Mad cow disease: Could it be here? 2001 revisited 2026
Man's stubborn crusade attracts experts' notice
By Carol Christian, Copyright 2001 Houston Chronicle Aug 5, 2001
https://www.chron.com/news/houston-texas/article/mad-cow-disease-could-it-be-here-2042860.php
Like Paul Revere with e-mail, Terry Singeltary Sr. is on a mission to sound an alarm: Beware of mad cow disease.
As is true of many crusaders, however, his pleas often fall on deaf ears.
Health officials here and abroad insist that bovine spongiform encephalopathy -- popularly known as mad cow disease, a fatal brain disorder that can make cows shake uncontrollably -- has been kept out of this country through surveillance of the cattle industry.
But since his mother's death in December 1997, the Galveston County man has been obsessed with possible connections between her deadly brain disorder, sporadic Creutzfeldt-Jakob Disease, and mad cow disease.
And after much persistence on his part, people are taking notice of this former machinist and high school dropout who jokes that he has a Ph.D. -- a Pool Hall Degree. "They called me Chicken Little for four years," he said. "Now they're calling back, asking for more information." For the past year he has been U.S. co-coordinator of an international monitoring group called CJD Watch. He regularly gets e-mail from scientists and journalists around the world.
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Debora MacKenzie, a reporter for the British magazine New Scientist, described Singeltary, 47, as a "dogged unearther and tabulator of government documents."
Singeltary monitors "every word written about CJD/BSE," said Anita Manning of USA Today, also by e-mail. "He's passionate, opinionated and not always tactful, although I like him because he's such a character and he is so transparent," Manning said. "He is what he appears to be."
Science and environment writer Jonathan Leake of the Sunday Times in London said Singeltary has helped him track down families of people with CJD along with academic research papers. "I strongly suspect he is right in thinking the USA has had BSE cases," Leake said by e-mail "The American government is making the same mistake as the British in putting the short-term commercial interests of its farmers before health considerations," he added. "It should start formal and widespread testing of cattle plus compulsory autopsies for all human CJD victims at the state's expense. If there is BSE, then leaving it to spread will kill people -- and that would eventually destroy the industry, too."
Texas Department of Health epidemiologist Julie Rawlings said Singeltary's careful monitoring of the disease had proven useful. "Terry has been helpful in providing contact information regarding suspect CJD cases so that the Health Department can initiate case investigations and learn more about CJD in Texas," she said.
Noting that the department cannot release records on individual patients, she added, "I think we learn more from him than he does from us."
Mad cow disease surfaced in England in 1986 and quickly became an epidemic. It since has been reported in 15 European countries, most recently Greece on July 2, and the Czech Republic on June 14. Two German-born cows tested positive for BSE in November.
Singeltary said he became convinced that BSE is here as he watched his mother, Barbara Poulter of Crystal Beach, dying of sporadic Creutzfeldt-Jakob Disease. The rare, fatal brain disease is sometimes accompanied by severe jerking.
"She would jerk so bad at times, it would take three of us to hold her down," Singeltary said. "They can call it whatever they want, but I know what I saw, and what she went through. `Sporadic' simply means they don't know."
Poulter, a retired telephone-company field worker, had a form of sporadic CJD -- Haidenhain variant -- that is even less common than the typical sporadic case. One of its first symptoms is loss of vision.
She started seeing brown spots in September 1997 and was virtually blind within two weeks. By the eighth week of the illness Poulter was bedridden, and in the 10th week she died. Before that she had been in good health.
In many countries and most U.S. states, physicians are not required to report CJD cases to health officials. Texas made the disease reportable in 1998. Through 2000, there were 17 probable or confirmed cases, according to the Texas Department of Health.
In mid-June, a case of sporadic CJD was confirmed through brain biopsy at Christus Spohn Hospital Shoreline in Corpus Christi, said Jane Bakos, hospital vice president. The patient has since died, the hospital reported.
CJD and mad cow disease leave their victims' brains full of holes like a sponge. Although not contagious, the illnesses are thought to be transmissible through prions, or nearly indestructible abnormal proteins.
Because the prion protein is not killed by standard sterilization, sporadic CJD can be spread by contaminated surgical instruments.
