candace K. Mathiason</div>
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Department of Microbiology, Immunology, and Pathology, Colorado State University, Fort Collins, CO, USA</div>
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<b>CONTACT</b> Amy V. Nalls <a href="mailto:amy.nalls@colostate.edu" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank" ymailto="mailto:amy.nalls@colostate.edu">amy.nalls@colostate.edu</a></div>
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<b>ABSTRACT</b></div>
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Blood contains the infectious agent associated with prion disease affecting several mammalian species, including humans, cervids, sheep, and cattle. It has been confirmed that sufficient prion agent is present in the blood of both symptomatic and asymptomatic carriers to initiate the amyloid templating and accumulation process that results in this fatal neurodegenerative disease. Yet, to date, the ability to detect blood-borne prions by <i>in vitro</i> methods remains difficult.</div>
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We have capitalized on blood samples collected from longitudinal chronic wasting disease (CWD) studies in the native white-tailed deer host to examine hematogenous prion load in blood collected minutes, days, weeks and months post exposure. Our work has focused on refinement of the amplification methods RT-QuIC and PMCA. We demonstrate enhanced <i>in vitro</i> detection of amyloid seeding activity (prions) in blood cell fractions harvested from deer orally-exposed to 300 ng CWD positive brain or saliva.</div>
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These findings permit assessment of the role hematogenous prions play in the pathogenesis of CWD and provide tools to assess the same for prion diseases of other mammalian species.</div>
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<a fg_scanned="1" href="https://www.tandfonline.com/doi/full/10.1080/19336896.2019.1615197" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://www.tandfonline.com/doi/full/10.1080/19336896.2019.1615197</a></div>
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<span style="color: #333333; font-family: sans-serif; font-size: 17.6px;">Considering the oral secretion of prions, saliva from CWD-infected deer was shown to transmit disease to other susceptible naïve deer when harvested from the animals in both the </span><span class="yiv1437632715ref-lnk" style="color: #333333; font-family: sans-serif; font-size: 17.6px;"><span class="yiv1437632715ref-overlay yiv1437632715scrollable-ref" style="line-height: 1.5; max-height: 150px; text-align: justify; transition: all 0s ease 0s; width: 263.833px; z-index: 200;"><span class="yiv1437632715NLM_article-title">prions in the saliva and blood of deer with chronic wasting disease</span>. </span></span></div>
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<span style="color: #333333; font-family: sans-serif; font-size: 17.6px;"> and preclinical stages</span><span class="yiv1437632715ref-lnk" style="color: #333333; font-family: sans-serif; font-size: 17.6px;"><a fg_scanned="1" href="https://www.tandfonline.com/doi/full/10.4161/pri.4.4.13678#" rel="noopener noreferrer" shape="rect" style="color: #10147e; cursor: pointer;" target="_blank">69</a></span></div>
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<span style="color: #333333; font-family: sans-serif; font-size: 17.6px;"> of infection, albeit within relatively large volumes of saliva (50 ml). In sheep with preclinical, natural scrapie infections, sPMCA facilitated the detection of PrP</span><span style="color: #333333; font-family: sans-serif; font-size: 13.2px; line-height: 0; position: relative; vertical-align: baseline;">Sc</span><span style="color: #333333; font-family: sans-serif; font-size: 17.6px;"> within buccal swabs throughout most of the incubation period of the disease with an apparent peak in prion secretion around the mid-term of disease progression.</span><span class="yiv1437632715ref-lnk" style="color: #333333; font-family: sans-serif; font-size: 17.6px;"><a fg_scanned="1" href="https://www.tandfonline.com/doi/full/10.4161/pri.4.4.13678#" rel="noopener noreferrer" shape="rect" style="color: #10147e; cursor: pointer;" target="_blank">70</a></span></div>
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<span style="color: #333333; font-family: sans-serif; font-size: 17.6px;"> The amounts of prion present in saliva are likely to be low as indicated by CWD-infected saliva producing prolonged incubation periods and incomplete attack rates within the transgenic mouse bioassay.</span><span class="yiv1437632715ref-lnk" style="color: #333333; font-family: sans-serif; font-size: 17.6px;"><a fg_scanned="1" href="https://www.tandfonline.com/doi/full/10.4161/pri.4.4.13678#" rel="noopener noreferrer" shape="rect" style="color: #10147e; cursor: pointer;" target="_blank">41</a></span></div>
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<span style="color: #666666; font-family: "arial" , "helvetica" , sans-serif; font-size: 15px;">Indeed, it has also been shown that the scrapie and CWD prions are excreted in urine, feces and saliva and are likely to be excreted from skin. While levels of prion within these excreta/secreta are very low, they are produced throughout long periods of preclinical disease as well as clinical disease. Furthermore, the levels of prion in such materials are likely to be increased by concurrent inflammatory conditions affecting the relevant secretory organ or site. Such dissemination of prion into the environment is very likely to facilitate the repeat exposure of flockmates to low levels of the disease agent, possibly over years.</span></div>
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<span style="color: #333333; font-family: sans-serif; font-size: 17.6px;">Given the res</span><span style="color: #333333; font-family: sans-serif; font-size: 17.6px;">ults with scrapie-contaminated milk and CWD-contaminated saliva, it seems very likely that these low levels of prion in different secreta/excreta are capable of transmitting disease upon prolonged exposure, either through direct animal-to-animal contact or through environmental reservoirs of infectivity.</span></div>
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<a fg_scanned="1" href="https://www.tandfonline.com/doi/full/10.4161/pri.4.4.13678" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://www.tandfonline.com/doi/full/10.4161/pri.4.4.13678</a></div>
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the other part, these tissues and things in the body then shed or secrete prions which then are the route to other animals into the environment, so in particular, the things, the secretions that are infectious are salvia, feces, blood and urine. so pretty much anything that comes out of a deer is going to be infectious and potential for transmitting disease.</div>
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<a href="https://www.youtube.com/watch?v=bItnEElzuKo&index=6&list=PL7ZG8MkruQh3wI96XQ8_EymytO828rGxj" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://www.youtube.com/watch?v=bItnEElzuKo&index=6&list=PL7ZG8MkruQh3wI96XQ8_EymytO828rGxj</a></div>
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<span style="font-family: "times new roman" , serif;"><span style="font-size: 16px;">***>>> Recently, we have been using PMCA to study the role of environmental prion contamination on the horizontal spreading of TSEs. These experiments have focused on the study of the interaction of prions with plants and environmentally relevant surfaces. Our results show that plants (both leaves and roots) bind tightly to prions present in brain extracts and excreta (urine and feces) and retain even small quantities of PrPSc for long periods of time. Strikingly, ingestion of prioncontaminated leaves and roots produced disease with a 100% attack rate and an incubation period not substantially longer than feeding animals directly with scrapie brain homogenate. Furthermore, plants can uptake prions from contaminated soil and transport them to different parts of the plant tissue (stem and leaves). Similarly, prions bind tightly to a variety of environmentally relevant surfaces, including stones, wood, metals, plastic, glass, cement, etc. Prion contaminated surfaces efficiently transmit prion disease when these materials were directly injected into the brain of animals and strikingly when the contaminated surfaces were just placed in the animal cage. These findings demonstrate that environmental materials can efficiently bind infectious prions and act as carriers of infectivity, suggesting that they may play an important role in the horizontal transmission of the disease.</span></span></div>
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<span style="font-family: "times new roman" , serif;"><span style="font-size: 16px;">Since its invention 13 years ago, PMCA has helped to answer fundamental questions of prion propagation and has broad applications in research areas including the food industry, blood bank safety and human and veterinary disease diagnosis. </span></span></div>
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<a href="https://prion2015.files.wordpress.com/2015/05/programguide1.pdf" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://prion2015.files.wordpress.com/2015/05/programguide1.pdf</a></div>
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HUNTERS, CWD TSE PRION, THIS SHOULD A WAKE UP CALL TO ALL OF YOU GUTTING AND BONING OUT YOUR KILL IN THE FIELD, AND YOUR TOOLS YOU USE...</div>
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<em style="background: transparent; border: 0px; margin: 0px; padding: 0px; vertical-align: baseline;">*</em> 1: J Neurol Neurosurg Psychiatry 1994 Jun;57(6):757-8</div>
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Transmission of Creutzfeldt-Jakob disease to a chimpanzee by electrodes contaminated during neurosurgery.</div>
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Gibbs CJ Jr, Asher DM, Kobrine A, Amyx HL, Sulima MP, Gajdusek DC.</div>
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Laboratory of Central Nervous System Studies, National Institute of</div>
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Neurological Disorders and Stroke, National Institutes of Health,</div>
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Bethesda, MD 20892.</div>
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Stereotactic multicontact electrodes used to probe the cerebral cortex of a middle aged woman with progressive dementia were previously implicated in the accidental transmission of Creutzfeldt-Jakob disease (CJD) to two younger patients. The diagnoses of CJD have been confirmed for all three cases. More than two years after their last use in humans, after three cleanings and repeated sterilisation in ethanol and formaldehyde vapour, the electrodes were implanted in the cortex of a chimpanzee. Eighteen months later the animal became ill with CJD. This finding serves to re-emphasise the potential danger posed by reuse of instruments contaminated with the agents of spongiform encephalopathies, even after scrupulous attempts to clean them.</div>
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PMID: 8006664 [PubMed - indexed for MEDLINE]</div>
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<a fg_scanned="1" href="http://jnnp.bmj.com/content/57/6/757.long" rel="noopener noreferrer" shape="rect" style="background: transparent; border: 0px; color: #162a3a; cursor: pointer; margin: 0px; padding: 0px; vertical-align: baseline;" target="_blank">http://jnnp.bmj.com/content/57/6/757.long</a></div>
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Wednesday, September 11, 2019 </div>
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Is the re-use of sterilized implant abutments safe enough? (Implant abutment safety) iatrogenic TSE Prion</div>
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<a fg_scanned="1" href="https://prionprp.blogspot.com/2019/09/is-re-use-of-sterilized-implant.html" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">https://prionprp.blogspot.com/2019/09/is-re-use-of-sterilized-implant.html</a></div>
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<span style="font-family: "georgia";"><span style="font-size: 13px;">SATURDAY, MARCH 16, 2019 </span></span></div>
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<span style="font-family: "georgia";"><span style="font-size: 13px;">Medical Devices Containing Materials Derived from Animal Sources (Except for In Vitro Diagnostic Devices) Guidance for Industry and Food and Drug Administration Staff Document issued on March 15, 2019 Singeltary Submission</span></span></div>
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<span style="font-family: "georgia";"><span style="font-size: 13px;"><a fg_scanned="1" href="https://bovineprp.blogspot.com/2019/03/medical-devices-containing-materials.html" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://bovineprp.blogspot.com/2019/03/medical-devices-containing-materials.html</a></span></span></div>
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<span style="font-family: "arial" , "helvetica";">THURSDAY, SEPTEMBER 27, 2018 </span></div>
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<span style="font-family: "arial" , "helvetica";"><span style="font-size: x-small;">***> Estimating the impact on food and edible materials of changing scrapie control measures: The scrapie control model</span></span></div>
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<span style="font-family: "arial" , "helvetica";"><span style="font-size: x-small;"><a fg_scanned="1" href="http://scrapie-usa.blogspot.com/2018/09/estimating-impact-on-food-and-edible.html" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">http://scrapie-usa.blogspot.com/2018/09/estimating-impact-on-food-and-edible.html</a></span></span></div>
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<span style="font-family: "arial"; font-size: 13.3333px; line-height: 1.22em;">THE tse prion aka mad cow type disease is not your normal pathogen. </span></div>
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<span style="font-size: 13.3333px; line-height: 1.22em;">The TSE prion disease survives ashing to 600 degrees celsius, that’s around 1112 degrees farenheit. </span></div>
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<span style="font-size: 13.3333px; line-height: 1.22em;">you cannot cook the TSE prion disease out of meat. </span></div>
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<span style="font-size: 13.3333px; line-height: 1.22em;">you can take the ash and mix it with saline and inject that ash into a mouse, and the mouse will go down with TSE. </span></div>
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<span style="font-size: 13.3333px; line-height: 1.22em;">Prion Infected Meat-and-Bone Meal Is Still Infectious after Biodiesel Production as well. </span></div>
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<span style="font-size: 13.3333px; line-height: 1.22em;">the TSE prion agent also survives Simulated Wastewater Treatment Processes. </span></div>
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<span style="font-size: 13.3333px; line-height: 1.22em;">IN fact, you should also know that the TSE Prion agent will survive in the environment for years, if not decades. </span></div>
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<span style="font-size: 13.3333px; line-height: 1.22em;">you can bury it and it will not go away. </span></div>
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<span style="font-size: 13.3333px; line-height: 1.22em;">The TSE agent is capable of infected your water table i.e. Detection of protease-resistant cervid prion protein in water from a CWD-endemic area. </span></div>
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<span style="font-size: 13.3333px; line-height: 1.22em;">it’s not your ordinary pathogen you can just cook it out and be done with. </span></div>
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<span style="font-size: 13.3333px; line-height: 1.22em;">***> that’s what’s so worrisome about Iatrogenic mode of transmission, a simple autoclave will not kill this TSE prion agent.</span></div>
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<span style="font-size: 13.3333px; line-height: 1.22em;">1: J Neurol Neurosurg Psychiatry 1994 Jun;57(6):757-8 </span></div>
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<span style="font-size: 13.3333px; line-height: 1.22em;">***> Transmission of Creutzfeldt-Jakob disease to a chimpanzee by electrodes contaminated during neurosurgery. </span></div>
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<span style="font-size: 13.3333px; line-height: 1.22em;">Gibbs CJ Jr, Asher DM, Kobrine A, Amyx HL, Sulima MP, Gajdusek DC. </span></div>
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<span style="font-size: 13.3333px; line-height: 1.22em;">Laboratory of Central Nervous System Studies, National Institute of </span></div>
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<span style="font-size: 13.3333px; line-height: 1.22em;">Neurological Disorders and Stroke, National Institutes of Health, </span></div>
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<span style="font-size: 13.3333px; line-height: 1.22em;">Bethesda, MD 20892. </span></div>
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<span style="font-size: 13.3333px; line-height: 1.22em;">Stereotactic multicontact electrodes used to probe the cerebral cortex of a middle aged woman with progressive dementia were previously implicated in the accidental transmission of Creutzfeldt-Jakob disease (CJD) to two younger patients. The diagnoses of CJD have been confirmed for all three cases. More than two years after their last use in humans, after three cleanings and repeated sterilisation in ethanol and formaldehyde vapour, the electrodes were implanted in the cortex of a chimpanzee. Eighteen months later the animal became ill with CJD. This finding serves to re-emphasise the potential danger posed by reuse of instruments contaminated with the agents of spongiform encephalopathies, even after scrupulous attempts to clean them. </span></div>
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<span style="font-size: 13.3333px; line-height: 1.22em;">PMID: 8006664 [PubMed - indexed for MEDLINE] </span></div>
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<a fg_scanned="1" href="https://www.ncbi.nlm.nih.gov/pubmed/8006664?dopt=Abstract" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">https://www.ncbi.nlm.nih.gov/pubmed/8006664?dopt=Abstract</a></div>
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***> This is very likely to have parallels with control efforts for CWD in cervids.</div>
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Rapid recontamination of a farm building occurs after attempted prion removal</div>
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<a fg_scanned="1" href="http://dx.doi.org/10.1136/vr.105054" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">http://dx.doi.org/10.1136/vr.105054</a></div>
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Kevin Christopher Gough, BSc (Hons), PhD1, Claire Alison Baker, BSc (Hons)2, Steve Hawkins, MIBiol3, Hugh Simmons, BVSc, MRCVS, MBA, MA3, Timm Konold, DrMedVet, PhD, MRCVS3 and Ben Charles Maddison, BSc (Hons), PhD2</div>
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The transmissible spongiform encephalopathy scrapie of sheep/goats and chronic wasting disease of cervids are associated with environmental reservoirs of infectivity. </div>
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Preventing environmental prions acting as a source of infectivity to healthy animals is of major concern to farms that have had outbreaks of scrapie and also to the health management of wild and farmed cervids. </div>
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Here, an efficient scrapie decontamination protocol was applied to a farm with high levels of environmental contamination with the scrapie agent. </div>
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Post-decontamination, no prion material was detected within samples taken from the farm buildings as determined using a sensitive in vitro replication assay (sPMCA). </div>
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A bioassay consisting of 25 newborn lambs of highly susceptible prion protein genotype VRQ/VRQ introduced into this decontaminated barn was carried out in addition to sampling and analysis of dust samples that were collected during the bioassay. </div>
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Twenty-four of the animals examined by immunohistochemical analysis of lymphatic tissues were scrapie-positive during the bioassay, samples of dust collected within the barn were positive by month 3. </div>
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The data illustrates the difficulty in decontaminating farm buildings from scrapie, and demonstrates the likely contribution of farm dust to the recontamination of these environments to levels that are capable of causing disease.</div>
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As in the authors' previous study,12 the decontamination of this sheep barn was not effective at removing scrapie infectivity, and despite the extra measures brought into this study (more effective chemical treatment and removal of sources of dust) the overall rates of disease transmission mirror previous results on this farm. With such apparently effective decontamination (assuming that at least some sPMCA seeding ability is coincident with infectivity), how was infectivity able to persist within the environment and where does infectivity reside? Dust samples were collected in both the bioassay barn and also a barn subject to the same decontamination regime within the same farm (but remaining unoccupied). Within both of these barns dust had accumulated for three months that was able to seed sPMCA, indicating the accumulation of scrapie-containing material that was independent of the presence of sheep that may have been incubating and possibly shedding low amounts of infectivity.</div>
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This study clearly demonstrates the difficulty in removing scrapie infectivity from the farm environment. Practical and effective prion decontamination methods are still urgently required for decontamination of scrapie infectivity from farms that have had cases of scrapie and this is particularly relevant for scrapiepositive goatherds, which currently have limited genetic resistance to scrapie within commercial breeds.24 This is very likely to have parallels with control efforts for CWD in cervids.</div>
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Acknowledgements The authors thank the APHA farm staff, Tony Duarte, Olly Roberts and Margaret Newlands for preparation of the sheep pens and animal husbandry during the study. The authors also thank the APHA pathology team for RAMALT and postmortem examination.</div>
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Funding This study was funded by DEFRA within project SE1865. </div>
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Competing interests None declared. </div>
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<a fg_scanned="1" href="https://veterinaryrecord.bmj.com/content/early/2019/01/02/vr.105054.long" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://veterinaryrecord.bmj.com/content/early/2019/01/02/vr.105054.long</a></div>
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Saturday, January 5, 2019 </div>
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Rapid recontamination of a farm building occurs after attempted prion removal </div>
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<a fg_scanned="1" href="https://prionprp.blogspot.com/2019/01/rapid-recontamination-of-farm-building.html" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://prionprp.blogspot.com/2019/01/rapid-recontamination-of-farm-building.html</a></div>
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<span style="font-size: 13.3333px; line-height: 1.22em;">BSE infectivity survives burial for five years with only limited spread</span></div>
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<a fg_scanned="1" href="https://bovineprp.blogspot.com/2019/02/bse-infectivity-survives-burial-for.html" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">https://bovineprp.blogspot.com/2019/02/bse-infectivity-survives-burial-for.html</a></div>
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<span style="font-family: "times new roman" , serif;"><span style="font-size: 16px;">***> CONGRESSIONAL ABSTRACTS PRION CONFERENCE 2018</span></span></div>
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<span style="font-size: 16px;">P69 Experimental transmission of CWD from white-tailed deer to co-housed reindeer </span></div>
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<span style="font-family: "times new roman" , serif;"><span style="font-size: 16px;">Mitchell G (1), Walther I (1), Staskevicius A (1), Soutyrine A (1), Balachandran A (1) </span></span></div>
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<span style="font-family: "times new roman" , serif;"><span style="font-size: 16px;">(1) National & OIE Reference Laboratory for Scrapie and CWD, Canadian Food Inspection Agency, Ottawa, Ontario, Canada. </span></span></div>
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<span style="font-family: "times new roman" , serif;"><span style="font-size: 16px;">Chronic wasting disease (CWD) continues to be detected in wild and farmed cervid populations of North America, affecting predominantly white-tailed deer, mule deer and elk. Extensive herds of wild caribou exist in northern regions of Canada, although surveillance has not detected the presence of CWD in this population. Oral experimental transmission has demonstrated that reindeer, a species closely related to caribou, are susceptible to CWD. Recently, CWD was detected for the first time in Europe, in wild Norwegian reindeer, advancing the possibility that caribou in North America could also become infected. Given the potential overlap in habitat between wild CWD-infected cervids and wild caribou herds in Canada, we sought to investigate the horizontal transmissibility of CWD from white-tailed deer to reindeer. </span></span></div>
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<span style="font-family: "times new roman" , serif;"><span style="font-size: 16px;">Two white-tailed deer were orally inoculated with a brain homogenate prepared from a farmed Canadian white-tailed deer previously diagnosed with CWD. Two reindeer, with no history of exposure to CWD, were housed in the same enclosure as the white-tailed deer, 3.5 months after the deer were orally inoculated. The white-tailed deer developed clinical signs consistent with CWD beginning at 15.2 and 21 months post-inoculation (mpi), and were euthanized at 18.7 and 23.1 mpi, respectively. Confirmatory testing by immunohistochemistry (IHC) and western blot demonstrated widespread aggregates of pathological prion protein (PrPCWD) in the central nervous system and lymphoid tissues of both inoculated white-tailed deer. Both reindeer were subjected to recto-anal mucosal associated lymphoid tissue (RAMALT) biopsy at 20 months post-exposure (mpe) to the white-tailed deer. The biopsy from one reindeer contained PrPCWD confirmed by IHC. This reindeer displayed only subtle clinical evidence of disease prior to a rapid decline in condition requiring euthanasia at 22.5 mpe. Analysis of tissues from this reindeer by IHC revealed widespread PrPCWD deposition, predominantly in central nervous system and lymphoreticular tissues. Western blot molecular profiles were similar between both orally inoculated white-tailed deer and the CWD positive reindeer. Despite sharing the same enclosure, the other reindeer was RAMALT negative at 20 mpe, and PrPCWD was not detected in brainstem and lymphoid tissues following necropsy at 35 mpe. Sequencing of the prion protein gene from both reindeer revealed differences at several codons, which may have influenced susceptibility to infection. </span></span></div>
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<span style="font-family: "times new roman" , serif;"><span style="font-size: 16px;">Natural transmission of CWD occurs relatively efficiently amongst cervids, supporting the expanding geographic distribution of disease and the potential for transmission to previously naive populations. The efficient horizontal transmission of CWD from white-tailed deer to reindeer observed here highlights the potential for reindeer to become infected if exposed to other cervids or environments infected with CWD. </span></span></div>
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<a fg_scanned="1" href="https://prion2018.org/" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://prion2018.org/</a></div>
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<span style="font-size: 16px; letter-spacing: 0px;">***> Infectious agent of sheep scrapie may persist in the environment for at least 16 years</span></div>
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<div class="yiv1437632715aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;">
<span style="font-size: 16px;">***> Nine of these recurrences occurred 14–21 years after culling, apparently as the result of environmental contamination, </span><span style="font-size: 16px;">but outside entry could not always be absolutely excluded. </span></div>
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<span style="font-family: "times new roman" , serif;"><span style="font-size: 16px;"><br clear="none" /></span></span></div>
<div class="yiv1437632715aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;">
<span style="font-family: "times new roman" , serif;"><span style="font-size: 16px;">Gudmundur Georgsson,1 Sigurdur Sigurdarson2 and Paul Brown3</span></span></div>
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<span style="font-family: "times new roman" , serif;"><span style="font-size: 16px;"><br clear="none" /></span></span></div>
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<span style="font-family: "times new roman" , serif;"><span style="font-size: 16px;">Correspondence</span></span></div>
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<span style="font-family: "times new roman" , serif;"><span style="font-size: 16px;"><br clear="none" /></span></span></div>
<div class="yiv1437632715aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;">
<span style="font-family: "times new roman" , serif;"><span style="font-size: 16px;">Gudmundur Georgsson <a href="mailto:ggeorgs@hi.is" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank" ymailto="mailto:ggeorgs@hi.is">ggeorgs@hi.is</a></span></span></div>
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<span style="font-family: "times new roman" , serif;"><span style="font-size: 16px;"><br clear="none" /></span></span></div>
<div class="yiv1437632715aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;">
<span style="font-family: "times new roman" , serif;"><span style="font-size: 16px;">1 Institute for Experimental Pathology, University of Iceland, Keldur v/vesturlandsveg, IS-112 Reykjavı´k, Iceland</span></span></div>
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<span style="font-family: "times new roman" , serif;"><span style="font-size: 16px;"><br clear="none" /></span></span></div>
<div class="yiv1437632715aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;">
<span style="font-family: "times new roman" , serif;"><span style="font-size: 16px;">2 Laboratory of the Chief Veterinary Officer, Keldur, Iceland</span></span></div>
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<span style="font-family: "times new roman" , serif;"><span style="font-size: 16px;">3 Bethesda, Maryland, USA</span></span></div>
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<span style="font-family: "times new roman" , serif;"><span style="font-size: 16px;">Received 7 March 2006 Accepted 6 August 2006</span></span></div>
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<span style="font-family: "times new roman" , serif;"><span style="font-size: 16px;"><br clear="none" /></span></span></div>
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<span style="font-family: "times new roman" , serif;"><span style="font-size: 16px;">In 1978, a rigorous programme was implemented to stop the spread of, and subsequently eradicate, sheep scrapie in Iceland. Affected flocks were culled, premises were disinfected and, after 2–3 years, restocked with lambs from scrapie-free areas. Between 1978 and 2004, scrapie recurred on 33 farms. Nine of these recurrences occurred 14–21 years after culling, apparently as the result of environmental contamination, but outside entry could not always be absolutely excluded. Of special interest was one farm with a small, completely self-contained flock where scrapie recurred 18 years after culling, 2 years after some lambs had been housed in an old sheephouse that had never been disinfected. Epidemiological investigation established with near certitude that the disease had not been introduced from the outside and it is concluded that the agent may have persisted in the old sheep-house for at least 16 years.</span></span></div>
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<span style="font-family: "times new roman" , serif;"><span style="font-size: 16px;"><br clear="none" /></span></span></div>
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<span style="font-family: "times new roman" , serif;"><span style="font-size: 16px;"><a href="http://www.microbiologyresearch.org/docserver/fulltext/jgv/87/12/3737.pdf?expires=1540908280&id=id&accname=guest&checksum=ED0572E1E5B272C100A32212A3E3761A" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">http://www.microbiologyresearch.org/docserver/fulltext/jgv/87/12/3737.pdf?expires=1540908280&id=id&accname=guest&checksum=ED0572E1E5B272C100A32212A3E3761A</a></span></span></div>
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<span style="font-size: 16px;">TITLE: PATHOLOGICAL FEATURES OF CHRONIC WASTING DISEASE IN REINDEER AND DEMONSTRATION OF HORIZONTAL TRANSMISSION </span></div>
<div class="yiv1437632715aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;">
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<span style="font-family: "times new roman" , serif;"><span style="font-size: 16px;"><a fg_scanned="1" href="https://www.ars.usda.gov/research/publications/publication/?seqNo115=328261" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://www.ars.usda.gov/research/publications/publication/?seqNo115=328261</a></span></span></div>
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<span style="font-family: "times new roman" , serif;"><span style="font-size: 16px;"> *** DECEMBER 2016 CDC EMERGING INFECTIOUS DISEASE JOURNAL CWD HORIZONTAL TRANSMISSION </span></span></div>
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<span style="font-family: "times new roman" , serif;"><span style="font-size: 16px;"><a fg_scanned="1" href="http://wwwnc.cdc.gov/eid/article/22/12/16-0635_article" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">http://wwwnc.cdc.gov/eid/article/22/12/16-0635_article</a></span></span></div>
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<span style="font-family: "times new roman" , serif;"><span style="font-size: 16px;">SEE;</span></span></div>
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<span style="font-family: "times new roman" , serif;"><span style="font-size: 16px;"><br clear="none" /></span></span></div>
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<span style="font-family: "times new roman" , serif;"><span style="font-size: 16px;">Back around 2000, 2001, or so, I was corresponding with officials abroad during the bse inquiry, passing info back and forth, and some officials from here inside USDA aphis FSIS et al. In fact helped me get into the USA 50 state emergency BSE conference call way back. That one was a doozy. But I always remember what “deep throat” I never knew who they were, but I never forgot;</span></span></div>
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<span style="font-family: "times new roman" , serif;"><span style="font-size: 16px;"><br clear="none" /></span></span></div>
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<span style="font-family: "times new roman" , serif;"><span style="font-size: 16px;">Some unofficial information from a source on the inside looking out -</span></span></div>
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<span style="font-family: "times new roman" , serif;"><span style="font-size: 16px;"><br clear="none" /></span></span></div>
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<span style="font-family: "times new roman" , serif;"><span style="font-size: 16px;">Confidential!!!!</span></span></div>
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<span style="font-family: "times new roman" , serif;"><span style="font-size: 16px;"><br clear="none" /></span></span></div>
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<span style="font-family: "times new roman" , serif;"><span style="font-size: 16px;">As early as 1992-3 there had been long studies conducted on small pastures containing scrapie infected sheep at the sheep research station associated with the Neuropathogenesis Unit in Edinburgh, Scotland. Whether these are documented...I don't know. But personal recounts both heard and recorded in a daily journal indicate that leaving the pastures free and replacing the topsoil completely at least 2 feet of thickness each year for SEVEN years....and then when very clean (proven scrapie free) sheep were placed on these small pastures.... the new sheep also broke out with scrapie and passed it to offspring. I am not sure that TSE contaminated ground could ever be free of the agent!! A very frightening revelation!!!</span></span></div>
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<span style="font-family: "times new roman" , serif;"><span style="font-size: 16px;"><br clear="none" /></span></span></div>
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<span style="font-family: "times new roman" , serif;"><span style="font-size: 16px;">---end personal email---end...tss</span></span></div>
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<a fg_scanned="1" href="http://scrapie-usa.blogspot.com/2018/04/scrapie-transmits-to-pigs-by-oral-route.html" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">http://scrapie-usa.blogspot.com/2018/04/scrapie-transmits-to-pigs-by-oral-route.html</a></div>
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Infectivity surviving ashing to 600*C is (in my opinion) degradable but infective. based on Bown & Gajdusek, (1991), landfill and burial may be assumed to have a reduction factor of 98% (i.e. a factor of 50) over 3 years. CJD-infected brain-tissue remained infectious after storing at room-temperature for 22 months (Tateishi et al, 1988). Scrapie agent is known to remain viable after at least 30 months of desiccation (Wilson et al, 1950). and pastures that had been grazed by scrapie-infected sheep still appeared to be contaminated with scrapie agent three years after they were last occupied by sheep (Palsson, 1979).</div>
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<a href="http://europa.eu.int/comm/food/fs/sc/ssc/out58_en.pdf" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">http://europa.eu.int/comm/food/fs/sc/ssc/out58_en.pdf</a></div>
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Dr. Paul Brown Scrapie Soil Test BSE Inquiry Document</div>
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<a href="https://web.archive.org/web/20090505211734/http://www.bseinquiry.gov.uk/files/sc/Seac07/tab03.pdf" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://web.archive.org/web/20090505211734/http://www.bseinquiry.gov.uk/files/sc/Seac07/tab03.pdf</a></div>
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THURSDAY, FEBRUARY 28, 2019 </div>
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BSE infectivity survives burial for five years with only limited spread</div>
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<a fg_scanned="1" href="https://bovineprp.blogspot.com/2019/02/bse-infectivity-survives-burial-for.html" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://bovineprp.blogspot.com/2019/02/bse-infectivity-survives-burial-for.html</a></div>
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<span style="font-family: "times new roman" , serif;"><span style="font-size: 16px;">Using in vitro Prion replication for high sensitive detection of prions and prionlike proteins and for understanding mechanisms of transmission. </span></span></div>
<div class="yiv1437632715aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;">
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<span style="font-family: "times new roman" , serif;"><span style="font-size: 16px;">Claudio Soto Mitchell Center for Alzheimer's diseases and related Brain disorders, Department of Neurology, University of Texas Medical School at Houston. </span></span></div>
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<span style="font-family: "times new roman" , serif;"><span style="font-size: 16px;">Prion and prion-like proteins are misfolded protein aggregates with the ability to selfpropagate to spread disease between cells, organs and in some cases across individuals. I n T r a n s m i s s i b l e s p o n g i f o r m encephalopathies (TSEs), prions are mostly composed by a misfolded form of the prion protein (PrPSc), which propagates by transmitting its misfolding to the normal prion protein (PrPC). The availability of a procedure to replicate prions in the laboratory may be important to study the mechanism of prion and prion-like spreading and to develop high sensitive detection of small quantities of misfolded proteins in biological fluids, tissues and environmental samples. Protein Misfolding Cyclic Amplification (PMCA) is a simple, fast and efficient methodology to mimic prion replication in the test tube. PMCA is a platform technology that may enable amplification of any prion-like misfolded protein aggregating through a seeding/nucleation process. In TSEs, PMCA is able to detect the equivalent of one single molecule of infectious PrPSc and propagate prions that maintain high infectivity, strain properties and species specificity. Using PMCA we have been able to detect PrPSc in blood and urine of experimentally infected animals and humans affected by vCJD with high sensitivity and specificity. Recently, we have expanded the principles of PMCA to amplify amyloid-beta (Aβ) and alphasynuclein (α-syn) aggregates implicated in Alzheimer's and Parkinson's diseases, respectively. Experiments are ongoing to study the utility of this technology to detect Aβ and α-syn aggregates in samples of CSF and blood from patients affected by these diseases.</span></span></div>
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<span style="font-family: "times new roman" , serif;"><span style="font-size: 16px;">=========================</span></span></div>
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<span style="font-family: "times new roman" , serif;"><span style="font-size: 16px;">***>>> Recently, we have been using PMCA to study the role of environmental prion contamination on the horizontal spreading of TSEs. These experiments have focused on the study of the interaction of prions with plants and environmentally relevant surfaces. Our results show that plants (both leaves and roots) bind tightly to prions present in brain extracts and excreta (urine and feces) and retain even small quantities of PrPSc for long periods of time. Strikingly, ingestion of prioncontaminated leaves and roots produced disease with a 100% attack rate and an incubation period not substantially longer than feeding animals directly with scrapie brain homogenate. Furthermore, plants can uptake prions from contaminated soil and transport them to different parts of the plant tissue (stem and leaves). Similarly, prions bind tightly to a variety of environmentally relevant surfaces, including stones, wood, metals, plastic, glass, cement, etc. Prion contaminated surfaces efficiently transmit prion disease when these materials were directly injected into the brain of animals and strikingly when the contaminated surfaces were just placed in the animal cage. These findings demonstrate that environmental materials can efficiently bind infectious prions and act as carriers of infectivity, suggesting that they may play an important role in the horizontal transmission of the disease.</span></span></div>
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<span style="font-family: "times new roman" , serif;"><span style="font-size: 16px;">========================</span></span></div>
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<span style="font-family: "times new roman" , serif;"><span style="font-size: 16px;">Since its invention 13 years ago, PMCA has helped to answer fundamental questions of prion propagation and has broad applications in research areas including the food industry, blood bank safety and human and veterinary disease diagnosis. </span></span></div>
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<a href="https://prion2015.files.wordpress.com/2015/05/programguide1.pdf" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://prion2015.files.wordpress.com/2015/05/programguide1.pdf</a></div>
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<span style="font-family: "times new roman" , serif;"><span style="font-size: 16px;">Survival and Limited Spread of TSE Infectivity after Burial </span></span></div>
<div class="yiv1437632715aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;">
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<a href="http://www.neuroprion.org/resources/pdf_docs/conferences/prion2010/prion_2010_programme.pdf" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">http://www.neuroprion.org/resources/pdf_docs/conferences/prion2010/prion_2010_programme.pdf</a></div>
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<a fg_scanned="1" href="http://chronic-wasting-disease.blogspot.com/2010/09/cwd-prion-2010.html" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">http://chronic-wasting-disease.blogspot.com/2010/09/cwd-prion-2010.html</a></div>
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<div class="yiv1437632715aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;">
<span style="font-family: "times new roman" , serif;"><span style="font-size: 16px;">Discussion Classical scrapie is an environmentally transmissible disease because it has been reported in naïve, supposedly previously unexposed sheep placed in pastures formerly occupied by scrapie-infected sheep (4, 19, 20). </span></span></div>
<div class="yiv1437632715aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;">
<span style="font-family: "times new roman" , serif;"><span style="font-size: 16px;"><br clear="none" /></span></span></div>
<div class="yiv1437632715aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;">
<span style="font-family: "times new roman" , serif;"><span style="font-size: 16px;">Although the vector for disease transmission is not known, soil is likely to be an important reservoir for prions (2) where – based on studies in rodents – prions can adhere to minerals as a biologically active form (21) and remain infectious for more than 2 years (22). </span></span></div>
<div class="yiv1437632715aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;">
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<div class="yiv1437632715aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;">
<span style="font-family: "times new roman" , serif;"><span style="font-size: 16px;">Similarly, chronic wasting disease (CWD) has re-occurred in mule deer housed in paddocks used by infected deer 2 years earlier, which was assumed to be through foraging and soil consumption (23). </span></span></div>
<div class="yiv1437632715aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;">
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<span style="font-family: "times new roman" , serif;"><span style="font-size: 16px;">Our study suggested that the risk of acquiring scrapie infection was greater through exposure to contaminated wooden, plastic, and metal surfaces via water or food troughs, fencing, and hurdles than through grazing. </span></span></div>
<div class="yiv1437632715aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;">
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<span style="font-family: "times new roman" , serif;"><span style="font-size: 16px;">Drinking from a water trough used by the scrapie flock was sufficient to cause infection in sheep in a clean building. </span></span></div>
<div class="yiv1437632715aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;">
<span style="font-family: "times new roman" , serif;"><span style="font-size: 16px;"><br clear="none" /></span></span></div>
<div class="yiv1437632715aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;">
<span style="font-family: "times new roman" , serif;"><span style="font-size: 16px;">Exposure to fences and other objects used for rubbing also led to infection, which supported the hypothesis that skin may be a vector for disease transmission (9). </span></span></div>
<div class="yiv1437632715aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;">
<span style="font-family: "times new roman" , serif;"><span style="font-size: 16px;"><br clear="none" /></span></span></div>
<div class="yiv1437632715aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;">
<span style="font-family: "times new roman" , serif;"><span style="font-size: 16px;">The risk of these objects to cause infection was further demonstrated when 87% of 23 sheep presented with PrPSc in lymphoid tissue after grazing on one of the paddocks, which contained metal hurdles, a metal lamb creep and a water trough in contact with the scrapie flock up to 8 weeks earlier, whereas no infection had been demonstrated previously in sheep grazing on this paddock, when equipped with new fencing and field furniture. </span></span></div>
<div class="yiv1437632715aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;">
<span style="font-family: "times new roman" , serif;"><span style="font-size: 16px;"><br clear="none" /></span></span></div>
<div class="yiv1437632715aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;">
<span style="font-family: "times new roman" , serif;"><span style="font-size: 16px;">When the contaminated furniture and fencing were removed, the infection rate dropped significantly to 8% of 12 sheep, with soil of the paddock as the most likely source of infection caused by shedding of prions from the scrapie-infected sheep in this paddock up to a week earlier. </span></span></div>
<div class="yiv1437632715aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;">
<span style="font-family: "times new roman" , serif;"><span style="font-size: 16px;"><br clear="none" /></span></span></div>
<div class="yiv1437632715aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;">
<span style="font-family: "times new roman" , serif;"><span style="font-size: 16px;">This study also indicated that the level of contamination of field furniture sufficient to cause infection was dependent on two factors: stage of incubation period and time of last use by scrapie-infected sheep. </span></span></div>
<div class="yiv1437632715aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;">
<span style="font-family: "times new roman" , serif;"><span style="font-size: 16px;"><br clear="none" /></span></span></div>
<div class="yiv1437632715aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;">
<span style="font-family: "times new roman" , serif;"><span style="font-size: 16px;">Drinking from a water trough that had been used by scrapie sheep in the predominantly pre-clinical phase did not appear to cause infection, whereas infection was shown in sheep drinking from the water trough used by scrapie sheep in the later stage of the disease. </span></span></div>
<div class="yiv1437632715aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;">
<span style="font-family: "times new roman" , serif;"><span style="font-size: 16px;"><br clear="none" /></span></span></div>
<div class="yiv1437632715aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;">
<span style="font-family: "times new roman" , serif;"><span style="font-size: 16px;">It is possible that contamination occurred through shedding of prions in saliva, which may have contaminated the surface of the water trough and subsequently the water when it was refilled. </span></span></div>
<div class="yiv1437632715aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;">
<span style="font-family: "times new roman" , serif;"><span style="font-size: 16px;"><br clear="none" /></span></span></div>
<div class="yiv1437632715aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;">
<span style="font-family: "times new roman" , serif;"><span style="font-size: 16px;">Contamination appeared to be sufficient to cause infection only if the trough was in contact with sheep that included clinical cases. </span></span></div>
<div class="yiv1437632715aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;">
<span style="font-family: "times new roman" , serif;"><span style="font-size: 16px;"><br clear="none" /></span></span></div>
<div class="yiv1437632715aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;">
<span style="font-family: "times new roman" , serif;"><span style="font-size: 16px;">Indeed, there is an increased risk of bodily fluid infectivity with disease progression in scrapie (24) and CWD (25) based on PrPSc detection by sPMCA. </span></span></div>
<div class="yiv1437632715aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;">
<span style="font-family: "times new roman" , serif;"><span style="font-size: 16px;"><br clear="none" /></span></span></div>
<div class="yiv1437632715aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;">
<span style="font-family: "times new roman" , serif;"><span style="font-size: 16px;">Although ultraviolet light and heat under natural conditions do not inactivate prions (26), furniture in contact with the scrapie flock, which was assumed to be sufficiently contaminated to cause infection, did not act as vector for disease if not used for 18 months, which suggest that the weathering process alone was sufficient to inactivate prions. </span></span></div>
<div class="yiv1437632715aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;">
<span style="font-family: "times new roman" , serif;"><span style="font-size: 16px;"><br clear="none" /></span></span></div>
<div class="yiv1437632715aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;">
<span style="font-family: "times new roman" , serif;"><span style="font-size: 16px;">PrPSc detection by sPMCA is increasingly used as a surrogate for infectivity measurements by bioassay in sheep or mice. </span></span></div>
<div class="yiv1437632715aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;">
<span style="font-family: "times new roman" , serif;"><span style="font-size: 16px;"><br clear="none" /></span></span></div>
<div class="yiv1437632715aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;">
<span style="font-family: "times new roman" , serif;"><span style="font-size: 16px;">In this reported study, however, the levels of PrPSc present in the environment were below the limit of detection of the sPMCA method, yet were still sufficient to cause infection of in-contact animals. </span></span></div>
<div class="yiv1437632715aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;">
<span style="font-family: "times new roman" , serif;"><span style="font-size: 16px;"><br clear="none" /></span></span></div>
<div class="yiv1437632715aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;">
<span style="font-family: "times new roman" , serif;"><span style="font-size: 16px;">In the present study, the outdoor objects were removed from the infected flock 8 weeks prior to sampling and were positive by sPMCA at very low levels (2 out of 37 reactions). </span></span></div>
<div class="yiv1437632715aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;">
<span style="font-family: "times new roman" , serif;"><span style="font-size: 16px;"><br clear="none" /></span></span></div>
<div class="yiv1437632715aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;">
<span style="font-family: "times new roman" , serif;"><span style="font-size: 16px;">As this sPMCA assay also yielded 2 positive reactions out of 139 in samples from the scrapie-free farm, the sPMCA assay could not detect PrPSc on any of the objects above the background of the assay. </span></span></div>
<div class="yiv1437632715aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;">
<span style="font-family: "times new roman" , serif;"><span style="font-size: 16px;"><br clear="none" /></span></span></div>
<div class="yiv1437632715aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;">
<span style="font-family: "times new roman" , serif;"><span style="font-size: 16px;">False positive reactions with sPMCA at a low frequency associated with de novo formation of infectious prions have been reported (27, 28). </span></span></div>
<div class="yiv1437632715aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;">
<span style="font-family: "times new roman" , serif;"><span style="font-size: 16px;"><br clear="none" /></span></span></div>
<div class="yiv1437632715aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;">
<span style="font-family: "times new roman" , serif;"><span style="font-size: 16px;">This is in contrast to our previous study where we demonstrated that outdoor objects that had been in contact with the scrapie-infected flock up to 20 days prior to sampling harbored PrPSc that was detectable by sPMCA analysis [4 out of 15 reactions (12)] and was significantly more positive by the assay compared to analogous samples from the scrapie-free farm. </span></span></div>
<div class="yiv1437632715aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;">
<span style="font-family: "times new roman" , serif;"><span style="font-size: 16px;"><br clear="none" /></span></span></div>
<div class="yiv1437632715aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;">
<span style="font-family: "times new roman" , serif;"><span style="font-size: 16px;">This discrepancy could be due to the use of a different sPMCA substrate between the studies that may alter the efficiency of amplification of the environmental PrPSc. </span></span></div>
<div class="yiv1437632715aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;">
<span style="font-family: "times new roman" , serif;"><span style="font-size: 16px;"><br clear="none" /></span></span></div>
<div class="yiv1437632715aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;">
<span style="font-family: "times new roman" , serif;"><span style="font-size: 16px;">In addition, the present study had a longer timeframe between the objects being in contact with the infected flock and sampling, which may affect the levels of extractable PrPSc. </span></span></div>
<div class="yiv1437632715aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;">
<span style="font-family: "times new roman" , serif;"><span style="font-size: 16px;"><br clear="none" /></span></span></div>
<div class="yiv1437632715aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;">
<span style="font-family: "times new roman" , serif;"><span style="font-size: 16px;">Alternatively, there may be potentially patchy contamination of this furniture with PrPSc, which may have been missed by swabbing. </span></span></div>
<div class="yiv1437632715aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;">
<span style="font-family: "times new roman" , serif;"><span style="font-size: 16px;"><br clear="none" /></span></span></div>
<div class="yiv1437632715aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;">
<span style="font-family: "times new roman" , serif;"><span style="font-size: 16px;">The failure of sPMCA to detect CWD-associated PrP in saliva from clinically affected deer despite confirmation of infectivity in saliva-inoculated transgenic mice was associated with as yet unidentified inhibitors in saliva (29), and it is possible that the sensitivity of sPMCA is affected by other substances in the tested material. </span></span></div>
<div class="yiv1437632715aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;">
<span style="font-family: "times new roman" , serif;"><span style="font-size: 16px;"><br clear="none" /></span></span></div>
<div class="yiv1437632715aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;">
<span style="font-family: "times new roman" , serif;"><span style="font-size: 16px;">In addition, sampling of amplifiable PrPSc and subsequent detection by sPMCA may be more difficult from furniture exposed to weather, which is supported by the observation that PrPSc was detected by sPMCA more frequently in indoor than outdoor furniture (12). </span></span></div>
<div class="yiv1437632715aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;">
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<span style="font-family: "times new roman" , serif;"><span style="font-size: 16px;">A recent experimental study has demonstrated that repeated cycles of drying and wetting of prion-contaminated soil, equivalent to what is expected under natural weathering conditions, could reduce PMCA amplification efficiency and extend the incubation period in hamsters inoculated with soil samples (30). </span></span></div>
<div class="yiv1437632715aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;">
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<div class="yiv1437632715aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;">
<span style="font-family: "times new roman" , serif;"><span style="font-size: 16px;">This seems to apply also to this study even though the reduction in infectivity was more dramatic in the sPMCA assays than in the sheep model. </span></span></div>
<div class="yiv1437632715aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;">
<span style="font-family: "times new roman" , serif;"><span style="font-size: 16px;"><br clear="none" /></span></span></div>
<div class="yiv1437632715aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;">
<span style="font-family: "times new roman" , serif;"><span style="font-size: 16px;">Sheep were not kept until clinical end-point, which would have enabled us to compare incubation periods, but the lack of infection in sheep exposed to furniture that had not been in contact with scrapie sheep for a longer time period supports the hypothesis that prion degradation and subsequent loss of infectivity occurs even under natural conditions. </span></span></div>
<div class="yiv1437632715aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;">
<span style="font-family: "times new roman" , serif;"><span style="font-size: 16px;"><br clear="none" /></span></span></div>
<div class="yiv1437632715aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;">
<span style="font-family: "times new roman" , serif;"><span style="font-size: 16px;">In conclusion, the results in the current study indicate that removal of furniture that had been in contact with scrapie-infected animals should be recommended, particularly since cleaning and decontamination may not effectively remove scrapie infectivity (31), even though infectivity declines considerably if the pasture and the field furniture have not been in contact with scrapie-infected sheep for several months. As sPMCA failed to detect PrPSc in furniture that was subjected to weathering, even though exposure led to infection in sheep, this method may not always be reliable in predicting the risk of scrapie infection through environmental contamination. </span></span></div>
<div class="yiv1437632715aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;">
<span style="font-family: "times new roman" , serif;"><span style="font-size: 16px;"><br clear="none" /></span></span></div>
<div class="yiv1437632715aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;">
<span style="font-family: "times new roman" , serif;"><span style="font-size: 16px;">These results suggest that the VRQ/VRQ sheep model may be more sensitive than sPMCA for the detection of environmentally associated scrapie, and suggest that extremely low levels of scrapie contamination are able to cause infection in susceptible sheep genotypes. </span></span></div>
<div class="yiv1437632715aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;">
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<span style="font-family: "times new roman" , serif;"><span style="font-size: 16px;">Keywords: classical scrapie, prion, transmissible spongiform encephalopathy, sheep, field furniture, reservoir, serial protein misfolding cyclic amplification </span></span></div>
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<a fg_scanned="1" href="http://journal.frontiersin.org/article/10.3389/fvets.2015.00032/full" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">http://journal.frontiersin.org/article/10.3389/fvets.2015.00032/full</a></div>
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<span style="font-family: "times new roman" , serif;"><span style="font-size: 16px;">Wednesday, December 16, 2015 </span></span></div>
<div class="yiv1437632715aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;">
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<span style="font-family: "times new roman" , serif;"><span style="font-size: 16px;">*** Objects in contact with classical scrapie sheep act as a reservoir for scrapie transmission *** </span></span></div>
<div class="yiv1437632715aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;">
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<a fg_scanned="1" href="http://scrapie-usa.blogspot.com/2015/12/objects-in-contact-with-classical.html" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">http://scrapie-usa.blogspot.com/2015/12/objects-in-contact-with-classical.html</a></div>
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<span style="font-family: "georgia";">WEDNESDAY, MARCH 13, 2019 </span></div>
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<span style="font-family: "georgia";">CWD, TSE, PRION, MATERNAL mother to offspring, testes, epididymis, seminal fluid, and blood</span></div>
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<span style="font-family: "georgia";"><a fg_scanned="1" href="https://chronic-wasting-disease.blogspot.com/2019/03/cwd-tse-prion-maternal-mother-to.html" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://chronic-wasting-disease.blogspot.com/2019/03/cwd-tse-prion-maternal-mother-to.html</a></span></div>
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Subject: Prion 2019 Conference</div>
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See full Prion 2019 Conference Abstracts</div>
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<span style="color: #0096ef;"><a fg_scanned="1" href="https://www.tandfonline.com/doi/full/10.1080/19336896.2019.1615197" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://www.tandfonline.com/doi/full/10.1080/19336896.2019.1615197</a></span></div>
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see scientific program and follow the cwd studies here;</div>
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Thursday, May 23, 2019 </div>
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Prion 2019 Emerging Concepts CWD, BSE, SCRAPIE, CJD, SCIENTIFIC PROGRAM Schedule and Abstracts</div>
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TSE surveillance statistics exotic species and domestic cats Update December 2019</div>
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<a fg_scanned="1" href="https://transmissiblespongiformencephalopathy.blogspot.com/2019/12/tse-surveillance-statistics-exotic.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://transmissiblespongiformencephalopathy.blogspot.com/2019/12/tse-surveillance-statistics-exotic.html</a></div>
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MONDAY, DECEMBER 16, 2019 </div>
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Chronic Wasting Disease CWD TSE Prion aka mad cow type disease in cervid Zoonosis Update</div>
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***> ''In particular the US data do not clearly exclude the possibility of human (sporadic or familial) TSE development due to consumption of venison. The Working Group thus recognizes a potential risk to consumers if a TSE would be present in European cervids.'' Scientific opinion on chronic wasting disease (II) <***</div>
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What if?</div>
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<a fg_scanned="1" href="https://chronic-wasting-disease.blogspot.com/2019/12/chronic-wasting-disease-cwd-tse-prion.html" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://chronic-wasting-disease.blogspot.com/2019/12/chronic-wasting-disease-cwd-tse-prion.html</a></div>
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> However, to date, no CWD infections have been reported in people.</div>
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key word here is ‘reported’. science has shown that CWD in humans will look like sporadic CJD. SO, how can one assume that CWD has not already transmitted to humans? they can’t, and it’s as simple as that. from all recorded science to date, CWD has already transmitted to humans, and it’s being misdiagnosed as sporadic CJD. …terry</div>
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*** LOOKING FOR CWD IN HUMANS AS nvCJD or as an ATYPICAL CJD, LOOKING IN ALL THE WRONG PLACES $$$ ***</div>
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*** These results would seem to suggest that CWD does indeed have zoonotic potential, at least as judged by the compatibility of CWD prions and their human PrPC target. Furthermore, extrapolation from this simple in vitro assay suggests that if zoonotic CWD occurred, it would most likely effect those of the PRNP codon 129-MM genotype and that the PrPres type would be similar to that found in the most common subtype of sCJD (MM1).***</div>
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<a fg_scanned="1" href="http://www.tandfonline.com/doi/full/10.4161/pri.28124?src=recsys" rel="noopener noreferrer" shape="rect" style="background-color: inherit; color: #222222; cursor: pointer; transition: all 0s ease-in-out 0s;" target="_blank">http://www.tandfonline.com/doi/full/10.4161/pri.28124?src=recsys</a></div>
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<a fg_scanned="1" href="http://www.tandfonline.com/doi/pdf/10.4161/pri.28124?needAccess=true" rel="noopener noreferrer" shape="rect" style="background-color: inherit; color: #222222; cursor: pointer; transition: all 0s ease-in-out 0s;" target="_blank">http://www.tandfonline.com/doi/pdf/10.4161/pri.28124?needAccess=true</a></div>
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<a fg_scanned="1" href="https://wwwnc.cdc.gov/eid/article/20/1/13-0858_article" rel="noopener noreferrer" shape="rect" style="background-color: inherit; color: #222222; cursor: pointer; transition: all 0s ease-in-out 0s;" target="_blank">https://wwwnc.cdc.gov/eid/article/20/1/13-0858_article</a></div>
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Chronic Wasting Disease CWD TSE Prion aka mad deer disease zoonosis</div>
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We hypothesize that:</div>
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(1) The classic CWD prion strain can infect humans at low levels in the brain and peripheral lymphoid tissues;</div>
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(2) The cervid-to-human transmission barrier is dependent on the cervid prion strain and influenced by the host (human) prion protein (PrP) primary sequence;</div>
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(3) Reliable essays can be established to detect CWD infection in humans; and</div>
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(4) CWD transmission to humans has already occurred. We will test these hypotheses in 4 Aims using transgenic (Tg) mouse models and complementary in vitro approaches.</div>
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<a fg_scanned="1" href="http://grantome.com/grant/NIH/R01-NS088604-04" rel="noopener noreferrer" shape="rect" style="background-color: inherit; color: #222222; cursor: pointer; transition: all 0s ease-in-out 0s;" target="_blank">http://grantome.com/grant/NIH/R01-NS088604-04</a></div>
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ZOONOTIC CHRONIC WASTING DISEASE CWD TSE PRION UPDATE</div>
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<span style="color: #222222; font-size: 16px;">First evidence of intracranial and peroral transmission of Chronic Wasting Disease (CWD) into Cynomolgus macaques: a work in progress Stefanie Czub1, Walter Schulz-Schaeffer2, Christiane Stahl-Hennig3, Michael Beekes4, Hermann Schaetzl5 and Dirk Motzkus6 1 </span></div>
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<span style="color: #222222; font-size: 16px;">University of Calgary Faculty of Veterinary Medicine/Canadian Food Inspection Agency; 2Universitatsklinikum des Saarlandes und Medizinische Fakultat der Universitat des Saarlandes; 3 Deutsches Primaten Zentrum/Goettingen; 4 Robert-Koch-Institut Berlin; 5 University of Calgary Faculty of Veterinary Medicine; 6 presently: Boehringer Ingelheim Veterinary Research Center; previously: Deutsches Primaten Zentrum/Goettingen </span></div>
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<span style="color: #222222; font-size: 16px;">This is a progress report of a project which started in 2009. 21 cynomolgus macaques were challenged with characterized CWD material from white-tailed deer (WTD) or elk by intracerebral (ic), oral, and skin exposure routes. Additional blood transfusion experiments are supposed to assess the CWD contamination risk of human blood product. Challenge materials originated from symptomatic cervids for ic, skin scarification and partially per oral routes (WTD brain). Challenge material for feeding of muscle derived from preclinical WTD and from preclinical macaques for blood transfusion experiments. We have confirmed that the CWD challenge material contained at least two different CWD agents (brain material) as well as CWD prions in muscle-associated nerves. </span></div>
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<span style="color: #222222; font-size: 16px;">Here we present first data on a group of animals either challenged ic with steel wires or per orally and sacrificed with incubation times ranging from 4.5 to 6.9 years at postmortem. Three animals displayed signs of mild clinical disease, including anxiety, apathy, ataxia and/or tremor. In four animals wasting was observed, two of those had confirmed diabetes. All animals have variable signs of prion neuropathology in spinal cords and brains and by supersensitive IHC, reaction was detected in spinal cord segments of all animals. Protein misfolding cyclic amplification (PMCA), real-time quaking-induced conversion (RT-QuiC) and PET-blot assays to further substantiate these findings are on the way, as well as bioassays in bank voles and transgenic mice. </span></div>
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<span style="color: #222222; font-size: 16px;">At present, a total of 10 animals are sacrificed and read-outs are ongoing. Preclinical incubation of the remaining macaques covers a range from 6.4 to 7.10 years. Based on the species barrier and an incubation time of > 5 years for BSE in macaques and about 10 years for scrapie in macaques, we expected an onset of clinical disease beyond 6 years post inoculation. </span></div>
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<span style="color: #222222; font-size: 16px;">PRION 2017 DECIPHERING NEURODEGENERATIVE DISORDERS </span></div>
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PRION 2018 CONFERENCE</div>
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Oral transmission of CWD into Cynomolgus macaques: signs of atypical disease, prion conversion and infectivity in macaques and bio-assayed transgenic mice</div>
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Hermann M. Schatzl, Samia Hannaoui, Yo-Ching Cheng, Sabine Gilch (Calgary Prion Research Unit, University of Calgary, Calgary, Canada) Michael Beekes (RKI Berlin), Walter Schulz-Schaeffer (University of Homburg/Saar, Germany), Christiane Stahl-Hennig (German Primate Center) & Stefanie Czub (CFIA Lethbridge).</div>
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To date, BSE is the only example of interspecies transmission of an animal prion disease into humans. The potential zoonotic transmission of CWD is an alarming issue and was addressed by many groups using a variety of in vitro and in vivo experimental systems. Evidence from these studies indicated a substantial, if not absolute, species barrier, aligning with the absence of epidemiological evidence suggesting transmission into humans. Studies in non-human primates were not conclusive so far, with oral transmission into new-world monkeys and no transmission into old-world monkeys. Our consortium has challenged 18 Cynomolgus macaques with characterized CWD material, focusing on oral transmission with muscle tissue. Some macaques have orally received a total of 5 kg of muscle material over a period of 2 years.</div>
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After 5-7 years of incubation time some animals showed clinical symptoms indicative of prion disease, and prion neuropathology and PrPSc deposition were detected in spinal cord and brain of some euthanized animals. PrPSc in immunoblot was weakly detected in some spinal cord materials and various tissues tested positive in RT-QuIC, including lymph node and spleen homogenates. To prove prion infectivity in the macaque tissues, we have intracerebrally inoculated 2 lines of transgenic mice, expressing either elk or human PrP. At least 3 TgElk mice, receiving tissues from 2 different macaques, showed clinical signs of a progressive prion disease and brains were positive in immunoblot and RT-QuIC. Tissues (brain, spinal cord and spleen) from these and pre-clinical mice are currently tested using various read-outs and by second passage in mice. Transgenic mice expressing human PrP were so far negative for clear clinical prion disease (some mice >300 days p.i.). In parallel, the same macaque materials are inoculated into bank voles.</div>
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Taken together, there is strong evidence of transmissibility of CWD orally into macaques and from macaque tissues into transgenic mouse models, although with an incomplete attack rate.</div>
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The clinical and pathological presentation in macaques was mostly atypical, with a strong emphasis on spinal cord pathology.<br />
Our ongoing studies will show whether the transmission of CWD into macaques and passage in transgenic mice represents a form of non-adaptive prion amplification, and whether macaque-adapted prions have the potential to infect mice expressing human PrP.</div>
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The notion that CWD can be transmitted orally into both new-world and old-world non-human primates asks for a careful reevaluation of the zoonotic risk of CWD..</div>
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***> The notion that CWD can be transmitted orally into both new-world and old-world non-human primates asks for a careful reevaluation of the zoonotic risk of CWD. <***</div>
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<a fg_scanned="1" href="https://prion2018.org/" rel="noopener noreferrer" shape="rect" style="background-color: inherit; color: #222222; cursor: pointer; transition: all 0s ease-in-out 0s;" target="_blank">https://prion2018.org/</a></div>
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READING OVER THE PRION 2018 ABSTRACT BOOK, LOOKS LIKE THEY FOUND THAT from this study ;</div>
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P190 Human prion disease mortality rates by occurrence of chronic wasting disease in freeranging cervids, United States</div>
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Abrams JY (1), Maddox RA (1), Schonberger LB (1), Person MK (1), Appleby BS (2), Belay ED (1) (1) Centers for Disease Control and Prevention (CDC), National Center for Emerging and Zoonotic Infectious Diseases, Atlanta, GA, USA (2) Case Western Reserve University, National Prion Disease Pathology Surveillance Center (NPDPSC), Cleveland, OH, USA..</div>
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SEEMS THAT THEY FOUND Highly endemic states had a higher rate of prion disease mortality compared to non-CWD<br />
states.</div>
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AND ANOTHER STUDY;</div>
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P172 Peripheral Neuropathy in Patients with Prion Disease</div>
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Wang H(1), Cohen M(1), Appleby BS(1,2) (1) University Hospitals Cleveland Medical Center, Cleveland, Ohio (2) National Prion Disease Pathology Surveillance Center, Cleveland, Ohio..</div>
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IN THIS STUDY, THERE WERE autopsy-proven prion cases from the National Prion Disease Pathology Surveillance Center that were diagnosed between September 2016 to March 2017,</div>
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AND</div>
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included 104 patients. SEEMS THEY FOUND THAT The most common sCJD subtype was MV1-2 (30%), followed by MM1-2 (20%),</div>
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AND</div>
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THAT The Majority of cases were male (60%), AND half of them had exposure to wild game.</div>
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snip…</div>
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see more on Prion 2017 Macaque study from Prion 2017 Conference and other updated science on cwd tse prion zoonosis below…terry</div>
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<a href="https://prion2018.org/wp-content/uploads/2018/05/program.pdf" rel="noopener noreferrer" shape="rect" style="background-color: inherit; color: #222222; cursor: pointer; transition: all 0s ease-in-out 0s;" target="_blank">https://prion2018.org/wp-content/uploads/2018/05/program.pdf</a></div>
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PRION 2019 ABSTRACTS </div>
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1. Interspecies transmission of the chronic wasting disease agent</div>
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Justin Greenlee</div>
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Virus and Prion Research Unit, National Animal Disease Center, USDA Agriculture Research Service</div>
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The presentation will summarize the results of various studies conducted at our research center that assess the transmissibility of the chronic wasting disease (CWD) agent to cattle, pigs, raccoons, goats, and sheep. This will include specifics of the relative attack rates, clinical signs, and microscopic lesions with emphasis on how to differentiate cross-species transmission of the CWD agent from the prion diseases that naturally occur in hosts such as cattle or sheep. Briefly, the relative difficulty of transmitting the CWD agent to sheep and goats will be contrasted with the relative ease of transmitting the scrapie agent to white-tailed deer.</div>
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53. Evaluation of the inter-species transmission potential of different CWD isolates</div>
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Rodrigo Moralesa, Carlos Kramma,b, Paulina Sotoa, Adam Lyona, Sandra Pritzkowa, Claudio Sotoa</div>
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aMitchell Center for Alzheimer’s disease and Related Brain Disorders, Dept. of Neurology, McGovern School of Medicine University of Texas Health Science Center at Houston, TX, USA; bFacultad de Medicina, Universidad de los Andes, Santiago, Chile</div>
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Chronic Wasting Disease (CWD) has reached epidemic proportions in North America and has been identified in South Korea and Northern Europe. CWD-susceptible cervid species are known to share habitats with humans and other animals entering the human food chain. At present, the potential of CWD to infect humans and other animal species is not completely clear. The exploration of this issue acquires further complexity considering the differences in the prion protein sequence due to species-specific variations and polymorphic changes within species. While several species of cervids are naturally affected by CWD, white-tailed deer (WTD) is perhaps the most relevant due to its extensive use in hunting and as a source of food. Evaluation of inter-species prion infections using animals or mouse models is costly and time consuming. We and others have shown that the Protein Misfolding Cyclic Amplification (PMCA) technology reproduces, in an accelerated and inexpensive manner, the inter-species transmission of prions while preserving the strain features of the input PrPSc. In this work, we tested the potential of different WTD-derived CWD isolates to transmit to humans and other animal species relevant for human consumption using PMCA. For these experiments, CWD isolates homozygous for the most common WTD-PrP polymorphic changes (G96S) were used (96SS variant obtained from a pre-symptomatic prion infected WTD). Briefly, 96GG and 96SS CWD prions were adapted in homologous or heterologous substrate by PMCA through several (15) rounds. End products, as well as intermediates across the process, were tested for their inter-species transmission potentials. A similar process was followed to assess seed-templated misfolding of ovine, porcine, and bovine PrPC. Our results show differences on the inter-species transmission potentials of the four adapted materials generated (PrPC/PrPSc polymorphic combinations), being the homologous combinations of seed/substrate the ones with the greater apparent zoonotic potential. Surprisingly, 96SS prions adapted in homologous substrate were the ones showing the easiest potential to template PrPC misfolding from other animal species. In summary, our results show that a plethora of different CWD isolates, each comprising different potentials for inter-species transmission, may exist in the environment. These experiments may help to clarify an uncertain and potentially worrisome public health issue. Additional research in this area may be useful to advise on the design of regulations intended to stop the spread of CWD and predict unwanted zoonotic events.</div>
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56. Understanding chronic wasting disease spread potential for at-risk species</div>
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Catherine I. Cullingham, Anh Dao, Debbie McKenzie and David W. Coltman</div>
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Department of Biological Sciences, University of Alberta, Edmonton AB, Canada</div>
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CONTACT Catherine I. Cullingham <a href="mailto:cathy.cullingham@ualberta.ca" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank" ymailto="mailto:cathy.cullingham@ualberta.ca">cathy.cullingham@ualberta.ca</a></div>
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ABSTRACT</div>
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Genetic variation can be linked to susceptibility or resistance to a disease, and this information can help to better understand spread-risk in a population. Wildlife disease incidence is increasing, and this is resulting in negative impacts on the economy, biodiversity, and in some instances, human health. If we can find genetic variation that helps to inform which individuals are susceptible, then we can use this information on at-risk populations to better manage negative consequences. Chronic wasting disease, a fatal, transmissible spongiform encephalopathy of cervids (both wild and captive), continues to spread geographically, which has resulted in an increasing host-range. The disease agent (PrPCWD) is a misfolded conformer of native cellular protein (PrPC). In Canada, the disease is endemic in Alberta and Saskatchewan, infecting primarily mule deer and white-tail deer, with a smaller impact on elk and moose populations. As the extent of the endemic area continues to expand, additional species will be exposed to this disease, including bison, bighorn sheep, mountain goat, and pronghorn antelope. To better understand the potential spread-risk among these species, we reviewed the current literature on species that have been orally exposed to CWD to identify susceptible and resistant species. We then compared the amino acid polymorphisms of PrPC among these species to determine whether any sites were linked to susceptibility or resistance to CWD infection. We sequenced the entire PrP coding region in 578 individuals across at-risk populations to evaluate their potential susceptibility. Three amino acid sites (97, 170, and 174; human numbering) were significantly associated with susceptibility, but these were not fully discriminating. All but one species among the resistant group shared the same haplotype, and the same for the susceptible species. For the at-risk species, bison had the resistant haplotype, while bighorn sheep and mountain goats were closely associated with the resistant type. Pronghorn antelope and a newly identified haplotype in moose differed from the susceptible haplotype, but were still closely associated with it. These data suggest pronghorn antelope will be susceptible to CWD while bison are likely to be resistant. Based on this data, recommendations can be made regarding species to be monitored for possible CWD infection.</div>
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KEYWORDS: Chronic wasting disease; Prnp; wildlife disease; population genetics; ungulates</div>
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Thursday, May 23, 2019 </div>
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Prion 2019 Emerging Concepts CWD, BSE, SCRAPIE, CJD, SCIENTIFIC PROGRAM Schedule and Abstracts</div>
