Tennessee CWD TSE Prion 2019 to 2020 Sample 148 Positive So Far
Tennessee CWD TSE Prion 2019 to 2020 Sample 148 Positive So Far
Tennessee CWD TSE Prion 2019 to 2020 To Date 148 Positive
https://youtu.be/LBgOt8z8mPM?t=1264
T ennessee cwd distribution map
https://youtu.be/LBgOt8z8mPM?t=814
https://www.youtube.com/watch?v=LBgOt8z8mPM&feature=youtu.be&t=512&fbclid=IwAR3P5UymDKfcR7i8ssj9p8RR8nv_ZMdG0F3sgoUMw_WQy2aHCBRYo_AHt8Y
FRIDAY, NOVEMBER 22, 2019
Tennessee CWD TSE Prion Positive Deer Harvested in Shelby County
https://chronic-wasting-disease.blogspot.com/2019/11/tennessee-cwd-tse-prion-positive-deer.html
THURSDAY, OCTOBER 03, 2019
Tennessee Madison County deer sampled within 10 miles of Crockett and Gibson counties has tested positive for CWD, Declared High Risk
https://chronic-wasting-disease.blogspot.com/2019/10/tennessee-madison-county-deer-sampled.html
MONDAY, SEPTEMBER 23, 2019
Tennessee More deer test positive for Chronic Wasting Disease in Tennessee, sharp rise expected
https://chronic-wasting-disease.blogspot.com/2019/09/tennessee-more-deer-test-positive-for.html
MONDAY, JUNE 03, 2019 Tennessee
NEW CWD UNIT HUNTING REGULATIONS ESTABLISHED TO AID IN EFFORTS FOR DISEASE MANAGEMENT
https://chronic-wasting-disease.blogspot.com/2019/06/tennessee-new-cwd-unit-hunting.html
FRIDAY, FEBRUARY 22, 2019
Tennessee Reports 2 More CWD TSE Positives, Total To Date Now At 185 Cases Confirmed
https://chronic-wasting-disease.blogspot.com/2019/02/tennessee-reports-2-more-cwd-tse.html
THURSDAY, FEBRUARY 21, 2019
Tennessee officials concerned after 183 deer test positive for CWD TSE Prion
https://chronic-wasting-disease.blogspot.com/2019/02/tennessee-officials-concerned-after-183.html
MONDAY, FEBRUARY 11, 2019
Tennessee CWD TSE Prion Cases Mount Total To Date 168 cases with more samples pending
https://chronic-wasting-disease.blogspot.com/2019/02/tennessee-cwd-tse-prion-cases-mount.html
SATURDAY, JANUARY 26, 2019
Tennessee Potential Expansion of CWD Zone as 91 CWD Positive To Date
https://chronic-wasting-disease.blogspot.com/2019/01/tennessee-potential-expansion-of-cwd.html
Here is the latest on the cwd tse prion…terry
FRIDAY, NOVEMBER 08, 2019 ***> EFSA Panel on Biological Hazards (BIOHAZ) Update on chronic wasting disease (CWD) III https://chronic-wasting-disease.blogspot.com/2019/11/efsa-panel-on-biological-hazards-biohaz.html WEDNESDAY, NOVEMBER 20, 2019 Sheep Are Susceptible to the Bovine Adapted Transmissible Mink Encephalopathy agent by Intracranial Inoculation and Have Evidence of Infectivity in Lymphoid Tissues ***> ”indicating that sheep inoculated with the bovine TME agent harbor infectivity in their lymph nodes despite a lack of detection with conventional immunoassays.” https://transmissible-mink-encephalopathy.blogspot.com/2019/11/sheep-are-susceptible-to-bovine-adapted.html WEDNESDAY, NOVEMBER 20, 2019 Review: Update on Classical and Atypical Scrapie in Sheep and Goats https://chronic-wasting-disease.blogspot.com/2019/11/review-update-on-classical-and-atypical.html FRIDAY, NOVEMBER 15, 2019 Southwest Wisconsin CWD, Deer and Predator Study https://chronic-wasting-disease.blogspot.com/2019/11/southwest-wisconsin-cwd-deer-and.html THURSDAY, OCTOBER 17, 2019 Europe’s uneven laws threaten scavengers and Spread Transmissible Spongiform Encephalopathy TSE Prion https://chronic-wasting-disease.blogspot.com/2019/10/europes-uneven-laws-threaten-scavengers.html UESDAY, OCTOBER 29, 2019 America BSE 589.2001 FEED REGULATIONS, BSE SURVEILLANCE, BSE TESTING, and CJD TSE Prion https://bovineprp.blogspot.com/2019/10/america-bse-5892001-feed-regulations.html MONDAY, FEBRUARY 25, 2019 ***> MAD DOGS AND ENGLISHMEN BSE, SCRAPIE, CWD, CJD, TSE PRION A REVIEW 2019 https://bseinquiry.blogspot.com/2019/02/mad-dogs-and-englishmen-bse-scrapie-cwd.html ***> cattle, pigs, sheep, cwd, tse, prion, oh my! ***> 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). 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. https://assets.publishing.service.gov.uk/government/uploads/system/uploads/attachment_data/file/733407/DEFRA_QRA_TSE_in_cervids_June2018_v1.pdf http://chronic-wasting-disease.blogspot.com/2012/08/susceptibility-of-cattle-to-agent-of.html cwd scrapie pigs oral routes ***> 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. 