In March 1996, the British government announced the discovery of a new variant of CJD, most likely explained by exposure to bovine spongiform encephalopathy.
Through June, 101 cases of new-variant CJD have been reported in the United Kingdom, three in France and one in Ireland. In contrast to sporadic CJD, the new variant usually affects younger patients and lasts longer.
No cases of new-variant CJD or BSE have been reported in the United States. No relationship has been shown between sporadic CJD and mad cow disease.
There is no indication that new-variant CJD can be spread through blood transfusions, but a U.S. Food and Drug Administration advisory committee voted in June to broaden the categories for excluding potential donors. The recommendations have not yet been approved by the FDA.
The American Red Cross has announced that on Sept. 17 it will begin rejecting potential blood donors who, since 1980, have spent at least three months in the United Kingdom or at least six months in any European country or combination of countries. Those who have received a blood transfusion in Britain since 1980 also will be rejected.
The primary collector of local blood donations is the Gulf Coast Regional Blood Center, which will follow the FDA's guidelines, said Bill Teague, president and chief executive officer.
Singeltary said it's naive to think that U.S. prevention efforts have kept mad cow and new-variant CJD out of the United States.
"They haven't found it," he said, "because they haven't looked."
For one thing, he said, too few cows are tested for the disease. In the first six months of this year, the European Union tested more than 3.2 million cows, David Byrne of the European Commission said in a speech last month.
By contrast, it took the U.S. Department of Agriculture nearly 10 years to analyze about 13,000 cow brains, according to the department's Web site.
With more than 68 million cattle slaughtered since 1990 in the United States, according to the USDA, checking about 13,000 falls far short, Singeltary said.
Though not a scholar, Singeltary has collected voluminous material on mad cow and CJD. Disabled from a neck injury, Singeltary never used a computer until 1998. He now spends hours each day on the Internet while his wife, Bonnie Singeltary, runs a flower shop in their home in Bacliff, in north Galveston County.
His challenge to the CJD/BSE establishment is courageous and refreshing, said Dr. Lynette Dumble, former visiting professor of surgery at University of Texas Medical School at Houston and a former senior research fellow in the history and philosophy of science at the University of Melbourne in Australia. "I certainly have no problem with Terry's ideas on BSE/CJD," said Dumble, who coordinates the Global Sisterhood Network, a computer service that posts media reports on developments affecting women. "His research skills are excellent, and he is abreast of each and every development in the field."
Among Singeltary's worries now, he said, are widespread violations of an August 1997 ban on feeding animal products to U.S. cattle. The FDA reported in January that hundreds of feed manufacturers were not complying with regulations designed to keep BSE out of this country.
(That same month, a Purina Mills feedlot near San Antonio told the FDA that a "very low level" of cow parts had been found in cattle feed. The company voluntarily removed 1,222 animals who had been fed the prohibited materials.)
He obtained copies of FDA letters to various feed mills that had been found in violation of the regulations and immediately sent them by e-mail to hundreds of people around the world.
Singeltary might not be so zealous in getting the word out if he weren't convinced that someone is covering up the truth.
"They used to say BSE would never transmit to humans," he said, "and it has. They lied about the feed ban being in place. "I've lost faith in the whole process. I've discovered too many things."
Aug 5, 2001…end…TSS
2026
2026, we have BSE, last confirmed mad cow was 2023, a new case of scrapie 2026, CWD running rampant, they can’t stop, studies now show CWD of cervid transmits to sheep, and a cwd spillover outbreak in wild pigs in Texas and Arkansas. cwd will transmit, by oral routes to cattle, sheep, pigs, cervid, and primates, mad cow feed ban of 1997, woefully lacking, will not stop TSE in all those species, PLUS, new TSE prion disease in a new livestock species, the CAMEL, rather large outbreak in the Middle east. Professor John Collinge MRC cjd prion unit, now states, Globally, CJD is now 1 in 5,000. sporadic cjd now linked to BSE, CWD, and Scrapie, and most likely so will pigs and camels. it’s just science, nobody likes science, but on my mothers grave, 85%+ of all human TSE prion disease, sporadic CJD, is not all spontaneous, or a happenstance of bad luck, that’s just horseshit science, and you can take that to the bank. oh, not to mention Alzheimer’s disease, tried warning that Alzheimer’s was a TSE Prion back in 2001 on the BSE-list and published in PloS in 2003.