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<a fg_scanned="1" href="https://prionconference.blogspot.com/2019/05/prion-2019-emerging-concepts-cwd-bse.html" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://prionconference.blogspot.com/2019/05/prion-2019-emerging-concepts-cwd-bse.html</a></div>
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see full Prion 2019 Conference Abstracts</div>
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<span style="color: #0096ef;"><a fg_scanned="1" href="https://www.tandfonline.com/doi/full/10.1080/19336896.2019.1615197" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://www.tandfonline.com/doi/full/10.1080/19336896.2019.1615197</a></span></div>
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THURSDAY, OCTOBER 04, 2018</div>
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Cervid to human prion transmission 5R01NS088604-04 Update</div>
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<a fg_scanned="1" href="http://grantome.com/grant/NIH/R01-NS088604-04" rel="noopener noreferrer" shape="rect" style="background-color: inherit; color: #222222; cursor: pointer; transition: all 0s ease-in-out 0s;" target="_blank">http://grantome.com/grant/NIH/R01-NS088604-04</a></div>
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<a fg_scanned="1" href="http://chronic-wasting-disease.blogspot.com/2018/10/cervid-to-human-prion-transmission.html" rel="noopener noreferrer" shape="rect" style="background-color: inherit; color: #222222; cursor: pointer; transition: all 0s ease-in-out 0s;" target="_blank">http://chronic-wasting-disease.blogspot.com/2018/10/cervid-to-human-prion-transmission.html</a></div>
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snip…full text;</div>
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SATURDAY, FEBRUARY 09, 2019</div>
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Experts: Yes, chronic wasting disease in deer is a public health issue — for people</div>
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<a fg_scanned="1" href="https://chronic-wasting-disease.blogspot.com/2019/02/experts-yes-chronic-wasting-disease-in.html" rel="noopener noreferrer" shape="rect" style="background-color: inherit; color: #222222; cursor: pointer; transition: all 0s ease-in-out 0s;" target="_blank">https://chronic-wasting-disease.blogspot.com/2019/02/experts-yes-chronic-wasting-disease-in.html</a></div>
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SATURDAY, FEBRUARY 23, 2019 </div>
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Chronic Wasting Disease CWD TSE Prion and THE FEAST 2003 CDC an updated review of the science 2019</div>
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TUESDAY, NOVEMBER 04, 2014 </div>
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Six-year follow-up of a point-source exposure to CWD contaminated venison in an Upstate New York community: risk behaviours and health outcomes 2005–2011</div>
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Authors, though, acknowledged the study was limited in geography and sample size and so it couldn't draw a conclusion about the risk to humans. They recommended more study. Dr. Ermias Belay was the report's principal author but he said New York and Oneida County officials are following the proper course by not launching a study. "There's really nothing to monitor presently. No one's sick," Belay said, noting the disease's incubation period in deer and elk is measured in years. "</div>
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Transmission Studies</div>
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Mule deer transmissions of CWD were by intracerebral inoculation and compared with natural cases {the following was written but with a single line marked through it ''first passage (by this route)}....TSS</div>
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resulted in a more rapidly progressive clinical disease with repeated episodes of synocopy ending in coma. One control animal became affected, it is believed through contamination of inoculum (?saline). Further CWD transmissions were carried out by Dick Marsh into ferret, mink and squirrel monkey. Transmission occurred in ALL of these species with the shortest incubation period in the ferret.</div>
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snip.... </div>
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<a href="https://web.archive.org/web/20090506002237/http://www.bseinquiry.gov.uk/files/mb/m11b/tab01.pdf" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">https://web.archive.org/web/20090506002237/http://www..bseinquiry.gov.uk/files/mb/m11b/tab01.pdf</a></div>
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Prion Infectivity in Fat of Deer with Chronic Wasting Disease▿ </div>
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Brent Race#, Kimberly Meade-White#, Richard Race and Bruce Chesebro* + Author Affiliations</div>
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In mice, prion infectivity was recently detected in fat. Since ruminant fat is consumed by humans and fed to animals, we determined infectivity titers in fat from two CWD-infected deer. Deer fat devoid of muscle contained low levels of CWD infectivity and might be a risk factor for prion infection of other species. </div>
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<a fg_scanned="1" href="http://jvi.asm.org/content/83/18/9608.full" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">http://jvi.asm.org/content/83/18/9608.full</a> </div>
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Prions in Skeletal Muscles of Deer with Chronic Wasting Disease </div>
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Here bioassays in transgenic mice expressing cervid prion protein revealed the presence of infectious prions in skeletal muscles of CWD-infected deer, demonstrating that humans consuming or handling meat from CWD-infected deer are at risk to prion exposure. </div>
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<a fg_scanned="1" href="http://science.sciencemag.org/content/311/5764/1117..long" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">http://science.sciencemag.org/content/311/5764/1117..long</a> </div>
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*** now, let’s see what the authors said about this casual link, personal communications years ago, and then the latest on the zoonotic potential from CWD to humans from the TOKYO PRION 2016 CONFERENCE.</div>
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see where it is stated NO STRONG evidence. so, does this mean there IS casual evidence ???? “Our conclusion stating that we found no strong evidence of CWD transmission to humans”</div>
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From: TSS (<a class="yiv1437632715linkified" fg_scanned="1" href="http://216-119-163-189.ipset45.wt.net/" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">216-119-163-189.ipset45.wt.net</a>)</div>
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Subject: CWD aka MAD DEER/ELK TO HUMANS ???</div>
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Date: September 30, 2002 at 7:06 am PST</div>
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From: "Belay, Ermias"</div>
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To: Cc: "Race, Richard (NIH)" ; ; "Belay, Ermias"</div>
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Sent: Monday, September 30, 2002 9:22 AM</div>
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Subject: RE: TO CDC AND NIH - PUB MED- 3 MORE DEATHS - CWD - YOUNG HUNTERS</div>
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Dear Sir/Madam,</div>
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In the Archives of Neurology you quoted (the abstract of which was attached to your email), we did not say CWD in humans will present like variant CJD.. That assumption would be wrong. I encourage you to read the whole article and call me if you have questions or need more clarification (phone: 404-639-3091). Also, we do not claim that "no-one has ever been infected with prion disease from eating venison." Our conclusion stating that we found no strong evidence of CWD transmission to humans in the article you quoted or in any other forum is limited to the patients we investigated.</div>
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Ermias Belay, M.D. Centers for Disease Control and Prevention</div>
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-----Original Message-----</div>
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From: Sent: Sunday, September 29, 2002 10:15 AM</div>
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To: <a href="mailto:rr26k@nih.gov" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank" ymailto="mailto:rr26k@nih.gov">rr26k@nih.gov</a>; <a href="mailto:rrace@niaid.nih.gov" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank" ymailto="mailto:rrace@niaid.nih.gov">rrace@niaid.nih.gov</a>; <a href="mailto:ebb8@CDC.GOV" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank" ymailto="mailto:ebb8@CDC.GOV">ebb8@CDC.GOV</a></div>
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Subject: TO CDC AND NIH - PUB MED- 3 MORE DEATHS - CWD - YOUNG HUNTERS</div>
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Sunday, November 10, 2002 6:26 PM .......snip........end..............TSS</div>
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Thursday, April 03, 2008</div>
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A prion disease of cervids: Chronic wasting disease 2008 1: Vet Res. 2008 Apr 3;39(4):41 A prion disease of cervids: Chronic wasting disease Sigurdson CJ.</div>
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snip...</div>
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*** twenty-seven CJD patients who regularly consumed venison were reported to the Surveillance Center***,</div>
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snip... full text ; </div>
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> However, to date, no CWD infections have been reported in people. </div>
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sporadic, spontaneous CJD, 85%+ of all human TSE, just not just happen. never in scientific literature has this been proven.</div>
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if one looks up the word sporadic or spontaneous at pubmed, you will get a laundry list of disease that are classified in such a way;</div>
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sporadic = 54,983 hits <a fg_scanned="1" href="https://www.ncbi.nlm.nih.gov/pubmed/?term=sporadic" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">https://www.ncbi.nlm.nih.gov/pubmed/?term=sporadic</a></div>
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spontaneous = 325,650 hits <a fg_scanned="1" href="https://www.ncbi.nlm.nih.gov/pubmed/?term=spontaneous" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">https://www.ncbi.nlm.nih.gov/pubmed/?term=spontaneous</a></div>
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key word here is 'reported'. science has shown that CWD in humans will look like sporadic CJD. SO, how can one assume that CWD has not already transmitted to humans? they can't, and it's as simple as that. from all recorded science to date, CWD has already transmitted to humans, and it's being misdiagnosed as sporadic CJD. ...terry </div>
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*** LOOKING FOR CWD IN HUMANS AS nvCJD or as an ATYPICAL CJD, LOOKING IN ALL THE WRONG PLACES $$$ ***</div>
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*** These results would seem to suggest that CWD does indeed have zoonotic potential, at least as judged by the compatibility of CWD prions and their human PrPC target. Furthermore, extrapolation from this simple in vitro assay suggests that if zoonotic CWD occurred, it would most likely effect those of the PRNP codon 129-MM genotype and that the PrPres type would be similar to that found in the most common subtype of sCJD (MM1).*** </div>
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FRIDAY, JULY 26, 2019 </div>
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Chronic Wasting Disease in Cervids: Implications for Prion Transmission to Humans and Other Animal Species</div>
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TUESDAY, JANUARY 21, 2020 </div>
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***> 2004 European Commission Chronic wasting disease AND TISSUES THAT MIGHT CARRY A RISK FOR HUMAN FOOD AND ANIMAL FEED CHAINS REPORT UPDATED 2020</div>
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<span style="font-family: "arial" , "helvetica";">***> In conclusion, sensory symptoms and loss of reflexes in Gerstmann-Sträussler-Scheinker syndrome can be explained by neuropathological changes in the spinal cord. We conclude that the sensory symptoms and loss of lower limb reflexes in Gerstmann-Sträussler-Scheinker syndrome is due to pathology in the caudal spinal cord. <***</span></div>
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<span style="font-size: 13.3333px;">***> The clinical and pathological presentation in macaques was mostly atypical, with a strong emphasis on spinal cord pathology.<*** </span></div>
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<span style="font-size: 13.3333px;">***> The notion that CWD can be transmitted orally into both new-world and old-world non-human primates asks for a careful reevaluation of the zoonotic risk of CWD. <***</span></div>
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<span style="font-size: 13.3333px;">***> All animals have variable signs of prion neuropathology in spinal cords and brains and by supersensitive IHC, reaction was detected in spinal cord segments of all animals.<*** </span></div>
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<span style="font-family: "arial" , "helvetica";">***> In particular the US data do not clearly exclude the possibility of human (sporadic or familial) TSE development due to consumption of venison. The Working Group thus recognizes a potential risk to consumers if a TSE would be present in European cervids.'' Scientific opinion on chronic wasting disease (II) <***</span></div>
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<span style="background-color: white; color: black; font-family: "arial"; font-size: 10pt;">FRIDAY, OCTOBER 25, 2019 </span></div>
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<span style="background-color: white; color: black; font-family: "arial"; font-size: 10pt;">Experts testify United States is underprepared for bioterrorism threats Transmissible Spongiform Encephalopathy TSE Prion disease </span></div>
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<span style="color: #222222;">THURSDAY, JANUARY 23, 2020 </span></div>
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<span style="color: #222222;">USDA Consolidates Regulations for NAHLN Laboratory Testing USDA Animal and Plant Health Inspection Service sent this bulletin at 01/23/2020 02:15 PM EST</span></div>
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Terry S. Singeltary Sr.</div>
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WEDNESDAY, FEBRUARY 5, 2020 </div>
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Switzerland OIE Bovine spongiform encephalopathy atypical BSE type L TSE Prion</div>
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THURSDAY, DECEMBER 12, 2019 </div>
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Heidenhain Variant Creutzfeldt Jakob Disease hvCJD, sporadic spontaneous CJD and the TSE Prion December 14, 2019</div>
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<span style="font-family: "helvetica" , "arial" , sans-serif;">MONDAY, JANUARY 20, 2020</span></div>
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<span style="font-family: "helvetica" , "arial" , sans-serif;">sporadic CJD one in a million, FAKE NEWS PEOPLE!</span></div>
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<span style="font-family: "helvetica" , "arial" , sans-serif;">this myth has been incorrect for decades, and had been stated as such by a few, but again, the media is too lazy to do it's job and print the facts.</span></div>
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<span style="font-family: "helvetica" , "arial" , sans-serif;">bottom line, science shows human tse prion is 1 in 5,000...</span></div>
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MONDAY, FEBRUARY 25, 2019</div>
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***> MAD DOGS AND ENGLISHMEN BSE, SCRAPIE, CWD, CJD, TSE PRION A REVIEW 2019</div>
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CONFIDENTIAL</div>
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<span style="background-color: rgba(255, 255, 255, 0);">>>> The only tenable public line will be that "more research is required’’ <<< </span></div>
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<span style="background-color: rgba(255, 255, 255, 0);">>>> possibility on a transmissible prion remains open<<< </span></div>
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<span style="background-color: rgba(255, 255, 255, 0);"><span style="line-height: 1.22em;">O.K., so it’s about 23 years later, so somebody please tell me, when is "more research is required’’ enough time for evaluation ? </span></span></div>
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<span style="background-color: rgba(255, 255, 255, 0);">Re-Evidence for human transmission of amyloid-β pathology and cerebral amyloid angiopathy </span></div>
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<span style="background-color: rgba(255, 255, 255, 0);">Nature 525, 247?250 (10 September 2015) doi:10.1038/nature15369 Received 26 April 2015 Accepted 14 August 2015 Published online 09 September 2015 Updated online 11 September 2015 Erratum (October, 2015) </span></div>
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<span style="background-color: rgba(255, 255, 255, 0);">snip...see full Singeltary Nature comment here; </span></div>
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<span style="background-color: rgba(255, 255, 255, 0);">Alzheimer's disease</span></div>
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<span style="background-color: rgba(255, 255, 255, 0);">let's not forget the elephant in the room. curing Alzheimer's would be a great and wonderful thing, but for starters, why not start with the obvious, lets prove the cause or causes, and then start to stop that. think iatrogenic, friendly fire, or the pass it forward mode of transmission. think medical, surgical, dental, tissue, blood, related transmission. think transmissible spongiform encephalopathy aka tse prion disease aka mad cow type disease... </span></div>
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<span style="background-color: rgba(255, 255, 255, 0);">Commentary: Evidence for human transmission of amyloid-β pathology and cerebral amyloid angiopathy</span></div>
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<span style="color: black;"><span style="background-color: rgba(255, 255, 255, 0);"><a fg_scanned="1" href="http://journals.plos.org/plosone/article/comment?id=info:doi/10.1371/annotation/933cc83a-a384-45c3-b3b2-336882c30f9d" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">http://journals.plos.org/plosone/article/comment?id=info:doi/10.1371/annotation/933cc83a-a384-45c3-b3b2-336882c30f9d</a></span></span></div>
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<span style="color: black;"><span style="background-color: rgba(255, 255, 255, 0);"><a fg_scanned="1" href="http://journals.plos.org/plosone/article/comments?id=10.1371/journal.pone.0111492" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">http://journals.plos.org/plosone/article/comments?id=10.1371/journal.pone.0111492</a></span></span></div>
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<span style="color: black;"><span style="background-color: rgba(255, 255, 255, 0);"><a fg_scanned="1" href="https://www.frontiersin.org/articles/10.3389/fnagi.2016.00005/full" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">https://www.frontiersin.org/articles/10.3389/fnagi.2016.00005/full</a></span></span></div>
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<span style="background-color: rgba(255, 255, 255, 0);">Self-Propagative Replication of Ab Oligomers Suggests Potential Transmissibility in Alzheimer Disease </span></div>
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<span style="background-color: rgba(255, 255, 255, 0);">*** Singeltary comment PLoS *** </span></div>
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<span style="background-color: rgba(255, 255, 255, 0);">Alzheimer’s disease and Transmissible Spongiform Encephalopathy prion disease, Iatrogenic, what if ? </span></div>
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<span style="background-color: rgba(255, 255, 255, 0);">Posted by flounder on 05 Nov 2014 at 21:27 GMT </span></div>
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<span style="color: black;"><span style="background-color: rgba(255, 255, 255, 0);"><a fg_scanned="1" href="http://www.plosone.org/annotation/listThread.action?root=82860" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">http://www.plosone.org/annotation/listThread.action?root=82860</a></span></span></div>
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<span style="background-color: rgba(255, 255, 255, 0);">IN CONFIDENCE</span></div>
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<span style="background-color: rgba(255, 255, 255, 0);">5 NOVEMBER 1992</span></div>
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<span style="background-color: rgba(255, 255, 255, 0);">TRANSMISSION OF ALZHEIMER TYPE PLAQUES TO PRIMATES</span></div>
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<span style="background-color: rgba(255, 255, 255, 0);">[9. Whilst this matter is not at the moment directly concerned with the iatrogenic CJD cases from hgH, there remains a possibility of litigation here, and this presents an added complication. </span></div>
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<span style="background-color: rgba(255, 255, 255, 0);">There are also results to be made available shortly </span></div>
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<span style="background-color: rgba(255, 255, 255, 0);">(1) concerning a farmer with CJD who had BSE animals, </span></div>
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<span style="background-color: rgba(255, 255, 255, 0);">(2) on the possible transmissibility of Alzheimer’s and </span></div>
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<span style="background-color: rgba(255, 255, 255, 0);">(3) a CMO letter on prevention of iatrogenic CJD transmission in neurosurgery, all of which will serve to increase media interest.]</span></div>
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<span style="color: black;"><span style="background-color: rgba(255, 255, 255, 0);"><a href="https://web.archive.org/web/20170126060344/http://collections.europarchive.org/tna/20080102232842/http://www.bseinquiry.gov.uk/files/yb/1992/11/04001001.pdf" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">https://web.archive.org/web/20170126060344/http://collections.europarchive.org/tna/20080102232842/http://www.bseinquiry.gov.uk/files/yb/1992/11/04001001.pdf</a></span></span></div>
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<span style="color: black;"><span style="background-color: rgba(255, 255, 255, 0);"><a href="https://web.archive.org/web/20040315075058/http://www.bseinquiry.gov.uk/files/yb/1992/12/16005001.pdf" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">https://web.archive.org/web/20040315075058/http://www.bseinquiry.gov.uk/files/yb/1992/12/16005001.pdf</a></span></span></div>
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<span style="font-family: "helvetica" , "arial" , sans-serif;">''From a large array of bioassays, we conclude that AD, PD, MSA, and the frontotemporal dementias, including PSP and CBD, are all prion diseases'' 11. Arguments for Alzheimer’s and Parkinson’s diseases caused by prions</span></div>
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<span style="font-family: "helvetica" , "arial" , sans-serif;">Stanley B. Prusiner</span></div>
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<span style="font-family: "helvetica" , "arial" , sans-serif;">Institute of Neurodegenerative Diseases, and Professor of Neurology and Biochemistry, University of California San Francisco</span></div>
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<span style="font-family: "helvetica" , "arial" , sans-serif;">ABSTRACT</span></div>
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<span style="font-family: "helvetica" , "arial" , sans-serif;">Arguments for Alzheimer’s (AD) and Parkinson’s diseases (PD) being caused by prions continue to advance with new evidence. Findings in the brains of deceased AD patients argue that both Aβ and tau prions can be demonstrated by bioassays in cultured cells as well as in transgenic (Tg) mice. Likewise, studies of the brains of deceased MSA patients have been found to contain α-synuclein prions by bioassays in cultured cells and Tg mice. Conversely, the brains of AD patients do not contain α-synuclein prions, and the brains of MSA patients do not contain Aβ or tau prions. Additionally, while the brains of patients who died of either progressive supranuclear palsy (PSP) or corticobasal degeneration (CBD) contained tau prions, neither Aβ nor α-synuclein prions were detectable. Merely measuring the levels of Aβ, tau, and α-synuclein appears to give misleading information about the etiology and pathogenesis of neurodegenerative diseases (NDs). From a large array of bioassays, we conclude that AD, PD, MSA, and the frontotemporal dementias, including PSP and CBD, are all prion diseases. Our findings argue that changes in the conformations of Aβ, tau, and α-synuclein underlie the acquisition of prion infectivity in all of these NDs.</span></div>
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<a fg_scanned="1" href="https://www.tandfonline.com/doi/full/10.1080/19336896.2019.1615197" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://www.tandfonline.com/doi/full/10.1080/19336896.2019.1615197</a></div>
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P132 Aged cattle brain displays Alzheimer’s-like pathology that can be propagated in a prionlike manner</div>
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Ines Moreno-Gonzalez (1), George Edwards III (1), Rodrigo Morales (1), Claudia Duran-Aniotz (1), Mercedes Marquez (2), Marti Pumarola (2), Claudio Soto (1) </div>
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These results may contribute to uncover a previously unsuspected etiology surrounding some cases of sporadic AD. However, the early and controversial stage of the field of prion-like transmission in non-prion diseases added to the artificial nature of the animal models utilized for these studies, indicate that extrapolation of the results to humans should not be done without further experiments. </div>
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P75 Determining transmissibility and proteome changes associated with abnormal bovine prionopathy </div>
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Dudas S (1,2), Seuberlich T (3), Czub S (1,2) </div>
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In prion diseases, it is believed that altered protein conformation encodes for different pathogenic strains. Currently 3 different strains of bovine spongiform encephalopathy (BSE) are confirmed. Diagnostic tests for BSE are able to identify animals infected with all 3 strains, however, several diagnostic laboratories have reported samples with inconclusive results which are challenging to classify. It was suggested that these may be novel strains of BSE; to determine transmissibility, brain material from index cases were inoculated into cattle. </div>
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In the first passage, cattle were intra-cranially challenged with brain homogenate from 2 Swiss animals with abnormal prionopathy. The challenged cattle incubated for 3 years and were euthanized with no clinical signs of neurologic disease. Animals were negative when tested on validated diagnostic tests but several research methods demonstrated changes in the prion conformation in these cattle, including density gradient centrifugation and immunohistochemistry. Currently, samples from the P1 animals are being tested for changes in protein levels using 2-D Fluorescence Difference Gel Electrophoresis (2D DIGE) and mass spectrometry. It is anticipated that, if a prionopathy is present, this approach should identify pathways and targets to decipher the source of altered protein conformation. In addition, a second set of cattle have been challenged with brain material from the first passage. Ideally, these cattle will be given a sufficient incubation period to provide a definitive answer to the question of transmissibility. </div>
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=====prion 2018=== </div>
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<a href="https://prion2018.org/wp-content/uploads/2018/05/program.pdf" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://prion2018.org/wp-content/uploads/2018/05/program.pdf</a></div>
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***however in 1 C-type challenged animal, Prion 2015 Poster Abstracts </div>
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S67 PrPsc was not detected using rapid tests for BSE.</div>
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***Subsequent testing resulted in the detection of pathologic lesion in unusual brain location and PrPsc detection by PMCA only.</div>
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*** IBNC Tauopathy or TSE Prion disease, it appears, no one is sure ***</div>
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Posted by Terry S. Singeltary Sr. on 03 Jul 2015 at 16:53 GMT</div>
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<a fg_scanned="1" href="http://www.plosone.org/annotation/listThread.action?root=86610" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://www.plosone.org/annotation/listThread.action?root=86610</a></div>
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Molecular characterization of BSE in Canada</div>
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Jianmin Yang 1 , Sandor Dudas 2 , Catherine Graham 2 , Markus Czub 3 , Tim McAllister 1 , Stefanie Czub 1 1 Agriculture and Agri-Food Canada Research Centre, Canada; 2 National and OIE BSE Reference Laboratory, Canada; 3 University of Calgary, Canada</div>
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Background: Three BSE types (classical and two atypical) have been identified on the basis of molecular characteristics of the misfolded protein associated with the disease. To date, each of these three types have been detected in Canadian cattle. Objectives: This study was conducted to further characterize the 16 Canadian BSE cases based on the biochemical properties of there associated PrPres.</div>
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Methods: Immuno-reactivity, molecular weight, glycoform profiles and relative proteinase K sensitivity of the PrPres from each of the 16 confirmed Canadian BSE cases was determined using modified Western blot analysis.</div>
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Results: Fourteen of the 16 Canadian BSE cases were C type, 1 was H type and 1 was L type. The Canadian H and L-type BSE cases exhibited size shifts and changes in glycosylation similar to other atypical BSE cases. PK digestion under mild and stringent conditions revealed a reduced protease resistance of the atypical cases compared to the C-type cases. N terminal-specific antibodies bound to PrPres from H type but not from C or L type. The C-terminal-specific antibodies resulted in a shift in the glycoform profile and detected a fourth band in the Canadian H-type BSE.</div>
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Discussion: The C, L and H type BSE cases in Canada exhibit molecular characteristics similar to those described for classical and atypical BSE cases from Europe and Japan. This supports the theory that the importation of BSE contaminated feedstuff is the source of C-type BSE in Canada. It also suggests a similar cause or source for atypical BSE in these countries.</div>
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Discussion: The C, L and H type BSE cases in Canada exhibit molecular characteristics similar to those described for classical and atypical BSE cases from Europe and Japan.</div>
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*** This supports the theory that the importation of BSE contaminated feedstuff is the source of C-type BSE in Canada.</div>
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*** It also suggests a similar cause or source for atypical BSE in these countries. ***</div>
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see page 176 of 201 pages...tss</div>
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<a href="http://www.neuroprion.org/resources/pdf_docs/conferences/prion2009/prion2009_bookofabstracts.pdf" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://www.neuroprion.org/resources/pdf_docs/conferences/prion2009/prion2009_bookofabstracts.pdf</a></div>
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*** Singeltary reply ; Molecular, Biochemical and Genetic Characteristics of BSE in Canada Singeltary reply;</div>
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On behalf of the Scientific Committee, I am pleased to inform you that your abstract</div>
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'Transmissible Spongiform encephalopathy (TSE) animal and human TSE in North America update October 2009'</div>
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WAS accepted for inclusion in the INTERNATIONAL SCIENTIFIC EXCHANGE (ISE) section of the 14th International Congress on Infectious Diseases. Accordingly, your abstract will be included in the "Intl. Scientific Exchange abstract CD-rom" of the Congress which will be distributed to all participants.</div>
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Abstracts accepted for INTERNATIONAL SCIENTIFIC EXCHANGE are NOT PRESENTED in the oral OR poster sessions.</div>
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Your abstract below was accepted for: INTERNATIONAL SCIENTIFIC EXCHANGE</div>
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#0670: Transmissible Spongiform encephalopathy (TSE) animal and human TSE in North America update October 2009</div>
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Author: T. Singeltary; Bacliff, TX/US</div>
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Topic: Emerging Infectious Diseases Preferred type of presentation: International Scientific Exchange</div>
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This abstract has been ACCEPTED.</div>
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#0670: Transmissible Spongiform encephalopathy (TSE) animal and human TSE in North America update October 2009</div>
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Authors: T. Singeltary; Bacliff, TX/US</div>
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Title: Transmissible Spongiform encephalopathy (TSE) animal and human TSE in North America update October 2009</div>
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Body: Background</div>
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An update on atypical BSE and other TSE in North America. Please remember, the typical U.K. c-BSE, the atypical l-BSE (BASE), and h-BSE have all been documented in North America, along with the typical scrapie's, and atypical Nor-98 Scrapie, and to date, 2 different strains of CWD, and also TME. All these TSE in different species have been rendered and fed to food producing animals for humans and animals in North America (TSE in cats and dogs ?), and that the trading of these TSEs via animals and products via the USA and Canada has been immense over the years, decades.</div>
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Methods</div>
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12 years independent research of available data</div>
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Results</div>
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I propose that the current diagnostic criteria for human TSEs only enhances and helps the spreading of human TSE from the continued belief of the UKBSEnvCJD only theory in 2009. With all the science to date refuting it, to continue to validate this old myth, will only spread this TSE agent through a multitude of potential routes and sources i.e. consumption, medical i.e., surgical, blood, dental, endoscopy, optical, nutritional supplements, cosmetics etc.</div>
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Conclusion</div>
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I would like to submit a review of past CJD surveillance in the USA, and the urgent need to make all human TSE in the USA a reportable disease, in every state, of every age group, and to make this mandatory immediately without further delay. The ramifications of not doing so will only allow this agent to spread further in the medical, dental, surgical arena's. Restricting the reporting of CJD and or any human TSE is NOT scientific. Iatrogenic CJD knows NO age group, TSE knows no boundaries.</div>
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I propose as with Aguzzi, Asante, Collinge, Caughey, Deslys, Dormont, Gibbs, Gajdusek, Ironside, Manuelidis, Marsh, et al and many more, that the world of TSE Transmissible Spongiform Encephalopathy is far from an exact science, but there is enough proven science to date that this myth should be put to rest once and for all, and that we move forward with a new classification for human and animal TSE that would properly identify the infected species, the source species, and then the route.</div>
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Keywords: Transmissible Spongiform Encephalopathy Creutzfeldt Jakob Disease Prion</div>
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THURSDAY, AUGUST 17, 2017 </div>
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*** Monitoring the occurrence of emerging forms of Creutzfeldt-Jakob disease in the United States revisited 2017</div>
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Tuesday, March 20, 2018 </div>
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Variably protease-sensitive prionopathy (VPSPr), sporadic creutzfeldt jakob disease sCJD, the same disease, what if?</div>
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UNDAY, MARCH 10, 2019 </div>
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National Prion Disease Pathology Surveillance Center Cases Examined¹ Updated Feb 1, 2019 Variably protease-sensitive prionopathy VPSPr</div>
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wasted days and wasted nights...Freddy Fender</div>
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Terry S. Singeltary Sr.</div>
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Terry S. Singeltary Sr.http://www.blogger.com/profile/06986622967539963260noreply@blogger.com0tag:blogger.com,1999:blog-6404950019984350027.post-73045056180360259962019-09-18T14:22:00.000-07:002019-09-18T14:22:30.089-07:00USDA Modernizes Swine Slaughter Inspection for the First Time in Over 50 Years and TSE Prion Risk Factors<div style="background-color: white; font-family: arial; font-size: 13.3333px;">
USDA Modernizes Swine Slaughter Inspection for the First Time in Over 50 Years </div>
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Release & Contact Info Press Release Release No. 0139.19 Contact: USDA Press Email: <a href="mailto:press@oc.usda.gov" rel="noopener noreferrer" style="color: blue; cursor: pointer;">press@oc.usda.gov</a></div>
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WASHINGTON, September 17, 2019 — The U.S. Department of Agriculture (USDA) today announced a final rule to modernize swine slaughter inspection and bring it into the 21st century. For the first time in more than five decades, the USDA’s Food Safety and Inspection Service (FSIS) is modernizing inspection at market hog slaughter establishments with a goal of protecting public health while allowing for food safety innovations.</div>
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“This regulatory change allows us to ensure food safety while eliminating outdated rules and allowing for companies to innovate,” Secretary Sonny Perdue said. “The final rule is the culmination of a science-based and data-driven rule making process which builds on the food safety improvements made in 1997, when USDA introduced a system of preventive controls for industry. With this rule, FSIS will finally begin full implementation of that program in swine establishments.”</div>
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Background: The final rule has new requirements for microbial testing that apply to all swine slaughterhouses to demonstrate that they are controlling for pathogens throughout the slaughter system. Additionally, FSIS is amending its meat inspection regulations to establish a new inspection system for market hog establishments called the New Swine Slaughter Inspection System (NSIS).</div>
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In the final rule, FSIS amends the regulations to require all swine slaughter establishments to develop written sanitary dressing plans and implement microbial sampling to monitor process control for enteric pathogens that can cause foodborne illness. The final rule also allows market hog establishments to choose if they will operate under NSIS or continue to operate under traditional inspection.</div>
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FSIS will continue to conduct 100% inspection of animals before slaughter and 100% carcass-by-carcass inspection, as mandated by Congress. FSIS inspectors will also retain the authority to stop or slow the line as necessary to ensure that food safety and inspection are achieved. Under the NSIS, FSIS offline inspectors will conduct more food safety and humane handling verification tasks to protect the food supply and animal welfare.</div>
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To view the final rule, visit the FSIS website at: <a fg_scanned="1" href="http://go.usa.gov/xVPVK" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">go.usa.gov/xVPVK</a></div>
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<span style="color: #262626; font-family: Helvetica; font-size: 17px;">The new rule will end limits on how fast slaughterhouses can kill pigs. It will also shift responsibility for removing defective meat during the slaughtering process from government inspectors to plant workers. The USDA will still inspect live pigs and the final pork products.</span></div>
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<span style="color: #262626; font-family: Helvetica; font-size: 17px;"><a fg_scanned="1" href="https://www.ecowatch.com/trump-hog-slaughtering-rule-2640414342.html?rebelltitem=1#rebelltitem1" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://www.ecowatch.com/trump-hog-slaughtering-rule-2640414342.html?rebelltitem=1#rebelltitem1</a></span></div>
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As line speeds increase, meatpacking workers are in ever more danger Don't expect the Trump administration to improve conditions in this already brutal industry. Matt McConnell Opinion contributor </div>
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President Trump and his attack on our our safe guards from food to the environment and every thing in between for corporate greed will come back to haunt all of us in time.</div>
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the feds just released this statement and you should read this very carefully about the mad cow feed ban that never was, and still isn't, and why this is so important, since USDA APHIS ARS Scientist recent transmitted Chronic Wasting Disease CWD TSE Prion, BY ORAL ROUTES, to PIGS AND SHEEP. this is terrible news, and proves the mad cow feed ban never worked, especially since it really never existed;</div>
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ponder this; ***> Adriano Aguzzi...''We even showed that a prion AEROSOL will infect 100% of mice within 10 seconds of exposure''</div>
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FDA Reports on VFD Compliance</div>
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Before and after the current Veterinary Feed Directive (VFD) rules took full effect in January, 2017, the FDA focused primarily on education and outreach to help feed mills, veterinarians and producers understand and comply with the requirements. Since then, FDA has gradually increased the number of VFD inspections and initiated enforcement actions when necessary.</div>
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***> cattle, pigs, sheep, cwd, tse, prion, oh my!</div>
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***> In contrast, cattle are highly susceptible to white-tailed deer CWD and mule deer CWD in experimental conditions but no natural CWD infections in cattle have been reported (Sigurdson, 2008; Hamir et al., 2006). </div>
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<span style="font-family: arial, helvetica; font-size: x-small;">Sheep and cattle may be exposed to CWD via common grazing areas with affected deer but so far, appear to be poorly susceptible to mule deer CWD (Sigurdson, 2008). In contrast, cattle are highly susceptible to white-tailed deer CWD and mule deer CWD in experimental conditions but no natural CWD infections in cattle have been reported (Sigurdson, 2008; Hamir et al., 2006). It is not known how susceptible humans are to CWD but given that the prion can be present in muscle, it is likely that humans have been exposed to the agent via consumption of venison (Sigurdson, 2008). Initial experimental research suggests that human susceptibility to CWD is low and there may be a robust species barrier for CWD transmission to humans (Sigurdson, 2008), however the risk appetite for a public health threat may still find this level unacceptable.</span><div style="font-family: arial, helvetica; font-size: small;">
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<a href="https://assets.publishing.service.gov.uk/government/uploads/system/uploads/attachment_data/file/733407/DEFRA_QRA_TSE_in_cervids_June2018_v1.pdf" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://assets.publishing.service.gov.uk/government/uploads/system/uploads/attachment_data/file/733407/DEFRA_QRA_TSE_in_cervids_June2018_v1.pdf</a></div>
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cwd scrapie pigs oral routes</div>
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***> However, at 51 months of incubation or greater, 5 animals were positive by one or more diagnostic methods. Furthermore, positive bioassay results were obtained from all inoculated groups (oral and intracranial; market weight and end of study) suggesting that swine are potential hosts for the agent of scrapie. <*** </div>
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>*** Although the current U.S. feed ban is based on keeping tissues from TSE infected cattle from contaminating animal feed, swine rations in the U.S. could contain animal derived components including materials from scrapie infected sheep and goats. These results indicating the susceptibility of pigs to sheep scrapie, coupled with the limitations of the current feed ban, indicates that a revision of the feed ban may be necessary to protect swine production and potentially human health. <*** </div>
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***> Results: PrPSc was not detected by EIA and IHC in any RPLNs. All tonsils and MLNs were negative by IHC, though the MLN from one pig in the oral <6 5="" 6="" at="" by="" detected="" eia.="" examined="" group="" in="" intracranial="" least="" lymphoid="" month="" months="" of="" one="" pigs="" positive="" prpsc="" quic="" the="" tissues="" was="">6 months group, 5/6 pigs in the oral <6 4="" and="" group="" months="" oral="">6 months group. Overall, the MLN was positive in 14/19 (74%) of samples examined, the RPLN in 8/18 (44%), and the tonsil in 10/25 (40%). </6></6></div>
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***> Conclusions: This study demonstrates that PrPSc accumulates in lymphoid tissues from pigs challenged intracranially or orally with the CWD agent, and can be detected as early as 4 months after challenge. CWD-infected pigs rarely develop clinical disease and if they do, they do so after a long incubation period. </div>
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This raises the possibility that CWD-infected pigs could shed prions into their environment long before they develop clinical disease. </div>
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Furthermore, lymphoid tissues from CWD-infected pigs could present a potential source of CWD infectivity in the animal and human food chains. </div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">Friday, December 14, 2012</span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">DEFRA U.K. What is the risk of Chronic Wasting Disease CWD being introduced into Great Britain? A Qualitative Risk Assessment October 2012</span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">In the USA, under the Food and Drug Administration's BSE Feed Regulation (21 CFR 589.2000) most material (exceptions include milk, tallow, and gelatin) from deer and elk is prohibited for use in feed for ruminant animals. With regards to feed for non-ruminant animals, under FDA law, CWD positive deer may not be used for any animal feed or feed ingredients. For elk and deer considered at high risk for CWD, the FDA recommends that these animals do not enter the animal feed system. However, this recommendation is guidance and not a requirement by law.</span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">Animals considered at high risk for CWD include:</span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">1) animals from areas declared to be endemic for CWD and/or to be CWD eradication zones and</span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">2) deer and elk that at some time during the 60-month period prior to slaughter were in a captive herd that contained a CWD-positive animal.</span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">Therefore, in the USA, materials from cervids other than CWD positive animals may be used in animal feed and feed ingredients for non-ruminants.</span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">The amount of animal PAP that is of deer and/or elk origin imported from the USA to GB can not be determined, however, as it is not specified in TRACES. It may constitute a small percentage of the 8412 kilos of non-fish origin processed animal proteins that were imported from US into GB in 2011.</span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">Overall, therefore, it is considered there is a __greater than negligible risk___ that (nonruminant) animal feed and pet food containing deer and/or elk protein is imported into GB.</span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">There is uncertainty associated with this estimate given the lack of data on the amount of deer and/or elk protein possibly being imported in these products.</span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">36% in 2007 (Almberg et al., 2011). In such areas, population declines of deer of up to 30 to 50% have been observed (Almberg et al., 2011). In areas of Colorado, the prevalence can be as high as 30% (EFSA, 2011).</span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">The clinical signs of CWD in affected adults are weight loss and behavioural changes that can span weeks or months (Williams, 2005). In addition, signs might include excessive salivation, behavioural alterations including a fixed stare and changes in interaction with other animals in the herd, and an altered stance (Williams, 2005). These signs are indistinguishable from cervids experimentally infected with bovine spongiform encephalopathy (BSE).</span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">Given this, if CWD was to be introduced into countries with BSE such as GB, for example, infected deer populations would need to be tested to differentiate if they were infected with CWD or BSE to minimise the risk of BSE entering the human food-chain via affected venison.</span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">The rate of transmission of CWD has been reported to be as high as 30% and can approach 100% among captive animals in endemic areas (Safar et al., 2008).</span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">In summary, in endemic areas, there is a medium probability that the soil and surrounding environment is contaminated with CWD prions and in a bioavailable form. In rural areas where CWD has not been reported and deer are present, there is a greater than negligible risk the soil is contaminated with CWD prion.</span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">In summary, given the volume of tourists, hunters and servicemen moving between GB and North America, the probability of at least one person travelling to/from a CWD affected area and, in doing so, contaminating their clothing, footwear and/or equipment prior to arriving in GB is greater than negligible... For deer hunters, specifically, the risk is likely to be greater given the increased contact with deer and their environment. However, there is significant uncertainty associated with these estimates.</span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">Therefore, it is considered that farmed and park deer may have a higher probability of exposure to CWD transferred to the environment than wild deer given the restricted habitat range and higher frequency of contact with tourists and returning GB residents.</span></div>
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<a href="https://web.archive.org/web/20170404125557/http://webarchive.nationalarchives.gov.uk/20130822084033/http://www.defra.gov.uk/animal-diseases/files/qra_chronic-wasting-disease-121029.pdf" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">https://web.archive.org/web/20170404125557/http://webarchive.nationalarchives.gov.uk/20130822084033/http://www.defra.gov.uk/animal-diseases/files/qra_chronic-wasting-disease-121029.pdf</a></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">TUESDAY, APRIL 18, 2017 </span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">*** EXTREME USA FDA PART 589 TSE PRION FEED LOOP HOLE STILL EXIST, AND PRICE OF POKER GOES UP ***</span></div>
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<a fg_scanned="1" href="http://usdameatexport.blogspot.com/2017/04/extreme-usa-fda-part-589-tse-prion-feed.html" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">http://usdameatexport.blogspot.com/2017/04/extreme-usa-fda-part-589-tse-prion-feed.html</a></div>
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THURSDAY, AUGUST 08, 2019 </div>
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Raccoons accumulate PrPSc after intracranial inoculation with the agents of chronic wasting disease (CWD) or transmissible mink encephalopathy (TME) but not atypical scrapie</div>
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<a fg_scanned="1" href="https://chronic-wasting-disease.blogspot.com/2019/08/raccoons-accumulate-prpsc-after.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://chronic-wasting-disease.blogspot.com/2019/08/raccoons-accumulate-prpsc-after.html</a></div>
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FRIDAY, JULY 26, 2019 </div>
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Chronic Wasting Disease in Cervids: Implications for Prion Transmission to Humans and Other Animal Species</div>
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SUNDAY, SEPTEMBER 08, 2019 </div>
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Wisconsin Laboratory Testing Options for Prion Diseases, Wisconsin Neurologists, Clinical Laboratory Directors, and Infection Preventionists, Please Distribute Widely</div>
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Preparing for the Storm</div>
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<a fg_scanned="1" href="https://creutzfeldt-jakob-disease.blogspot.com/2019/09/wisconsin-laboratory-testing-options.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://creutzfeldt-jakob-disease.blogspot.com/2019/09/wisconsin-laboratory-testing-options.html</a></div>
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<span style="background-color: #dddd99; color: #333333;">The prions from the Texas deer were a lot harder to destroy than the ones from the Colorado elk. In fact, the guanidine barely damaged them at all. “We’ve never seen that before in any prion strain, which means that it has a completely different structure than we've ever seen before,” says Zabel. And that suggests that it might be a very different kind of chronic wasting disease. The researchers ran the same test on another Texas deer, with the same results.</span></div>
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THURSDAY, SEPTEMBER 05, 2019 </div>
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Unique Profile of The Texas CWD TSE Prion isolates, the TSE Prion CWD, Scrapie, BSE in Livestock, and CJD in Humans</div>
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<span style="font-size: 10pt;">WEDNESDAY, JULY 31, 2019 </span></div>
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The agent of transmissible mink encephalopathy passaged in sheep is similar to BSE-L</div>
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<a fg_scanned="1" href="https://transmissible-mink-encephalopathy.blogspot.com/2019/07/the-agent-of-transmissible-mink.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://transmissible-mink-encephalopathy.blogspot.com/2019/07/the-agent-of-transmissible-mink.html</a></div>
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<span style="color: #191919; font-family: Verdana, Arial, sans-serif; font-size: 15px;">FSIS [Docket No. FSIS–2019–0021] Notice of Request To Renew an Approved Information Collection: Specified Risk Materials Singeltary Submission</span></div>
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<span style="color: #191919; font-family: Verdana, Arial, sans-serif; font-size: 15px;"><a fg_scanned="1" href="https://specifiedriskmaterial.blogspot.com/2019/09/fsis-docket-no-fsis20190021-notice-of.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://specifiedriskmaterial.blogspot.com/2019/09/fsis-docket-no-fsis20190021-notice-of.html</a></span></div>
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<span style="font-size: 12pt;">MONDAY, FEBRUARY 25, 2019</span></div>
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<span style="font-size: 12pt;">MAD DOGS AND ENGLISHMEN BSE, SCRAPIE, CWD, CJD, TSE PRION A REVIEW 2019</span></div>
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<span style="font-size: 12pt;"><a fg_scanned="1" href="https://bseinquiry.blogspot.com/2019/02/mad-dogs-and-englishmen-bse-scrapie-cwd.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://bseinquiry.blogspot.com/2019/02/mad-dogs-and-englishmen-bse-scrapie-cwd.html</a></span></div>
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<span style="font-family: Helvetica;"><span style="font-size: 12px;">TUESDAY, JULY 10, 2018 </span></span></div>
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<span style="font-family: Helvetica;"><span style="font-size: 12px;">CONFIDENTIAL </span></span></div>
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<span style="font-family: Helvetica;"><span style="font-size: 12px;">IN CONFIDENCE </span></span></div>
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<span style="font-family: Helvetica;"><span style="font-size: 12px;">SPONGIFORM ENCEPHALOPATHY OF PIGS </span></span></div>
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<span style="font-family: Helvetica;"><span style="font-size: 12px;">*** ''but feeding of other ruminant protein, including scrapie-infected sheep, can continue to pigs.''</span></span></div>
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<span style="font-family: Helvetica;"><span style="font-size: 12px;">CONFIDENTIAL SPONGIFORM ENCEPHALOPATHY OF PIGS</span></span></div>
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<span style="font-family: Helvetica;"><span style="font-size: 12px;">Ref: Pigs10i</span></span></div>
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<a href="https://madporcinedisease.blogspot.com/2018/07/confidential-in-confidence-spongiform.html">https://madporcinedisease.blogspot.com/2018/07/confidential-in-confidence-spongiform.html</a></div>
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TUESDAY, SEPTEMBER 17, 2019 </div>
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Michigan House Bill 4687 State Legislators Turn To Draft Dodger Ted Nugent To Make Scientific Decisions over DNR on CWD TSE Prion</div>
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<a fg_scanned="1" href="https://chronic-wasting-disease.blogspot.com/2019/09/michigan-house-bill-4687-state.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://chronic-wasting-disease.blogspot.com/2019/09/michigan-house-bill-4687-state.html</a></div>
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<span style="font-size: 13.3333px;">SUNDAY, MARCH 10, 2019 </span></div>
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<span style="font-size: 13.3333px;">National Prion Disease Pathology Surveillance Center Cases Examined¹ Updated Feb 1, 2019 Variably protease-sensitive prionopathy VPSPr</span></div>
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<a fg_scanned="1" href="https://prionunitusaupdate.blogspot.com/2019/03/national-prion-disease-pathology.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://prionunitusaupdate.blogspot.com/2019/03/national-prion-disease-pathology.html</a></div>
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MONDAY, AUGUST 26, 2019 </div>
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Creutzfeldt Jakob Disease CJD, TSE, Prion, Surveillance Update August 2019</div>
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<a fg_scanned="1" href="https://creutzfeldt-jakob-disease.blogspot.com/2019/08/creutzfeldt-jakob-disease-cjd-tse-prion.html" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">https://creutzfeldt-jakob-disease.blogspot.com/2019/08/creutzfeldt-jakob-disease-cjd-tse-prion.html</a></div>
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Friendly Fire...Pass it forward...IATROGENIC TSE PRION</div>
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Wednesday, September 11, 2019 </div>
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Is the re-use of sterilized implant abutments safe enough? (Implant abutment safety) iatrogenic TSE Prion</div>
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Terry S. Singeltary Sr.</div>
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Bacliff, Texas USA 77518 <a href="mailto:flounder9@verizon.net" rel="noopener noreferrer" style="color: blue; cursor: pointer;">flounder9@verizon.net</a> Galveston Bay, on the bottom...</div>
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Terry S. Singeltary Sr.http://www.blogger.com/profile/06986622967539963260noreply@blogger.com0tag:blogger.com,1999:blog-6404950019984350027.post-83690399097916206242018-10-31T14:45:00.001-07:002018-11-05T08:40:38.221-08:00PIG HEART VALVES and Potential Iatrogenic Transmissible Spongiform Encephalopathy TSE Prion Disease in Humans, what if?<span style="font-family: "arial" , "helvetica"; font-size: 10pt;">Subject: PIG HEART VALVES</span><br />
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<span style="background-color: white; color: #1d2129; font-family: "helvetica" , "arial" , sans-serif; font-size: 14px;">Did you know that porcine heart valves are commonly used in human patients who require replacement valves? </span></div>
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<span style="background-color: white; color: #1d2129; font-family: "helvetica" , "arial" , sans-serif; font-size: 14px;">There is also hope that one day pigs could provide a step in helping to treat or to cure diabetes because of the similarities between the human and porcine pancreas. </span></div>
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<span style="background-color: white; color: #1d2129; font-family: "helvetica" , "arial" , sans-serif; font-size: 14px;">Read more about </span><a class="aolmail__58cn" href="https://www.facebook.com/hashtag/porktober?source=feed_text&__xts__%5B0%5D=68.ARBUKDMIpUMhF7nP3M8eu43lBifJ47fG3a4PG1VjtDtdKLn-YbGmsmzjxojzwOSdrB7rwzoK9zVWmNVRHMbXlhXgjx7PIPZaYTNhxZgp8Xiecb3tPFah_eh-cvjMlyrGR2U_eDRQ7DC0HflzfAPOvE1ujM6WU-uAaIlsdZkHnmJQfbO-BbnUc5r07eFCrL-vG9JmlY_kG4vrzwIGeNULmf1sEqU&__tn__=%2ANK-R" rel="noopener noreferrer" style="background-color: white; color: #365899; cursor: pointer; font-family: Helvetica, Arial, sans-serif; font-size: 14px; text-decoration-line: none;" target="_blank"><span class="aolmail__5afx" style="direction: ltr; font-family: inherit;"><span class="aolmail__58cl aolmail__5afz" style="font-family: inherit; unicode-bidi: isolate;">#</span><span class="aolmail__58cm" style="font-family: inherit;">PORKtober</span></span></a><span style="background-color: white; color: #1d2129; font-family: "helvetica" , "arial" , sans-serif; font-size: 14px;"> at </span><a href="https://www.porkbusiness.com/article/our-top-7-posts-trending-porktober?fbclid=IwAR1hFE5FgfsOq8-qir0pyl7GdZOhdWMPSjqU16KzHkpRrtJPLPPd7qjCCRg" rel="noopener noreferrer" style="background-color: white; color: #365899; cursor: pointer; font-family: Helvetica, Arial, sans-serif; font-size: 14px; text-decoration-line: none;" target="_blank">https://www.porkbusiness.com/…/our-top-7-posts-trending-por…</a></div>
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<a href="https://www.porkbusiness.com/article/how-quickly-can-you-provide-information-event-fad#comment-12013" rel="noopener noreferrer" style="color: #0096ef; cursor: pointer; text-decoration-line: none;" target="_blank">https://www.porkbusiness.com/article/how-quickly-can-you-provide-information-event-fad#comment-12013</a></div>
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<span style="font-size: 10pt; line-height: 1.22em;">O3 Experimental studies on prion transmission barrier and TSE pathogenesis in large animals </span></div>
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Rosa Bolea(1), Acín C(1)Marín B(1), Hedman C(1), Raksa H(1), Barrio T(1), Otero A(1), LópezPérez O(1), Monleón E(1),Martín-Burriel(1), Monzón M(1), Garza MC(1), Filali H(1),Pitarch JL(1), Garcés M(1), Betancor M(1), GuijarroIM(1), GarcíaM(1), Moreno B(1),Vargas A(1), Vidal E(2), Pumarola M(2), Castilla J(3), Andréoletti O(4), Espinosa JC(5), Torres JM(5), Badiola JJ(1). </div>
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<span style="font-size: 10pt; line-height: 1.22em;">1Centro de Investigación en Encefalopatías y Enfermedades Transmisibles Emergentes, VeterinaryFaculty, Universidad de Zaragoza; Zaragoza,Spain.2 RTA, Centre de Recerca en Sanitat Animal (CReSA, IRTA-UAB) 3 4 INRA, ÉcoleVétérinaire, Toulouse, France.5CIC bioGUNE, Prion researchlab, Derio, Spain CISA- INIA, Valdeolmos, Madrid 28130, Spain. </span></div>
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Experimental transmission of Transmissible Spongiform Encephalopathies (TSE) has been understood and related with several factors that could modify the natural development of these diseases. In fact, the behaviour of the natural disease does not match exactly in each animal, being modified by parameters such as the age at infection, the genotype, the breed or the causative strain. Moreover, different TSE strains can target different animal species or tissues, what complicate the prediction of its transmissibility when is tested in a different species of the origin source. The aim of the experimental studies in large animals is to homogenize all those factors, trying to minimize as much as possible variations between individuals. These effects can be flattened by experimental transmission in mice, in which a specific strain can be selected after several passages. With this objective, several experimental studies in large animals have been developed by the presenter research team. </div>
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Classical scrapie agent has been inoculated in cow, with the aim of demonstrate the resistance or susceptibility of this species to the first well known TSE; Atypical scrapie has been inoculated in sheep (using several routes of infection), cow and pig, with the objective of evaluating the potential pathogenicity of this strain; Classical Bovine Spongiform Encephalopathy (BSE) has been inoculated in goats aiming to demonstrate if the genetic background of this species could protect against this strain; goat BSE and sheep BSE have been inoculated in goats and pigs respectively to evaluate the effect of species barrier; and finally atypical BSE has been inoculated in cattle to assess the transmissibility properties of this newly introduced strain. </div>
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Once the experiments have been carried out on large animal species, a collection of samples from animals studied were inoculated in different types of tg mice overexpressing PrPcin order to study the infectivity of the tissues, and also were studied using PMCA. </div>
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In summary, the parameters that have been controlled are the species, the strain, the route of inoculation, the time at infection, the genotype, the age, and the environmental conditions. </div>
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To date, </div>
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***> eleven of the atypical scrapie intracerebrally inoculated sheep have succumbed to atypical scrapie disease; </div>
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***> six pigs to sheep BSE; </div>
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***> one cow to classical scrapie; </div>
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***> nine goats to goat BSE and </div>
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***> five goats to classical BSE. </div>
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***> PrPSC has been demonstrated in all cases by immunohistochemistry and western blot. </div>
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=====> <span style="font-size: 10pt; line-height: 1.22em;">PRION CONFERENCE 2018</span></div>
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SCRAPIE AND CWD HAS NOW BEEN FOUND TO TRANSMIT TO PIGS BY ORAL ROUTE...TSS</div>
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<span style="color: #333333; font-size: 17px; line-height: 1.22em;"><span style="font-family: "arial" , "helvetica" , sans-serif; line-height: 1.22em;">***> </span></span><span style="color: #333333; font-family: "helvetica neue" , "helvetica" , "arial" , sans-serif; font-size: 17px; line-height: 1.22em;">However, at 51 months of incubation or greater, 5 animals were positive by one or more diagnostic methods. Furthermore, positive bioassay results were obtained from all inoculated groups (oral and intracranial; market weight and end of study) suggesting that swine are potential hosts for the agent of scrapie. </span><span style="color: #333333; font-size: 17px; line-height: 1.22em;"><span style="font-family: "arial" , "helvetica" , sans-serif; line-height: 1.22em;"><***</span></span></div>
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<span style="color: #333333; font-size: 17px; line-height: 1.22em;"><span style="font-family: "arial" , "helvetica" , sans-serif; line-height: 1.22em;">>*** </span></span><span style="color: #333333; font-family: "helvetica neue" , "helvetica" , "arial" , sans-serif; font-size: 17px; line-height: 1.22em;">Although the current U.S. feed ban is based on keeping tissues from TSE infected cattle from contaminating animal feed, swine rations in the U.S. could contain animal derived components including materials from scrapie infected sheep and goats. These results indicating the susceptibility of pigs to sheep scrapie, coupled with the limitations of the current feed ban, indicates that a revision of the feed ban may be necessary to protect swine production and potentially human health.</span><span style="color: #333333; font-size: 17px; line-height: 1.22em;"><span style="font-family: "arial" , "helvetica" , sans-serif; line-height: 1.22em;"> <***</span></span></div>
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40,000 human heart valves a year from BSE herds</h3>
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<pre style="font-family: arial, helvetica; font-size: 10pt;">Sun, 3 Sep 2000. Unpublished Inquiry documents obtained by CJD activist <a href="mailto:flounder@WT.NET" style="color: #0096ef; cursor: pointer; text-decoration-line: none;">Terry S. Singeltary Sr.</a> of Bacliff, Texas
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<b>Opinion</b><span style="background-color: #fffdd3;"> (webmaster): Below are some shocking documents. Here is a British company preparing 40,000 heart valves a year from bovine pericardium, primarily for export, and they are not required to source this material from BSE-free herds even in peak epidemic years. It is amazing to watch health "authorities" grovelling on their bellies to wring petty concessions from middle management at obscure little companies. The main worry is not the practise of using 800 potentially infected cows a week for human heart transplant material but that the press or recipients will get wind of it, hurting business.</span><br />
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BSE wasn't the problem, it was awkward queries from importing countries like the US. The cows are stunned using brain penetration -- can't do anything about the chunks of bovine brain blasted into the circulatory system, it's the norm. Can't use younger lower-risk animals either, patch would not be big enough. It is fascinating to see the British government worrying about, but doing nothing, with pigs with BSE 10 years ago.<br />
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While scrapie was long used as an excuse for continuing with human use of BSE-tainted material, little sheep material was used medically. Bovine transplants, vaccines, insulin doeses, etc. are<span style="color: #990099;"> far more dangerous than dietary materia</span>l as injections, and are done on a very wide scale. So scrapie was never a valid analogy to BSE, as MAFF knew full well.<br />
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The British government deferred to the manufacturer's rep for an opinion on how contaminated pericardium might be, just as this appeared showing that this tissue is extremely dangerous:</div>
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CJD in a patient who received homograft [was it really?] tissue for tympanic membrane </h4>
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<pre style="font-family: arial, helvetica; font-size: 10pt;">Eur Arch Otorhinolaryngol 1990;247(4):199-201</pre>
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<span style="background-color: #fffdd3;">We report the case history of a 54-year-old man who developed a fatal neurological disorder 4 years after a successful tympanoplasty with homograft pericardium...</span><br />
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<pre style="font-size: 10pt;">Heidenhain variant of Creutzfeldt-Jakob disease in a patient who had bovine bioprosthetic valve implantation<div style="background-color: white; font-family: arial; font-size: small; white-space: normal;">
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<span style="font-size: 13.3333px;">Indian J Ophthalmol. 2016 Oct; 64(10): 767–769. doi: [10.4103/0301-4738.195003] PMCID: PMC5168920 PMID: 27905341 </span><br />
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<span style="font-size: 13.3333px;">Heidenhain variant of Creutzfeldt–Jakob disease in a patient who had bovine bioprosthetic valve implantation </span></div>
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<span style="font-size: 13.3333px;">Jehard Hashoul, Waleed Saliba,1 Irina Bloch,2 and Haneen Jabaly-Habib </span><br />
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<span style="font-size: 13.3333px;">Author information Article notes Copyright and License information Disclaimer </span><br />
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<span style="font-size: 13.3333px;">Creutzfeldt–Jakob disease (CJD) is a rare neurodegenerative disorder characterized by rapidly progressing dementia, general neurologic deterioration, and death. When the leading symptoms are visual disturbances, it is termed as the Heidenhain variant of CJD (HvCJD). CJD was reported following prion-contaminated pericardium transplants but never after bovine bioprosthetic cardiac valve. In this case report, we describe HvCJD in a patient who had a bovine bioprosthetic cardiac valve implant. An 82-year-old-woman was referred to neuro-ophthalmology clinic for unexplained visual loss that started 1 month previously. Medical history included aortic valve replacement with bovine bioprosthetic valve. On examination, best-corrected visual acuity was 20/120 in the right eye and 20/200 in the left eye; otherwise, the eye examination was normal. Humphrey visual fields revealed complete right homonymous hemianopsia. Magnetic resonance imaging (MRI) demonstrated nonspecific white matter changes. A week later, she was hospitalized due to memory impairment; repeated MRI and total body computed tomography scan showed no significant findings. </span><br />
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<span style="font-size: 13.3333px;">Electroencephalography recordings and extremely elevated cerebrospinal fluid tau protein were compatible with CJD. The patient died 3 weeks later; autopsy was not performed. The patient had HvCJD. Ophthalmologists being first to see these patients should be aware of this diagnosis. Contaminated bovine bioprosthetic valve might be another source for prion disease. Further research is required to establish this issue.</span><br />
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<span style="font-size: 13.3333px;">Creutzfeldt–Jakob disease (CJD) is the most common human prion disease with an incidence of 1 case per 1 million populations per year; it is a rare neurodegenerative disease associated with severe neuronal loss, spongiform changes, and accumulation of the abnormal prion protein. About 85% of CJD cases are sporadic CJD (sCJD), 5%–15% are familial CJD, and <1 3.9="" 30="" 70="" a="" about="" accounts="" advanced="" age="" and="" any="" are="" associated="" at="" been="" cases.="" cases="" cjd.="" cjd="" classic="" clinical="" cognitive="" decline="" dementia="" duration="" early-prominent="" even="" few="" for="" have="" heidenhain="" iatrogenic="" illness="" in="" includes="" is="" isolated="" it="" may="" mean="" months="" mv1="" myoclonic="" myoclonus="" of="" onset="" persist="" phenotype="" phenotypes="" precede="" presents="" progressive="" rapidly="" reported="" scjd="" severe="" short="" signs="" six="" span="" symptoms="" termed="" the="" variant.="" variant="" visual="" weeks="" when="" which="" with="" without=""></1></span><br />
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<span style="font-size: 13.3333px;">Go to: Case Report An 82-year-old Jewish woman, Ukrainian descendant, was referred to neuro-ophthalmology clinic for unexplained progressive visual loss over the past month with a significant deterioration in the last few days. The patients and her son denied any behavioral change or memory impairment at this point.</span><br />
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<span style="font-size: 13.3333px;">Medical history included hypertension and aortic valve replacement with bovine 19 mm bioprosthetic valve, performed 5 years before her current presentation.</span><br />
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<span style="font-size: 13.3333px;">On examination, her best-corrected visual acuity was 20/120 in the right eye and 20/200 in the left eye, pupillary reactions and eye movement were normal, and applanation tonometry was 11/11; after dilating the pupils, both eyes revealed nonsignificant cataract, normal optic disc and retina. Humphrey visual fields revealed complete right homonymous hemianopsia with bilateral macular involvement [Fig. 1]. Brain magnetic resonance imaging (MRI) demonstrated diffuse atrophic and nonspecific white matter changes along with small cystic lesions and anatomical distortion at the basal ganglia level, no cortical pathology [Fig. 2].</span></div>
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<span style="font-size: 13.3333px;">One week later, the patient was admitted to the hospital due to memory impairment; repeated complete blood count, chemistry and rheumatologic panel were within normal limits. Electroencephalography (EEG) revealed diffuse slowing and periodic sharp wave discharges along with triphasic wave complexes [Fig. 3]; repeated brain MRI and total body computed tomography showed no significant changes compared to previous studies; cerebrospinal fluid (CSF) revealed extremely elevated tau protein >1200 pg/ml compatible with CJD.</span></div>
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<span style="font-size: 13.3333px;">During her hospitalization, the patient developed rapid loss of short and long memory, disorientation, incontinence, and brisk reflexes. She was discharged home according to her family request and died 3 weeks later. Unfortunately, autopsy was not performed. </span><br />
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<span style="font-size: 13.3333px;">Our patient presented with progressive visual decline over 5 weeks, followed by rapidly progressive dementia and extrapyramidal tract dysfunction. The patient died 2.5 months after her presenting symptoms. According to the World Health Organization, the definite diagnosis of CJD is made by tissue diagnosis not performed in our patient.[2] Considering the disease course, rapidly progressive dementia (</span><span style="font-size: 13.3333px;">Human-to-human transmission of CJD was first reported in 1974 in a 55-year-old woman who developed symptoms 18 months after corneal transplantation from a donor who died of the disease. CJD transmission had been also reported following cadaveric dural graft transplants, radiographic embolization procedures with dura mater, liver transplants, administration of cadaveric human pituitary hormones, and by contaminated neurosurgical instruments. In 1989, a 54-year-old patient who received homograft pericardium for tympanic membrane closure 4 years earlier developed CJD.[3]</span></div>
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<span style="font-size: 13.3333px;">Although the definite pathogenesis is unknown, the primary component associated with the infection of CJD is an isoform of a normal host membrane glycoprotein called cellular prion protein (PrPC). The normal prion protein PrPC is protease sensitive, soluble and has a high α-helix content.[4] PrPC can undergo conversion into a conformationally altered isoform (scrapie prion protein [PrPSc]) widely believed to be the pathogenic agent of transmissible spongiform encephalopathies. The PrPSc is protease-resistant, insoluble, forms of amyloid fibrils and has high β-sheet content.[5]</span><br />
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<span style="font-size: 13.3333px;">The tissue-specific expression of PrPC is crucial considering that cells expressing high levels of PrPC bear a risk for conversion and accumulation of PrPSc. Quantitative and qualitative analysis of PrPC revealed that widespread tissue expression pattern of PrPC in bovine somatic tissues includes heart and myocardium;[6] it was found also in sheep,[7] hamster, and other nonhuman primates. Furthermore, expression of PrPSc was demonstrated in the hearts of transgenic mice as amyloid deposits that led to myocardial stiffness and cardiac disease.[8] PrPSc has been reported in the heart tissue of one sCJD patient.[9]</span><br />
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<span style="font-size: 13.3333px;">Prions exhibit an unusual resistance to conventional disinfection and sterilization methods; the procedures for sterilization of prion-contaminated medical instruments have been controversial for many years. Guidelines for sterilization that appear to be effective have been reported.[10] We presume that all of these guidelines may dismantle any biological tissue.</span><br />
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<span style="font-size: 13.3333px;">According to the manufacturer, our patient bioprosthetic aortic valve leaflets were made of bovine pericardium, and no information of bovine PrPSc screening of the pericardium leaflets was available.</span><br />
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<span style="font-size: 13.3333px;">We are unable to offer definite proof of the transmission of CJD by the bovine pericardium-made bioprosthetic aortic valve since autopsy was not performed. Still, the interval between the valve replacement surgery and the symptoms of the disease suggests that the pericardium was the conceivable vehicle for the transmission of the patient with CJD.</span><br />
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<span style="font-size: 13.3333px;">The patient's diagnosis was probable Heidenhain variant of CJD (HvCJD), suspected to be transmitted by the bovine valve transplantation never reported before. Bovine bioprosthetic valve made of pericardium might be another source for prion disease. Although this is a rare disease, ophthalmologists should be aware of the diagnosis being first to see the HvCJD of the CJD patients. Thorough medical history and good clinical examination and patients’ follow-up may lead to the correct investigation and diagnosis. Further research is required to establish this issue.</span><br />
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<span style="font-size: 13.3333px;">Keywords: Bovine bioprosthetic cardiac valve, Heidenhain variant of Creutzfeldt–Jakob disease, prion, unexplained visual loss</span></div>
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<span style="font-size: 13.3333px;"><a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5168920/" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5168920/</a></span></div>
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<pre><span style="font-family: "arial" , "helvetica" , sans-serif;"><span style="font-size: 13.3333px;">BSE offals used in cosmetics, toiletry and perfume industry Sun, 3 Sep 2000. </span></span></pre>
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<pre><span style="font-family: "arial" , "helvetica" , sans-serif;"><span style="font-size: 13.3333px;">Unpublished Inquiry documents obtained by CJD activist Terry S. Singeltary Sr. of Bacliff, Texas</span></span></pre>
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<pre><span style="font-family: "arial" , "helvetica" , sans-serif;">back then, i was getting things via Her <span style="font-size: 13.3333px;">Majesty Air Mail FOIA request, now they are online, if you can keep up with the different</span></span></pre>
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<pre><span style="font-family: "arial" , "helvetica" , sans-serif;"><a href="https://web.archive.org/web/20090505223320/http://www.bseinquiry.gov.uk/files/yb/1990/02/01014001.pdf" style="color: #0096ef; cursor: pointer; text-decoration-line: none;">https://web.archive.org/web/20090505223320/http://www.bseinquiry.gov.uk/files/yb/1990/02/01014001.pdf</a></span></pre>
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<pre><span style="font-family: "arial" , "helvetica" , sans-serif;"><a href="http://webarchive.nationalarchives.gov.uk/20080102182541/http://www.bseinquiry.gov.uk/files/yb/1990/01/29019001.pdf" style="color: #0096ef; cursor: pointer; text-decoration-line: none;">http://webarchive.nationalarchives.gov.uk/20080102182541/http://www.bseinquiry.gov.uk/files/yb/1990/01/29019001.pdf</a></span></pre>
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<pre><a href="http://webarchive.nationalarchives.gov.uk/20080103004803/http://www.bseinquiry.gov.uk/files/yb/1989/12/12008001.pdf" style="color: #0096ef; cursor: pointer; text-decoration-line: none;">http://webarchive.nationalarchives.gov.uk/20080103004803/http://www.bseinquiry.gov.uk/files/yb/1989/12/12008001.pdf</a></pre>
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<pre><a href="https://web.archive.org/web/20090506011945/http://www.bseinquiry.gov.uk/files/yb/1990/01/26020001.pdf" style="color: #0096ef; cursor: pointer; text-decoration-line: none;">https://web.archive.org/web/20090506011945/http://www.bseinquiry.gov.uk/files/yb/1990/01/26020001.pdf</a></pre>
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<pre><span style="font-family: "arial" , "helvetica" , sans-serif;"><span style="font-size: 13.3333px;">7 OF 10 LITTLE PIGGIES WENT ON TO DEVELOP BSE;
1: J Comp Pathol. 2000 Feb-Apr; 122(2-3): 131-43. Related Articles,
The neuropathology of experimental bovine spongiform encephalopathy in the pig.
Ryder SJ, Hawkins SA, Dawson M, Wells GA.
Veterinary Laboratories Agency Weybridge, Woodham Lane, New Haw, Addlestone, Surrey, KT15 3NB, UK.
In an experimental study of the transmissibility of BSE to the pig, seven of 10 pigs, infected at 1-2 weeks of age by
multiple-route parenteral inoculation with a homogenate of bovine brain from natural BSE cases developed lesions typical of
spongiform encephalopathy. The lesions consisted principally of severe neuropil vacuolation affecting most areas of the brain,
but mainly the forebrain. In addition, some vacuolar change was identified in the rostral colliculi and hypothalamic areas of
normal control pigs. PrP accumulations were detected immunocytochemically in the brains of BSE-infected animals. PrP
accumulation was sparse in many areas and its density was not obviously related to the degree of vacuolation. The patterns
of PrP immunolabelling in control pigs differed strikingly from those in the infected animals.