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%). ***> 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. https://www.ars.usda.gov/research/publications/publication/?seqNo115=353091 https://www.ars.usda.gov/research/project/?accnNo=432011&fy=2017 https://www.ars.usda.gov/research/publications/publication/?seqNo115=337105 Friday, December 14, 2012 DEFRA U.K. What is the risk of Chronic Wasting Disease CWD being introduced into Great Britain? A Qualitative Risk Assessment October 2012 snip 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: 1) animals from areas declared to be endemic for CWD and/or to be CWD eradication zones and 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. Therefore, in the USA, materials from cervids other than CWD positive animals may be used in animal feed and feed ingredients for non-ruminants. 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. 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. 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. snip 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). snip 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. snip 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. s nip 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 ***> 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; BSE TESTING (failed terribly and proven to be a sham) BSE SURVEILLANCE (failed terribly and proven to be a sham) BSE 589.2001 FEED REGULATIONS (another colossal failure, and proven to be a sham) these are facts folks. trump et al just admitted it with the feed ban. see; FDA Reports on VFD Compliance John Maday August 30, 2019 09:46 AM VFD-Form 007 (640×427) 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. https://www.fda.gov/media/130382/download SUNDAY, SEPTEMBER 1, 2019 ***> FDA Reports on VFD Compliance https://bovineprp.blogspot.com/2019/09/fda-reports-on-vfd-compliance.html TUESDAY, APRIL 18, 2017 *** EXTREME USA FDA PART 589 TSE PRION FEED LOOP HOLE STILL EXIST, AND PRICE OF POKER GOES UP *** http://usdameatexport.blogspot.com/2017/04/extreme-usa-fda-part-589-tse-prion-feed.html MONDAY, MAY 20, 2019 Tracking and clarifying differential traits of classical- and atypical L-type bovine spongiform encephalopathy prions after transmission from cattle to cynomolgus monkeys https://bse-atypical.blogspot.com/2019/05/tracking-and-clarifying-differential.html SUNDAY, APRIL 14, 2019 Estimation of prion infectivity in tissues of cattle infected with atypical BSE by real time-quaking induced conversion assay https://bse-atypical.blogspot.com/2019/04/estimation-of-prion-infectivity-in.html WEDNESDAY, APRIL 24, 2019 USDA Announces Atypical Bovine Spongiform Encephalopathy Detection Aug 29, 2018 A Review of Science 2019 https://bse-atypical.blogspot.com/2019/04/usda-announces-atypical-bovine.html WEDNESDAY, JULY 31, 2019 The agent of transmissible mink encephalopathy passaged in sheep is similar to BSE-L https://transmissible-mink-encephalopathy.blogspot.com/2019/07/the-agent-of-transmissible-mink.html TUESDAY, OCTOBER 29, 2019 USDA Abruptly Halts Animal ID Plan As Experts Testify USA Underprepared For Bioterrorism Threats Such As BSE TSE Prion aka Mad Cow Disease https://animalhealthreportpriontse.blogspot.com/2019/10/usda-abruptly-halts-animal-id-plan-as.html FRIDAY, OCTOBER 11, 2019 CattleTrace to Host First-Ever Industry Symposium https://naiscoolyes.blogspot.com/2019/10/cattletrace-to-host-first-ever-industry.html TUESDAY, MARCH 26, 2019 USDA ARS 2018 USAHA RESOLUTIONS TWO PRONGED APPROACH NEEDED FOR ADVANCING CATTLE TRACEABILITY RESOLUTION NUMBER: 34 APPROVED SOURCE: COMMITTEE ON CATTLE AND BISON https://naiscoolyes.blogspot.com/2019/03/usda-ars-2018-usaha-resolutions-two.html THURSDAY, AUGUST 08, 2019 Raccoons accumulate PrPSc after intracranial inoculation with the agents of chronic wasting disease (CWD) or transmissible mink encephalopathy (TME) but not atypical scrapie https://chronic-wasting-disease.blogspot.com/2019/08/raccoons-accumulate-prpsc-after.html MONDAY, NOVEMBER 04, 2019 Minnesota Legislators legislating, or throwing away your money for battling cwd tse prion, State Rep. Steve Green, R-Fosston more money to deer farms for antibiotics? https://chronic-wasting-disease.blogspot.com/2019/11/legislators-legislating-or-throwing.html