let’s look at the latest science on TSE PrP, shall we, please pay attention this time around, the iatrogenic threat from all these different TSE prion strains in different species, is a great threat to humanity…p.s. i don’t make this stuff up, it’s just science…
with kindest regards, terry
Jonh Collinge MRC on sporadic CJD;
***> 2023 Professor John Collinge on tackling prion diseases <***
“The best-known human prion disease is sporadic Creutzfeldt-Jakob disease (sCJD), a rapidly progressive dementia which accounts for around 1 in 5000 deaths worldwide.” There is accumulating evidence also for iatrogenic AD. Understanding prion biology, and in particular how propagation of prions leads to neurodegeneration, is therefore of central research importance in medicine.
https://www.ucl.ac.uk/brain-sciences/research/dementia-ucl-priority/professor-john-collinge-tackling-prion-diseases
Front. Public Health, 12 June 2024 Sec. Infectious Diseases: Epidemiology and Prevention Volume 12 - 2024 | https://doi.org/10.3389/fpubh.2024.1411489
Updated global epidemiology atlas of human prion diseases
The top seven countries in PrD cases were the USA (n = 5,156), France (n = 3,276), Germany (n = 3,212), Italy (n = 2,995), China (n = 2,662), the UK (n = 2,521), Spain (n = 1,657), and Canada (n = 1,311).
https://www.frontiersin.org/journals/public-health/articles/10.3389/fpubh.2024.1411489/full
Research Letter December 11, 2023
Change in Epidemiology of Creutzfeldt-Jakob Disease in the US, 2007-2020
Matthew A. Crane, BS1; Sameer Nair-Desai, BS2; Alison Gemmill, PhD3; et al John A. Romley, PhD4; John C. Probasco, MD5 Author Affiliations Article Information JAMA Neurol. 2024;81(2):195-197. doi:10.1001/jamaneurol.2023.4678
Creutzfeldt-Jakob disease (CJD) is a rapidly progressive and universally fatal prion disease.1 Research on CJD in the US showed stable incidence from 1979 to 2006, though recent trends are not as well described.2 The incidence of sporadic CJD, the most common type, is higher among older patients.1,2 Due to aging populations worldwide, the epidemiology of CJD is evolving.3 We examined death certificate data from 2007 to 2020 to better understand recent US trends of CJD. Snip… Discussion Our findings indicate the reported incidence of CJD has risen considerably, disproportionately affecting older and female individuals. These trends align with data from Japan3 and could be influenced by changing demographics. However, our findings may also reflect improved detection of CJD with new diagnostic tools, such as magnetic resonance imaging and real-time quaking-induced conversion testing. This study is limited by a reliance on death certificate data for estimating CJD incidence. While research supports this approach,5 such data may be subject to miscoding or misdiagnosis. Results from both neuropathologic and genetic testing may complement death certificate data and enhance surveillance.6 The findings underscore the changing landscape of CJD and suggest a need for monitoring among the aging US population.
https://jamanetwork.com/journals/jamaneurology/fullarticle/2812784
Eur J Epidemiol. 2023; 38(7): 757–764. Published online 2023 May 16. doi: 10.1007/s10654-023-01004-5 PMCID: PMC10276107PMID: 37191829 Received: 31 January 2023 / Accepted: 6 April 2023 / Published online: 16 May 2023 © The Author(s) 2023
The role of environmental factors on sporadic Creutzfeldt-Jakob disease mortality: evidence from an age-period-cohort analysis
Abstract
Sporadic Creutzfeldt-Jakob disease (sCJD) is the most common form of prion diseases. The causes of sCJD are still unknown and exogenous factors may play a role. Worldwide, the number of patients with sCJD has progressively increased over time. This increase can be partly explained by increasing life expectancy and better case ascertainment, but a true increase in the number of sCJD cases cannot be excluded. We estimated mortality rates from sCJD in France (1992–2016) and studied variation in mortality rates by age, period, and time.
snip... The overall sCJD mortality rate was 4.58 per 1,000,000 person-years (95% CI=4.39–4.78) (Table S1).
snip...