PMID: 10684682 [PubMed - indexed for MEDLINE]
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<pre><span style="font-family: "arial" , "helvetica" , sans-serif;"><span style="font-size: 13.3333px;"><a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?holding=npg&cmd=Retrieve&db=PubMed&list_uids=10684682&dopt=Abstract" style="cursor: pointer;">http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?holding=npg&cmd=Retrieve&db=PubMed&list_uids=10684682&dopt=Abstract</a></span></span></pre>
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<pre><a href="http://madporcinedisease.blogspot.com/2015/07/porcine-prion-protein-amyloid-or-mad.html" style="color: #0096ef; cursor: pointer; text-decoration-line: none;">http://madporcinedisease.blogspot.com/2015/07/porcine-prion-protein-amyloid-or-mad.html</a></pre>
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<pre>----Original Message-----</pre>
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<span style="font-family: "arial" , "helvetica"; font-size: 10pt; line-height: 1.22em; white-space: normal;">From: Terry Singeltary <<a href="mailto:flounder9@verizon.net" rel="noopener noreferrer" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">flounder9@verizon.net</a>> </span><br />
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<span style="font-family: "arial" , "helvetica"; font-size: 10pt; line-height: 1.22em; white-space: normal;">To: bse-l <bse- a="" href="mailto:l@lists.aegee.org" rel="noopener noreferrer" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">l@lists.aegee.org</bse-></span></div>
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Cc: cjdvoice <<a href="mailto:cjdvoice@yahoogroups.com" rel="noopener noreferrer" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">cjdvoice@yahoogroups..com</a>>; bloodcjd <<a href="mailto:bloodcjd@yahoogroups.com" rel="noopener noreferrer" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">bloodcjd@yahoogroups.com</a>><br />
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Sent: Fri, Apr 20, 2018 3:54 pm<br />
Subject: Scrapie Transmits To Pigs By Oral Route, what about the terribly flawed USA tse prion feed ban?<br />
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<div id="aolmail_aolmail_aolmail_aolmail_aolmail_AOLMsgPart_1.2.1_f124af85-5d60-497b-b08a-c6376bc44717" style="line-height: 1.22em;">
<span style="font-size: 10pt; line-height: 1.22em; white-space: normal;"><span style="color: black; font-family: "arial" , "helvetica"; font-size: x-small; line-height: 1.22em;"></span></span><br />
<div class="aolmail_aolmail_aolmail_aolmail_aolmail_aolReplacedBody" style="line-height: 1.22em;">
<span style="color: black; font-family: "arial" , "helvetica"; font-size: 10pt; line-height: 1.22em; white-space: normal;"><span style="color: black; font-family: "arial"; font-size: x-small; line-height: 1.22em;"><span style="color: #333333; font-family: "verdana" , "geneva" , "arial" , "helvetica" , sans-serif; line-height: 1.22em;"><strong style="line-height: 1.22em;">Research Project: </strong><a href="https://www.ars.usda.gov/research/project/?accnNo=432011" rel="noopener noreferrer" style="background-color: transparent; color: #4c2c92; cursor: pointer; line-height: 1.22em;" target="_blank">Pathobiology, Genetics, and Detection of Transmissible Spongiform Encephalopathies</a></span></span></span><br />
<span style="color: black; font-family: "arial" , "helvetica"; font-size: 10pt; line-height: 1.22em; white-space: normal;"><span style="color: black; font-family: "arial"; font-size: x-small; line-height: 1.22em;"><br /></span></span>
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<span style="color: black; font-family: "arial" , "helvetica"; font-size: 10pt; line-height: 1.22em; white-space: normal;"><span style="color: black; font-family: "arial"; font-size: x-small; line-height: 1.22em;"><span style="color: #333333; font-family: "verdana" , "geneva" , "arial" , "helvetica" , sans-serif; line-height: 1.22em;"><strong style="line-height: 1.22em;">Location: <a href="https://www.ars.usda.gov/midwest-area/ames/nadc/virus-and-prion-research/" id="aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_anch_62" rel="noopener noreferrer" style="background-color: transparent; color: #4c2c92; cursor: pointer; line-height: 1.22em;" target="_blank">Virus and Prion Research</a></strong></span></span></span></div>
<span style="color: black; font-family: "arial" , "helvetica"; font-size: 10pt; line-height: 1.22em; white-space: normal;"><span style="color: black; font-family: "arial"; font-size: x-small; line-height: 1.22em;"><span style="color: #333333; font-family: "verdana" , "geneva" , "arial" , "helvetica" , sans-serif; line-height: 1.22em;">
</span><span style="color: #333333; font-family: "helvetica neue" , "helvetica" , "arial" , sans-serif; font-size: 17px; line-height: 1.22em;"></span><b style="color: #333333; font-family: "Helvetica Neue", Helvetica, Arial, sans-serif; font-size: 17px; line-height: 1.22em;"><span style="color: navy; font-family: "arial" , "helvetica"; line-height: 1.22em;">2017 Annual Report</span></b><span style="color: #333333; font-family: "helvetica neue" , "helvetica" , "arial" , sans-serif; font-size: 17px; line-height: 1.22em;"></span></span></span><br />
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<span style="color: black; font-family: "arial" , "helvetica"; font-size: 10pt; line-height: 1.22em; white-space: normal;"><span style="color: black; font-family: "arial"; font-size: x-small; line-height: 1.22em;"><br style="line-height: 1.22em;" /></span></span>
<span style="color: black; font-family: "arial" , "helvetica"; font-size: 10pt; line-height: 1.22em; white-space: normal;"><span style="color: black; font-family: "arial"; font-size: x-small; line-height: 1.22em;"><strong style="line-height: 1.22em;">1a. Objectives (from AD-416):</strong></span></span><br />
<span style="color: black; font-family: "arial" , "helvetica"; font-size: 10pt; line-height: 1.22em; white-space: normal;"><span style="color: black; font-family: "arial"; font-size: x-small; line-height: 1.22em;">Objective 1: Investigate the mechanisms of protein misfolding in prion disease, including the genetic determinants of misfolding of the prion protein and the environmental influences on protein misfolding as it relates to prion diseases. Subobjective 1.A: Investigate the differences in the unfolded state of wild-type and disease associated prion proteins to better understand the mechanism of misfolding in genetic prion disease. Subobjective 1.B: Investigate the influence of metal ions on the misfolding of the prion protein in vitro to determine if environmental exposure to metal ions may alter disease progression. Objective 2: Investigate the pathobiology of prion strains in natural hosts, including the influence of prion source genotype on interspecies transmission and the pathobiology of atypical transmissible spongiform encephalopathies (TSEs). Subobjective 2.A: Investigate the pathobiology of atypical TSEs. Subobjective 2.B: Investigate the influence of prion source genotype on interspecies transmission. Objective 3: Investigate sampling methodologies for antemortem detection of prion disease, including the utility of blood sampling as a means to assess prion disease status of affected animals and the utility of environmental sampling for monitoring herd prion disease status. Subobjective 3.A: Investigate the utility of blood sampling as a means to assess prion disease status of affected animals. Subobjective 3.B: Investigate the utility of environmental sampling for monitoring herd prion disease status.</span></span></div>
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<span style="color: black; font-family: "arial" , "helvetica"; font-size: 10pt; line-height: 1.22em; white-space: normal;"><span style="color: black; font-family: "arial"; font-size: x-small; line-height: 1.22em;"><br style="line-height: 1.22em;" /></span></span>
<span style="color: black; font-family: "arial" , "helvetica"; font-size: 10pt; line-height: 1.22em; white-space: normal;"><span style="color: black; font-family: "arial"; font-size: x-small; line-height: 1.22em;"><strong style="line-height: 1.22em;">1b. Approach (from AD-416):</strong></span></span><br />
<span style="color: black; font-family: "arial" , "helvetica"; font-size: 10pt; line-height: 1.22em; white-space: normal;"><span style="color: black; font-family: "arial"; font-size: x-small; line-height: 1.22em;">The studies will focus on three animal transmissible spongiform encephalopathy (TSE) agents found in the United States: bovine spongiform encephalopathy (BSE); scrapie of sheep and goats; and chronic wasting disease (CWD) of deer, elk, and moose. The research will address sites of protein folding and misfolding as it relates to prion disease, accumulation of misfolded protein in the host, routes of infection, and ante mortem diagnostics with an emphasis on controlled conditions and natural routes of infection. Techniques used will include spectroscopic monitoring of protein folding/misfolding, clinical exams, histopathology, immunohistochemistry, and biochemical analysis of proteins. The enhanced knowledge gained from this work will help understand the underlying mechanisms of prion disease and mitigate the potential for unrecognized epidemic expansions of these diseases in populations of animals that could either directly or indirectly affect food animals.</span></span></div>
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<strong style="line-height: 1.22em;">3. Progress Report:</strong><br />
All 8 project plan milestones for FY17 were fully met. Research efforts directed toward meeting objective 1 of our project plan center around the production of recombinant prion protein from either bacteria or mammalian tissue culture systems and collection of thermodynamic data on the folding of the recombinant prion protein produced. Both bacterial and mammalian expression systems have been established. Thermodynamic data addressing the denatured state of wild-type and a disease associated variant of bovine prion protein has been collected and a manuscript is in preparation. In research pertaining to objective 2, all studies have been initiated and animals are under observation for the development of clinical signs. The animal studies for this objective are long term and will continue until onset of clinical signs. In vitro studies planned in parallel to the animals studies have similarly been initiated and are ongoing. Objective 3 of the project plan focuses on the detection of disease associated prion protein in body fluids and feces collected from a time course study of chronic wasting disease inoculated animals. At this time samples are being collected as planned and methods for analysis are under development.</div>
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<strong style="line-height: 1.22em;">4. Accomplishments</strong><br />
1. Showed that swine are potential hosts for the scrapie agent. A naturally occurring prion disease has not been recognized in swine, but the agent of bovine spongiform encephalopathy does transmit to swine by experimental routes. Swine are thought to have a robust species barrier when exposed to the naturally occurring prion diseases of other species, but the susceptibility of swine to the agent of sheep scrapie has not been thoroughly tested. ARS researchers at Ames, Iowa conducted this experiment to test the susceptibility of swine to U.S. scrapie isolates by intracranial and oral inoculation. Necropsies were done on a subset of animals at approximately 6 months post inoculation (PI): the time the pigs were expected to reach market weight. Remaining pigs were maintained and monitored for clinical signs of transmissible spongiform encephalopathies (TSE) until study termination at 80 months PI or when removed due to intercurrent disease. Brain samples were examined by multiple diagnostic approaches, and for a subset of pigs in each inoculation group, bioassay in mice expressing porcine prion protein. At 6 months PI, no evidence of scrapie infection was noted by any diagnostic method. However, at 51 months of incubation or greater, 5 animals were positive by one or more diagnostic methods. Furthermore, positive bioassay results were obtained from all inoculated groups (oral and intracranial; market weight and end of study) suggesting that swine are potential hosts for the agent of scrapie. Although the current U.S. feed ban is based on keeping tissues from TSE infected cattle from contaminating animal feed, swine rations in the U.S. could contain animal derived components including materials from scrapie infected sheep and goats. These results indicating the susceptibility of pigs to sheep scrapie, coupled with the limitations of the current feed ban, indicates that a revision of the feed ban may be necessary to protect swine production and potentially human health.</div>
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2. Determined that pigs naturally exposed to chronic wasting disease (CWD) may act as a reservoir of CWD infectivity. Chronic wasting disease is a naturally occurring, fatal, neurodegenerative disease of cervids. The potential for swine to serve as a host for the agent of CWD disease is unknown. The purpose of this study was to investigate the susceptibility of swine to the CWD agent following experimental oral or intracranial inoculation. Pigs were assigned to 1 of 3 groups: intracranially inoculated; orally inoculated; or non-inoculated. At market weight age, half of the pigs in each group were tested ('market weight' groups). The remaining pigs ('aged' groups) were allowed to incubate for up to 73 months post inoculation (MPI). Tissues collected at necropsy were examined for disease-associated prion protein (PrPSc) by multiple diagnostic methods. Brain samples from selected pigs were bioassayed in mice expressing porcine prion protein. Some pigs from each inoculated group were positive by one or more tests.. Bioassay was positive in 4 out of 5 pigs assayed. Although only small amounts of PrPSc were detected using sensitive methods, this study demonstrates that pigs can serve as hosts for CWD. Detection of infectivity in orally inoculated pigs using mouse bioassay raises the possibility that naturally exposed pigs could act as a reservoir of CWD infectivity. Currently, swine rations in the U.S. could contain animal derived components including materials from deer or elk. In addition, feral swine could be exposed to infected carcasses in areas where CWD is present in wildlife populations. The current feed ban in the U.S. is based exclusively on keeping tissues from TSE infected cattle from entering animal feeds. These results indicating the susceptibility of pigs to CWD, coupled with the limitations of the current feed ban, indicates that a revision of the feed ban may be necessary to protect swine production and potentially human health.</div>
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3. Developed a method for amplification and discrimination of the 3 forms of BSE in cattle. The prion protein (PrP) is a protein that is the causative agent of transmissible spongiform encephalopathies (TSEs). The disease process involves conversion of the normal cellular PrP to a pathogenic misfolded conformation. This conversion process can be recreated in the lab using a misfolding amplification process known as real-time quaking induced conversion (RT-QuIC). RT-QuIC allows the detection of minute amounts of the abnormal infectious form of the prion protein by inducing misfolding in a supplied substrate. Although RT-QuIC has been successfully used to detect pathogenic PrP with substrates from a variety of host species, prior to this work bovine prion protein had not been proven for its practical uses for RT-QuIC. We demonstrated that prions from transmissible mink encephalopathy (TME) and BSE-infected cattle can be detected with using bovine prion proteins with RT-QuIC, and developed an RT-QuIC based approach to discriminate different forms of BSE. This rapid and robust method, both to detect and discriminate BSE types, is of importance as the economic implications for different types of BSE vary greatly.</div>
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<strong style="line-height: 1.22em;">Review Publications</strong><br />
<em style="line-height: 1.22em;"><a href="https://www.ars.usda.gov/research/publications/publication/?seqNo115=333896" id="aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_anch_60" rel="noopener noreferrer" style="background-color: transparent; color: #4c2c92; cursor: pointer; line-height: 1.22em;" target="_blank">Hwang, S., Greenlee, J.J., Nicholson, E..M. 2017. Use of bovine recombinant prion protein and real-time quaking-induced conversion to detect cattle transmissible mink encephalopathy prions and discriminate classical and atypical L- and H-type bovine spongiform encephalopathy. PLoS One. 12(2):e0172391.</a></em></div>
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<em style="color: #333333; font-family: "Helvetica Neue", Helvetica, Arial, sans-serif; font-size: 17px; line-height: 1.22em;"><a href="https://www.ars.usda.gov/research/publications/publication/?seqNo115=328261" id="aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_anch_60" rel="noopener noreferrer" style="background-color: transparent; color: #4c2c92; cursor: pointer; line-height: 1.22em;" target="_blank">Moore, S., Kunkle, R., Greenlee, M., Nicholson, E., Richt, J., Hamir, A., Waters, W., Greenlee, J. 2016. Horizontal transmission of chronic wasting disease in reindeer. Emerging Infectious Diseases. 22(12):2142-2145. doi:10.3201/eid2212.160635.</a></em><span style="color: #333333; font-family: "helvetica neue" , "helvetica" , "arial" , sans-serif; font-size: 17px; line-height: 1.22em;"></span><div style="color: #333333; font-family: "Helvetica Neue", Helvetica, Arial, sans-serif; font-size: 17px; line-height: 1.22em; margin-bottom: 1em; margin-top: 1em; max-width: none;">
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<em style="color: #333333; font-family: "Helvetica Neue", Helvetica, Arial, sans-serif; font-size: 17px; line-height: 1.22em;"><a href="https://www.ars.usda.gov/research/publications/publication/?seqNo115=326785" id="aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_anch_60" rel="noopener noreferrer" style="background-color: transparent; color: #4c2c92; cursor: pointer; line-height: 1.22em;" target="_blank">Moore, S.J., West Greenlee, M.H., Smith, J.D., Vrentas, C.E., Nicholson, E.M., Greenlee, J.J. 2016. A comparison of classical and H-type bovine spongiform encephalopathy associated with E211K prion protein polymorphism in wild type and EK211 cattle following intracranial inoculation. Frontiers in Veterinary Science. 3:78.</a></em><span style="color: #333333; font-family: "helvetica neue" , "helvetica" , "arial" , sans-serif; font-size: 17px; line-height: 1.22em;"></span><div style="color: #333333; font-family: "Helvetica Neue", Helvetica, Arial, sans-serif; font-size: 17px; line-height: 1.22em; margin-bottom: 1em; margin-top: 1em; max-width: none;">
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<em style="color: #333333; font-family: "Helvetica Neue", Helvetica, Arial, sans-serif; font-size: 17px; line-height: 1.22em;"><a href="https://www.ars.usda.gov/research/publications/publication/?seqNo115=331559" id="aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_anch_60" rel="noopener noreferrer" style="background-color: transparent; color: #4c2c92; cursor: pointer; line-height: 1.22em;" target="_blank">Greenlee, J.J., Kunkle, R.A., Smith, J.D., West Greenlee, M.H. 2016. Scrapie in swine: a diagnostic challenge. Food Safety. 4(4):110-114.</a></em><span style="color: #333333; font-family: "helvetica neue" , "helvetica" , "arial" , sans-serif; font-size: 17px; line-height: 1.22em;"></span><div style="color: #333333; font-family: "Helvetica Neue", Helvetica, Arial, sans-serif; font-size: 17px; line-height: 1.22em; margin-bottom: 1em; margin-top: 1em; max-width: none;">
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<em style="color: #333333; font-family: "Helvetica Neue", Helvetica, Arial, sans-serif; font-size: 17px; line-height: 1.22em;"><a href="https://www.ars.usda.gov/research/publications/publication/?seqNo115=332347" id="aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_anch_60" rel="noopener noreferrer" style="background-color: transparent; color: #4c2c92; cursor: pointer; line-height: 1.22em;" target="_blank">Kondru, N., Manne, S., Greenlee, J., West Greenlee, H., Anantharam, V., Halbur, P., Kanthasamy, A., Kanthasamy, A. 2017. Integrated organotypic slice cultures and RT-QuIC (OSCAR) assay: implications for translational discovery in protein misfolding diseases. Scientific Reports. 7:43155. doi:10.1038/srep43155.</a></em><span style="color: #333333; font-family: "helvetica neue" , "helvetica" , "arial" , sans-serif; font-size: 17px; line-height: 1.22em;"></span><div style="color: #333333; font-family: "Helvetica Neue", Helvetica, Arial, sans-serif; font-size: 17px; line-height: 1.22em; margin-bottom: 1em; margin-top: 1em; max-width: none;">
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<em style="color: #333333; font-family: "Helvetica Neue", Helvetica, Arial, sans-serif; font-size: 17px; line-height: 1.22em;"><a href="https://www.ars.usda.gov/research/publications/publication/?seqNo115=327234" id="aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_anch_60" rel="noopener noreferrer" style="background-color: transparent; color: #4c2c92; cursor: pointer; line-height: 1.22em;" target="_blank">Mammadova, N., Ghaisas, S., Zenitsky, G., Sakaguchi, D.S., Kanthasamy, A.G., Greenlee, J.J., West Greenlee, M.H. 2017. Lasting retinal injury in a mouse model of blast-induced trauma. American Journal of Pathology. 187(7):1459-1472. doi:10.1016/j.ajpath.2017.03.005.</a></em><div style="line-height: 1.22em;">
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<span style="color: #333333; font-size: 17px; line-height: 1.22em;"><span style="font-family: "arial" , "helvetica" , sans-serif; line-height: 1.22em;">***> </span></span><span style="color: #333333; font-family: "helvetica neue" , "helvetica" , "arial" , sans-serif; font-size: 17px; line-height: 1.22em;">However, at 51 months of incubation or greater, 5 animals were positive by one or more diagnostic methods. Furthermore, positive bioassay results were obtained from all inoculated groups (oral and intracranial; market weight and end of study) suggesting that swine are potential hosts for the agent of scrapie. </span><span style="color: #333333; font-size: 17px; line-height: 1.22em;"><span style="font-family: "arial" , "helvetica" , sans-serif; line-height: 1.22em;"><***</span></span></div>
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<span style="color: #333333; font-size: 17px; line-height: 1.22em;"><span style="font-family: "arial" , "helvetica" , sans-serif; line-height: 1.22em;">>*** </span></span><span style="color: #333333; font-family: "helvetica neue" , "helvetica" , "arial" , sans-serif; font-size: 17px; line-height: 1.22em;">Although the current U.S. feed ban is based on keeping tissues from TSE infected cattle from contaminating animal feed, swine rations in the U.S. could contain animal derived components including materials from scrapie infected sheep and goats. These results indicating the susceptibility of pigs to sheep scrapie, coupled with the limitations of the current feed ban, indicates that a revision of the feed ban may be necessary to protect swine production and potentially human health.</span><span style="color: #333333; font-size: 17px; line-height: 1.22em;"><span style="font-family: "arial" , "helvetica" , sans-serif; line-height: 1.22em;"> <***</span></span></div>
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THE Aug. 1997 mad cow feed ban was/is a joke, BSE surveillance also was proven to be terribly flawed, along with BSE testing, shown to be flawed as well. </div>
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ALSO, WHAT ABOUT CWD TRANSMITTING TO PIGS AS WELL, AND MAD CAMEL DISEASE NOW, BIG OUTBREAK, NOT SPONTANEOUS, WHAT ABOUT THAT, and the feed ban concern there as well? AND what about Scrapie transmission to the Macaque recently. seems the tse prion poker continue to goes up. very worrying...terry</div>
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please see these facts below...thank you///</div>
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<span style="line-height: 1.22em;"><span style="line-height: 1.22em;"><span style="line-height: 1.22em;">***> CWD TO PIGS <***</span></span></span></div>
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<span style="line-height: 1.22em;"><span style="line-height: 1.22em;"><span style="line-height: 1.22em;">Research Project: TRANSMISSION, DIFFERENTIATION, AND PATHOBIOLOGY OF TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES</span></span></span></div>
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<span style="line-height: 1.22em;">Location: Virus and Prion Research</span></div>
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<span style="line-height: 1.22em;">Title: Disease-associated prion protein detected in lymphoid tissues from pigs challenged with the agent of chronic wasting disease</span></div>
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<span style="line-height: 1.22em;">Author item Moore, Sarah item Kunkle, Robert item Kondru, Naveen item Manne, Sireesha item Smith, Jodi item Kanthasamy, Anumantha item West Greenlee, M item Greenlee, Justin</span></div>
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<span style="line-height: 1.22em;">Submitted to: Prion Publication Type: Abstract Only Publication Acceptance Date: 3/15/2017 Publication Date: N/A Citation: N/A Interpretive Summary:</span></div>
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<span style="line-height: 1.22em;">Technical Abstract: Aims: Chronic wasting disease (CWD) is a naturally-occurring, fatal neurodegenerative disease of cervids. We previously demonstrated that disease-associated prion protein (PrPSc) can be detected in the brain and retina from pigs challenged intracranially or orally with the CWD agent. In that study, neurological signs consistent with prion disease were observed only in one pig: an intracranially challenged pig that was euthanized at 64 months post-challenge. The purpose of this study was to use an antigen-capture immunoassay (EIA) and real-time quaking-induced conversion (QuIC) to determine whether PrPSc is present in lymphoid tissues from pigs challenged with the CWD agent.</span></div>
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<span style="line-height: 1.22em;">Methods: At two months of age, crossbred pigs were challenged by the intracranial route (n=20), oral route (n=19), or were left unchallenged (n=9). At approximately 6 months of age, the time at which commercial pigs reach market weight, half of the pigs in each group were culled (<6 challenge="" groups="" month="" pigs="" remaining="" the="">6 month challenge groups) were allowed to incubate for up to 73 months post challenge (mpc). The retropharyngeal lymph node (RPLN) was screened for the presence of PrPSc by EIA and immunohistochemistry (IHC). The RPLN, palatine tonsil, and mesenteric lymph node (MLN) from 6-7 pigs per challenge group were also tested using EIA and QuIC.</6></span></div>
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<span style="line-height: 1.22em;">Results: PrPSc was not detected by EIA and IHC in any RPLNs. All tonsils and MLNs were negative by IHC, though the MLN from one pig in the oral <6 5="" 6="" at="" by="" detected="" eia.="" examined="" group="" in="" intracranial="" least="" lymphoid="" month="" months="" of="" one="" pigs="" positive="" prpsc="" quic="" the="" tissues="" was="">6 months group, 5/6 pigs in the oral <6 4="" and="" group="" months="" oral="">6 months group. Overall, the MLN was positive in 14/19 (74%) of samples examined, the RPLN in 8/18 (44%), and the tonsil in 10/25 (40%). Conclusions:</6></6></span></div>
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<span style="line-height: 1.22em;">This study demonstrates that PrPSc accumulates in lymphoid tissues from pigs challenged intracranially or orally with the CWD agent, and can be detected as early as 4 months after challenge.</span></div>
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<span style="line-height: 1.22em;">CWD-infected pigs rarely develop clinical disease and if they do, they do so after a long incubation period. This raises the possibility that CWD-infected pigs could shed prions into their environment long before they develop clinical disease.</span></div>
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<span style="line-height: 1.22em;">Furthermore, lymphoid tissues from CWD-infected pigs could present a potential source of CWD infectivity in the animal and human food chains.</span></div>
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<span style="line-height: 1.22em;">CONFIDENTIAL</span></div>
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<span style="line-height: 1.22em;">Subject: CONFIDENTIAL IN CONFIDENCE SPONGIFORM ENCEPHALOPATHY OF PIGS</span><br />
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<span style="line-height: 1.22em;">*** ''but feeding of other ruminant protein, including scrapie-infected sheep, can continue to pigs.''</span><br />
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CONFIDENTIAL SPONGIFORM ENCEPHALOPATHY OF PIGS<br />
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CONFIDENTIAL<br />
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Ref: Pigs10i<br />
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IN CONFIDENCE<br />
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From Dr. H Pickles Med ISD/3<br />
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Date 10 September 1990<br />
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Copy: Dr G Jones Mr D Hagger Mr T Murray (o/r) Dr D Harper Dr Richardson Mrs Shersby<br />
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SPONGIFORM ENCEPHALOPATHY OF PIGS<br />
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1. There has been a preliminary meeting of the Tyrrell committee today to discuss the significance of the pig experiment in the light of other evidence, for example on feline spongiform encephalopathy.<br />
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2. The preliminary conclusions were:<br />
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we now know pigs are capable of expressing spongiform encephalopathy. Previously this had been doubted. </div>
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the clinical picture in pigs exposed to agent by these doses/routes is fairly distinctive and unlikely to have gone unrecognised.<br />
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even so improved monitoring/surveillance of neurological disease in older pigs should be considered. </div>
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feeding of the "specified offal" (ie nervous/lymphoid tissue from cattle) should no longer be permitted, to pigs or to any other species.<br />
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*** but feeding of other ruminant protein, including scrapie-infected sheep, can continue to pigs. </div>
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if one natural field case of spongiform encephalopathy were described in a pig, we would need a ban on offal from for human consumption.<br />
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we cannot rule out the possibility that unrecognised subclinical spongiform encephalopathy could be present in British pigs though there is no evidence for this: only with parenteral/implantable pharmaceuticals/devices is the theoretical risk to humans of sufficient concern to consider any action.<br />
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whilst any such action on pharmaceuticals/devices is for others to decide, this group (which includes 4 key members of the CSM group) suggests non-UK sources should now be used, at least for "high risk" pharmaceuticals and devices (ie for those from nervous or RE System)<br />
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3. The full committee will meet on the 19th to confirm these conclusions, to review experimental protocols of transmission experiments, to reconsider the cat position in the light of additional cases and to consider scrapie in sheep and goats. In view of Mr Gummer's earlier commitments, we assume he willI want to go public on the pig soon after, so the Tyrrell committee will also prepare a brief written statement.<br />
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4. You may want to consider with the MCA and the Medical Device Agency what preparatory action is appropriate in anticipation of the formal advice from the Tyrrell group. The CSM subgroup not due to meet until the 31 October.<br />
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Hilary Pickles Room 414 Eileen House Ext: 22832<br />
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<span style="line-height: 1.22em;">EXPERIMENTAL PORCINE SPONGIFORM ENCEPHALOPATHY</span></div>
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<span style="line-height: 1.22em;">While this clearly is a cause for concern we should not jump to the conclusion that this means that pigs will necessarily be infected by bone and meat meal fed by the oral route as is the case with cattle. ...</span></div>
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<a href="http://web.archive.org/web/20031026000118/www.bseinquiry..gov.uk/files/yb/1990/08/23004001.pdf" rel="noopener noreferrer" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">http://web.archive.org/web/20031026000118/www.bseinquiry.gov.uk/files/yb/1990/08/23004001.pdf</a></div>
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<span style="line-height: 1.22em;">we cannot rule out the possibility that unrecognised subclinical spongiform encephalopathy could be present in British pigs though there is no evidence for this: only with parenteral/implantable pharmaceuticals/devices is the theoretical risk to humans of sufficient concern to consider any action.</span></div>
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<a href="http://web.archive.org/web/20030822031154/www.bseinquiry..gov.uk/files/yb/1990/09/10007001.pdf" rel="noopener noreferrer" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">http://web.archive.org/web/20030822031154/www.bseinquiry.gov.uk/files/yb/1990/09/10007001.pdf</a><br />
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<span style="line-height: 1.22em;">Our records show that while some use is made of porcine materials in medicinal products, the only products which would appear to be in a hypothetically ''higher risk'' area are the adrenocorticotrophic hormone for which the source material comes from outside the United Kingdom, namely America China Sweden France and Germany. The products are manufactured by Ferring and Armour. A further product, ''Zenoderm Corium implant'' manufactured by Ethicon, makes use of porcine skin - which is not considered to be a ''high risk'' tissue, but one of its uses is described in the data sheet as ''in dural replacement''. This product is sourced from the United Kingdom.....</span></div>
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<a href="http://web.archive.org/web/20030822054419/www.bseinquiry..gov.uk/files/yb/1990/09/21009001.pdf" rel="noopener noreferrer" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">http://web.archive.org/web/20030822054419/www.bseinquiry.gov.uk/files/yb/1990/09/21009001.pdf</a><br />
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<span style="line-height: 1.22em;">snip...see much more here ;</span></div>
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<span style="line-height: 1.22em;">WEDNESDAY, APRIL 05, 2017</span></div>
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<span style="line-height: 1.22em;">Disease-associated prion protein detected in lymphoid tissues from pigs challenged with the agent of chronic wasting disease</span></div>
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<a href="http://chronic-wasting-disease.blogspot.com/2017/04/disease-associated-prion-protein.html" rel="noopener noreferrer" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">http://chronic-wasting-disease.blogspot.com/2017/04/disease-associated-prion-protein.html</a><br />
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<span style="line-height: 1.22em;">WEDNESDAY, APRIL 05, 2017</span></div>
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<span style="line-height: 1.22em;">*** Disease-associated prion protein detected in lymphoid tissues from pigs challenged with the agent of chronic wasting disease ***</span></div>
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<span style="line-height: 1.22em;"><a href="http://chronic-wasting-disease.blogspot.com/2017/04/disease-associated-prion-protein.html" rel="noopener noreferrer" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">http://chronic-wasting-disease.blogspot.com/2017/04/disease-associated-prion-protein.html</a> </span><br />
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<span style="line-height: 1.22em;"><span style="font-family: "georgia";"><span style="font-size: 13.3333px; white-space: normal;">FRIDAY, APRIL 20, 2018 </span></span></span></div>
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<span style="line-height: 1.22em;"><span style="font-family: "georgia";"><span style="font-size: 13.3333px; white-space: normal;">Scrapie Transmits To Pigs By Oral Route, what about the terribly flawed USA tse prion feed ban?</span></span></span></div>
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<span style="line-height: 1.22em;"><span style="font-family: "georgia";"><span style="font-size: 13.3333px; white-space: normal;"><a href="http://scrapie-usa.blogspot.com/2018/04/scrapie-transmits-to-pigs-by-oral-route.html" style="color: #0096ef; cursor: pointer; text-decoration-line: none;">http://scrapie-usa.blogspot.com/2018/04/scrapie-transmits-to-pigs-by-oral-route.html</a></span></span></span><br />
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<span style="font-family: "arial" , sans-serif; line-height: 1.22em;">WEDNESDAY, JULY 11, 2018 </span></div>
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<span style="font-family: "arial" , sans-serif; line-height: 1.22em;">CONFIDENTIAL IN CONFIDENCE SPONGIFORM ENCEPHALOPATHY OF PIGS FDA EMERGENCY REQUEST FOR RULE CHANGE USA Section 21 C.F.R. 589.2000</span></div>
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<span style="font-family: "arial" , sans-serif; line-height: 1.22em;"><a href="http://transmissiblespongiformencephalopathy.blogspot.com/2018/07/confidential-in-confidence-spongiform.html" rel="noopener noreferrer" style="color: purple; cursor: pointer; line-height: 1.22em;" target="_blank">http://transmissiblespongiformencephalopathy.blogspot.com/2018/07/confidential-in-confidence-spongiform.html</a></span><br />
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<span style="font-family: "arial" , sans-serif; font-size: 10pt; line-height: 1.22em;">TUESDAY, JULY 10, 2018</span></div>
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<span style="font-family: "arial" , sans-serif; font-size: 10pt; line-height: 1.22em;">CONFIDENTIAL IN CONFIDENCE SPONGIFORM ENCEPHALOPATHY OF PIGS</span></div>
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<span style="font-family: "arial" , sans-serif; font-size: 10pt; line-height: 1.22em;">*** ''but feeding of other ruminant protein, including scrapie-infected sheep, can continue to pigs.''</span></div>
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<span style="font-family: "arial" , sans-serif; font-size: 10pt; line-height: 1.22em;">CONFIDENTIAL SPONGIFORM ENCEPHALOPATHY OF PIGS</span></div>
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<span style="font-family: "arial" , sans-serif; font-size: 10pt; line-height: 1.22em;"><a href="http://madporcinedisease.blogspot.com/2018/07/confidential-in-confidence-spongiform.html" rel="noopener noreferrer" style="color: purple; cursor: pointer; line-height: 1.22em;" target="_blank">http://madporcinedisease.blogspot.com/2018/07/confidential-in-confidence-spongiform.html</a></span><br />
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<pre><div class="aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="background-attachment: initial; background-color: white; background-repeat: initial; line-height: 1.22em; margin: 0in 0in 0.0001pt;">
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<span style="color: #29303b; font-family: "arial"; font-size: xx-small; white-space: normal;">Porcine prion protein amyloid </span><span style="white-space: normal;">
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Per Hammarstr€om and Sofie Nystr€om* IFM-Department of Chemistry; Link€oping University; Link€oping, Sweden<br />
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ABSTRACT.<br />
Mammalian prions are composed of misfolded aggregated prion protein (PrP) with amyloid-like features.</div>
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Prions are zoonotic disease agents that infect a wide variety of mammalian species including humans. Mammals and by-products thereof which are frequently encountered in daily life are most important for human health. It is established that bovine prions (BSE) can infect humans while there is no such evidence for any other prion susceptible species in the human food chain (sheep, goat, elk, deer) and largely prion resistant species (pig) or susceptible and resistant pets (cat and dogs, respectively). PrPs from these species have been characterized using biochemistry, biophysics and neurobiology. Recently we studied PrPs from several mammals in vitro and found evidence for generic amyloidogenicity as well as cross-seeding fibril formation activity of all PrPs on the human PrP sequence regardless if the original species was resistant or susceptible to prion disease. Porcine PrP amyloidogenicity was among the studied. Experimentally inoculated pigs as well as transgenic mouse lines overexpressing porcine PrP have, in the past, been used to investigate the possibility of prion transmission in pigs. The pig is a species with extraordinarily wide use within human daily life with over a billion pigs harvested for human consumption each year. Here we discuss the possibility that the largely prion disease resistant pig can be a clinically silent carrier of replicating prions.<br />
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KEYWORDS. prion, pig, amyloid fibril, misfolding, transmissibility, seeding, TSE, prion strain, strain adaptation<br />
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snip...<br />
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What about pigs?<br />
In several recent papers which in our view have not received sufficient attention the notion of prion resistant pigs was challenged by generation of transgenic mice with knocked out endogenous PrP and overexpressed PoPrP. Different lines of tgPoPrP mouse were proven to be susceptible to clinical disease triggered by a variety of prion strains, suggesting that the surrogate host species (mouse) and prion strain are more important than what PrP sequence it expresses for neurotoxicity to commence. In more detail, Torres and colleagues experimentally subjected transgenic mouse lines expressing porcine PrP to a number of different TSE isolates.24-26 Their studies demonstrate that prion infection is strain specific when porcine PrP is overexpressed (4x) and used as in vivo substrate. PoTg001 mice inoculated with classical scrapie, regardless of donor genotype, resisted prion disease both at first and second passage (Fig. 3b). On the other hand, Nor98 scrapie (Atypical scrapie) as well as BSE from both cattle and BoTg mouse model resulted in clinical disease in the PoTg001 mice. However, in the first generation, disease progression was slow. Incubation time until death was as long as 600 d and the hit rate was low. This indicates that disease has barely developed by the time the mice reach their natural life span limit which in this study was set to 650 d Already in the second passage the hit rate was 100 % and the incubation time was cut in half (Fig. 3b). No further shortening of incubation time was observed upon third passage. This shows that PoPrP is capable of forming infectious and neurotoxic prions in vivo if triggered by a compatible prion strain and if given enough time to develop. Both BSE and Nor98 rapidly adapts to the PoPrP host sequence, resulting in higher penetrance as well as in markedly shorter life span already in the second passage, well within the limits of normal life span for a mouse.<br />
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There are several crucial variables which impact the susceptibility of prion diseases and transmission studies.27 PrP sequence of host, PrP sequence of prion, prion strain, prion dosage, PrP expression level of host, host genetic background, route of transmission and neuroinvasiveness if peripherally infected.28 Importantly the PrP expression level corresponds to the rate of prion disease onset.1 This likely reflects 2 converging variables: a) PrP as a substrate to the prion misfolding reaction i.e. selfcatalyzed conversion and b) PrP as a mediator of neurotoxicity through interactions with misfolded PrP within prions.<br />
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The non-homologous recPrPs presented here and in,12 easily adapt to each other and form amyloid fibrils in accordance with what is seen in vivo when inoculum composed of BoPrP used to challenge mice expressing PoPrP (Fig. 3b).24-26 A review of the literature showed that BSE strains have a high degree of penetrance in both experimental and accidental transmission. Over 50% of the species reported to be susceptible to prion disease were infected by a BSE strain.19 Recent data form our lab shows that the promiscuity of BoPrP fibrils holds true also in the case of recombinant in vitro experiments. When cross-seeding human, bovine, porcine, feline and canine PrPs with any of the other, the recBoPrP seed outcompetes the other seeds in all instances except when the HuPrP acted as substrate (Data not shown). In this case recPoPrP fibrils have the highest seeding efficiency (Fig. 1). These findings in combination with the Torres experiments,24-26 implicate that a PoPrP substrate in vivo (in pigs) could adapt to an amyloidogenic prion strain of bovine or ovine prion disease and hence replicate in the new host.<br />
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For adaptation of experimental strains through multiple passages, donors are selected based on neurotoxicity (that is on TSE disease phenotype) not on basis of amyloid fibril formation. Hence the traits of transmissible amyloidotypic prion strains may be largely unexplored if these strains require more time to transform to neurotoxic strains e.g. as proposed by Baskakov’s model of deformed templating.8 There is experimental evidence for BSE transmission into pig via parenteral routes.16 with an incubation period of 2–3 years, well within what is to be considered normal lifespan. For a breeding sow in industrial scale pig farming that is 3–5 y (Bojne Andersson, personal communication).29,30 In small scale and hobby farming both sows and boars may be kept significantly longer. Collinge and Clarke.31 describe how prion titers reach transmissibility levels well before the prion burden is high enough to be neurotoxic and cause clinical disease. It is known that prion strains need time and serial passages to adapt. Knowing that pigs in modern farming are rarely kept for enough time for clinical signs to emerge in prion infected pigs it is important to be vigilant if there is a sporadic porcine spongiform encephalopathy (PSE) as has been seen in cattle (BASE) and sheep (Nor98). Hypothetically such a sporadic and then infectious event could further adapt and over a few generations have reached the point where clinical PSE is established within the time frame where pigs are being slaughtered for human consumption (Fig. 4).<br />
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FIGURE 4. Potential prion strain adaptation in pig. The red horizontal gradient indicates the hietherto unkown prion toxicity tolerance threshold for pigs, the blue vertical line indicates normal slaughter age for industrial pig farming, the green vertical line indicates the normal lifespan of a breeding sow in industrial scale pig farming, orange areas indicate window of neurotoxic prions before onset of clinical disease (dark orange indicates subclinical BSE as reported by Wells et al,16 pale orange indicate hypothetic outcome of PSE and strain adaptation. On the outmost right a potential subclinical sporadic PSE.<br />
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USE OF MATERIALS DERIVED FROM PIG IN VIEW OF PORCINE PrP AMYLOID<br />
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The pig is the most versatile species used by humans for food and other applications. Over 1,5 billion pigs are slaughtered each year worldwide for human use.32 Besides juicy pork sirloin other parts from pig are used for making remarkably diverse things such as musical instruments, china, leather, explosives, lubricants etc. Pig offal is used for human medicine, e.g., hormone preparations such as insulin and cerebrolysin, in xenographs, sutures, heparin and in gelatin for drug capsules.33,34<br />
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And that means not only pork, it means your pigskin wallet, catgut surgical suture...in tallow, in butter. It is undoubtedly in the blood supply. DC Gajdusek (From R. Rhodes ''Deadly Feast'' 35)<br />
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While the late Carleton Gajdusek had strong views in diverse areas of prion biology, according to journalist Richard Rhodes,35 he was correct on his prediction on BSE prions (vCJD) in the blood supply18 (see text box above). An opinionated scientist can sometimes be ignored due to a judgment of character and Gajdusek was certainly provocative. Notwithstanding society should remain vigilant on the possibility that Gajdusek was also prophetic on porcine prions given the exceptionally wide spread use of pigs in everyday human life and medicine.<br />
As discussed previously it is currently not established what relations transmissible neurotoxic prion strains and amyloid morphotypic mature APrP strains have. Given the hypotheses that amyloidotypic PrP conformations can transmit with low neurotoxicity.7,36 it is interesting to reflect on possible implications. Pigs are slaughtered at 6–8 months of age. Because amyloid deposition is associated with old age, this is likely far too young for spontaneous development of APrP amyloid from PoPrP as well as other amyloidogenic proteins. From the perspective of seeded amyloidogenesis it is however a potential ideal case for highly transmissible titers of APrP (Fig. 4). In such a scenario the potential of porcine prions constitutes the perfect storm, clinically silent due to neurotoxic resistance and with high titers of transmissibility. When it comes to prions CNS material is most heavily infected.<br />
In addition, however, fat tissue (to make lard and tallow) is known to harbor extraordinary amounts of amyloid in systemic amyloidoses.37 Amyloid fibrils of misfolded large proteins (AA, AL, ATTR) are notoriously hydrophobic due to the abnormal exposure of hydrophobic residues which <span style="font-family: "arial" , "helvetica"; font-size: 10pt; line-height: 1.22em;">normally in the folded structure being hidden in the protein core. The amyloid accumulation in fat tissue is likely a phase-separation from a rather hydrophilic environment in circulation toward the hydrophobic environment provided by adipocytes. Adipose tissue could in addition represent an in vivo environment well suitable for fibril formation. </span><br />
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<span style="line-height: 1.22em;">In analysis of mice expressing Glycophosphatidylinositol, (GPI)-anchorless PrP, abdominal fat contains appreciable amounts of infectious prions in APrP isoform stained with ThS.38 Notably mice overexpressing anchorless PrP provides a silent carrier status for a long time prior to presenting symptoms and is severely afflicted by amyloid fibril formation following scrapie (RML) infection.39 Recall that this study showed that GPI-anchored PrP is needed to present clinical neurotoxicity. Evidently circulating anchorless-PrP (analogous to recPrP) is more amyloidogenic compared to GPI-anchored PrP and is poorly neuroinvasive.28 Amyloidosis is systemic in anchorless-PrP mice and is not limited to fat but is also found as extensive cardiac amyloid deposits.39 Interestingly cardiac APrP was recently reported in one BSE inoculated rhesus macaque which showed symptoms of cardiac distress prior to death from prion neurotoxicity.40 It is noteworthy that transgenic mice expressing PoPrP appear sensitive to strains with biochemical features of amyloidogenic prion strains i.e., BSE and Nor98.25,26,36 (Fig. 3b). We recently adopted the parallel inregister intermolecular b-sheet structural model of the APrP fibril from the Caughey lab to rationalize cross-seeding between various PrP sequences.12,41 It is tempting to use this structural model to speculate on the adaptation of mono-N-glycolsylated PoPrP at the expense of double-N-glycolylated PrP in the original BSE inoculum reported in the Torres experiments.25,26 In this APrP model monoglycosylated PrP at N197 is structurally compatible while N181 is not, due to burial in the in-register intermolecular cross-beta sheet (Fig. 5).</span><br />
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<span style="line-height: 1.22em;">It appears that amyloidotypic prion strains, APrP, are transmissible but associated with lower neurotoxicity compared to diffuse aggregated PrP associated with synaptic PrP accumulations. It is possible that the amino acid substitutions in PoPrP compared to HuPrP and BoPrP are important for neurotoxic signal transmission (Fig. 2b, 5). The main issue hereby is that transmissibility of APrP will remain undetected unless used for surveillance. AA amyloidosis is frequent in many animals (e.g. cattle and birds) but is exceptionally rare in pigs.42 suggesting that APrP should it reside in pig fat would be traceable using newly developed screening methods.37</span><br />
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<span style="line-height: 1.22em;">Should the topic of porcine PrP amyloid be more of a worry than of mere academic interest? Well perhaps. Prions are particularly insidious pathogens. A recent outbreak of peripheral neuropathy in human, suggests that exposure to aerosolized porcine brain is deleterious for human health.43,44 Aerosolization is a known vector for prions at least under experimental conditions.45-47 where a mere single exposure was enough for transmission in transgenic mice. HuPrP is seedable with BoPrP seeds and even more so with PoPrP seed (Fig. 1), indicating that humans could be infected by porcine APrP prions while neurotoxicity associated with spongiform encephalopathy if such a disease existed is even less clear. Importantly transgenic mice over-expressing PoPrP are susceptible to BSE and BSE passaged through domestic pigs implicating that efficient downstream neurotoxicity pathways in the mouse, a susceptible host for prion disease neurotoxicity is augmenting the TSE phenotype.25,26 Prions in silent carrier hosts can be infectious to a third species. Data from Collinge and coworkers.21 propose that species considered to be prion free may be carriers of replicating prions. Especially this may be of concern for promiscuous prion strains such as BSE.19,48 It is rather established that prions can exist in both replicating and neurotoxic conformations.49,50 and this can alter the way in which new host organisms can react upon cross-species transmission.51 The na€ıve host can either be totally resistant to prion infection as well as remain non-infectious, become a silent non-symptomatic but infectious carrier of disease or be afflicted by disease with short or long incubation time. The host can harbor and/or propagate the donor strain or convert the strain conformation to adapt it to the na€ıve host species. The latter would facilitate infection and shorten the incubation time in a consecutive event of intra-species transmission.</span><br />
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<span style="line-height: 1.22em;">It may be advisable to avoid procedures and exposure without proper biosafety precautions as the knowledge of silence carrier species is poor.</span><br />
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<span style="line-height: 1.22em;">One case of iatrogenic CJD in recipient of porcine dura mater graft has been reported in the literature.52 The significance of this finding is still unknown.</span><br />
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<span style="line-height: 1.22em;">The low public awareness in this matter is exemplified by the practice of using proteolytic peptide mixtures prepared from porcine brains (Cerebrolysin) as a nootropic drug. While Cerebrolysin may be beneficial for treatment of severe diseases such as vascular dementia,53 a long term follow-up of such a product for recreational use is recommended.</span><br />
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DISCLOSURE OF POTENTIAL CONFLICTS OF INTEREST<br />
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No potential conflicts of interest were disclosed<br />
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FUNDING<br />
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This work was supported by G€oran Gustafsson foundation, the Swedish research council Grant #2011-5804 (PH) and the Swedish Alzheimer association (SN).<br />
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REFERENCES<br />
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<a href="http://www.tandfonline.com/doi/full/10.1080/19336896.2015.1065373" rel="noopener noreferrer" style="color: #956839; cursor: pointer; font-family: arial, helvetica, clean, sans-serif; line-height: 1.22em;" target="_blank">http://www.tandfonline.com/doi/full/10.1080/19336896.2015.1065373</a><br />
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<a href="http://www.tandfonline.com/doi/pdf/10.1080/19336896.2015.1065373?needAccess=true" rel="noopener noreferrer" style="color: #956839; cursor: pointer; font-family: arial, helvetica, clean, sans-serif; line-height: 1.22em;" target="_blank">http://www.tandfonline.com/doi/pdf/10.1080/19336896.2015.1065373?needAccess=true</a><br />
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<a href="https://madporcinedisease.blogspot.com/2017/04/disease-associated-prion-protein.html" style="color: #0096ef; cursor: pointer; text-decoration-line: none;">https://madporcinedisease.blogspot.com/2017/04/disease-associated-prion-protein.html</a><br />
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<span style="color: #29303b; font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px; white-space: normal;">J Neurol Neurosurg Psychiatry. 2006 Jul; 77(7): 880–882. Published online 2006 Apr 20. doi: [10.1136/jnnp.2005.073395] PMCID: PMC2117491 PMID: 16627534 </span></span><br />
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<span style="color: #29303b; font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px; white-space: normal;">Dura mater‐associated Creutzfeldt–Jakob disease: experience from surveillance in the UK </span></span><br />
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<span style="color: #29303b; font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px; white-space: normal;">C A Heath, R A Barker, T F G Esmonde, P Harvey, R Roberts, P Trend, M W Head, C Smith, J E Bell, J W Ironside, R G Will, and R S G Knight Author information Article notes Copyright and License information Disclaimer This article has been cited by other articles in PMC. Go to: </span></span><br />
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<span style="color: #29303b; font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px; white-space: normal;">Between 1970 and 2003, seven cases of human dura mater‐associated Creutzfeldt–Jakob disease (CJD) were identified in the UK. Furthermore, we identified a case of CJD in a porcine dura graft recipient. The mean incubation period of the human dura mater cases was 93 (range 45–177) months. The clinico‐pathological features of the cases are described and compared with cases previously reported in the world literature.</span></span></div>
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<span style="color: #29303b; font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px; white-space: normal;">Creutzfeldt–Jakob disease (CJD) exists in four clinical forms: sporadic, genetic, iatrogenic and variant. The cause of sporadic CJD, the most common form worldwide, is unknown and case–control studies have failed to identify any consistent risk factor, although two studies have implicated previous surgical interventions.1,2 Genetic forms of the disease are associated with underlying mutations of the prion protein gene (PRNP), which are generally considered to be directly causative. Mutations, however, possibly increase liability to some, as of yet unrecognised, source of infection. The two remaining forms of CJD are acquired. Variant CJD is considered to be caused by bovine spongiform encephalopathy through contaminated food products3,4,5; iatrogenic CJD results from the inadvertent transmission of CJD during the course of medical or surgical treatment. The two most numerically significant instances of iatrogenic CJD resulted from treatment with cadaveric human growth hormone and the use of dura mater grafts in surgery. Corneal grafts, depth electrodes and neurosurgical instruments have also rarely been implicated.6,7</span></span><br />
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<span style="color: #29303b; font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px; white-space: normal;">The first report of dura mater‐associated CJD was published in 1987,8 with a more detailed report appearing the following year;9 to date, 164 cases have been recognised worldwide (P Brown, personal communication, 2006). This paper reports and describes the seven cases of human dura mater graft‐associated CJD identified during surveillance in the UK and, for the first time, reports a case of CJD in a porcine dura graft recipient.</span></span><br />
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<span style="color: #29303b; font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px; white-space: normal;">Discussion Human dura mater is a rare, but important source of transmission of human prion disease, with only seven cases recognised in a 33‐year period. Surveillance systems worldwide have identified 164 cases of CJD in people previously exposed to human dura mater. Prevalence is particularly high in Japan and probably reflects neurosurgical practice, with an estimated 20 000 grafts used each year.15 The overall risk of CJD associated with human dura grafts in the UK is unknown because an accurate estimation of human dura graft use and thus a denominator for calculation of risk is not available. The estimated risk after exposure in Japan has been estimated to be approximately 1 per 2000 patients treated between 1979 and 2000 and approximately 1 per 1000 between 1983 and 1987.16 Neurosurgical practice in Japan, with widespread use of dura mater, may be different from other countries throughout the industrialised world and therefore it is unreasonable to extrapolate any estimated risk from these data. If neurosurgical practices in the UK were more akin to those in Australia, then a subsequent study by Brooke and co‐workers would help provide additional information pertaining to estimated risk. By using information from the Australian CJD Surveillance system, Brooke and co‐workers estimated the risk associated with exposure to human dura mater to be approximately 1 per 500 patients treated between 1978 and 2003.17 </span></span><span style="color: #29303b; font-family: "arial" , "helvetica"; font-size: 10pt; white-space: normal;">Clearly, the risk of developing CJD in this patient population is considerably higher than we would expect by chance. </span><br />
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<span style="color: #29303b; font-family: "arial" , "helvetica"; font-size: 10pt; white-space: normal;"> The human dura mater implicated in the transmission of CJD was processed, almost exclusively, by B Braun Melsungen in Germany and traded under the name Lyodura. Over 100 Japanese cases, and all but one of the UK cases (the source of the first case identified in the UK is unknown), have been associated with this particular product and only rarely has dura processed by other manufacturers been associated with transmission.18,19 Although the first case in the UK was exposed to potentially infectious dura in 1969, a disproportionately large number of cases were exposed between 1983 and 1987 (80% of those identified worldwide and six of the seven cases in the UK). Interestingly, the apparent reduction in the number of cases post‐1987 coincided with the introduction of stringent donor selection criteria and the introduction of sodium hydroxide immersion techniques in the manufacturing process. </span><br />
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<span style="color: #29303b; font-family: "arial" , "helvetica"; font-size: 10pt; white-space: normal;"> We found no temporal or geographical association between any of the dura‐associated cases, or any other case of CJD identified in the UK, despite potential contamination of neurosurgical instruments. </span><br />
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<span style="color: #29303b; font-family: "arial" , "helvetica"; font-size: 10pt; white-space: normal;"> It has been proposed that clinical features at onset are dependent on the site of graft placement or underlying parenchymal damage20,21,22 and our findings may support such a proposition. The explanation for this observation is unclear. We, could, speculate that the pathological process starts within a region adjacent to the graft and that this is reflected in the early clinical features. This proposition may also be supported by findings obtained at autopsy, with severe pathological changes identified adjacent to graft placement in three cases. Overall, the pathology is consistent for that previously described in dura mater‐associated CJD.9,18 We did not identify either “kuru‐type” or florid PrP plaques. The florid PrP plaques were previously noted in limited distribution in a small number of dural graft‐associated iatrogenic CJD cases in Japan.21,23,24 </span><br />
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<span style="color: #29303b; font-family: "arial" , "helvetica"; font-size: 10pt; white-space: normal;"> We believe case VIII represents the first reported case of CJD in a person previously exposed to a graft from a non‐human source. The age at onset, duration of illness, clinical and investigative features were similar to a typical case of sporadic CJD. Furthermore, the pathological features were also considered characteristic of sporadic CJD, with type 1 PrPres identified. Neither finding can definitively exclude the possibility of transmission of a yet unidentified pathogen. As natural transmissible spongiform encephalopathies are, however, as yet unrecognised in pigs, despite experimental transmission in animal models,25 a chance association seems the most plausible explanation.</span><br />
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<span style="color: #29303b; font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px; white-space: normal;"><a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2117491/" style="color: #0096ef; cursor: pointer; text-decoration-line: none;">https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2117491/</a></span></span><br />
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<span style="color: #29303b; font-family: "arial" , "helvetica";"><a href="https://madporcinedisease.blogspot.com/" style="color: #0096ef; cursor: pointer; text-decoration-line: none;">https://madporcinedisease.blogspot.com/</a></span><br />
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BSE INQUIRY DFA 17 Medicines and medical devices<br />
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<a href="http://bseinquiry.blogspot.com/2017/08/bse-inquiry-dfa-17-medicines-and.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://bseinquiry.blogspot.com/2017/08/bse-inquiry-dfa-17-medicines-and.html</a><br />
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<span style="font-size: x-small; line-height: 1.22em;"><span style="font-family: "arial" , "helvetica"; line-height: 1.22em;">Could diabetes spread like mad cow disease?</span></span><br />
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<span style="font-size: x-small; line-height: 1.22em;"><span style="font-family: "arial" , "helvetica"; line-height: 1.22em;"><a href="http://betaamyloidcjd.blogspot.com/2017/08/could-diabetes-spread-like-mad-cow.html" rel="noopener noreferrer" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">http://betaamyloidcjd.blogspot.com/2017/08/could-diabetes-spread-like-mad-cow.html</a></span></span><br />
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<span style="font-size: x-small; line-height: 1.22em;">Could Insulin be contaminated with and potentially spread, Transmissible Spongiform Encephalopathy TSE Prion, what if?</span><br />
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<span style="font-size: x-small; line-height: 1.22em;"><a href="http://bovineprp.blogspot.com/2017/08/could-insulin-be-contaminated-with-and.html" rel="noopener noreferrer" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">http://bovineprp.blogspot.com/2017/08/could-insulin-be-contaminated-with-and.html</a></span><br />
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<span style="color: #29303b; font-family: "arial" , "helvetica";">PRION 2015 CONFERENCE</span></div>
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<span style="font-family: "georgia" , serif; white-space: normal;"><span style="font-family: "georgia" , serif; font-size: 10pt;">O.05: Transmission of prions to primates after extended silent incubation periods: Implications for BSE and scrapie risk assessment in human populations </span></span><br />
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<span style="font-family: "georgia" , serif; font-size: 10pt;">O.05: Transmission of prions to primates after extended silent incubation periods: Implications for BSE and scrapie risk assessment in human populations </span><br />
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<span style="font-family: "georgia" , serif; font-size: 10pt;"><span style="background-attachment: initial; background-clip: initial; background-image: initial; background-origin: initial; background-position: initial; background-repeat: initial; background-size: initial;">Prion diseases (PD) are the unique neurodegenerative proteinopathies reputed to be transmissible under field conditions since decades. The transmission of Bovine Spongiform Encephalopathy (BSE) to humans evidenced that an animal PD might be zoonotic under appropriate conditions. Contrarily, in the absence of obvious (epidemiological or experimental) elements supporting a transmission or genetic predispositions, PD, like the other proteinopathies, are reputed to occur spontaneously (atpical animal prion strains, sporadic CJD summing 80% of human prion cases). </span>
<span style="background-attachment: initial; background-clip: initial; background-image: initial; background-origin: initial; background-position: initial; background-repeat: initial; background-size: initial;">Non-human primate models provided the first evidences supporting the transmissibiity of human prion strains and the zoonotic potential of BSE. Among them, cynomolgus macaques brought major information for BSE risk assessment for human health (Chen, 2014), according to their phylogenetic proximity to humans and extended lifetime. We used this model to assess the zoonotic potential of other animal PD from bovine, ovine and cervid origins even after very long silent incubation periods. </span> </span><br />
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<span style="font-family: "georgia" , serif; font-size: 10pt;"><span style="background-attachment: initial; background-clip: initial; background-image: initial; background-origin: initial; background-position: initial; background-repeat: initial; background-size: initial;">***is the third potentially zoonotic PD (with BSE and L-type BSE), </span> </span><br />
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<span style="font-family: "georgia" , serif; font-size: 10pt;"><span style="background-attachment: initial; background-clip: initial; background-image: initial; background-origin: initial; background-position: initial; background-repeat: initial; background-size: initial;">*</span></span><span style="font-family: "georgia" , serif; font-size: 10pt;">**thus questioning the origin of human sporadic cases. </span><span style="font-family: "georgia" , serif; font-size: 10pt;"> </span><br />
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<span style="font-family: "georgia" , serif; font-size: 10pt;"><span style="background-attachment: initial; background-clip: initial; background-image: initial; background-origin: initial; background-position: initial; background-repeat: initial; background-size: initial;">We will present an updated panorama of our different transmission studies and discuss the implications of such extended incubation periods on risk assessment of animal PD for human health. </span> </span><br />
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<span style="font-family: "georgia" , serif; font-size: 10pt;"><span style="background-attachment: initial; background-clip: initial; background-image: initial; background-origin: initial; background-position: initial; background-repeat: initial; background-size: initial;">***thus questioning the origin of human sporadic cases*** </span> </span><br />
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<span style="font-family: "georgia" , serif; font-size: 10pt;"><span style="background-attachment: initial; background-clip: initial; background-image: initial; background-origin: initial; background-position: initial; background-repeat: initial; background-size: initial;">
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<span style="font-family: "georgia" , serif; font-size: 10pt;"><span style="background-attachment: initial; background-clip: initial; background-image: initial; background-origin: initial; background-position: initial; background-repeat: initial; background-size: initial;">***our findings suggest that possible transmission risk of H-type BSE to sheep and human. Bioassay will be required to determine whether the PMCA products are infectious to these animals. </span> </span><br />
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<span style="font-family: "arial" , sans-serif; font-size: 10pt;"><a href="https://prion2015.files.wordpress.com/2015/05/prion2015abstracts.pdf" rel="noopener noreferrer" style="color: purple; cursor: pointer;" target="_blank"><span style="background-attachment: initial; background-clip: initial; background-image: initial; background-origin: initial; background-position: initial; background-repeat: initial; background-size: initial; font-family: "verdana" , sans-serif;"></span></a><a href="https://prion2015.files.wordpress.com/2015/05/prion2015abstracts.pdf" rel="noopener noreferrer" style="color: purple; cursor: pointer;" target="_blank">https://prion2015.files.wordpress.com/2015/05/prion2015abstracts.pdf</a></span><br />
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<span style="font-family: "georgia" , serif; font-size: 10pt;"><span style="background-attachment: initial; background-clip: initial; background-image: initial; background-origin: initial; background-position: initial; background-repeat: initial; background-size: initial;">
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<span style="font-family: "georgia" , serif; font-size: 10pt;"><span style="background-attachment: initial; background-clip: initial; background-image: initial; background-origin: initial; background-position: initial; background-repeat: initial; background-size: initial;">***Transmission data also revealed that several scrapie prions propagate in HuPrP-Tg mice with efficiency comparable to that of cattle BSE. While the efficiency of transmission at primary passage was low, subsequent passages resulted in a highly virulent prion disease in both Met129 and Val129 mice. </span> </span><br />
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<span style="font-family: "georgia" , serif; font-size: 10pt;"><span style="background-attachment: initial; background-clip: initial; background-image: initial; background-origin: initial; background-position: initial; background-repeat: initial; background-size: initial;">
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<span style="font-family: "georgia" , serif; font-size: 10pt;"><span style="background-attachment: initial; background-clip: initial; background-image: initial; background-origin: initial; background-position: initial; background-repeat: initial; background-size: initial;">*</span></span><span style="font-family: georgia, serif; font-size: 10pt;">**Transmission of the different scrapie isolates in these mice leads to the emergence of prion strain phenotypes that showed similar characteristics to those displayed by MM1 or VV2 sCJD prion. </span><span style="font-family: georgia, serif; font-size: 10pt;"> </span><br />
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<span style="font-family: "georgia" , serif; font-size: 10pt;"><span style="background-attachment: initial; background-clip: initial; background-image: initial; background-origin: initial; background-position: initial; background-repeat: initial; background-size: initial;">
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<span style="font-family: "georgia" , serif; font-size: 10pt;"><span style="background-attachment: initial; background-clip: initial; background-image: initial; background-origin: initial; background-position: initial; background-repeat: initial; background-size: initial;">***These results demonstrate that scrapie prions have a zoonotic potential and raise new questions about the possible link between animal and human prions.</span></span><br />
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<span style="font-family: "arial" , sans-serif; font-size: 10pt;"><a href="http://www.tandfonline.com/doi/abs/10.1080/19336896.2016.1163048?journalCode=kprn20" rel="noopener noreferrer" style="color: purple; cursor: pointer;" target="_blank">http://www.tandfonline.com/doi/abs/10.1080/19336896.2016.1163048?journalCode=kprn20</a></span><span style="font-family: "georgia" , serif; font-size: 10pt;"> </span><br />
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<span style="background-attachment: initial; background-clip: initial; background-image: initial; background-origin: initial; background-position: initial; background-repeat: initial; background-size: initial;">PRION 2016 TOKYO</span> </span><br />
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<span style="font-family: "georgia" , serif; font-size: 10pt;"><span style="background-attachment: initial; background-clip: initial; background-image: initial; background-origin: initial; background-position: initial; background-repeat: initial; background-size: initial;">Saturday, April 23, 2016</span> </span><br />
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<span style="font-family: "georgia" , serif; font-size: 10pt;"><span style="background-attachment: initial; background-clip: initial; background-image: initial; background-origin: initial; background-position: initial; background-repeat: initial; background-size: initial;">SCRAPIE WS-01: Prion diseases in animals and zoonotic potential </span></span><br />
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<span style="background-attachment: initial; background-clip: initial; background-image: initial; background-origin: initial; background-position: initial; background-repeat: initial; background-size: initial;">Prion. 10:S15-S21. 2016 ISSN: 1933-6896 printl 1933-690X online</span>
<span style="background-attachment: initial; background-clip: initial; background-image: initial; background-origin: initial; background-position: initial; background-repeat: initial; background-size: initial;">Taylor & Francis</span> </span><br />
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<span style="background-attachment: initial; background-clip: initial; background-image: initial; background-origin: initial; background-position: initial; background-repeat: initial; background-size: initial;">WS-01: </span></span><br />
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<span style="font-family: "georgia" , serif; font-size: 10pt;"><span style="background-attachment: initial; background-clip: initial; background-image: initial; background-origin: initial; background-position: initial; background-repeat: initial; background-size: initial;">Prion diseases in animals and zoonotic potential</span> </span><br />
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<span style="font-family: "georgia" , serif; font-size: 10pt;"><span style="background-attachment: initial; background-clip: initial; background-image: initial; background-origin: initial; background-position: initial; background-repeat: initial; background-size: initial;">Juan Maria Torres a, Olivier Andreoletti b, J uan-Carlos Espinosa a. Vincent Beringue c. Patricia Aguilar a,</span>
<span style="background-attachment: initial; background-clip: initial; background-image: initial; background-origin: initial; background-position: initial; background-repeat: initial; background-size: initial;">Natalia Fernandez-Borges a. and Alba Marin-Moreno a</span>
<span style="background-attachment: initial; background-clip: initial; background-image: initial; background-origin: initial; background-position: initial; background-repeat: initial; background-size: initial;">"Centro de Investigacion en Sanidad Animal ( CISA-INIA ). Valdeolmos, Madrid. Spain; b UMR INRA -ENVT 1225 Interactions Holes Agents Pathogenes. ENVT. Toulouse. France: "UR892. Virologie lmmunologie MolécuIaires, Jouy-en-Josas. France</span> </span><br />
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<span style="font-family: "georgia" , serif; font-size: 10pt;"><span style="background-attachment: initial; background-clip: initial; background-image: initial; background-origin: initial; background-position: initial; background-repeat: initial; background-size: initial;">Dietary exposure to bovine spongiform encephalopathy (BSE) contaminated bovine tissues is</span></span><span style="font-family: georgia, serif; font-size: 10pt;"> considered as the origin of variant Creutzfeldt Jakob (vCJD) disease in human. To date, BSE agent is the only recognized zoonotic prion.. Despite the variety of Transmissible Spongiform Encephalopathy (TSE) agents that have been circulating for centuries in farmed ruminants there is no apparent epidemiological link between exposure to ruminant products and the occurrence of other form of TSE in human like sporadic Creutzfeldt Jakob Disease (sCJD). However, the zoonotic potential of the diversity of circulating TSE agents has never been systematically assessed. The major issue in experimental assessment of TSEs zoonotic potential lies in the modeling of the ‘species barrier‘, the biological phenomenon that limits TSE agents’ propagation from a species to another. In the last decade, mice genetically engineered to express normal forms of the human prion protein has proved essential in studying human prions pathogenesis and modeling the capacity of TSEs to cross the human species barrier.</span><span style="font-family: georgia, serif; font-size: 10pt;">
</span><span style="font-family: georgia, serif; font-size: 10pt;">To assess the zoonotic potential of prions circulating in farmed ruminants, we study their transmission ability in transgenic mice expressing human PrPC (HuPrP-Tg). Two lines of mice expressing different forms of the human PrPC (129Met or 129Val) are used to determine the role of the Met129Val dimorphism in susceptibility/resistance to the different agents.</span><span style="font-family: georgia, serif; font-size: 10pt;"> </span><br />
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<span style="font-family: "georgia" , serif; font-size: 10pt;"><span style="background-attachment: initial; background-clip: initial; background-image: initial; background-origin: initial; background-position: initial; background-repeat: initial; background-size: initial;">These transmission experiments confirm the ability of BSE prions to propagate in 129M- HuPrP-Tg mice and demonstrate that Met129 homozygotes may be susceptible to BSE in sheep or goat to a greater degree than the BSE agent in cattle and that these agents can convey molecular properties and neuropathological indistinguishable from vCJD. However homozygous 129V mice are resistant to all tested BSE derived prions independently of the originating species suggesting a higher transmission barrier for 129V-PrP variant.</span> </span><br />
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<span style="font-family: "georgia" , serif; font-size: 10pt;"><span style="background-attachment: initial; background-clip: initial; background-image: initial; background-origin: initial; background-position: initial; background-repeat: initial; background-size: initial;">Transmission data also revealed that several scrapie prions propagate in HuPrP-Tg mice with efficiency comparable to that of cattle BSE. While the efficiency of transmission at primary passage was low, subsequent passages resulted in a highly virulent prion disease in both Met129 and Val129 mice. </span></span><br />
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<span style="background-attachment: initial; background-clip: initial; background-image: initial; background-origin: initial; background-position: initial; background-repeat: initial; background-size: initial;">Transmission of the different scrapie isolates in these mice leads to the emergence of prion strain phenotypes that showed similar characteristics to those displayed by MM1 or VV2 sCJD prion. </span> </span><br />
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<span style="background-attachment: initial; background-clip: initial; background-image: initial; background-origin: initial; background-position: initial; background-repeat: initial; background-size: initial; font-family: "georgia" , serif;">why do we not want to do TSE transmission studies on chimpanzees $</span>
<span style="background-attachment: initial; background-clip: initial; background-image: initial; background-origin: initial; background-position: initial; background-repeat: initial; background-size: initial; font-family: "georgia" , serif;">5. A positive result from a chimpanzee challenged severly would likely create alarm in some circles even if the result could not be interpreted for man. I have a view that all these agents could be transmitted provided a large enough dose by appropriate routes was given and the animals kept long enough. Until the mechanisms of the species barrier are more clearly understood it might be best to retain that hypothesis.</span> </span><br />
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<span style="background-attachment: initial; background-clip: initial; background-image: initial; background-origin: initial; background-position: initial; background-repeat: initial; background-size: initial; font-family: "georgia" , serif;">R. BRADLEY</span> </span><br />
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<span style="font-family: "arial" , sans-serif; font-size: 10pt;"><a href="https://web.archive.org/web/20170126051158/http:/collections.europarchive.org/tna/20080102222950/http:/www.bseinquiry.gov.uk/files/yb/1990/09/23001001.pdf" rel="noopener noreferrer" style="color: purple; cursor: pointer;" target="_blank"><span style="background-attachment: initial; background-clip: initial; background-image: initial; background-origin: initial; background-position: initial; background-repeat: initial; background-size: initial; font-family: "verdana" , sans-serif;"></span></a><a href="https://web.archive.org/web/20170126051158/http://collections.europarchive.org/tna/20080102222950/http://www.bseinquiry.gov.uk/files/yb/1990/09/23001001.pdf" rel="noopener noreferrer" style="color: purple; cursor: pointer;" target="_blank">https://web.archive.org/web/20170126051158/http://collections.europarchive.org/tna/20080102222950/http://www.bseinquiry.gov.uk/files/yb/1990/09/23001001.pdf</a></span><br />
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<span style="background-attachment: initial; background-clip: initial; background-image: initial; background-origin: initial; background-position: initial; background-repeat: initial; background-size: initial; font-family: "georgia" , serif;">Title: Transmission of scrapie prions to primate after an extended silent incubation period) </span> </span><br />
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<span style="font-size: 10pt;"><span style="background-attachment: initial; background-clip: initial; background-image: initial; background-origin: initial; background-position: initial; background-repeat: initial; background-size: initial; font-family: "georgia" , serif;">
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<span style="font-size: 10pt;"><span style="background-attachment: initial; background-clip: initial; background-image: initial; background-origin: initial; background-position: initial; background-repeat: initial; background-size: initial; font-family: "georgia" , serif;">*** In complement to the recent demonstration that humanized mice are susceptible to scrapie, we report here the first observation of direct transmission of a natural classical scrapie isolate to a macaque after a 10-year incubation period. Neuropathologic examination revealed all of the features of a prion disease: spongiform change, neuronal loss, and accumulation of PrPres throughout the CNS. </span> </span><br />
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<span style="font-size: 10pt;"><span style="background-attachment: initial; background-clip: initial; background-image: initial; background-origin: initial; background-position: initial; background-repeat: initial; background-size: initial; font-family: "georgia" , serif;">*** This observation strengthens the questioning of the harmlessness of scrapie to humans, at a time when protective measures for human and animal health are being dismantled and reduced as c-BSE is considered controlled and being eradicated. </span> </span><br />
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</span><span style="font-family: "arial" , sans-serif; font-size: 10pt;"><a href="http://www.ars.usda.gov/research/publications/publications.htm?SEQ_NO_115=313160" rel="noopener noreferrer" style="color: purple; cursor: pointer;" target="_blank"><span style="background-attachment: initial; background-clip: initial; background-image: initial; background-origin: initial; background-position: initial; background-repeat: initial; background-size: initial; font-family: "verdana" , sans-serif;"></span></a><a href="http://www.ars.usda.gov/research/publications/publications.htm?SEQ_NO_115=313160" rel="noopener noreferrer" style="color: purple; cursor: pointer;" target="_blank">http://www.ars.usda.gov/research/publications/publications.htm?SEQ_NO_115=313160</a></span><br />
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<span style="color: #222222; font-size: 17px; letter-spacing: 0.17px; line-height: 1.22em;"><span style="font-family: "arial" , "helvetica" , sans-serif; line-height: 1.22em;">***> </span></span><span style="color: #222222; font-family: "lora" , "palatino" , "times" , "times new roman" , serif; font-size: 17px; letter-spacing: 0.17px; line-height: 1.22em;">Moreover, sporadic disease has never been observed in breeding colonies or primate research laboratories, most notably among hundreds of animals over several decades of study at the National Institutes of Health</span><span style="color: #222222; font-family: "lora" , "palatino" , "times" , "times new roman" , serif; font-size: 12.75px; letter-spacing: 0.17px; line-height: 1.22em; vertical-align: baseline;"><a href="https://www.nature.com/articles/srep11573#ref25" id="aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_ref-link-section-34" rel="noopener noreferrer" style="background-color: transparent; color: #006699; cursor: pointer; line-height: 1.22em; vertical-align: baseline;" target="_blank" title="Brown, P. et al. Human spongiform encephalopathy: the National Institutes of Health series of 300 cases of experimentally transmitted disease. Ann Neurol 35, 513–529, 10.1002/ana.410350504 (1994).">25</a></span><span style="color: #222222; font-family: "lora" , "palatino" , "times" , "times new roman" , serif; font-size: 17px; letter-spacing: 0.17px; line-height: 1.22em;">, and in nearly twenty older animals continuously housed in our own facility.</span><span style="color: #222222; font-size: 17px; letter-spacing: 0.17px; line-height: 1.22em;"><span style="font-family: "arial" , "helvetica" , sans-serif; line-height: 1.22em;"> <***</span></span><br />
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<span style="font-size: x-small; line-height: 1.22em;">Transmission of scrapie prions to primate after an extended silent incubation period </span><br />
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<span style="font-size: x-small; line-height: 1.22em;">Emmanuel E. Comoy, Jacqueline Mikol, Sophie Luccantoni-Freire, Evelyne Correia, Nathalie Lescoutra-Etchegaray, Valérie Durand, Capucine Dehen, Olivier Andreoletti, Cristina Casalone, Juergen A. Richt, Justin J. Greenlee, Thierry Baron, Sylvie L. Benestad, Paul Brown & Jean-Philippe Deslys Scientific Reports volume 5, Article number: 11573 (2015) | Download Citation</span><br />
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<span style="font-size: x-small; line-height: 1.22em;">Classical bovine spongiform encephalopathy (c-BSE) is the only animal prion disease reputed to be zoonotic, causing variant Creutzfeldt-Jakob disease (vCJD) in humans and having guided protective measures for animal and human health against animal prion diseases. Recently, partial transmissions to humanized mice showed that the zoonotic potential of scrapie might be similar to c-BSE. We here report the direct transmission of a natural classical scrapie isolate to cynomolgus macaque, a highly relevant model for human prion diseases, after a 10-year silent incubation period, with features similar to those reported for human cases of sporadic CJD. Scrapie is thus actually transmissible to primates with incubation periods compatible with their life expectancy, although fourfold longer than BSE. Long-term experimental transmission studies are necessary to better assess the zoonotic potential of other prion diseases with high prevalence, notably Chronic Wasting Disease of deer and elk and atypical/Nor98 scrapie.</span><br />
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<span style="font-size: x-small; line-height: 1.22em;">Discussion We describe the transmission of spongiform encephalopathy in a non-human primate inoculated 10 years earlier with a strain of sheep c-scrapie. Because of this extended incubation period in a facility in which other prion diseases are under study, we are obliged to consider two alternative possibilities that might explain its occurrence. We first considered the possibility of a sporadic origin (like CJD in humans). Such an event is extremely improbable because the inoculated animal was 14 years old when the clinical signs appeared, i.e. about 40% through the expected natural lifetime of this species, compared to a peak age incidence of 60–65 years in human sporadic CJD, or about 80% through their expected lifetimes. Moreover, sporadic disease has never been observed in breeding colonies or primate research laboratories, most notably among hundreds of animals over several decades of study at the National Institutes of Health25, and in nearly twenty older animals continuously housed in our own facility.</span><br />
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<span style="font-size: x-small; line-height: 1.22em;">The second possibility is a laboratory cross-contamination. Three facts make this possibility equally unlikely. First, handling of specimens in our laboratory is performed with fastidious attention to the avoidance of any such cross-contamination. Second, no laboratory cross-contamination has ever been documented in other primate laboratories, including the NIH, even between infected and uninfected animals housed in the same or adjacent cages with daily intimate contact (P. Brown, personal communication). </span><br />
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<span style="font-size: x-small; line-height: 1.22em;">Third, the cerebral lesion profile is different from all the other prion diseases we have studied in this model19, with a correlation between cerebellar lesions (massive spongiform change of Purkinje cells, intense PrPres staining and reactive gliosis26) and ataxia. The iron deposits present in the globus pallidus are a non specific finding that have been reported previously in neurodegenerative diseases and aging27. Conversely, the thalamic lesion was reminiscent of a metabolic disease due to thiamine deficiency28 but blood thiamine levels were within normal limits (data not shown). </span><br />