THE tse prion aka mad cow type disease is not your normal pathogen. The TSE prion disease survives ashing to 600 degrees celsius, that’s around 1112 degrees farenheit. you cannot cook the TSE prion disease out of meat. 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. Prion Infected Meat-and-Bone Meal Is Still Infectious after Biodiesel Production as well. the TSE prion agent also survives Simulated Wastewater Treatment Processes. IN fact, you should also know that the TSE Prion agent will survive in the environment for years, if not decades. you can bury it and it will not go away. 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. 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. 1: J Neurol Neurosurg Psychiatry 1994 Jun;57(6):757-8 ***> Transmission of Creutzfeldt-Jakob disease to a chimpanzee by electrodes contaminated during neurosurgery. 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. 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. PMID: 8006664 [PubMed – indexed for MEDLINE] https://www.ncbi.nlm.nih.gov/pubmed/8006664?dopt=Abstract 2018 – 2019 ***> This is very likely to have parallels with control efforts for CWD in cervids. Rapid recontamination of a farm building occurs after attempted prion removal http://dx.doi.org/10.1136/vr.105054 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 Abstract The transmissible spongiform encephalopathy scrapie of sheep/goats and chronic wasting disease of cervids are associated with environmental reservoirs of infectivity. 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. Here, an efficient scrapie decontamination protocol was applied to a farm with high levels of environmental contamination with the scrapie agent. Post-decontamination, no prion material was detected within samples taken from the farm buildings as determined using a sensitive in vitro replication assay (sPMCA). 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. 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. 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. snip… 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. 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. 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. Funding This study was funded by DEFRA within project SE1865. Competing interests None declared. https://veterinaryrecord.bmj.com/content/early/2019/01/02/vr.105054.long Saturday, January 5, 2019 Rapid recontamination of a farm building occurs after attempted prion removal https://prionprp.blogspot.com/2019/01/rapid-recontamination-of-farm-building.html THURSDAY, FEBRUARY 28, 2019 BSE infectivity survives burial for five years with only limited spread https://bovineprp.blogspot.com/2019/02/bse-infectivity-survives-burial-for.html ***> CONGRESSIONAL ABSTRACTS PRION CONFERENCE 2018 P69 Experimental transmission of CWD from white-tailed deer to co-housed reindeer Mitchell G (1), Walther I (1), Staskevicius A (1), Soutyrine A (1), Balachandran A (1) (1) National & OIE Reference Laboratory for Scrapie and CWD, Canadian Food Inspection Agency, Ottawa, Ontario, Canada. 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. 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. 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. https://prion2018.org/ ***> Infectious agent of sheep scrapie may persist in the environment for at least 16 years ***> 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. Gudmundur Georgsson,1 Sigurdur Sigurdarson2 and Paul Brown3 Correspondence Gudmundur Georgsson ggeorgs@hi.is 1 Institute for Experimental Pathology, University of Iceland, Keldur v/vesturlandsveg, IS-112 Reykjavı´k, Iceland 2 Laboratory of the Chief Veterinary Officer, Keldur, Iceland 3 Bethesda, Maryland, USA Received 7 March 2006 Accepted 6 August 2006 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. http://www.microbiologyresearch.org/docserver/fulltext/jgv/87/12/3737.pdf?expires=1540908280&id=id&accname=guest&checksum=ED0572E1E5B272C100A32212A3E3761A TITLE: PATHOLOGICAL FEATURES OF CHRONIC WASTING DISEASE IN REINDEER AND DEMONSTRATION OF HORIZONTAL TRANSMISSION https://www.ars.usda.gov/research/publications/publication/?seqNo115=328261 *** DECEMBER 2016 CDC EMERGING INFECTIOUS DISEASE JOURNAL CWD HORIZONTAL TRANSMISSION http://wwwnc.cdc.gov/eid/article/22/12/16-0635_article SEE; 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; Some unofficial information from a source on the inside looking out – Confidential!!!! 