Besides risk factors explored in case-control studies, the possibility of zoonotic risk factors remains a possibility that could account for an exogenous origin in some sCJD cases. Research on atypical forms of BSE (L-BSE, H-BSE) has revealed molecular similarities between the L-BSE strain and molecular subtypes of human sCJD, in particular the MV2 subtype [39].
Furthermore, L-BSE has been experimentally transmitted to non-human primates as efficiently as classical BSE responsible for vCJD in humans, and could be even more virulent [40–42].
The zoonotic risk associated with natural sheep scrapie has also been recently updated with the demonstration of an intracerebral transmission of scrapie to mice expressing the human prion protein during serial passages, as well as transmission of scrapie to primates.
These observations highlight the possibility of a causal link between exposure to sheep scrapie and sCJD in some cases [43, 44].
A large increase in animal product consumption and the generalization of mechanically separated meat in developed countries over the last century may have contribute to increase the zoonotic prion pressure [45].
It would be of interest to observe the effect of safety measures implemented since the “mad cow crisis” to avoid population prion exposure on sCJD mortality in the next decades.
https://link.springer.com/article/10.1007/s10654-023-01004-5
US NATIONAL PRION DISEASE PATHOLOGY SURVEILLANCE CENTER CJD TSE REPORT SEPTEMBER 2025
From the first full year of reporting CJD TSE in the US in 2000, where 90 cases of CJD was reported that year, to today, where in September 2025, the number of CJD cases reported in the last full year reporting, which would have been 2024, the number of CJD cases for 2024 was 249 cases. So, from the first full year 2000 CJD cases were 90 cases confirmed in that year, to 2024, where 2024 CJD statistics rose to 249 confirmed CJD cases in a single year. A dramatic increase in deaths, from figures that don’t seem to be dramatic. But thes figures today, they are not from “better surveillance”, that dog don’t hunt no more. They have been saying this for over 25 years, year after year, well it’s time to call it for what it is, Human Transmissible Spongiform Encephalopathy TSE Prion cases are rising, and it’s NOT because of better surveillance, or just a “happenstance of bad luck, that 85%+ of all human cases, sporadic CJD, including VPSPr, just happen spontaneously, no, it’s because of unknown environmental factors, and or iatrogenic factors, imho…terry
US NATIONAL PRION DISEASE PATHOLOGY SURVEILLANCE CENTER CJD TSE REPORT SEPTEMBER 2025
https://prionunitusaupdate.blogspot.com/2025/10/us-national-prion-disease-pathology.html
MONDAY, JUNE 1, 2026
NATIONAL PRION DISEASE PATHOLOGY SURVEILLANCE CENTER CJD SURVEILLANCE TABLES OF CASES EXAMINED NPDPSC Last updated March 31st, 2026
https://prionunitusaupdate.blogspot.com/2026/06/national-prion-disease-pathology.html
TUESDAY, DECEMBER 12, 2023
CREUTZFELDT JAKOB DISEASE TSE PRION DISEASE UPDATE USA DECEMBER 2023
https://creutzfeldt-jakob-disease.blogspot.com/2023/12/creutzfeldt-jakob-disease-tse-prion.html
2023 CJD Prion
https://creutzfeldt-jakob-disease.blogspot.com/2023/09/professor-john-collinge-on-tackling.html
Bovine Spongiform Encephalopathy BSE
USA BSE Testing and Surveillance?
Bottom line, USA is testing so few cows for BSE (<25k tested annually), you don’t find much mad cow disease testing only less than 25k a year, the mad cows have to find you, and the did in 2023, South Carolina BSE
https://www.aphis.usda.gov/livestock-poultry-disease/cattle/bse/bse-surveillance-program
BUT, even at those low testing figures, the USA did just confirm another case of BSE just here recently. Feed ban has failed terribly, and CWD is spreading in the USA, at an alarming rate. Recent transmission studies show oral transmission of CWD of Cervid to cattle. Studies also show links of sporadic CJD to BSE, Scrapie, and CWD. It’s a Whole new game of Prion poker now$$$
The U.S. has reported an atypical case of Bovine Spongiform Encephalopathy (BSE) in a beef cow approximately five years old or older at a slaughter plant in South Carolina. The animal never entered slaughter channels and at no time presented a risk to the food supply or to human health in the U.S. The radio frequency identification tag present on the animal is associated with a herd in Tennessee. APHIS and veterinary officials in South Carolina and Tennessee are gathering more information during this ongoing investigation.