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<span style="font-size: x-small; line-height: 1.22em;">The preferential distribution of spongiform change in cortex associated with a limited distribution in the brainstem is reminiscent of the lesion profile in MM2c and VV1 sCJD patients29, but interspecies comparison of lesion profiles should be interpreted with caution. </span><br />
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<span style="font-size: x-small; line-height: 1.22em;">It is of note that the same classical scrapie isolate induced TSE in C57Bl/6 mice with similar incubation periods and lesional profiles as a sample derived from a MM1 sCJD patient30.</span><br />
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<span style="font-size: x-small; line-height: 1.22em;">We are therefore confident that the illness in this cynomolgus macaque represents a true transmission of a sheep c-scrapie isolate directly to an old-world monkey, which taxonomically resides in the primate subdivision (parvorder of catarrhini) that includes humans. </span><br />
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<span style="font-size: x-small; line-height: 1.22em;">With an homology of its PrP protein with humans of 96.4%31, cynomolgus macaque constitutes a highly relevant model for assessing zoonotic risk of prion diseases. </span><br />
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<span style="font-size: x-small; line-height: 1.22em;">Since our initial aim was to show the absence of transmission of scrapie to macaques in the worst-case scenario, we obtained materials from a flock of naturally-infected sheep, affecting animals with different genotypes32. This c-scrapie isolate exhibited complete transmission in ARQ/ARQ sheep (332 ± 56 days) and Tg338 transgenic mice expressing ovine VRQ/VRQ prion protein (220 ± 5 days) (O. Andreoletti, personal communication). From the standpoint of zoonotic risk, it is important to note that sheep with c-scrapie (including the isolate used in our study) have demonstrable infectivity throughout their lymphoreticular system early in the incubation period of the disease (3 months-old for all the lymphoid organs, and as early as 2 months-old in gut-associated lymph nodes)33. </span><br />
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<span style="font-size: x-small; line-height: 1.22em;">In addition, scrapie infectivity has been identified in blood34, milk35 and skeletal muscle36 from asymptomatic but scrapie infected small ruminants which implies a potential dietary exposure for consumers.</span><br />
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<span style="font-size: x-small; line-height: 1.22em;">Two earlier studies have reported the occurrence of clinical TSE in cynomolgus macaques after exposures to scrapie isolates. In the first study, the “Compton” scrapie isolate (derived from an English sheep) and serially propagated for 9 passages in goats did not transmit TSE in cynomolgus macaque, rhesus macaque or chimpanzee within 7 years following intracerebral challenge1; conversely, after 8 supplementary passages in conventional mice, this “Compton” isolate induced TSE in a cynomolgus macaque 5 years after intracerebral challenge, but rhesus macaques and chimpanzee remained asymptomatic 8.5 years post-exposure8. However, multiple successive passages that are classically used to select laboratory-adapted prion strains can significantly modify the initial properties of a scrapie isolate, thus questioning the relevance of zoonotic potential for the initial sheep-derived isolate. The same isolate had also induced disease into squirrel monkeys (new-world monkey)9. A second historical observation reported that a cynomolgus macaque developed TSE 6 years post-inoculation with brain homogenate from a scrapie-infected Suffolk ewe (derived from USA), whereas a rhesus macaque and a chimpanzee exposed to the same inoculum remained healthy 9 years post-exposure1. This inoculum also induced TSE in squirrel monkeys after 4 passages in mice. Other scrapie transmission attempts in macaque failed but had more shorter periods of observation in comparison to the current study. Further, it is possible that there are differences in the zoonotic potential of different scrapie strains.</span><br />
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<span style="font-size: x-small; line-height: 1.22em;">The most striking observation in our study is the extended incubation period of scrapie in the macaque model, which has several implications. </span><br />
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<span style="font-size: x-small; line-height: 1.22em;">Firstly, our observations constitute experimental evidence in favor of the zoonotic potential of c-scrapie, at least for this isolate that has been extensively studied32,33,34,35,36. The cross-species zoonotic ability of this isolate should be confirmed by performing duplicate intracerebral exposures and assessing the transmissibility by the oral route (a successful transmission of prion strains through the intracerebral route may not necessarily indicate the potential for oral transmission37). However, such confirmatory experiments may require more than one decade, which is hardly compatible with current general management and support of scientific projects; thus this study should be rather considered as a case report.</span><br />
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<span style="font-size: x-small; line-height: 1.22em;">Secondly, transmission of c-BSE to primates occurred within 8 years post exposure for the lowest doses able to transmit the disease (the survival period after inoculation is inversely proportional to the initial amount of infectious inoculum). The occurrence of scrapie 10 years after exposure to a high dose (25 mg) of scrapie-infected sheep brain suggests that the macaque has a higher species barrier for sheep c-scrapie than c-BSE, although it is notable that previous studies based on in vitro conversion of PrP suggested that BSE and scrapie prions would have a similar conversion potential for human PrP38.</span><br />
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<span style="font-size: x-small; line-height: 1.22em;">Thirdly, prion diseases typically have longer incubation periods after oral exposure than after intracerebral inoculations: since humans can develop Kuru 47 years after oral exposure39, an incubation time of several decades after oral exposure to scrapie would therefore be expected, leading the disease to occur in older adults, i.e. the peak age for cases considered to be sporadic disease, and making a distinction between scrapie-associated and truly sporadic disease extremely difficult to appreciate.</span><br />
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<span style="font-size: x-small; line-height: 1.22em;">Fourthly, epidemiologic evidence is necessary to confirm the zoonotic potential of an animal disease suggested by experimental studies. A relatively short incubation period and a peculiar epidemiological situation (e.g., all the first vCJD cases occurring in the country with the most important ongoing c-BSE epizootic) led to a high degree of suspicion that c-BSE was the cause of vCJD. Sporadic CJD are considered spontaneous diseases with an almost stable and constant worldwide prevalence (0.5–2 cases per million inhabitants per year), and previous epidemiological studies were unable to draw a link between sCJD and classical scrapie6,7,40,41, even though external causes were hypothesized to explain the occurrence of some sCJD clusters42,43,44. However, extended incubation periods exceeding several decades would impair the predictive values of epidemiological surveillance for prion diseases, already weakened by a limited prevalence of prion diseases and the multiplicity of isolates gathered under the phenotypes of “scrapie” and “sporadic CJD”.</span><br />
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<span style="font-size: x-small; line-height: 1.22em;">Fifthly, considering this 10 year-long incubation period, together with both laboratory and epidemiological evidence of decade or longer intervals between infection and clinical onset of disease, no premature conclusions should be drawn from negative transmission studies in cynomolgus macaques with less than a decade of observation, as in the aforementioned historical transmission studies of scrapie to primates1,8,9. Our observations and those of others45,46 to date are unable to provide definitive evidence regarding the zoonotic potential of CWD, atypical/Nor98 scrapie or H-type BSE. The extended incubation period of the scrapie-affected macaque in the current study also underscores the limitations of rodent models expressing human PrP for assessing the zoonotic potential of some prion diseases since their lifespan remains limited to approximately two years21,47,48. This point is illustrated by the fact that the recently reported transmission of scrapie to humanized mice was not associated with clinical signs for up to 750 days and occurred in an extreme minority of mice with only a marginal increase in attack rate upon second passage13. The low attack rate in these studies is certainly linked to the limited lifespan of mice compared to the very long periods of observation necessary to demonstrate the development of scrapie. Alternatively, one could estimate that a successful second passage is the result of strain adaptation to the species barrier, thus poorly relevant of the real zoonotic potential of the original scrapie isolate of sheep origin49. </span><br />
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<span style="font-size: x-small; line-height: 1.22em;">The development of scrapie in this primate after an incubation period compatible with its lifespan complements the study conducted in transgenic (humanized) mice; taken together these studies suggest that some isolates of sheep scrapie can promote misfolding of the human prion protein and that scrapie can develop within the lifespan of some primate species.</span><br />
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<span style="font-size: x-small; line-height: 1.22em;">In addition to previous studies on scrapie transmission to primate1,8,9 and the recently published study on transgenic humanized mice13, our results constitute new evidence for recommending that the potential risk of scrapie for human health should not be dismissed. Indeed, human PrP transgenic mice and primates are the most relevant models for investigating the human transmission barrier. To what extent such models are informative for measuring the zoonotic potential of an animal TSE under field exposure conditions is unknown. During the past decades, many protective measures have been successfully implemented to protect cattle from the spread of c-BSE, and some of these measures have been extended to sheep and goats to protect from scrapie according to the principle of precaution. </span><br />
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<span style="font-size: x-small; line-height: 1.22em;">Since cases of c-BSE have greatly reduced in number, those protective measures are currently being challenged and relaxed in the absence of other known zoonotic animal prion disease. We recommend that risk managers should be aware of the long term potential risk to human health of at least certain scrapie isolates, notably for lymphotropic strains like the classical scrapie strain used in the current study. Relatively high amounts of infectivity in peripheral lymphoid organs in animals infected with these strains could lead to contamination of food products produced for human consumption. </span><br />
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<span style="font-size: x-small; line-height: 1.22em;">Efforts should also be maintained to further assess the zoonotic potential of other animal prion strains in long-term studies, notably lymphotropic strains with high prevalence like CWD, which is spreading across North America, and atypical/Nor98 scrapie (Nor98)50 that was first detected in the past two decades and now represents approximately half of all reported cases of prion diseases in small ruminants worldwide, including territories previously considered as scrapie free.. </span><br />
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<span style="font-size: x-small; line-height: 1.22em;">Even if the prevailing view is that sporadic CJD is due to the spontane</span><span style="font-size: x-small;">ous formation of CJD prions, it remains possible that its apparent sporadic nature may, at least in part, result from our limited capacity to identify an environmental origin.</span><br />
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<span style="font-size: x-small; line-height: 1.22em;"><a href="https://www.nature.com/articles/srep11573" rel="noopener noreferrer" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">https://www.nature.com/articles/srep11573</a></span><br />
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<a href="http://www.mad-cow.org/UKCJD/CJD_news52.html#29%20Mar%2001%20-%20CJD%20-%20Suspect%20symptoms" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://www.mad-cow.org/UKCJD/CJD_news52.html#29%20Mar%2001%20-%20CJD%20-%20Suspect%20symptoms</a><br />
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<span style="color: #191919; font-family: "verdana" , sans-serif; font-size: 10.5pt; line-height: 1.22em;">here is the latest;</span><br />
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<span style="color: #191919; font-family: "verdana" , sans-serif; font-size: 10.5pt;">PRION 2018 CONFERENCE</span><br />
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<span style="color: #191919; font-family: "verdana" , sans-serif; font-size: 10.5pt; line-height: 1.22em;">Oral transmission of CWD into Cynomolgus macaques: signs of atypical disease, prion conversion and infectivity in macaques and bio-assayed transgenic mice </span><span style="font-family: "arial" , sans-serif; font-size: 10pt; line-height: 1.22em;"></span><br />
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<span style="color: #191919; font-family: "verdana" , sans-serif; font-size: 10.5pt; line-height: 1.22em;">Hermann M. Schatzl, Samia Hannaoui, Yo-Ching Cheng, Sabine Gilch (Calgary Prion Research Unit, University of Calgary, Calgary, Canada) Michael Beekes (RKI Berlin), Walter Schulz-Schaeffer (University of Homburg/Saar, Germany), Christiane Stahl-Hennig (German Primate Center) & Stefanie Czub (CFIA Lethbridge). </span><span style="font-family: "arial" , sans-serif; font-size: 10pt; line-height: 1.22em;"></span><br />
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<span style="color: #191919; font-family: "verdana" , sans-serif; font-size: 10.5pt; line-height: 1.22em;">To date, BSE is the only example of interspecies transmission of an animal prion disease into humans. The potential zoonotic transmission of CWD is an alarming issue and was addressed by many groups using a variety of in vitro and in vivo experimental systems. Evidence from these studies indicated a substantial, if not absolute, species barrier, aligning with the absence of epidemiological evidence suggesting transmission into humans. Studies in non-human primates were not conclusive so far, with oral transmission into new-world monkeys and no transmission into old-world monkeys. </span><span style="font-family: "arial" , sans-serif; font-size: 10pt; line-height: 1.22em;"></span><br />
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<span style="color: #191919; font-family: "verdana" , sans-serif; font-size: 10.5pt; line-height: 1.22em;">Our consortium has challenged 18 Cynomolgus macaques with characterized CWD material, focusing on oral transmission with muscle tissue. Some macaques have orally received a total of 5 kg of muscle material over a period of 2 years. After 5-7 years of incubation time some animals showed clinical symptoms indicative of prion disease, and prion neuropathology and PrPSc deposition were detected in spinal cord and brain of some euthanized animals. PrPSc in immunoblot was weakly detected in some spinal cord materials and various tissues tested positive in RT-QuIC, including lymph node and spleen homogenates. To prove prion infectivity in the macaque tissues, we have intracerebrally inoculated 2 lines of transgenic mice, expressing either elk or human PrP. At least 3 TgElk mice, receiving tissues from 2 different macaques, showed clinical signs of a progressive prion disease and brains were positive in immunoblot and RT-QuIC. Tissues (brain, spinal cord and spleen) from these and pre-clinical mice are currently tested using various read-outs and by second passage in mice. Transgenic mice expressing human PrP were so far negative for clear clinical prion disease (some mice >300 days p.i.). In parallel, the same macaque materials are inoculated into bank voles. </span><span style="font-family: "arial" , sans-serif; font-size: 10pt; line-height: 1.22em;"></span><br />
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<span style="color: #191919; font-family: "verdana" , sans-serif; font-size: 10.5pt; line-height: 1.22em;">Taken together, there is strong evidence of transmissibility of CWD orally into macaques and from macaque tissues into transgenic mouse models, although with an incomplete attack rate. The clinical and pathological presentation in macaques was mostly atypical, with a strong emphasis on spinal cord pathology. Our ongoing studies will show whether the transmission of CWD into macaques and passage in transgenic mice represents a form of non-adaptive prion amplification, and whether macaque-adapted prions have the potential to infect mice expressing human PrP. </span><br />
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<span style="color: #191919; font-family: "verdana" , sans-serif; font-size: 10.5pt; line-height: 1.22em;">The notion that CWD can be transmitted orally into both new-world and old-world non-human primates asks for a careful reevaluation of the zoonotic risk of CWD.</span><span style="font-family: "arial" , sans-serif; font-size: 10pt; line-height: 1.22em;"></span><br />
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<span style="color: #191919; font-family: "verdana" , sans-serif; font-size: 10.5pt; line-height: 1.22em;">***> The notion that CWD can be transmitted orally into both new-world and old-world non-human primates asks for a careful reevaluation of the zoonotic risk of CWD. <***</span><span style="font-family: "arial" , sans-serif; font-size: 10pt; line-height: 1.22em;"></span><br />
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<span style="font-family: "arial" , sans-serif; font-size: 10pt; line-height: 1.22em;"><a href="https://prion2018.org/" rel="noopener noreferrer" style="color: purple; cursor: pointer; line-height: 1.22em;" target="_blank">https://prion2018.org/</a></span><br />
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<span style="color: #191919; font-family: "verdana" , sans-serif; font-size: 10.5pt;">READING OVER THE PRION 2018 ABSTRACT BOOK, LOOKS LIKE THEY FOUND THAT from this study ;</span><br />
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<span style="color: #191919; font-family: "verdana" , sans-serif; font-size: 10.5pt; line-height: 1.22em;">P190 Human prion disease mortality rates by occurrence of chronic wasting disease in freeranging cervids, United States </span><span style="font-family: "arial" , sans-serif; font-size: 10pt; line-height: 1.22em;"></span><br />
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<span style="color: #191919; font-family: "verdana" , sans-serif; font-size: 10.5pt; line-height: 1.22em;">Abrams JY (1), Maddox RA (1), Schonberger LB (1), Person MK (1), Appleby BS (2), Belay ED (1) (1) Centers for Disease Control and Prevention (CDC), National Center for Emerging and Zoonotic Infectious Diseases, Atlanta, GA, USA (2) Case Western Reserve University, National Prion Disease Pathology Surveillance Center (NPDPSC), Cleveland, OH, USA. </span><span style="font-family: "arial" , sans-serif; font-size: 10pt; line-height: 1.22em;"></span><br />
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<span style="color: #191919; font-family: "verdana" , sans-serif; font-size: 10.5pt; line-height: 1.22em;">SEEMS THAT THEY FOUND Highly endemic states had a higher rate of prion disease mortality compared to non-CWD states.</span><span style="font-family: "arial" , sans-serif; font-size: 10pt; line-height: 1.22em;"></span><br />
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<span style="color: #191919; font-family: "verdana" , sans-serif; font-size: 10.5pt; line-height: 1.22em;">AND ANOTHER STUDY;</span><span style="font-family: "arial" , sans-serif; font-size: 10pt; line-height: 1.22em;"></span><br />
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<span style="color: #191919; font-family: "verdana" , sans-serif; font-size: 10.5pt; line-height: 1.22em;">P172 Peripheral Neuropathy in Patients with Prion Disease </span><span style="font-family: "arial" , sans-serif; font-size: 10pt; line-height: 1.22em;"></span><br />
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<span style="color: #191919; font-family: "verdana" , sans-serif; font-size: 10.5pt; line-height: 1.22em;">Wang H(1), Cohen M(1), Appleby BS(1,2) (1) University Hospitals Cleveland Medical Center, Cleveland, Ohio (2) National Prion Disease Pathology Surveillance Center, Cleveland, Ohio..</span><span style="font-family: "arial" , sans-serif; font-size: 10pt; line-height: 1.22em;"></span><br />
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<span style="color: #191919; font-family: "verdana" , sans-serif; font-size: 10.5pt; line-height: 1.22em;">IN THIS STUDY, THERE WERE autopsy-proven prion cases from the National Prion Disease Pathology Surveillance Center that were diagnosed between September 2016 to March 2017, AND included 104 patients.</span><span style="font-family: "arial" , sans-serif; font-size: 10pt; line-height: 1.22em;"></span><br />
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<span style="color: #191919; font-family: "verdana" , sans-serif; font-size: 10.5pt; line-height: 1.22em;">SEEMS THEY FOUND THAT The most common sCJD subtype was MV1-2 (30%), followed by MM1-2 (20%), AND THAT The Majority of cases were male (60%), AND half of them had exposure to wild game.</span><span style="font-family: "arial" , sans-serif; font-size: 10pt; line-height: 1.22em;"></span><br />
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<span style="color: #191919; font-family: "verdana" , sans-serif; font-size: 10.5pt; line-height: 1.22em;">see more on Prion 2017 Macaque study from Prion 2017 Conference and other updated science on cwd tse prion zoonosis below...terry</span><span style="font-family: "arial" , sans-serif; font-size: 10pt; line-height: 1.22em;"></span><br />
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<span style="color: #191919; font-family: "verdana" , sans-serif; font-size: 10.5pt; line-height: 1.22em;"><a href="https://prion2018.org/wp-content/uploads/2018/05/program.pdf" rel="noopener noreferrer" style="color: purple; cursor: pointer; line-height: 1.22em;" target="_blank">https://prion2018.org/wp-content/uploads/2018/05/program.pdf</a></span><span style="font-family: "arial" , sans-serif; font-size: 10pt; line-height: 1.22em;"></span><br />
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<span style="font-family: "arial" , sans-serif; font-size: 10pt; line-height: 1.22em;"><a href="https://prion2018.org/" rel="noopener noreferrer" style="color: purple; cursor: pointer; line-height: 1.22em;" target="_blank">https://prion2018.org/</a></span><br />
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<span style="color: #191919; font-family: "verdana" , sans-serif; font-size: 10.5pt; line-height: 1.22em;">Research</span><span style="font-family: "arial" , sans-serif; font-size: 10pt; line-height: 1.22em;"></span><br />
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<span style="color: #191919; font-family: "verdana" , sans-serif; font-size: 10.5pt; line-height: 1.22em;">Susceptibility of Human Prion Protein to Conversion by Chronic Wasting Disease Prions</span><span style="font-family: "arial" , sans-serif; font-size: 10pt; line-height: 1.22em;"></span><br />
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<span style="color: #191919; font-family: "verdana" , sans-serif; font-size: 10.5pt; line-height: 1.22em;">Marcelo A. BarriaComments to Author , Adriana Libori, Gordon Mitchell, and Mark W. Head Author affiliations: National CJD Research and Surveillance Unit, University of Edinburgh, Edinburgh, Scotland, UK (M.A. Barria, A. Libori, M.W. Head); National and OIE Reference Laboratory for Scrapie and CWD, Canadian Food Inspection Agency, Ottawa, Ontario, Canada (G. Mitchell)</span><span style="font-family: "arial" , sans-serif; font-size: 10pt; line-height: 1.22em;"></span></div>
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<span style="color: #191919; font-family: "verdana" , sans-serif; font-size: 10.5pt; line-height: 1.22em;">M. A. Barria et al.</span><span style="font-family: "arial" , sans-serif; font-size: 10pt; line-height: 1.22em;"></span><br />
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<span style="color: #191919; font-family: "verdana" , sans-serif; font-size: 10.5pt; line-height: 1.22em;">ABSTRACT</span><span style="font-family: "arial" , sans-serif; font-size: 10pt; line-height: 1.22em;"></span><br />
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<span style="color: #191919; font-family: "verdana" , sans-serif; font-size: 10.5pt; line-height: 1.22em;">Chronic wasting disease (CWD) is a contagious and fatal neurodegenerative disease and a serious animal health issue for deer and elk in North America. The identification of the first cases of CWD among free-ranging reindeer and moose in Europe brings back into focus the unresolved issue of whether CWD can be zoonotic like bovine spongiform encephalopathy. We used a cell-free seeded protein misfolding assay to determine whether CWD prions from elk, white-tailed deer, and reindeer in North America can convert the human prion protein to the disease-associated form. We found that prions can convert, but the efficiency of conversion is affected by polymorphic variation in the cervid and human prion protein genes. In view of the similarity of reindeer, elk, and white-tailed deer in North America to reindeer, red deer, and roe deer, respectively, in Europe, a more comprehensive and thorough assessment of the zoonotic potential of CWD might be warranted. </span><span style="font-family: "arial" , sans-serif; font-size: 10pt; line-height: 1.22em;"></span><br />
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<span style="font-family: "arial" , sans-serif; font-size: 10pt; line-height: 1.22em;"><a href="https://wwwnc.cdc.gov/eid/article/24/8/16-1888_article" rel="noopener noreferrer" style="color: purple; cursor: pointer; line-height: 1.22em;" target="_blank">https://wwwnc.cdc.gov/eid/article/24/8/16-1888_article</a></span><br />
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<span style="color: #191919; font-family: "verdana" , sans-serif; font-size: 10.5pt;">Molecular Barriers to Zoonotic Transmission of Prions </span><br />
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<span style="color: #191919; font-family: "verdana" , sans-serif; font-size: 10.5pt; line-height: 1.22em;">Marcelo A. Barria, Aru Balachandran, Masanori Morita, Tetsuyuki Kitamoto, Rona Barron, Jean Manson, Richard Knight, James W. Ironside, and Mark W. Headcorresponding author </span><span style="font-family: "arial" , sans-serif; font-size: 10pt; line-height: 1.22em;"></span><br />
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<span style="color: #191919; font-family: "verdana" , sans-serif; font-size: 10.5pt; line-height: 1.22em;">The conversion of human PrPC by CWD brain homogenate in PMCA reactions was less efficient when the amino acid at position 129 was valine rather than methionine. </span><span style="font-family: "arial" , sans-serif; font-size: 10pt; line-height: 1.22em;"></span><br />
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<span style="color: #191919; font-family: "verdana" , sans-serif; font-size: 10.5pt; line-height: 1.22em;">***Furthermore, the form of human PrPres produced in this in vitro assay when seeded with CWD, resembles that found in the most common human prion disease, namely sCJD of the MM1 subtype. </span><span style="font-family: "arial" , sans-serif; font-size: 10pt; line-height: 1.22em;"></span><br />
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<span style="color: #191919; font-family: "verdana" , sans-serif; font-size: 10.5pt; line-height: 1.22em;">snip... </span><span style="font-family: "arial" , sans-serif; font-size: 10pt; line-height: 1.22em;"></span><br />
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<span style="color: #191919; font-family: "verdana" , sans-serif; font-size: 10.5pt; line-height: 1.22em;">However, we can say with confidence that under the conditions used here, none of the animal isolates tested were as efficient as C-type BSE in converting human PrPC, which is reassuring. </span><span style="font-family: "arial" , sans-serif; font-size: 10pt; line-height: 1.22em;"></span><br />
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<span style="color: #191919; font-family: "verdana" , sans-serif; font-size: 10.5pt; line-height: 1.22em;">***Less reassuring is the finding that there is no absolute barrier to the conversion of human PrPC by CWD prions in a protocol using a single round of PMCA and an entirely human substrate prepared from the target organ of prion diseases, the brain. </span><span style="font-family: "arial" , sans-serif; font-size: 10pt; line-height: 1.22em;"></span><br />
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<span style="color: #191919; font-family: "verdana" , sans-serif; font-size: 10.5pt; line-height: 1.22em;"><a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3884726/" rel="noopener noreferrer" style="color: purple; cursor: pointer; line-height: 1.22em;" target="_blank">https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3884726/</a> </span><span style="font-family: "arial" , sans-serif; font-size: 10pt; line-height: 1.22em;"></span><br />
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<span style="color: #191919; font-family: "verdana" , sans-serif; font-size: 10.5pt;">Prion 2017 </span><br />
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<span style="color: #191919; font-family: "verdana" , sans-serif; font-size: 10.5pt; line-height: 1.22em;">Conference Abstracts CWD 2017 PRION CONFERENCE </span><span style="font-family: "arial" , sans-serif; font-size: 10pt; line-height: 1.22em;"></span><br />
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<span style="color: #191919; font-family: "verdana" , sans-serif; font-size: 10.5pt; line-height: 1.22em;">First evidence of intracranial and peroral transmission of Chronic Wasting Disease (CWD) into Cynomolgus macaques: a work in progress </span><span style="font-family: "arial" , sans-serif; font-size: 10pt; line-height: 1.22em;"></span><br />
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<span style="color: #191919; font-family: "verdana" , sans-serif; font-size: 10.5pt; line-height: 1.22em;">Stefanie Czub1, Walter Schulz-Schaeffer2, Christiane Stahl-Hennig3, Michael Beekes4, Hermann Schaetzl5 and Dirk Motzkus6 1 </span><span style="font-family: "arial" , sans-serif; font-size: 10pt; line-height: 1.22em;"></span><br />
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<span style="color: #191919; font-family: "verdana" , sans-serif; font-size: 10.5pt; line-height: 1.22em;">University of Calgary Faculty of Veterinary Medicine/Canadian Food Inspection Agency; 2Universitatsklinikum des Saarlandes und Medizinische Fakultat der Universitat des Saarlandes; 3 Deutsches Primaten Zentrum/Goettingen; 4 Robert-Koch-Institut Berlin; 5 University of Calgary Faculty of Veterinary Medicine; 6 presently: Boehringer Ingelheim Veterinary Research Center; previously: Deutsches Primaten Zentrum/Goettingen </span><span style="font-family: "arial" , sans-serif; font-size: 10pt; line-height: 1.22em;"></span><br />
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<span style="color: #191919; font-family: "verdana" , sans-serif; font-size: 10.5pt; line-height: 1.22em;">This is a progress report of a project which started in 2009. 21 cynomolgus macaques were challenged with characterized CWD material from white-tailed deer (WTD) or elk by intracerebral (ic), oral, and skin exposure routes. </span><br />
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<span style="color: #191919; font-family: "verdana" , sans-serif; font-size: 10.5pt; line-height: 1.22em;">Additional blood transfusion experiments are supposed to assess the CWD contamination risk of human blood product. </span><br />
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<span style="color: #191919; font-family: "verdana" , sans-serif; font-size: 10.5pt; line-height: 1.22em;">Challenge materials originated from symptomatic cervids for ic, skin scarification and partially per oral routes (WTD brain). Challenge material for feeding of muscle derived from preclinical WTD and from preclinical macaques for blood transfusion experiments. </span><br />
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<span style="color: #191919; font-family: "verdana" , sans-serif; font-size: 10.5pt; line-height: 1.22em;">We have confirmed that the CWD challenge material contained at least two different CWD agents (brain material) as well as CWD prions in muscle-associated nerves. </span><br />
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<span style="color: #191919; font-family: "verdana" , sans-serif; font-size: 10.5pt; line-height: 1.22em;">Here we present first data on a group of animals either challenged ic with steel wires or per orally and sacrificed with incubation times ranging from 4.5 to 6.9 years at postmortem. </span><br />
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<span style="color: #191919; font-family: "verdana" , sans-serif; font-size: 10.5pt; line-height: 1.22em;">Three animals displayed signs of mild clinical disease, including anxiety, apathy, ataxia and/or tremor. In four animals wasting was observed, two of those had confirmed diabetes. </span><br />
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<span style="color: #191919; font-family: "verdana" , sans-serif; font-size: 10.5pt; line-height: 1.22em;">All animals have variable signs of prion neuropathology in spinal cords and brains and by supersensitive IHC, reaction was detected in spinal cord segments of all animals. Protein misfolding cyclic amplification (PMCA), real-time quaking-induced conversion (RT-QuiC) and PET-blot assays to further substantiate these findings are on the way, as well as bioassays in bank voles and transgenic mice. </span><br />
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<span style="color: #191919; font-family: "verdana" , sans-serif; font-size: 10.5pt; line-height: 1.22em;">At present, a total of 10 animals are sacrificed and read-outs are ongoing. Preclinical incubation of the remaining macaques covers a range from 6.4 to 7.10 years. </span><br />
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<span style="color: #191919; font-family: "verdana" , sans-serif; font-size: 10.5pt; line-height: 1.22em;">Based on the species barrier and an incubation time of > 5 years for BSE in macaques and about 10 years for scrapie in macaques, we expected an onset of clinical disease beyond 6 years post inoculation. </span><span style="font-family: "arial" , sans-serif; font-size: 10pt; line-height: 1.22em;"></span><br />
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<span style="color: #191919; font-family: "verdana" , sans-serif; font-size: 10.5pt; line-height: 1.22em;">PRION 2017 </span><span style="font-family: "arial" , sans-serif; font-size: 10pt; line-height: 1.22em;"></span><br />
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<span style="color: #191919; font-family: "verdana" , sans-serif; font-size: 10.5pt; line-height: 1.22em;">DECIPHERING NEURODEGENERATIVE DISORDERS </span><span style="font-family: "arial" , sans-serif; font-size: 10pt; line-height: 1.22em;"></span><br />
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<span style="color: #191919; font-family: "verdana" , sans-serif; font-size: 10.5pt; line-height: 1.22em;">Subject: PRION 2017 CONFERENCE DECIPHERING NEURODEGENERATIVE DISORDERS VIDEO </span><span style="font-family: "arial" , sans-serif; font-size: 10pt; line-height: 1.22em;"></span><br />
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<span style="color: #191919; font-family: "verdana" , sans-serif; font-size: 10.5pt; line-height: 1.22em;">PRION 2017 </span><span style="font-family: "arial" , sans-serif; font-size: 10pt; line-height: 1.22em;"></span><br />
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<span style="color: #191919; font-family: "verdana" , sans-serif; font-size: 10.5pt; line-height: 1.22em;">CONFERENCE DECIPHERING NEURODEGENERATIVE DISORDERS </span><span style="font-family: "arial" , sans-serif; font-size: 10pt; line-height: 1.22em;"></span><br />
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<span style="color: #191919; font-family: "verdana" , sans-serif; font-size: 10.5pt; line-height: 1.22em;">*** PRION 2017 CONFERENCE VIDEO </span><span style="font-family: "arial" , sans-serif; font-size: 10pt; line-height: 1.22em;"></span><br />
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<span style="font-size: 13.3333px;">Cervid to human prion transmission </span><br />
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<span style="font-size: 13.3333px;">Prion disease is transmissible and invariably fatal. Chronic wasting disease (CWD) is the prion disease affecting deer, elk and moose, and it is a widespread and expanding epidemic affecting 22 US States and 2 Canadian provinces so far. CWD poses the most serious zoonotic prion transmission risks in North America because of huge venison consumption (>6 million deer/elk hunted and consumed annually in the USA alone), significant prion infectivity in muscles and other tissues/fluids from CWD-affected cervids, and usually high levels of individual exposure to CWD resulting from consumption of the affected animal among often just family and friends. However, we still do not know whether CWD prions can infect humans in the brain or peripheral tissues or whether clinical/asymptomatic CWD zoonosis has already occurred, and we have no essays to reliably detect CWD infection in humans. </span><br />
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<span style="font-size: 13.3333px;">We hypothesize that: </span><br />
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<span style="font-size: 13.3333px;">(1) The classic CWD prion strain can infect humans at low levels in the brain and peripheral lymphoid tissues; </span><br />
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<span style="font-size: 13.3333px;">(2) The cervid-to-human transmission barrier is dependent on the cervid prion strain and influenced by the host (human) prion protein (PrP) primary sequence; </span><br />
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<span style="font-size: 13.3333px;">(3) Reliable essays can be established to detect CWD infection in humans; and </span><br />
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<span style="font-size: 13.3333px;">(4) CWD transmission to humans has already occurred. We will test these hypotheses in 4 Aims using transgenic (Tg) mouse models and complementary in vitro approaches. </span><br />
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<span style="font-size: 13.3333px;">Aim 1 will prove that the classical CWD strain may infect humans in brain or peripheral lymphoid tissues at low levels by conducting systemic bioassays in a set of humanized Tg mouse lines expressing common human PrP variants using a number of CWD isolates at varying doses and routes. Experimental human CWD samples will also be generated for Aim 3. </span><br />
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<span style="font-size: 13.3333px;">Aim 2 will test the hypothesis that the cervid-to-human prion transmission barrier is dependent on prion strain and influenced by the host (human) PrP sequence by examining and comparing the transmission efficiency and phenotypes of several atypical/unusual CWD isolates/strains as well as a few prion strains from other species that have adapted to cervid PrP sequence, utilizing the same panel of humanized Tg mouse lines as in Aim 1. </span><br />
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<span style="font-size: 13.3333px;">Aim 3 will establish reliable essays for detection and surveillance of CWD infection in humans by examining in details the clinical, pathological, biochemical and in vitro seeding properties of existing and future experimental human CWD samples generated from Aims 1-2 and compare them with those of common sporadic human Creutzfeldt-Jakob disease (sCJD) prions. </span><br />
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<span style="font-size: 13.3333px;">Aim 4 will attempt to detect clinical CWD-affected human cases by examining a significant number of brain samples from prion-affected human subjects in the USA and Canada who have consumed venison from CWD-endemic areas utilizing the criteria and essays established in Aim 3. The findings from this proposal will greatly advance our understandings on the potential and characteristics of cervid prion transmission in humans, establish reliable essays for CWD zoonosis and potentially discover the first case(s) of CWD infection in humans.</span><br />
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<span style="font-size: 13.3333px;">There are significant and increasing human exposure to cervid prions because chronic wasting disease (CWD, a widespread and highly infectious prion disease among deer and elk in North America) continues spreading and consumption of venison remains popular, but our understanding on cervid-to-human prion transmission is still very limited, raising public health concerns. This proposal aims to define the zoonotic risks of cervid prions and set up and apply essays to detect CWD zoonosis using mouse models and in vitro methods. The findings will greatly expand our knowledge on the potentials and characteristics of cervid prion transmission in humans, establish reliable essays for such infections and may discover the first case(s) of CWD infection in humans.</span><br />
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<span style="font-size: 13.3333px;">National Institute of Health (NIH)</span><br />
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<span style="font-size: 13.3333px;">National Institute of Neurological Disorders and Stroke (NINDS)</span><br />
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<span style="font-size: 13.3333px;">5R01NS088604-04</span><br />
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<span style="font-size: 13.3333px;">9517118</span><br />
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<span style="font-size: 13.3333px;">Cellular and Molecular Biology of Neurodegeneration Study Section (CMND)</span><br />
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<span style="font-size: 13.3333px;">Program Officer Wong, May</span><br />
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<span style="font-size: 13.3333px;">Project Start 2015-09-30 Project End 2019-07-31 Budget Start 2018-08-01 Budget End 2019-07-31 Support Year 4 Fiscal Year 2018 Total Cost Indirect Cost Institution Name Case Western Reserve University </span><br />
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<span style="font-size: 13.3333px;">Department Pathology Type Schools of Medicine DUNS # 077758407 City Cleveland State OH Country United States Zip Code 44106</span><br />
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<span style="font-size: 13.3333px;">NIH 2018 R01 NS Cervid to human prion transmission Kong, Qingzhong / Case Western Reserve University </span><br />
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<span style="font-size: 13.3333px;">NIH 2017 R01 NS Cervid to human prion transmission Kong, Qingzhong / Case Western Reserve University </span><br />
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<span style="font-size: 13.3333px;">NIH 2016 R01 NS Cervid to human prion transmission Kong, Qingzhong / Case Western Reserve University </span><br />
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<span style="font-size: 13.3333px;">NIH 2015 R01 NS Cervid to human prion transmission Kong, Qingzhong / Case Western Reserve University </span><br />
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<span style="font-size: 13.3333px;"><a href="http://grantome.com/grant/NIH/R01-NS088604-04" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://grantome.com/grant/NIH/R01-NS088604-04</a></span><br />
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<span style="background-attachment: initial; background-repeat: initial; line-height: 1.22em;">10. ZOONOTIC, ZOONOSIS, CHRONIC WASTING DISEASE CWD TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHY TSE PRION AKA MAD DEER ELK DISEASE IN HUMANS, has it already happened, that should be the question... </span> </span></span><br />
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<span style="font-family: "arial"; font-size: 13.3333px; line-height: 1.22em;"><span style="font-family: "georgia" , serif; font-size: 10pt; line-height: 1.22em;"><span style="background-attachment: initial; background-repeat: initial; line-height: 1.22em;">Scientific opinion on chronic wasting disease (II)</span>
<span style="background-attachment: initial; background-repeat: initial; line-height: 1.22em;">EFSA Panel on Biological Hazards (BIOHAZ) Antonia Ricci Ana Allende Declan Bolton Marianne Chemaly Robert Davies Pablo Salvador Fernández Escámez ... </span></span></span><br />
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<span style="background-attachment: initial; background-repeat: initial; line-height: 1.22em;">First published: 17 January 2018 </span></span></span><br />
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<span style="font-family: "arial"; font-size: 13.3333px; line-height: 1.22em;"><span style="font-family: "arial" , sans-serif; font-size: 10pt; line-height: 1.22em;"><a href="https://doi.org/10.2903/j.efsa.2018.5132" rel="noopener noreferrer" style="color: purple; cursor: pointer; line-height: 1.22em;" target="_blank"><span style="font-family: "verdana" , sans-serif; line-height: 1.22em;"></span></a><a href="https://doi.org/10.2903/j.efsa.2018.5132" rel="noopener noreferrer" style="color: purple; cursor: pointer; line-height: 1.22em;" target="_blank">https://doi.org/10.2903/j.efsa.2018.5132</a></span></span><br />
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<span style="font-family: "arial"; font-size: 13.3333px; line-height: 1.22em;"><span style="font-family: "georgia" , serif; font-size: 10pt; line-height: 1.22em;"><span style="background-attachment: initial; background-repeat: initial; line-height: 1.22em;">also, see; </span> </span></span><br />
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<span style="font-family: "arial"; font-size: 13.3333px; line-height: 1.22em;"><span style="font-family: "georgia" , serif; font-size: 10pt; line-height: 1.22em;"><span style="background-attachment: initial; background-repeat: initial; line-height: 1.22em;">8. Even though human TSE</span></span><span style="font-family: "cambria math" , serif; font-size: 10pt; line-height: 1.22em;">‐</span><span style="font-family: "georgia" , serif; font-size: 10pt; line-height: 1.22em;">exposure risk through consumption of game from European cervids can be assumed to be minor, if at all existing, no final conclusion can be drawn due to the overall lack of scientific data. In particular the US data do not clearly exclude the possibility of human (sporadic or familial) TSE development due to consumption of venison. The Working Group thus recognizes a potential risk to consumers if a TSE would be present in European cervids. It might be prudent considering appropriate measures to reduce such a risk, e.g. excluding tissues such as CNS and lymphoid tissues from the human food chain, which would greatly reduce any potential risk for consumers. However, it is stressed that currently, no data regarding a risk of TSE infections from cervid products are available. </span><span style="font-family: "georgia" , serif; font-size: 10pt; line-height: 1.22em;"> </span></span><br />
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<span style="font-family: "arial"; font-size: 13.3333px; line-height: 1.22em;"><span style="font-family: "georgia" , serif; font-size: 10pt; line-height: 1.22em;"><span style="background-attachment: initial; background-repeat: initial; line-height: 1.22em;">The tissue distribution of infectivity in CWD</span></span><span style="font-family: "cambria math" , serif; font-size: 10pt; line-height: 1.22em;">‐</span><span style="font-family: "georgia" , serif; font-size: 10pt; line-height: 1.22em;">infected cervids is now known to extend beyond CNS and lymphoid tissues. While the removal of these specific tissues from the food chain would reduce human dietary exposure to infectivity, exclusion from the food chain of the whole carcass of any infected animal would be required to eliminate human dietary exposure. </span><span style="font-family: "georgia" , serif; font-size: 10pt; line-height: 1.22em;"> </span></span><br />
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</span><span style="font-family: "georgia" , serif; line-height: 1.22em;">zoonosis zoonotic cervid tse prion cwd to humans, preparing for the storm </span> </span></span><br />
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<span style="font-family: "arial"; font-size: 13.3333px; line-height: 1.22em;"><span style="font-size: 10pt; line-height: 1.22em;"><span style="font-family: "georgia" , serif; line-height: 1.22em;">***An alternative to modeling the species barrier is the cell-free conversion assay which points to CWD as the animal prion disease with the greatest zoonotic potential, after (and very much less than) BSE.116*** </span> </span></span><br />
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<span style="font-family: "arial"; font-size: 13.3333px; line-height: 1.22em;"><span style="font-family: "arial" , sans-serif; font-size: 10pt; line-height: 1.22em;"><a href="https://www.tandfonline.com/doi/pdf/10.4161/pri.29237" rel="noopener noreferrer" style="color: purple; cursor: pointer; line-height: 1.22em;" target="_blank"><span style="font-family: "verdana" , sans-serif; line-height: 1.22em;"></span></a><a href="https://www.tandfonline.com/doi/pdf/10.4161/pri.29237" rel="noopener noreferrer" style="color: purple; cursor: pointer; line-height: 1.22em;" target="_blank">https://www.tandfonline.com/doi/pdf/10.4161/pri.29237</a></span></span><br />
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<span style="background-attachment: initial; background-repeat: initial; line-height: 1.22em;">To date there is no direct evidence that CWD has been or can be transmitted from animals to humans. </span>
<span style="background-attachment: initial; background-repeat: initial; line-height: 1.22em;">However, initial findings from a laboratory research project funded by the Alberta Prion Research Institute (APRI) and Alberta Livestock Meat Agency (ALMA), and led by a Canadian Food Inspection Agency (CFIA) scientist indicate that CWD has been transmitted to cynomolgus macaques (the non-human primate species most closely related to humans that may be used in research), through both the intracranial and oral routes of exposure. </span>
<span style="background-attachment: initial; background-repeat: initial; line-height: 1.22em;">Both infected brain and muscle tissues were found to transmit disease. </span>
<span style="background-attachment: initial; background-repeat: initial; line-height: 1.22em;">Health Canada’s Health Products and Food Branch (HPFB) was asked to consider the impact of these findings on the Branch’s current position on CWD in health products and foods. </span>
<span style="background-attachment: initial; background-repeat: initial; line-height: 1.22em;">Summary and Recommendation: </span>
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<span style="background-attachment: initial; background-repeat: initial; line-height: 1.22em;">Health Portfolio partners were recently made aware of initial findings from a research project led by a CFIA scientist that have demonstrated that cynomolgus macaques can be infected via intracranial exposure and oral gavage with CWD infected muscle. </span>
<span style="background-attachment: initial; background-repeat: initial; line-height: 1.22em;">These findings suggest that CWD, under specific experimental conditions, has the potential to cross the human species barrier, including by enteral feeding of CWD infected muscle. </span> </span></span><br />
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<span style="font-family: "arial"; font-size: 13.3333px; line-height: 1.22em;"><span style="font-family: "arial" , sans-serif; font-size: 10pt; line-height: 1.22em;"><a href="https://www.thetyee.ca/Documents/2017/06/24/Risk-Advisory-Opinion-CWD-2017.pdf" rel="noopener noreferrer" style="color: purple; cursor: pointer; line-height: 1.22em;" target="_blank"><span style="font-family: "verdana" , sans-serif; line-height: 1.22em;"></span></a><a href="https://www.thetyee.ca/Documents/2017/06/24/Risk-Advisory-Opinion-CWD-2017.pdf" rel="noopener noreferrer" style="color: purple; cursor: pointer; line-height: 1.22em;" target="_blank">https://www.thetyee.ca/Documents/2017/06/24/Risk-Advisory-Opinion-CWD-2017.pdf</a></span></span><br />
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<span style="font-family: "arial"; font-size: 13.3333px; line-height: 1.22em;"><span style="font-size: 10pt; line-height: 1.22em;"><span style="font-family: "georgia" , serif; line-height: 1.22em;">*** WDA 2016 NEW YORK *** </span> </span></span><br />
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<span style="font-family: "arial"; font-size: 13.3333px; line-height: 1.22em;"><span style="font-size: 10pt; line-height: 1.22em;"><span style="font-family: "georgia" , serif; line-height: 1.22em;">
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<span style="font-family: "arial"; font-size: 13.3333px; line-height: 1.22em;"><span style="font-size: 10pt; line-height: 1.22em;"><span style="font-family: "georgia" , serif; line-height: 1.22em;">We found that CWD adapts to a new host more readily than BSE and that human PrP was unexpectedly prone to misfolding by CWD prions. </span>
<span style="font-family: "georgia" , serif; line-height: 1.22em;">In addition, we investigated the role of specific regions of the bovine, deer and human PrP protein in resistance to conversion by prions from another species. </span> </span></span><br />
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<span style="font-family: "arial"; font-size: 13.3333px; line-height: 1.22em;"><span style="font-size: 10pt; line-height: 1.22em;"><span style="font-family: "georgia" , serif; line-height: 1.22em;">***We have concluded that the human protein has a region that confers unusual susceptibility to conversion by CWD prions. </span> </span></span><br />
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<span style="font-family: "arial"; font-size: 13.3333px; line-height: 1.22em;"><span style="font-size: 10pt; line-height: 1.22em;"><span style="font-family: "georgia" , serif; line-height: 1.22em;">Student Presentations </span></span></span><br />
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<span style="font-family: "arial"; font-size: 13.3333px; line-height: 1.22em;"><span style="font-size: 10pt; line-height: 1.22em;"><span style="font-family: "georgia" , serif; line-height: 1.22em;">Session 2 </span> </span></span><br />
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<span style="font-family: "arial"; font-size: 13.3333px; line-height: 1.22em;"><span style="font-size: 10pt; line-height: 1.22em;"><span style="font-family: "georgia" , serif; line-height: 1.22em;">
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<span style="font-family: "arial"; font-size: 13.3333px; line-height: 1.22em;"><span style="font-size: 10pt; line-height: 1.22em;"><span style="font-family: "georgia" , serif; line-height: 1.22em;">The species barriers and public health threat of CWD and BSE prions </span> </span></span><br />
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<span style="font-family: "arial"; font-size: 13.3333px; line-height: 1.22em;"><span style="font-size: 10pt; line-height: 1.22em;"><span style="font-family: "georgia" , serif; line-height: 1.22em;">Ms. Kristen Davenport1, Dr. Davin Henderson1, Dr. Candace Mathiason1, Dr. Edward Hoover1 1Colorado State University </span> </span></span><br />
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<span style="font-family: "arial"; font-size: 13.3333px; line-height: 1.22em;"><span style="font-size: 10pt; line-height: 1.22em;"><span style="font-family: "georgia" , serif; line-height: 1.22em;">
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<span style="font-family: "arial"; font-size: 13.3333px; line-height: 1.22em;"><span style="font-size: 10pt; line-height: 1.22em;"><span style="font-family: "georgia" , serif; line-height: 1.22em;">Chronic wasting disease (CWD) is spreading rapidly through cervid populations in the USA. </span></span></span><br />
<span style="font-family: "arial"; font-size: 13.3333px; line-height: 1.22em;"><span style="font-size: 10pt; line-height: 1.22em;"><span style="font-family: "georgia" , serif; line-height: 1.22em;">
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<span style="font-family: "arial"; font-size: 13.3333px; line-height: 1.22em;"><span style="font-size: 10pt; line-height: 1.22em;"><span style="font-family: "georgia" , serif; line-height: 1.22em;">Bovine </span></span></span><span style="font-family: "georgia" , serif; font-size: 10pt; line-height: 1.22em;">spongiform encephalopathy (BSE, mad cow disease) arose in the 1980s because cattle were fed recycled animal protein. </span><span style="font-family: "arial"; font-size: 10pt;">
</span><span style="font-family: "georgia" , serif; font-size: 10pt; line-height: 1.22em;">These and other prion diseases are caused by abnormal folding of the normal prion protein (PrP) into a disease causing form (PrPd), which is pathogenic to nervous system cells and can cause subsequent PrP to misfold. CWD spreads among cervids very efficiently, but it has not yet infected humans. On the other hand, BSE was spread only when cattle consumed infected bovine or ovine tissue, but did infect humans and other species. </span><span style="font-family: "arial"; font-size: 10pt;">
</span><span style="font-family: "georgia" , serif; font-size: 10pt; line-height: 1.22em;">The objective of this research is to understand the role of PrP structure in cross-species infection by CWD and BSE. To study the propensity of each species’ PrP to be induced to misfold by the presence of PrPd from verious species, we have used an in vitro system that permits detection of PrPd in real-time. </span><span style="font-family: "arial"; font-size: 10pt;">
</span><span style="font-family: "georgia" , serif; font-size: 10pt; line-height: 1.22em;">We measured the conversion efficiency of various combinations of PrPd seeds and PrP substrate combinations. </span><span style="font-family: "arial"; font-size: 10pt;"> </span><br />
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<span style="font-family: "arial"; font-size: 10pt;"></span><span style="font-family: "georgia" , serif; font-size: 10pt; line-height: 1.22em;">We observed the cross-species behavior of CWD and BSE, in addition to feline-adapted CWD and BSE. </span><br />
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<span style="font-family: "georgia" , serif; font-size: 10pt; line-height: 1.22em;">We found that CWD adapts to a new host more readily than BSE and that human PrP was unexpectedly prone to misfolding by CWD prions. In addition, we investigated the role of specific regions of the bovine, deer and human PrP protein in resistance to conversion by prions from another species. </span><span style="font-family: "arial"; font-size: 10pt;"> </span><br />
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<span style="font-family: "arial"; font-size: 13.3333px; line-height: 1.22em;"><span style="font-size: 10pt; line-height: 1.22em;"><span style="font-family: "georgia" , serif; line-height: 1.22em;">
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<span style="font-family: "arial"; font-size: 13.3333px; line-height: 1.22em;"><span style="font-size: 10pt; line-height: 1.22em;"><span style="font-family: "georgia" , serif; line-height: 1.22em;">***We have concluded that the human protein has a region that confers unusual susceptibility to conversion by CWD prions. </span></span></span><br />
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<span style="font-family: "arial"; font-size: 13.3333px; line-height: 1.22em;"><span style="font-size: 10pt; line-height: 1.22em;"><span style="font-family: "georgia" , serif; line-height: 1.22em;">
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<span style="font-family: "arial"; font-size: 13.3333px; line-height: 1.22em;"><span style="font-size: 10pt; line-height: 1.22em;"><span style="font-family: "georgia" , serif; line-height: 1.22em;">CWD is unique among prion diseases in its rapid spread in natural populations. BSE prions are essentially unaltered upon passage to a new species, while CWD adapts to the new species. </span></span></span><br />
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<span style="font-family: "arial"; font-size: 13.3333px; line-height: 1.22em;"><span style="font-size: 10pt; line-height: 1.22em;"><span style="font-family: "georgia" , serif; line-height: 1.22em;">
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<span style="font-family: "arial"; font-size: 13.3333px; line-height: 1.22em;"><span style="font-size: 10pt; line-height: 1.22em;"><span style="font-family: "georgia" , serif; line-height: 1.22em;">This adaptation has consequences for surveillance of humans exposed to CWD. </span></span></span><br />
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<span style="font-family: "arial"; font-size: 13.3333px; line-height: 1.22em;"><span style="font-size: 10pt; line-height: 1.22em;"><span style="font-family: "georgia" , serif; line-height: 1.22em;">Wildlife Disease Risk Communication Research Contributes to Wildlife Trust Administration Exploring perceptions about chronic wasting disease risks among wildlife and agriculture professionals and stakeholders</span></span></span><br />
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</span><span style="font-family: "arial" , sans-serif; font-size: 10pt; line-height: 1.22em;"><a href="http://www.wda2016.org/uploads/5/8/6/1/58613359/wda_2016_conference_proceedings_low_res.pdf" rel="noopener noreferrer" style="color: purple; cursor: pointer; line-height: 1.22em;" target="_blank"><span style="font-family: "verdana" , sans-serif; line-height: 1.22em;"></span></a><a href="http://www.wda2016.org/uploads/5/8/6/1/58613359/wda_2016_conference_proceedings_low_res.pdf" rel="noopener noreferrer" style="color: purple; cursor: pointer; line-height: 1.22em;" target="_blank">http://www.wda2016.org/uploads/5/8/6/1/58613359/wda_2016_conference_proceedings_low_res.pdf</a></span></span><br />
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</span><span style="font-family: "arial" , sans-serif; font-size: 10pt; line-height: 1.22em;"><a href="https://www.cdc.gov/prions/cwd/transmission.html" rel="noopener noreferrer" style="color: purple; cursor: pointer; line-height: 1.22em;" target="_blank"><span style="font-family: "verdana" , sans-serif; line-height: 1.22em;"></span></a><a href="https://www.cdc.gov/prions/cwd/transmission.html" rel="noopener noreferrer" style="color: purple; cursor: pointer; line-height: 1.22em;" target="_blank">https://www.cdc.gov/prions/cwd/transmission.html</a></span></span><br />
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<span style="font-family: "arial"; font-size: 13.3333px; line-height: 1.22em;"><span style="font-size: 10pt; line-height: 1.22em;"><span style="font-family: "georgia" , serif; line-height: 1.22em;">TUESDAY, SEPTEMBER 12, 2017 </span> </span></span><br />
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<span style="font-family: "arial"; font-size: 13.3333px; line-height: 1.22em;"><span style="font-size: 10pt; line-height: 1.22em;"><span style="font-family: "georgia" , serif; line-height: 1.22em;">CDC Now Recommends Strongly consider having the deer or elk tested for CWD before you eat the meat</span></span></span><br />
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<span style="font-family: "arial"; font-size: 13.3333px; line-height: 1.22em;"><span style="font-family: "arial" , sans-serif; font-size: 10pt; line-height: 1.22em;"><a href="http://chronic-wasting-disease.blogspot.com/2017/09/cdc-now-recommends-strongly-consider.html" rel="noopener noreferrer" style="color: purple; cursor: pointer; line-height: 1.22em;" target="_blank">http://chronic-wasting-disease.blogspot.com/2017/09/cdc-now-recommends-strongly-consider.html</a></span></span><br />
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</span><span style="font-family: "georgia" , serif; line-height: 1.22em;">SATURDAY, JANUARY 27, 2018</span></span></span><br />
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<span style="font-family: "arial"; font-size: 13.3333px; line-height: 1.22em;"><span style="font-size: 10pt; line-height: 1.22em;"><span style="font-family: "georgia" , serif; line-height: 1.22em;"></span></span></span><span style="font-family: "arial"; font-size: 13.3333px; line-height: 1.22em;"><span style="font-size: 10pt; line-height: 1.22em;"><span style="font-family: "georgia" , serif; line-height: 1.22em;">CDC CHRONIC WASTING DISEASE CWD TSE PRION UPDATE REPORT USA JANUARY 2018</span> </span></span><br />
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<span style="font-family: "arial"; font-size: 13.3333px; line-height: 1.22em;"><span style="font-family: "arial" , sans-serif; font-size: 10pt; line-height: 1.22em;"><a href="http://chronic-wasting-disease.blogspot.com/2018/01/cdc-chronic-wasting-disease-cwd-tse.html" rel="noopener noreferrer" style="color: purple; cursor: pointer; line-height: 1.22em;" target="_blank"><span style="font-family: "verdana" , sans-serif; line-height: 1.22em;"></span></a><a href="http://chronic-wasting-disease.blogspot.com/2018/01/cdc-chronic-wasting-disease-cwd-tse.html" rel="noopener noreferrer" style="color: purple; cursor: pointer; line-height: 1.22em;" target="_blank">http://chronic-wasting-disease.blogspot.com/2018/01/cdc-chronic-wasting-disease-cwd-tse.html</a></span></span><br />
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<span style="font-family: "arial"; font-size: 13.3333px; line-height: 1.22em;"><span style="font-size: 10pt; line-height: 1.22em;"><span style="font-family: "georgia" , serif; line-height: 1.22em;">Subject: CDC CHRONIC WASTING DISEASE CWD TSE PRION UPDATE REPORT USA JANUARY 2018</span>
<span style="font-family: "georgia" , serif; line-height: 1.22em;">CHRONIC WASTING DISEASE CWD TSE PRION IS THE USA AND NORTH AMERICA'S MAD COW DISEASE. </span>
<span style="font-family: "georgia" , serif; line-height: 1.22em;">THE USDA INC ET AL WORKED VERY HARD CONCEALING BSE TSE PRION IN CATTLE. they almost succeeded $$$</span>
<span style="font-family: "georgia" , serif; line-height: 1.22em;">BUT CWD TSE PRION IN CERVIDS IS A DIFFERENT BEAST, THE COVER UP THERE, USDA INC COULD NOT CONTAIN.</span>
<span style="font-family: "georgia" , serif; line-height: 1.22em;">SPORADIC CJD IS 85%+ OF ALL HUMAN TSE PRION DISEASE.</span>
<span style="font-family: "georgia" , serif; line-height: 1.22em;">SPORADIC CJD HAS NOW BEEN LINKED TO TYPICAL AND ATYPICAL BSE, SCRAPIE, AND CWD.</span>
<span style="font-family: "georgia" , serif; line-height: 1.22em;">SPORADIC/SPONTANEOUS TSE HAS NEVER BEEN PROVEN.</span> </span></span><br />
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<span style="font-family: "arial"; font-size: 13.3333px; line-height: 1.22em;"><span style="font-size: 10pt; line-height: 1.22em;"><span style="font-family: "georgia" , serif; line-height: 1.22em;">***Moreover, sporadic disease has never been observed in breeding colonies or primate research laboratories, most notably among hundreds of animals over several decades of study at the National Institutes of Health25, and in nearly twenty older animals continuously housed in our own facility.***</span></span></span><br />
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</span><span style="font-family: "arial" , sans-serif; font-size: 10pt; line-height: 1.22em;"><a href="https://www.nature.com/articles/srep11573" rel="noopener noreferrer" style="color: purple; cursor: pointer; line-height: 1.22em;" target="_blank"><span style="font-family: "verdana" , sans-serif; line-height: 1.22em;"></span></a><a href="https://www.nature.com/articles/srep11573" rel="noopener noreferrer" style="color: purple; cursor: pointer; line-height: 1.22em;" target="_blank">https://www.nature.com/articles/srep11573</a></span></span><br />
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<span style="background-attachment: initial; background-repeat: initial; line-height: 1.22em;">CDC CWD TSE PRION UPDATE USA JANUARY 2018</span> </span></span><br />
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<span style="font-family: "arial"; font-size: 13.3333px; line-height: 1.22em;"><span style="font-family: "georgia" , serif; font-size: 10pt; line-height: 1.22em;"><span style="background-attachment: initial; background-repeat: initial; line-height: 1.22em;">
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<span style="font-family: "arial"; font-size: 13.3333px; line-height: 1.22em;"><span style="font-family: "georgia" , serif; font-size: 10pt; line-height: 1.22em;"><span style="background-attachment: initial; background-repeat: initial; line-height: 1.22em;">As of January 2018, CWD in free-ranging deer, elk and/or moose has been reported in at least 22 states in the continental United States, as well as two provinces in Canada. In addition, CWD has been reported in reindeer and moose in Norway, and a small number of imported cases have been reported in South Korea. The disease has also been found in farmed deer and elk. CWD was first identified in captive deer in the late 1960s in Colorado and in wild deer in 1981. By the 1990s, it had been reported in surrounding areas in northern Colorado and southern Wyoming. Since 2000, the area known to be affected by CWD in free-ranging animals has increased to at least 22 states, including states in the Midwest, Southwest, and limited areas on the East Coast.. It is possible that CWD may also occur in other states without strong animal surveillance systems, but that cases haven’t been detected yet. Once CWD is established in an area, the risk can remain for a long time in the environment. The affected areas are likely to continue to expand. Nationwide, the overall occurrence of CWD in free-ranging deer and elk is relatively low. However, in several locations where the disease is established, infection rates may exceed 10 percent (1 in 10), and localized infection rates of more than 25 percent (1 in 4) have been reported. The infection rates among some captive deer can be much higher, with a rate of 79% (nearly 4 in 5) reported from at least one captive herd. </span></span></span><br />
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<span style="font-family: "arial"; font-size: 13.3333px; line-height: 1.22em;"><span style="font-family: "georgia" , serif; font-size: 10pt; line-height: 1.22em;"><span style="background-attachment: initial; background-repeat: initial; line-height: 1.22em;">As of January 2018, there were 186 counties in 22 states with reported CWD in free-ranging cervids... </span> </span></span><br />
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<span style="font-family: "arial"; font-size: 13.3333px; line-height: 1.22em;"><span style="font-family: "georgia" , serif; font-size: 10pt; line-height: 1.22em;"><span style="background-attachment: initial; background-repeat: initial; line-height: 1.22em;">Chronic Wasting Disease Among Free-Ranging Cervids by County, United States, January 2018 </span> </span></span><br />
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<span style="font-family: "arial"; font-size: 13.3333px; line-height: 1.22em;"><span style="font-family: "arial" , sans-serif; font-size: 10pt; line-height: 1.22em;"><a href="https://www.cdc.gov/prions/cwd/occurrence.html" rel="noopener noreferrer" style="color: purple; cursor: pointer; line-height: 1.22em;" target="_blank"><span style="font-family: "verdana" , sans-serif; line-height: 1.22em;"></span></a><a href="https://www.cdc.gov/prions/cwd/occurrence.html" rel="noopener noreferrer" style="color: purple; cursor: pointer; line-height: 1.22em;" target="_blank">https://www.cdc.gov/prions/cwd/occurrence.html</a></span></span><br />
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<span style="font-family: "georgia" , serif; line-height: 1.22em;">*** 2017-2018 CWD TSE Prion UPDATE</span> </span></span><br />
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<span style="font-family: "arial"; font-size: 13.3333px; line-height: 1.22em;"><span style="font-family: "arial" , sans-serif; font-size: 10pt; line-height: 1.22em;"><a href="https://www.cdc.gov/prions/cwd/occurrence.html" rel="noopener noreferrer" style="color: purple; cursor: pointer; line-height: 1.22em;" target="_blank"><span style="font-family: "verdana" , sans-serif; line-height: 1.22em;"></span></a><a href="https://www.cdc.gov/prions/cwd/occurrence.html" rel="noopener noreferrer" style="color: purple; cursor: pointer; line-height: 1.22em;" target="_blank">https://www.cdc.gov/prions/cwd/occurrence.html</a></span></span><br />
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<span style="font-family: "arial"; font-size: 13.3333px; line-height: 1.22em;"><span style="font-size: 10pt; line-height: 1.22em;"><span style="font-family: "georgia" , serif; line-height: 1.22em;">*** The potential impact of prion diseases on human health was greatly magnified by the recognition that interspecies transfer of BSE to humans by beef ingestion resulted in vCJD. While changes in animal feed constituents and slaughter practices appear to have curtailed vCJD, there is concern that CWD of free-ranging deer and elk in the U.S. might also cross the species barrier. Thus, consuming venison could be a source of human prion disease. Whether BSE and CWD represent interspecies scrapie transfer or are newly arisen prion diseases is unknown. Therefore, the possibility of transmission of prion disease through other food animals cannot be ruled out. There is evidence that vCJD can be transmitted through blood transfusion. There is likely a pool of unknown size of asymptomatic individuals infected with vCJD, and there may be asymptomatic individuals infected with the CWD equivalent. These circumstances represent a potential threat to blood, blood products, and plasma supplies. </span> </span></span><br />
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<span style="font-family: "arial"; font-size: 13.3333px; line-height: 1.22em;"><span style="font-family: "arial" , sans-serif; font-size: 10pt; line-height: 1.22em;"><a href="http://cdmrp.army.mil/prevfunded/nprp/NPRP_Summit_Final_Report.pdf" rel="noopener noreferrer" style="color: purple; cursor: pointer; line-height: 1.22em;" target="_blank"><span style="font-family: "verdana" , sans-serif; line-height: 1.22em;"></span></a><a href="http://cdmrp.army.mil/prevfunded/nprp/NPRP_Summit_Final_Report.pdf" rel="noopener noreferrer" style="color: purple; cursor: pointer; line-height: 1.22em;" target="_blank">http://cdmrp.army.mil/prevfunded/nprp/NPRP_Summit_Final_Report.pdf</a></span></span><br />
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<span style="font-family: "georgia" , serif; line-height: 1.22em;">Transmission Studies</span>
<span style="font-family: "georgia" , serif; line-height: 1.22em;">Mule deer transmissions of CWD were by intracerebral inoculation and compared with natural cases {the following was written but with a single line marked through it ''first passage (by this route)}....TSS</span>
<span style="font-family: "georgia" , serif; line-height: 1.22em;">resulted in a more rapidly progressive clinical disease with repeated episodes of synocopy ending in coma. One control animal became affected, it is believed through contamination of inoculum (?saline). Further CWD transmissions were carried out by Dick Marsh into ferret, mink and squirrel monkey. Transmission occurred in ALL of these species with the shortest incubation period in the ferret.</span> </span></span><br />
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<span style="font-family: "arial"; font-size: 13.3333px; line-height: 1.22em;"><span style="font-family: "arial" , sans-serif; font-size: 10pt; line-height: 1.22em;"><a href="https://web.archive.org/web/20090506002237/http:/www.bseinquiry.gov.uk/files/mb/m11b/tab01.pdf" rel="noopener noreferrer" style="color: purple; cursor: pointer; line-height: 1.22em;" target="_blank"><span style="font-family: "verdana" , sans-serif; line-height: 1.22em;"></span></a><a href="https://web.archive.org/web/20090506002237/http://www.bseinquiry.gov.uk/files/mb/m11b/tab01.pdf" rel="noopener noreferrer" style="color: purple; cursor: pointer; line-height: 1.22em;" target="_blank">https://web.archive.org/web/20090506002237/http://www.bseinquiry.gov.uk/files/mb/m11b/tab01.pdf</a></span></span><br />
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</span><span style="font-family: "arial" , sans-serif; font-size: 10pt; line-height: 1.22em;"><a href="http://www.fsis.usda.gov/OPPDE/Comments/03-025IFA/03-025IFA-2.pdf" rel="noopener noreferrer" style="color: purple; cursor: pointer; line-height: 1.22em;" target="_blank"><span style="font-family: "verdana" , sans-serif; line-height: 1.22em;"></span></a><a href="http://www.fsis.usda.gov/OPPDE/Comments/03-025IFA/03-025IFA-2.pdf" rel="noopener noreferrer" style="color: purple; cursor: pointer; line-height: 1.22em;" target="_blank">http://www.fsis.usda.gov/OPPDE/Comments/03-025IFA/03-025IFA-2.pdf</a></span></span><br />
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</span><span style="font-family: "georgia" , serif; line-height: 1.22em;">Prion Infectivity in Fat of Deer with Chronic Wasting Disease</span></span><span style="font-family: "ms gothic"; font-size: 10pt; line-height: 1.22em;">▿</span><span style="font-family: "georgia" , serif; font-size: 10pt; line-height: 1.22em;"> </span><span style="font-family: "georgia" , serif; font-size: 10pt; line-height: 1.22em;"> </span></span><br />
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<span style="font-family: "arial"; font-size: 13.3333px; line-height: 1.22em;"><span style="font-family: "georgia" , serif; font-size: 10pt; line-height: 1.22em;"><span style="background-attachment: initial; background-repeat: initial; line-height: 1.22em;">Brent Race#, Kimberly Meade-White#, Richard Race and Bruce Chesebro* + Author Affiliations</span> </span></span><br />
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<span style="font-family: "arial"; font-size: 13.3333px; line-height: 1.22em;"><span style="font-family: "georgia" , serif; font-size: 10pt; line-height: 1.22em;"><span style="background-attachment: initial; background-repeat: initial; line-height: 1.22em;">
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<span style="font-family: "arial"; font-size: 13.3333px; line-height: 1.22em;"><span style="font-family: "georgia" , serif; font-size: 10pt; line-height: 1.22em;"><span style="background-attachment: initial; background-repeat: initial; line-height: 1.22em;">In mice, prion infectivity was recently detected in fat. Since ruminant fat is consumed by humans and fed to animals, we determined infectivity titers in fat from two CWD-infected deer. Deer fat devoid of muscle contained low levels of CWD infectivity and might be a risk factor for prion infection of other species.</span> </span></span><br />
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<span style="font-family: "arial"; font-size: 13.3333px; line-height: 1.22em;"><span style="font-family: "arial" , sans-serif; font-size: 10pt; line-height: 1.22em;"><a href="http://jvi.asm.org/content/83/18/9608.full" rel="noopener noreferrer" style="color: purple; cursor: pointer; line-height: 1.22em;" target="_blank"><span style="font-family: "verdana" , sans-serif; line-height: 1.22em;"></span></a><a href="http://jvi.asm.org/content/83/18/9608.full" rel="noopener noreferrer" style="color: purple; cursor: pointer; line-height: 1.22em;" target="_blank">http://jvi.asm.org/content/83/18/9608.full</a></span></span><br />
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<span style="font-family: "georgia" , serif; line-height: 1.22em;">Prions in Skeletal Muscles of Deer with Chronic Wasting Disease </span> </span></span><br />
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<span style="font-family: "arial"; font-size: 13.3333px; line-height: 1.22em;"><span style="font-size: 10pt; line-height: 1.22em;"><span style="font-family: "georgia" , serif; line-height: 1.22em;">
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<span style="font-family: "arial"; font-size: 13.3333px; line-height: 1.22em;"><span style="font-size: 10pt; line-height: 1.22em;"><span style="font-family: "georgia" , serif; line-height: 1.22em;">Here bioassays in transgenic mice expressing cervid prion protein revealed the presence of infectious prions in skeletal muscles of CWD-infected deer, demonstrating that humans consuming or handling meat from CWD-infected deer are at risk to prion exposure.</span> </span></span><br />
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<span style="font-family: "arial"; font-size: 13.3333px; line-height: 1.22em;"><span style="font-family: "arial" , sans-serif; font-size: 10pt; line-height: 1.22em;"><a href="http://science.sciencemag.org/content/311/5764/1117.long" rel="noopener noreferrer" style="color: purple; cursor: pointer; line-height: 1.22em;" target="_blank"><span style="font-family: "verdana" , sans-serif; line-height: 1.22em;"></span></a><a href="http://science.sciencemag.org/content/311/5764/1117.long" rel="noopener noreferrer" style="color: purple; cursor: pointer; line-height: 1.22em;" target="_blank">http://science.sciencemag.org/content/311/5764/1117.long</a></span></span><br />
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</span><span style="font-family: "georgia" , serif; line-height: 1.22em;">*** now, let’s see what the authors said about this casual link, personal communications years ago, and then the latest on the zoonotic potential from CWD to humans from the TOKYO PRION 2016 CONFERENCE.</span> </span></span><br />
<span style="font-family: "arial"; font-size: 13.3333px; line-height: 1.22em;"><span style="font-size: 10pt; line-height: 1.22em;"><span style="font-family: "georgia" , serif; line-height: 1.22em;">
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<span style="font-family: "arial"; font-size: 13.3333px; line-height: 1.22em;"><span style="font-size: 10pt; line-height: 1.22em;"><span style="font-family: "georgia" , serif; line-height: 1.22em;">see where it is stated NO STRONG evidence. </span></span></span><br />
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<span style="font-family: "arial"; font-size: 13.3333px; line-height: 1.22em;"><span style="font-size: 10pt; line-height: 1.22em;"><span style="font-family: "georgia" , serif; line-height: 1.22em;">so, does this mean there IS casual evidence ???? </span></span></span><br />
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<span style="font-family: "arial"; font-size: 13.3333px; line-height: 1.22em;"><span style="font-size: 10pt; line-height: 1.22em;"><span style="font-family: "georgia" , serif; line-height: 1.22em;">“Our conclusion stating that we found no strong evidence of CWD transmission to humans”</span> </span></span><br />
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<span style="font-family: "arial"; font-size: 13.3333px; line-height: 1.22em;"><span style="font-size: 10pt; line-height: 1.22em;"><span style="font-family: "georgia" , serif; line-height: 1.22em;">
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<span style="font-family: "arial"; font-size: 13.3333px; line-height: 1.22em;"><span style="font-size: 10pt; line-height: 1.22em;"><span style="font-family: "georgia" , serif; line-height: 1.22em;">From: TSS (216-119-163-189.ipset45.wt.net)</span> </span></span><br />
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<span style="font-family: "arial"; font-size: 13.3333px; line-height: 1.22em;"><span style="font-size: 10pt; line-height: 1.22em;"><span style="font-family: "georgia" , serif; line-height: 1.22em;">Subject: CWD aka MAD DEER/ELK TO HUMANS ???</span> </span></span><br />
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<span style="font-family: "arial"; font-size: 13.3333px; line-height: 1.22em;"><span style="font-size: 10pt; line-height: 1.22em;"><span style="font-family: "georgia" , serif; line-height: 1.22em;">
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<span style="font-family: "arial"; font-size: 13.3333px; line-height: 1.22em;"><span style="font-size: 10pt; line-height: 1.22em;"><span style="font-family: "georgia" , serif; line-height: 1.22em;">Date: September 30, 2002 at 7:06 am PST</span> </span></span><br />
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<span style="font-family: "arial"; font-size: 13.3333px; line-height: 1.22em;"><span style="font-size: 10pt; line-height: 1.22em;"><span style="font-family: "georgia" , serif; line-height: 1.22em;">
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<span style="font-family: "arial"; font-size: 13.3333px; line-height: 1.22em;"><span style="font-size: 10pt; line-height: 1.22em;"><span style="font-family: "georgia" , serif; line-height: 1.22em;">From: "Belay, Ermias"</span>
<span style="font-family: "georgia" , serif; line-height: 1.22em;">To: Cc: "Race, Richard (NIH)" ; ; "Belay, Ermias"</span> </span></span><br />
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<span style="font-family: "arial"; font-size: 13.3333px; line-height: 1.22em;"><span style="font-size: 10pt; line-height: 1.22em;"><span style="font-family: "georgia" , serif; line-height: 1.22em;">
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<span style="font-family: "arial"; font-size: 13.3333px; line-height: 1.22em;"><span style="font-size: 10pt; line-height: 1.22em;"><span style="font-family: "georgia" , serif; line-height: 1.22em;">Sent: Monday, September 30, 2002 9:22 AM</span> </span></span><br />
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<span style="font-family: "arial"; font-size: 13.3333px; line-height: 1.22em;"><span style="font-size: 10pt; line-height: 1.22em;"><span style="font-family: "georgia" , serif; line-height: 1.22em;">
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<span style="font-family: "arial"; font-size: 13.3333px; line-height: 1.22em;"><span style="font-size: 10pt; line-height: 1.22em;"><span style="font-family: "georgia" , serif; line-height: 1.22em;">S</span></span></span><span style="font-family: "georgia" , serif; font-size: 10pt; line-height: 1.22em;">ubject: RE: TO CDC AND NIH - PUB MED- 3 MORE DEATHS - CWD - YOUNG HUNTERS</span><span style="font-family: "arial"; font-size: 10pt;"> </span><br />
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<span style="font-family: "arial"; font-size: 13.3333px; line-height: 1.22em;"><span style="font-size: 10pt; line-height: 1.22em;"><span style="font-family: "georgia" , serif; line-height: 1.22em;">
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<span style="font-family: "arial"; font-size: 13.3333px; line-height: 1.22em;"><span style="font-size: 10pt; line-height: 1.22em;"><span style="font-family: "georgia" , serif; line-height: 1.22em;">Dear Sir/Madam,</span> </span></span><br />
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<span style="font-family: "arial"; font-size: 13.3333px; line-height: 1.22em;"><span style="font-size: 10pt; line-height: 1.22em;"><span style="font-family: "georgia" , serif; line-height: 1.22em;">
</span></span></span>
<span style="font-family: "arial"; font-size: 13.3333px; line-height: 1.22em;"><span style="font-size: 10pt; line-height: 1.22em;"><span style="font-family: "georgia" , serif; line-height: 1.22em;">In the Archives of Neurology you quoted (the abstract of which was attached to your email), we did not say CWD in humans will present like variant CJD.. That assumption would be wrong. I encourage you to read the whole article and call me if you have questions or need more clarification (phone: 404-639-3091). Also, we do not claim that "no-one has ever been infected with prion disease from eating venison." Our conclusion stating that we found no strong evidence of CWD transmission to humans in the article you quoted or in any other forum is limited to the patients we investigated.</span>
<span style="font-family: "georgia" , serif; line-height: 1.22em;">Ermias Belay, M.D. Centers for Disease Control and Prevention</span> </span></span><br />
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<span style="font-family: "arial"; font-size: 13.3333px; line-height: 1.22em;"><span style="font-size: 10pt; line-height: 1.22em;"><span style="font-family: "georgia" , serif; line-height: 1.22em;">
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<span style="font-family: "arial"; font-size: 13.3333px; line-height: 1.22em;"><span style="font-size: 10pt; line-height: 1.22em;"><span style="font-family: "georgia" , serif; line-height: 1.22em;">-----Original Message-----</span> </span></span><br />
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<span style="font-family: "arial"; font-size: 13.3333px; line-height: 1.22em;"><span style="font-size: 10pt; line-height: 1.22em;"><span style="font-family: "georgia" , serif; line-height: 1.22em;">From: </span></span></span><br />
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<span style="font-family: "arial"; font-size: 13.3333px; line-height: 1.22em;"><span style="font-size: 10pt; line-height: 1.22em;"><span style="font-family: "georgia" , serif; line-height: 1.22em;">
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<span style="font-family: "arial"; font-size: 13.3333px; line-height: 1.22em;"><span style="font-size: 10pt; line-height: 1.22em;"><span style="font-family: "georgia" , serif; line-height: 1.22em;">
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<span style="font-family: "arial"; font-size: 13.3333px; line-height: 1.22em;"><span style="font-size: 10pt; line-height: 1.22em;"><span style="font-family: "georgia" , serif; line-height: 1.22em;">Sent: Sunday, September 29, 2002 10:15 AM</span> </span></span><br />
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<span style="font-family: "arial"; font-size: 13.3333px; line-height: 1.22em;"><span style="font-size: 10pt; line-height: 1.22em;"><span style="font-family: "georgia" , serif; line-height: 1.22em;">
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<span style="font-family: "arial"; font-size: 13.3333px; line-height: 1.22em;"><span style="font-size: 10pt; line-height: 1.22em;"><span style="font-family: "georgia" , serif; line-height: 1.22em;">To: </span></span><span style="font-family: "arial" , sans-serif; font-size: 10pt; line-height: 1.22em;"><a href="mailto:rr26k@nih.gov" rel="noopener noreferrer" style="color: purple; cursor: pointer; line-height: 1.22em;" target="_blank"><span style="font-family: "verdana" , sans-serif; line-height: 1.22em;"></span></a><a href="mailto:rr26k@nih.gov" rel="noopener noreferrer" style="color: purple; cursor: pointer; line-height: 1.22em;" target="_blank">rr26k@nih.gov</a></span><span style="font-family: "georgia" , serif; font-size: 10pt; line-height: 1.22em;">; </span><span style="font-family: "arial" , sans-serif; font-size: 10pt; line-height: 1.22em;"><a href="mailto:rrace@niaid.nih.gov" rel="noopener noreferrer" style="color: purple; cursor: pointer; line-height: 1.22em;" target="_blank"><span style="font-family: "verdana" , sans-serif; line-height: 1.22em;"></span></a><a href="mailto:rrace@niaid.nih.gov" rel="noopener noreferrer" style="color: purple; cursor: pointer; line-height: 1.22em;" target="_blank">rrace@niaid.nih.gov</a></span><span style="font-family: "georgia" , serif; font-size: 10pt; line-height: 1.22em;">; </span><span style="font-family: "arial" , sans-serif; font-size: 10pt; line-height: 1.22em;"><a href="mailto:ebb8@CDC.GOV" rel="noopener noreferrer" style="color: purple; cursor: pointer; line-height: 1.22em;" target="_blank"><span style="font-family: "verdana" , sans-serif; line-height: 1.22em;"></span></a><a href="mailto:ebb8@CDC.GOV" rel="noopener noreferrer" style="color: purple; cursor: pointer; line-height: 1.22em;" target="_blank">ebb8@CDC.GOV</a></span><span style="font-family: "georgia" , serif; font-size: 10pt; line-height: 1.22em;"> </span></span><br />
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<span style="font-family: "arial"; font-size: 13.3333px; line-height: 1.22em;"><span style="font-family: "georgia" , serif; font-size: 10pt; line-height: 1.22em;"><span style="background-attachment: initial; background-repeat: initial; line-height: 1.22em;">Subject: TO CDC AND NIH - PUB MED- 3 MORE DEATHS - CWD - YOUNG HUNTERS</span> </span></span><br />
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<span style="font-family: "arial"; font-size: 13.3333px; line-height: 1.22em;"><span style="font-family: "georgia" , serif; font-size: 10pt; line-height: 1.22em;"><span style="background-attachment: initial; background-repeat: initial; line-height: 1.22em;">Sunday, November 10, 2002 6:26 PM </span></span></span><br />
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<span style="font-family: "arial"; font-size: 13.3333px; line-height: 1.22em;"><span style="font-family: "georgia" , serif; font-size: 10pt; line-height: 1.22em;"><span style="background-attachment: initial; background-repeat: initial; line-height: 1.22em;">Thursday, April 03, 2008</span> </span></span><br />
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<span style="font-family: "arial"; font-size: 13.3333px; line-height: 1.22em;"><span style="font-family: "georgia" , serif; font-size: 10pt; line-height: 1.22em;"><span style="background-attachment: initial; background-repeat: initial; line-height: 1.22em;">
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<span style="font-family: "arial"; font-size: 13.3333px; line-height: 1.22em;"><span style="font-family: "georgia" , serif; font-size: 10pt; line-height: 1.22em;"><span style="background-attachment: initial; background-repeat: initial; line-height: 1.22em;">A prion disease of cervids: Chronic wasting disease 2008 1: Vet Res. 2008 Apr 3;39(4):41 A prion disease of cervids: Chronic wasting disease Sigurdson CJ.</span> </span></span><br />
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<span style="font-family: "arial"; font-size: 13.3333px; line-height: 1.22em;"><span style="font-family: "georgia" , serif; font-size: 10pt; line-height: 1.22em;"><span style="background-attachment: initial; background-repeat: initial; line-height: 1.22em;">*** twenty-seven CJD patients who regularly consumed venison were reported to the Surveillance Center***,</span></span></span><br />
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<span style="background-attachment: initial; background-repeat: initial; line-height: 1.22em;">key word here is 'reported'. science has shown that CWD in humans will look like sporadic CJD. SO, how can one assume that CWD has not already transmitted to humans? they can't, and it's as simple as that. from all recorded science to date, CWD has already transmitted to humans, and it's being misdiagnosed as sporadic CJD. ...terry </span> </span></span><br />
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<span style="font-family: "arial"; font-size: 13.3333px; line-height: 1.22em;"><span style="font-family: "georgia" , serif; font-size: 10pt; line-height: 1.22em;"><span style="background-attachment: initial; background-repeat: initial; line-height: 1.22em;">*** LOOKING FOR CWD IN HUMANS AS nvCJD or as an ATYPICAL CJD, LOOKING IN ALL THE WRONG PLACES $$$ ***</span> </span></span><br />
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<span style="font-family: "arial"; font-size: 13.3333px; line-height: 1.22em;"><span style="font-family: "georgia" , serif; font-size: 10pt; line-height: 1.22em;"><span style="background-attachment: initial; background-repeat: initial; line-height: 1.22em;">*** These results would seem to suggest that CWD does indeed have zoonotic potential, at least as judged by the compatibility of CWD prions and their human PrPC target. </span></span></span><br />
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<span style="font-family: "arial"; font-size: 13.3333px; line-height: 1.22em;"><span style="font-family: "georgia" , serif; font-size: 10pt; line-height: 1.22em;"><span style="background-attachment: initial; background-repeat: initial; line-height: 1.22em;">***Furthermore, extrapolation from this simple in vitro assay suggests that if zoonotic CWD occurred, it would most likely effect those of the PRNP codon 129-MM genotype and that the PrPres type would be similar to that found in the most common subtype of sCJD (MM1).*** </span> </span></span><br />