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!!! —end personal email—end…tss http://scrapie-usa.blogspot.com/2018/04/scrapie-transmits-to-pigs-by-oral-route.html 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). http://europa.eu.int/comm/food/fs/sc/ssc/out58_en.pdf Dr. Paul Brown Scrapie Soil Test BSE Inquiry Document https://web.archive.org/web/20090505211734/http://www.bseinquiry.gov.uk/files/sc/Seac07/tab03.pdf THURSDAY, FEBRUARY 28, 2019 BSE infectivity survives burial for five years with only limited spread https://bovineprp.blogspot.com/2019/02/bse-infectivity-survives-burial-for.html Using in vitro Prion replication for high sensitive detection of prions and prionlike proteins and for understanding mechanisms of transmission. Claudio Soto Mitchell Center for Alzheimer’s diseases and related Brain disorders, Department of Neurology, University of Texas Medical School at Houston. 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. ***>>> 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. 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. https://prion2015.files.wordpress.com/2015/05/programguide1.pdf New studies on the heat resistance of hamster-adapted scrapie agent: Threshold survival after ashing at 600°C suggests an inorganic template of replication http://www.pnas.org/content/97/7/3418.full Prion Infected Meat-and-Bone Meal Is Still Infectious after Biodiesel Production http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2493038/ Detection of protease-resistant cervid prion protein in water from a CWD-endemic area https://www.ncbi…nlm.nih.gov/pmc/articles/PMC2802782/pdf/prion0303_0171.pdf A Quantitative Assessment of the Amount of Prion Diverted to Category 1 Materials and Wastewater During Processing http://onlinelibrary.wiley.com/doi/10.1111/j.1539-6924.2012.01922.x/abstract Rapid assessment of bovine spongiform encephalopathy prion inactivation by heat treatment in yellow grease produced in the industrial manufacturing process of meat and bone meals http://transmissiblespongiformencephalopathy.blogspot.com/2013/07/rapid-assessment-of-bovine-spongiform.html PPo4-4: Survival and Limited Spread of TSE Infectivity after Burial http://www.neuroprion.org/resources/pdf_docs/conferences/prion2010/prion_2010_programme.pdf http://chronic-wasting-disease.blogspot.com/2010/09/cwd-prion-2010.html 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). 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). 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). 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. Drinking from a water trough used by the scrapie flock was sufficient to cause infection in sheep in a clean building. 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). 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. 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. 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. 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. 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. Contamination appeared to be sufficient to cause infection only if the trough was in contact with sheep that included clinical cases. 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. 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. PrPSc detection by sPMCA is increasingly used as a surrogate for infectivity measurements by bioassay in sheep or mice. 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. 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). 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. False positive reactions with sPMCA at a low frequency associated with de novo formation of infectious prions have been reported (27, 28). 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. 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. 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. Alternatively, there may be potentially patchy contamination of this furniture with PrPSc, which may have been missed by swabbing. 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. 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). 