This is the nation’s 7th detection of BSE, of the six previous U.S. cases, the first, in 2003 was the only case of classical BSE, which was from a cow imported from Canada. The rest of the cases have been atypical BSE. The animal was tested as part of the USDA’s Animal and Plant Health Inspection Service’s routine surveillance of cattle that are deemed unsuitable for slaughter.
National Cattlemen’s Beef Association chief veterinarian Dr. Kathy Simmons says USDA’s ongoing BSE surveillance program has tested more than one million cattle since the program began, ensuring that the agency’s interlocking supply chain safety products are working. She says the incidence of BSE in the U.S. is extremely low and will remain so.
U.S. Cattlemen’s Association president Justin Tupper says the swift detection of this case proves that the systems and protocols put in place are working. He says the organization is grateful to the nationwide team of veterinarians, animal health officials, meat inspectors, and others who ensure the well-being of the U.S. cattle herd.
Atypical BSE generally occurs in older cattle and seems to arise rarely and spontaneously in all cattle populations.
The World Organization for Animal Health (WOAH) recognizes the U.S. as negligible risk for BSE, the lowest possible risk in the world. Per WOAH guidelines in determining this status, atypical BSE cases do not impact official BSE risk status and this finding of an atypical case will not change the negligible risk status of the U.S., and should not lead to any trade issues.
0 comments Tags: Animal and Plant Health Inspection Service, animal health, bovine spongiform encephalopathy, BSE, cattle beef, US Cattlemen's Association, USCA, USDA
https://www.brownfieldagnews.com/news/atypical-case-of-bse-detected-in-south-carolina/
Wednesday, May 24, 2023
***> WAHIS, WOAH, OIE, United States of America Bovine spongiform encephalopathy Immediate notification
https://wahis.woah.org/#/in-review/5067
https://woahoie.blogspot.com/2023/05/wahis-woah-oie-united-states-of-america.html
https://prpsc.proboards.com/thread/125/wahis-woah-oie-immediate-notification
SATURDAY, MAY 20, 2023
***> Tennessee State Veterinarian Alerts Cattle Owners to Disease Detection Mad Cow atypical L-Type BSE
https://bse-atypical.blogspot.com/2023/05/tennessee-state-veterinarian-alerts.html
https://prpsc.proboards.com/thread/123/tennessee-veterinarian-alerts-cattle-confirmed
MAY 19, 2023
https://www.aphis.usda.gov/aphis/newsroom/stakeholder-info/sa_by_date/sa-2023/bse
2 weeks before the announcement of this recent mad cow case in the USA, i submitted this to the APHIS et al;
***> APPRX. 2 weeks before the recent mad cow case was confirmed in the USA, in Tennessee, atypical L-Type BSE, I submitted this to the APHIS et al;
Document APHIS-2023-0027-0001 BSE Singeltary Comment Submission May 2, 2023
''said 'burden' cost, will be a heavy burden to bear, if we fail with Bovine Spongiform Encephalopathy BSE TSE Prion disease, that is why this information collection is so critical''...
https://www.regulations.gov/comment/APHIS-2023-0027-0002
https://downloads.regulations.gov/APHIS-2023-0027-0002/attachment_1.pdf
Bovine Spongiform Encephalopathy BSE TSE Prion Origin USA?, what if?