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</span><span style="font-family: "arial" , sans-serif; font-size: 10pt; line-height: 1.22em;"><a href="https://wwwnc.cdc.gov/eid/article/20/1/13-0858_article" rel="noopener noreferrer" style="color: purple; cursor: pointer; line-height: 1.22em;" target="_blank"><span style="font-family: "verdana" , sans-serif; line-height: 1.22em;"></span></a><a href="https://wwwnc.cdc.gov/eid/article/20/1/13-0858_article" rel="noopener noreferrer" style="color: purple; cursor: pointer; line-height: 1.22em;" target="_blank">https://wwwnc.cdc.gov/eid/article/20/1/13-0858_article</a></span></span><br />
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<span style="font-family: "georgia" , serif; line-height: 1.22em;">SEE; Travel History, Hunting, and Venison Consumption Related to Prion Disease Exposure, 2006-2007 FoodNet Population Survey</span> </span></span><br />
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<span style="font-family: "arial"; font-size: 13.3333px; line-height: 1.22em;"><span style="font-size: 10pt; line-height: 1.22em;"><span style="font-family: "georgia" , serif; line-height: 1.22em;">CDC Assesses Potential Human Exposure to Prion Diseases Travel Warning</span>
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<span style="font-family: "arial"; font-size: 13.3333px; line-height: 1.22em;"><span style="font-size: 10pt; line-height: 1.22em;"><span style="font-family: "georgia" , serif; line-height: 1.22em;">release date: 23-May-2011</span>
<span style="font-family: "georgia" , serif; line-height: 1.22em;">Contact: Francesca Costanzo </span></span><span style="font-family: "arial" , sans-serif; font-size: 10pt; line-height: 1.22em;"><a href="mailto:adajmedia@elsevier.com" rel="noopener noreferrer" style="color: purple; cursor: pointer; line-height: 1.22em;" target="_blank"><span style="font-family: "verdana" , sans-serif; line-height: 1.22em;"></span></a><a href="mailto:adajmedia@elsevier.com" rel="noopener noreferrer" style="color: purple; cursor: pointer; line-height: 1.22em;" target="_blank">adajmedia@elsevier.com</a></span><span style="font-family: "georgia" , serif; font-size: 10pt; line-height: 1.22em;"> 215-239-3249 Elsevier Health Sciences</span><span style="font-family: "georgia" , serif; font-size: 10pt; line-height: 1.22em;"> </span></span><br />
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<span style="font-family: "arial"; font-size: 13.3333px; line-height: 1.22em;"><span style="font-family: "georgia" , serif; font-size: 10pt; line-height: 1.22em;"><span style="background-attachment: initial; background-repeat: initial; line-height: 1.22em;">
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<span style="font-family: "arial"; font-size: 13.3333px; line-height: 1.22em;"><span style="font-family: "georgia" , serif; font-size: 10pt; line-height: 1.22em;"><span style="background-attachment: initial; background-repeat: initial; line-height: 1.22em;">CDC assesses potential human exposure to prion diseases Study results reported in the Journal of the American Dietetic Association Philadelphia, PA, May 23, 2011 – Researchers from the Centers for Disease Control and Prevention (CDC) have examined the potential for human exposure to prion diseases, looking at hunting, venison consumption, and travel to areas in which prion diseases have been reported in animals. Three prion diseases in particular – bovine spongiform encephalopathy (BSE or “Mad Cow Disease”), variant Creutzfeldt-Jakob disease (vCJD), and chronic wasting disease (CWD) – were specified in the investigation. </span></span></span><br />
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<span style="font-family: "arial"; font-size: 13.3333px; line-height: 1.22em;"><span style="font-family: "georgia" , serif; font-size: 10pt; line-height: 1.22em;"><span style="background-attachment: initial; background-repeat: initial; line-height: 1.22em;">The results of this investigation are published in the June issue of the Journal of the American Dietetic Association.</span>
<span style="background-attachment: initial; background-repeat: initial; line-height: 1.22em;">“While prion diseases are rare, they are generally fatal for anyone who becomes infected. More than anything else, the results of this study support the need for continued surveillance of prion diseases,” commented lead investigator Joseph Y. Abrams, MPH, National Center for Emerging and Zoonotic Infectious Diseases, CDC, Atlanta.”But it’s also important that people know the facts about these diseases, especially since this study shows that a good number of people have participated in activities that may expose them to infection-causing agents.”</span>
<span style="background-attachment: initial; background-repeat: initial; line-height: 1.22em;">Although rare, human prion diseases such as CJD may be related to BSE. Prion (proteinaceous infectious particles) diseases are a group of rare brain diseases that affect humans and animals. When a person gets a prion disease, brain function is impaired. This causes memory and personality changes, dementia, and problems with movement. All of these worsen over time. These diseases are invariably fatal. Since these diseases may take years to manifest, knowing the extent of human exposure to possible prion diseases could become important in the event of an outbreak.</span>
<span style="background-attachment: initial; background-repeat: initial; line-height: 1.22em;">CDC investigators evaluated the results of the 2006-2007 population survey conducted by the Foodborne Diseases Active Surveillance Network (FoodNet). </span></span></span><br />
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<span style="font-family: "arial"; font-size: 13.3333px; line-height: 1.22em;"><span style="font-family: "georgia" , serif; font-size: 10pt; line-height: 1.22em;"><span style="background-attachment: initial; background-repeat: initial; line-height: 1.22em;">This survey collects information on food consumption practices, health outcomes, and demographic characteristics of residents of the participating Emerging Infections Program sites. The survey was conducted in Connecticut, Georgia, Maryland, Minnesota, New Mexico, Oregon, and Tennessee, as well as five counties in the San Francisco Bay area, seven counties in the Greater Denver area, and 34 counties in western and northeastern New York.</span>
<span style="background-attachment: initial; background-repeat: initial; line-height: 1.22em;">Survey participants were asked about behaviors that could be associated with exposure to the agents causing BSE and CWD, including travel to the nine countries considered to be BSE-endemic (United Kingdom, Republic of Ireland, France, Portugal, Switzerland, Italy, the Netherlands, Germany, Spain) and the cumulative length of stay in each of those countries. Respondents were asked if they ever had hunted for deer or elk, and if that hunting had taken place in areas considered to be CWD-endemic (northeastern Colorado, southeastern Wyoming or southwestern Nebraska). They were also asked if they had ever consumed venison, the frequency of consumption, and whether the meat came from the wild.</span>
<span style="background-attachment: initial; background-repeat: initial; line-height: 1.22em;">The proportion of survey respondents who reported travel to at least one of the nine BSE endemic countries since 1980 was 29.5%. Travel to the United Kingdom was reported by 19.4% of respondents, higher than to any other BSE-endemic country. Among those who traveled, the median duration of travel to the United Kingdom (14 days) was longer than that of any other BSE-endemic country. Travelers to the UK were more likely to have spent at least 30 days in the country (24.9%) compared to travelers to any other BSE endemic country. The prevalence and extent of travel to the UK indicate that health concerns in the UK may also become issues for US residents.</span>
<span style="background-attachment: initial; background-repeat: initial; line-height: 1.22em;">The proportion of survey respondents reporting having hunted for deer or elk was 18.5% and 1.2% reported having hunted for deer or elk in CWD-endemic areas. Venison consumption was reported by 67.4% of FoodNet respondents, and 88.6% of those reporting venison consumption had obtained all of their meat from the wild. </span></span></span><br />
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<span style="font-family: "georgia" , serif; font-size: 10pt; line-height: 1.22em;"><span style="background-attachment: initial; background-repeat: initial; line-height: 1.22em;">These findings reinforce the importance of CWD surveillance and control programs for wild deer and elk to reduce human exposure to the CWD agent. Hunters in CWD-endemic areas are advised to take simple precautions such as: avoiding consuming meat from sickly deer or elk, avoiding consuming brain or spinal cord tissues, minimizing the handling of brain and spinal cord tissues, and wearing gloves when field-dressing carcasses.</span>
<span style="background-attachment: initial; background-repeat: initial; line-height: 1.22em;">According to Abrams, “The 2006-2007 FoodNet population survey provides useful information should foodborne prion infection become an increasing public health concern in the future. The data presented describe the prevalence of important behaviors and their associations with demographic characteristics. Surveillance of BSE, CWD, and human prion diseases are critical aspects of addressing the burden of these diseases in animal populations and how that may relate to human health.”</span>
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<span style="background-attachment: initial; background-repeat: initial; line-height: 1.22em;">The article is “Travel history, hunting, and venison consumption related to prion disease exposure, 2006-2007 FoodNet population survey” by Joseph Y. Abrams, MPH; Ryan A. Maddox, MPH; Alexis R Harvey, MPH; Lawrence B. Schonberger, MD; and Ermias D. Belay, MD. It appears in the Journal of the American Dietetic Association, Volume 111, Issue 6 (June 2011) published by Elsevier.</span>
<span style="background-attachment: initial; background-repeat: initial; line-height: 1.22em;">In an accompanying podcast CDC’s Joseph Y. Abrams discusses travel, hunting, and eating venison in relation to prion diseases. It is available at </span></span><br />
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<span style="font-family: "arial" , sans-serif; font-size: 10pt; line-height: 1.22em;"><a href="http://adajournal.org/content/podcast" rel="noopener noreferrer" style="color: purple; cursor: pointer; line-height: 1.22em;" target="_blank"><span style="font-family: "verdana" , sans-serif; line-height: 1.22em;"></span></a><a href="http://adajournal.org/content/podcast" rel="noopener noreferrer" style="color: purple; cursor: pointer; line-height: 1.22em;" target="_blank">http://adajournal.org/content/podcast</a></span><span style="font-family: "georgia" , serif; font-size: 10pt; line-height: 1.22em;">.</span><span style="font-family: "georgia" , serif; font-size: 10pt; line-height: 1.22em;">
</span><span style="font-family: "arial" , sans-serif; font-size: 10pt; line-height: 1.22em;"><a href="http://www.eurekalert.org/pub_releases/2011-05/ehs-cap051811.php" rel="noopener noreferrer" style="color: purple; cursor: pointer; line-height: 1.22em;" target="_blank"><span style="font-family: "verdana" , sans-serif; line-height: 1.22em;"></span></a><a href="http://www.eurekalert.org/pub_releases/2011-05/ehs-cap051811.php" rel="noopener noreferrer" style="color: purple; cursor: pointer; line-height: 1.22em;" target="_blank">http://www.eurekalert.org/pub_releases/2011-05/ehs-cap051811.php</a></span><br />
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<span style="font-family: "arial"; font-size: 13.3333px; line-height: 1.22em;"><span style="font-size: 10pt; line-height: 1.22em;"><span style="font-family: "georgia" , serif; line-height: 1.22em;">Travel History, Hunting, and Venison Consumption Related to Prion Disease Exposure, 2006-2007 </span></span></span><br />
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<span style="font-family: "georgia" , serif; line-height: 1.22em;">Journal of the American Dietetic Association Volume 111, Issue 6 , Pages 858-863, June 2011.</span>
<span style="font-family: "georgia" , serif; line-height: 1.22em;">Travel History, Hunting, and Venison Consumption Related to Prion Disease Exposure, 2006-2007 FoodNet Population Survey</span>
<span style="font-family: "georgia" , serif; line-height: 1.22em;">Joseph Y. Abrams, MPH, Ryan A. Maddox, MPH , Alexis R. Harvey, MPH , Lawrence B. Schonberger, MD , Ermias D. Belay, MD</span>
<span style="font-family: "georgia" , serif; line-height: 1.22em;">Accepted 15 November 2010. </span></span></span><br />
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<span style="font-family: "arial"; font-size: 13.3333px; line-height: 1.22em;"><span style="font-size: 10pt; line-height: 1.22em;"><span style="font-family: "georgia" , serif; line-height: 1.22em;">Abstract</span> </span></span><br />
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<span style="font-family: "arial"; font-size: 13.3333px; line-height: 1.22em;"><span style="font-size: 10pt; line-height: 1.22em;"><span style="font-family: "georgia" , serif; line-height: 1.22em;">
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<span style="font-family: "arial"; font-size: 13.3333px; line-height: 1.22em;"><span style="font-size: 10pt; line-height: 1.22em;"><span style="font-family: "georgia" , serif; line-height: 1.22em;">The transmission of bovine spongiform encephalopathy (BSE) to human beings and the spread of chronic wasting disease (CWD) among cervids have prompted concerns about zoonotic transmission of prion diseases. Travel to the United Kingdom and other European countries, hunting for deer or elk, and venison consumption could result in the exposure of US residents to the agents that cause BSE and CWD. The Foodborne Diseases Active Surveillance Network 2006-2007 population survey was used to assess the prevalence of these behaviors among residents of 10 catchment areas across the United States. Of 17,372 survey respondents, 19.4% reported travel to the United Kingdom since 1980, and 29.5% reported travel to any of the nine European countries considered to be BSE-endemic since 1980. The proportion of respondents who had ever hunted deer or elk was 18.5%, and 1.2% had hunted deer or elk in a CWD–endemic area. </span></span></span><span style="font-family: "georgia" , serif; font-size: 10pt; line-height: 1.22em;">More than two thirds (67.4%) reported having ever eaten deer or elk meat. Respondents who traveled spent more time in the United Kingdom (median 14 days) than in any other BSE-endemic country. </span><span style="font-family: "georgia" , serif; font-size: 10pt; line-height: 1.22em;">Of the 11,635 respondents who had consumed venison, 59.8% ate venison at most one to two times during their year of highest consumption, and 88.6% had obtained all of their meat from the wild. The survey results were useful in determining the prevalence and frequency of behaviors that could be important factors for foodborne prion transmission.</span><span style="font-family: "arial"; font-size: 10pt;"> </span><br />
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<span style="font-family: "georgia" , serif; line-height: 1.22em;">Journal of the American Dietetic Association Volume 111, Issue 6 , Pages 858-863, June 2011.</span> </span></span><br />
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<span style="font-family: "arial"; font-size: 13.3333px; line-height: 1.22em;"><span style="font-family: "arial" , sans-serif; font-size: 10pt; line-height: 1.22em;"><a href="http://transmissiblespongiformencephalopathy.blogspot.com/2011/05/travel-history-hunting-and-venison.html" rel="noopener noreferrer" style="color: purple; cursor: pointer; line-height: 1.22em;" target="_blank"><span style="font-family: "verdana" , sans-serif; line-height: 1.22em;"></span></a><a href="http://transmissiblespongiformencephalopathy.blogspot.com/2011/05/travel-history-hunting-and-venison.html" rel="noopener noreferrer" style="color: purple; cursor: pointer; line-height: 1.22em;" target="_blank">http://transmissiblespongiformencephalopathy.blogspot.com/2011/05/travel-history-hunting-and-venison.html</a></span></span><br />
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</span><span style="font-family: "georgia" , serif; line-height: 1.22em;">NOR IS THE FDA recalling this CWD positive elk meat for the well being of the dead elk ;</span>
<span style="font-family: "georgia" , serif; line-height: 1.22em;">Wednesday, March 18, 2009</span>
<span style="font-family: "georgia" , serif; line-height: 1.22em;">Noah's Ark Holding, LLC, Dawson, MN </span></span></span><br />
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<span style="font-family: "arial"; font-size: 13.3333px; line-height: 1.22em;"><span style="font-family: "georgia" , serif; font-size: 10pt;">Transmissible Spongiform Encephalopathies</span></span><br />
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<span style="background-attachment: initial; background-repeat: initial; line-height: 1.22em;">Spongiform Encephalopathy in Captive Wild ZOO BSE INQUIRY</span> </span></span><br />
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<a href="https://web.archive.org/web/20090506001201/http://www.bseinquiry.gov.uk/files/mb/m09a/tab03.pdf" rel="noopener noreferrer" style="color: purple; cursor: pointer; font-family: arial, sans-serif; font-size: 10pt; line-height: 1.22em;" target="_blank">https://web.archive.org/web/20090506001201/http://www.bseinquiry.gov.uk/files/mb/m09a/tab03.pdf</a></span><br />
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<span style="font-family: "georgia" , serif; line-height: 1.22em;">BSE INQUIRY</span>
<span style="font-family: "georgia" , serif; line-height: 1.22em;">CJD9/10022</span>
<span style="font-family: "georgia" , serif; line-height: 1.22em;">October 1994</span>
<span style="font-family: "georgia" , serif; line-height: 1.22em;">Mr R.N. Elmhirst Chairman British Deer Farmers Association Holly Lodge Spencers Lane </span>
<span style="font-family: "georgia" , serif; line-height: 1.22em;">BerksWell Coventry CV7 7BZ</span> </span></span><br />
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<span style="font-size: 10pt; line-height: 1.22em;"><span style="font-family: "georgia" , serif; line-height: 1.22em;">Dear Mr Elmhirst,</span>
<span style="font-family: "georgia" , serif; line-height: 1.22em;">CREUTZFELDT-JAKOB DISEASE (CJD) SURVEILLANCE UNIT REPORT</span>
<span style="font-family: "georgia" , serif; line-height: 1.22em;">Thank you for your recent letter concerning the publication of the third annual report from the CJD Surveillance Unit. </span></span></span><br />
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<span style="font-size: 10pt; line-height: 1.22em;"><span style="font-family: "georgia" , serif; line-height: 1.22em;">I am sorry that you are dissatisfied with the way in which this report was published.</span> </span></span><br />
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<span style="font-size: 10pt; line-height: 1.22em;"><span style="font-family: "georgia" , serif; line-height: 1.22em;">The Surveillance Unit is a completely independant outside body and the Department of Health is committed to publishing their reports as soon as they become available. </span></span></span><br />
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<span style="font-size: 10pt; line-height: 1.22em;"><span style="font-family: "georgia" , serif; line-height: 1.22em;">In the circumstances it is not the practice to circulate the report for comment since the findings of the report would not be amended.. In future we can ensure that the British Deer Farmers Association receives a copy of the report in advance of publication.</span> </span></span><br />
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<span style="font-size: 10pt; line-height: 1.22em;"><span style="font-family: "georgia" , serif; line-height: 1.22em;">The Chief Medical Officer has undertaken to keep the public fully informed of the results of any research in respect of CJD. This report was entirely the work of the unit and was produced completely independantly of the the Department.</span> </span></span><br />
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<span style="font-size: 10pt; line-height: 1.22em;"><span style="font-family: "georgia" , serif; line-height: 1.22em;">The statistical results reqarding the consumption of venison was put into perspective in the body of the report and was not mentioned at all in the press release. Media attention regarding this report was low key but gave a realistic presentation of the statistical findings of the Unit. </span></span></span><br />
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<span style="font-size: 10pt; line-height: 1.22em;"><span style="font-family: "georgia" , serif; line-height: 1.22em;">This approach to publication was successful in that consumption of venison was highlighted only once by the media ie. in the News at one television proqramme.</span> </span></span><br />
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<span style="font-size: 10pt; line-height: 1.22em;"><span style="font-family: "georgia" , serif; line-height: 1.22em;">I believe that a further statement about the report, or indeed statistical links between CJD and consumption of venison, would increase, and quite possibly give damaging credence, to the whole issue. </span></span></span><br />
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<span style="font-size: 10pt; line-height: 1.22em;"><span style="font-family: "georgia" , serif; line-height: 1.22em;">From the low key media reports of which I am aware it seems unlikely that venison consumption will suffer adversely, if at all.</span> </span></span><br />
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<span style="font-family: "arial" , sans-serif; font-size: 10pt; line-height: 1.22em;"><a href="http://web.archive.org/web/20030511010117/http:/www.bseinquiry.gov.uk/files/yb/1994/10/00003001.pdf" rel="noopener noreferrer" style="color: purple; cursor: pointer; line-height: 1.22em;" target="_blank"><span style="font-family: "verdana" , sans-serif; line-height: 1.22em;"></span></a><a href="http://web.archive.org/web/20030511010117/http://www.bseinquiry.gov.uk/files/yb/1994/10/00003001.pdf" rel="noopener noreferrer" style="color: purple; cursor: pointer; line-height: 1.22em;" target="_blank">http://web.archive.org/web/20030511010117/http://www.bseinquiry.gov.uk/files/yb/1994/10/00003001.pdf</a></span></span></div>
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</span><span style="font-family: "georgia" , serif; line-height: 1.22em;">*** The association between venison eating and risk of CJD shows similar pattern, with regular venison eating associated with a 9 FOLD INCREASE IN RISK OF CJD (p = 0.04). ***</span> </span></span><br />
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<span style="font-size: 10pt; line-height: 1.22em;"><span style="font-family: "georgia" , serif; line-height: 1.22em;">*** The association between venison eating and risk of CJD shows similar pattern, with regular venison eating associated with a 9 FOLD INCREASE IN RISK OF CJD (p = 0.04). ***</span> </span></span><br />
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<span style="font-size: 10pt; line-height: 1.22em;"><span style="font-family: "georgia" , serif; line-height: 1.22em;">*** The association between venison eating and risk of CJD shows similar pattern, with regular venison eating associated with a 9 FOLD INCREASE IN RISK OF CJD (p = 0.04). ***</span> </span></span><br />
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<span style="font-size: 10pt; line-height: 1.22em;"><span style="font-family: "georgia" , serif; line-height: 1.22em;">There is some evidence that risk of CJD INCREASES WITH INCREASING FREQUENCY OF LAMB EATING (p = 0.02).</span>
<span style="font-family: "georgia" , serif; line-height: 1.22em;">The evidence for such an association between beef eating and CJD is weaker (p = 0.14). When only controls for whom a relative was interviewed are included, this evidence becomes a little STRONGER (p = 0.08).</span> </span></span><br />
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<span style="font-size: 10pt; line-height: 1.22em;"><span style="font-family: "georgia" , serif; line-height: 1.22em;">It was found that when veal was included in the model with another exposure, the association between veal and CJD remained statistically significant (p = < 0.05 for all exposures), while the other exposures ceased to be statistically significant (p = > 0.05).</span> </span></span><br />
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<span style="font-size: 10pt; line-height: 1.22em;"><span style="font-family: "georgia" , serif; line-height: 1.22em;">In conclusion, an analysis of dietary histories revealed statistical associations between various meats/animal products and INCREASED RISK OF CJD. </span></span></span><br />
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<span style="font-size: 10pt; line-height: 1.22em;"><span style="font-family: "georgia" , serif; line-height: 1.22em;">When some account was taken of possible confounding, the association between VEAL EATING AND RISK OF CJD EMERGED AS THE STRONGEST OF THESE ASSOCIATIONS STATISTICALLY. ...</span> </span></span><br />
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<span style="font-size: 10pt; line-height: 1.22em;"><span style="font-family: "georgia" , serif; line-height: 1.22em;">In the study in the USA, a range of foodstuffs were associated with an increased risk of CJD, including liver consumption which was associated with an apparent SIX-FOLD INCREASE IN THE RISK OF CJD. </span></span></span><br />
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<span style="font-size: 10pt; line-height: 1.22em;"><span style="font-family: "georgia" , serif; line-height: 1.22em;">By comparing the data from 3 studies in relation to this particular dietary factor, the risk of liver consumption became non-significant with an odds ratio of 1.2 (PERSONAL COMMUNICATION, PROFESSOR A. HOFMAN. ERASMUS UNIVERSITY, ROTTERDAM). (???...TSS)</span> </span></span><br />
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</span><span style="font-family: "arial" , sans-serif; font-size: 10pt; line-height: 1.22em;"><a href="https://web.archive.org/web/20170126073306/http:/collections..europarchive..org/tna/20090505194948/http:/bseinquiry.gov.uk/files/yb/1994/08/00004001.pdf" rel="noopener noreferrer" style="color: purple; cursor: pointer; line-height: 1.22em;" target="_blank"><span style="font-family: "verdana" , sans-serif; line-height: 1.22em;"></span></a><a href="https://web.archive.org/web/20170126073306/http://collections..europarchive..org/tna/20090505194948/http://bseinquiry.gov.uk/files/yb/1994/08/00004001.pdf" rel="noopener noreferrer" style="color: purple; cursor: pointer; line-height: 1.22em;" target="_blank">https://web.archive.org/web/20170126073306/http://collections..europarchive..org/tna/20090505194948/http://bseinquiry.gov.uk/files/yb/1994/08/00004001.pdf</a></span></span><br />
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<span style="font-family: "arial"; font-size: 13.3333px; line-height: 1.22em;">the tse prion aka mad cow type disease is not your normal pathogen. </span><br />
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<span style="font-size: 13.3333px; line-height: 1.22em;">The TSE prion disease survives ashing to 600 degrees celsius, that’s around 1112 degrees farenheit. </span><br />
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<span style="font-size: 13.3333px; line-height: 1.22em;">you cannot cook the TSE prion disease out of meat. </span><br />
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<span style="font-size: 13.3333px; line-height: 1.22em;">you can take the ash and mix it with saline and inject that ash into a mouse, and the mouse will go down with TSE. </span><br />
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<span style="font-size: 13.3333px; line-height: 1.22em;">Prion Infected Meat-and-Bone Meal Is Still Infectious after Biodiesel Production as well. </span><br />
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<span style="font-size: 13.3333px; line-height: 1.22em;">the TSE prion agent also survives Simulated Wastewater Treatment Processes. </span><br />
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<span style="font-size: 13.3333px; line-height: 1.22em;">IN fact, you should also know that the TSE Prion agent will survive in the environment for years, if not decades. </span><br />
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<span style="font-size: 13.3333px; line-height: 1.22em;">you can bury it and it will not go away. </span><br />
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<span style="font-size: 13.3333px; line-height: 1.22em;">The TSE agent is capable of infected your water table i.e. Detection of protease-resistant cervid prion protein in water from a CWD-endemic area. </span><br />
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<span style="font-size: 13.3333px; line-height: 1.22em;">it’s not your ordinary pathogen you can just cook it out and be done with. </span><br />
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<span style="font-size: 13.3333px; line-height: 1.22em;">***> that’s what’s so worrisome about Iatrogenic mode of transmission, a simple autoclave will not kill this TSE prion agent.</span><br />
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<span style="font-size: 13.3333px;">1: J Neurol Neurosurg Psychiatry 1994 Jun;57(6):757-8 </span><br />
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<span style="font-size: 13.3333px; line-height: 1.22em;">***> Transmission of Creutzfeldt-Jakob disease to a chimpanzee by electrodes contaminated during neurosurgery. </span><br />
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<span style="font-size: 13.3333px; line-height: 1.22em;">Gibbs CJ Jr, Asher DM, Kobrine A, Amyx HL, Sulima MP, Gajdusek DC. </span><br />
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<span style="font-size: 13.3333px; line-height: 1.22em;">Laboratory of Central Nervous System Studies, National Institute of </span></div>
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<span style="font-size: 13.3333px; line-height: 1.22em;">Neurological Disorders and Stroke, National Institutes of Health, </span><br />
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<span style="font-size: 13.3333px; line-height: 1.22em;">Bethesda, MD 20892. </span><br />
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<span style="font-size: 13.3333px; line-height: 1.22em;">Stereotactic multicontact electrodes used to probe the cerebral cortex of a middle aged woman with progressive dementia were previously implicated in the accidental transmission of Creutzfeldt-Jakob disease (CJD) to two younger patients. The diagnoses of CJD have been confirmed for all three cases. More than two years after their last use in humans, after three cleanings and repeated sterilisation in ethanol and formaldehyde vapour, the electrodes were implanted in the cortex of a chimpanzee. Eighteen months later the animal became ill with CJD. This finding serves to re-emphasise the potential danger posed by reuse of instruments contaminated with the agents of spongiform encephalopathies, even after scrupulous attempts to clean them. </span><br />
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<span style="font-size: 13.3333px; line-height: 1.22em;">PMID: 8006664 [PubMed - indexed for MEDLINE] </span><br />
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<a href="https://www.ncbi.nlm.nih.gov/pubmed/8006664?dopt=Abstract" rel="noopener noreferrer" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">https://www.ncbi.nlm.nih.gov/pubmed/8006664?dopt=Abstract</a><br />
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<span style="font-family: "times new roman" , serif;"><span style="font-size: 16px; white-space: normal;">New Outbreak of TSE Prion in NEW LIVESTOCK SPECIES</span></span><br />
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<span style="font-family: "times new roman" , serif;"><span style="font-size: 16px; white-space: normal;">Mad Camel Disease</span></span><br />
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<span style="font-family: "times new roman" , serif;"><span style="font-size: 16px; white-space: normal;"><a href="https://wwwnc.cdc.gov/eid/article/24/6/17-2007_article" style="color: #0096ef; cursor: pointer; text-decoration-line: none;">https://wwwnc.cdc.gov/eid/article/24/6/17-2007_article</a> </span></span><br />
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<span style="font-family: "times new roman" , serif;"><span style="font-size: 16px; white-space: normal;">***> IMPORTS AND EXPORTS <***</span></span><br />
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<span style="font-family: "times new roman" , serif;"><span style="font-size: 16px; white-space: normal;">***SEE MASSIVE AMOUNTS OF BANNED ANIMAL PROTEIN AKA MAD COW FEED IN COMMERCE USA DECADES AFTER POST BAN ***</span></span><br />
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<a href="http://camelusprp.blogspot.com/2018/04/dromedary-camels-algeria-prion-mad.html" style="color: #0096ef; cursor: pointer; text-decoration-line: none;">http://camelusprp.blogspot.com/2018/04/dromedary-camels-algeria-prion-mad.html</a><br />
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<span style="font-family: "times new roman" , serif; line-height: 1.22em;">TUESDAY, SEPTEMBER 4, 2018 </span></div>
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<span style="font-family: "times new roman" , serif; line-height: 1.22em;"><span style="font-size: x-small; line-height: 1.22em;">USA CJD, BSE, SCRAPIE, CWD, TSE PRION END OF YEAR REPORTS September 4, 2018</span></span></div>
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<span style="font-family: "times new roman" , serif; line-height: 1.22em;">prepare for the storm...</span></div>
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<span style="font-family: "times new roman" , serif; line-height: 1.22em;"><span style="font-size: x-small; line-height: 1.22em;"><a href="http://transmissiblespongiformencephalopathy.blogspot.com/2018/09/usa-cjd-bse-scrapie-cwd-tse-prion-end.html" rel="noopener noreferrer" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">http://transmissiblespongiformencephalopathy.blogspot.com/2018/09/usa-cjd-bse-scrapie-cwd-tse-prion-end.html</a></span></span></div>
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THURSDAY, OCTOBER 04, 2018 <span style="font-family: "arial" , "helvetica"; font-size: x-small;">
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<span style="font-size: 13.3333px;">Cervid to human prion transmission 5R01NS088604-04 Update</span></div>
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<span style="font-size: 13.3333px; line-height: 1.22em;"><a href="http://chronic-wasting-disease.blogspot.com/2018/10/cervid-to-human-prion-transmission.html" rel="noopener noreferrer" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">http://chronic-wasting-disease.blogspot.com/2018/10/cervid-to-human-prion-transmission.html</a></span></div>
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<span style="font-family: "arial"; font-size: x-small; line-height: 1.22em;">WEDNESDAY, SEPTEMBER 26, 2018 </span></div>
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<span style="font-family: "arial"; font-size: x-small; line-height: 1.22em;">J</span><span style="font-family: "arial"; font-size: x-small; line-height: 1.22em;">AVMA In Short Update USDA announces detection of atypical BSE</span><br />
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<a href="http://bovineprp.blogspot.com/2018/09/javma-in-short-update-usda-announces.html" rel="noopener noreferrer" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">http://bovineprp.blogspot.com/2018/09/javma-in-short-update-usda-announces.html</a><br />
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WEDNESDAY, OCTOBER 17, 2018 </div>
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PRICE OF TSE PRION POKER GOES UP spectrum of human prion diseases may extend the current field and may notably include spinal cord diseases </div>
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<a href="https://creutzfeldt-jakob-disease.blogspot.com/2018/10/price-of-tse-prion-poker-goes-up.html" rel="noopener noreferrer" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">https://creutzfeldt-jakob-disease.blogspot.com/2018/10/price-of-tse-prion-poker-goes-up.html</a><br />
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SATURDAY, OCTOBER 06, 2018<br />
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Evaluation of iatrogenic risk of CJD transmission associated with corneal transplantation<br />
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<a href="http://creutzfeldt-jakob-disease.blogspot.com/2018/10/evaluation-of-iatrogenic-risk-of-cjd.html" rel="noopener noreferrer" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">http://creutzfeldt-jakob-disease.blogspot.com/2018/10/evaluation-of-iatrogenic-risk-of-cjd.html</a><br />
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<span style="font-family: "arial" , "helvetica"; line-height: 1.22em;"><span style="font-size: 13.3333px; line-height: 1.22em;">Emerging Diseases, Infection Control & California Dental Practice Act</span></span></div>
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<span style="font-family: "arial" , "helvetica"; line-height: 1.22em;"><span style="font-size: 13.3333px; line-height: 1.22em;"><a href="https://transmissiblespongiformencephalopathy.blogspot.com/2018/09/emerging-diseases-infection-control.html" rel="noopener noreferrer" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">https://transmissiblespongiformencephalopathy.blogspot.com/2018/09/emerging-diseases-infection-control.html</a></span></span><br />
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<span style="font-family: "arial" , "helvetica"; font-size: x-small; line-height: 1.22em;">THURSDAY, OCTOBER 04, 2018 </span></div>
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<span style="font-family: "arial" , "helvetica"; font-size: x-small; line-height: 1.22em;">Case Western Reserve researchers to examine skin prions in fatal neurodegenerative disease $2.9 million NIH grant focuses on transmission and diagnostic testing</span></div>
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<span style="font-family: "arial" , "helvetica"; font-size: x-small; line-height: 1.22em;"><a href="http://creutzfeldt-jakob-disease.blogspot.com/2018/10/case-western-reserve-researchers-to.html" rel="noopener noreferrer" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">http://creutzfeldt-jakob-disease.blogspot.com/2018/10/case-western-reserve-researchers-to.html</a></span><br />
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WEDNESDAY, JULY 04, 2018<br />
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CREUTZFELDT-JAKOB DISEASE: GUIDELINES FOR SOCIAL WORKERS IN ENGLAND June 2018<br />
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<a href="https://creutzfeldt-jakob-disease.blogspot.com/2018/07/creutzfeldt-jakob-disease-guidelines.html" rel="noopener noreferrer" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">https://creutzfeldt-jakob-disease.blogspot.com/2018/07/creutzfeldt-jakob-disease-guidelines.html</a><br />
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MONDAY, JUNE 18, 2018<br />
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Ecuador Six Case series of Creutzfeldt-Jakob disease in a third-level hospital in Quito<br />
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<a href="https://creutzfeldt-jakob-disease.blogspot.com/2018/06/ecuador-six-case-series-of-creutzfeldt.html" rel="noopener noreferrer" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">https://creutzfeldt-jakob-disease.blogspot.com/2018/06/ecuador-six-case-series-of-creutzfeldt.html</a><br />
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<span style="font-family: "arial" , "helvetica"; line-height: 1.22em;"><span style="font-size: 13.3333px; line-height: 1.22em;">WEDNESDAY, SEPTEMBER 26, 2018 </span></span><br />
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<span style="font-family: "arial" , "helvetica"; line-height: 1.22em;"><span style="font-size: 13.3333px; line-height: 1.22em;">A new variant of Creutzfeldt-Jakob disease in the UK 1995 revisited 2018 a review of science</span></span><br />
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<span style="font-family: "arial" , "helvetica"; line-height: 1.22em;"><span style="font-size: 13.3333px; line-height: 1.22em;"><a href="http://creutzfeldt-jakob-disease.blogspot.com/2018/09/a-new-variant-of-creutzfeldt-jakob.html" rel="noopener noreferrer" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">http://creutzfeldt-jakob-disease.blogspot.com/2018/09/a-new-variant-of-creutzfeldt-jakob.html</a></span></span><br />
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<span style="font-family: "arial" , "helvetica"; line-height: 1.22em;">Terry S. Singeltary Sr.</span></div>
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Terry S. Singeltary Sr.http://www.blogger.com/profile/06986622967539963260noreply@blogger.com0tag:blogger.com,1999:blog-6404950019984350027.post-78099174005089566662018-07-10T09:17:00.001-07:002018-07-10T09:17:11.802-07:00CONFIDENTIAL IN CONFIDENCE SPONGIFORM ENCEPHALOPATHY OF PIGS<div style="font-family: arial; font-size: 13.3333px;">
<span style="font-size: 10pt;">*** ''but feeding of other ruminant protein, including scrapie-infected sheep, can continue to pigs.''</span></div>
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CONFIDENTIAL SPONGIFORM ENCEPHALOPATHY OF PIGS</div>
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CONFIDENTIAL</div>
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Ref: Pigs10i</div>
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IN CONFIDENCE</div>
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Dr. Metters </div>
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From Dr. H Pickles Med ISD/3</div>
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Date 10 September 1990</div>
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Copy: Dr G Jones Mr D Hagger Mr T Murray (o/r) Dr D Harper Dr Richardson Mrs Shersby </div>
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SPONGIFORM ENCEPHALOPATHY OF PIGS</div>
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1. There has been a preliminary meeting of the Tyrrell committee today to discuss the significance of the pig experiment in the light of other evidence, for example on feline spongiform encephalopathy. </div>
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2. The preliminary conclusions were: </div>
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we now know pigs are capable of expressing spongiform encephalopathy. Previously this had been doubted. </div>
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the clinical picture in pigs exposed to agent by these doses/routes is fairly distinctive and unlikely to have gone unrecognised. </div>
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even so improved monitoring/surveillance of neurological disease in older pigs should be considered. </div>
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feeding of the "specified offal" (ie nervous/lymphoid tissue from cattle) should no longer be permitted, to pigs or to any other species. </div>
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*** but feeding of other ruminant protein, including scrapie-infected sheep, can continue to pigs. </div>
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if one natural field case of spongiform encephalopathy were described in a pig, we would need a ban on offal from for human consumption. </div>
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we cannot rule out the possibility that unrecognised subclinical spongiform encephalopathy could be present in British pigs though there is no evidence for this: only with parenteral/implantable pharmaceuticals/devices is the theoretical risk to humans of sufficient concern to consider any action.</div>
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whilst any such action on pharmaceuticals/devices is for others to decide, this group (which includes 4 key members of the CSM group) suggests non-UK sources should now be used, at least for "high risk" pharmaceuticals and devices (ie for those from nervous or RE System)</div>
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3. The full committee will meet on the 19th to confirm these conclusions, to review experimental protocols of transmission experiments, to reconsider the cat position in the light of additional cases and to consider scrapie in sheep and goats. In view of Mr Gummer's earlier commitments, we assume he willI want to go public on the pig soon after, so the Tyrrell committee will also prepare a brief written statement. </div>
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4. You may want to consider with the MCA and the Medical Device Agency what preparatory action is appropriate in anticipation of the formal advice from the Tyrrell group. The CSM subgroup not due to meet until the 31 October. </div>
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Hilary Pickles Room 414 Eileen House Ext: 22832 </div>
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<a href="http://web.archive.org/web/20030822031154/www.bseinquiry.gov.uk/files/yb/1990/09/10007001.pdf" style="color: #0096ef; cursor: pointer; text-decoration-line: none;">http://web.archive.org/web/20030822031154/www.bseinquiry.gov.uk/files/yb/1990/09/10007001.pdf</a></div>
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<span style="color: #3c63af; font-family: Arial, Helvetica, sans-serif;"><span style="font-size: 20px;">Detection of PrPres in peripheral tissue in pigs with clinical disease induced by intracerebral challenge with sheep-passaged bovine spongiform encephalopathy agent</span></span></div>
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<span style="color: #3c63af; font-family: Arial, Helvetica, sans-serif;"><span style="font-size: 20px;">Published: July 5, </span></span><span style="color: #3c63af; font-family: Arial, Helvetica, sans-serif; font-size: 20px;">2018</span></div>
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Abstract</h2>
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Bovine spongiform encephalopathy (BSE) can be efficiently transmitted to pigs via intracerebral inoculation. A clear link has been established between the consumption of products of bovine origin contaminated with the BSE agent and the development of variant Creutzfeldt-Jakob disease in humans. Small ruminants can also naturally develop BSE, and sheep-adapted BSE (Sh-BSE) propagates more efficiently than cattle BSE in pigs and in mouse models expressing porcine prion protein. In addition, Sh-BSE shows greater efficiency of transmission to human models than original cow BSE. While infectivity and/or abnormal PrP accumulation have been reported in the central nervous system in BSE-infected pigs, the ability of the agent to replicate in peripheral tissues has not been fully investigated. We previously characterized the presence of prions in a panel of tissues collected at the clinical stage of disease from pigs experimentally infected with Sh-BSE. Western blot revealed low levels of PrP<span style="bottom: 1ex; box-sizing: border-box; position: relative; vertical-align: 0px;">res</span> accumulation in lymphoid tissues, nerves, and skeletal muscles from 4 of the 5 animals analysed. Using protein misfolding cyclic amplification (PMCA), which we found to be 6 log fold more sensitive than direct WB for the detection of pig BSE, we confirmed the presence of the Sh-BSE agent in lymphoid organs, nerves, ileum, and striated muscles from all 5 inoculated pigs. Surprisingly, PrP<span style="bottom: 1ex; box-sizing: border-box; position: relative; vertical-align: 0px;">res</span> positivity was also detected in white blood cells from one pig using this method. The presence of infectivity in lymphoid tissues, striated muscles, and peripheral nerves was confirmed by bioassay in bovine PrP transgenic mice. These results demonstrate the ability of BSE-derived agents to replicate efficiently in various peripheral tissues in pigs. Although no prion transmission has been reported in pigs following oral BSE challenge, our data support the continuation of the Feed Ban measure implemented to prevent entry of the BSE agent into the feed chain.</div>
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<span style="color: #3c63af; font-family: Arial, Helvetica, sans-serif; font-size: 20px;"><a href="http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0199914" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0199914</a></span></div>
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Singeltary's comment;</div>
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cwd and scrapie transmits to pigs orally and the USA Section 21 C.F.R. 589.2000, Animal Proteins Prohibited in Ruminant Feed ban WARNING</h3>
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Posted by <span class="aolmail_aolmail_aolmail_aolmail_userlink aolmail_aolmail_aolmail_aolmail_user aolmail_aolmail_aolmail_aolmail_icon aolmail_aolmail_aolmail_aolmail_replyCreator" style="box-sizing: border-box; font-size: 13px; font-weight: bold;">flounder</span> on <span class="aolmail_aolmail_aolmail_aolmail_replyTimestamp" style="box-sizing: border-box; font-size: 13px;"><strong style="box-sizing: border-box; line-height: inherit;">08 Jul 2018 at 21:05 GMT</strong></span></h4>
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>>>Although no prion transmission has been reported in pigs following oral BSE challenge, our data support the continuation of the Feed Ban measure implemented to prevent entry of the BSE agent into the feed chain.<<<<br style="box-sizing: border-box;" /><br style="box-sizing: border-box;" />I would kindly like to bring urgent awareness to PLOS and the authors of this study, and the globe, the USA Section 21 C.F.R. 589.2000, Animal Proteins Prohibited in Ruminant Feed ban has been a failed policy since inception imo (see DEFRA report below), also, cervid that are potentially at risk of Chronic Wasting Disease CWD TSE Prion, are still allowed to be used as protein feed for livestock. But foremost, CWD and Scrapie TRANSMITS TO PIGS BY ORAL ROUTE. please see many many more tonnages of 589.2000, Animal Proteins Prohibited in Ruminant Feed right up to 2017. this is an extremely dangerous situation for the globe, especially with this new outbreak of TSE Prion disease in a new livestock species, i.e. camels in Nigeria, this is an extremely dangerous situation that has global ramifications and needs to be addressed asap, or risk spreading cwd tse prion from the USA and Canada further around the globe. please see;</div>
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<span style="color: #3c63af; font-family: Arial, Helvetica, sans-serif; font-size: 20px;"><a href="http://journals.plos.org/plosone/article/comment?id=10.1371/annotation/a02528e2-6b60-49b2-8719-17927c1a2d60" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://journals.plos.org/plosone/article/comment?id=10.1371/annotation/a02528e2-6b60-49b2-8719-17927c1a2d60</a></span></div>
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<span style="font-size: x-small;">Scrapie Transmits To Pigs By Oral Route, what about the terribly flawed USA tse prion feed ban?</span></div>
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<span style="font-size: x-small;">Research Project: Pathobiology, Genetics, and Detection of Transmissible Spongiform Encephalopathies</span></div>
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<span style="font-size: x-small;">2017 Annual Report</span></div>
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<span style="font-size: x-small;">1a. Objectives (from AD-416):</span></div>
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<span style="font-size: x-small;">Objective 1: Investigate the mechanisms of protein misfolding in prion disease, including the genetic determinants of misfolding of the prion protein and the environmental influences on protein misfolding as it relates to prion diseases. Subobjective 1.A: Investigate the differences in the unfolded state of wild-type and disease associated prion proteins to better understand the mechanism of misfolding in genetic prion disease. Subobjective 1.B: Investigate the influence of metal ions on the misfolding of the prion protein in vitro to determine if environmental exposure to metal ions may alter disease progression. Objective 2: Investigate the pathobiology of prion strains in natural hosts, including the influence of prion source genotype on interspecies transmission and the pathobiology of atypical transmissible spongiform encephalopathies (TSEs). Subobjective 2.A: Investigate the pathobiology of atypical TSEs. Subobjective 2.B: Investigate the influence of prion source genotype on interspecies transmission. Objective 3: Investigate sampling methodologies for antemortem detection of prion disease, including the utility of blood sampling as a means to assess prion disease status of affected animals and the utility of environmental sampling for monitoring herd prion disease status. Subobjective 3.A: Investigate the utility of blood sampling as a means to assess prion disease status of affected animals. Subobjective 3.B: Investigate the utility of environmental sampling for monitoring herd prion disease status.</span></div>
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<span style="font-size: x-small;">1b. Approach (from AD-416):</span></div>
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<span style="font-size: x-small;">The studies will focus on three animal transmissible spongiform encephalopathy (TSE) agents found in the United States: bovine spongiform encephalopathy (BSE); scrapie of sheep and goats; and chronic wasting disease (CWD) of deer, elk, and moose. The research will address sites of protein folding and misfolding as it relates to prion disease, accumulation of misfolded protein in the host, routes of infection, and ante mortem diagnostics with an emphasis on controlled conditions and natural routes of infection. Techniques used will include spectroscopic monitoring of protein folding/misfolding, clinical exams, histopathology, immunohistochemistry, and biochemical analysis of proteins. The enhanced knowledge gained from this work will help understand the underlying mechanisms of prion disease and mitigate the potential for unrecognized epidemic expansions of these diseases in populations of animals that could either directly or indirectly affect food animals.</span></div>
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<span style="font-size: x-small;">All 8 project plan milestones for FY17 were fully met. Research efforts directed toward meeting objective 1 of our project plan center around the production of recombinant prion protein from either bacteria or mammalian tissue culture systems and collection of thermodynamic data on the folding of the recombinant prion protein produced. Both bacterial and mammalian expression systems have been established. Thermodynamic data addressing the denatured state of wild-type and a disease associated variant of bovine prion protein has been collected and a manuscript is in preparation. In research pertaining to objective 2, all studies have been initiated and animals are under observation for the development of clinical signs. The animal studies for this objective are long term and will continue until onset of clinical signs. In vitro studies planned in parallel to the animals studies have similarly been initiated and are ongoing. Objective 3 of the project plan focuses on the detection of disease associated prion protein in body fluids and feces collected from a time course study of chronic wasting disease inoculated animals. At this time samples are being collected as planned and methods for analysis are under development.</span></div>
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<span style="font-size: x-small;">4. Accomplishments</span></div>
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<span style="font-size: x-small;">1. Showed that swine are potential hosts for the scrapie agent. A naturally occurring prion disease has not been recognized in swine, but the agent of bovine spongiform encephalopathy does transmit to swine by experimental routes. Swine are thought to have a robust species barrier when exposed to the naturally occurring prion diseases of other species, but the susceptibility of swine to the agent of sheep scrapie has not been thoroughly tested. ARS researchers at Ames, Iowa conducted this experiment to test the susceptibility of swine to U.S. scrapie isolates by intracranial and oral inoculation. Necropsies were done on a subset of animals at approximately 6 months post inoculation (PI): the time the pigs were expected to reach market weight. Remaining pigs were maintained and monitored for clinical signs of transmissible spongiform encephalopathies (TSE) until study termination at 80 months PI or when removed due to intercurrent disease. Brain samples were examined by multiple diagnostic approaches, and for a subset of pigs in each inoculation group, bioassay in mice expressing porcine prion protein. At 6 months PI, no evidence of scrapie infection was noted by any diagnostic method. </span></div>
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<span style="font-size: x-small;">***However, at 51 months of incubation or greater, 5 animals were positive by one or more diagnostic methods. </span></div>
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<span style="font-size: x-small;">***Furthermore, positive bioassay results were obtained from all inoculated groups (oral and intracranial; market weight and end of study) suggesting that swine are potential hosts for the agent of scrapie. Although the current U.S. feed ban is based on keeping tissues from TSE infected cattle from contaminating animal feed, swine rations in the U.S. could contain animal derived components including materials from scrapie infected sheep and goats. </span></div>
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<span style="font-size: x-small;">***These results indicating the susceptibility of pigs to sheep scrapie, coupled with the limitations of the current feed ban, indicates that a revision of the feed ban may be necessary to protect swine production and potentially human health.</span></div>
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<span style="font-size: x-small;">2. Determined that pigs naturally exposed to chronic wasting disease (CWD) may act as a reservoir of CWD infectivity. Chronic wasting disease is a naturally occurring, fatal, neurodegenerative disease of cervids. The potential for swine to serve as a host for the agent of CWD disease is unknown. The purpose of this study was to investigate the susceptibility of swine to the CWD agent following experimental oral or intracranial inoculation. Pigs were assigned to 1 of 3 groups: intracranially inoculated; orally inoculated; or non-inoculated. At market weight age, half of the pigs in each group were tested ('market weight' groups). The remaining pigs ('aged' groups) were allowed to incubate for up to 73 months post inoculation (MPI). Tissues collected at necropsy were examined for disease-associated prion protein (PrPSc) by multiple diagnostic methods. Brain samples from selected pigs were bioassayed in mice expressing porcine prion protein. Some pigs from each inoculated group were positive by one or more tests. Bioassay was positive in 4 out of 5 pigs assayed. Although only small amounts of PrPSc were detected using sensitive methods, this study demonstrates that pigs can serve as hosts for CWD. Detection of infectivity in orally inoculated pigs using mouse bioassay raises the possibility that naturally exposed pigs could act as a reservoir of CWD infectivity. Currently, swine rations in the U.S. could contain animal derived components including materials from deer or elk. In addition, feral swine could be exposed to infected carcasses in areas where CWD is present in wildlife populations. The current feed ban in the U.S. is based exclusively on keeping tissues from TSE infected cattle from entering animal feeds. </span></div>
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<span style="font-size: x-small;">***These results indicating the susceptibility of pigs to CWD, coupled with the limitations of the current feed ban, indicates that a revision of the feed ban may be necessary to protect swine production and potentially human health.</span></div>
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<span style="font-size: x-small;">3. Developed a method for amplification and discrimination of the 3 forms of BSE in cattle. The prion protein (PrP) is a protein that is the causative agent of transmissible spongiform encephalopathies (TSEs). The disease process involves conversion of the normal cellular PrP to a pathogenic misfolded conformation. This conversion process can be recreated in the lab using a misfolding amplification process known as real-time quaking induced conversion (RT-QuIC). RT-QuIC allows the detection of minute amounts of the abnormal infectious form of the prion protein by inducing misfolding in a supplied substrate. Although RT-QuIC has been successfully used to detect pathogenic PrP with substrates from a variety of host species, prior to this work bovine prion protein had not been proven for its practical uses for RT-QuIC. We demonstrated that prions from transmissible mink encephalopathy (TME) and BSE-infected cattle can be detected with using bovine prion proteins with RT-QuIC, and developed an RT-QuIC based approach to discriminate different forms of BSE. This rapid and robust method, both to detect and discriminate BSE types, is of importance as the economic implications for different types of BSE vary greatly.</span></div>
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<span style="font-size: x-small;">Hwang, S., Greenlee, J.J., Nicholson, E.M. 2017. Use of bovine recombinant prion protein and real-time quaking-induced conversion to detect cattle transmissible mink encephalopathy prions and discriminate classical and atypical L- and H-type bovine spongiform encephalopathy. PLoS One. 12(2):e0172391.</span></div>
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<span style="font-size: x-small;">Moore, S., Kunkle, R., Greenlee, M., Nicholson, E., Richt, J., Hamir, A., Waters, W., Greenlee, J. 2016. Horizontal transmission of chronic wasting disease in reindeer. Emerging Infectious Diseases. 22(12):2142-2145. doi:10.3201/eid2212.160635.</span></div>
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<span style="font-size: x-small;">Moore, S.J., West Greenlee, M.H., Smith, J.D., Vrentas, C.E., Nicholson, E.M., Greenlee, J.J. 2016. A comparison of classical and H-type bovine spongiform encephalopathy associated with E211K prion protein polymorphism in wild type and EK211 cattle following intracranial inoculation. Frontiers in Veterinary Science. 3:78.</span></div>
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<span style="font-size: x-small;">Greenlee, J.J., Kunkle, R.A., Smith, J.D., West Greenlee, M.H. 2016. Scrapie in swine: a diagnostic challenge. Food Safety. 4(4):110-114. Kondru, N., Manne, S., Greenlee, J., West Greenlee, H., Anantharam, V., Halbur, P., Kanthasamy, A., Kanthasamy, A. 2017. Integrated organotypic slice cultures and RT-QuIC (OSCAR) assay: implications for translational discovery in protein misfolding diseases. Scientific Reports. 7:43155. doi:10.1038/srep43155.</span></div>
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<span style="font-size: x-small;">Mammadova, N., Ghaisas, S., Zenitsky, G., Sakaguchi, D.S., Kanthasamy, A.G., Greenlee, J.J., West Greenlee, M.H. 2017. Lasting retinal injury in a mouse model of blast-induced trauma. American Journal of Pathology. 187(7):1459-1472. doi:10.1016/j.ajpath.2017.03.005. </span></div>
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<span style="font-size: x-small;"><a href="https://www.ars.usda.gov/research/project/?accnNo=432011&fy=2017" style="color: #0096ef; cursor: pointer; text-decoration-line: none;">https://www.ars.usda.gov/research/project/?accnNo=432011&fy=2017</a> </span></div>
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<span style="font-size: x-small;">***> However, at 51 months of incubation or greater, 5 animals were positive by one or more diagnostic methods. Furthermore, positive bioassay results were obtained from all inoculated groups (oral and intracranial; market weight and end of study) suggesting that swine are potential hosts for the agent of scrapie. <*** </span></div>
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<span style="font-size: x-small;"> >*** Although the current U.S. feed ban is based on keeping tissues from TSE infected cattle from contaminating animal feed, swine rations in the U.S. could contain animal derived components including materials from scrapie infected sheep and goats. These results indicating the susceptibility of pigs to sheep scrapie, coupled with the limitations of the current feed ban, indicates that a revision of the feed ban may be necessary to protect swine production and potentially human health. <*** </span></div>
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<span style="font-size: 13.3333px;">***> CWD TO PIGS <***</span></div>
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<span style="font-size: 13.3333px;">Research Project: TRANSMISSION, DIFFERENTIATION, AND PATHOBIOLOGY OF TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES</span></div>
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<span style="font-size: 13.3333px;">Location: Virus and Prion Research</span></div>
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<span style="font-size: 13.3333px;">Title: Disease-associated prion protein detected in lymphoid tissues from pigs challenged with the agent of chronic wasting disease</span></div>
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<span style="font-size: 13.3333px;">Author item Moore, Sarah item Kunkle, Robert item Kondru, Naveen item Manne, Sireesha item Smith, Jodi item Kanthasamy, Anumantha item West Greenlee, M item Greenlee, Justin</span></div>
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<span style="font-size: 13.3333px;">Submitted to: Prion Publication Type: Abstract Only Publication Acceptance Date: 3/15/2017 Publication Date: N/A Citation: N/A Interpretive Summary:</span></div>
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<span style="font-size: 13.3333px;">Technical Abstract: Aims: Chronic wasting disease (CWD) is a naturally-occurring, fatal neurodegenerative disease of cervids. We previously demonstrated that disease-associated prion protein (PrPSc) can be detected in the brain and retina from pigs challenged intracranially or orally with the CWD agent. In that study, neurological signs consistent with prion disease were observed only in one pig: an intracranially challenged pig that was euthanized at 64 months post-challenge. The purpose of this study was to use an antigen-capture immunoassay (EIA) and real-time quaking-induced conversion (QuIC) to determine whether PrPSc is present in lymphoid tissues from pigs challenged with the CWD agent.</span></div>
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<span style="font-size: 13.3333px;">Methods: At two months of age, crossbred pigs were challenged by the intracranial route (n=20), oral route (n=19), or were left unchallenged (n=9). At approximately 6 months of age, the time at which commercial pigs reach market weight, half of the pigs in each group were culled (<6 challenge="" groups="" month="" pigs="" remaining="" the="">6 month challenge groups) were allowed to incubate for up to 73 months post challenge (mpc). The retropharyngeal lymph node (RPLN) was screened for the presence of PrPSc by EIA and immunohistochemistry (IHC). The RPLN, palatine tonsil, and mesenteric lymph node (MLN) from 6-7 pigs per challenge group were also tested using EIA and QuIC.</6></span></div>
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<span style="font-size: 13.3333px;">Results: PrPSc was not detected by EIA and IHC in any RPLNs. All tonsils and MLNs were negative by IHC, though the MLN from one pig in the oral <6 5="" 6="" at="" by="" detected="" eia.="" examined="" group="" in="" intracranial="" least="" lymphoid="" month="" months="" of="" one="" pigs="" positive="" prpsc="" quic="" the="" tissues="" was="">6 months group, 5/6 pigs in the oral <6 4="" and="" group="" months="" oral="">6 months group. Overall, the MLN was positive in 14/19 (74%) of samples examined, the RPLN in 8/18 (44%), and the tonsil in 10/25 (40%). Conclusions:</6></6></span></div>
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<span style="font-size: 13.3333px;">This study demonstrates that PrPSc accumulates in lymphoid tissues from pigs challenged intracranially or orally with the CWD agent, and can be detected as early as 4 months after challenge.</span></div>
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<span style="font-size: 13.3333px;">CWD-infected pigs rarely develop clinical disease and if they do, they do so after a long incubation period. This raises the possibility that CWD-infected pigs could shed prions into their environment long before they develop clinical disease.</span></div>
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<span style="font-size: 13.3333px;">Furthermore, lymphoid tissues from CWD-infected pigs could present a potential source of CWD infectivity in the animal and human food chains.</span></div>
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<span style="font-size: 13.3333px;"><a href="https://www.ars.usda.gov/research/publications/publication/?seqNo115=337105" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://www.ars.usda.gov/research/publications/publication/?seqNo115=337105</a> </span></div>
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CONFIDENTIAL</div>
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<span style="font-size: 10pt;">EXPERIMENTAL PORCINE SPONGIFORM ENCEPHALOPATHY</span></div>
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<span style="font-size: 10pt;">While this clearly is a cause for concern we should not jump to the conclusion that this means that pigs will necessarily be infected by bone and meat meal fed by the oral route as is the case with cattle. ...</span></div>
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<a href="http://web.archive.org/web/20031026000118/www.bseinquiry.gov.uk/files/yb/1990/08/23004001.pdf" style="color: blue; cursor: pointer; font-size: 10pt; font-weight: bold; text-decoration-line: none;" target="_blank">http://web.archive.org/web/20031026000118/www.bseinquiry.gov.uk/files/yb/1990/08/23004001.pdf</a></div>
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<span style="font-size: 10pt;">we cannot rule out the possibility that unrecognised subclinical spongiform encephalopathy could be present in British pigs though there is no evidence for this: only with parenteral/implantable pharmaceuticals/devices is the theoretical risk to humans of sufficient concern to consider any action.</span></div>
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<a href="http://web.archive.org/web/20030822031154/www.bseinquiry.gov.uk/files/yb/1990/09/10007001.pdf" style="color: blue; cursor: pointer; font-size: 10pt; font-weight: bold; text-decoration-line: none;" target="_blank">http://web.archive.org/web/20030822031154/www.bseinquiry.gov.uk/files/yb/1990/09/10007001.pdf</a></div>
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<span style="font-size: 10pt;">May I, at the outset, reiterate that we should avoid dissemination of papers relating to this experimental finding to prevent premature release of the information. ...</span></div>
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<a href="http://web.archive.org/web/20030822052332/www.bseinquiry.gov.uk/files/yb/1990/09/11005001.pdf" style="color: blue; cursor: pointer; font-size: 10pt; font-weight: bold; text-decoration-line: none;" target="_blank">http://web.archive.org/web/20030822052332/www.bseinquiry.gov.uk/files/yb/1990/09/11005001.pdf</a></div>
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<span style="font-size: 10pt;">3. It is particularly important that this information is not passed outside the Department, until Ministers have decided how they wish it to be handled. ...</span></div>
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<a href="http://web.archive.org/web/20030822052438/www.bseinquiry.gov.uk/files/yb/1990/09/12002001.pdf" style="color: blue; cursor: pointer; font-size: 10pt; font-weight: bold; text-decoration-line: none;" target="_blank">http://web.archive.org/web/20030822052438/www.bseinquiry.gov.uk/files/yb/1990/09/12002001.pdf</a></div>
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<span style="font-size: 10pt;">But it would be easier for us if pharmaceuticals/devices are not directly mentioned at all. ...</span></div>
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<a href="http://web.archive.org/web/20030518170213/www.bseinquiry.gov.uk/files/yb/1990/09/13004001.pdf" style="color: blue; cursor: pointer; font-size: 10pt; font-weight: bold; text-decoration-line: none;" target="_blank">http://web.archive.org/web/20030518170213/www.bseinquiry.gov.uk/files/yb/1990/09/13004001.pdf</a></div>
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<span style="font-size: 10pt;">Our records show that while some use is made of porcine materials in medicinal products, the only products which would appear to be in a hypothetically ''higher risk'' area are the adrenocorticotrophic hormone for which the source material comes from outside the United Kingdom, namely America China Sweden France and Germany. The products are manufactured by Ferring and Armour. A further product, ''Zenoderm Corium implant'' manufactured by Ethicon, makes use of porcine skin - which is not considered to be a ''high risk'' tissue, but one of its uses is described in the data sheet as ''in dural replacement''. This product is sourced from the United Kingdom.....</span></div>
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<a href="http://web.archive.org/web/20030822054419/www.bseinquiry.gov.uk/files/yb/1990/09/21009001.pdf" style="color: blue; cursor: pointer; font-size: 10pt; font-weight: bold; text-decoration-line: none;" target="_blank">http://web.archive.org/web/20030822054419/www.bseinquiry.gov.uk/files/yb/1990/09/21009001.pdf</a></div>
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<span style="font-size: 10pt;">snip...</span></div>
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<span style="font-size: 10pt;">It was not until . . . August 1990, that the result from the pig persuaded both SEAC and us to change our view and to take out of pig rations any residual infectivity that might have arisen from the SBOs.</span></div>
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<a href="http://web.archive.org/web/20071014143511/http://www.bseinquiry.gov.uk/files/tr/tab69.pdf" style="color: blue; cursor: pointer; font-size: 10pt; font-weight: bold; text-decoration-line: none;" target="_blank">http://web.archive.org/web/20071014143511/http://www.bseinquiry.gov.uk/files/tr/tab69.pdf</a></div>
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<span style="font-size: 10pt;">4.303 The minutes of the meeting record that:</span></div>
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<span style="font-size: 10pt;">It was very difficult to draw conclusions from one experimental result for what may happen in the field. However it would be prudent to exclude specified bovine offals from the pig diet. Although any relationship between BSE and the finding of a spongiform encephalopathy in cats had yet to be demonstrated, the fact that this had occurred suggested that a cautious view should be taken of those species which might be susceptible. The 'specified offals' of bovines should therefore be excluded from the feed of all species. 17</span></div>
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<a href="http://web.archive.org/web/20031026084516/http://www.bseinquiry.gov.uk/files/yb/1990/09/07001001.pdf" style="color: blue; cursor: pointer; font-size: 10pt; font-weight: bold; text-decoration-line: none;" target="_blank">http://web.archive.org/web/20031026084516/http://www.bseinquiry.gov.uk/files/yb/1990/09/07001001.pdf</a></div>
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<span style="font-size: 10pt;">IN CONFIENCE</span></div>
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<span style="font-size: 10pt;">1. CMO should be aware that a pig inoculated experimentally (ic, iv, and ip) with BSE brain suspension has after 15 months developed an illness, now confirmed as a spongiform encephalopathy. This is the first ever description of such a disease in a pig, although it seems there ar no previous attempts at experimental inoculation with animal material. The Southwood group had thought igs would not be susceptible. Most pigs are slaughtered when a few weeks old but there have been no reports of relevant neurological illness in breeding sows or other elderly pigs. ...see full text ;</span></div>
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<a href="http://web.archive.org/web/20040302031004/www.bseinquiry.gov.uk/files/yb/1990/08/23001001.pdf" style="color: blue; cursor: pointer; font-size: 10pt; font-weight: bold; text-decoration-line: none;" target="_blank">http://web.archive.org/web/20040302031004/www.bseinquiry.gov.uk/files/yb/1990/08/23001001.pdf</a></div>
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<span style="font-size: 10pt;">IN CONFIDENCE</span></div>
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<span style="font-size: 10pt;">So it is plausible pigs could be preclinically affected with BSE but since so few are allowed to reach adulthood this has not been recognised through clinical disease. ...</span></div>
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<a href="http://web.archive.org/web/20040904150118/www.bseinquiry.gov.uk/files/yb/1990/08/23002001.pdf" style="color: blue; cursor: pointer; font-size: 10pt; font-weight: bold; text-decoration-line: none;" target="_blank">http://web.archive.org/web/20040904150118/www.bseinquiry.gov.uk/files/yb/1990/08/23002001.pdf</a></div>
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<span style="font-size: 10pt;">CONFIDENTIAL</span></div>
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<span style="font-size: 10pt;">EXPERIMENTAL PORCINE SPONGIFORM ENCEPHALOPATHY</span></div>
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<span style="font-size: 10pt;">While this clearly is a cause for concern we should not jump to the conclusion that this means that pigs will necessarily be infected by bone and meat meal fed by the oral route as is the case with cattle. ...</span></div>
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<a href="http://web.archive.org/web/20031026000118/www.bseinquiry.gov.uk/files/yb/1990/08/23004001.pdf" style="color: blue; cursor: pointer; font-size: 10pt; font-weight: bold; text-decoration-line: none;" target="_blank">http://web.archive.org/web/20031026000118/www.bseinquiry.gov.uk/files/yb/1990/08/23004001.pdf</a></div>
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<span style="font-size: 10pt;">we cannot rule out the possibility that unrecognised subclinical spongiform encephalopathy could be present in British pigs though there is no evidence for this: only with parenteral/implantable pharmaceuticals/devices is the theoretical risk to humans of sufficient concern to consider any action.</span></div>
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<a href="http://web.archive.org/web/20030822031154/www.bseinquiry.gov.uk/files/yb/1990/09/10007001.pdf" style="color: blue; cursor: pointer; font-size: 10pt; font-weight: bold; text-decoration-line: none;" target="_blank">http://web.archive.org/web/20030822031154/www.bseinquiry.gov.uk/files/yb/1990/09/10007001.pdf</a></div>
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<span style="font-size: 10pt;">May I, at the outset, reiterate that we should avoid dissemination of papers relating to this experimental finding to prevent premature release of the information. ...</span></div>
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<a href="http://web.archive.org/web/20030822052332/www.bseinquiry.gov.uk/files/yb/1990/09/11005001.pdf" style="color: blue; cursor: pointer; font-size: 10pt; font-weight: bold; text-decoration-line: none;" target="_blank">http://web.archive.org/web/20030822052332/www.bseinquiry.gov.uk/files/yb/1990/09/11005001.pdf</a></div>
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<span style="font-size: 10pt;">3. It is particularly important that this information is not passed outside the Department, until Ministers have decided how they wish it to be handled. ...</span></div>
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<a href="http://web.archive.org/web/20030822052438/www.bseinquiry.gov.uk/files/yb/1990/09/12002001.pdf" style="color: blue; cursor: pointer; font-size: 10pt; font-weight: bold; text-decoration-line: none;" target="_blank">http://web.archive.org/web/20030822052438/www.bseinquiry.gov.uk/files/yb/1990/09/12002001.pdf</a></div>
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<span style="font-size: 10pt;">But it would be easier for us if pharmaceuticals/devices are not directly mentioned at all. ...</span></div>
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<a href="http://web.archive.org/web/20030518170213/www.bseinquiry.gov.uk/files/yb/1990/09/13004001.pdf" style="color: blue; cursor: pointer; font-size: 10pt; font-weight: bold; text-decoration-line: none;" target="_blank">http://web.archive.org/web/20030518170213/www.bseinquiry.gov.uk/files/yb/1990/09/13004001.pdf</a></div>
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<span style="font-size: 10pt;">Our records show that while some use is made of porcine materials in medicinal products, the only products which would appear to be in a hypothetically ''higher risk'' area are the adrenocorticotrophic hormone for which the source material comes from outside the United Kingdom, namely America China Sweden France and Germany. The products are manufactured by Ferring and Armour. A further product, ''Zenoderm Corium implant'' manufactured by Ethicon, makes use of porcine skin - which is not considered to be a ''high risk'' tissue, but one of its uses is described in the data sheet as ''in dural replacement''. This product is sourced from the United Kingdom.....</span></div>
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<a href="http://web.archive.org/web/20030822054419/www.bseinquiry.gov.uk/files/yb/1990/09/21009001.pdf" style="color: blue; cursor: pointer; font-size: 10pt; font-weight: bold; text-decoration-line: none;" target="_blank">http://web.archive.org/web/20030822054419/www.bseinquiry.gov.uk/files/yb/1990/09/21009001.pdf</a></div>
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<span style="font-size: 10pt;">BSE TO PIGS NEWS RELEASE</span></div>
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<a href="http://web.archive.org/web/20030822162313/www.bseinquiry.gov.uk/files/yb/1990/09/24001001.pdf" style="color: blue; cursor: pointer; font-size: 10pt; font-weight: bold; text-decoration-line: none;" target="_blank">http://web.archive.org/web/20030822162313/www.bseinquiry.gov.uk/files/yb/1990/09/24001001.pdf</a></div>
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<span style="font-size: 10pt;">CONFIDENTIAL</span></div>
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<span style="font-size: 10pt;">BSE: PRESS PRESENTATION</span></div>
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<a href="http://web.archive.org/web/20030822160958/www.bseinquiry.gov.uk/files/yb/1990/09/20003001.pdf" style="color: blue; cursor: pointer; font-size: 10pt; font-weight: bold; text-decoration-line: none;" target="_blank">http://web.archive.org/web/20030822160958/www.bseinquiry.gov.uk/files/yb/1990/09/20003001.pdf</a></div>
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<a href="http://web.archive.org/web/20040623191707/www.bseinquiry.gov.uk/files/yb/1990/09/24013001.pdf" style="color: blue; cursor: pointer; font-size: 10pt; font-weight: bold; text-decoration-line: none;" target="_blank">http://web.archive.org/web/20040623191707/www.bseinquiry.gov.uk/files/yb/1990/09/24013001.pdf</a></div>
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<a href="http://web.archive.org/web/20030820195733/http://www.bseinquiry.gov.uk/files/yb/1990/09/20010001.pdf" style="color: blue; cursor: pointer; font-size: 10pt; font-weight: bold; text-decoration-line: none;" target="_blank">http://web.archive.org/web/20030820195733/http://www.bseinquiry.gov.uk/files/yb/1990/09/20010001.pdf</a></div>
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<a href="http://web.archive.org/web/20030820195733/http://www.bseinquiry.gov.uk/files/yb/1990/09/25013001.pdf" style="color: blue; cursor: pointer; font-size: 10pt; font-weight: bold; text-decoration-line: none;" target="_blank">http://web.archive.org/web/20030820195733/http://www.bseinquiry.gov.uk/files/yb/1990/09/25013001.pdf</a></div>
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<a href="http://web.archive.org/web/20030820195733/http://www.bseinquiry.gov.uk/files/yb/1990/09/25015001.pdf" style="color: blue; cursor: pointer; font-size: 10pt; font-weight: bold; text-decoration-line: none;" target="_blank">http://web.archive.org/web/20030820195733/http://www.bseinquiry.gov.uk/files/yb/1990/09/25015001.pdf</a></div>
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<span style="font-size: 10pt;">INDUSTRY RESPONSE TYPICAL</span></div>
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<a href="http://web.archive.org/web/20030822055917/www.bseinquiry.gov.uk/files/yb/1990/09/25007001.pdf" style="color: blue; cursor: pointer; font-size: 10pt; font-weight: bold; text-decoration-line: none;" target="_blank">http://web.archive.org/web/20030822055917/www.bseinquiry.gov.uk/files/yb/1990/09/25007001.pdf</a></div>
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<span style="font-size: 10pt;">DEFENSIVE BRIEFING</span></div>
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<a href="http://web.archive.org/web/20030820195733/http://www.bseinquiry.gov.uk/files/yb/1990/09/25016001.pdf" style="color: blue; cursor: pointer; font-size: 10pt; font-weight: bold; text-decoration-line: none;" target="_blank">http://web.archive.org/web/20030820195733/http://www.bseinquiry.gov.uk/files/yb/1990/09/25016001.pdf</a></div>
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<span style="font-size: 10pt;">CONFIDENTIAL</span></div>
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<span style="font-size: 10pt;">pigs & pharmaceuticals</span></div>
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<a href="http://web.archive.org/web/20010305223234/www.bseinquiry.gov.uk/files/yb/1990/09/10007001.pdf" style="color: blue; cursor: pointer; font-size: 10pt; font-weight: bold; text-decoration-line: none;" target="_blank">http://web.archive.org/web/20010305223234/www.bseinquiry.gov.uk/files/yb/1990/09/10007001.pdf</a></div>
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<a href="http://web.archive.org/web/20010305223234/www.bseinquiry.gov.uk/files/yb/1990/08/23002001.pdf" style="color: blue; cursor: pointer; font-size: 10pt; font-weight: bold; text-decoration-line: none;" target="_blank">http://web.archive.org/web/20010305223234/www.bseinquiry.gov.uk/files/yb/1990/08/23002001.pdf</a></div>
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<a href="http://web.archive.org/web/20010305223234/www.bseinquiry.gov.uk/files/yb/1990/08/23004001.pdf" style="color: blue; cursor: pointer; font-size: 10pt; font-weight: bold; text-decoration-line: none;" target="_blank">http://web.archive.org/web/20010305223234/www.bseinquiry.gov.uk/files/yb/1990/08/23004001.pdf</a></div>
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<a href="http://web.archive.org/web/20010305223234/www.bseinquiry.gov.uk/files/yb/1990/08/29003001.pdf" style="color: blue; cursor: pointer; font-size: 10pt; font-weight: bold; text-decoration-line: none;" target="_blank">http://web.archive.org/web/20010305223234/www.bseinquiry.gov.uk/files/yb/1990/08/29003001.pdf</a></div>
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<span style="font-size: 10pt;">COMMERCIAL IN CONFIDENCE COMMITTEE ON SAFETY OF MEDICINE NOT FOR PUBLICATION BOVINE SPONGIFORM ENCEPHALOPATHY WORKING GROUP</span></div>
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<span style="font-size: 10pt;">There are only two products using porcine brain and these use corticotrophin BP, made from porcine pituitary, source from outside the UK.............</span></div>
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<a href="http://web.archive.org/web/20040622220349/www.bseinquiry.gov.uk/files/yb/1990/10/31003001.pdf" style="color: blue; cursor: pointer; font-size: 10pt; font-weight: bold; text-decoration-line: none;" target="_blank">http://web.archive.org/web/20040622220349/www.bseinquiry.gov.uk/files/yb/1990/10/31003001.pdf</a></div>
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<span style="font-size: 10pt;">snip...</span></div>
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7 OF 10 LITTLE PIGGIES WENT ON TO DEVELOP BSE;</div>
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1: J Comp Pathol. 2000 Feb-Apr; 122(2-3): 131-43. Related Articles,</div>
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The neuropathology of experimental bovine spongiform encephalopathy in the pig.</div>
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Ryder SJ, Hawkins SA, Dawson M, Wells GA.</div>
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Veterinary Laboratories Agency Weybridge, Woodham Lane, New Haw, Addlestone, Surrey, KT15 3NB, UK.</div>
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In an experimental study of the transmissibility of BSE to the pig, seven of 10 pigs, infected at 1-2 weeks of age by multiple-route parenteral inoculation with a homogenate of bovine brain from natural BSE cases developed lesions typical of spongiform encephalopathy. The lesions consisted principally of severe neuropil vacuolation affecting most areas of the brain, but mainly the forebrain. In addition, some vacuolar change was identified in the rostral colliculi and hypothalamic areas of normal control pigs. PrP accumulations were detected immunocytochemically in the brains of BSE-infected animals. PrP accumulation was sparse in many areas and its density was not obviously related to the degree of vacuolation. The patterns of PrP immunolabelling in control pigs differed strikingly from those in the infected animals.</div>
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PMID: 10684682 [PubMed - indexed for MEDLINE]</div>
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<a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?holding=npg&cmd=Retrieve&db=PubMed&list_uids=10684682&dopt=Abstract" style="color: blue; cursor: pointer; font-weight: bold; text-decoration-line: none;" target="_blank">http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?holding=npg&cmd=Retrieve&db=PubMed&list_uids=10684682&dopt=Abstract</a></div>
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snip...</div>
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In the United States, feeding of ruminant by-products to ruminants is prohibited, but feeding of ruminant materials to swine and poultry still occurs. The potential for swine to have access to scrapie-contaminated feedstuffs exists, but the potential for swine to serve as a host for replication/accumulation of the agent of scrapie is unknown. The purpose of this study was to perform oral and intracerebral inoculation of the U.S. scrapie agent to determine the potential of swine as a host for the scrapie agent and their clinical susceptibility.</div>
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see full text and more transmission studies here ;</div>
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<a href="http://chronic-wasting-disease.blogspot.com/2011/07/swine-are-susceptible-to-chronic.html" style="color: blue; cursor: pointer; font-weight: bold; text-decoration-line: none;" target="_blank">http://chronic-wasting-disease.blogspot.com/2011/07/swine-are-susceptible-to-chronic.html</a></div>
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Transgenic mice expressing porcine prion protein resistant to classical scrapie but susceptible to sheep bovine spongiform encephalopathy and atypical scrapie.</div>
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Emerg Infect Dis. 2009 Aug; [Epub ahead of print]</div>
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<a href="http://nor-98.blogspot.com/2009/07/transgenic-mice-expressing-porcine.html" style="color: blue; cursor: pointer; font-weight: bold; text-decoration-line: none;" target="_blank">http://nor-98.blogspot.com/2009/07/transgenic-mice-expressing-porcine.html</a></div>
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<a href="http://madporcinedisease.blogspot.com/" style="color: #cc6600; cursor: pointer; font-weight: bold;">http://madporcinedisease.blogspot.com/</a></div>
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<span style="font-family: Georgia;">NEW TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHY TSE PRION DISEASE (MAD CAMEL DISEASE) IN A NEW SPECIES</span><br style="font-family: Georgia; line-height: 1.22em;" /><br style="font-family: Georgia; line-height: 1.22em;" /><span style="font-family: Georgia;">NEW OUTBREAK OF TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHY TSE PRION DISEASE IN A NEW SPECIES</span><br style="font-family: Georgia; line-height: 1.22em;" /><br style="font-family: Georgia; line-height: 1.22em;" /><span style="font-family: Georgia;">Subject: Prion Disease in Dromedary Camels, Algeria</span><br style="font-family: Georgia; line-height: 1.22em;" /><br style="font-family: Georgia; line-height: 1.22em;" /><span style="font-family: Georgia;">Our identification of this prion disease in a geographically widespread livestock species requires urgent enforcement of surveillance and assessment of the potential risks to human and animal health.</span><br style="font-family: Georgia; line-height: 1.22em;" /><br style="font-family: Georgia; line-height: 1.22em;" /><a href="https://wwwnc.cdc.gov/eid/article/24/6/17-2007_article" rel="noopener noreferrer" style="color: blue; cursor: pointer; font-family: Verdana; line-height: 1.22em;" target="_blank">https://wwwnc.cdc.gov/eid/article/24/6/17-2007_article</a><br style="font-family: Georgia; line-height: 1.22em;" /><br style="font-family: Georgia; line-height: 1.22em;" /><a href="http://camelusprp.blogspot.com/2018/04/tse-prion-disease-in-dromedary-camels.html" rel="noopener noreferrer" style="color: blue; cursor: pointer; font-family: Verdana; line-height: 1.22em;" target="_blank">http://camelusprp.blogspot.com/2018/04/tse-prion-disease-in-dromedary-camels.html</a><br style="font-family: Georgia; line-height: 1.22em;" /><br style="font-family: Georgia; line-height: 1.22em;" /><span style="font-family: Georgia;">***> IMPORTS AND EXPORTS <***</span><br style="font-family: Georgia; line-height: 1.22em;" /><br style="font-family: Georgia; line-height: 1.22em;" /><a href="http://camelusprp.blogspot.com/2018/04/dromedary-camels-algeria-prion-mad.html" rel="noopener noreferrer" style="color: blue; cursor: pointer; font-family: Verdana; line-height: 1.22em;" target="_blank">http://camelusprp.blogspot.com/2018/04/dromedary-camels-algeria-prion-mad.html</a><span style="font-size: 10pt;"><br /></span></div>
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<span style="font-family: Georgia;">2017 USAHA RESOLUTION</span><br style="font-family: Georgia; line-height: 1.22em;" /><br style="font-family: Georgia; line-height: 1.22em;" /><span style="font-family: Georgia;">RESOLUTION NUMBER: 1 Combined with 6, 13, 16, and 22 APPROVED</span><br style="font-family: Georgia; line-height: 1.22em;" /><br style="font-family: Georgia; line-height: 1.22em;" /><span style="font-family: Georgia;">SUBJECT MATTER: Adequate Funding for Prevention, Diagnosis, and Response for Foreign Animal Disease Outbreaks </span><br style="font-family: Georgia; line-height: 1.22em;" /><br style="font-family: Georgia; line-height: 1.22em;" /><a href="http://www.usaha.org/upload/Resolution/2017/Resolution_1_6_13_16_22_FAD_Sup..pdf" rel="noopener noreferrer" style="color: blue; cursor: pointer; font-family: Verdana; line-height: 1.22em;" target="_blank">http://www.usaha.org/upload/Resolution/2017/Resolution_1_6_13_16_22_FAD_Sup..pdf</a><br style="font-family: Georgia; line-height: 1.22em;" /><br style="font-family: Georgia; line-height: 1.22em;" /><a href="http://camelusprp.blogspot.com/2018/04/genetic-variation-of-prion-protein-gene.html" rel="noopener noreferrer" style="color: blue; cursor: pointer; font-family: Verdana; line-height: 1.22em;" target="_blank">http://camelusprp.blogspot.com/2018/04/genetic-variation-of-prion-protein-gene.html</a></div>
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<span style="font-family: arial;">O.05: Transmission of prions to primates after extended silent incubation periods: Implications for BSE and scrapie risk assessment in human populations </span></div>
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Emmanuel Comoy, Jacqueline Mikol, Valerie Durand, Sophie Luccantoni, Evelyne Correia, Nathalie Lescoutra, Capucine Dehen, and Jean-Philippe Deslys Atomic Energy Commission; Fontenay-aux-Roses, France </div>