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). 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. 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. 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. 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. Keywords: classical scrapie, prion, transmissible spongiform encephalopathy, sheep, field furniture, reservoir, serial protein misfolding cyclic amplification http://journal.frontiersin.org/article/10.3389/fvets.2015.00032/full Wednesday, December 16, 2015 *** Objects in contact with classical scrapie sheep act as a reservoir for scrapie transmission *** http://scrapie-usa.blogspot.com/2015/12/objects-in-contact-with-classical.html WEDNESDAY, MARCH 13, 2019 CWD, TSE, PRION, MATERNAL mother to offspring, testes, epididymis, seminal fluid, and blood https://chronic-wasting-disease.blogspot.com/2019/03/cwd-tse-prion-maternal-mother-to.html Subject: Prion 2019 Conference See full Prion 2019 Conference Abstracts https://www.tandfonline.com/doi/full/10.1080/19336896.2019.1615197 see scientific program and follow the cwd studies here; Thursday, May 23, 2019 Prion 2019 Emerging Concepts CWD, BSE, SCRAPIE, CJD, SCIENTIFIC PROGRAM Schedule and Abstracts https://prionconference.blogspot.com/2019/05/prion-2019-emerging-concepts-cwd-bse.html FRIDAY, MAY 24, 2019 Assessing chronic wasting disease strain differences in free-ranging cervids across the United States https://chronic-wasting-disease.blogspot.com/2019/05/assessing-chronic-wasting-disease.html MONDAY, MAY 20, 2019 APHIS, USDA, Announces the Finalized Chronic Wasting Disease Herd Certification Program Standards Singeltary Submissions https://chronic-wasting-disease.blogspot.com/2019/05/aphis-usda-announces-finalized-chronic.html
SUNDAY, JULY 14, 2019 Korea Chronic Wasting Disease CWD TSE Prion additional cases were observed in red deer, sika deer, and their crossbred deer in 2010 and 2016, beyond that, anyone’s guess https://chronic-wasting-disease.blogspot.com/2019/07/korea-chronic-wasting-disease-cwd-tse.html
Korea Chronic Wasting Disease CWD TSE Prion additional cases were observed in red deer, sika deer, and their crossbred deer in 2010 and 2016
In Korea, CWD was only confirmed in elk in 2001, 2004, and 2005 [13]; however, additional cases were observed in red deer, sika deer, and their crossbred deer in 2010 and 2016 [14]. Therefore, it is important to prevent CWD recurrence in the Republic of Korea, and farmers that have experienced a CWD outbreak are required to disinfect the farm before reintroducing the cervids. Thus, farmers require a disinfectant solution that is marketed and readily available to effectively inactivate prions.
[14] Sohn HJ, Roh IS, Kim HJ, et al. Epidemiology of chronic wasting disease in Korea. Prion. 2106;10 (supp1):S16–S17
https://www.tandfonline.com/doi/pdf/10.1080/19336896.2019.1617623 WS-03: Epidemiology of chronic wasting disease in Korea Hyun Joo Sohn In Soon Roh Hyo Jin Kim Tae Young Suh Kyung Je Park Hoo Chang Park Byounghan Kim Foreign Animal Disease Division (FADD), Animal and Plant Quarantine Agency (QIA), Gimcheon, Korea Transmissible spongiform encephalopathy (TSE) is a fatal neurodegenerative disorder, which is so-called as prion diseases due to the causative agents (PrP Sc ). TSEs are believed to be due to the template-directed accumulation of disease-associated prion protein, generally designated PrP Sc . Based on export information of Chronic wasting disease (CWD) suspected elk from Canada to Korea, CWD surveilance program was initiated by the Ministry of Agriculture, Food and Rural Affairs (MAFRA) in 2001. CWD control measures included stamping out of all animals in the affected farm, and through cleaning and disinfection of the premises. In addition, nationwide clinical surveillance of Korean native cervid and improved measures to ensure reporting of CWD suspect cases were implemented. Total of 9 elks were found to be affected. CWD was designated as a notifiable disease under the Act for Prevention of Livestock Epidemics in 2002. Additional CWD cases– 12 elks and 2 elks – were diagnosed in 2004 and 2005. On 2010, 6 elks, 7 sika deer, one red deer and 5 cross-breeds were confirmed as positive. Further epidemiological investigations showed