Research Project: Pathobiology, Genetics, and Detection of Transmissible Spongiform Encephalopathies Location: Virus and Prion Research
Title: Sheep are susceptible to the agent of TME by intracranial inoculation and have evidence of infectivity in lymphoid tissues
Author item CASSMANN, ERIC - Oak Ridge Institute For Science And Education (ORISE) item MOORE, SARA - Oak Ridge Institute For Science And Education (ORISE) item SMITH, JODI - Iowa State University item Greenlee, Justin
Submitted to: Frontiers in Veterinary Science Publication Type: Peer Reviewed Journal Publication Acceptance Date: 11/14/2019 Publication Date: 11/29/2019 Citation: Cassmann, E.D., Moore, S.J., Smith, J.D., Greenlee, J.J. 2019.
Sheep are susceptible to the agent of TME by intracranial inoculation and have evidence of infectivity in lymphoid tissues.
Frontiers in Veterinary Science. 6:430. https://doi.org/10.3389/fvets.2019.00430. DOI: https://doi.org/10.3389/fvets.2019.00430
Interpretive Summary: Prion diseases are protein misfolding diseases that are transmissible between animals. The outcome of prion infection is irreversible brain damage and death. Transmission can occur between animals of the same or different species, however, transmission between different species is usually less efficient due to the species barrier, which results from differences in the amino acid sequence of the prion protein between the donor and recipient species. The present work evaluated whether transmissible mink encephalopathy (TME) can infect sheep. Our results demonstrate that sheep are susceptible to the TME agent and that the TME agent has similar properties to the agent of L-type atypical bovine spongiform encephalopathy (L-BSE). This work supports the ideas that L-BSE is a possible source for TME in mink and that the practice of feeding cattle with neurologic disease to mink should be avoided. This information is important to farmers who raise cattle, sheep, or mink.
Technical Abstract: Transmissible mink encephalopathy (TME) is a food borne prion disease. Epidemiological and experimental evidence suggests similarities between the agent of TME and L-BSE. This experiment demonstrates the susceptibility of four different genotypes of sheep to the agent of TME by intracranial inoculation. The four genotypes of sheep used in this experiment had polymorphisms corresponding to codons 136 and 171 of the prion gene: VV136QQ171, AV136QQ171, AA136QQ171, and AA136QR171. All intracranially inoculated sheep without comorbidities (15/15) developed clinical scrapie and had detectable PrPSc by immunohistochemistry, western blot, and enzyme immunoassay (EIA). The mean incubation periods in TME infected sheep correlated with their relative genotypic susceptibility. There was peripheral distribution of PrPSc in the trigeminal ganglion and neuromuscular spindles; however, unlike classical scrapie and C-BSE in sheep, ovine TME did not accumulate in the lymphoid tissue. To rule out the presence of infectious, but proteinase K susceptible PrPSc, the lymph nodes of two sheep genotypes, VV136QQ171 and AA136QQ171, were bioassayed in transgenic ovinized mice. None of the mice (0/32) inoculated by the intraperitoneal route had detectable PrPSc by EIA. Interestingly, mice intracranially inoculated with RPLN tissue from a VV136QQ171 sheep were EIA positive (3/17) indicating that sheep inoculated with TME harbor infectivity in their lymph nodes. Western blot analysis demonstrated similarities in the migration patterns between ovine TME and the bovine TME inoculum. Overall, these results demonstrate that sheep are susceptible to the agent of TME, and that the tissue distribution of PrPSc in TME infected sheep is distinct from classical scrapie.
https://www.ars.usda.gov/research/publications/publication/?seqNo115=363305
https://www.ars.usda.gov/research/publications/publication/?seqNo115=360665
https://www.ars.usda.gov/research/publications/publication/?seqNo115=373668
Previous work has shown that the Stetsonville, WI outbreak of TME could have been precipitated by feeding mink a downer cow with atypical BSE; therefore, it very well may have originated from a cow with L-BSE. The agent of TME appears to remain stable, and it has a high transmission efficiency after a sequence of interspecies transmission events. Although C-BSE is the archetypal foodborne TSE, our findings indicate that L-BSE and bTME have greater transmission efficiencies in bovinized mice. Previous work has demonstrated that L-BSE also is more virulent than C-BSE in mice expressing the human prion protein [46, 55]. Although the documented incidence of L-BSE is low, the propensity of L-BSE and the TME agent to cross species barriers support the continued monitoring for atypical BSE.
https://bmcvetres.biomedcentral.com/articles/10.1186/s12917-020-02611-0
***>This work supports the ideas that L-BSE is a possible source for TME in mink and that the practice of feeding cattle with neurologic disease to mink should be avoided. This information is important to farmers who raise cattle, sheep, or mink.<***
1985
Evidence That Transmissible Mink Encephalopathy Results from Feeding Infected Cattle Over the next 8-10 weeks, approximately 40% of all the adult mink on the farm died from TME.
snip...