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Prion diseases (PD) are the unique neurodegenerative proteinopathies reputed to be transmissible under field conditions since decades. The transmission of Bovine Spongiform Encephalopathy (BSE) to humans evidenced that an animal PD might be zoonotic under appropriate conditions. Contrarily, in the absence of obvious (epidemiological or experimental) elements supporting a transmission or genetic predispositions, PD, like the other proteinopathies, are reputed to occur spontaneously (atpical animal prion strains, sporadic CJD summing 80% of human prion cases). Non-human primate models provided the first evidences supporting the transmissibiity of human prion strains and the zoonotic potential of BSE. Among them, cynomolgus macaques brought major information for BSE risk assessment for human health (Chen, 2014), according to their phylogenetic proximity to humans and extended lifetime. We used this model to assess the zoonotic potential of other animal PD from bovine, ovine and cervid origins even after very long silent incubation periods. </div>
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*** We recently observed the direct transmission of a natural classical scrapie isolate to macaque after a 10-year silent incubation period, </div>
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***with features similar to some reported for human cases of sporadic CJD, albeit requiring fourfold long incubation than BSE. Scrapie, as recently evoked in humanized mice (Cassard, 2014), </div>
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***is the third potentially zoonotic PD (with BSE and L-type BSE), </div>
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***thus questioning the origin of human sporadic cases. </div>
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We will present an updated panorama of our different transmission studies and discuss the implications of such extended incubation periods on risk assessment of animal PD for human health. </div>
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=============== </div>
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***thus questioning the origin of human sporadic cases*** </div>
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=============== </div>
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***our findings suggest that possible transmission risk of H-type BSE to sheep and human. Bioassay will be required to determine whether the PMCA products are infectious to these animals. </div>
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============== </div>
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<a href="https://prion2015.files.wordpress.com/2015/05/prion2015abstracts.pdf" rel="noopener noreferrer" style="color: blue; cursor: pointer; text-size-adjust: 100%;" target="_blank">https://prion2015.files.wordpress.com/2015/05/prion2015abstracts.pdf</a> </div>
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***Transmission data also revealed that several scrapie prions propagate in HuPrP-Tg mice with efficiency comparable to that of cattle BSE. While the efficiency of transmission at primary passage was low, subsequent passages resulted in a highly virulent prion disease in both Met129 and Val129 mice. </div>
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***Transmission of the different scrapie isolates in these mice leads to the emergence of prion strain phenotypes that showed similar characteristics to those displayed by MM1 or VV2 sCJD prion. </div>
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***These results demonstrate that scrapie prions have a zoonotic potential and raise new questions about the possible link between animal and human prions. </div>
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<a href="http://www.tandfonline.com/doi/abs/10.1080/19336896.2016.1163048?journalCode=kprn20" rel="noopener noreferrer" style="color: blue; cursor: pointer; text-size-adjust: 100%;" target="_blank">http://www.tandfonline.com/doi/abs/10.1080/19336896.2016.1163048?journalCode=kprn20</a> </div>
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PRION 2016 TOKYO</div>
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SCRAPIE WS-01: Prion diseases in animals and zoonotic potential 2016</div>
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Prion. 10:S15-S21. 2016 ISSN: 1933-6896 printl 1933-690X online</div>
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Taylor & Francis</div>
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Prion 2016 Animal Prion Disease Workshop Abstracts</div>
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WS-01: Prion diseases in animals and zoonotic potential</div>
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Juan Maria Torres a, Olivier Andreoletti b, J uan-Carlos Espinosa a. Vincent Beringue c. Patricia Aguilar a,</div>
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Natalia Fernandez-Borges a. and Alba Marin-Moreno a</div>
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"Centro de Investigacion en Sanidad Animal ( CISA-INIA ). Valdeolmos, Madrid. Spain; b UMR INRA -ENVT 1225 Interactions Holes Agents Pathogenes. ENVT. Toulouse. France: "UR892. Virologie lmmunologie MolécuIaires, Jouy-en-Josas. France</div>
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Dietary exposure to bovine spongiform encephalopathy (BSE) contaminated bovine tissues is considered as the origin of variant Creutzfeldt Jakob (vCJD) disease in human. To date, BSE agent is the only recognized zoonotic prion. Despite the variety of Transmissible Spongiform Encephalopathy (TSE) agents that have been circulating for centuries in farmed ruminants there is no apparent epidemiological link between exposure to ruminant products and the occurrence of other form of TSE in human like sporadic Creutzfeldt Jakob Disease (sCJD). However, the zoonotic potential of the diversity of circulating TSE agents has never been systematically assessed. The major issue in experimental assessment of TSEs zoonotic potential lies in the modeling of the ‘species barrier‘, the biological phenomenon that limits TSE agents’ propagation from a species to another. In the last decade, mice genetically engineered to express normal forms of the human prion protein has proved essential in studying human prions pathogenesis and modeling the capacity of TSEs to cross the human species barrier.</div>
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To assess the zoonotic potential of prions circulating in farmed ruminants, we study their transmission ability in transgenic mice expressing human PrPC (HuPrP-Tg). Two lines of mice expressing different forms of the human PrPC (129Met or 129Val) are used to determine the role of the Met129Val dimorphism in susceptibility/resistance to the different agents.</div>
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These transmission experiments confirm the ability of BSE prions to propagate in 129M- HuPrP-Tg mice and demonstrate that Met129 homozygotes may be susceptible to BSE in sheep or goat to a greater degree than the BSE agent in cattle and that these agents can convey molecular properties and neuropathological indistinguishable from vCJD. However homozygous 129V mice are resistant to all tested BSE derived prions independently of the originating species suggesting a higher transmission barrier for 129V-PrP variant.</div>
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Transmission data also revealed that several scrapie prions propagate in HuPrP-Tg mice with efficiency comparable to that of cattle BSE. While the efficiency of transmission at primary passage was low, subsequent passages resulted in a highly virulent prion disease in both Met129 and Val129 mice. </div>
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Transmission of the different scrapie isolates in these mice leads to the emergence of prion strain phenotypes that showed similar characteristics to those displayed by MM1 or VV2 sCJD prion. </div>
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These results demonstrate that scrapie prions have a zoonotic potential and raise new questions about the possible link between animal and human prions. </div>
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<a href="http://www.tandfonline.com/doi/abs/10.1080/19336896.2016.1163048?journalCode=kprn20" rel="noopener noreferrer" style="color: blue; cursor: pointer; font-size: 10pt; text-size-adjust: 100%;" target="_blank">http://www.tandfonline.com/doi/abs/10.1080/19336896.2016.1163048?journalCode=kprn20</a></div>
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why do we not want to do TSE transmission studies on chimpanzees $</div>
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5. A positive result from a chimpanzee challenged severly would likely create alarm in some circles even if the result could not be interpreted for man. I have a view that all these agents could be transmitted provided a large enough dose by appropriate routes was given and the animals kept long enough. Until the mechanisms of the species barrier are more clearly understood it might be best to retain that hypothesis.</div>
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snip...</div>
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R. BRADLEY</div>
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<a href="https://web.archive.org/web/20170126051158/http://collections.europarchive.org/tna/20080102222950/http://www.bseinquiry.gov.uk/files/yb/1990/09/23001001.pdf" rel="noopener noreferrer" style="color: blue; cursor: pointer; font-size: 10pt; text-size-adjust: 100%;" target="_blank">https://web.archive.org/web/20170126051158/http://collections.europarchive.org/tna/20080102222950/http://www.bseinquiry.gov.uk/files/yb/1990/09/23001001.pdf</a></div>
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Title: Transmission of scrapie prions to primate after an extended silent incubation period) </div>
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*** In complement to the recent demonstration that humanized mice are susceptible to scrapie, we report here the first observation of direct transmission of a natural classical scrapie isolate to a macaque after a 10-year incubation period. Neuropathologic examination revealed all of the features of a prion disease: spongiform change, neuronal loss, and accumulation of PrPres throughout the CNS. </div>
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*** This observation strengthens the questioning of the harmlessness of scrapie to humans, at a time when protective measures for human and animal health are being dismantled and reduced as c-BSE is considered controlled and being eradicated. </div>
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*** Our results underscore the importance of precautionary and protective measures and the necessity for long-term experimental transmission studies to assess the zoonotic potential of other animal prion strains. </div>
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<a href="http://www.ars.usda.gov/research/publications/publications.htm?SEQ_NO_115=313160" rel="noopener noreferrer" style="color: blue; cursor: pointer; text-size-adjust: 100%;" target="_blank">http://www.ars.usda.gov/research/publications/publications.htm?SEQ_NO_115=313160</a></div>
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<span style="font-family: Georgia;">I urge everyone to watch this video closely...terry </span></div>
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*** you can see video here and interview with Jeff's Mom, and scientist telling you to test everything and potential risk factors for humans ***</div>
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<a href="https://histodb11.usz.ch/Images/videos/video-004/video-004.html" rel="noopener noreferrer" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">https://histodb11.usz.ch/Images/videos/video-004/video-004.html</a></div>
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<span style="color: #191919; font-family: Verdana, Arial, sans-serif; font-size: 14px;">ZOONOTIC CHRONIC WASTING DISEASE CWD TSE PRION UPDATE ???</span><br style="color: #191919; font-family: Verdana, Arial, sans-serif; font-size: 14px;" /><br style="color: #191919; font-family: Verdana, Arial, sans-serif; font-size: 14px;" /><span style="color: #191919; font-family: Verdana, Arial, sans-serif; font-size: 14px;">here is the latest;</span></div>
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SEE CZUB CWD TSE Prion Zoonosis to squirrel monkey by oral route to macaque, RACE et al study, and other studies that show that indeed CWD is a increasingly zoonosis risk factor for humans...terry</div>
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<a href="https://www.cste2.org/Webinars/files/CWD_Slides_FINAL.pdf" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://www.cste2.org/Webinars/files/CWD_Slides_FINAL.pdf</a></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;"><span style="font-size: 13.3333px; line-height: 1.22em;">9:35 Candace Mathiason (Colorado State University): An Overview-Chronic Wasting</span></span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;"><span style="font-size: 13.3333px; line-height: 1.22em;">Disease mother to offspring transmission studies conducted at Colorado State University.</span></span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;"><span style="font-size: 13.3333px; line-height: 1.22em;">10:05 Hermann Schätzl/Sandor Dudas (University of Calgary): Oral transmission of CWD</span></span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;"><span style="font-size: 13.3333px; line-height: 1.22em;">into Cynomolgus macaques: signs of atypical disease, prion conversion and infectivity in</span></span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;"><span style="font-size: 13.3333px; line-height: 1.22em;">macaques and bio-assayed transgenic mice.</span></span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;"><span style="font-size: 13.3333px; line-height: 1.22em;">16:30 Jo Moore (USDA, Ames): The agent of chronic wasting disease from pigs is infectious</span></span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;"><span style="font-size: 13.3333px; line-height: 1.22em;">in transgenic mice expressing human PRNP.</span></span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;"><span style="font-size: 13.3333px; line-height: 1.22em;"><a href="https://prion2018.org/wp-content/uploads/2018/05/program.pdf" rel="noopener noreferrer" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">https://prion2018.org/wp-content/uploads/2018/05/program.pdf</a></span></span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;"><a href="http://prionconference.blogspot.com/2018/02/prion-round-table-conference-2018-may.html" rel="noopener noreferrer" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">http://prionconference.blogspot.com/2018/02/prion-round-table-conference-2018-may.html</a></span></div>
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<span style="font-family: Georgia; font-size: x-small;">***We have concluded that the human protein has a region that confers unusual susceptibility to conversion by CWD prions. CWD is unique among prion diseases in its rapid spread in natural populations. BSE prions are essentially unaltered upon passage to a new species, while CWD adapts to the new species. This adaptation has consequences for surveillance of humans exposed to CWD. Wildlife Disease Risk Communication Research Contributes to Wildlife Trust Administration Exploring perceptions about chronic wasting disease risks among wildlife and agriculture professionals and stakeholders</span></div>
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<span style="font-family: Georgia; font-size: x-small;"><a href="http://www.wda2016.org/uploads/5/8/6/1/58613359/wda_2016_conference_proceedings_low_res.pdf" rel="noopener noreferrer" style="color: blue; cursor: pointer; text-size-adjust: 100%;" target="_blank">http://www.wda2016.org/uploads/5/8/6/1/58613359/wda_2016_conference_proceedings_low_res.pdf</a> </span></div>
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<span style="font-family: Georgia; font-size: x-small;">CDC CWD 2018 TRANSMISSION</span></div>
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<a href="https://www.cdc.gov/prions/cwd/transmission.html" rel="noopener noreferrer" style="color: blue; cursor: pointer; font-size: 10pt; text-size-adjust: 100%;" target="_blank">https://www.cdc.gov/prions/cwd/transmission.html</a></div>
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*** The potential impact of prion diseases on human health was greatly magnified by the recognition that interspecies transfer of BSE to humans by beef ingestion resulted in vCJD. While changes in animal feed constituents and slaughter practices appear to have curtailed vCJD, there is concern that CWD of free-ranging deer and elk in the U.S. might also cross the species barrier. Thus, consuming venison could be a source of human prion disease. Whether BSE and CWD represent interspecies scrapie transfer or are newly arisen prion diseases is unknown. Therefore, the possibility of transmission of prion disease through other food animals cannot be ruled out. There is evidence that vCJD can be transmitted through blood transfusion. There is likely a pool of unknown size of asymptomatic individuals infected with vCJD, and there may be asymptomatic individuals infected with the CWD equivalent. These circumstances represent a potential threat to blood, blood products, and plasma supplies. </div>
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<span style="line-height: 1.22em;"><a href="http://cdmrp.army.mil/prevfunded/nprp/NPRP_Summit_Final_Report.pdf" rel="noopener noreferrer" style="color: blue; cursor: pointer; line-height: 1.22em; text-size-adjust: 100%;" target="_blank">http://cdmrp.army.mil/prevfunded/nprp/NPRP_Summit_Final_Report.pdf</a></span></div>
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see more cwd zoonosis risk factors from updated science below...terry</div>
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<br style="color: #191919; font-family: Verdana, Arial, sans-serif; font-size: 14px;" /><span style="color: #191919; font-family: Verdana, Arial, sans-serif; font-size: 14px;">Cervid to human prion transmission </span><br style="color: #191919; font-family: Verdana, Arial, sans-serif; font-size: 14px;" /><br style="color: #191919; font-family: Verdana, Arial, sans-serif; font-size: 14px;" /><span style="color: #191919; font-family: Verdana, Arial, sans-serif; font-size: 14px;">Kong, Qingzhong </span><br style="color: #191919; font-family: Verdana, Arial, sans-serif; font-size: 14px;" /><br style="color: #191919; font-family: Verdana, Arial, sans-serif; font-size: 14px;" /><span style="color: #191919; font-family: Verdana, Arial, sans-serif; font-size: 14px;">Case Western Reserve University, Cleveland, OH, United States </span><br style="color: #191919; font-family: Verdana, Arial, sans-serif; font-size: 14px;" /><br style="color: #191919; font-family: Verdana, Arial, sans-serif; font-size: 14px;" /><span style="color: #191919; font-family: Verdana, Arial, sans-serif; font-size: 14px;">Abstract </span><br style="color: #191919; font-family: Verdana, Arial, sans-serif; font-size: 14px;" /><br style="color: #191919; font-family: Verdana, Arial, sans-serif; font-size: 14px;" /><span style="color: #191919; font-family: Verdana, Arial, sans-serif; font-size: 14px;">Prion disease is transmissible and invariably fatal. Chronic wasting disease (CWD) is the prion disease affecting deer, elk and moose, and it is a widespread and expanding epidemic affecting 22 US States and 2 Canadian provinces so far. CWD poses the most serious zoonotic prion transmission risks in North America because of huge venison consumption (>6 million deer/elk hunted and consumed annually in the USA alone), significant prion infectivity in muscles and other tissues/fluids from CWD-affected cervids, and usually high levels of individual exposure to CWD resulting from consumption of the affected animal among often just family and friends. However, we still do not know whether CWD prions can infect humans in the brain or peripheral tissues or whether clinical/asymptomatic CWD zoonosis has already occurred, and we have no essays to reliably detect CWD infection in humans. We hypothesize that: </span><br style="color: #191919; font-family: Verdana, Arial, sans-serif; font-size: 14px;" /><br style="color: #191919; font-family: Verdana, Arial, sans-serif; font-size: 14px;" /><span style="color: #191919; font-family: Verdana, Arial, sans-serif; font-size: 14px;">(1) The classic CWD prion strain can infect humans at low levels in the brain and peripheral lymphoid tissues; </span><br style="color: #191919; font-family: Verdana, Arial, sans-serif; font-size: 14px;" /><br style="color: #191919; font-family: Verdana, Arial, sans-serif; font-size: 14px;" /><span style="color: #191919; font-family: Verdana, Arial, sans-serif; font-size: 14px;">(2) The cervid-to-human transmission barrier is dependent on the cervid prion strain and influenced by the host (human) prion protein (PrP) primary sequence; </span><br style="color: #191919; font-family: Verdana, Arial, sans-serif; font-size: 14px;" /><br style="color: #191919; font-family: Verdana, Arial, sans-serif; font-size: 14px;" /><span style="color: #191919; font-family: Verdana, Arial, sans-serif; font-size: 14px;">(3) Reliable essays can be established to detect CWD infection in humans;and </span></div>
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<br style="color: #191919; font-family: Verdana, Arial, sans-serif; font-size: 14px;" /><span style="color: #191919; font-family: Verdana, Arial, sans-serif; font-size: 14px;">*** (4) CWD transmission to humans has already occurred. </span><br style="color: #191919; font-family: Verdana, Arial, sans-serif; font-size: 14px;" /><br style="color: #191919; font-family: Verdana, Arial, sans-serif; font-size: 14px;" /><span style="color: #191919; font-family: Verdana, Arial, sans-serif; font-size: 14px;">We will test these hypotheses in 4 Aims using transgenic (Tg) mouse models and complementary in vitro approaches. </span><br style="color: #191919; font-family: Verdana, Arial, sans-serif; font-size: 14px;" /><br style="color: #191919; font-family: Verdana, Arial, sans-serif; font-size: 14px;" /><span style="color: #191919; font-family: Verdana, Arial, sans-serif; font-size: 14px;">Aim 1 will prove that the classical CWD strain may infect humans in brain or peripheral lymphoid tissues at low levels by conducting systemic bioassays in a set of "humanized" Tg mouse lines expressing common human PrP variants using a number of CWD isolates at varying doses and routes. Experimental "human CWD" samples will also be generated for Aim 3. </span><br style="color: #191919; font-family: Verdana, Arial, sans-serif; font-size: 14px;" /><br style="color: #191919; font-family: Verdana, Arial, sans-serif; font-size: 14px;" /><span style="color: #191919; font-family: Verdana, Arial, sans-serif; font-size: 14px;">Aim 2 will test the hypothesis that the cervid-to-human prion transmission barrier is dependent on prion strain and influenced by the host (human) PrP sequence by examining and comparing the transmission efficiency and phenotypes of several atypical/unusual CWD isolates/strains as well as a few prion strains from other species that have adapted to cervid PrP sequence, utilizing the same panel of humanized Tg mouse lines as in Aim 1. </span><br style="color: #191919; font-family: Verdana, Arial, sans-serif; font-size: 14px;" /><span style="color: #191919; font-family: Verdana, Arial, sans-serif; font-size: 14px;">Aim 3 will establish reliable essays for detection and surveillance of CWD infection in humans by examining in details the clinical, pathological, biochemical and in vitro seeding properties of existing and future experimental "human CWD" samples generated from Aims 1-2 and compare them with those of common sporadic human Creutzfeldt-Jakob disease (sCJD) prions. </span><br style="color: #191919; font-family: Verdana, Arial, sans-serif; font-size: 14px;" /><br style="color: #191919; font-family: Verdana, Arial, sans-serif; font-size: 14px;" /><span style="color: #191919; font-family: Verdana, Arial, sans-serif; font-size: 14px;">Aim 4 will attempt to detect clinical CWD-affected human cases by examining a significant number of brain samples from prion-affected human subjects in the USA and Canada who have consumed venison from CWD-endemic areas utilizing the criteria and essays established in Aim 3. The findings from this proposal will greatly advance our understandings on the potential and characteristics of cervid prion transmission in humans, establish reliable essays for CWD zoonosis and potentially discover the first case(s) of CWD infection in humans. </span></div>
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<br style="color: #191919; font-family: Verdana, Arial, sans-serif; font-size: 14px;" /><span style="color: #191919; font-family: Verdana, Arial, sans-serif; font-size: 14px;">Public Health Relevance There are significant and increasing human exposure to cervid prions because chronic wasting disease (CWD, a widespread and highly infectious prion disease among deer and elk in North America) continues spreading and consumption of venison remains popular, but our understanding on cervid-to-human prion transmission is still very limited, raising public health concerns. This proposal aims to define the zoonotic risks of cervid prions and set up and apply essays to detect CWD zoonosis using mouse models and in vitro methods. The findings will greatly expand our knowledge on the potentials and characteristics of cervid prion transmission in humans, establish reliable essays for such infections and may discover the first case(s) of CWD infection in humans. </span></div>
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<br style="color: #191919; font-family: Verdana, Arial, sans-serif; font-size: 14px;" /><span style="color: #191919; font-family: Verdana, Arial, sans-serif; font-size: 14px;">Funding Agency Agency National Institute of Health (NIH) </span><br style="color: #191919; font-family: Verdana, Arial, sans-serif; font-size: 14px;" /><br style="color: #191919; font-family: Verdana, Arial, sans-serif; font-size: 14px;" /><span style="color: #191919; font-family: Verdana, Arial, sans-serif; font-size: 14px;">Institute National Institute of Neurological Disorders and Stroke (NINDS) </span><br style="color: #191919; font-family: Verdana, Arial, sans-serif; font-size: 14px;" /><span style="color: #191919; font-family: Verdana, Arial, sans-serif; font-size: 14px;">Type Research Project (R01) </span><br style="color: #191919; font-family: Verdana, Arial, sans-serif; font-size: 14px;" /><span style="color: #191919; font-family: Verdana, Arial, sans-serif; font-size: 14px;">Project # 1R01NS088604-01A1 </span><br style="color: #191919; font-family: Verdana, Arial, sans-serif; font-size: 14px;" /><span style="color: #191919; font-family: Verdana, Arial, sans-serif; font-size: 14px;">Application # 9037884 </span><br style="color: #191919; font-family: Verdana, Arial, sans-serif; font-size: 14px;" /><span style="color: #191919; font-family: Verdana, Arial, sans-serif; font-size: 14px;">Study Section Cellular and Molecular Biology of Neurodegeneration Study Section (CMND) </span><br style="color: #191919; font-family: Verdana, Arial, sans-serif; font-size: 14px;" /><span style="color: #191919; font-family: Verdana, Arial, sans-serif; font-size: 14px;">Program Officer Wong, May </span><br style="color: #191919; font-family: Verdana, Arial, sans-serif; font-size: 14px;" /><span style="color: #191919; font-family: Verdana, Arial, sans-serif; font-size: 14px;">Project Start 2015-09-30 </span><br style="color: #191919; font-family: Verdana, Arial, sans-serif; font-size: 14px;" /><span style="color: #191919; font-family: Verdana, Arial, sans-serif; font-size: 14px;">Project End 2019-07-31 </span><br style="color: #191919; font-family: Verdana, Arial, sans-serif; font-size: 14px;" /><span style="color: #191919; font-family: Verdana, Arial, sans-serif; font-size: 14px;">Budget Start 2015-09-30 </span><br style="color: #191919; font-family: Verdana, Arial, sans-serif; font-size: 14px;" /><span style="color: #191919; font-family: Verdana, Arial, sans-serif; font-size: 14px;">Budget End 2016-07-31 </span><br style="color: #191919; font-family: Verdana, Arial, sans-serif; font-size: 14px;" /><span style="color: #191919; font-family: Verdana, Arial, sans-serif; font-size: 14px;">Support Year 1 </span><br style="color: #191919; font-family: Verdana, Arial, sans-serif; font-size: 14px;" /><span style="color: #191919; font-family: Verdana, Arial, sans-serif; font-size: 14px;">Fiscal Year 2015 </span><br style="color: #191919; font-family: Verdana, Arial, sans-serif; font-size: 14px;" /><span style="color: #191919; font-family: Verdana, Arial, sans-serif; font-size: 14px;">Total Cost $337,507 </span><br style="color: #191919; font-family: Verdana, Arial, sans-serif; font-size: 14px;" /><span style="color: #191919; font-family: Verdana, Arial, sans-serif; font-size: 14px;">Indirect Cost $118,756 </span><br style="color: #191919; font-family: Verdana, Arial, sans-serif; font-size: 14px;" /><span style="color: #191919; font-family: Verdana, Arial, sans-serif; font-size: 14px;">Institution </span><br style="color: #191919; font-family: Verdana, Arial, sans-serif; font-size: 14px;" /><span style="color: #191919; font-family: Verdana, Arial, sans-serif; font-size: 14px;">Name Case Western Reserve University </span><br style="color: #191919; font-family: Verdana, Arial, sans-serif; font-size: 14px;" /><span style="color: #191919; font-family: Verdana, Arial, sans-serif; font-size: 14px;">Department Pathology </span><br style="color: #191919; font-family: Verdana, Arial, sans-serif; font-size: 14px;" /><span style="color: #191919; font-family: Verdana, Arial, sans-serif; font-size: 14px;">Type Schools of Medicine </span><br style="color: #191919; font-family: Verdana, Arial, sans-serif; font-size: 14px;" /><span style="color: #191919; font-family: Verdana, Arial, sans-serif; font-size: 14px;">DUNS # 077758407 </span><br style="color: #191919; font-family: Verdana, Arial, sans-serif; font-size: 14px;" /><span style="color: #191919; font-family: Verdana, Arial, sans-serif; font-size: 14px;">City Cleveland </span><br style="color: #191919; font-family: Verdana, Arial, sans-serif; font-size: 14px;" /><span style="color: #191919; font-family: Verdana, Arial, sans-serif; font-size: 14px;">State OH </span><br style="color: #191919; font-family: Verdana, Arial, sans-serif; font-size: 14px;" /><span style="color: #191919; font-family: Verdana, Arial, sans-serif; font-size: 14px;">Country United States </span><br style="color: #191919; font-family: Verdana, Arial, sans-serif; font-size: 14px;" /><span style="color: #191919; font-family: Verdana, Arial, sans-serif; font-size: 14px;">Zip Code 44106 </span><br style="color: #191919; font-family: Verdana, Arial, sans-serif; font-size: 14px;" /><br style="color: #191919; font-family: Verdana, Arial, sans-serif; font-size: 14px;" /><a class="aolmail_aolmail_aolmail_externalLink aolmail_aolmail_aolmail_ProxyLink" href="http://grantome.com/grant/NIH/R01-NS088604-01A1%20http://grantome.com/grant/NIH/R01-NS088604-01A1" rel="noopener noreferrer" style="border-radius: 0px; color: #1d6f23; cursor: pointer; font-family: Verdana, Arial, sans-serif; font-size: 14px; margin: 0px -3px; padding: 0px 3px;" target="_blank">http://grantome.com/grant/NIH/R01-NS088604-01A1 http://grantome.com/grant/NIH/R01-NS088604-01A1</a></div>
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<span style="font-size: 10pt;">CWD TSE Prion Zoonosis to squirrel monkey and macaque</span></div>
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<a href="https://www.cste2.org/Webinars/files/CWD_Slides_FINAL.pdf" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://www.cste2.org/Webinars/files/CWD_Slides_FINAL.pdf</a></div>
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Prion 2017 Conference Abstracts CWD</div>
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<span style="line-height: 1.22em;"> 2017 PRION CONFERENCE </span></div>
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<span style="line-height: 1.22em;">First evidence of intracranial and peroral transmission of Chronic Wasting Disease (CWD) into Cynomolgus macaques: a work in progress </span></div>
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<span style="line-height: 1.22em;">Stefanie Czub1, Walter Schulz-Schaeffer2, Christiane Stahl-Hennig3, Michael Beekes4, Hermann Schaetzl5 and Dirk Motzkus6 1 </span></div>
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<span style="line-height: 1.22em;">University of Calgary Faculty of Veterinary Medicine/Canadian Food Inspection Agency; 2Universitatsklinikum des Saarlandes und Medizinische Fakultat der Universitat des Saarlandes; 3 Deutsches Primaten Zentrum/Goettingen; 4 Robert-Koch-Institut Berlin; 5 University of Calgary Faculty of Veterinary Medicine; 6 presently: Boehringer Ingelheim Veterinary Research Center; previously: Deutsches Primaten Zentrum/Goettingen </span></div>
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<span style="line-height: 1.22em;">This is a progress report of a project which started in 2009. 21 cynomolgus macaques were challenged with characterized CWD material from white-tailed deer (WTD) or elk by intracerebral (ic), oral, and skin exposure routes. Additional blood transfusion experiments are supposed to assess the CWD contamination risk of human blood product. Challenge materials originated from symptomatic cervids for ic, skin scarification and partially per oral routes (WTD brain). Challenge material for feeding of muscle derived from preclinical WTD and from preclinical macaques for blood transfusion experiments. We have confirmed that the CWD challenge material contained at least two different CWD agents (brain material) as well as CWD prions in muscle-associated nerves. </span></div>
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<span style="line-height: 1.22em;">Here we present first data on a group of animals either challenged ic with steel wires or per orally and sacrificed with incubation times ranging from 4.5 to 6.9 years at postmortem. Three animals displayed signs of mild clinical disease, including anxiety, apathy, ataxia and/or tremor. In four animals wasting was observed, two of those had confirmed diabetes. All animals have variable signs of prion neuropathology in spinal cords and brains and by supersensitive IHC, reaction was detected in spinal cord segments of all animals. Protein misfolding cyclic amplification (PMCA), real-time quaking-induced conversion (RT-QuiC) and PET-blot assays to further substantiate these findings are on the way, as well as bioassays in bank voles and transgenic mice. </span></div>
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<span style="line-height: 1.22em;">At present, a total of 10 animals are sacrificed and read-outs are ongoing. Preclinical incubation of the remaining macaques covers a range from 6.4 to 7.10 years. Based on the species barrier and an incubation time of > 5 years for BSE in macaques and about 10 years for scrapie in macaques, we expected an onset of clinical disease beyond 6 years post inoculation. </span></div>
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<span style="line-height: 1.22em;">PRION 2017 DECIPHERING NEURODEGENERATIVE DISORDERS </span></div>
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<span style="line-height: 1.22em;">Subject: PRION 2017 CONFERENCE DECIPHERING NEURODEGENERATIVE DISORDERS VIDEO </span></div>
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<span style="line-height: 1.22em;">*** PRION 2017 CONFERENCE VIDEO </span></div>
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<a href="https://www.youtube.com/embed/Vtt1kAVDhDQ" rel="noopener noreferrer" style="color: blue; cursor: pointer; line-height: 1.22em; text-size-adjust: 100%;" target="_blank">https://www.youtube.com/embed/Vtt1kAVDhDQ</a></div>
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<a href="http://prion2017.org/programme/" rel="noopener noreferrer" style="color: blue; cursor: pointer; line-height: 1.22em; text-size-adjust: 100%;" target="_blank">http://prion2017.org/programme/</a></div>
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<span style="color: blue; text-decoration-line: underline;"><a href="https://www.cste2.org/Webinars/files/CWD_Slides_FINAL.pdf" rel="noopener noreferrer" style="color: blue; cursor: pointer; text-decoration-line: none;" target="_blank">https://www.cste2.org/Webinars/files/CWD_Slides_FINAL.pdf</a></span></div>
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TUESDAY, JUNE 13, 2017</div>
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<span style="line-height: 1.22em;">PRION 2017 CONFERENCE ABSTRACT </span></div>
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<span style="line-height: 1.22em;">First evidence of intracranial and peroral transmission of Chronic Wasting Disease (CWD) into Cynomolgus macaques: a work in progress</span></div>
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<a href="http://chronic-wasting-disease.blogspot.com/2017/06/prion-2017-conference-abstract-first.html" rel="noopener noreferrer" style="color: blue; cursor: pointer; line-height: 1.22em; text-size-adjust: 100%;" target="_blank">http://chronic-wasting-disease.blogspot.com/2017/06/prion-2017-conference-abstract-first.html</a></div>
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<span style="color: blue; text-decoration-line: underline;"><a href="https://www.cste2.org/Webinars/files/CWD_Slides_FINAL.pdf" rel="noopener noreferrer" style="color: blue; cursor: pointer; text-decoration-line: none;" target="_blank">https://www.cste2.org/Webinars/files/CWD_Slides_FINAL.pdf</a></span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;"><span style="font-size: 13.3333px; line-height: 1.22em;">9:35 Candace Mathiason (Colorado State University): An Overview-Chronic Wasting</span></span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;"><span style="font-size: 13.3333px; line-height: 1.22em;">Disease mother to offspring transmission studies conducted at Colorado State University.</span></span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;"><span style="font-size: 13.3333px; line-height: 1.22em;">10:05 Hermann Schätzl/Sandor Dudas (University of Calgary): Oral transmission of CWD</span></span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;"><span style="font-size: 13.3333px; line-height: 1.22em;"><a href="https://prion2018.org/wp-content/uploads/2018/05/program.pdf" rel="noopener noreferrer" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">https://prion2018.org/wp-content/uploads/2018/05/program.pdf</a></span></span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;"><a href="http://prionconference.blogspot.com/2018/02/prion-round-table-conference-2018-may.html" rel="noopener noreferrer" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">http://prionconference.blogspot.com/2018/02/prion-round-table-conference-2018-may.html</a></span></div>
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SATURDAY, JULY 29, 2017 </div>
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Risk Advisory Opinion: Potential Human Health Risks from Chronic Wasting Disease CFIA, PHAC, HC (HPFB and FNIHB), INAC, Parks Canada, ECCC and AAFC </div>
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<a href="http://chronic-wasting-disease.blogspot.com/2017/07/risk-advisory-opinion-potential-human.html" rel="noopener noreferrer" style="color: blue; cursor: pointer; text-size-adjust: 100%;" target="_blank">http://chronic-wasting-disease.blogspot.com/2017/07/risk-advisory-opinion-potential-human.html</a></div>
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<span style="color: blue; font-family: Georgia; text-decoration-line: underline;"><a href="https://www.cste2.org/Webinars/files/CWD_Slides_FINAL.pdf" rel="noopener noreferrer" style="color: blue; cursor: pointer; text-decoration-line: none;" target="_blank">https://www.cste2.org/Webinars/files/CWD_Slides_FINAL.pdf</a></span></div>
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<a href="http://chronic-wasting-disease.blogspot.com/2017/07/risk-advisory-opinion-potential-human.html" rel="noopener noreferrer" style="color: blue; cursor: pointer; text-size-adjust: 100%;" target="_blank">http://chronic-wasting-disease.blogspot.com/2017/07/risk-advisory-opinion-potential-human.html</a></div>
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ZOONOTIC, ZOONOSIS, CHRONIC WASTING DISEASE CWD TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHY TSE PRION </div>
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10. ZOONOTIC, ZOONOSIS, CHRONIC WASTING DISEASE CWD TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHY TSE PRION AKA MAD DEER ELK DISEASE IN HUMANS, has it already happened, that should be the question... </div>
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''In particular the US data do not clearly exclude the possibility of human (sporadic or familial) TSE development due to consumption of venison. The Working Group thus recognizes a potential risk to consumers if a TSE would be present in European cervids.'' Scientific opinion on chronic wasting disease (II)</div>
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EFSA Panel on Biological Hazards (BIOHAZ) Antonia Ricci Ana Allende Declan Bolton Marianne Chemaly Robert Davies Pablo Salvador Fernández Escámez ... See all authors </div>
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First published: 17 January 2018 <a href="https://doi.org/10.2903/j.efsa.2018.5132" rel="noopener noreferrer" style="color: blue; cursor: pointer; text-size-adjust: 100%;" target="_blank">https://doi.org/10.2903/j.efsa.2018.5132</a> ;</div>
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8. Even though human TSE‐exposure risk through consumption of game from European cervids can be assumed to be minor, if at all existing, no final conclusion can be drawn due to the overall lack of scientific data. In particular the US data do not clearly exclude the possibility of human (sporadic or familial) TSE development due to consumption of venison. The Working Group thus recognizes a potential risk to consumers if a TSE would be present in European cervids. It might be prudent considering appropriate measures to reduce such a risk, e.g. excluding tissues such as CNS and lymphoid tissues from the human food chain, which would greatly reduce any potential risk for consumers. However, it is stressed that currently, no data regarding a risk of TSE infections from cervid products are available. </div>
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The tissue distribution of infectivity in CWD‐infected cervids is now known to extend beyond CNS and lymphoid tissues. While the removal of these specific tissues from the food chain would reduce human dietary exposure to infectivity, exclusion from the food chain of the whole carcass of any infected animal would be required to eliminate human dietary exposure. </div>
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<a href="https://efsa.onlinelibrary.wiley.com/doi/full/10.2903/j.efsa.2018.5132" rel="noopener noreferrer" style="color: blue; cursor: pointer; text-size-adjust: 100%;" target="_blank">https://efsa.onlinelibrary.wiley.com/doi/full/10.2903/j.efsa.2018.5132</a></div>
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zoonosis zoonotic cervid tse prion cwd to humans, preparing for the storm </div>
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***An alternative to modeling the species barrier is the cell-free conversion assay which points to CWD as the animal prion disease with the greatest zoonotic potential, after (and very much less than) BSE.116*** </div>
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<a href="https://www.tandfonline.com/doi/pdf/10.4161/pri.29237" rel="noopener noreferrer" style="color: blue; cursor: pointer; text-size-adjust: 100%;" target="_blank">https://www.tandfonline.com/doi/pdf/10.4161/pri.29237</a> </div>
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<span style="color: #663300; font-family: Arial, Helvetica, sans-serif; font-size: medium;"><br /></span><span style="color: #663300; font-family: "Times New Roman"; font-size: small;"><b>4. The link between BSE and vCJD</b> </span></div>
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<span style="color: #663300; font-family: Arial, Helvetica, sans-serif;"><br /></span><span style="font-family: Times New Roman;"><a href="https://www.blogger.com/null" name="aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_814097" style="color: blue; cursor: pointer; text-decoration-line: underline;"></a></span><span style="color: #663300; font-family: "Times New Roman";"><b>Summary</b> </span></div>
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<a href="https://www.blogger.com/null" name="aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_814098" style="color: blue; cursor: pointer; text-decoration-line: underline;"></a><span style="color: #663300; font-family: Arial, Helvetica, sans-serif;"><b>4.29 </b></span><span style="color: black; font-family: Arial, Helvetica, sans-serif;">The evidence discussed above that vCJD is caused by BSE seems overwhelming. Uncertainties exist about the cause of CJD in farmers, their wives and in several abattoir workers. It seems that farmers at least might be at higher risk than others in the general population. <a href="http://webarchive.nationalarchives.gov.uk/20090505202857/http://www.bseinquiry.gov.uk/report/volume2/chapteb6.htm#814101" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank" title="Click here to goto footnote/return to text"><sup>1</sup></a> Increased ascertainment (ie, increased identification of cases as a result of greater awareness of the condition) seems unlikely, as other groups exposed to risk, such as butchers and veterinarians, do not appear to have been affected. The CJD in farmers seems to be similar to other sporadic CJD in age of onset, in respect to glycosylation patterns, and in strain-typing in experimental mice. Some farmers are heterozygous for the methionine/valine variant at codon 129, and their lymphoreticular system (LRS) does not contain the high levels of PrP<sup>Sc</sup> found in vCJD. It remains a remote possibility that when older people contract CJD from BSE the resulting phenotype is like sporadic CJD and is distinct from the vCJD phenotype in younger people...</span><span style="font-family: Arial, Helvetica, sans-serif; font-size: x-small;">BSE INQUIRY</span></div>
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<span style="font-family: Georgia; font-size: x-small;">Health Portfolio partners were recently made aware of initial findings from a research project led by a CFIA scientist that have demonstrated that cynomolgus macaques can be infected via intracranial exposure and oral gavage with CWD infected muscle. </span></div>
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<span style="font-family: Georgia; font-size: x-small;">These findings suggest that CWD, under specific experimental conditions, has the potential to cross the human species barrier, including by enteral feeding of CWD infected muscle. </span></div>
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<a href="https://www.thetyee.ca/Documents/2017/06/24/Risk-Advisory-Opinion-CWD-2017.pdf" rel="noopener noreferrer" style="color: blue; cursor: pointer; text-size-adjust: 100%;" target="_blank">https://www.thetyee.ca/Documents/2017/06/24/Risk-Advisory-Opinion-CWD-2017.pdf</a></div>
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<span style="font-family: Georgia; font-size: x-small;">*** WDA 2016 NEW YORK *** </span></div>
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<span style="font-family: Georgia; font-size: x-small;">We found that CWD adapts to a new host more readily than BSE and that human PrP was unexpectedly prone to misfolding by CWD prions. </span></div>
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<span style="font-family: Georgia; font-size: x-small;">In addition, we investigated the role of specific regions of the bovine, deer and human PrP protein in resistance to conversion by prions from another species. </span></div>
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<span style="font-family: Georgia; font-size: x-small;">***We have concluded that the human protein has a region that confers unusual susceptibility to conversion by CWD prions. </span></div>
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<span style="font-family: Georgia; font-size: x-small;">The species barriers and public health threat of CWD and BSE prions </span></div>
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<span style="font-family: Georgia; font-size: x-small;">Ms. Kristen Davenport1, Dr. Davin Henderson1, Dr. Candace Mathiason1, Dr. Edward Hoover1 1Colorado State University </span></div>
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<span style="font-family: Georgia; font-size: x-small;">Chronic wasting disease (CWD) is spreading rapidly through cervid populations in the USA. Bovine spongiform encephalopathy (BSE, mad cow disease) arose in the 1980s because cattle were fed recycled animal protein. </span></div>
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<span style="font-family: Georgia; font-size: x-small;">These and other prion diseases are caused by abnormal folding of the normal prion protein (PrP) into a disease causing form (PrPd), which is pathogenic to nervous system cells and can cause subsequent PrP to misfold. CWD spreads among cervids very efficiently, but it has not yet infected humans. On the other hand, BSE was spread only when cattle consumed infected bovine or ovine tissue, but did infect humans and other species. </span></div>
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<span style="font-family: Georgia; font-size: x-small;">The objective of this research is to understand the role of PrP structure in cross-species infection by CWD and BSE. To study the propensity of each species’ PrP to be induced to misfold by the presence of PrPd from verious species, we have used an in vitro system that permits detection of PrPd in real-time. </span></div>
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<span style="font-family: Georgia; font-size: x-small;">We measured the conversion efficiency of various combinations of PrPd seeds and PrP substrate combinations. </span></div>
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<span style="font-family: Georgia; font-size: x-small;">We observed the cross-species behavior of CWD and BSE, in addition to feline-adapted CWD and BSE. We found that CWD adapts to a new host more readily than BSE and that human PrP was unexpectedly prone to misfolding by CWD prions. In addition, we investigated the role of specific regions of the bovine, deer and human PrP protein in resistance to conversion by prions from another species. </span></div>
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<span style="font-family: Georgia; font-size: x-small;">***We have concluded that the human protein has a region that confers unusual susceptibility to conversion by CWD prions. CWD is unique among prion diseases in its rapid spread in natural populations. BSE prions are essentially unaltered upon passage to a new species, while CWD adapts to the new species. This adaptation has consequences for surveillance of humans exposed to CWD. Wildlife Disease Risk Communication Research Contributes to Wildlife Trust Administration Exploring perceptions about chronic wasting disease risks among wildlife and agriculture professionals and stakeholders</span></div>
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<span style="font-family: Georgia; font-size: x-small;"><a href="http://www.wda2016.org/uploads/5/8/6/1/58613359/wda_2016_conference_proceedings_low_res.pdf" rel="noopener noreferrer" style="color: blue; cursor: pointer; text-size-adjust: 100%;" target="_blank">http://www.wda2016.org/uploads/5/8/6/1/58613359/wda_2016_conference_proceedings_low_res.pdf</a> </span></div>
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*** The potential impact of prion diseases on human health was greatly magnified by the recognition that interspecies transfer of BSE to humans by beef ingestion resulted in vCJD. While changes in animal feed constituents and slaughter practices appear to have curtailed vCJD, there is concern that CWD of free-ranging deer and elk in the U.S. might also cross the species barrier. Thus, consuming venison could be a source of human prion disease. Whether BSE and CWD represent interspecies scrapie transfer or are newly arisen prion diseases is unknown. Therefore, the possibility of transmission of prion disease through other food animals cannot be ruled out. There is evidence that vCJD can be transmitted through blood transfusion. There is likely a pool of unknown size of asymptomatic individuals infected with vCJD, and there may be asymptomatic individuals infected with the CWD equivalent. These circumstances represent a potential threat to blood, blood products, and plasma supplies. </div>
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<span style="font-family: Georgia; font-size: x-small;">Mule deer transmissions of CWD were by intracerebral inoculation and compared with natural cases {the following was written but with a single line marked through it ''first passage (by this route)}...TSS</span></div>
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<span style="font-family: Georgia; font-size: x-small;">resulted in a more rapidly progressive clinical disease with repeated episodes of synocopy ending in coma. One control animal became affected, it is believed through contamination of inoculum (?saline). Further CWD transmissions were carried out by Dick Marsh into ferret, mink and squirrel monkey. Transmission occurred in ALL of these species with the shortest incubation period in the ferret.</span></div>
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<a href="https://web.archive.org/web/20090506002237/http://www.bseinquiry.gov.uk/files/mb/m11b/tab01.pdf" rel="noopener noreferrer" style="color: blue; cursor: pointer; text-size-adjust: 100%;" target="_blank">https://web.archive.org/web/20090506002237/http://www.bseinquiry.gov.uk/files/mb/m11b/tab01.pdf</a></div>
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<span style="font-size: x-small;">Prion Infectivity in Fat of Deer with Chronic Wasting Disease▿ </span></div>
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<span style="font-size: x-small;">Brent Race#, Kimberly Meade-White#, Richard Race and Bruce Chesebro* + Author Affiliations</span></div>
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<span style="font-size: x-small;">In mice, prion infectivity was recently detected in fat. Since ruminant fat is consumed by humans and fed to animals, we determined infectivity titers in fat from two CWD-infected deer. Deer fat devoid of muscle contained low levels of CWD infectivity and might be a risk factor for prion infection of other species.</span></div>
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<span style="font-size: x-small;">Prions in Skeletal Muscles of Deer with Chronic Wasting Disease </span></div>
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<span style="font-size: x-small;">Here bioassays in transgenic mice expressing cervid prion protein revealed the presence of infectious prions in skeletal muscles of CWD-infected deer, demonstrating that humans consuming or handling meat from CWD-infected deer are at risk to prion exposure.</span></div>
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<span style="font-size: x-small;"> </span><span style="font-family: Georgia;">*** now, let’s see what the authors said about this casual link, personal communications years ago, and then the latest on the zoonotic potential from CWD to humans from the TOKYO PRION 2016 CONFERENCE.</span></div>
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see where it is stated NO STRONG evidence. so, does this mean there IS casual evidence ???? “Our conclusion stating that we found no strong evidence of CWD transmission to humans”</div>
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From: TSS (<a href="http://216-119-163-189.ipset45.wt.net/" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">216-119-163-189.ipset45.wt.net</a>)</div>
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Subject: CWD aka MAD DEER/ELK TO HUMANS ???</div>
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Date: September 30, 2002 at 7:06 am PST</div>
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From: "Belay, Ermias"</div>
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To: Cc: "Race, Richard (NIH)" ; ; "Belay, Ermias"</div>
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Sent: Monday, September 30, 2002 9:22 AM</div>
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Subject: RE: TO CDC AND NIH - PUB MED- 3 MORE DEATHS - CWD - YOUNG HUNTERS</div>
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Dear Sir/Madam,</div>
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In the Archives of Neurology you quoted (the abstract of which was attached to your email), we did not say CWD in humans will present like variant CJD. That assumption would be wrong. I encourage you to read the whole article and call me if you have questions or need more clarification (phone: 404-639-3091). Also, we do not claim that "no-one has ever been infected with prion disease from eating venison." Our conclusion stating that we found no strong evidence of CWD transmission to humans in the article you quoted or in any other forum is limited to the patients we investigated.</div>
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Ermias Belay, M.D. Centers for Disease Control and Prevention</div>
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-----Original Message-----</div>
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From: Sent: Sunday, September 29, 2002 10:15 AM</div>
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To: <a href="mailto:rr26k@nih.gov" rel="noopener noreferrer" style="color: blue; cursor: pointer; line-height: 1.22em; text-size-adjust: 100%;" target="_blank">rr26k@nih.gov</a>; <a href="mailto:rrace@niaid.nih.gov" rel="noopener noreferrer" style="color: blue; cursor: pointer; line-height: 1.22em; text-size-adjust: 100%;" target="_blank">rrace@niaid.nih.gov</a>; <a href="mailto:ebb8@CDC.GOV" rel="noopener noreferrer" style="color: blue; cursor: pointer; line-height: 1.22em; text-size-adjust: 100%;" target="_blank">ebb8@CDC.GOV</a></div>
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Subject: TO CDC AND NIH - PUB MED- 3 MORE DEATHS - CWD - YOUNG HUNTERS</div>
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Sunday, November 10, 2002 6:26 PM ......snip........end..............TSS</div>
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Thursday, April 03, 2008</div>
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A prion disease of cervids: Chronic wasting disease 2008 1: Vet Res. 2008 Apr 3;39(4):41 A prion disease of cervids: Chronic wasting disease Sigurdson CJ.</div>
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*** twenty-seven CJD patients who regularly consumed venison were reported to the Surveillance Center***,</div>
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snip... full text ;</div>
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<a href="http://chronic-wasting-disease.blogspot.com/2008/04/prion-disease-of-cervids-chronic.html" rel="noopener noreferrer" style="color: blue; cursor: pointer; line-height: 1.22em; text-size-adjust: 100%;" target="_blank">http://chronic-wasting-disease.blogspot.com/2008/04/prion-disease-of-cervids-chronic.html</a></div>
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<span style="line-height: 1.22em;">> However, to date, no CWD infections have been reported in people. </span></div>
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key word here is 'reported'. science has shown that CWD in humans will look like sporadic CJD. SO, how can one assume that CWD has not already transmitted to humans? they can't, and it's as simple as that. from all recorded science to date, CWD has already transmitted to humans, and it's being misdiagnosed as sporadic CJD. ...terry </div>
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<span style="line-height: 1.22em;">*** LOOKING FOR CWD IN HUMANS AS nvCJD or as an ATYPICAL CJD, LOOKING IN ALL THE WRONG PLACES $$$ ***</span></div>
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<span style="line-height: 1.22em;">*** These results would seem to suggest that CWD does indeed have zoonotic potential, at least as judged by the compatibility of CWD prions and their human PrPC target. Furthermore, extrapolation from this simple in vitro assay suggests that if zoonotic CWD occurred, it would most likely effect those of the PRNP codon 129-MM genotype and that the PrPres type would be similar to that found in the most common subtype of sCJD (MM1).*** </span></div>
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<a href="https://wwwnc.cdc.gov/eid/article/20/1/13-0858_article" rel="noopener noreferrer" style="color: blue; cursor: pointer; text-size-adjust: 100%;" target="_blank">https://wwwnc.cdc.gov/eid/article/20/1/13-0858_article</a></div>
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Missouri Donald Hill, et al., Respondents, vs. Missouri Department of Conservation, et al., Appellants SC96739 </div>
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<a href="http://chronic-wasting-disease.blogspot.com/2018/07/missouri-donald-hill-et-al-respondents.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://chronic-wasting-disease.blogspot.com/2018/07/missouri-donald-hill-et-al-respondents.html</a></div>
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<span style="font-family: arial, helvetica;"><span style="font-size: 13.3333px;">Chronic Wasting Disease CWD TSE Prion Global Report Update, USA, CANADA, KOREA, NORWAY, FINLAND, Game Farms and Fake news</span></span></div>
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<span style="font-family: arial, helvetica;">Terry S. Singeltary Sr.</span></div>
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Terry S. Singeltary Sr.http://www.blogger.com/profile/06986622967539963260noreply@blogger.com0tag:blogger.com,1999:blog-6404950019984350027.post-2886101429064656312017-08-14T15:53:00.001-07:002017-08-14T15:53:38.181-07:00Experimental transmission of the chronic wasting disease agent to swine after oral or intracranial inoculation<div style="font-family: arial; font-size: 13.3333px;">
Experimental transmission of the chronic wasting disease agent to swine after oral or intracranial inoculation</div>
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S. Jo Moore1,2, M. Heather West Greenlee3, Naveen Kondru3, Sireesha Manne3, Jodi D. Smith1, Robert A. Kunkle1, Anumantha Kanthasamy3 and Justin J. Greenlee1* + Author Affiliations</div>
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1Virus and Prion Research Unit, National Animal Disease Center, USDA, Agricultural Research Service, Ames, Iowa, United States of America 2Oak Ridge Institute for Science and Education, Oak Ridge, Tennessee, United States of America 3Department of Biomedical Sciences, Iowa State University College of Veterinary Medicine, Ames, Iowa, United States of America</div>
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Chronic wasting disease (CWD) is a naturally occurring, fatal neurodegenerative disease of cervids. The potential for swine to serve as a host for the agent of chronic wasting disease is unknown. The purpose of this study was to investigate the susceptibility of swine to the CWD agent following experimental oral or intracranial inoculation. Crossbred piglets were assigned to one of three groups: intracranially inoculated (n=20), orally inoculated (n=19), or non-inoculated (n=9). At approximately the age at which commercial pigs reach market weight, half of the pigs in each group were culled (‘market weight’ groups). The remaining pigs (‘aged’ groups) were allowed to incubate for up to 73 months post inoculation (MPI). Tissues collected at necropsy were examined for disease-associated prion protein (PrPSc) by western blotting (WB), antigen-capture immunoassay (EIA), immunohistochemistry (IHC) and in vitro real-time quaking induced conversion (RT-QuIC). Brain samples from selected pigs were also bioassayed in mice expressing porcine prion protein. Four intracranially inoculated aged pigs and one orally inoculated aged pig were positive by EIA, IHC and/or WB. Using RT-QuIC, PrPSc was detected in lymphoid and/or brain tissue from one or more pigs in each inoculated group. Bioassay was positive in 4 out of 5 pigs assayed. This study demonstrates that pigs can support low-level amplification of CWD prions, although the species barrier to CWD infection is relatively high. However, detection of infectivity in orally inoculated pigs using mouse bioassay raises the possibility that naturally exposed pigs could act as a reservoir of CWD infectivity.</div>
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IMPORTANCE We challenged domestic swine with the chronic wasting disease agent by inoculation directly into the brain (intracranially) or by oral gavage (orally). Disease-associated prion protein (PrPSc) was detected in brain and lymphoid tissues from intracranially and orally inoculated pigs as early as 8 months of age (6 months post-inoculation). Only one pig developed clinical neurologic signs suggestive of prion disease. The amount of PrPSc in the brains and lymphoid tissues of positive pigs was small, especially in orally inoculated pigs. Regardless, positive results in orally inoculated pigs suggest that it may be possible for swine to serve as a reservoir for prion disease under natural conditions.</div>
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FOOTNOTES</div>
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↵*Corresponding author: Email: justin.greenlee@ars.usda.gov This is a work of the U.S. Government and is not subject to copyright protection in the United States. Foreign copyrights may apply.</div>
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Research Project: TRANSMISSION, DIFFERENTIATION, AND PATHOBIOLOGY OF TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES</div>
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Location: Virus and Prion Research</div>
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Title: Disease-associated prion protein detected in lymphoid tissues from pigs challenged with the agent of chronic wasting disease</div>
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Author item Moore, Sarah item Kunkle, Robert item Kondru, Naveen item Manne, Sireesha item Smith, Jodi item Kanthasamy, Anumantha item West Greenlee, M item Greenlee, Justin</div>
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Submitted to: Prion Publication Type: Abstract Only Publication Acceptance Date: 3/15/2017 Publication Date: N/A Citation: N/A Interpretive Summary:</div>
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Technical Abstract: Aims: Chronic wasting disease (CWD) is a naturally-occurring, fatal neurodegenerative disease of cervids. We previously demonstrated that disease-associated prion protein (PrPSc) can be detected in the brain and retina from pigs challenged intracranially or orally with the CWD agent. In that study, neurological signs consistent with prion disease were observed only in one pig: an intracranially challenged pig that was euthanized at 64 months post-challenge. The purpose of this study was to use an antigen-capture immunoassay (EIA) and real-time quaking-induced conversion (QuIC) to determine whether PrPSc is present in lymphoid tissues from pigs challenged with the CWD agent.</div>
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Methods: At two months of age, crossbred pigs were challenged by the intracranial route (n=20), oral route (n=19), or were left unchallenged (n=9). At approximately 6 months of age, the time at which commercial pigs reach market weight, half of the pigs in each group were culled (<6 challenge="" groups="" month="" pigs="" remaining="" the="">6 month challenge groups) were allowed to incubate for up to 73 months post challenge (mpc). The retropharyngeal lymph node (RPLN) was screened for the presence of PrPSc by EIA and immunohistochemistry (IHC). The RPLN, palatine tonsil, and mesenteric lymph node (MLN) from 6-7 pigs per challenge group were also tested using EIA and QuIC.</6></div>
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Results: PrPSc was not detected by EIA and IHC in any RPLNs. All tonsils and MLNs were negative by IHC, though the MLN from one pig in the oral <6 5="" 6="" at="" by="" detected="" eia.="" examined="" group="" in="" intracranial="" least="" lymphoid="" month="" months="" of="" one="" pigs="" positive="" prpsc="" quic="" the="" tissues="" was="">6 months group, 5/6 pigs in the oral <6 4="" and="" group="" months="" oral="">6 months group. Overall, the MLN was positive in 14/19 (74%) of samples examined, the RPLN in 8/18 (44%), and the tonsil in 10/25 (40%). Conclusions:</6></6></div>
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This study demonstrates that PrPSc accumulates in lymphoid tissues from pigs challenged intracranially or orally with the CWD agent, and can be detected as early as 4 months after challenge.</div>
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CWD-infected pigs rarely develop clinical disease and if they do, they do so after a long incubation period. This raises the possibility that CWD-infected pigs could shed prions into their environment long before they develop clinical disease.</div>
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Furthermore, lymphoid tissues from CWD-infected pigs could present a potential source of CWD infectivity in the animal and human food chains.</div>
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<a href="https://www.ars.usda.gov/research/publications/publication/?seqNo115=337105" style="color: blue; cursor: pointer;" target="_blank">https://www.ars.usda.gov/research/publications/publication/?seqNo115=337105</a></div>
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EXPERIMENTAL PORCINE SPONGIFORM ENCEPHALOPATHY</div>
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While this clearly is a cause for concern we should not jump to the conclusion that this means that pigs will necessarily be infected by bone and meat meal fed by the oral route as is the case with cattle. ...</div>
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<a href="http://web.archive.org/web/20031026000118/www.bseinquiry.gov.uk/files/yb/1990/08/23004001.pdf" style="color: blue; cursor: pointer;" target="_blank">http://web.archive.org/web/20031026000118/www.bseinquiry.gov.uk/files/yb/1990/08/23004001.pdf</a></div>
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we cannot rule out the possibility that unrecognised subclinical spongiform encephalopathy could be present in British pigs though there is no evidence for this: only with parenteral/implantable pharmaceuticals/devices is the theoretical risk to humans of sufficient concern to consider any action.</div>
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<a href="http://web.archive.org/web/20030822031154/www.bseinquiry.gov.uk/files/yb/1990/09/10007001.pdf" style="color: blue; cursor: pointer;" target="_blank">http://web.archive.org/web/20030822031154/www.bseinquiry.gov.uk/files/yb/1990/09/10007001.pdf</a></div>
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Our records show that while some use is made of porcine materials in medicinal products, the only products which would appear to be in a hypothetically ''higher risk'' area are the adrenocorticotrophic hormone for which the source material comes from outside the United Kingdom, namely America China Sweden France and Germany. The products are manufactured by Ferring and Armour. A further product, ''Zenoderm Corium implant'' manufactured by Ethicon, makes use of porcine skin - which is not considered to be a ''high risk'' tissue, but one of its uses is described in the data sheet as ''in dural replacement''. This product is sourced from the United Kingdom.....</div>
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<a href="http://web.archive.org/web/20030822054419/www.bseinquiry.gov.uk/files/yb/1990/09/21009001.pdf" style="color: blue; cursor: pointer;" target="_blank">http://web.archive.org/web/20030822054419/www.bseinquiry.gov.uk/files/yb/1990/09/21009001.pdf</a></div>
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snip...see much more here ;</div>
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WEDNESDAY, APRIL 05, 2017</div>
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Disease-associated prion protein detected in lymphoid tissues from pigs challenged with the agent of chronic wasting disease</div>
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<a href="http://chronic-wasting-disease.blogspot.com/2017/04/disease-associated-prion-protein.html" style="color: blue; cursor: pointer;" target="_blank">http://chronic-wasting-disease.blogspot.com/2017/04/disease-associated-prion-protein.html</a></div>
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TUESDAY, APRIL 18, 2017 </div>
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*** EXTREME USA FDA PART 589 TSE PRION FEED LOOP HOLE STILL EXIST, AND PRICE OF POKER GOES UP ***</div>
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<a href="http://usdameatexport.blogspot.com/2017/04/extreme-usa-fda-part-589-tse-prion-feed.html" style="color: blue; cursor: pointer;" target="_blank">http://usdameatexport.blogspot.com/2017/04/extreme-usa-fda-part-589-tse-prion-feed.html</a></div>
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TUESDAY, MARCH 28, 2017 </div>
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*** Passage of scrapie to deer results in a new phenotype upon return passage to sheep ***</div>
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<a href="http://chronic-wasting-disease.blogspot.com/2017/03/passage-of-scrapie-to-deer-results-in.html" style="color: blue; cursor: pointer;" target="_blank">http://chronic-wasting-disease.blogspot.com/2017/03/passage-of-scrapie-to-deer-results-in.html</a></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">National Scrapie Eradication Program May 2017 Monthly Report Fiscal Year 2017</span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;"><a href="http://nor-98.blogspot.com/2017/07/national-scrapie-eradication-program.html" rel="noopener noreferrer" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">http://nor-98.blogspot.com/2017/07/national-scrapie-eradication-program.html</a></span></div>
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WEDNESDAY, JULY 26, 2017 </div>
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APHIS USDA Emerging Animal Disease Preparedness and Response Plan July 2017</div>
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<a href="http://animalhealthreportpriontse.blogspot.com/2017/07/aphis-usda-emerging-animal-disease.html" rel="noopener noreferrer" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">http://animalhealthreportpriontse.blogspot.com/2017/07/aphis-usda-emerging-animal-disease.html</a></div>
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<span style="font-family: arial, helvetica;"><span style="font-size: 13.3333px;">MINK FARMING USA TRANSMISSIBLE MINK ENCEPHALOPATHY TSE PRION DISEASE SURVEILLANCE AND TESTING</span></span></div>
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<span style="font-family: arial, helvetica;"><span style="font-size: 13.3333px;"><a href="http://transmissible-mink-encephalopathy.blogspot.com/2017/07/mink-farming-usa-transmissible-mink.html" rel="noopener noreferrer" style="color: purple; cursor: pointer;" target="_blank">http://transmissible-mink-encephalopathy.blogspot.com/2017/07/mink-farming-usa-transmissible-mink.html</a></span></span></div>
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<a href="http://transmissible-mink-encephalopathy.blogspot.com/" rel="noopener noreferrer" style="color: purple; cursor: pointer;" target="_blank">http://transmissible-mink-encephalopathy.blogspot.com/</a></div>
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THURSDAY, JULY 13, 2017 </div>
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EFSA BSE Sixty cases of mad cow disease since 2001 breached feed ban likely the cause </div>
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Scientists investigate origin of isolated BSE cases</div>
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<a href="http://bovineprp.blogspot.com/2017/07/efsa-bse-sixty-cases-of-mad-cow-disease.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://bovineprp.blogspot.com/2017/07/efsa-bse-sixty-cases-of-mad-cow-disease.html</a></div>
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*** The potential impact of prion diseases on human health was greatly magnified by the recognition that interspecies transfer of BSE to humans by beef ingestion resulted in vCJD. While changes in animal feed constituents and slaughter practices appear to have curtailed vCJD, there is concern that CWD of free-ranging deer and elk in the U.S. might also cross the species barrier. Thus, consuming venison could be a source of human prion disease. Whether BSE and CWD represent interspecies scrapie transfer or are newly arisen prion diseases is unknown. Therefore, the possibility of transmission of prion disease through other food animals cannot be ruled out. There is evidence that vCJD can be transmitted through blood transfusion. There is likely a pool of unknown size of asymptomatic individuals infected with vCJD, and there may be asymptomatic individuals infected with the CWD equivalent. These circumstances represent a potential threat to blood, blood products, and plasma supplies. </div>
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<a href="http://cdmrp.army.mil/prevfunded/nprp/NPRP_Summit_Final_Report.pdf" style="color: blue; cursor: pointer;" target="_blank">http://cdmrp.army.mil/prevfunded/nprp/NPRP_Summit_Final_Report.pdf</a></div>
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<a href="http://chronic-wasting-disease.blogspot.com/%C2%A0" style="color: blue; cursor: pointer;" target="_blank">http://chronic-wasting-disease.blogspot.com/</a></div>
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SUNDAY, AUGUST 06, 2017 </div>
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USA Chronic Wasting Disease CWD TSE Prion Emergency Response Plan Singeltary et al </div>
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<a href="http://chronic-wasting-disease.blogspot.com/2017/08/usa-chronic-wasting-disease-cwd-tse.html" style="color: blue; cursor: pointer;" target="_blank">http://chronic-wasting-disease.blogspot.com/2017/08/usa-chronic-wasting-disease-cwd-tse.html</a></div>
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Prion Infectivity in Fat of Deer with Chronic Wasting Disease▿ Brent Race#, Kimberly Meade-White#, Richard Race and Bruce Chesebro* + Author Affiliations</div>
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Rocky Mountain Laboratories, 903 South 4th Street, Hamilton, Montana 59840 Next Section ABSTRACT</div>
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Chronic wasting disease (CWD) is a neurodegenerative prion disease of cervids. Some animal prion diseases, such as bovine spongiform encephalopathy, can infect humans; however, human susceptibility to CWD is unknown. In ruminants, prion infectivity is found in central nervous system and lymphoid tissues, with smaller amounts in intestine and muscle. In mice, prion infectivity was recently detected in fat. Since ruminant fat is consumed by humans and fed to animals, we determined infectivity titers in fat from two CWD-infected deer. Deer fat devoid of muscle contained low levels of CWD infectivity and might be a risk factor for prion infection of other species.</div>
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<a href="http://jvi.asm.org/content/83/18/9608.full" style="color: blue; cursor: pointer;" target="_blank">http://jvi.asm.org/content/83/18/9608.full</a></div>
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Prions in Skeletal Muscles of Deer with Chronic Wasting Disease Rachel C. Angers1,*, Shawn R. Browning1,*,†, Tanya S. Seward2, Christina J. Sigurdson4,‡, Michael W. Miller5, Edward A. Hoover4, Glenn C. Telling1,2,3,§ ↵* These authors contributed equally to this work. ↵† Present address: Department of Infectology, Scripps Research Institute, 5353 Parkside Drive, RF-2, Jupiter, FL 33458, USA. ↵‡ Present address: Institute of Neuropathology, University of Zurich, Schmelzbergstrasse 12, 8091 Zurich, Switzerland. + See all authors and affiliations Science 24 Feb 2006: Vol. 311, Issue 5764, pp. 1117 DOI: 10.1126/science.1122864 Article Figures & Data Info & Metrics eLetters PDF You are currently viewing the abstract.</div>
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Abstract</div>
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The emergence of chronic wasting disease (CWD) in deer and elk in an increasingly wide geographic area, as well as the interspecies transmission of bovine spongiform encephalopathy to humans in the form of variant Creutzfeldt Jakob disease, have raised concerns about the zoonotic potential of CWD. Because meat consumption is the most likely means of exposure, it is important to determine whether skeletal muscle of diseased cervids contains prion infectivity. Here bioassays in transgenic mice expressing cervid prion protein revealed the presence of infectious prions in skeletal muscles of CWD-infected deer, demonstrating that humans consuming or handling meat from CWD-infected deer are at risk to prion exposure.</div>
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<a href="http://science.sciencemag.org/content/311/5764/1117.long" style="color: #0096ef; cursor: pointer; text-decoration-line: none;">http://science.sciencemag.org/content/311/5764/1117.long</a></div>
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First evidence of intracranial and peroral transmission of Chronic Wasting Disease (CWD) into Cynomolgus macaques: a work in progress </div>
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Stefanie Czub1, Walter Schulz-Schaeffer2, Christiane Stahl-Hennig3, Michael Beekes4, Hermann Schaetzl5 and Dirk Motzkus6 1 </div>
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University of Calgary Faculty of Veterinary Medicine/Canadian Food Inspection Agency; 2Universitatsklinikum des Saarlandes und Medizinische Fakultat der Universitat des Saarlandes; 3 Deutsches Primaten Zentrum/Goettingen; 4 Robert-Koch-Institut Berlin; 5 University of Calgary Faculty of Veterinary Medicine; 6 presently: Boehringer Ingelheim Veterinary Research Center; previously: Deutsches Primaten Zentrum/Goettingen </div>
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This is a progress report of a project which started in 2009. 21 cynomolgus macaques were challenged with characterized CWD material from white-tailed deer (WTD) or elk by intracerebral (ic), oral, and skin exposure routes. Additional blood transfusion experiments are supposed to assess the CWD contamination risk of human blood product. Challenge materials originated from symptomatic cervids for ic, skin scarification and partially per oral routes (WTD brain). Challenge material for feeding of muscle derived from preclinical WTD and from preclinical macaques for blood transfusion experiments. We have confirmed that the CWD challenge material contained at least two different CWD agents (brain material) as well as CWD prions in muscle-associated nerves. </div>
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Here we present first data on a group of animals either challenged ic with steel wires or per orally and sacrificed with incubation times ranging from 4.5 to 6.9 years at postmortem. Three animals displayed signs of mild clinical disease, including anxiety, apathy, ataxia and/or tremor. In four animals wasting was observed, two of those had confirmed diabetes. All animals have variable signs of prion neuropathology in spinal cords and brains and by supersensitive IHC, reaction was detected in spinal cord segments of all animals. Protein misfolding cyclic amplification (PMCA), real-time quaking-induced conversion (RT-QuiC) and PET-blot assays to further substantiate these findings are on the way, as well as bioassays in bank voles and transgenic mice. </div>
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At present, a total of 10 animals are sacrificed and read-outs are ongoing. Preclinical incubation of the remaining macaques covers a range from 6.4 to 7.10 years. Based on the species barrier and an incubation time of > 5 years for BSE in macaques and about 10 years for scrapie in macaques, we expected an onset of clinical disease beyond 6 years post inoculation. </div>
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PRION 2017 DECIPHERING NEURODEGENERATIVE DISORDERS </div>
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Subject: PRION 2017 CONFERENCE DECIPHERING NEURODEGENERATIVE DISORDERS VIDEO</div>
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PRION 2017 CONFERENCE DECIPHERING NEURODEGENERATIVE DISORDERS</div>
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PRION 2017 CONFERENCE VIDEO</div>
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<a href="https://www.youtube.com/embed/Vtt1kAVDhDQ" style="color: blue; cursor: pointer;" target="_blank">https://www.youtube.com/embed/Vtt1kAVDhDQ</a></div>
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<a href="http://prion2017.org/programme/" style="color: blue; cursor: pointer;" target="_blank">http://prion2017.org/programme/</a></div>
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Chronic Wasting Disease CWD TSE Prion to Humans, who makes that final call, when, or, has it already happened?</div>
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SATURDAY, JULY 29, 2017</div>
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Risk Advisory Opinion: Potential Human Health Risks from Chronic Wasting Disease CFIA, PHAC, HC (HPFB and FNIHB), INAC, Parks Canada, ECCC and AAFC</div>
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<a href="http://chronic-wasting-disease.blogspot.com/2017/07/risk-advisory-opinion-potential-human.html" style="color: blue; cursor: pointer;" target="_blank">http://chronic-wasting-disease.blogspot.com/2017/07/risk-advisory-opinion-potential-human.html</a></div>
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TUESDAY, JUNE 13, 2017</div>
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PRION 2017 CONFERENCE ABSTRACT First evidence of intracranial and peroral transmission of Chronic Wasting Disease (CWD) into Cynomolgus macaques: a work in progress</div>
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<a href="http://chronic-wasting-disease.blogspot.com/2017/06/prion-2017-conference-abstract-first.html" style="color: blue; cursor: pointer;" target="_blank">http://chronic-wasting-disease.blogspot.com/2017/06/prion-2017-conference-abstract-first.html</a></div>
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TUESDAY, JUNE 13, 2017</div>
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PRION 2017 CONFERENCE ABSTRACT Chronic Wasting Disease in European moose is associated with PrPSc features different from North American CWD</div>
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<a href="http://chronic-wasting-disease.blogspot.com/2017/06/prion-2017-conference-abstract-chronic.html" style="color: blue; cursor: pointer;" target="_blank">http://chronic-wasting-disease.blogspot.com/2017/06/prion-2017-conference-abstract-chronic.html</a></div>
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TUESDAY, JULY 04, 2017</div>
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*** PRION 2017 CONFERENCE ABSTRACTS ON CHRONIC WASTING DISEASE CWD TSE PRION ***</div>
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<a href="http://chronic-wasting-disease.blogspot.com/2017/07/prion-2017-conference-abstracts-on.html" style="color: blue; cursor: pointer;" target="_blank">http://chronic-wasting-disease.blogspot.com/2017/07/prion-2017-conference-abstracts-on.html</a></div>
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URINE</div>
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SUNDAY, JULY 16, 2017</div>
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*** Temporal patterns of chronic wasting disease prion excretion in three cervid species ***</div>
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<a href="http://chronic-wasting-disease.blogspot.com/2017/07/temporal-patterns-of-chronic-wasting.html" style="color: blue; cursor: pointer;" target="_blank">http://chronic-wasting-disease.blogspot.com/2017/07/temporal-patterns-of-chronic-wasting.html</a></div>
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PAGE 25 </div>
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Transmission Studies </div>
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Mule deer transmissions of CWD were by intracerebral inoculation and compared with natural cases resulted in a more rapidly progressive clinical disease with repeated episodes of synocopy ending in coma. One control animal became affected, it is believed through contamination of inoculam (?saline). </div>
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Further CWD transmissions were carried out by Dick Marsh into ferret, mink and squirrel monkey. Transmission occurred in all of these species with the shortest incubation period in the ferret. </div>
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<a href="http://collections.europarchive.org/tna/20080102193705/http://www.bseinquiry.gov.uk/files/mb/m11b/tab01.pdf" style="color: blue; cursor: pointer;" target="_blank">http://collections.europarchive.org/tna/20080102193705/http://www.bseinquiry.gov.uk/files/mb/m11b/tab01.pdf</a></div>
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LOOKING FOR CWD IN HUMANS AS nvCJD or as an ATYPICAL CJD, LOOKING IN ALL THE WRONG PLACES $$$</div>
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*** These results would seem to suggest that CWD does indeed have zoonotic potential, at least as judged by the compatibility of CWD prions and their human PrPC target. Furthermore, extrapolation from this simple in vitro assay suggests that if zoonotic CWD occurred, it would most likely effect those of the PRNP codon 129-MM genotype and that the PrPres type would be similar to that found in the most common subtype of sCJD (MM1).***</div>
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<a href="http://www.tandfonline.com/doi/full/10.4161/pri.28124?src=recsys" style="color: blue; cursor: pointer;" target="_blank">http://www.tandfonline.com/doi/full/10.4161/pri.28124?src=recsys</a></div>
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<a href="http://www.tandfonline.com/doi/pdf/10.4161/pri.28124?needAccess=true" style="color: blue; cursor: pointer;" target="_blank">http://www.tandfonline.com/doi/pdf/10.4161/pri.28124?needAccess=true</a></div>
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Molecular Barriers to Zoonotic Transmission of Prions</div>
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*** chronic wasting disease, there was no absolute barrier to conversion of the human prion protein.</div>
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*** Furthermore, the form of human PrPres produced in this in vitro assay when seeded with CWD, resembles that found in the most common human prion disease, namely sCJD of the MM1 subtype.</div>
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<a href="http://wwwnc.cdc.gov/eid/article/20/1/13-0858_article.htm" style="color: blue; cursor: pointer;" target="_blank">http://wwwnc.cdc.gov/eid/article/20/1/13-0858_article.htm</a></div>
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<a href="http://chronic-wasting-disease.blogspot.com/2014/01/molecular-barriers-to-zoonotic.html" style="color: blue; cursor: pointer;" target="_blank">http://chronic-wasting-disease.blogspot.com/2014/01/molecular-barriers-to-zoonotic.html</a></div>
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SPONTANEOUS ATYPICAL BOVINE SPONGIFORM ENCEPHALOPATHY </div>
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***Moreover, sporadic disease has never been observed in breeding colonies or primate research laboratories, most notably among hundreds of animals over several decades of study at the National Institutes of Health25, and in nearly twenty older animals continuously housed in our own facility.*** </div>
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<a href="https://www.nature.com/articles/srep11573" style="color: blue; cursor: pointer;" target="_blank">https://www.nature.com/articles/srep11573</a></div>
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Envt.07: </div>
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Pathological Prion Protein (PrPTSE) in Skeletal Muscles of Farmed and Free Ranging White-Tailed Deer Infected with Chronic Wasting Disease </div>
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***The presence and seeding activity of PrPTSE in skeletal muscle from CWD-infected cervids suggests prevention of such tissue in the human diet as a precautionary measure for food safety, pending on further clarification of whether CWD may be transmissible to humans. </div>
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Yet, it has to be noted that our assessments of PrPTSE levels in skeletal muscles were based on findings in presumably pre- or subclinically infected animals. Therefore, the concentration of PrPTSE in skeletal muscles of WTD with clinically manifest CWD may possibly exceed our estimate which refers to clinically inconspicuous animals that are more likely to enter the human food chain. Our tissue blot findings in skeletal muscles from CWD-infected WTD would be consistent with an anterograde spread of CWD prions via motor nerve fibres to muscle tissue (figure 4A). Similar neural spreading pathways of muscle infection were previously found in hamsters orally challenged with scrapie [28] and suggested by the detection of PrPTSE in muscle fibres and muscle-associated nerve fascicles of clinically-ill non-human primates challenged with BSE prions [29]. Whether the absence of detectable PrPTSE in myofibers observed in our study is a specific feature of CWD in WTD, or was due to a pre- or subclinical stage of infection in the examined animals, remains to be established. In any case, our observations support previous findings suggesting the precautionary prevention of muscle tissue from CWD-infected WTD in the human diet, and highlight the need to comprehensively elucidate of whether CWD may be transmissible to humans. While the understanding of TSEs in cervids has made substantial progress during the past few years, the assessment and management of risks possibly emanating from prions in skeletal muscles of CWD-infected cervids requires further research. </div>
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<a href="http://www.landesbioscience.com/journals/prion/Prion5-Supp-PrionEnvironment.pdf?nocache=1333529975" style="color: blue; cursor: pointer;" target="_blank">http://www.landesbioscience.com/journals/prion/Prion5-Supp-PrionEnvironment.pdf?nocache=1333529975</a></div>
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<a href="http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3069970/" style="color: blue; cursor: pointer;" target="_blank">http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3069970/</a></div>
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*** WDA 2016 NEW YORK </div>
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*** We found that CWD adapts to a new host more readily than BSE and that human PrP was unexpectedly prone to misfolding by CWD prions. </div>
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In addition, we investigated the role of specific regions of the bovine, deer and human PrP protein in resistance to conversion by prions from another species. </div>
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We have concluded that the human protein has a region that confers unusual susceptibility to conversion by CWD prions. </div>
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Student Presentations Session 2 </div>
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The species barriers and public health threat of CWD and BSE prions </div>
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Ms. Kristen Davenport1, Dr. Davin Henderson1, Dr. Candace Mathiason1, Dr. Edward Hoover1 1Colorado State University </div>
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Chronic wasting disease (CWD) is spreading rapidly through cervid populations in the USA. Bovine spongiform encephalopathy (BSE, mad cow disease) arose in the 1980s because cattle were fed recycled animal protein. These and other prion diseases are caused by abnormal folding of the normal prion protein (PrP) into a disease causing form (PrPd), which is pathogenic to nervous system cells and can cause subsequent PrP to misfold. CWD spreads among cervids very efficiently, but it has not yet infected humans. On the other hand, BSE was spread only when cattle consumed infected bovine or ovine tissue, but did infect humans and other species. </div>
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The objective of this research is to understand the role of PrP structure in cross-species infection by CWD and BSE. To study the propensity of each species’ PrP to be induced to misfold by the presence of PrPd from verious species, we have used an in vitro system that permits detection of PrPd in real-time. We measured the conversion efficiency of various combinations of PrPd seeds and PrP substrate combinations. </div>