that these CWD outbreaks were linked to the importation of elks from Canada in 1994 based on circumstantial evidences. CWD is the prion disease that is known spread horizontally. The experimental studies have shown that PrP CWD is capable of transmitting CWD through saliva and blood. We conducted sPMCA and animal biosassy using contaminated soils in the playground of farm 2 which considered horizontal transmission between cervid and have been confirmed infectious PrP CWD . This result suggests PrP CWD shedding in the CWD contaminated soil is progressive through the disease course. Keywords: CWD, soil, sPMCA https://www.tandfonline.com/doi/full/10.1080/19336896.2016.1163048 WEDNESDAY, OCTOBER 16, 2019 Australia Assessment of bulk wheat from Canada Part B: Animal biosecurity risk advice, CWD TSE Prion concerns are mounting https://chronic-wasting-disease.blogspot.com/2019/10/australia-assessment-of-bulk-wheat-from.html
THURSDAY, AUGUST 08, 2019 Raccoons accumulate PrPSc after intracranial inoculation with the agents of chronic wasting disease (CWD) or transmissible mink encephalopathy (TME) but not atypical scrapie https://chronic-wasting-disease.blogspot.com/2019/08/raccoons-accumulate-prpsc-after.html
*** 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).*** http://www.tandfonline.com/doi/full/10.4161/pri.28124?src=recsys http://www.tandfonline.com/doi/pdf/10.4161/pri.28124?needAccess=true https://wwwnc.cdc.gov/eid/article/20/1/13-0858_article FRIDAY, JULY 26, 2019 Chronic Wasting Disease in Cervids: Implications for Prion Transmission to Humans and Other Animal Species https://chronic-wasting-disease.blogspot.com/2019/07/chronic-wasting-disease-in-cervids.html
atypical and typical BSE and Scrapie Zoonosis O.05: Transmission of prions to primates after extended silent incubation periods: Implications for BSE and scrapie risk assessment in human populations 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 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. *** We recently observed the direct transmission of a natural classical scrapie isolate to macaque after a 10-year silent incubation period, ***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), ***is the third potentially zoonotic PD (with BSE and L-type BSE), ***thus questioning the origin of human sporadic cases. 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. ***thus questioning the origin of human sporadic cases*** ***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. https://prion2015.files.wordpress.com/2015/05/prion2015abstracts.pdf ***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. ***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. ***These results demonstrate that scrapie prions have a zoonotic potential and raise new questions about the possible link between animal and human prions. http://www.tandfonline.com/doi/abs/10.1080/19336896.2016.1163048?journalCode=kprn20 PRION 2016 TOKYO Saturday, April 23, 2016 SCRAPIE WS-01: Prion diseases in animals and zoonotic potential 2016 Prion. 10:S15-S21. 2016 ISSN: 1933-6896 printl 1933-690X online Taylor & Francis Prion 2016 Animal Prion Disease Workshop Abstracts WS-01: Prion diseases in animals and zoonotic potential Juan Maria Torres a, Olivier Andreoletti b, J uan-Carlos Espinosa a. Vincent Beringue c. Patricia Aguilar a, Natalia Fernandez-Borges a. and Alba Marin-Moreno a “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 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. 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. 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. 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. 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. These results demonstrate that scrapie prions have a zoonotic potential and raise new questions about the possible link between animal and human prions. http://www.tandfonline.com/doi/abs/10.1080/19336896.2016.1163048?journalCode=kprn20 ***> why do we not want to do TSE transmission studies on chimpanzees $ 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. snip… R. BRADLEY https://web.archive.org/web/20170126051158/http://collections.europarchive.org/tna/20080102222950/http://www.bseinquiry.gov.uk/files/yb/1990/09/23001001.pdf Title: Transmission of scrapie prions to primate after an extended silent incubation period) *** 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. *** 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. *** 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. http://www.ars.usda.gov/research/publications/publications.htm?SEQ_NO_115=313160 ***> 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. However, to date, no CWD infections have been reported in people. 