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We observed the cross-species behavior of CWD and BSE, in addition to feline-adapted CWD and BSE. We found that CWD adapts to a new host more readily than BSE and that human PrP was unexpectedly prone to misfolding by CWD prions. </div>
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In addition, we investigated the role of specific regions of the bovine, deer and human PrP protein in resistance to conversion by prions from another species. </div>
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***We have concluded that the human protein has a region that confers unusual susceptibility to conversion by CWD prions. CWD is unique among prion diseases in its rapid spread in natural populations. </div>
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BSE prions are essentially unaltered upon passage to a new species, while CWD adapts to the new species. </div>
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This adaptation has consequences for surveillance of humans exposed to CWD. Wildlife Disease Risk Communication Research Contributes to Wildlife Trust Administration Exploring perceptions about chronic wasting disease risks among wildlife and agriculture professionals and stakeholders </div>
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<a href="http://www.wda2016.org/uploads/5/8/6/1/58613359/wda_2016_conference_proceedings_low_res.pdf" style="color: blue; cursor: pointer;" target="_blank">http://www.wda2016.org/uploads/5/8/6/1/58613359/wda_2016_conference_proceedings_low_res.pdf</a> </div>
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PRION 2016 TOKYO </div>
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Zoonotic Potential of CWD Prions: An Update Chronic wasting disease (CWD) is a widespread and highly transmissible prion disease in free-ranging and captive cervid species in North America. The zoonotic potential of CWD prions is a serious public health concern, but the susceptibility of human CNS and peripheral organs to CWD prions remains largely unresolved. </div>
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***We reported earlier that peripheral and CNS infections were detected in transgenic mice expressing human PrP129M or PrP129V. </div>
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Here we will present an update on this project, including evidence for strain dependence and influence of cervid PrP polymorphisms on CWD zoonosis as well as the characteristics of experimental human CWD prions. </div>
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PRION 2016 TOKYO In Conjunction with Asia Pacific Prion Symposium 2016 PRION 2016 Tokyo Prion 2016 </div>
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<a href="http://prion2016.org/dl/newsletter_03.pdf" style="color: blue; cursor: pointer;" target="_blank">http://prion2016.org/dl/newsletter_03.pdf</a> </div>
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*** The association between venison eating and risk of CJD shows similar pattern, with regular venison eating associated with a 9 FOLD INCREASE IN RISK OF CJD (p = 0.04). ***</div>
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*** The association between venison eating and risk of CJD shows similar pattern, with regular venison eating associated with a 9 FOLD INCREASE IN RISK OF CJD (p = 0.04). ***</div>
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*** The association between venison eating and risk of CJD shows similar pattern, with regular venison eating associated with a 9 FOLD INCREASE IN RISK OF CJD (p = 0.04). ***</div>
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There is some evidence that risk of CJD INCREASES WITH INCREASING FREQUENCY OF LAMB EATING (p = 0.02).</div>
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The evidence for such an association between beef eating and CJD is weaker (p = 0.14). When only controls for whom a relative was interviewed are included, this evidence becomes a little STRONGER (p = 0.08).</div>
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snip...</div>
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It was found that when veal was included in the model with another exposure, the association between veal and CJD remained statistically significant (p = < 0.05 for all exposures), while the other exposures ceased to be statistically significant (p = > 0.05).</div>
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snip...</div>
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In conclusion, an analysis of dietary histories revealed statistical associations between various meats/animal products and INCREASED RISK OF CJD. When some account was taken of possible confounding, the association between VEAL EATING AND RISK OF CJD EMERGED AS THE STRONGEST OF THESE ASSOCIATIONS STATISTICALLY. ...</div>
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snip...</div>
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In the study in the USA, a range of foodstuffs were associated with an increased risk of CJD, including liver consumption which was associated with an apparent SIX-FOLD INCREASE IN THE RISK OF CJD. By comparing the data from 3 studies in relation to this particular dietary factor, the risk of liver consumption became non-significant with an odds ratio of 1.2 (PERSONAL COMMUNICATION, PROFESSOR A. HOFMAN. ERASMUS UNIVERSITY, ROTTERDAM). (???...TSS)</div>
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snip...see full report ;</div>
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<a href="http://collections.europarchive.org/tna/20090505194948/http://bseinquiry.gov.uk/files/yb/1994/08/00004001.pdf" style="color: blue; cursor: pointer;" target="_blank">http://collections.europarchive.org/tna/20090505194948/http://bseinquiry.gov.uk/files/yb/1994/08/00004001.pdf</a></div>
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<br /></div>
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you can see more evidence here ;</div>
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<a href="http://chronic-wasting-disease.blogspot.com/2016/05/zoonotic-potential-of-cwd-prions-update.html" style="color: blue; cursor: pointer;" target="_blank">http://chronic-wasting-disease.blogspot.com/2016/05/zoonotic-potential-of-cwd-prions-update.html</a></div>
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<div>
TUESDAY, AUGUST 8, 2017 </div>
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<br /></div>
<div>
Concurrence With OIE Risk Designations for Bovine Spongiform Encephalopathy [Docket No. APHIS-2016-0092]</div>
<div>
<br /></div>
<div>
<a href="http://animalhealthreportpriontse.blogspot.com/2017/08/concurrence-with-oie-risk-designations.html%C2%A0" style="color: blue; cursor: pointer;" target="_blank">http://animalhealthreportpriontse.blogspot.com/2017/08/concurrence-with-oie-risk-designations.html</a></div>
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<br /></div>
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<span style="font-family: arial, helvetica; font-size: x-small;">Terry S. Singeltary Sr.</span></div>
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<span style="font-family: arial, helvetica; font-size: x-small;"><br /></span></div>
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<span style="font-family: arial, helvetica; font-size: x-small;">FRIDAY, AUGUST 11, 2017 </span></div>
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<span style="font-family: arial, helvetica; font-size: x-small;"><br /></span></div>
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<span style="font-family: arial, helvetica; font-size: x-small;">Infectivity in bone marrow from sporadic CJD patients</span></div>
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<span style="font-family: arial, helvetica; font-size: x-small;"><br /></span></div>
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<b style="color: #767676; font-family: Arial, Helvetica, sans-serif; font-size: 18.6667px;">Bioassays in transgenic mice expressing the human prion protein revealed the presence of unexpectedly high levels of infectivity in the bone marrow from seven out of eight sCJD cases. These findings may explain the presence of blood-borne infectivity in sCJD patients. They also suggest that the distribution of prion infectivity in peripheral tissues in sCJD patients could be wider than currently believed, with potential implications for the iatrogenic transmission risk of this disease. </b><span style="font-family: arial, helvetica; font-size: x-small;"><br /></span></div>
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<span style="font-family: arial, helvetica; font-size: x-small;"><br /></span></div>
<div>
<span style="font-family: arial, helvetica; font-size: x-small;"><a href="http://creutzfeldt-jakob-disease.blogspot.com/2017/08/infectivity-in-bone-marrow-from.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://creutzfeldt-jakob-disease.blogspot.com/2017/08/infectivity-in-bone-marrow-from.html</a></span></div>
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<div>
<span style="font-family: arial, helvetica;"><span style="font-size: 13.3333px;">THURSDAY, AUGUST 10, 2017 </span></span></div>
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<span style="font-family: arial, helvetica;"><span style="font-size: 13.3333px;"><br /></span></span></div>
<div>
<span style="font-family: arial, helvetica;"><span style="font-size: 13.3333px;">Minimise transmission risk of CJD and vCJD in healthcare settings Updated 10 August 2017</span></span></div>
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<span style="font-family: arial, helvetica;"><span style="font-size: 13.3333px;"><br /></span></span></div>
<div>
<span style="font-family: arial, helvetica;"><span style="font-size: 13.3333px;"><a href="http://creutzfeldt-jakob-disease.blogspot.com/2017/08/minimise-transmission-risk-of-cjd-and.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://creutzfeldt-jakob-disease.blogspot.com/2017/08/minimise-transmission-risk-of-cjd-and.html</a></span></span></div>
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<span style="font-family: arial, helvetica;"><br /></span></div>
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<div style="font-family: arial, helvetica; font-size: 13.3333px;">
<span style="font-size: 13.3333px;">*** Transmission of Creutzfeldt-Jakob disease to a chimpanzee by electrodes contaminated during neurosurgery *** </span></div>
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<span style="font-size: 13.3333px;"><br /></span></div>
<div style="font-family: arial, helvetica; font-size: 13.3333px;">
<span style="font-size: 13.3333px;">Gibbs CJ Jr, Asher DM, Kobrine A, Amyx HL, Sulima MP, Gajdusek DC. Laboratory of Central Nervous System Studies, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892. </span></div>
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<span style="font-size: 13.3333px;"><br /></span></div>
<div style="font-family: arial, helvetica; font-size: 13.3333px;">
<span style="font-size: 13.3333px;">Stereotactic multicontact electrodes used to probe the cerebral cortex of a middle aged woman with progressive dementia were previously implicated in the accidental transmission of Creutzfeldt-Jakob disease (CJD) to two younger patients. The diagnoses of CJD have been confirmed for all three cases. More than two years after their last use in humans, after three cleanings and repeated sterilisation in ethanol and formaldehyde vapour, the electrodes were implanted in the cortex of a chimpanzee. Eighteen months later the animal became ill with CJD. This finding serves to re-emphasise the potential danger posed by reuse of instruments contaminated with the agents of spongiform encephalopathies, even after scrupulous attempts to clean them. </span></div>
<div style="font-family: arial, helvetica; font-size: 13.3333px;">
<span style="font-size: 13.3333px;"><br /></span></div>
<div style="font-family: arial, helvetica; font-size: 13.3333px;">
<a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8006664&dopt=Abstract" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8006664&dopt=Abstract</a></div>
<div style="font-family: arial, helvetica; font-size: 13.3333px;">
<span style="font-size: 13.3333px;"><br /></span></div>
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<span style="font-size: 13.3333px;">THURSDAY, JULY 13, 2017 </span></div>
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<span style="font-size: 13.3333px;"><br /></span></div>
<div style="font-size: 13.3333px;">
<span style="font-size: 13.3333px;">TEXAS CREUTZFELDT JAKOB DISEASE CJD TSE PRION</span></div>
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<span style="font-size: 13.3333px;"><br /></span></div>
<div style="font-size: 13.3333px;">
<span style="font-size: 13.3333px;"><a href="http://cjdtexas.blogspot.com/2017/07/texas-creutzfeldt-jakob-disease-cjd-tse.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://cjdtexas.blogspot.com/2017/07/texas-creutzfeldt-jakob-disease-cjd-tse.html</a></span></div>
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<span style="font-size: 13.3333px;"><br /></span></div>
<div style="font-size: 13.3333px;">
<span style="font-size: 13.3333px;">National Prion Center could lose all funding just as concern about CWD jumping to humans rises</span></div>
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<span style="font-size: 13.3333px;"><br /></span></div>
<div style="font-size: 13.3333px;">
<span style="font-size: 13.3333px;">SATURDAY, JULY 15, 2017 </span></div>
<div style="font-size: 13.3333px;">
<span style="font-size: 13.3333px;"><br /></span></div>
<div style="font-size: 13.3333px;">
<span style="font-size: 13.3333px;">*** National Prion Center could lose all funding just as concern about CWD jumping to humans rises</span></div>
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<span style="font-size: 13.3333px;"><br /></span></div>
<div style="font-size: 13.3333px;">
<span style="font-size: 13.3333px;"><a href="http://creutzfeldt-jakob-disease.blogspot.com/2017/07/national-prion-center-could-lose-all.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://creutzfeldt-jakob-disease.blogspot.com/2017/07/national-prion-center-could-lose-all.html</a></span></div>
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<span style="font-size: 13.3333px;"><br /></span></div>
<div style="font-size: 13.3333px;">
<span style="font-size: 13.3333px;">*** I URGE YOU ALL TO WATCH THESE VIDEOS ***</span></div>
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<span style="font-size: 13.3333px;"><br /></span></div>
<div style="font-size: 13.3333px;">
<span style="font-size: 13.3333px;"><a href="http://creutzfeldt-jakob-disease.blogspot.com/2009/07/usa-hiding-mad-cow-disease-victims-as.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://creutzfeldt-jakob-disease.blogspot.com/2009/07/usa-hiding-mad-cow-disease-victims-as.html</a></span></div>
<div style="font-size: 13.3333px;">
<span style="font-size: 13.3333px;"><br /></span></div>
<div style="font-size: 13.3333px;">
<span style="font-size: 13.3333px;"><a href="http://madcowusda.blogspot.com/2009/09/mad-cow-usa-1997-video.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://madcowusda.blogspot.com/2009/09/mad-cow-usa-1997-video.html</a></span></div>
<div style="font-size: 13.3333px;">
<span style="font-size: 13.3333px;"><br /></span></div>
<div style="font-size: 13.3333px;">
<span style="font-size: 13.3333px;">Tracking spongiform encephalopathies in North America</span></div>
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<span style="font-size: 13.3333px;"><br /></span></div>
<div style="font-size: 13.3333px;">
<span style="font-size: 13.3333px;">Xavier Bosch</span></div>
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<span style="font-size: 13.3333px;"><br /></span></div>
<div style="font-size: 13.3333px;">
<span style="font-size: 13.3333px;">Published: August 2003</span></div>
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<span style="font-size: 13.3333px;"><br /></span></div>
<div style="font-size: 13.3333px;">
<span style="font-size: 13.3333px;">DOI: <a href="http://dx.doi.org/10.1016/S1473-3099(03)00715-1" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://dx.doi.org/10.1016/S1473-3099(03)00715-1</a></span></div>
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<span style="font-size: 13.3333px;"><br /></span></div>
<div style="font-size: 13.3333px;">
<span style="font-size: 13.3333px;">Summary;</span></div>
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<span style="font-size: 13.3333px;"><br /></span></div>
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<span style="font-size: 13.3333px;">“My name is Terry S Singeltary Sr, and I live in Bacliff, Texas. I lost my mom to hvCJD (Heidenhain variant CJD) and have been searching for answers ever since. What I have found is that we have not been told the truth. CWD in deer and elk is a small portion of a much bigger problem.”</span></div>
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<span style="font-size: 13.3333px;">49-year-old Singeltary is one of a number of people who have remained largely unsatisfied after being told that a close relative died from a rapidly progressive dementia compatible with spontaneous Creutzfeldt-Jakob disease (CJD). So he decided to gather hundreds of documents on transmissible spongiform encephalopathies (TSE) and realised that if Britons could get variant CJD from bovine spongiform encephalopathy (BSE), Americans might get a similar disorder from chronic wasting disease (CWD) the relative of mad cow disease seen among deer and elk in the USA. Although his feverish search did not lead him to the smoking gun linking CWD to a similar disease in North American people, it did uncover a largely disappointing situation.</span></div>
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<span style="font-size: 13.3333px;">Singeltary was greatly demoralised at the few attempts to monitor the occurrence of CJD and CWD in the USA. Only a few states have made CJD reportable. Human and animal TSEs should be reportable nationwide and internationally, he complained in a letter to the Journal of the American Medical Association (JAMA 2003; 285: 733). "I hope that the CDC does not continue to expect us to still believe that the 85% plus of all CJD cases which are sporadic are all spontaneous, without route or source."</span></div>
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<span style="font-size: 13.3333px;">Singeltary, Sr et al. JAMA.2001; 285: 733-734. Vol. 285 No. 6, February 14, 2001 JAMA</span></div>
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<span style="font-size: 13.3333px;">To the Editor: In their Research Letter, Dr Gibbons and colleagues1 reported that the annual US death rate due to Creutzfeldt-Jakob disease (CJD) has been stable since 1985. These estimates, however, are based only on reported cases, and do not include misdiagnosed or preclinical cases. It seems to me that misdiagnosis alone would drastically change these figures. An unknown number of persons with a diagnosis of Alzheimer disease in fact may have CJD, although only a small number of these patients receive the postmortem examination necessary to make this diagnosis. Furthermore, only a few states have made CJD reportable. Human and animal transmissible spongiform encephalopathies should be reportable nationwide and internationally.</span></div>
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<span style="font-size: 13.3333px;">Terry S. Singeltary, Sr Bacliff, Tex</span></div>
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<span style="font-size: 13.3333px;">1. Gibbons RV, Holman RC, Belay ED, Schonberger LB. Creutzfeldt-Jakob disease in the United States: 1979-1998. JAMA. 2000;284:2322-2323.</span></div>
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<a href="http://jama.jamanetwork.com/article.aspx?articleid=1031186" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://jama.jamanetwork.com/article.aspx?articleid=1031186</a></div>
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<span style="font-size: 13.3333px;">Until recently, CWD was thought to be confined to the wild in a small region in Colorado. But since early 2002, it has been reported in other areas, including Wisconsin, South Dakota, and the Canadian province of Saskatchewan. Indeed, the occurrence of CWD in states that were not endemic previously increased concern about a widespread outbreak and possible transmission to people and cattle.</span></div>
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<span style="font-size: 13.3333px;">To date, experimental studies have proven that the CWD agent can be transmitted to cattle by intracerebral inoculation and that it can cross the mucous membranes of the digestive tract to initiate infection in lymphoid tissue before invasion of the central nervous system. Yet the plausibility of CWD spreading to people has remained elusive.</span></div>
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<span style="font-size: 13.3333px;">Part of the problem seems to stem from the US surveillance system. CJD is only reported in those areas known to be endemic foci of CWD. Moreover, US authorities have been criticised for not having performed enough prionic tests in farm deer and elk.</span></div>
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<span style="font-size: 13.3333px;">Although in November last year the US Food and Drug Administration issued a directive to state public-health and agriculture officials prohibiting material from CWD-positive animals from being used as an ingredient in feed for any animal species, epidemiological control and research in the USA has been quite different from the situation in the UK and Europe regarding BSE.</span></div>
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<span style="font-size: 13.3333px;">"Getting data on TSEs in the USA from the government is like pulling teeth", Singeltary argues. "You get it when they want you to have it, and only what they want you to have."</span></div>
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<span style="font-size: 13.3333px;">Norman Foster, director of the Cognitive Disorders Clinic at the University of Michigan (Ann Arbor, MI, USA), says that "current surveillance of prion disease in people in the USA is inadequate to detect whether CWD is occurring in human beings"; adding that, "the cases that we know about are reassuring, because they do not suggest the appearance of a new variant of CJD in the USA or atypical features in patients that might be exposed to CWD. However, until we establish a system that identifies and analyses a high proportion of suspected prion disease cases we will not know for sure". The USA should develop a system modelled on that established in the UK, he points out.</span></div>
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<span style="font-size: 13.3333px;">Ali Samii, a neurologist at Seattle VA Medical Center who recently reported the cases of three hunters "two of whom were friends" who died from pathologically confirmed CJD, says that "at present there are insufficient data to claim transmission of CWD into humans"; adding that "[only] by asking [the questions of venison consumption and deer/elk hunting] in every case can we collect suspect cases and look into the plausibility of transmission further". Samii argues that by making both doctors and hunters more aware of the possibility of prions spreading through eating venison, doctors treating hunters with dementia can consider a possible prion disease, and doctors treating CJD patients will know to ask whether they ate venison.</span></div>
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<span style="font-size: 13.3333px;">CDC spokesman Ermias Belay says that the CDC "will not be investigating the [Samii] cases because there is no evidence that the men ate CWD-infected meat". He notes that although "the likelihood of CWD jumping the species barrier to infect humans cannot be ruled out 100%" and that "[we] cannot be 100% sure that CWD does not exist in humans& the data seeking evidence of CWD transmission to humans have been very limited". </span></div>
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<span style="font-size: 13.3333px;"><a href="http://infection.thelancet.com/" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://infection.thelancet.com/</a></span></div>
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<a href="http://www.thelancet.com/pdfs/journals/laninf/PIIS1473-3099(03)00715-1.pdf" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://www.thelancet.com/pdfs/journals/laninf/PIIS1473-3099(03)00715-1.pdf</a></div>
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<span style="font-size: 13.3333px;">Terry S. Singeltary, retired (medically) CJD WATCH </span></div>
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<span style="font-size: 13.3333px;">I lost my mother to hvCJD (Heidenhain Variant CJD). I would like to comment on the CDC's attempts to monitor the occurrence of emerging forms of CJD. Asante, Collinge et al [1] have reported that BSE transmission to the 129-methionine genotype can lead to an alternate phenotype that is indistinguishable from type 2 PrPSc, the commonest sporadic CJD. However, CJD and all human TSEs are not reportable nationally. CJD and all human TSEs must be made reportable in every state and internationally. I hope that the CDC does not continue to expect us to still believe that the 85%+ of all CJD cases which are sporadic are all spontaneous, without route/source. We have many TSEs in the USA in both animal and man. CWD in deer/elk is spreading rapidly and CWD does transmit to mink, ferret, cattle, and squirrel monkey by intracerebral inoculation. With the known incubation periods in other TSEs, oral transmission studies of CWD may take much longer. Every victim/family of CJD/TSEs should be asked about route and source of this agent. To prolong this will only spread the agent and needlessly expose others. In light of the findings of Asante and Collinge et al, there should be drastic measures to safeguard the medical and surgical arena from sporadic CJDs and all human TSEs. I only ponder how many sporadic CJDs in the USA are type 2 PrPSc? </span></div>
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<a href="http://www.neurology.org/content/60/2/176/reply#neurology_el_535" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://www.neurology.org/content/60/2/176/reply#neurology_el_535</a></div>
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<span style="font-size: 13.3333px;">2 January 2000 British Medical Journal U.S. </span></div>
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<span style="font-size: 13.3333px;">Scientist should be concerned with a CJD epidemic in the U.S., as well </span></div>
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<a href="http://www.bmj.com/rapid-response/2011/10/28/us-scientist-should-be-concerned-cjd-epidemic-us-well" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://www.bmj.com/rapid-response/2011/10/28/us-scientist-should-be-concerned-cjd-epidemic-us-well</a></div>
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<span style="font-size: 13.3333px;">15 November 1999 British Medical Journal hvCJD in the USA * BSE in U.S. </span></div>
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<a href="http://www.bmj.com/rapid-response/2011/10/28/re-vcjd-usa-bse-us" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://www.bmj.com/rapid-response/2011/10/28/re-vcjd-usa-bse-us</a></div>
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<span style="font-size: 13.3333px;">*** U.S.A. 50 STATE BSE MAD COW CONFERENCE CALL Jan. 9, 2001 </span></div>
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<a href="http://tseac.blogspot.com/2011/02/usa-50-state-bse-mad-cow-conference.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://tseac.blogspot.com/2011/02/usa-50-state-bse-mad-cow-conference.html</a></div>
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Terry S. Singeltary Sr.http://www.blogger.com/profile/06986622967539963260noreply@blogger.com0tag:blogger.com,1999:blog-6404950019984350027.post-59268996701942523252017-04-10T11:39:00.000-07:002017-05-24T12:57:12.927-07:00Disease-associated prion protein detected in lymphoid tissues from pigs challenged with the agent of chronic wasting disease<span style="color: #1d2129;"><span style="background-color: white; font-size: 12px; white-space: pre-wrap;">Disease-associated prion protein detected in lymphoid tissues from pigs challenged with the agent of chronic wasting disease </span></span><br />
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<span style="color: #1d2129;"><span style="background-color: white; font-size: 12px; white-space: pre-wrap;">Research Project: TRANSMISSION, DIFFERENTIATION, AND PATHOBIOLOGY OF TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES</span></span><br />
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<span style="color: #1d2129;"><span style="background-color: white; font-size: 12px; white-space: pre-wrap;">Location: Virus and Prion Research</span></span><br />
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<span style="color: #1d2129;"><span style="background-color: white; font-size: 12px; white-space: pre-wrap;">Title: Disease-associated prion protein detected in lymphoid tissues from pigs challenged with the agent of chronic wasting disease</span></span><br />
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<span style="color: #1d2129;"><span style="background-color: white; font-size: 12px; white-space: pre-wrap;">Author item Moore, Sarah item Kunkle, Robert item Kondru, Naveen item Manne, Sireesha item Smith, Jodi item Kanthasamy, Anumantha item West Greenlee, M item Greenlee, Justin</span></span><br />
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<span style="color: #1d2129;"><span style="background-color: white; font-size: 12px; white-space: pre-wrap;">Submitted to: Prion Publication Type: Abstract Only Publication Acceptance Date: 3/15/2017 Publication Date: N/A Citation: N/A Interpretive Summary:</span></span><br />
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<span style="color: #1d2129;"><span style="background-color: white; font-size: 12px; white-space: pre-wrap;">Technical Abstract: Aims: Chronic wasting disease (CWD) is a naturally-occurring, fatal neurodegenerative disease of cervids. We previously demonstrated that disease-associated prion protein (PrPSc) can be detected in the brain and retina from pigs challenged intracranially or orally with the CWD agent. In that study, neurological signs consistent with prion disease were observed only in one pig: an intracranially challenged pig that was euthanized at 64 months post-challenge. The purpose of this study was to use an antigen-capture immunoassay (EIA) and real-time quaking-induced conversion (QuIC) to determine whether PrPSc is present in lymphoid tissues from pigs challenged with the CWD agent. Methods: At two months of age, crossbred pigs were challenged by the intracranial route (n=20), oral route (n=19), or were left unchallenged (n=9). At approximately 6 months of age, the time at which commercial pigs reach market weight, half of the pigs in each group were culled (6 month challenge groups) were allowed to incubate for up to 73 months post challenge (mpc). The retropharyngeal lymph node (RPLN) was screened for the presence of PrPSc by EIA and immunohistochemistry (IHC). The RPLN, palatine tonsil, and mesenteric lymph node (MLN) from 6-7 pigs per challenge group were also tested using EIA and QuIC. Results: PrPSc was not detected by EIA and IHC in any RPLNs. All tonsils and MLNs were negative by IHC, though the MLN from one pig in the oral 6 months group, 5/6 pigs in the oral 6 months group. Overall, the MLN was positive in 14/19 (74%) of samples examined, the RPLN in 8/18 (44%), and the tonsil in 10/25 (40%). </span></span><br />
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<span style="color: #1d2129;"><span style="background-color: white; font-size: 12px; white-space: pre-wrap;">Conclusions: This study demonstrates that PrPSc accumulates in lymphoid tissues from pigs challenged intracranially or orally with the CWD agent, and can be detected as early as 4 months after challenge. CWD-infected pigs rarely develop clinical disease and if they do, they do so after a long incubation period. This raises the possibility that CWD-infected pigs could shed prions into their environment long before they develop clinical disease. Furthermore, lymphoid tissues from CWD-infected pigs could present a potential source of CWD infectivity in the animal and human food chains.</span></span><br />
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<a href="https://www.ars.usda.gov/research/publications/publication/?seqNo115=337105">https://www.ars.usda.gov/research/publications/publication/?seqNo115=337105</a><br />
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<span style="color: #1d2129;"><span style="background-color: white; font-size: 12px; white-space: pre-wrap;">CONFIDENTIAL</span></span><br />
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<span style="color: #1d2129;"><span style="background-color: white; font-size: 12px; white-space: pre-wrap;">EXPERIMENTAL PORCINE SPONGIFORM ENCEPHALOPATHY</span></span><br />
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<span style="color: #1d2129;"><span style="background-color: white; font-size: 12px; white-space: pre-wrap;">While this clearly is a cause for concern we should not jump to the conclusion that this means that pigs will necessarily be infected by bone and meat meal fed by the oral route as is the case with cattle. ...</span></span><br />
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<a href="http://web.archive.org/web/20031026000118/www.bseinquiry.gov.uk/files/yb/1990/08/23004001.pdf"> http://web.archive.org/web/20031026000118/www.bseinquiry.gov.uk/files/yb/1990/08/23004001.pdf</a><br />
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<span style="color: #1d2129;"><span style="background-color: white; font-size: 12px; white-space: pre-wrap;">we cannot rule out the possibility that unrecognised subclinical spongiform encephalopathy could be present in British pigs though there is no evidence for this: only with parenteral/implantable pharmaceuticals/devices is the theoretical risk to humans of sufficient concern to consider any action.</span></span><br />
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<a href="http://web.archive.org/web/20030822031154/www.bseinquiry.gov.uk/files/yb/1990/09/10007001.pdf">http://web.archive.org/web/20030822031154/www.bseinquiry.gov.uk/files/yb/1990/09/10007001.pdf</a><br />
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<span style="color: #1d2129;"><span style="background-color: white; font-size: 12px; white-space: pre-wrap;">May I, at the outset, reiterate that we should avoid dissemination of papers relating to this experimental finding to prevent premature release of the information. ...</span></span><br />
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<a href="http://web.archive.org/web/20030822052332/www.bseinquiry.gov.uk/files/yb/1990/09/11005001.pdf">http://web.archive.org/web/20030822052332/www.bseinquiry.gov.uk/files/yb/1990/09/11005001.pdf</a><br />
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<span style="color: #1d2129;"><span style="background-color: white; font-size: 12px; white-space: pre-wrap;">3. It is particularly important that this information is not passed outside the Department, until Ministers have decided how they wish it to be handled. ...</span></span><br />
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<a href="http://web.archive.org/web/20030822052438/www.bseinquiry.gov.uk/files/yb/1990/09/12002001.pdf">http://web.archive.org/web/20030822052438/www.bseinquiry.gov.uk/files/yb/1990/09/12002001.pdf</a><br />
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<span style="color: #1d2129;"><span style="background-color: white; font-size: 12px; white-space: pre-wrap;">But it would be easier for us if pharmaceuticals/devices are not directly mentioned at all. ...</span></span><br />
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<a href="http://web.archive.org/web/20030518170213/www.bseinquiry.gov.uk/files/yb/1990/09/13004001.pdf">http://web.archive.org/web/20030518170213/www.bseinquiry.gov.uk/files/yb/1990/09/13004001.pdf</a><br />
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<span style="color: #1d2129;"><span style="background-color: white; font-size: 12px; white-space: pre-wrap;">Our records show that while some use is made of porcine materials in medicinal products, the only products which would appear to be in a hypothetically ''higher risk'' area are the adrenocorticotrophic hormone for which the source material comes from outside the United Kingdom, namely America China Sweden France and Germany. The products are manufactured by Ferring and Armour. A further product, ''Zenoderm Corium implant'' manufactured by Ethicon, makes use of porcine skin - which is not considered to be a ''high risk'' tissue, but one of its uses is described in the data sheet as ''in dural replacement''. This product is sourced from the United Kingdom.....</span></span><br />
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<a href="http://web.archive.org/web/20030822054419/www.bseinquiry.gov.uk/files/yb/1990/09/21009001.pdf">http://web.archive.org/web/20030822054419/www.bseinquiry.gov.uk/files/yb/1990/09/21009001.pdf</a><br />
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<span style="background-color: white; font-family: arial; font-size: x-small;">Porcine prion protein amyloid </span><br />
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Per Hammarstr€om and Sofie Nystr€om* IFM-Department of Chemistry; Link€oping University; Link€oping, Sweden </div>
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ABSTRACT. Mammalian prions are composed of misfolded aggregated prion protein (PrP) with amyloid-like features. </div>
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Prions are zoonotic disease agents that infect a wide variety of mammalian species including humans. Mammals and by-products thereof which are frequently encountered in daily life are most important for human health. It is established that bovine prions (BSE) can infect humans while there is no such evidence for any other prion susceptible species in the human food chain (sheep, goat, elk, deer) and largely prion resistant species (pig) or susceptible and resistant pets (cat and dogs, respectively). PrPs from these species have been characterized using biochemistry, biophysics and neurobiology. Recently we studied PrPs from several mammals in vitro and found evidence for generic amyloidogenicity as well as cross-seeding fibril formation activity of all PrPs on the human PrP sequence regardless if the original species was resistant or susceptible to prion disease. Porcine PrP amyloidogenicity was among the studied. Experimentally inoculated pigs as well as transgenic mouse lines overexpressing porcine PrP have, in the past, been used to investigate the possibility of prion transmission in pigs. The pig is a species with extraordinarily wide use within human daily life with over a billion pigs harvested for human consumption each year. Here we discuss the possibility that the largely prion disease resistant pig can be a clinically silent carrier of replicating prions. </div>
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KEYWORDS. prion, pig, amyloid fibril, misfolding, transmissibility, seeding, TSE, prion strain, strain adaptation</div>
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What about pigs? In several recent papers which in our view have not received sufficient attention the notion of prion resistant pigs was challenged by generation of transgenic mice with knocked out endogenous PrP and overexpressed PoPrP. Different lines of tgPoPrP mouse were proven to be susceptible to clinical disease triggered by a variety of prion strains, suggesting that the surrogate host species (mouse) and prion strain are more important than what PrP sequence it expresses for neurotoxicity to commence. In more detail, Torres and colleagues experimentally subjected transgenic mouse lines expressing porcine PrP to a number of different TSE isolates.24-26 Their studies demonstrate that prion infection is strain specific when porcine PrP is overexpressed (4x) and used as in vivo substrate. PoTg001 mice inoculated with classical scrapie, regardless of donor genotype, resisted prion disease both at first and second passage (Fig. 3b). On the other hand, Nor98 scrapie (Atypical scrapie) as well as BSE from both cattle and BoTg mouse model resulted in clinical disease in the PoTg001 mice. However, in the first generation, disease progression was slow. Incubation time until death was as long as 600 d and the hit rate was low. This indicates that disease has barely developed by the time the mice reach their natural life span limit which in this study was set to 650 d Already in the second passage the hit rate was 100 % and the incubation time was cut in half (Fig. 3b). No further shortening of incubation time was observed upon third passage. This shows that PoPrP is capable of forming infectious and neurotoxic prions in vivo if triggered by a compatible prion strain and if given enough time to develop. Both BSE and Nor98 rapidly adapts to the PoPrP host sequence, resulting in higher penetrance as well as in markedly shorter life span already in the second passage, well within the limits of normal life span for a mouse.</div>
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There are several crucial variables which impact the susceptibility of prion diseases and transmission studies.27 PrP sequence of host, PrP sequence of prion, prion strain, prion dosage, PrP expression level of host, host genetic background, route of transmission and neuroinvasiveness if peripherally infected.28 Importantly the PrP expression level corresponds to the rate of prion disease onset.1 This likely reflects 2 converging variables: a) PrP as a substrate to the prion misfolding reaction i.e. selfcatalyzed conversion and b) PrP as a mediator of neurotoxicity through interactions with misfolded PrP within prions.</div>
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The non-homologous recPrPs presented here and in,12 easily adapt to each other and form amyloid fibrils in accordance with what is seen in vivo when inoculum composed of BoPrP used to challenge mice expressing PoPrP (Fig. 3b).24-26 A review of the literature showed that BSE strains have a high degree of penetrance in both experimental and accidental transmission. Over 50% of the species reported to be susceptible to prion disease were infected by a BSE strain.19 Recent data form our lab shows that the promiscuity of BoPrP fibrils holds true also in the case of recombinant in vitro experiments. When cross-seeding human, bovine, porcine, feline and canine PrPs with any of the other, the recBoPrP seed outcompetes the other seeds in all instances except when the HuPrP acted as substrate (Data not shown). In this case recPoPrP fibrils have the highest seeding efficiency (Fig. 1). These findings in combination with the Torres experiments,24-26 implicate that a PoPrP substrate in vivo (in pigs) could adapt to an amyloidogenic prion strain of bovine or ovine prion disease and hence replicate in the new host.</div>
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For adaptation of experimental strains through multiple passages, donors are selected based on neurotoxicity (that is on TSE disease phenotype) not on basis of amyloid fibril formation. Hence the traits of transmissible amyloidotypic prion strains may be largely unexplored if these strains require more time to transform to neurotoxic strains e.g. as proposed by Baskakov’s model of deformed templating.8 There is experimental evidence for BSE transmission into pig via parenteral routes.16 with an incubation period of 2–3 years, well within what is to be considered normal lifespan. For a breeding sow in industrial scale pig farming that is 3–5 y (Bojne Andersson, personal communication).29,30 In small scale and hobby farming both sows and boars may be kept significantly longer. Collinge and Clarke.31 describe how prion titers reach transmissibility levels well before the prion burden is high enough to be neurotoxic and cause clinical disease. It is known that prion strains need time and serial passages to adapt. Knowing that pigs in modern farming are rarely kept for enough time for clinical signs to emerge in prion infected pigs it is important to be vigilant if there is a sporadic porcine spongiform encephalopathy (PSE) as has been seen in cattle (BASE) and sheep (Nor98). Hypothetically such a sporadic and then infectious event could further adapt and over a few generations have reached the point where clinical PSE is established within the time frame where pigs are being slaughtered for human consumption (Fig. 4).</div>
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FIGURE 4. Potential prion strain adaptation in pig. The red horizontal gradient indicates the hietherto unkown prion toxicity tolerance threshold for pigs, the blue vertical line indicates normal slaughter age for industrial pig farming, the green vertical line indicates the normal lifespan of a breeding sow in industrial scale pig farming, orange areas indicate window of neurotoxic prions before onset of clinical disease (dark orange indicates subclinical BSE as reported by Wells et al,16 pale orange indicate hypothetic outcome of PSE and strain adaptation. On the outmost right a potential subclinical sporadic PSE.</div>
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USE OF MATERIALS DERIVED FROM PIG IN VIEW OF PORCINE PrP AMYLOID</div>
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The pig is the most versatile species used by humans for food and other applications. Over 1,5 billion pigs are slaughtered each year worldwide for human use.32 Besides juicy pork sirloin other parts from pig are used for making remarkably diverse things such as musical instruments, china, leather, explosives, lubricants etc. Pig offal is used for human medicine, e.g., hormone preparations such as insulin and cerebrolysin, in xenographs, sutures, heparin and in gelatin for drug capsules.33,34</div>
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And that means not only pork, it means your pigskin wallet, catgut surgical suture...in tallow, in butter. It is undoubtedly in the blood supply. DC Gajdusek (From R. Rhodes ''Deadly Feast'' 35)</div>
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While the late Carleton Gajdusek had strong views in diverse areas of prion biology, according to journalist Richard Rhodes,35 he was correct on his prediction on BSE prions (vCJD) in the blood supply18 (see text box above). An opinionated scientist can sometimes be ignored due to a judgment of character and Gajdusek was certainly provocative. Notwithstanding society should remain vigilant on the possibility that Gajdusek was also prophetic on porcine prions given the exceptionally wide spread use of pigs in everyday human life and medicine. As discussed previously it is currently not established what relations transmissible neurotoxic prion strains and amyloid morphotypic mature APrP strains have. Given the hypotheses that amyloidotypic PrP conformations can transmit with low neurotoxicity.7,36 it is interesting to reflect on possible implications. Pigs are slaughtered at 6–8 months of age. Because amyloid deposition is associated with old age, this is likely far too young for spontaneous development of APrP amyloid from PoPrP as well as other amyloidogenic proteins. From the perspective of seeded amyloidogenesis it is however a potential ideal case for highly transmissible titers of APrP (Fig. 4). In such a scenario the potential of porcine prions constitutes the perfect storm, clinically silent due to neurotoxic resistance and with high titers of transmissibility. When it comes to prions CNS material is most heavily infected. In addition, however, fat tissue (to make lard and tallow) is known to harbor extraordinary amounts of amyloid in systemic amyloidoses.37 Amyloid fibrils of misfolded large proteins (AA, AL, ATTR) are notoriously hydrophobic due to the abnormal exposure of hydrophobic residues which <span style="font-family: arial, helvetica; font-size: 10pt; line-height: 1.22em;">normally in the folded structure being hidden in the protein core. The amyloid accumulation in fat tissue is likely a phase-separation from a rather hydrophilic environment in circulation toward the hydrophobic environment provided by adipocytes. Adipose tissue could in addition represent an in vivo environment well suitable for fibril formation. What about APrP?</span></div>
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<span style="line-height: 1.22em;">In analysis of mice expressing Glycophosphatidylinositol, (GPI)-anchorless PrP, abdominal fat contains appreciable amounts of infectious prions in APrP isoform stained with ThS.38 Notably mice overexpressing anchorless PrP provides a silent carrier status for a long time prior to presenting symptoms and is severely afflicted by amyloid fibril formation following scrapie (RML) infection.39 Recall that this study showed that GPI-anchored PrP is needed to present clinical neurotoxicity. Evidently circulating anchorless-PrP (analogous to recPrP) is more amyloidogenic compared to GPI-anchored PrP and is poorly neuroinvasive.28 Amyloidosis is systemic in anchorless-PrP mice and is not limited to fat but is also found as extensive cardiac amyloid deposits.39 Interestingly cardiac APrP was recently reported in one BSE inoculated rhesus macaque which showed symptoms of cardiac distress prior to death from prion neurotoxicity.40 It is noteworthy that transgenic mice expressing PoPrP appear sensitive to strains with biochemical features of amyloidogenic prion strains i.e., BSE and Nor98.25,26,36 (Fig. 3b). We recently adopted the parallel inregister intermolecular b-sheet structural model of the APrP fibril from the Caughey lab to rationalize cross-seeding between various PrP sequences.12,41 It is tempting to use this structural model to speculate on the adaptation of mono-N-glycolsylated PoPrP at the expense of double-N-glycolylated PrP in the original BSE inoculum reported in the Torres experiments.25,26 In this APrP model monoglycosylated PrP at N197 is structurally compatible while N181 is not, due to burial in the in-register intermolecular cross-beta sheet (Fig. 5).</span></div>
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<span style="line-height: 1.22em;">It appears that amyloidotypic prion strains, APrP, are transmissible but associated with lower neurotoxicity compared to diffuse aggregated PrP associated with synaptic PrP accumulations. It is possible that the amino acid substitutions in PoPrP compared to HuPrP and BoPrP are important for neurotoxic signal transmission (Fig. 2b, 5). The main issue hereby is that transmissibility of APrP will remain undetected unless used for surveillance. AA amyloidosis is frequent in many animals (e.g. cattle and birds) but is exceptionally rare in pigs.42 suggesting that APrP should it reside in pig fat would be traceable using newly developed screening methods.37</span></div>
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CONCLUDING REMARKS </div>
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Should the topic of porcine PrP amyloid be more of a worry than of mere academic interest? Well perhaps. Prions are particularly insidious pathogens. A recent outbreak of peripheral neuropathy in human, suggests that exposure to aerosolized porcine brain is deleterious for human health.43,44 Aerosolization is a known vector for prions at least under experimental conditions.45-47 where a mere single exposure was enough for transmission in transgenic mice. HuPrP is seedable with BoPrP seeds and even more so with PoPrP seed (Fig. 1), indicating that humans could be infected by porcine APrP prions while neurotoxicity associated with spongiform encephalopathy if such a disease existed is even less clear. Importantly transgenic mice over-expressing PoPrP are susceptible to BSE and BSE passaged through domestic pigs implicating that efficient downstream neurotoxicity pathways in the mouse, a susceptible host for prion disease neurotoxicity is augmenting the TSE phenotype.25,26 Prions in silent carrier hosts can be infectious to a third species. Data from Collinge and coworkers.21 propose that species considered to be prion free may be carriers of replicating prions. Especially this may be of concern for promiscuous prion strains such as BSE.19,48 It is rather established that prions can exist in both replicating and neurotoxic conformations.49,50 and this can alter the way in which new host organisms can react upon cross-species transmission.51 The na€ıve host can either be totally resistant to prion infection as well as remain non-infectious, become a silent non-symptomatic but infectious carrier of disease or be afflicted by disease with short or long incubation time. The host can harbor and/or propagate the donor strain or convert the strain conformation to adapt it to the na€ıve host species. The latter would facilitate infection and shorten the incubation time in a consecutive event of intra-species transmission. It may be advisable to avoid procedures and exposure without proper biosafety precautions as the knowledge of silence carrier species is poor. One case of iatrogenic CJD in recipient of porcine dura mater graft has been reported in the literature.52 The significance of this finding is still unknown. The low public awareness in this matter is exemplified by the practice of using proteolytic peptide mixtures prepared from porcine brains (Cerebrolysin) as a nootropic drug. While Cerebrolysin may be beneficial for treatment of severe diseases such as vascular dementia,53 a long term follow-up of such a product for recreational use is recommended.</div>
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DISCLOSURE OF POTENTIAL CONFLICTS OF INTEREST</div>
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No potential conflicts of interest were disclosed</div>
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FUNDING</div>
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This work was supported by G€oran Gustafsson foundation, the Swedish research council Grant #2011-5804 (PH) and the Swedish Alzheimer association (SN).</div>
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REFERENCES</div>
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<a href="http://www.tandfonline.com/doi/full/10.1080/19336896.2015.1065373" rel="noopener noreferrer" style="cursor: pointer; font-family: arial, helvetica, clean, sans-serif; line-height: 1.22em;" target="_blank">http://www.tandfonline.com/doi/full/10.1080/19336896.2015.1065373</a></div>
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<a href="http://www.tandfonline.com/doi/pdf/10.1080/19336896.2015.1065373?needAccess=true" rel="noopener noreferrer" style="cursor: pointer; font-family: arial, helvetica, clean, sans-serif; line-height: 1.22em;" target="_blank">http://www.tandfonline.com/doi/pdf/10.1080/19336896.2015.1065373?needAccess=true</a></div>
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TUESDAY, APRIL 18, 2017 </div>
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*** EXTREME USA FDA PART 589 TSE PRION FEED LOOP HOLE STILL EXIST, AND PRICE OF POKER GOES UP ***</div>
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<a href="http://usdameatexport.blogspot.com/2017/04/extreme-usa-fda-part-589-tse-prion-feed.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://usdameatexport.blogspot.com/2017/04/extreme-usa-fda-part-589-tse-prion-feed.html</a></div>
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WEDNESDAY, MAY 17, 2017 </div>
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SHIC FUNDED STUDY SUGGESTS POTENTIAL FOR PATHOGEN TRANSMISSION VIA FEED</div>
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<a href="http://transmissiblespongiformencephalopathy.blogspot.com/2017/05/shic-funded-study-suggests-potential.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://transmissiblespongiformencephalopathy.blogspot.com/2017/05/shic-funded-study-suggests-potential.html</a></div>
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<span style="color: #1d2129;"><span style="background-color: white; font-size: 12px; white-space: pre-wrap;">snip... see much more here ;</span></span><br />
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<span style="color: #1d2129;"><span style="background-color: white; font-size: 12px; white-space: pre-wrap;">WEDNESDAY, APRIL 05, 2017 </span></span><br />
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<span style="color: #1d2129;"><span style="background-color: white; font-size: 12px; white-space: pre-wrap;">Disease-associated prion protein detected in lymphoid tissues from pigs challenged with the agent of chronic wasting disease</span></span><br />
<span style="color: #1d2129;"><span style="background-color: white; font-size: 12px; white-space: pre-wrap;"><br /></span></span>
<a href="http://chronic-wasting-disease.blogspot.com/2017/04/disease-associated-prion-protein.html">http://chronic-wasting-disease.blogspot.com/2017/04/disease-associated-prion-protein.html</a><br />
<span style="color: #1d2129;"><span style="background-color: white; font-size: 12px; white-space: pre-wrap;"><br /></span></span>
<span style="color: #1d2129;"><span style="background-color: white; font-size: 12px; white-space: pre-wrap;">Terry S. Singeltary Sr.</span></span><br />
<span style="color: #1d2129;"><span style="background-color: white; font-size: 12px; white-space: pre-wrap;"><br /></span></span>
<span style="color: #1d2129;"><span style="background-color: white; font-size: 12px; white-space: pre-wrap;">Bacliff, Texas USA 77518</span></span><br />
<span style="color: #1d2129;"><span style="background-color: white; font-size: 12px; white-space: pre-wrap;"><br /></span></span>
<span style="color: #1d2129;"><span style="background-color: white; font-size: 12px; white-space: pre-wrap;"><flounder9@verizon.net> </span></span><br />
<br />Terry S. Singeltary Sr.http://www.blogger.com/profile/06986622967539963260noreply@blogger.com0tag:blogger.com,1999:blog-6404950019984350027.post-20219493554685362252016-01-09T13:28:00.002-08:002016-01-09T13:28:31.811-08:00Transmission of sheep-bovine spongiform encephalopathy to pigs <div>
Saturday, January 9, 2016</div>
<br />
<div>
</div>
Transmission of sheep-bovine spongiform encephalopathy to pigs <br />
<br />
<div>
</div>
Research article <br />
<br />
<div>
</div>
<a href="http://transmissiblespongiformencephalopathy.blogspot.com/2016/01/transmission-of-sheep-bovine-spongiform.html" title="http://transmissiblespongiformencephalopathy.blogspot.com/2016/01/transmission-of-sheep-bovine-spongiform.html">http://transmissiblespongiformencephalopathy.blogspot.com/2016/01/transmission-of-sheep-bovine-spongiform.html</a><br />
<br />
<br />
<div>
</div>
Terry S. Singeltary Sr.http://www.blogger.com/profile/06986622967539963260noreply@blogger.com0tag:blogger.com,1999:blog-6404950019984350027.post-40379544202227645572015-07-29T11:16:00.001-07:002015-07-29T11:16:49.371-07:00Porcine Prion Protein Amyloid or mad pig disease PSE<div>
Porcine Prion Protein Amyloid</div>
<br />
<div>
</div>
<br />
<div>
DOI:</div>
<br />
<div>
</div>
<br />
<div>
10.1080/19336896.2015.1065373</div>
<br />
<div>
</div>
<br />
<div>
Received: 1 Jun 2015</div>
<br />
<div>
</div>
<br />
<div>
Accepted: 17 Jun 2015</div>
<br />
<div>
</div>
<br />
<div>
Accepted author version posted online: 28 Jul 2015</div>
<br />
<div>
</div>
<br />
<div>
Abstract</div>
<br />
<div>
</div>
<br />
<div>
Mammalian prions are composed of misfolded aggregated prion protein (PrP)
with amyloid-like features. Prions are zoonotic disease agents that infect a
wide variety of mammalian species including humans. Mammals and by-products
thereof which are frequently encountered in daily life are most important for
human health. It is established that bovine prions (BSE) can infect humans while
there is no such evidence for any other prion susceptible species in the human
food chain (sheep, goat, elk, deer) and largely prion resistant species (pig) or
susceptible and resistant pets (cat and dogs respectively). PrPs from these
species have been characterized using biochemistry, biophysics and neurobiology.
Recently we studied PrPs from several mammals in vitro and found evidence for
generic amyloidogenicity as well as cross-seeding fibril formation activity of
all PrPs on the human PrP sequence regardless if the original species was
resistant or susceptible to prion disease. Porcine PrP amyloidogenicity was
among the studied. Experimentally inoculated pigs as well as transgenic mouse
lines overexpressing porcine PrP have, in the past, been used to investigate the
possibility of prion transmission in pigs. The pig is a species with
extraordinarily wide use within human daily life with over a billion pigs
harvested for human consumption each year. *** Here we discuss the possibility
that the largely prion disease resistant pig can be a clinically silent carrier
of replicating prions. </div>
<br />
<div>
</div>
<br />
<div>
<a href="http://www.tandfonline.com/doi/abs/10.1080/19336896.2015.1065373#.VbjxKf3bI5s">http://www.tandfonline.com/doi/abs/10.1080/19336896.2015.1065373#.VbjxKf3bI5s</a>
</div>
<br />
<div>
</div>
<br />
<div>
PORCINE SPONGIFORM ENCEPHALOPATHY PSE AND DEADSTOCK DOWNER PIGS </div>
<br />
<div>
</div>
<br />
<div>
EXPERIMENTAL INTRACEREBRAL AND ORAL INOCULATION OF SCRAPIE TO SWINE:
PRELIMINARY REPORT</div>
<br />
<div>
</div>
<br />
<div>
Date: February 6, 2006 at 12:33 pm PST </div>
<br />
<div>
</div>
<br />
<div>
Title: EXPERIMENTAL INTRACEREBRAL AND ORAL INOCULATION OF SCRAPIE TO SWINE:
PRELIMINARY REPORT </div>
<br />
<div>
</div>
<br />
<div>
SEE MORE HERE ; </div>
<br />
<div>
</div>
<br />
<div>
PORCINE SPONGIFORM ENCEPHALOPATHY PSE </div>
<br />
<div>
</div>
<br />
<div>
<a href="http://madporcinedisease.blogspot.com/">http://madporcinedisease.blogspot.com/</a>
</div>
<br />
<div>
</div>
<br />
<div>
Wednesday, July 06, 2011</div>
<br />
<div>
</div>
<br />
<div>
Swine Are Susceptible to Chronic Wasting Disease by Intracerebral
Inoculation</div>
<br />
<div>
</div>
<br />
<div>
snip...</div>
<br />
<div>
</div>
<br />
<div>
In the US, feeding of ruminant by-products to ruminants is prohibited, but
feeding of ruminant materials to swine, mink and poultry still occurs. Although
unlikely, the potential for swine to have access to TSE-contaminated feedstuffs
exists.</div>
<br />
<div>
</div>
<br />
<div>
snip...</div>
<br />
<div>
</div>
<br />
<div>
<a href="http://www.prion2011.ca/files/PRION_2011_-_Posters_(May_5-11).pdf">http://www.prion2011.ca/files/PRION_2011_-_Posters_(May_5-11).pdf</a>
</div>
<br />
<div>
</div>
<br />
<div>
Wednesday, July 06, 2011</div>
<br />
<div>
</div>
<br />
<div>
Swine Are Susceptible to Chronic Wasting Disease by Intracerebral
Inoculation </div>
<br />
<div>
</div>
<br />
<div>
(see tonnage of mad cow feed in commerce USA...tss) </div>
<br />
<div>
</div>
<br />
<div>
<a href="http://chronic-wasting-disease.blogspot.com/2011/07/swine-are-susceptible-to-chronic.html">http://chronic-wasting-disease.blogspot.com/2011/07/swine-are-susceptible-to-chronic.html</a>
</div>
<br />
<div>
</div>
<br />
<div>
In an experimental study of the transmissibility of BSE to the pig, seven
of 10 pigs, infected at 1-2 weeks of age by multiple-route parenteral
inoculation with a homogenate of bovine brain from natural BSE cases developed
lesions typical of spongiform encephalopathy.</div>
<br />
<div>
</div>
<br />
<div>
<a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?holding=npg&cmd=Retrieve&db=PubMed&list_uids=10684682&dopt=Abstract">http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?holding=npg&cmd=Retrieve&db=PubMed&list_uids=10684682&dopt=Abstract</a>
</div>
<br />
<div>
</div>
<br />
<div>
Title: Experimental Intracerebral and Oral Inoculation of Scrapie to Swine:
Preliminary Report</div>
<br />
<div>
</div>
<br />
<div>
In the United States, feeding of ruminant by-products to ruminants is
prohibited, but feeding of ruminant materials to swine and poultry still occurs.
The potential for swine to have access to scrapie-contaminated feedstuffs
exists, but the potential for swine to serve as a host for
replication/accumulation of the agent of scrapie is unknown. The purpose of this
study was to perform oral and intracerebral inoculation of the U.S. scrapie
agent to determine the potential of swine as a host for the scrapie agent and
their clinical susceptibility.</div>
<br />
<div>
</div>
<br />
<div>
snip...</div>
<br />
<div>
</div>
<br />
<div>
IN CONFIDENCE</div>
<br />
<div>
</div>
<br />
<div>
EXPERIMENTAL PORCINE SPONGIFORM ENCEPHALOPATHY</div>
<br />
<div>
</div>
<br />
<div>
1. CMO should be aware that a pig inoculated experimentally (ic, iv, and
ip) with BSE brain suspension has after 15 months developed an illness, now
confirmed as a spongiform encephalopathy. This is the first ever description of
such a disease in a pig, although it seems there ar no previous attempts at
experimental inoculation with animal material. The Southwood group had thought
igs would not be susceptible. Most pigs are slaughtered when a few weeks old but
there have been no reports of relevant neurological illness in breeding sows or
other elderly pigs. ...see full text ;</div>
<br />
<div>
</div>
<br />
<div>
<a href="http://web.archive.org/web/20040302031004/www.bseinquiry.gov.uk/files/yb/1990/08/23001001.pdf">http://web.archive.org/web/20040302031004/www.bseinquiry.gov.uk/files/yb/1990/08/23001001.pdf</a>
</div>
<br />
<div>
</div>
<br />
<div>
IN CONFIDENCE</div>
<br />
<div>
</div>
<br />
<div>
So it is plausible pigs could be preclinically affected with BSE but since
so few are allowed to reach adulthood this has not been recognised through
clinical disease. ...</div>
<br />
<div>
</div>
<br />
<div>
<a href="http://web.archive.org/web/20040904150118/www.bseinquiry.gov.uk/files/yb/1990/08/23002001.pdf">http://web.archive.org/web/20040904150118/www.bseinquiry.gov.uk/files/yb/1990/08/23002001.pdf</a>
</div>
<br />
<div>
</div>
<br />
<div>
snip... </div>
<br />
<div>
</div>
<br />
<div>
CONFIDENTIAL</div>
<br />
<div>
</div>
<br />
<div>
EXPERIMENTAL PORCINE SPONGIFORM ENCEPHALOPATHY</div>
<br />
<div>
</div>
<br />
<div>
While this clearly is a cause for concern we should not jump to the
conclusion that this means that pigs will necessarily be infected by bone and
meat meal fed by the oral route as is the case with cattle. ...</div>
<br />
<div>
</div>
<br />
<div>
<a href="http://web.archive.org/web/20031026000118/www.bseinquiry.gov.uk/files/yb/1990/08/23004001.pdf">http://web.archive.org/web/20031026000118/www.bseinquiry.gov.uk/files/yb/1990/08/23004001.pdf</a>
</div>
<br />
<div>
</div>
<br />
<div>
we cannot rule out the possibility that unrecognised subclinical spongiform
encephalopathy could be present in British pigs though there is no evidence for
this: only with parenteral/implantable pharmaceuticals/devices is the
theoretical risk to humans of sufficient concern to consider any action.</div>
<br />
<div>
</div>
<br />
<div>
<a href="http://web.archive.org/web/20030822031154/www.bseinquiry.gov.uk/files/yb/1990/09/10007001.pdf">http://web.archive.org/web/20030822031154/www.bseinquiry.gov.uk/files/yb/1990/09/10007001.pdf</a>
</div>
<br />
<div>
</div>
<br />
<div>
May I, at the outset, reiterate that we should avoid dissemination of
papers relating to this experimental finding to prevent premature release of the
information. ...</div>
<br />
<div>
</div>
<br />
<div>
<a href="http://web.archive.org/web/20030822052332/www.bseinquiry.gov.uk/files/yb/1990/09/11005001.pdf">http://web.archive.org/web/20030822052332/www.bseinquiry.gov.uk/files/yb/1990/09/11005001.pdf</a>
</div>
<br />
<div>
</div>
<br />
<div>
3. It is particularly important that this information is not passed outside
the Department, until Ministers have decided how they wish it to be handled.
...</div>
<br />
<div>
</div>
<br />
<div>
<a href="http://web.archive.org/web/20030822052438/www.bseinquiry.gov.uk/files/yb/1990/09/12002001.pdf">http://web.archive.org/web/20030822052438/www.bseinquiry.gov.uk/files/yb/1990/09/12002001.pdf</a>
</div>
<br />
<div>
</div>
<br />
<div>
But it would be easier for us if pharmaceuticals/devices are not directly
mentioned at all. ...</div>
<br />
<div>
</div>
<br />
<div>
<a href="http://web.archive.org/web/20030518170213/www.bseinquiry.gov.uk/files/yb/1990/09/13004001.pdf">http://web.archive.org/web/20030518170213/www.bseinquiry.gov.uk/files/yb/1990/09/13004001.pdf</a>
</div>
<br />
<div>
</div>
<br />
<div>
Our records show that while some use is made of porcine materials in
medicinal products, the only products which would appear to be in a
hypothetically ''higher risk'' area are the adrenocorticotrophic hormone for
which the source material comes from outside the United Kingdom, namely America
China Sweden France and Germany. The products are manufactured by Ferring and
Armour. A further product, ''Zenoderm Corium implant'' manufactured by Ethicon,
makes use of porcine skin - which is not considered to be a ''high risk''
tissue, but one of its uses is described in the data sheet as ''in dural
replacement''. This product is sourced from the United Kingdom.....</div>
<br />
<div>
</div>
<br />
<div>
<a href="http://web.archive.org/web/20030822054419/www.bseinquiry.gov.uk/files/yb/1990/09/21009001.pdf">http://web.archive.org/web/20030822054419/www.bseinquiry.gov.uk/files/yb/1990/09/21009001.pdf</a>
</div>
<br />
<div>
</div>
<br />
<div>
snip...</div>
<br />
<div>
</div>
<br />
<div>
It was not until . . . August 1990, that the result from the pig persuaded
both SEAC and us to change our view and to take out of pig rations any residual
infectivity that might have arisen from the SBOs.</div>
<br />
<div>
</div>
<br />
<div>
<a href="http://web.archive.org/web/20071014143511/http://www.bseinquiry.gov.uk/files/tr/tab69.pdf">http://web.archive.org/web/20071014143511/http://www.bseinquiry.gov.uk/files/tr/tab69.pdf</a>
</div>
<br />
<div>
</div>
<br />
<div>
4.303 The minutes of the meeting record that:</div>
<br />
<div>
</div>
<br />
<div>
It was very difficult to draw conclusions from one experimental result for
what may happen in the field. However it would be prudent to exclude specified
bovine offals from the pig diet. Although any relationship between BSE and the
finding of a spongiform encephalopathy in cats had yet to be demonstrated, the
fact that this had occurred suggested that a cautious view should be taken of
those species which might be susceptible. The 'specified offals' of bovines
should therefore be excluded from the feed of all species. 17</div>
<br />
<div>
</div>
<br />
<div>
<a href="http://web.archive.org/web/20031026084516/http://www.bseinquiry.gov.uk/files/yb/1990/09/07001001.pdf">http://web.archive.org/web/20031026084516/http://www.bseinquiry.gov.uk/files/yb/1990/09/07001001.pdf</a>
</div>
<br />
<div>
</div>
<br />
<div>
IN CONFIENCE</div>
<br />
<div>
</div>
<br />
<div>
EXPERIMENTAL PORCINE SPONGIFORM ENCEPHALOPATHY</div>
<br />
<div>
</div>
<br />
<div>
1. CMO should be aware that a pig inoculated experimentally (ic, iv, and
ip) with BSE brain suspension has after 15 months developed an illness, now
confirmed as a spongiform encephalopathy. This is the first ever description of
such a disease in a pig, although it seems there ar no previous attempts at
experimental inoculation with animal material. The Southwood group had thought
igs would not be susceptible. Most pigs are slaughtered when a few weeks old but
there have been no reports of relevant neurological illness in breeding sows or
other elderly pigs. ...see full text ;</div>
<br />
<div>
</div>
<br />
<div>
<a href="http://web.archive.org/web/20040302031004/www.bseinquiry.gov.uk/files/yb/1990/08/23001001.pdf">http://web.archive.org/web/20040302031004/www.bseinquiry.gov.uk/files/yb/1990/08/23001001.pdf</a>
</div>
<br />
<div>
</div>
<br />
<div>
IN CONFIDENCE</div>
<br />
<div>
</div>
<br />
<div>
So it is plausible pigs could be preclinically affected with BSE but since
so few are allowed to reach adulthood this has not been recognised through
clinical disease. ...</div>
<br />
<div>
</div>
<br />
<div>
<a href="http://web.archive.org/web/20040904150118/www.bseinquiry.gov.uk/files/yb/1990/08/23002001.pdf">http://web.archive.org/web/20040904150118/www.bseinquiry.gov.uk/files/yb/1990/08/23002001.pdf</a>
</div>
<br />
<div>
</div>
<br />
<div>
CONFIDENTIAL</div>
<br />
<div>
</div>
<br />
<div>
EXPERIMENTAL PORCINE SPONGIFORM ENCEPHALOPATHY</div>
<br />
<div>
</div>
<br />
<div>
While this clearly is a cause for concern we should not jump to the
conclusion that this means that pigs will necessarily be infected by bone and
meat meal fed by the oral route as is the case with cattle. ...</div>
<br />
<div>
</div>
<br />
<div>
<a href="http://web.archive.org/web/20031026000118/www.bseinquiry.gov.uk/files/yb/1990/08/23004001.pdf">http://web.archive.org/web/20031026000118/www.bseinquiry.gov.uk/files/yb/1990/08/23004001.pdf</a>
</div>
<br />
<div>
</div>
<br />
<div>
we cannot rule out the possibility that unrecognised subclinical spongiform
encephalopathy could be present in British pigs though there is no evidence for
this: only with parenteral/implantable pharmaceuticals/devices is the
theoretical risk to humans of sufficient concern to consider any action.</div>
<br />
<div>
</div>
<br />
<div>
<a href="http://web.archive.org/web/20030822031154/www.bseinquiry.gov.uk/files/yb/1990/09/10007001.pdf">http://web.archive.org/web/20030822031154/www.bseinquiry.gov.uk/files/yb/1990/09/10007001.pdf</a>
</div>
<br />
<div>
</div>
<br />
<div>
May I, at the outset, reiterate that we should avoid dissemination of
papers relating to this experimental finding to prevent premature release of the
information. ...</div>
<br />
<div>
</div>
<br />
<div>
<a href="http://web.archive.org/web/20030822052332/www.bseinquiry.gov.uk/files/yb/1990/09/11005001.pdf">http://web.archive.org/web/20030822052332/www.bseinquiry.gov.uk/files/yb/1990/09/11005001.pdf</a>
</div>
<br />
<div>
</div>
<br />
<div>
3. It is particularly important that this information is not passed outside
the Department, until Ministers have decided how they wish it to be handled.
...</div>
<br />
<div>
</div>
<br />
<div>
<a href="http://web.archive.org/web/20030822052438/www.bseinquiry.gov.uk/files/yb/1990/09/12002001.pdf">http://web.archive.org/web/20030822052438/www.bseinquiry.gov.uk/files/yb/1990/09/12002001.pdf</a>
</div>
<br />
<div>
</div>
<br />
<div>
But it would be easier for us if pharmaceuticals/devices are not directly
mentioned at all. ...</div>
<br />
<div>
</div>
<br />
<div>
<a href="http://web.archive.org/web/20030518170213/www.bseinquiry.gov.uk/files/yb/1990/09/13004001.pdf">http://web.archive.org/web/20030518170213/www.bseinquiry.gov.uk/files/yb/1990/09/13004001.pdf</a>
</div>
<br />
<div>
</div>
<br />
<div>
Our records show that while some use is made of porcine materials in
medicinal products, the only products which would appear to be in a
hypothetically ''higher risk'' area are the adrenocorticotrophic hormone for
which the source material comes from outside the United Kingdom, namely America
China Sweden France and Germany. The products are manufactured by Ferring and
Armour. A further product, ''Zenoderm Corium implant'' manufactured by Ethicon,
makes use of porcine skin - which is not considered to be a ''high risk''
tissue, but one of its uses is described in the data sheet as ''in dural
replacement''. This product is sourced from the United Kingdom.....</div>
<br />
<div>
</div>
<br />
<div>
<a href="http://web.archive.org/web/20030822054419/www.bseinquiry.gov.uk/files/yb/1990/09/21009001.pdf">http://web.archive.org/web/20030822054419/www.bseinquiry.gov.uk/files/yb/1990/09/21009001.pdf</a>
</div>
<br />
<div>
</div>
<br />
<div>
BSE TO PIGS NEWS RELEASE</div>
<br />
<div>
</div>
<br />
<div>
<a href="http://web.archive.org/web/20030822162313/www.bseinquiry.gov.uk/files/yb/1990/09/24001001.pdf">http://web.archive.org/web/20030822162313/www.bseinquiry.gov.uk/files/yb/1990/09/24001001.pdf</a>
</div>
<br />
<div>
</div>
<br />
<div>
CONFIDENTIAL</div>
<br />
<div>
</div>
<br />
<div>
BSE: PRESS PRESENTATION</div>
<br />
<div>
</div>
<br />
<div>
<a href="http://web.archive.org/web/20030822160958/www.bseinquiry.gov.uk/files/yb/1990/09/20003001.pdf">http://web.archive.org/web/20030822160958/www.bseinquiry.gov.uk/files/yb/1990/09/20003001.pdf</a>
</div>
<br />
<div>
</div>
<br />
<div>
<a href="http://web.archive.org/web/20040623191707/www.bseinquiry.gov.uk/files/yb/1990/09/24013001.pdf">http://web.archive.org/web/20040623191707/www.bseinquiry.gov.uk/files/yb/1990/09/24013001.pdf</a>
</div>
<br />
<div>
</div>
<br />
<div>
<a href="http://web.archive.org/web/20030820195733/http://www.bseinquiry.gov.uk/files/yb/1990/09/20010001.pdf">http://web.archive.org/web/20030820195733/http://www.bseinquiry.gov.uk/files/yb/1990/09/20010001.pdf</a>
</div>
<br />
<div>
</div>
<br />
<div>
<a href="http://web.archive.org/web/20030820195733/http://www.bseinquiry.gov.uk/files/yb/1990/09/25013001.pdf">http://web.archive.org/web/20030820195733/http://www.bseinquiry.gov.uk/files/yb/1990/09/25013001.pdf</a>
</div>
<br />
<div>
</div>
<br />
<div>
<a href="http://web.archive.org/web/20030820195733/http://www.bseinquiry.gov.uk/files/yb/1990/09/25015001.pdf">http://web.archive.org/web/20030820195733/http://www.bseinquiry.gov.uk/files/yb/1990/09/25015001.pdf</a>
</div>
<br />
<div>
</div>
<br />
<div>
INDUSTRY RESPONSE TYPICAL</div>
<br />
<div>
</div>
<br />
<div>
<a href="http://web.archive.org/web/20030822055917/www.bseinquiry.gov.uk/files/yb/1990/09/25007001.pdf">http://web.archive.org/web/20030822055917/www.bseinquiry.gov.uk/files/yb/1990/09/25007001.pdf</a>
</div>
<br />
<div>
</div>
<br />
<div>
DEFENSIVE BRIEFING</div>
<br />
<div>
</div>
<br />
<div>
<a href="http://web.archive.org/web/20030820195733/http://www.bseinquiry.gov.uk/files/yb/1990/09/25016001.pdf">http://web.archive.org/web/20030820195733/http://www.bseinquiry.gov.uk/files/yb/1990/09/25016001.pdf</a>
</div>
<br />
<div>
</div>
<br />
<div>
CONFIDENTIAL</div>
<br />
<div>
</div>
<br />
<div>
pigs & pharmaceuticals</div>
<br />
<div>
</div>
<br />
<div>
<a href="http://web.archive.org/web/20010305223234/www.bseinquiry.gov.uk/files/yb/1990/09/10007001.pdf">http://web.archive.org/web/20010305223234/www.bseinquiry.gov.uk/files/yb/1990/09/10007001.pdf</a>
</div>
<br />
<div>
</div>
<br />
<div>
<a href="http://web.archive.org/web/20010305223234/www.bseinquiry.gov.uk/files/yb/1990/08/23002001.pdf">http://web.archive.org/web/20010305223234/www.bseinquiry.gov.uk/files/yb/1990/08/23002001.pdf</a>
</div>
<br />
<div>
</div>
<br />
<div>
<a href="http://web.archive.org/web/20010305223234/www.bseinquiry.gov.uk/files/yb/1990/08/23004001.pdf">http://web.archive.org/web/20010305223234/www.bseinquiry.gov.uk/files/yb/1990/08/23004001.pdf</a>
</div>
<br />
<div>
</div>
<br />
<div>
<a href="http://web.archive.org/web/20010305223234/www.bseinquiry.gov.uk/files/yb/1990/08/29003001.pdf">http://web.archive.org/web/20010305223234/www.bseinquiry.gov.uk/files/yb/1990/08/29003001.pdf</a>
</div>
<br />
<div>
</div>
<br />
<div>
COMMERCIAL IN CONFIDENCE COMMITTEE ON SAFETY OF MEDICINE NOT FOR
PUBLICATION BOVINE SPONGIFORM ENCEPHALOPATHY WORKING GROUP</div>
<br />
<div>
</div>
<br />
<div>
There are only two products using porcine brain and these use
corticotrophin BP, made from porcine pituitary, source from outside the
UK.............</div>
<br />
<div>
</div>
<br />
<div>
<a href="http://web.archive.org/web/20040622220349/www.bseinquiry.gov.uk/files/yb/1990/10/31003001.pdf">http://web.archive.org/web/20040622220349/www.bseinquiry.gov.uk/files/yb/1990/10/31003001.pdf</a>
</div>
<br />
<div>
</div>
<br />
<div>
snip...</div>
<br />
<div>
</div>
<br />
<div>
7 OF 10 LITTLE PIGGIES WENT ON TO DEVELOP BSE;</div>
<br />
<div>
</div>
<br />
<div>
1: J Comp Pathol. 2000 Feb-Apr; 122(2-3): 131-43. Related Articles,</div>
<br />
<div>
</div>
<br />
<div>
Links</div>
<br />
<div>
</div>
<br />
<div>
Click here to read</div>
<br />
<div>
</div>
<br />
<div>
The neuropathology of experimental bovine spongiform encephalopathy in the
pig.</div>
<br />
<div>
</div>
<br />
<div>
Ryder SJ, Hawkins SA, Dawson M, Wells GA.</div>
<br />
<div>
</div>
<br />
<div>
Veterinary Laboratories Agency Weybridge, Woodham Lane, New Haw,
Addlestone, Surrey, KT15 3NB, UK.</div>
<br />
<div>
</div>
<br />
<div>
In an experimental study of the transmissibility of BSE to the pig, seven
of 10 pigs, infected at 1-2 weeks of age by multiple-route parenteral
inoculation with a homogenate of bovine brain from natural BSE cases developed
lesions typical of spongiform encephalopathy. The lesions consisted principally
of severe neuropil vacuolation affecting most areas of the brain, but mainly the
forebrain. In addition, some vacuolar change was identified in the rostral
colliculi and hypothalamic areas of normal control pigs. PrP accumulations were
detected immunocytochemically in the brains of BSE-infected animals. PrP
accumulation was sparse in many areas and its density was not obviously related
to the degree of vacuolation. The patterns of PrP immunolabelling in control
pigs differed strikingly from those in the infected animals.</div>
<br />
<div>
</div>
<br />
<div>
PMID: 10684682 [PubMed - indexed for MEDLINE]</div>
<br />
<div>
</div>
<br />
<div>
<a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?holding=npg&cmd=Retrieve&db=PubMed&list_uids=10684682&dopt=Abstract">http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?holding=npg&cmd=Retrieve&db=PubMed&list_uids=10684682&dopt=Abstract</a>
</div>
<br />
<div>
</div>
<br />
<div>
snip...</div>
<br />
<div>
</div>
<br />
<div>
In the United States, feeding of ruminant by-products to ruminants is
prohibited, but feeding of ruminant materials to swine and poultry still occurs.
The potential for swine to have access to scrapie-contaminated feedstuffs
exists, but the potential for swine to serve as a host for
replication/accumulation of the agent of scrapie is unknown. The purpose of this
study was to perform oral and intracerebral inoculation of the U.S. scrapie
agent to determine the potential of swine as a host for the scrapie agent and
their clinical susceptibility.</div>
<br />
<div>
</div>
<br />
<div>
see full text and more transmission studies here ;</div>
<br />
<div>
</div>
<br />
<div>
<a href="http://chronic-wasting-disease.blogspot.com/2011/07/swine-are-susceptible-to-chronic.html">http://chronic-wasting-disease.blogspot.com/2011/07/swine-are-susceptible-to-chronic.html</a>
</div>
<br />
<div>
</div>
<br />
<div>
Transgenic mice expressing porcine prion protein resistant to classical
scrapie but susceptible to sheep bovine spongiform encephalopathy and atypical
scrapie.</div>
<br />
<div>
</div>
<br />
<div>
Emerg Infect Dis. 2009 Aug; [Epub ahead of print]</div>
<br />
<div>
</div>
<br />
<div>
<a href="http://nor-98.blogspot.com/2009/07/transgenic-mice-expressing-porcine.html">http://nor-98.blogspot.com/2009/07/transgenic-mice-expressing-porcine.html</a>
</div>
<br />
<div>
</div>
<br />
<div>
The case for mad pigs in the US</div>
<br />
<div>
</div>
<br />
<div>
From the Consumer Policy Institute and Consumers Union: March 24,
1997</div>
<br />
<div>
</div>
<br />
<div>
Stephen F. Sundlof, D.V.M., Ph.D Center for Veterinary Medicine Food and
Drug Administration 7500 Standish Place, Room 482, HFV 1 RockvLIle, MD 20855
Dear Dr. Sundlof:</div>
<br />
<div>
</div>
<br />
<div>
We are writing to you to submit information that has recently come to our
attention which suggests that a TSE like disease (transmissible spongiform
encephalopathy) might exist in pigs in the U.S. We believe this new informantion
calls for intensive research and makes it urgent to ban the use of all mammalian
proteins, including swine, in the feed of all food animals, until better answers
are found.</div>
<br />
<div>
</div>
<br />
<div>
The evidence for the potential PSE (porcine spongiform encephalopathy ) is
as follows. In 1979, an FSQS veternarian, Dr. Masuo Doi, noticed some unusual
central nervous system (CNS) symptoms in young (about 6 months old) hogs coming
into a slaughter plant In Albany, New York. Since the plant received hogs from a
wide variety of sources (New York, Canada, Indiana, Illinois, Ohio, and other
Midwestern states) and was not a plant used to dealing with diseased animals,
Dr. Doi thought that the problem might be affecting hogs slaughtered nationwide.
So, he decided to conduct a detailed study on central nervous system (CNS)
symptoms/disease in young hogs coming into that slaughter plant. The study ran
for 15 months (January, 1979 to March, 1980) and consisted of extended
observations of the behavior of animals with suspected CNS symptoms at the
plant, followed by pathological, histopatholpgical, and microbiological work on
tissues from various organs of particular animals after slaughter.</div>
<br />
<div>
</div>
<br />
<div>
For his behavioral observational work, Dr. Doi extended the usual two day
observation period to three to four days, during which he took careful notes on
the animals' behavior and other vital signs. During the 15 month period of the
study, some 106 animals exhibiting CNS symptoms were retained during antemortem
inspection.</div>
<br />
<div>
</div>
<br />
<div>
A 1980 paper that summarized Dr. Doi's findings on the clinical symptoms
and incidence of the 'disease," contained descriptions of these symptoms that
sound remarkably similar to the symptoms noted for bovine spongiform
encephalopathy (BSE):</div>
<br />
<div>
</div>
<br />
<div>
"Excitable or nervous temperament to external stimuli such as touch to the
skin, handling and menacing approach to the animals is a common characteristic
sign among swine affected with the disease.... In the advanced stage of the
disease, manifestation of neurological signs are evidenced in the form of
general ataxia . . . Many animals have been found to be "downers' at first
observation; if the hindquarters of these downers are raised they may be able to
walk one or two steps and then fall to the ground" (Doi et al., 1980: 2, 4).
Indeed, a table of symptoms includes, for the early stage: "excitability and
nervousness (squealing, smacking of lips, grinding of teath, chewing, gnawing
ant foaming at mouth); stiffness of limbs . . . 'tic'; weakness of hindquarters;
focal tremors of skeletal muscles"; and for the advanced stage: depression;
ataxia; crossing over of limbs . . . kneeling posture . . . crawling". In
addition to his clinical observations, Dr. Doi also made an 8 mm film of
thirteen of the affected animals; film of two of the pigs was shown at the MPI
National Pathology Meeting in Seattle, Washington on flay 20, 1979.</div>
<br />
<div>
</div>
<br />
<div>
Dr. Doi sent tissue samples from suspect cases to the USDA's Eastern
Laboratory in Athens, GA for pathological, histopathogical and microbiological
work. Known infectious diseases were ruled out. As Dr. Doi points out,
"Histopathological studies of tissue collected from the brain and spinal cord of
these animals in the early stage of the disease show congestion, hemorrhage and
neuronal degeneration. All animals in the advanced stage of the disease have
been confined to have Encephalitis or Meningitis by MPI laboratory" (Doi et al.,
1980: 5). Eventually some 60 animals were confirmed by the MPI Laboratory to
have encephalitis or meningitis, with no ldentifiable cause. As pointed out in a
paper presented at the 1979 MPI National Pathology Meetings,</div>
<br />
<div>
</div>
<br />
<div>
"Since January, a number of hogs in this establishment have been found, in
antemortem, to show what appears to be CNS. Sets of tissue samples were sent to
the laboratory for examination, various tests were done which include
histological study (E H stain), fluorescence antibody technique, virus
neutralization and viral and bacteriological isolation. Differential diagnosis
was also done to exclude vitamin B deficiency, post vaccination reaction,
chlorinated hydrocarbon, arthritis, and transport stress" (Doi et al., 1979).
The brains of the 60 animals were examined. The brain of one of these pigs, on
histopathological analysis, exhibited signs reminiscent of a TSE. This
histopathological work was performed by Dr. Karl Langheinrich,
Pathologist-In-Charge at USDA's Eastern Laboratory in Athens, Georgia. According
to the USDA FSQS laboratory report, dated early November, 1979, Dr. Langheinrich
noted:</div>
<br />
<div>
</div>
<br />
<div>
"Microscopic examination of the barrow tissues revealed a encephalopathy
and diffuse gliosis characterized by vacuolated neurons, loss of neurons and
gliosis in a confined region (nucleus) of the brain stem (anterior ventral
midbrain). Only an empty sometimes divided vacuole was present instead of the
normal morphology of a nerve cell. Occasionally a shriveled neuron was seen.
According to . . . Pathology of Domestic Animals, . . . 'The degeneration of
neurons, the reactivity of the glia .... are the classical hallmarks of viral
infection of the central nervous system' .... Scrapie of sheep, and
encephalopathy of mink, according to the literature, all produce focal
vacuolation of the neurons similar to the kind as described for this pig. I was
unable to locate any lead as to the cause of this interesting phenomenon in
other species including swine'' (Langheinrich, 1979). Indeed, Dr. Langheinrich's
main diagnosis was, " Encephalopathy and diffuse gliosis of undetermined
etiology." Portions of the brain were sent for microbiological testing to a
neurologist at the University of Georgia, where they came up negative for
pseudo-rabies. The brain was unique enough that USDA scientists, such as Dr.
Langheinrich and Or. Dot, mentioned it to student and scientific colleagues over
the years.</div>
<br />
<div>
</div>
<br />
<div>
In 1979-1980, BSE was completely unknown. However, both the behavior of the
pigs, as well as the histopathology on at least one pig, both showed sign
consistent with a porcine TSE. This raises particular concern became the
affected animal was only 6 months old; in an animal this young, one would rust
expect to see any physical signs of TSE in the brain. Histopathology of TSEs can
be very variable, so that spongiform appearance (i.e. vacuolated neurons) are
not always present. Behavioral changes can be seen in TSE-infected animals
before any changes in brain morphology are visible. Dr. Clarence Gibbs, in
testimony before a Congressional hearing on the TSE issue on January 29, 1997
made just this point:</div>
<br />
<div>
</div>
<br />
<div>
''In the mid-1960s, we demonstrated with our French and English
collaborators that during the early incubation of the TSEs, when the virus titer
in the brain was very low, there were already marked functional changes, even
though no pathology was yet detectable, even ultrastructurally. A month or hero
later, polynucleation of neurons appeared in spider monkeys, incubating kuru,
and somewhat later, microvacuolation and membrane changes visible only by
electron microscopy. This preceded the pest appearance of astrogliosis and
spongiform change. It was only much later that the classical scrapie TSE
pathology appeared with virus titers in brain of 10 -5 or higher" (Gibbs, 1997;
pg. 4). Given that TSEs can cause behavioral changes in infected animals before
any physical changes in the brain can be seen, that the manifestation of TSE in
the brain can be quite variable, and that changes in brain morphology are not
usually seen in 6 month old animals, we are concerned that the brain of one pig
actually showed physical evidence consistent with a TSE.</div>
<br />
<div>
</div>
<br />
<div>
Following the announcement In March, 1996 of ten cases of new variant CJD
(Creutzfeldt-Jakob Disease) in the United Kingdom and their possible connection
to BSE, Drs. Doi, Langheinrich and others urged reinvestigation of this
case.</div>
<br />
<div>
</div>
<br />
<div>
In August, 1996, the USDA sent five slides, one of which was a
histopathology slide, to Dr. Janice Miller of USDA's Agricultural Research
Servicer . Dr. Miller stained four of the slides for prion protein (she didn't
stain the H&E slide). Dr. Miller told Consumers Union that Dr. Patrick
McCaskey, USDA/FSIS, in charge of the Research Center at Athens, GA, called her,
told her that he had five slides that all showed "problems" and asked her to
stain four of them. The H&E slide, which clearly show vacuoles in the
neurons (one sign of TSE), wasn't stained because to stain for PrP entails
removing the slide cover, baking the slide to destain it and then restaining it
for PrP; they didn't want to risk destroying the H&E slide.</div>
<br />
<div>
</div>
<br />
<div>
Dr. Doi had kept frozen samples of the brain and spinal chord of the
suspect PSE pig in case the Eastern lab wanted more material for analysis.
Unfortunately, these samples were discarded when the packing plant in Albany, NY
closed in 1991. It appears that the brain material sent to the Univcrsity of
Georgia may have been discarded. [pers com.. Dr. Doi 3/13/97]</div>
<br />
<div>
</div>
<br />
<div>
Dr. Miller found that the PrP stained in the four pig slides was found only
on the inside of neurons, while a positive control slide from a scrapie sheep
showed massive amounts of extraneuronal staining. In a letter summarizing her
results (copy attached), she concludes that the PrP stained in this pig was
normal: "In the pig sections you will see a small particulate type of staining
that is confined to neurons and as I indicated on the phone, I would interpret
as normal PrP. It is in marked contrast to the massive amount of extraneuronal
staining seen in the scrapie section" (Miller, 1996).</div>
<br />
<div>
</div>
<br />
<div>
Unfortunately, Dr. Miller's finding toes not conclusively rule out a TSE.
We are concerned that while British BSE and serapie create a massive amount of
extraneuronal staining, there are TSEs where this isn't the case. Three
experiments were done in He U.S. -- in Mission, TX (APHIS work), Pullman,
Washington (ARS work), and Ames, Iowa (ARS work) -- to see whether sheep scrapie
can possibly infect cows. In all the experiments, cattle were inoculated with
tissue from scrapie -infected sheep primarily by intra-cranial injection, but in
the case of the Texas and Iowa studies also by oral feeding -- to see if cattle
were susceptible to scrapie at all. In all three experiments, the majority of
cows injected in the brain with scrapie-infected sheep material (usually brains)
also developed a fatal spongiform encephalopathy.</div>
<br />
<div>
</div>
<br />
<div>
However, in all three examples, the symptoms of the spongifonn
encephalopathy differed from "mad cow" disease ~ England, as did the appearances
of slides from their brains. The brain lesions seen in all these animals were
more variable than those seen in England. When Dr. Miller did similar staining
for PrP from these brains (what she called "bovine scrapie") she only found PrP
stains on the inside of the neurons, not the massive extraneuronal staining seen
in BSE (Miller, pers. comm., March 7, 1997). Thus, Dr. Miller's finding of PrP
stains only inside the neurons in the suspect pigs is not particularly
reassuring.</div>
<br />
<div>
</div>
<br />
<div>
In November 1996, USDA sent the single histopathology slide to Dr. William
Hadlow, one of the foremost spongiform encephalopathy pathologists in the world.
(For unknown reasons, Dr. Hadlow was only sent the one slide; he was not told of
the existence of the other slides, nor of Dr. Miller's findings, nor was he told
or given the behavioral report from Dr. Doi or the morphology work by Dr.
Langheinrich, or shown film of the affected pigs [Dr. Hadlow, pers. com.,
3/13/97] From this single slide, Dr. Hadlow found some evidence consistent with
TSEs but not enough for a conclusive diagnosis. He noted that the slide
contained vacuoles inside neurons, one of the signs of a TSE (Dr. Langheinrich
had noted this as well).</div>
<br />
<div>
</div>
<br />
<div>
However, since such vacuoles occasionally occur normally in pigs, he
thought that was not something special: "About twelve (12) neurons in the
parasympathetic nucleus have unilocular optically empty vacuoles in the
perikaryon. This is the site where such vacuolated neurons have been seen in the
swine (as well as in cats and sheep) as an incidental finding. So I do not think
such cells have any significance in this pig" (Hadlow, 1996). However, he did
see evidence, Including changes in astrocytes, that suggested a TSE, but without
examining other parts of the brain to look for other evidence of TSE, he
couldn't be sure:</div>
<br />
<div>
</div>
<br />
<div>
"I am impressed, though, with what seems to be an increase in the number of
astrocytes in the section. Some astrocytes are in clusters, some are enlarged
and vesicular. Where they are most numerous, a few rod cells (activated
microglia) are seen. These findings suggest some perturbation of the nervous
tissue. Although such a global response occurs in the transmissible spongifonn
encephalopathies, I do no! know its significance in this case without examining
other parts of the brain for changes characteristic of these diseases. Thus,
from looking; at this one (1) section of brain, I cannot conclude that the pig
was affected with a scrapie-like spongiform encephalopathy" (Hadlow, 1996). In
sum, Dr. Hadlow~s letter does not rule out the possibility of a TSE. He says
that there is suggestive evidence, but that he would need to look at other
slides/sections of the brain, to make a conclusive diagnosis.</div>
<br />
<div>
</div>
<br />
<div>
In our view, the implications of this data are extremely serious.
Experiments in the United Kingdom have shown that pigs are susceptible to BSE.
Pigs inoculated with BSE develop a TSE (Dawson et al., 1990). Feeding
experiments are underway in the UK to see if BSE can be orally transmitted to
pigs; as of March, 1997, some 6 years after the start of the experiment, none of
the pigs fed BSE brain have come down with a TSE. Unfortunately the design of
this experiment severely limits what we will learn from it, and will most likely
not tell us conclusively if pigs can get BSE from feed. It turns out that the
pigs were not fed BSE brain continuously. Rather, the pigs were only fed BSE
brain material on three days, over a three week period (i.e.. one day each
week). Following these three doses, the pigs were never fed contaminated
material again. The total amount of infective material given to the pigs was
therefore quite small. Thus, a negative finding would be hard to interpret and
would not mean that BSE is not orally active in pigs.</div>
<br />
<div>
</div>
<br />
<div>
We believe that as a top priority USDA should conduct follow-up studies to
look for potential CNS/PSE cases in pigs (we plan to communicate about this to
USDA separately). In brief, we feel that the following kinds of studies need to
be done:</div>
<br />
<div>
</div>
<br />
<div>
i) TSE pathology experts should examine all the slides from the suspect pig
(2709). To our knowledge, at least 12 separate slides exist.</div>
<br />
<div>
</div>
<br />
<div>
ii) Determine if any brain material from the suspect pig (2709) still
exists at the Unlverslty of Georgia. If so, this material should be retrieved
and used for transmission studies. In particular, suckling pigs should be
inoculated with the material and then permitted to live unto they die of a
disease or old age, at which point their brains should be examined for physical
signs of a TSE as well as for immunchistochemical evidence (i.e. staining
looking for the abnormal PrP).</div>
<br />
<div>
</div>
<br />
<div>
iii) Increase antemortem inspection for CNS symptoms at hog facilities.
Inspectors should be trained to detect the subtle CNS symptoms seen in the Doi
et al. study. At a select number of slaughter facilities, animals exhibiting CNS
symptoms should be removed and held for observation until they die, at which
time their brains should be examined for evidence of a TSE.</div>
<br />
<div>
</div>
<br />
<div>
iv) Research on CNS symptoms among Me 6,000 or so breeding sows which are
permitted to live for 3+ years. Sows exhibiting CNS symptoms should be removed
and held for observation until they die, at which time then brains should be
exernined for evidence of a TSE.</div>
<br />
<div>
</div>
<br />
<div>
While such work is underway, given the above inforrnabon, we believe that
as a precutionary measure the FDA must expand the proposed ruminant plus
mink-to-ruminnant feed ban to prevent protein from any material, including hogs,
being fed to any food animal.</div>
<br />
<div>
</div>
<br />
<div>
Sincerely,</div>
<br />
<div>
</div>
<br />
<div>
Michael Hansen, Ph.D Research Associate</div>
<br />
<div>
</div>
<br />
<div>
Jean Halloran Director</div>
<br />
<div>
</div>
<br />
<div>
References</div>
<br />
<div>
</div>
<br />
<div>
Dawson, M., Wells, G.A.H., Parker, B.N;J. and A.C Scott. 1990. Primary
parental transmission of bovine spongiform encephalopathy to the pig. Veternary
Record, pg. 338.</div>
<br />
<div>
</div>
<br />
<div>
Doi, M., Matzner, N.D. and C. Rothaug. 1979. Observation of CNS disease in
market hogs at Est. 893 Tobin Packing Co., Inc. Albany, New York. United States
Department of Agriculture, Food Safety and Quality.Service, Meat and Poultry
Inspection Service. 7pp.</div>
<br />
<div>
</div>
<br />
<div>
Doi, M, Langheinrich, K. and F. Rellosa. 1980. Observations of CNS signs in
hogs at Est. 893 Tobin Packing C:o., Inc. Presented by Dr. Lngheinrich at the
MPI National Pathology Meeting in Seattle, Washington on July 20, 1979.</div>
<br />
<div>
</div>
<br />
<div>
Gibbs, C. 1997. Statement to the Committee on Governnent Reform and
Oversight, Subcommittee on Human Resources and Intergovernmental Relations, U.S.
House of Representatives. January 29,1997.</div>
<br />
<div>
</div>
<br />
<div>
Hadlow, WJ. 1996. Letter to Patrick McCaskey, USDA/FSIS/Eastem Lab, dated
November 13, 1996.</div>
<br />
<div>
</div>
<br />
<div>
Langheinrich, KA. 1979. USDA/FSQS Laboratory report on specimen 2709. Dated
November 8, 1979</div>
<br />
<div>
</div>
<br />
<div>
Miller, J. 1996. Letter to Patrick McCaskey, USDA/ESIS/Eastern Lab, dated
September 6, 1996.</div>
<br />
<div>
</div>
<br />
<div>
Dr. Janice Miller, ARS</div>
<br />
<div>
</div>
<br />
<div>
<a href="http://www.mad-cow.org/~tom/mad_pigs.html">http://www.mad-cow.org/~tom/mad_pigs.html</a>
</div>
<br />
<div>
</div>
<br />
<div>
HOUND STUDY</div>
<br />
<div>
</div>
<br />
<div>
*** AS implied in the Inset 25 we must not _ASSUME_ that transmission of
BSE to other species will invariably present pathology typical of a scrapie-like
disease. ***</div>
<br />
<div>
</div>
<br />
<div>
snip...</div>
<br />
<div>
</div>
<br />
<div>
<a href="http://web.archive.org/web/20010305222642/www.bseinquiry.gov.uk/files/yb/1991/01/04004001.pdf">http://web.archive.org/web/20010305222642/www.bseinquiry.gov.uk/files/yb/1991/01/04004001.pdf</a>
</div>
<br />
<div>
</div>
<br />
<div>
======================== </div>
<br />
<div>
</div>
<br />
<div>
2005</div>
<br />
<div>
</div>
<br />
<div>
DEFRA Department for Environment, Food & Rural Affairs</div>
<br />
<div>
</div>
<br />
<div>
Area 307, London, SW1P 4PQ Telephone: 0207 904 6000 Direct line: 0207 904
6287 E-mail: h.mcdonagh.defra.gsi.gov.uk</div>
<br />
<div>
</div>
<br />
<div>
GTN: FAX:</div>
<br />
<div>
</div>
<br />
<div>
Mr T S Singeltary P.O. Box 42 Bacliff Texas USA 77518</div>
<br />
<div>
</div>
<br />
<div>
21 November 2001</div>
<br />
<div>
</div>
<br />
<div>
Dear Mr Singeltary</div>
<br />
<div>
</div>
<br />
<div>
TSE IN HOUNDS</div>
<br />
<div>
</div>
<br />
<div>
Thank you for e-mail regarding the hounds survey. I am sorry for the long
delay in responding.</div>
<br />
<div>
</div>
<br />
<div>
As you note, the hound survey remains unpublished. However the Spongiform
Encephalopathy Advisory Committee (SEAC), the UK Government's independent
Advisory Committee on all aspects related to BSE-like disease, gave the hound
study detailed consideration at their meeting in January 1994. As a summary of
this meeting published in the BSE inquiry noted, the Committee were clearly
concerned about the work that had been carried out, concluding that there had
clearly been problems with it, particularly the control on the histology, and
that it was more or less inconclusive. However was agreed that there should be a
re-evaluation of the pathological material in the study.</div>
<br />
<div>
</div>
<br />
<div>
Later, at their meeting in June 95, The Committee re-evaluated the hound
study to see if any useful results could be gained from it. The Chairman
concluded that there were varying opinions within the Committee on further work.
It did not suggest any further transmission studies and thought that the lack of
clinical data was a major weakness.</div>
<br />
<div>
</div>
<br />
<div>
Overall, it is clear that SEAC had major concerns about the survey as
conducted. As a result it is likely that the authors felt that it would not
stand up to r~eer review and hence it was never published. As noted above, and
in the detailed minutes of the SEAC meeting in June 95, SEAC considered whether
additional work should be performed to examine dogs for evidence of TSE
infection. Although the Committee had mixed views about the merits of conducting
further work, the Chairman noted that when the Southwood Committee made their
recommendation to complete an assessment of possible spongiform disease in dogs,
no TSEs had been identified in other species and hence dogs were perceived as a
high risk population and worthy of study. However subsequent to the original
recommendation, made in 1990, a number of other species had been identified with
TSE ( e.g. cats) so a study in hounds was less</div>
<br />
<div>
</div>
<br />
<div>
critical. For more details see- <a href="http://www.bseinquiry/">http://www.bseinquiry</a>,
gov.uk/files/yb/1995/06/21005001 .pdf </div>
<br />
<div>
</div>
<br />
<div>
As this study remains unpublished, my understanding is that the ownership
of the data essentially remains with the original researchers. Thus
unfortunately, I am unable to help with your request to supply information on
the hound survey directly. My only suggestion is that you contact one of the
researchers originally involved in the project, such as Gerald Wells. He can be
contacted at the following address.</div>
<br />
<div>
</div>
<br />
<div>
Dr Gerald Wells, Veterinary Laboratories Agency, New Haw, Addlestone,
Surrey, KT 15 3NB, UK</div>
<br />
<div>
</div>
<br />
<div>
You may also wish to be aware that since November 1994 all suspected cases
of spongiform encephalopathy in animals and poultry were made notifiable. Hence
since that date there has been a requirement for vets to report any suspect SE
in dogs for further investigation. To date there has never been positive
identification of a TSE in a dog.</div>
<br />
<div>
</div>
<br />
<div>
I hope this is helpful</div>
<br />
<div>
</div>
<br />
<div>
Yours sincerely 4</div>
<br />
<div>
</div>
<br />
<div>
HUGH MCDONAGH BSE CORRESPONDENCE SECTION </div>
<br />
<div>
</div>
<br />
<div>
====================================== </div>
<br />
<div>
</div>
<br />
<div>
HOUND SURVEY</div>
<br />
<div>
</div>
<br />
<div>
I am sorry, but I really could have been a co-signatory of Gerald's
minute.</div>
<br />
<div>
</div>
<br />
<div>
I do NOT think that we can justify devoting any resources to this study,
especially as larger and more important projects such as the pathogenesis study
will be quite demanding.</div>
<br />
<div>
</div>
<br />
<div>
If there is a POLITICAL need to continue with the examination of hound
brains then it should be passed entirely to the VI Service. </div>
<br />
<div>
</div>
<br />
<div>
J W WILESMITH Epidemiology Unit 18 October 1991</div>
<br />
<div>
</div>
<br />
<div>
Mr. R Bradley</div>
<br />
<div>
</div>
<br />
<div>
cc: Mr. G A H Wells </div>
<br />
<div>
</div>
<br />
<div>
<a href="http://collections.europarchive.org/tna/20081106102318/http://www.bseinquiry.gov.uk/files/yb/1991/10/18001001.pdf">http://collections.europarchive.org/tna/20081106102318/http://www.bseinquiry.gov.uk/files/yb/1991/10/18001001.pdf</a>
</div>
<br />
<div>
</div>
<br />
<div>
3.3. Mr R J Higgins in conjunction with Mr G A Wells and Mr A C Scott would
by the end of the year, indentify the three brains that were from the
''POSITIVE'' end of the lesion spectrum. </div>
<br />
<div>
</div>
<br />
<div>
<a href="http://collections.europarchive.org/tna/20080103034308/http://www.bseinquiry.gov.uk/files/yb/1993/12/06001001.pdf">http://collections.europarchive.org/tna/20080103034308/http://www.bseinquiry.gov.uk/files/yb/1993/12/06001001.pdf</a>
</div>
<br />
<div>
</div>
<br />
<div>
*** OR-09: Canine spongiform encephalopathy—A new form of animal prion
disease ***</div>
<br />
<div>
</div>
<br />
<div>
Monique David, Mourad Tayebi UT Health; Houston, TX USA </div>
<br />
<div>
</div>
<br />
<div>
It was also hypothesized that BSE might have originated from an
unrecognized sporadic or genetic case of bovine prion disease incorporated into
cattle feed or even cattle feed contaminated with prion-infected human remains.1
However, strong support for a genetic origin of BSE has recently been
demonstrated in an H-type BSE case exhibiting the novel mutation E211K.2
Furthermore, a specific prion protein strain causing BSE in cattle is believed
to be the etiological agent responsible for the novel human prion disease,
variant Creutzfeldt-Jakob disease (vCJD).3 Cases of vCJD have been identified in
a number countries, including France, Italy, Ireland, the Netherlands, Canada,
Japan, US and the UK with the largest number of cases. Naturally occurring
feline spongiform encephalopathy of domestic cats4 and spongiform
encephalopathies of a number of zoo animals so-called exotic ungulate
encephalopathies5,6 are also recognized as animal prion diseases, and are
thought to have resulted from the same BSE-contaminated food given to cattle and
humans, although and at least in some of these cases, a sporadic and/or genetic
etiology cannot be ruled out. The canine species seems to display resistance to
prion disease and no single case has so far been reported.7,8 Here, we describe
a case of a 9 week old male Rottweiler puppy presenting neurological deficits;
and histological examination revealed spongiform vacuolation characteristic of
those associated with prion diseases.9 Initial biochemical studies using
anti-PrP antibodies revealed the presence of partially proteinase K-resistant
fragment by western blotting. Furthermore, immunohistochemistry revealed
spongiform degeneration consistent with those found in prion disease and
displayed staining for PrPSc in the cortex. </div>
<br />
<div>
</div>
<br />
<div>
Of major importance, PrPSc isolated from the Rottweiler was able to cross
the species barrier transmitted to hamster in vitro with PMCA and in vivo (one
hamster out of 5). Futhermore, second in vivo passage to hamsters, led to 100%
attack rate (n = 4) and animals displayed untypical lesional profile and shorter
incubation period. </div>
<br />
<div>
</div>
<br />
<div>
In this study, we show that the canine species might be sensitive to prion
disease and that PrPSc isolated from a dog can be transmitted to dogs and
hamsters in vitro using PMCA and in vivo to hamsters. </div>
<br />
<div>
</div>
<br />
<div>
If our preliminary results are confirmed, the proposal will have a major
impact on animal and public health and would certainly lead to implementing new
control measures for ‘canine spongiform encephalopathy’ (CSE). </div>
<br />
<div>
</div>
<br />
<div>
References 1. Colchester AC, Colchester NT. The origin of bovine spongiform
encephalopathy: the human prion disease hypothesis. Lancet 2005; 366:856-61;
PMID:16139661; <a href="http://%20dx.doi.org/10.1016/S0140-6736(05)67218-2">http://
dx.doi.org/10.1016/S0140-6736(05)67218-2</a>.</div>
<br />
<div>
</div>
<br />
<div>
2. Richt JA, Hall SM. BSE case associated with prion protein gene mutation.
PLoS Pathog 2008; 4:e1000156; PMID:18787697; <a href="http://dx.doi.org/10.1371/journal">http://dx.doi.org/10.1371/journal</a>.
ppat.1000156.</div>
<br />
<div>
</div>
<br />
<div>
3. Collinge J. Human prion diseases and bovine spongiform encephalopathy
(BSE). Hum Mol Genet 1997; 6:1699-705; PMID:9300662; <a href="http://dx.doi.org/10.1093/">http://dx.doi.org/10.1093/</a>
hmg/6.10.1699.</div>
<br />
<div>
</div>
<br />
<div>
4. Wyatt JM, Pearson GR, Smerdon TN, Gruffydd-Jones TJ, Wells GA, Wilesmith
JW. Naturally occurring scrapie-like spongiform encephalopathy in five domestic
cats. Vet Rec 1991; 129:233-6; PMID:1957458; <a href="http://dx.doi.org/10.1136/vr.129.11.233">http://dx.doi.org/10.1136/vr.129.11.233</a>.</div>
<br />
<div>
</div>
<br />
<div>
5. Jeffrey M, Wells GA. Spongiform encephalopathy in a nyala (Tragelaphus
angasi). Vet Pathol 1988; 25:398-9; PMID:3232315; <a href="http://dx.doi.org/10.1177/030098588802500514">http://dx.doi.org/10.1177/030098588802500514</a>.</div>
<br />
<div>
</div>
<br />
<div>
6. Kirkwood JK, Wells GA, Wilesmith JW, Cunningham AA, Jackson SI.
Spongiform encephalopathy in an arabian oryx (Oryx leucoryx) and a greater kudu
(Tragelaphus strepsiceros). Vet Rec 1990; 127:418-20; PMID:2264242.</div>
<br />
<div>
</div>
<br />
<div>
7. Bartz JC, McKenzie DI, Bessen RA, Marsh RF, Aiken JM. Transmissible mink
encephalopathy species barrier effect between ferret and mink: PrP gene and
protein analysis. J Gen Virol 1994; 75:2947-53; PMID:7964604; <a href="http://dx.doi.org/10.1099/0022-1317-">http://dx.doi.org/10.1099/0022-1317-</a>
75-11-2947.</div>
<br />
<div>
</div>
<br />
<div>
8. Lysek DA, Schorn C, Nivon LG, Esteve-Moya V, Christen B, Calzolai L, et
al. Prion protein NMR structures of cats, dogs, pigs, and sheep. Proc Natl Acad
Sci U S A 2005; 102:640-5; PMID:15647367; <a href="http://dx.doi.org/10.1073/pnas.0408937102">http://dx.doi.org/10.1073/pnas.0408937102</a>.</div>
<br />
<div>
</div>
<br />
<div>
9. Budka H. Neuropathology of prion diseases. Br Med Bull 2003; 66:121-30;
PMID:14522854; <a href="http://dx.doi.org/10.1093/bmb/66.1.121">http://dx.doi.org/10.1093/bmb/66.1.121</a>.
</div>
<br />
<div>
</div>
<br />
<div>
<a href="http://www.landesbioscience.com/journals/prion/01-Prion6-2-OralPresentations.pdf">http://www.landesbioscience.com/journals/prion/01-Prion6-2-OralPresentations.pdf</a>
</div>
<br />
<div>
</div>
<br />
<div>
Monday, March 26, 2012 </div>
<br />
<div>
</div>
<br />
<div>
CANINE SPONGIFORM ENCEPHALOPATHY: A NEW FORM OF ANIMAL PRION DISEASE </div>
<br />
<div>
</div>
<br />
<div>
<a href="http://caninespongiformencephalopathy.blogspot.com/2012/03/canine-spongiform-encephalopathy-new.html">http://caninespongiformencephalopathy.blogspot.com/2012/03/canine-spongiform-encephalopathy-new.html</a>
</div>
<br />
<div>
</div>
<br />
<div>
Monday, March 8, 2010 </div>
<br />
<div>
</div>
<br />
<div>
Canine Spongiform Encephalopathy aka MAD DOG DISEASE </div>
<br />
<div>
</div>
<br />
<div>
<a href="http://caninespongiformencephalopathy.blogspot.com/">http://caninespongiformencephalopathy.blogspot.com/</a>
</div>
<br />
<div>
</div>
<br />
<div>
Wednesday, July 29, 2015 </div>
<br />
<div>
</div>
<br />
<div>
Acquired transmissibility of sheep-passaged L-type bovine spongiform
encephalopathy prion to wild-type mice </div>
<br />
<div>
</div>
<br />
<div>
<a href="http://transmissiblespongiformencephalopathy.blogspot.com/2015/07/acquired-transmissibility-of-sheep.html" title="http://transmissiblespongiformencephalopathy.blogspot.com/2015/07/acquired-transmissibility-of-sheep.html">http://transmissiblespongiformencephalopathy.blogspot.com/2015/07/acquired-transmissibility-of-sheep.html</a></div>
<br />
<div>
</div>
<br />
<div>
Wednesday, July 15, 2015 </div>
<br />
<div>
</div>
<br />
<div>
*** Additional BSE TSE prion testing detects pathologic lesion in unusual
brain location and PrPsc by PMCA only, how many cases have we missed?</div>
<br />
<div>
</div>
<br />
<div>
<a href="http://transmissiblespongiformencephalopathy.blogspot.com/2015/07/additional-bse-tse-prion-testing.html">http://transmissiblespongiformencephalopathy.blogspot.com/2015/07/additional-bse-tse-prion-testing.html</a>
</div>
<br />
<div>
</div>
<br />
<div>
IBNC Tauopathy or TSE Prion disease, it appears, no one is sure</div>
<br />
<div>
</div>
<br />
<div>
Posted by flounder on 03 Jul 2015 at 16:53 GMT</div>
<br />
<div>
</div>
<br />
<div>
<a href="http://www.plosone.org/annotation/listThread.action?root=86610">http://www.plosone.org/annotation/listThread.action?root=86610</a>
</div>
<br />
<div>
</div>
<br />
<div>
SEE FULL TEXT ; </div>
<br />
<div>
</div>
<br />
<div>
<a href="http://madporcinedisease.blogspot.com/">http://madporcinedisease.blogspot.com/</a>
</div>
<br />
<div>
</div>
<br />
<div>
</div>
<br />
<div>
Terry S. Singeltary Sr. Bacliff, Texas USA 77518
flounder9@verizon.net</div>
Terry S. Singeltary Sr.http://www.blogger.com/profile/06986622967539963260noreply@blogger.com0tag:blogger.com,1999:blog-6404950019984350027.post-65426968856540335702012-04-20T18:36:00.002-07:002012-04-20T18:36:56.694-07:00Ultrastructural findings in pigs experimentally infected with bovine spongiform encephalopathy agent<div>
Ultrastructural findings in pigs experimentally infected with bovine
spongiform encephalopathy agent </div>
<br />
<div>
</div>
<br />
<div>
Pawel P. Liberski1, Beata Sikorska1, Gerald A.H. Wells2, Steve A.C.
Hawkins3, Michael Dawson3, Marion M. Simmons2 1Department of Molecular Pathology
and Neuropathology, Medical University of Lodz, Poland, 2TSE Department, and
3Specialist Scientific Services Department, Animal Health and Veterinary
Laboratories Agency, Weybridge, Addlestone, Surrey, United Kingdom Folia
Neuropathol 2012; 50 (1): 89-98 </div>
<br />
<div>
</div>
<br />
<div>
A b s t r a c t </div>
<br />
<div>
</div>
<br />
<div>
We report here an electron microscopic study of selected nervous system
tissues from pigs infected experimentally with the agent of bovine spongiform
encephalopathy (BSE). Generally, the ultrastructural neuropathology of
BSE-affected pig brain resembled that of BSE-affected cattle brain. Spongiform
change, in the form of membrane-bound vacuoles separated by septae into
secondary chambers, dominated the pathology. Numerous astrocytic processes were
visible in close conjunction with elongated microglial cells. Neuronal
degeneration presented as either dystrophic neurites or by the formation of
autophagic vacuoles. Altered subcellular organelles: mitochondria,
electron-dense bodies, autophagic vacuoles, neurofilaments and
“branching-cisterns” accumulated in abnormal neurites. Autophagic vacuoles
appeared as neuronal cytoplasm of increased electron-density sequestrated by
intracytoplasmic membranes. Tubulovesicular structures were numerous,
particularly in the cerebellum. Unusual crystalloids were observed in the white
matter. In conclusion, experimental BSE in pigs demonstrated ultrastructural
pathology in keeping with that observed in other spongiform encephalopathies.
</div>
<br />
<div>
</div>
<br />
<div>
Key words: prions, BSE, pigs, ultrastructure. </div>
<br />
<div>
</div>
<br />
<div>
snip... </div>
<br />
<div>
</div>
<br />
<div>
Material and methods</div>
<br />
<div>
</div>
<br />
<div>
Experiment design and inoculation procedure</div>
<br />
<div>
</div>
<br />
<div>
The pigs were infected at 1-2 weeks of age by multiple- route parenteral
inoculation with a homogenate of bovine brain from natural BSE cases, as
described in full previously [76,86,87]. All challenges were carried out in
accordance with the Animals (Scientific Procedures) Act, 1986, under licence
from the UK Home Office. Animals were sedated with azoperone (Stresnil; Janssen
Animal Health) and killed by the intravenous injection of pentobarbitone sodium
followed by exsanguination. When clinical disease developed, animals were killed
and samples collected immediately postmortem. </div>
<br />
<div>
</div>
<br />
<div>
</div>
<br />
<div>
</div>
<br />
<div>
snip... </div>
<br />
<div>
</div>
<br />
<div>
Electron microscopy </div>
<br />
<div>
</div>
<br />
<div>
Multiple samples, comprised 2-3 mm3, of cerebral cortex, brain stem at the
level of vestibular nuclei, ventral horns of the spinal cord, cerebellum and
dorsal root ganglia, selected on the basis of the previously determined
prevalence of light-microscopy changes [76,87], were fixed immediately after
dissection in 2.5% glutaraldehyde, freshly prepared in phosphate buffer (pH
7.4), then postfixed in 1% osmium tetroxide and processed for routine electron
microscopy. Comparable areas of brain from uninoculated pigs served as controls.
</div>
<br />
<div>
</div>
<br />
<div>
snip... </div>
<br />
<div>
</div>
<br />
<div>
Results </div>
<br />
<div>
</div>
<br />
<div>
In general, the ultrastructural features of BSE-affected pig brain were
similar to those of BSE-affected cattle [46,66,67] and humans with TSEs [60,61].
Spongiform change in the form of membrane-bound vacuoles (Fig. 1) separated by
membranes curled into secondary chambers dominated the pathology. A dense
astrocytic reaction was accompanied by abundant elongated microglial cells. Of
particular note was the finding of numerous astrocytic processes in close
conjunction with microglial cells. Neuronal degeneration presented as either
neuroaxonal dystrophy, as evidenced by dystro - phic neurites, or autophagic
vacuoles. Dystrophic neurites accumulated altered subcellular organelles:
mitochondria (Fig. 1B), electron-dense bodies, neurofilaments and
“branching-cisterns” (Fig. 2). Autopha - gic vacuoles appeared as a part or
parts of the neuronal cytoplasm sequestrated by intracytoplasmic membranes (Fig.
3). Sequestrated cytoplasm was of higher electron density than the remaining
cytosol. Discontinuity of plasma membranes was occasionally seen (Fig. 3B,
arrow). Tubulovesicular structures (TVS) were numerous with the highest number
of affected processes in the cerebellum (Fig. 4). Many large multivesicular
bodies were seen (Fig. 5). </div>
<br />
<div>
</div>
<br />
<div>
</div>
<br />
<div>
</div>
<br />
<div>
<a href="http://www.termedia.pl/Journal/-20/pdf-18394-10?filename=Ultrastructuralfindings.pdf">http://www.termedia.pl/Journal/-20/pdf-18394-10?filename=Ultrastructuralfindings.pdf</a>
</div>
<br />
<div>
</div>
<br />
<div>
</div>
<br />
<div>
<a href="http://www.termedia.pl/Review-article-Ultrastructural-findings-in-pigs-experimentally-infected-r-nwith-bovine-spongiform-encephalopathy-agent,20,18394,1,1.html">http://www.termedia.pl/Review-article-Ultrastructural-findings-in-pigs-experimentally-infected-r-nwith-bovine-spongiform-encephalopathy-agent,20,18394,1,1.html</a>
</div>
<br />
<div>
</div>
<br />
<div>
</div>
<br />
<div>
</div>
<br />
<div>
</div>
<br />
<div>
PORCINE SPONGIFORM ENCEPHALOPATHY PSE </div>
<br />
<div>
</div>
<br />
<div>
</div>
<br />
<div>
<a href="http://madporcinedisease.blogspot.com/">http://madporcinedisease.blogspot.com/</a>
</div>
<br />
<div>
</div>
<br />
<div>
</div>
<br />
<div>
</div>
<br />
<div>
</div>
<br />
<div>
TSS</div>
<br />
<div>
</div>
<br />
<div>
</div>
<br />
<div>
</div>
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</div>Terry S. Singeltary Sr.http://www.blogger.com/profile/06986622967539963260noreply@blogger.com0tag:blogger.com,1999:blog-6404950019984350027.post-15466690351749299502009-12-21T19:18:00.000-08:002009-12-21T19:20:43.148-08:00Distinct Molecular Signature of Bovine Spongiform Encephalopathy Prion in PigsDistinct Molecular Signature of Bovine Spongiform Encephalopathy Prion in Pigs<br /><br />To the Editor: In a recent article in Emerging Infectious Diseases, Espinosa et al. (1) investigated the porcine transmission barrier to infection with bovine and ovine transmissible spongiform encephalopathies (TSEs) in transgenic mice expressing the porcine prion protein. Bovine spongiform encepatholopathy of the classical type (BSE) derived from cattle and sheep, as well as atypical scrapie, transmitted to these mice, although with different effi - ciencies. Whereas sheep BSE showed a 100% attack rate, cattle BSE and atypical scrapie showed a higher transmission barrier in the fi rst passage. Unexpectedly, the electrophoretic profi le of the proteinase K–resistant prion protein (PrPres) in Western immunoblot (WB) analysis of all 3 TSEs shifted toward a common signature upon transmission. This was a 3-band pattern with a predominant monoglycosylated PrPres moiety and, therefore, clearly differed from those of the BSE and atypical scrapie inocula. The authors speculated that the porcine cellular prion protein (PrPc) might allow only for few options as it changes its conformation to the disease-associated prion protein. However, whether this effect is attributable to the porcine PrPc transgene or to the genetic background of the mouse model remains unknown.<br /><br />To our knowledge, BSE has been successfully transmitted to pigs in 1 study, but WB data were not reported (2). We had access to central nervous system tissues of 1 of these animals (kindly provided by the Veterinary Laboratories Agency TSE Archive, Weybridge, UK) and aimed at assessing whether a similar effect occurs when cattle BSE affects pigs. Our results show a PrPres signature in BSEinfected pigs similar to that described for the porcine PrPc transgenic mice and clearly different from that in cattle (Figure). These fi ndings support the fi nding by Espinosa et al. that the molecular shift most likely was due to intrinsic properties of the porcine PrPc. Therefore, in this respect the mouse model appears to refl ect the situation in the pig.<br /><br />BSE prions are considered to transmit to other species, such as exotic ruminants, cats, macaques, humans, sheep, and goats, without any obvious alterations of the molecular phenotype (3,4). Our study provides evidence that the molecular phenotype of classical BSE also may shift upon genuine interspecies transmission. Attempts to discriminate BSE from other prion diseases in humans and animals often rely at fi rst on the analysis of the PrPres signature in WB. Consequently, the situation described in our study complicates the interpretation of such disease surveillance data to assess public health risks for animal TSEs. Whether this applies to other TSEs and species remains to be addressed.<br /><br />Figure. Molecular signature of bovine spongiform encephalopathy (BSE) in pigs. A) Comparative Western immunoblot analysis of the proteinase K–resistant core fragment (PrPres) of the pathologic prion protein in BSE in cattle and in an experimentally BSE-infected pig using the monoclonal antibody 6H4 (Prionics, Schlieren, Switzerland). B) Average relative intensities of the diglycosylated (black bars), monoglycosylated (gray bars), and unglycosylated (white bars) PrPres moieties as determined by the Quantity One software package (Bio-Rad, Rheinach, Switzerland). Data are based on 4 independent runs, and error bars indicate SD. Note the different extent of PrPres glycosylation in bovine and porcine BSE. By contrast, the molecular masses of the unglycosylated PrPres were similar and scored 18.89 kDa (SD ± 0.28 kDa) and 18.90 kDa (SD ± 0.42 kDa) in bovine and porcine BSE, respectively. Molecular masses of the standards are indicated on the left in panel A.<br /><br />Emerging Infectious Diseases • www.cdc.gov/eid • Vol. 16, No. 1, January 2010<br /><br /><a href="http://www.cdc.gov/eid/content/16/1/pdfs/164.pdf">http://www.cdc.gov/eid/content/16/1/pdfs/164.pdf</a><br /><br /><br />Torsten Seuberlich and Andreas Zurbriggen Author affi liation: University of Berne, Berne, Switzerland DOI: 10.3201/eid1601.091104<br /><br />References<br /><br />1. Espinosa JC, Herva ME, Andreoletti O, Padilla D, Lacroux C, Cassard H, et al. Transgenic mice expressing porcine prion protein resistant to classical scrapie but susceptible to sheep bovine spongiform encephalopathy and atypical scrapie. Emerg Infect Dis. 2009;15:1214–21. DOI: 10.3201/eid1508.081218<br /><br />2. Wells GA, Hawkins SA, Austin AR, Ryder SJ, Done SH, Green RB, et al. Studies of the transmissibility of the agent of bovine spongiform encephalopathy to pigs. J Gen Virol. 2003;84:1021–31.<br /><br />3. Collinge J, Sidle KC, Meads J, Ironside J, Hill AF. Molecular analysis of prion strain variation and the aetiology of ‘new variant’ CJD. Nature. 1996;383:685–90.<br /><br />4. Hill AF, Desbruslais M, Joiner S, Sidle KC, Gowland I, Collinge J, et al. The same prion strain causes vCJD and BSE. Nature. 1997;389:448–50.<br /><br />Address for correspondence: Torsten Seuberlich, NeuroCentre, Reference Laboratory for TSE in Animals, University of Berne, Bremgartenstrasse 109a, CH-3001 Berne, Switzerland; email: torsten.seuberlich@itn.unibe.ch<br /><br /><a href="http://www.cdc.gov/eid/content/16/1/pdfs/164.pdf">http://www.cdc.gov/eid/content/16/1/pdfs/164.pdf</a><br /><br /><br />Thursday, October 15, 2009 Transmissibility studies of vacuolar changes in the rostral colliculus of pigs Research article Open Access T<br /><br />Transmissibility studies of vacuolar changes in the rostral colliculus of pigs<br /><br />Timm Konold*1,2, John Spiropoulos1, Melanie J Chaplin3, Leigh Thorne3, Yvonne I Spencer1, Gerald AH Wells1 and Steve AC Hawkins1 Address: 1Department of Pathology, Veterinary Laboratories Agency Weybridge, Woodham Lane, Addlestone, UK, 2Royal Veterinary College, Infection and Immunity Research Group, North Mymms, Hatfield, UK and 3Department of Molecular Pathogenesis and Genetics, Veterinary Laboratories Agency Weybridge, Woodham Lane, Addlestone, UK Email: Timm Konold* - t.konold@vla.defra.gsi.gov.uk; John Spiropoulos - j.spiropoulos@vla.defra.gsi.gov.uk; Melanie J Chaplin - m.j.chaplin@vla.defra.gsi.gov.uk; Leigh Thorne - l.thorne@vla.defra.gsi.gov.uk; Yvonne I Spencer - y.i.spencer@vla.defra.gsi.gov.uk; Gerald AH Wells - g.a.h.wells@vla.defra.gsi.gov.uk; Steve AC Hawkins - s.a.c.hawkins@vla.defra.gsi.gov.uk * Corresponding author<br /><br />Abstract Background:<br /><br />Histopathological examinations of brains from healthy pigs have revealed localised vacuolar changes, predominantly in the rostral colliculus, that are similar to the neuropil vacuolation featured in the transmissible spongiform encephalopathies and have been described in pigs challenged parenterally with the agent causing bovine spongiform encephalopathy (BSE). Feedstuff containing BSE-contaminated meat and bone meal (MBM) may have been fed to pigs prior to the ban of mammalian MBM in feed of farmed livestock in the United Kingdom in 1996, but there is no evidence of the natural occurrence of a transmissible spongiform encephalopathy (TSE) in the domestic pig. Furthermore, experimental transmission of BSE to pigs by the oral route has been unsuccessful. A study was conducted to investigate whether the localised vacuolar changes in the porcine brain were associated with a transmissible aetiology and therefore biologically significant. Two groups of ten pigs were inoculated parenterally with vacuolated rostral colliculus from healthy pigs either born before 1996 or born after 1996. Controls included ten pigs similarly inoculated with rostral colliculus from New Zealand-derived pigs and nine pigs inoculated with a bovine BSE brain homogenate. Results: None of the pigs inoculated with rostral colliculus developed a TSE-like neurological disease up to five years post inoculation when the study was terminated, and disease-associated prion protein, PrPd, was not detected in the brains of these pigs. By contrast, eight of nine BSE-inoculated pigs developed neurological signs, two of which had detectable PrPd by postmortem tests. No significant histopathological changes were detected to account for the clinical signs in the PrPd-negative, BSE-inoculated pigs. Conclusion: The findings in this study suggest that vacuolation in the porcine rostral colliculus is not caused by a transmissible agent and is probably a clinically insignificant change. The presence of neurological signs in pigs inoculated with BSE without detectable PrPd raises the possibility that the BSE agent may produce a prion disease in pigs that remains undetected by the current postmortem tests.<br /><br />SNIP...SEE FULL TEXT ;<br /><br /><a href="http://madporcinedisease.blogspot.com/2009/10/transmissibility-studies-of-vacuolar.html">http://madporcinedisease.blogspot.com/2009/10/transmissibility-studies-of-vacuolar.html</a><br /><br /><br />SNIP...SEE FULL TEXT ;<br /><br />7 OF 10 LITTLE PIGGIES WENT ON TO DEVELOP BSE;<br /><br />1: J Comp Pathol. 2000 Feb-Apr; 122(2-3): 131-43. Related Articles,<br /><br />Links<br /><br />Click here to read<br /><br />The neuropathology of experimental bovine spongiform encephalopathy in the pig.<br /><br />Ryder SJ, Hawkins SA, Dawson M, Wells GA.<br /><br />Veterinary Laboratories Agency Weybridge, Woodham Lane, New Haw, Addlestone, Surrey, KT15 3NB, UK.<br /><br />In an experimental study of the transmissibility of BSE to the pig, seven of 10 pigs, infected at 1-2 weeks of age by multiple-route parenteral inoculation with a homogenate of bovine brain from natural BSE cases developed lesions typical of spongiform encephalopathy. The lesions consisted principally of severe neuropil vacuolation affecting most areas of the brain, but mainly the forebrain. In addition, some vacuolar change was identified in the rostral colliculi and hypothalamic areas of normal control pigs. PrP accumulations were detected immunocytochemically in the brains of BSE-infected animals. PrP accumulation was sparse in many areas and its density was not obviously related to the degree of vacuolation. The patterns of PrP immunolabelling in control pigs differed strikingly from those in the infected animals.<br /><br />PMID: 10684682 [PubMed - indexed for MEDLINE]<br /><br /><a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?holding=npg&cmd=Retrieve&db=PubMed&list_uids=10684682&dopt=Abstract">http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?holding=npg&cmd=Retrieve&db=PubMed&list_uids=10684682&dopt=Abstract</a><br /><br /><br /><br />IN CONFIENCE<br /><br />EXPERIMENTAL PORCINE SPONGIFORM ENCEPHALOPATHY<br /><br />1. CMO should be aware that a pig inoculated experimentally (ic, iv, and ip) with BSE brain suspension has after 15 months developed an illness, now confirmed as a spongiform encephalopathy. This is the first ever description of such a disease in a pig, although it seems there ar no previous attempts at experimental inoculation with animal material. The Southwood group had thought igs would not be susceptible. Most pigs are slaughtered when a few weeks old but there have been no reports of relevant neurological illness in breeding sows or other elderly pigs. ...see full text ;<br /><br /><a href="http://web.archive.org/web/20040302031004/www.bseinquiry.gov.uk/files/yb/1990/08/23001001.pdf">http://web.archive.org/web/20040302031004/www.bseinquiry.gov.uk/files/yb/1990/08/23001001.pdf</a><br /><br /><br /><br />IN CONFIDENCE<br /><br />So it is plausible pigs could be preclinically affected with BSE but since so few are allowed to reach adulthood this has not been recognised through clinical disease. ...<br /><br /><a href="http://web.archive.org/web/20040904150118/www.bseinquiry.gov.uk/files/yb/1990/08/23002001.pdf">http://web.archive.org/web/20040904150118/www.bseinquiry.gov.uk/files/yb/1990/08/23002001.pdf</a><br /><br /><br /><br />CONFIDENTIAL<br /><br />EXPERIMENTAL PORCINE SPONGIFORM ENCEPHALOPATHY<br /><br />While this clearly is a cause for concern we should not jump to the conclusion that this means that pigs will necessarily be infected by bone and meat meal fed by the oral route as is the case with cattle. ...<br /><br /><a href="http://web.archive.org/web/20031026000118/www.bseinquiry.gov.uk/files/yb/1990/08/23004001.pdf">http://web.archive.org/web/20031026000118/www.bseinquiry.gov.uk/files/yb/1990/08/23004001.pdf</a><br /><br /><br /><br />we cannot rule out the possibility that unrecognised subclinical spongiform encephalopathy could be present in British pigs though there is no evidence for this: only with parenteral/implantable pharmaceuticals/devices is the theoretical risk to humans of sufficient concern to consider any action.<br /><br /><a href="http://web.archive.org/web/20030822031154/www.bseinquiry.gov.uk/files/yb/1990/09/10007001.pdf">http://web.archive.org/web/20030822031154/www.bseinquiry.gov.uk/files/yb/1990/09/10007001.pdf</a><br /><br /><br /><br />May I, at the outset, reiterate that we should avoid dissemination of papers relating to this experimental finding to prevent premature release of the information. ...<br /><br /><a href="http://web.archive.org/web/20030822052332/www.bseinquiry.gov.uk/files/yb/1990/09/11005001.pdf">http://web.archive.org/web/20030822052332/www.bseinquiry.gov.uk/files/yb/1990/09/11005001.pdf</a><br /><br /><br /><br />3. It is particularly important that this information is not passed outside the Department, until Ministers have decided how they wish it to be handled. ...<br /><br /><a href="http://web.archive.org/web/20030822052438/www.bseinquiry.gov.uk/files/yb/1990/09/12002001.pdf">http://web.archive.org/web/20030822052438/www.bseinquiry.gov.uk/files/yb/1990/09/12002001.pdf</a><br /><br /><br /><br />But it would be easier for us if pharmaceuticals/devices are not directly mentioned at all. ...<br /><br /><a href="http://web.archive.org/web/20030518170213/www.bseinquiry.gov.uk/files/yb/1990/09/13004001.pdf">http://web.archive.org/web/20030518170213/www.bseinquiry.gov.uk/files/yb/1990/09/13004001.pdf</a><br /><br /><br /><br />Our records show that while some use is made of porcine materials in medicinal products, the only products which would appear to be in a hypothetically ''higher risk'' area are the adrenocorticotrophic hormone for which the source material comes from outside the United Kingdom, namely America China Sweden France and Germany. The products are manufactured by Ferring and Armour. A further product, ''Zenoderm Corium implant'' manufactured by Ethicon, makes use of porcine skin - which is not considered to be a ''high risk'' tissue, but one of its uses is described in the data sheet as ''in dural replacement''. This product is sourced from the United Kingdom.....<br /><br /><a href="http://web.archive.org/web/20030822054419/www.bseinquiry.gov.uk/files/yb/1990/09/21009001.pdf">http://web.archive.org/web/20030822054419/www.bseinquiry.gov.uk/files/yb/1990/09/21009001.pdf</a><br /><br /><br /><br />BSE TO PIGS NEWS RELEASE<br /><br /><a href="http://web.archive.org/web/20030822162313/www.bseinquiry.gov.uk/files/yb/1990/09/24001001.pdf">http://web.archive.org/web/20030822162313/www.bseinquiry.gov.uk/files/yb/1990/09/24001001.pdf</a><br /><br /><br /><br />CONFIDENTIAL<br /><br />BSE: PRESS PRESENTATION<br /><br /><a href="http://web.archive.org/web/20030822160958/www.bseinquiry.gov.uk/files/yb/1990/09/20003001.pdf">http://web.archive.org/web/20030822160958/www.bseinquiry.gov.uk/files/yb/1990/09/20003001.pdf</a><br /><br /><br /><br /><a href="http://web.archive.org/web/20040623191707/www.bseinquiry.gov.uk/files/yb/1990/09/24013001.pdf">http://web.archive.org/web/20040623191707/www.bseinquiry.gov.uk/files/yb/1990/09/24013001.pdf</a><br /><br /><br /><br /><a href="http://web.archive.org/web/20030820195733/http://www.bseinquiry.gov.uk/files/yb/1990/09/20010001.pdf">http://web.archive.org/web/20030820195733/http://www.bseinquiry.gov.uk/files/yb/1990/09/20010001.pdf</a><br /><br /><br /><br /><a href="http://web.archive.org/web/20030820195733/http://www.bseinquiry.gov.uk/files/yb/1990/09/25013001.pdf">http://web.archive.org/web/20030820195733/http://www.bseinquiry.gov.uk/files/yb/1990/09/25013001.pdf</a><br /><br /><br /><br /><a href="http://web.archive.org/web/20030820195733/http://www.bseinquiry.gov.uk/files/yb/1990/09/25015001.pdf">http://web.archive.org/web/20030820195733/http://www.bseinquiry.gov.uk/files/yb/1990/09/25015001.pdf</a><br /><br /><br /><br />INDUSTRY RESPONSE TYPICAL<br /><br /><a href="http://web.archive.org/web/20030822055917/www.bseinquiry.gov.uk/files/yb/1990/09/25007001.pdf">http://web.archive.org/web/20030822055917/www.bseinquiry.gov.uk/files/yb/1990/09/25007001.pdf</a><br /><br /><br /><br />DEFENSIVE BRIEFING<br /><br /><a href="http://web.archive.org/web/20030820195733/http://www.bseinquiry.gov.uk/files/yb/1990/09/25016001.pdf">http://web.archive.org/web/20030820195733/http://www.bseinquiry.gov.uk/files/yb/1990/09/25016001.pdf</a><br /><br /><br /><br />CONFIDENTIAL<br /><br />pigs & pharmaceuticals<br /><br /><a href="http://web.archive.org/web/20010305223234/www.bseinquiry.gov.uk/files/yb/1990/09/10007001.pdf">http://web.archive.org/web/20010305223234/www.bseinquiry.gov.uk/files/yb/1990/09/10007001.pdf</a><br /><br /><br /><br /><a href="http://web.archive.org/web/20010305223234/www.bseinquiry.gov.uk/files/yb/1990/08/23002001.pdf">http://web.archive.org/web/20010305223234/www.bseinquiry.gov.uk/files/yb/1990/08/23002001.pdf</a><br /><br /><br /><br /><a href="http://web.archive.org/web/20010305223234/www.bseinquiry.gov.uk/files/yb/1990/08/23004001.pdf">http://web.archive.org/web/20010305223234/www.bseinquiry.gov.uk/files/yb/1990/08/23004001.pdf</a><br /><br /><br /><a href="http://web.archive.org/web/20010305223234/www.bseinquiry.gov.uk/files/yb/1990/08/29003001.pdf">http://web.archive.org/web/20010305223234/www.bseinquiry.gov.uk/files/yb/1990/08/29003001.pdf</a><br /><br /><br /><br />COMMERCIAL IN CONFIDENCE COMMITTEE ON SAFETY OF MEDICINE NOT FOR PUBLICATION BOVINE SPONGIFORM ENCEPHALOPATHY WORKING GROUP<br /><br />There are only two products using porcine brain and these use corticotrophin BP, made from porcine pituitary, source from outside the UK.............<br /><br /><a href="http://web.archive.org/web/20040622220349/www.bseinquiry.gov.uk/files/yb/1990/10/31003001.pdf">http://web.archive.org/web/20040622220349/www.bseinquiry.gov.uk/files/yb/1990/10/31003001.pdf</a><br /><br /><br />SEE FULL TEXT ;<br /><br /><a href="http://madporcinedisease.blogspot.com/">http://madporcinedisease.blogspot.com/</a><br /><br /><br /><br />TSSTerry S. Singeltary Sr.http://www.blogger.com/profile/06986622967539963260noreply@blogger.com0tag:blogger.com,1999:blog-6404950019984350027.post-44801144783733103322009-10-15T09:25:00.000-07:002009-12-21T19:18:19.243-08:00Transmissibility studies of vacuolar changes in the rostral colliculus of pigsResearch article Open Access T<br /><br />Transmissibility studies of vacuolar changes in the rostral colliculus of pigs<br /><br />Timm Konold*1,2, John Spiropoulos1, Melanie J Chaplin3, Leigh Thorne3, Yvonne I Spencer1, Gerald AH Wells1 and Steve AC Hawkins1 Address: 1Department of Pathology, Veterinary Laboratories Agency Weybridge, Woodham Lane, Addlestone, UK, 2Royal Veterinary College, Infection and Immunity Research Group, North Mymms, Hatfield, UK and 3Department of Molecular Pathogenesis and Genetics, Veterinary Laboratories Agency Weybridge, Woodham Lane, Addlestone, UK Email: Timm Konold* - t.konold@vla.defra.gsi.gov.uk; John Spiropoulos - j.spiropoulos@vla.defra.gsi.gov.uk; Melanie J Chaplin - m.j.chaplin@vla.defra.gsi.gov.uk; Leigh Thorne - l.thorne@vla.defra.gsi.gov.uk; Yvonne I Spencer - y.i.spencer@vla.defra.gsi.gov.uk; Gerald AH Wells - g.a.h.wells@vla.defra.gsi.gov.uk; Steve AC Hawkins - s.a.c.hawkins@vla.defra.gsi.gov.uk * Corresponding author<br /><br />Abstract Background:<br /><br />Histopathological examinations of brains from healthy pigs have revealed localised vacuolar changes, predominantly in the rostral colliculus, that are similar to the neuropil vacuolation featured in the transmissible spongiform encephalopathies and have been described in pigs challenged parenterally with the agent causing bovine spongiform encephalopathy (BSE). Feedstuff containing BSE-contaminated meat and bone meal (MBM) may have been fed to pigs prior to the ban of mammalian MBM in feed of farmed livestock in the United Kingdom in 1996, but there is no evidence of the natural occurrence of a transmissible spongiform encephalopathy (TSE) in the domestic pig. Furthermore, experimental transmission of BSE to pigs by the oral route has been unsuccessful. A study was conducted to investigate whether the localised vacuolar changes in the porcine brain were associated with a transmissible aetiology and therefore biologically significant. Two groups of ten pigs were inoculated parenterally with vacuolated rostral colliculus from healthy pigs either born before 1996 or born after 1996. Controls included ten pigs similarly inoculated with rostral colliculus from New Zealand-derived pigs and nine pigs inoculated with a bovine BSE brain homogenate. Results: None of the pigs inoculated with rostral colliculus developed a TSE-like neurological disease up to five years post inoculation when the study was terminated, and disease-associated prion protein, PrPd, was not detected in the brains of these pigs. By contrast, eight of nine BSE-inoculated pigs developed neurological signs, two of which had detectable PrPd by postmortem tests. No significant histopathological changes were detected to account for the clinical signs in the PrPd-negative, BSE-inoculated pigs. Conclusion: The findings in this study suggest that vacuolation in the porcine rostral colliculus is not caused by a transmissible agent and is probably a clinically insignificant change. The presence of neurological signs in pigs inoculated with BSE without detectable PrPd raises the possibility that the BSE agent may produce a prion disease in pigs that remains undetected by the current postmortem tests.<br /><br /><br />SNIP...<br /><br /><br />Conclusion The findings suggest that vacuolation in the rostral colliculus is a common feature of porcine brains without causing evident clinical signs and does not represent a localised form of a transmissible spongiform encephalopathy. The presence of neurological signs in pigs challenged with BSE in the absence of detectable disease-associated prion protein or other visible pathological changes raises the possibility that the BSE agent may cause a chronic disease that remains undetected by current prion disease phenotypic definitions and postmortem tests.<br /><br /><br /><a href="http://www.biomedcentral.com/content/pdf/1746-6148-5-35.pdf">http://www.biomedcentral.com/content/pdf/1746-6148-5-35.pdf</a><br /><br /><br /><br /><br /><br />CONFIDENTIAL TRANSMISSION (Day 4)<br /><br />6.1 BSE to pigs<br />SE1802/SE1816 - Transmissibility of BSE to pigs by injection with brain homogenate;<br />SE1803/SE1817 - Transmissibility of BSE to pigs by oral exposure with brain homogenate.<br /><br />6.1.3 The possibility that pigs could be recycling the BSE agent through<br />rendered material, which was then passed back to cattle via the<br />spreading of pig manure, was discussed. However, it was agreed that no<br />action was required (see para. 2.1.3).<br /><br />6.2 BSE to chickens<br />SE1805/SE1806 - Transmissibility of BSE to domestic fowl<br /><br />6.2.1 Material from a number of tissues including spleen in the<br />experimental chicken should be sub-passaged through further birds and<br />mice: by the intracerebral routes in birds and the intracerebral route<br />in mice. CSG would ask CVL to prepare a proposal.<br /><br />6.3 Scrapie to pigs SE1813/SE1822 - Transmissibility of scrapie to pigs by oral exposure to brain homogenate.<br /><br />6.3.1 SE1822 will replace SE1813. No amendment of this project was required.<br /><br />6.4 BSE to sheep<br />SE1402/SE1418 - Transmission of BSE and natural scrapie in sheep and goats by intracerebral and oral routes<br /><br />6.5 BSE to cattle via exposure to placenta<br /><br />95/5.11/1.19<br /><br /><br /><br /><br /><a href="http://www.mad-cow.org/00/aug00_late_news.html#ggg">http://www.mad-cow.org/00/aug00_late_news.html#ggg</a><br /><br /><br /><br /><br />7 OF 10 LITTLE PIGGIES WENT ON TO DEVELOP BSE;<br /><br />1: J Comp Pathol. 2000 Feb-Apr; 122(2-3): 131-43. Related Articles,<br /><br />Links<br /><br />Click here to read<br /><br />The neuropathology of experimental bovine spongiform encephalopathy in the pig.<br /><br />Ryder SJ, Hawkins SA, Dawson M, Wells GA.<br /><br />Veterinary Laboratories Agency Weybridge, Woodham Lane, New Haw, Addlestone, Surrey, KT15 3NB, UK.<br /><br />In an experimental study of the transmissibility of BSE to the pig, seven of 10 pigs, infected at 1-2 weeks of age by multiple-route parenteral inoculation with a homogenate of bovine brain from natural BSE cases developed lesions typical of spongiform encephalopathy. The lesions consisted principally of severe neuropil vacuolation affecting most areas of the brain, but mainly the forebrain. In addition, some vacuolar change was identified in the rostral colliculi and hypothalamic areas of normal control pigs. PrP accumulations were detected immunocytochemically in the brains of BSE-infected animals. PrP accumulation was sparse in many areas and its density was not obviously related to the degree of vacuolation. The patterns of PrP immunolabelling in control pigs differed strikingly from those in the infected animals.<br /><br />PMID: 10684682 [PubMed - indexed for MEDLINE]<br /><br /><br /><br /><br /><a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?holding=npg&cmd=Retrieve&db=PubMed&list_uids=10684682&dopt=Abstract">http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?holding=npg&cmd=Retrieve&db=PubMed&list_uids=10684682&dopt=Abstract</a><br /><br /><br /><br /><br />confindential<br /><br /><br />pigs & pharmaceuticals<br /><br /><br /><br /><br /><a href="http://web.archive.org/web/20010305223234/www.bseinquiry.gov.uk/files/yb/1990/09/10007001.pdf">http://web.archive.org/web/20010305223234/www.bseinquiry.gov.uk/files/yb/1990/09/10007001.pdf</a><br /><br /><br /><br /><br /><a href="http://web.archive.org/web/20010305223234/www.bseinquiry.gov.uk/files/yb/1990/08/23002001.pdf">http://web.archive.org/web/20010305223234/www.bseinquiry.gov.uk/files/yb/1990/08/23002001.pdf</a><br /><br /><br /><br /><br /><br /><a href="http://web.archive.org/web/20010305223234/www.bseinquiry.gov.uk/files/yb/1990/08/23004001.pdf">http://web.archive.org/web/20010305223234/www.bseinquiry.gov.uk/files/yb/1990/08/23004001.pdf</a><br /><br /><br /><br /><br /><a href="http://web.archive.org/web/20010305223234/www.bseinquiry.gov.uk/files/yb/1990/08/29003001.pdf">http://web.archive.org/web/20010305223234/www.bseinquiry.gov.uk/files/yb/1990/08/29003001.pdf</a><br /><br /><br /><br /><br />SEE FULL TEXT ;<br /><br /><br /><a href="http://chronic-wasting-disease.blogspot.com/2009/03/chronic-wasting-disease-prions-in-elk.html">http://chronic-wasting-disease.blogspot.com/2009/03/chronic-wasting-disease-prions-in-elk.html</a><br /><br /><br /><br /><br /><br /><br />The case for mad pigs in the US<br /><br />From the Consumer Policy Institute and Consumers Union: March 24, 1997<br /><br />Stephen F. Sundlof, D.V.M., Ph.D<br />Center for Veterinary Medicine<br />Food and Drug Administration<br />7500 Standish Place, Room 482, HFV 1<br />RockvLIle, MD 20855<br />Dear Dr. Sundlof:<br /><br />We are writing to you to submit information that has recently come to our attention which suggests that a TSE like disease (transmissible spongiform encephalopathy) might exist in pigs in the U.S. We believe this new informantion calls for intensive research and makes it urgent to ban the use of all mammalian proteins, including swine, in the feed of all food animals, until better answers are found.<br /><br />The evidence for the potential PSE (porcine spongiform encephalopathy ) is as follows. In 1979, an FSQS veternarian, Dr. Masuo Doi, noticed some unusual central nervous system (CNS) symptoms in young (about 6 months old) hogs coming into a slaughter plant In Albany, New York. Since the plant received hogs from a wide variety of sources (New York, Canada, Indiana, Illinois, Ohio, and other Midwestern states) and was not a plant used to dealing with diseased animals, Dr. Doi thought that the problem might be affecting hogs slaughtered nationwide. So, he decided to conduct a detailed study on central nervous system (CNS) symptoms/disease in young hogs coming into that slaughter plant. The study ran for 15 months (January, 1979 to March, 1980) and consisted of extended observations of the behavior of animals with suspected CNS symptoms at the plant, followed by pathological, histopatholpgical, and microbiological work on tissues from various organs of particular animals after slaughter.<br /><br />For his behavioral observational work, Dr. Doi extended the usual two day observation period to three to four days, during which he took careful notes on the animals' behavior and other vital signs. During the 15 month period of the study, some 106 animals exhibiting CNS symptoms were retained during antemortem inspection.<br /><br />A 1980 paper that summarized Dr. Doi's findings on the clinical symptoms and incidence of the 'disease," contained descriptions of these symptoms that sound remarkably similar to the symptoms noted for bovine spongiform encephalopathy (BSE):<br /><br />"Excitable or nervous temperament to external stimuli such as touch to the skin, handling and menacing approach to the animals is a common characteristic sign among swine affected with the disease.... In the advanced stage of the disease, manifestation of neurological signs are evidenced in the form of general ataxia . . . Many animals have been found to be "downers' at first observation; if the hindquarters of these downers are raised they may be able to walk one or two steps and then fall to the ground" (Doi et al., 1980: 2, 4).<br />Indeed, a table of symptoms includes, for the early stage: "excitability and nervousness (squealing, smacking of lips, grinding of teath, chewing, gnawing ant foaming at mouth); stiffness of limbs . . . 'tic'; weakness of hindquarters; focal tremors of skeletal muscles"; and for the advanced stage: depression; ataxia; crossing over of limbs . . . kneeling posture . . . crawling". In addition to his clinical observations, Dr. Doi also made an 8 mm film of thirteen of the affected animals; film of two of the pigs was shown at the MPI National Pathology Meeting in Seattle, Washington on flay 20, 1979.<br /><br />Dr. Doi sent tissue samples from suspect cases to the USDA's Eastern Laboratory in Athens, GA for pathological, histopathogical and microbiological work. Known infectious diseases were ruled out. As Dr. Doi points out, "Histopathological studies of tissue collected from the brain and spinal cord of these animals in the early stage of the disease show congestion, hemorrhage and neuronal degeneration. All animals in the advanced stage of the disease have been confined to have Encephalitis or Meningitis by MPI laboratory" (Doi et al., 1980: 5). Eventually some 60 animals were confirmed by the MPI Laboratory to have encephalitis or meningitis, with no ldentifiable cause. As pointed out in a paper presented at the 1979 MPI National Pathology Meetings,<br /><br /><br />"Since January, a number of hogs in this establishment have been found, in antemortem, to show what appears to be CNS. Sets of tissue samples were sent to the laboratory for examination, various tests were done which include histological study (E H stain), fluorescence antibody technique, virus neutralization and viral and bacteriological isolation. Differential diagnosis was also done to exclude vitamin B deficiency, post vaccination reaction, chlorinated hydrocarbon, arthritis, and transport stress" (Doi et al., 1979).<br />The brains of the 60 animals were examined. The brain of one of these pigs, on histopathological analysis, exhibited signs reminiscent of a TSE. This histopathological work was performed by Dr. Karl Langheinrich, Pathologist-In-Charge at USDA's Eastern Laboratory in Athens, Georgia. According to the USDA FSQS laboratory report, dated early November, 1979, Dr. Langheinrich noted:<br /><br /><br />"Microscopic examination of the barrow tissues revealed a encephalopathy and diffuse gliosis characterized by vacuolated neurons, loss of neurons and gliosis in a confined region (nucleus) of the brain stem (anterior ventral midbrain). Only an empty sometimes divided vacuole was present instead of the normal morphology of a nerve cell. Occasionally a shriveled neuron was seen. According to . . . Pathology of Domestic Animals, . . . 'The degeneration of neurons, the reactivity of the glia .... are the classical hallmarks of viral infection of the central nervous system' .... Scrapie of sheep, and encephalopathy of mink, according to the literature, all produce focal vacuolation of the neurons similar to the kind as described for this pig. I was unable to locate any lead as to the cause of this interesting phenomenon in other species including swine'' (Langheinrich, 1979).<br />Indeed, Dr. Langheinrich's main diagnosis was, " Encephalopathy and diffuse gliosis of undetermined etiology." Portions of the brain were sent for microbiological testing to a neurologist at the University of Georgia, where they came up negative for pseudo-rabies. The brain was unique enough that USDA scientists, such as Dr. Langheinrich and Or. Dot, mentioned it to student and scientific colleagues over the years.<br /><br />In 1979-1980, BSE was completely unknown. However, both the behavior of the pigs, as well as the histopathology on at least one pig, both showed sign consistent with a porcine TSE. This raises particular concern became the affected animal was only 6 months old; in an animal this young, one would rust expect to see any physical signs of TSE in the brain. Histopathology of TSEs can be very variable, so that spongiform appearance (i.e. vacuolated neurons) are not always present. Behavioral changes can be seen in TSE-infected animals before any changes in brain morphology are visible. Dr. Clarence Gibbs, in testimony before a Congressional hearing on the TSE issue on January 29, 1997 made just this point:<br /><br />''In the mid-1960s, we demonstrated with our French and English collaborators that during the early incubation of the TSEs, when the virus titer in the brain was very low, there were already marked functional changes, even though no pathology was yet detectable, even ultrastructurally. A month or hero later, polynucleation of neurons appeared in spider monkeys, incubating kuru, and somewhat later, microvacuolation and membrane changes visible only by electron microscopy. This preceded the pest appearance of astrogliosis and spongiform change. It was only much later that the classical scrapie TSE pathology appeared with virus titers in brain of 10 -5 or higher" (Gibbs, 1997; pg. 4).<br />Given that TSEs can cause behavioral changes in infected animals before any physical changes in the brain can be seen, that the manifestation of TSE in the brain can be quite variable, and that changes in brain morphology are not usually seen in 6 month old animals, we are concerned that the brain of one pig actually showed physical evidence consistent with a TSE.<br /><br />Following the announcement In March, 1996 of ten cases of new variant CJD (Creutzfeldt-Jakob Disease) in the United Kingdom and their possible connection to BSE, Drs. Doi, Langheinrich and others urged reinvestigation of this case.<br /><br />In August, 1996, the USDA sent five slides, one of which was a histopathology slide, to Dr. Janice Miller of USDA's Agricultural Research Servicer . Dr. Miller stained four of the slides for prion protein (she didn't stain the H&E slide). Dr. Miller told Consumers Union that Dr. Patrick McCaskey, USDA/FSIS, in charge of the Research Center at Athens, GA, called her, told her that he had five slides that all showed "problems" and asked her to stain four of them. The H&E slide, which clearly show vacuoles in the neurons (one sign of TSE), wasn't stained because to stain for PrP entails removing the slide cover, baking the slide to destain it and then restaining it for PrP; they didn't want to risk destroying the H&E slide.<br /><br />Dr. Doi had kept frozen samples of the brain and spinal chord of the suspect PSE pig in case the Eastern lab wanted more material for analysis. Unfortunately, these samples were discarded when the packing plant in Albany, NY closed in 1991. It appears that the brain material sent to the Univcrsity of Georgia may have been discarded. [pers com.. Dr. Doi 3/13/97]<br /><br />Dr. Miller found that the PrP stained in the four pig slides was found only on the inside of neurons, while a positive control slide from a scrapie sheep showed massive amounts of extraneuronal staining. In a letter summarizing her results (copy attached), she concludes that the PrP stained in this pig was normal: "In the pig sections you will see a small particulate type of staining that is confined to neurons and as I indicated on the phone, I would interpret as normal PrP. It is in marked contrast to the massive amount of extraneuronal staining seen in the scrapie section" (Miller, 1996).<br /><br />Unfortunately, Dr. Miller's finding toes not conclusively rule out a TSE. We are concerned that while British BSE and serapie create a massive amount of extraneuronal staining, there are TSEs where this isn't the case. Three experiments were done in He U.S. -- in Mission, TX (APHIS work), Pullman, Washington (ARS work), and Ames, Iowa (ARS work) -- to see whether sheep scrapie can possibly infect cows. In all the experiments, cattle were inoculated with tissue from scrapie -infected sheep primarily by intra-cranial injection, but in the case of the Texas and Iowa studies also by oral feeding -- to see if cattle were susceptible to scrapie at all. In all three experiments, the majority of cows injected in the brain with scrapie-infected sheep material (usually brains) also developed a fatal spongiform encephalopathy.<br /><br />However, in all three examples, the symptoms of the spongifonn encephalopathy differed from "mad cow" disease ~ England, as did the appearances of slides from their brains. The brain lesions seen in all these animals were more variable than those seen in England. When Dr. Miller did similar staining for PrP from these brains (what she called "bovine scrapie") she only found PrP stains on the inside of the neurons, not the massive extraneuronal staining seen in BSE (Miller, pers. comm., March 7, 1997). Thus, Dr. Miller's finding of PrP stains only inside the neurons in the suspect pigs is not particularly reassuring.<br /><br />In November 1996, USDA sent the single histopathology slide to Dr. William Hadlow, one of the foremost spongiform encephalopathy pathologists in the world. (For unknown reasons, Dr. Hadlow was only sent the one slide; he was not told of the existence of the other slides, nor of Dr. Miller's findings, nor was he told or given the behavioral report from Dr. Doi or the morphology work by Dr. Langheinrich, or shown film of the affected pigs [Dr. Hadlow, pers. com., 3/13/97] From this single slide, Dr. Hadlow found some evidence consistent with TSEs but not enough for a conclusive diagnosis. He noted that the slide contained vacuoles inside neurons, one of the signs of a TSE (Dr. Langheinrich had noted this as well).<br /><br />However, since such vacuoles occasionally occur normally in pigs, he thought that was not something special: "About twelve (12) neurons in the parasympathetic nucleus have unilocular optically empty vacuoles in the perikaryon. This is the site where such vacuolated neurons have been seen in the swine (as well as in cats and sheep) as an incidental finding. So I do not think such cells have any significance in this pig" (Hadlow, 1996). However, he did see evidence, Including changes in astrocytes, that suggested a TSE, but without examining other parts of the brain to look for other evidence of TSE, he couldn't be sure:<br /><br /><br />"I am impressed, though, with what seems to be an increase in the number of astrocytes in the section. Some astrocytes are in clusters, some are enlarged and vesicular. Where they are most numerous, a few rod cells (activated microglia) are seen. These findings suggest some perturbation of the nervous tissue. Although such a global response occurs in the transmissible spongifonn encephalopathies, I do no! know its significance in this case without examining other parts of the brain for changes characteristic of these diseases. Thus, from looking; at this one (1) section of brain, I cannot conclude that the pig was affected with a scrapie-like spongiform encephalopathy" (Hadlow, 1996).<br />In sum, Dr. Hadlow~s letter does not rule out the possibility of a TSE. He says that there is suggestive evidence, but that he would need to look at other slides/sections of the brain, to make a conclusive diagnosis.<br /><br />In our view, the implications of this data are extremely serious. Experiments in the United Kingdom have shown that pigs are susceptible to BSE. Pigs inoculated with BSE develop a TSE (Dawson et al., 1990). Feeding experiments are underway in the UK to see if BSE can be orally transmitted to pigs; as of March, 1997, some 6 years after the start of the experiment, none of the pigs fed BSE brain have come down with a TSE. Unfortunately the design of this experiment severely limits what we will learn from it, and will most likely not tell us conclusively if pigs can get BSE from feed. It turns out that the pigs were not fed BSE brain continuously. Rather, the pigs were only fed BSE brain material on three days, over a three week period (i.e.. one day each week). Following these three doses, the pigs were never fed contaminated material again. The total amount of infective material given to the pigs was therefore quite small. Thus, a negative finding would be hard to interpret and would not mean that BSE is not orally active in pigs.<br /><br />We believe that as a top priority USDA should conduct follow-up studies to look for potential CNS/PSE cases in pigs (we plan to communicate about this to USDA separately). In brief, we feel that the following kinds of studies need to be done:<br /><br />i) TSE pathology experts should examine all the slides from the suspect pig (2709). To our knowledge, at least 12 separate slides exist.<br /><br />ii) Determine if any brain material from the suspect pig (2709) still exists at the Unlverslty of Georgia. If so, this material should be retrieved and used for transmission studies. In particular, suckling pigs should be inoculated with the material and then permitted to live unto they die of a disease or old age, at which point their brains should be examined for physical signs of a TSE as well as for immunchistochemical evidence (i.e. staining looking for the abnormal PrP).<br /><br />iii) Increase antemortem inspection for CNS symptoms at hog facilities. Inspectors should be trained to detect the subtle CNS symptoms seen in the Doi et al. study. At a select number of slaughter facilities, animals exhibiting CNS symptoms should be removed and held for observation until they die, at which time their brains should be examined for evidence of a TSE.<br /><br />iv) Research on CNS symptoms among Me 6,000 or so breeding sows which are permitted to live for 3+ years. Sows exhibiting CNS symptoms should be removed and held for observation until they die, at which time then brains should be exernined for evidence of a TSE.<br /><br />While such work is underway, given the above inforrnabon, we believe that as a precutionary measure the FDA must expand the proposed ruminant plus mink-to-ruminnant feed ban to prevent protein from any material, including hogs, being fed to any food animal.<br /><br />Sincerely,<br /><br />Michael Hansen, Ph.D Research Associate<br /><br />Jean Halloran Director<br /><br />References<br /><br />Dawson, M., Wells, G.A.H., Parker, B.N;J. and A.C Scott. 1990. Primary parental transmission of bovine spongiform encephalopathy to the pig. Veternary Record, pg. 338.<br /><br />Doi, M., Matzner, N.D. and C. Rothaug. 1979. Observation of CNS disease in market hogs at Est. 893 Tobin Packing Co., Inc. Albany, New York. United States Department of Agriculture, Food Safety and Quality.Service, Meat and Poultry Inspection Service. 7pp.<br /><br />Doi, M, Langheinrich, K. and F. Rellosa. 1980. Observations of CNS signs in hogs at Est. 893 Tobin Packing C:o., Inc. Presented by Dr. Lngheinrich at the MPI National Pathology Meeting in Seattle, Washington on July 20, 1979.<br /><br />Gibbs, C. 1997. Statement to the Committee on Governnent Reform and Oversight, Subcommittee on Human Resources and Intergovernmental Relations, U.S. House of Representatives. January 29,1997.<br /><br />Hadlow, WJ. 1996. Letter to Patrick McCaskey, USDA/FSIS/Eastem Lab, dated November 13, 1996.<br /><br />Langheinrich, KA. 1979. USDA/FSQS Laboratory report on specimen 2709. Dated November 8, 1979<br /><br />Miller, J. 1996. Letter to Patrick McCaskey, USDA/ESIS/Eastern Lab, dated September 6, 1996.<br /><br /><br /><br /><br />Dr. Janice Miller, ARS<br /><br /><br /><a href="http://www.mad-cow.org/~tom/mad_pigs.html">http://www.mad-cow.org/~tom/mad_pigs.html</a><br /><br /><br /><br /><br /><br />Subject: EXPERIMENTAL INTRACEREBRAL AND ORAL INOCULATION OF SCRAPIE TO SWINE: PRELIMINARY REPORT<br />Date: February 6, 2006 at 12:33 pm PST<br />Title: EXPERIMENTAL INTRACEREBRAL AND ORAL INOCULATION OF SCRAPIE TO SWINE: PRELIMINARY REPORT<br /><br /><br />Authors<br /><br />Greenlee, Justin<br />Kunkle, Robert - bob<br />Hamir, Amirali<br /><br /><br />Submitted to: American Association Of Veterinary Laboratory Diagnosticians<br />Publication Acceptance Date: November 5, 2005<br />Publication Date: November 5, 2005<br />Citation: Greenlee, J.J., Kunkle, R.A., Hamir, A.N. 2005. Experimental Intracerebral And Oral Inoculation Of Scrapie To Swine: Preliminary Report [abstract]. Proceedings Of The American Association Of Veterinary Laboratory Diagnosticians 48th Annual Conference. P. 38.<br /><br />Technical Abstract: Transmissible spongiform encephalopathies (TSEs, prion diseases) are chronic neurodegenerative diseases that occur in humans, cattle, sheep, goats, cervids, and a number of laboratory animal models. In a laboratory setting, the host range of a given TSE can be tested by inoculating animals with brain tissue from affected animals through various routes including oral and intracranial. There is no evidence of the natural occurrence of any form of TSE in the pig, but pigs have been shown to be susceptible to bovine spongiform encephalopathy (BSE) infection by multiple-route parenteral challenge. However, pigs orally exposed at eight weeks of age to large amounts of brain from cattle clinically affected with BSE did not support infection after seven years of observation. In the United States, feeding of ruminant by-products to ruminants is prohibited, but feeding of ruminant materials to swine and poultry still occurs. The potential for swine to have access to scrapie-contaminated feedstuffs exists, but the potential for swine to serve as a host for replication/accumulation of the agent of scrapie is unknown. The purpose of this study was to perform oral and intracerebral inoculation of the U.S. scrapie agent to determine the potential of swine as a host for the scrapie agent and their clinical susceptibility. This study utilized 26 swine randomly divided into three groups: controls (n=6), oral inoculates (n=8), and intracranial inoculates (n=12). Brain homogenate (10%) derived from scrapie-affected sheep was given by a single intracranial injection of 0.75 ml or by oral inoculation of 15 ml on four consecutive days. Scrapie inoculum was derived from clinically ill sheep inoculated with material derived from 13 sheep in seven source flocks. A sample of this material was also inoculated back into sheep to assure infectivity. Necropsies were planned for six months post inoculation, at approximately the time the pigs were expected to reach market weight. Samples collected were examined microscopically after routine staining (hematoxylin and eosin) and staining by standard immunohistochemical methods for prion protein (PrP**Sc). After approximately six months incubation time, no histologic lesions<br /><br />suggestive of spongiform encephalopathy or immunohistochemical evidence of prion infection were obtained. No evidence of scrapie infection was demonstrated in this short-term study, but positive results after an incubation period of only six months would be uncharacteristic. The only TSE with an incubation of six months or less known at this time is transmissible mink encephalopathy in mink, skunk, or raccoon hosts. However, scrapie in the raccoon model has a two-year incubation period. A replicate of littermate pigs has been inoculated and will be studied after long-term (3-7 years) incubation, and a similar study is underway with pigs inoculated with material derived from elk, mule deer, and whitetail deer affected by chronic wasting disease (CWD).<br /><br /><br /><br />Project Team<br /><br />Kehrli, Marcus<br />Nicholson, Eric<br />Greenlee, Justin<br />Hamir, Amirali<br />Richt, Juergen<br />Kunkle, Robert - Bob<br /><br /><br /><br /><br /><a href="http://www.ars.usda.gov/research/publications/publications.htm?SEQ_NO_115=191555">http://www.ars.usda.gov/research/publications/publications.htm?SEQ_NO_115=191555</a><br /><br /><br /><br /><br />DOI: 10.3201/eid1508.081218<br /><br />Suggested citation for this article: Espinosa J-C, Herva M-E, Andréoletti O, Padilla D, Lacroux C, Cassard H, et al. Transgenic mice expressing porcine prion protein resistant to classical scrapie but susceptible to sheep bovine spongiform encephalopathy and atypical scrapie. Emerg Infect Dis. 2009 Aug; [Epub ahead of print]<br /><br />Transgenic Mice Expressing Porcine Prion Protein Resistant to Classical Scrapie but Susceptible to Sheep Bovine Spongiform Encephalopathy and Atypical Scrapie<br /><br />Juan-Carlos Espinosa,1 María-Eugenia Herva,1 Olivier Andréoletti, Danielle Padilla, Caroline Lacroux, Hervé Cassard, Isabelle Lantier, Joaquin Castilla, and Juan-María Torres<br />Author affiliations: Centro de Investigación en Sanidad Animal, Madrid, Spain (J.-C. Espinosa, M.-E. Herva, D. Padilla, J. Castilla, J.-M. Torres); École Nationale Vétérinaire de Toulouse, Toulouse, France (O. Andréoletti, C. Lacroux, H. Cassard); and Centre Institut National de la Recherche Agronomique de Tours, Nouzilly, France (I. Lantier)<br /><br />1These authors contributed equally to this article.<br /><br />How susceptible pigs are to infection with sheep prions is unknown. We show, through transmission experiments in transgenic mice expressing porcine prion protein (PrP), that the susceptibility of this mouse model to bovine spongiform encephalopathy (BSE) can be enhanced after its passage in ARQ sheep, indicating that the pathogenicity of the BSE agent is modified after passage in sheep. Transgenic mice expressing porcine PrP were, nevertheless, completely resistant to infection with a broad panel of classical scrapie isolates from different sheep PrP genotypes and with different biochemical characteristics. The atypical (Nor98 like) isolate (SC-PS152) was the only scrapie isolate capable of transmission in these mice, although with a marked transmission barrier. Unexpectedly, the atypical scrapie agent appeared to undergo a strain phenotype shift upon transmission to porcine-PrP transgenic mice and acquired new strain properties, suggesting that atypical scrapie agent may exhibit different phenotypes depending on the host cellular PrP or other genetic factors.<br /><br /><br />SNIP...<br /><br /><br />The atypical isolate SC-PS152 was the only scrapie isolate able to infect the Po-PrP mouse model after intracerebral inoculation (Table), albeit with a low efficiency of infection in the first passage (attack rate 16%). These results suggest the potential ability of atypical scrapie prions to infect pigs, although with a strong transmission barrier. Given the increasing number of atypical scrapie cases found in Europe and in North America, the potential ability of atypical scrapie to adapt to the pig becoming more easily transmitted could raise concerns about the potential danger of feeding ruminant meat and bone meal to swine.<br /><br /><br /><br /><br /><a href="http://www.cdc.gov/eid/content/15/8/pdfs/08-1218.pdf">http://www.cdc.gov/eid/content/15/8/pdfs/08-1218.pdf</a><br /><br /><br /><br /><br /><a href="http://nor-98.blogspot.com/2009/07/transgenic-mice-expressing-porcine.html">http://nor-98.blogspot.com/2009/07/transgenic-mice-expressing-porcine.html</a><br /><br /><br /><br /><br />Wednesday, July 1, 2009<br /><br />Nor98 scrapie identified in the United States J Vet Diagn Invest 21:454-463 (2009)<br /><br /><br /><br /><a href="http://nor-98.blogspot.com/2009/07/nor98-scrapie-identified-in-united.html">http://nor-98.blogspot.com/2009/07/nor98-scrapie-identified-in-united.html</a><br /><br /><br /><br /><br /><br /><br />TSSTerry S. Singeltary Sr.http://www.blogger.com/profile/06986622967539963260noreply@blogger.com0