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 *** LOOKING FOR CWD IN HUMANS AS nvCJD or as an ATYPICAL CJD, LOOKING IN ALL THE WRONG PLACES $$$ *** *** 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).*** http://www.tandfonline.com/doi/full/10.4161/pri.28124?src=recsys http://www.tandfonline.com/doi/pdf/10.4161/pri.28124?needAccess=true https://wwwnc.cdc.gov/eid/article/20/1/13-0858_article Chronic Wasting Disease CWD TSE Prion aka mad deer disease zoonosis 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. http://grantome.com/grant/NIH/R01-NS088604-04 ZOONOTIC CHRONIC WASTING DISEASE CWD TSE PRION UPDATE Prion 2017 Conference 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 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 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. 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. 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. PRION 2017 DECIPHERING NEURODEGENERATIVE DISORDERS PRION 2018 CONFERENCE Oral transmission of CWD into Cynomolgus macaques: signs of atypical disease, prion conversion and infectivity in macaques and bio-assayed transgenic mice 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). 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 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. 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.. ***> 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. Departmental Freedom of Information Act Regulations FOIA Dumbing Down of America Under the Trump Regime <*** https://usdameatexport.blogspot.com/2019/10/departmental-freedom-of-information-act.html THURSDAY, SEPTEMBER 26, 2019 Veterinary Biologics Guideline 3.32E: Guideline for minimising the risk of introducing transmissible spongiform encephalopathy prions and other infectious agents through veterinary biologics https://bovineprp.blogspot.com/2019/09/veterinary-biologics-guideline-332e.html U.S.A. 50 STATE BSE MAD COW CONFERENCE CALL Jan. 9, 2001 Subject: BSE–U.S. 50 STATE CONFERENCE CALL Jan. 9, 2001 Date: Tue, 9 Jan 2001 16:49:00 -0800 From: "Terry S. Singeltary Sr." Reply-To: Bovine Spongiform Encephalopathy To: BSE-L@uni-karlsruhe.de snip… [host Richard Barns] and now a question from Terry S. Singeltary of CJD Watch. [TSS] yes, thank you, U.S. cattle, what kind of guarantee can you give for serum or tissue donor herds? [no answer, you could hear in the back ground, mumbling and 'we can't. have him ask the question again.] [host Richard] could you repeat the question? [TSS] U.S. cattle, what kind of guarantee can you give for serum or tissue donor herds? [not sure whom ask this] what group are you with? [TSS] CJD Watch, my Mom died from hvCJD and we are tracking CJD world-wide. [not sure who is speaking] could you please disconnect Mr. Singeltary [TSS] you are not going to answer my question? [not sure whom speaking] NO snip…see full archive and more of this; http://tseac.blogspot.com/2011/02/usa-50-state-bse-mad-cow-conference.html FRIDAY, OCTOBER 25, 2019 27th ANNUAL REPORT 2018 CREUTZFELDT-JAKOB DISEASE SURVEILLANCE https://creutzfeldt-jakob-disease.blogspot.com/2019/10/27th-annual-report-2018-creutzfeldt.html TUESDAY, NOVEMBER 12, 2019 Woman is 3rd person this year diagnosed with Creutzfeldt-Jakob disease at the Moncton Hospital https://cjdmadcowbaseoct2007.blogspot.com/2019/11/woman-is-3rd-person-this-year-diagnosed.html
THURSDAY, DECEMBER 12, 2019
Heidenhain Variant Creutzfeldt Jakob Disease hvCJD, sporadic spontaneous CJD and the TSE Prion December 14, 2019
22 years, rip mom dod 12/14/97 confirmed hvcjd, just made a promise to mom, and you don't break those promises, never forget, and never let them forget, before we all do…this pearl's for you Mom! love terry
https://creutzfeldt-jakob-disease.blogspot.com/2019/12/heidenhain-variant-creutzfeldt-jakob.html
Terry S. Singeltary Sr.