The rancher was a ''dead stock'' feeder using mostly (>95%) downer or dead dairy cattle...
https://web.archive.org/web/20090506002258/http://www.bseinquiry.gov.uk/files/mb/m09/tab05.pdf
https://web.archive.org/web/20090506001031/http://www.bseinquiry.gov.uk/files/mb/m09a/tab01.pdf
https://web.archive.org/web/20090506024922/http://www.bseinquiry.gov.uk/files/yb/1987/06/10004001.pdf
Research and analysis Annual report to Parliament on the monitoring programme for transmissible spongiform encephalopathies (TSEs) – 2024 and 2025 Published 2 June 2026
https://efsaopinionbseanimalprotein.blogspot.com/2026/06/research-and-analysis-annual-report-to.html
TUESDAY, APRIL 28, 2026
Possible alignment of the EU BSE surveillance with the new WOAH provisions
https://efsaopinionbseanimalprotein.blogspot.com/2026/04/possible-alignment-of-eu-bse.html
https://efsaopinionbseanimalprotein.blogspot.com/2026/06/research-and-analysis-annual-report-to.html
The naturally occurring lysine to glutamic acid substitution (E211K in the bovine prion protein) results in short incubation periods for H-type bovine spongioform encephalopathy (BSE)
Component 6: Transmissible Spongiform Encephalopathies (TSEs)
Problem Statement 6A: Determine pathobiology of prion strains.
The naturally occurring lysine to glutamic acid substitution (E211K in the bovine prion protein) results in short incubation periods for H-type bovine spongioform encephalopathy (BSE).
Virus and Prion Research Unit, National Animal Disease Center, Ames, Iowa
Classical BSE (C-BSE) is a prion disease of cattle that was responsible for the "mad cow disease" epizootic in Europe in the 1980s. C-BSE was determined to cause the human prion disease vCJD. Since then, atypical spontaneous strains of BSE were identified. H-BSE is one of those strains. Much research has explored the origins of C-BSE, and strain emergence from atypical H-BSE is one hypothesis. An H-BSE case was determined to have a germline mutation, an E211K substitution in the prion protein gene, which is analogous to a hereditary human prion disease. ARS scientists in Ames, Iowa reported the transmission of H-BSE from cattle, with and without the germline prion protein amino acid substitution, to cattle with various prion genotypes: EE211 (wild-type), EK211, and KK211. Results indicated a significantly shorter incubation period in K containing cattle compared to prion wild-type cattle. The scientists also explored the possibility that the C-BSE strain might have occurred after serial passages of EK211 and KK211 containing H-BSE in cattle, but results did not support this concept. This information is important to prion researchers, veterinary diagnostic laboratories, and those involved with establishing regulatory guidelines.
https://www.ars.usda.gov/ARSUserFiles/np103/AnnualReports/Final%20NP103%20FY2024%20Annual%20Report.updated%205.30.25.pdf
Research Project: Elucidating the Pathobiology and Transmission of Transmissible Spongiform Encephalopathies Location: Virus and Prion Research
Title: Cattle with the EK211 PRNP polymorphism are susceptible to the H-type bovine spongiform encephalopathy agent from either E211K or wild type donors after oronasal inoculation
Author item Greenlee, Justin item Cassmann, Eric item MOORE, SARA JO - Oak Ridge Institute For Science And Education (ORISE) item WEST GREENLEE, HEATHER - Iowa State University
Submitted to: Meeting Abstract Publication Type: Abstract Only Publication Acceptance Date: 6/24/2022 Publication Date: 9/16/2022 Citation: Greenlee, J.J., Cassmann, E.D., Moore, S., West Greenlee, H.M. 2022.
Cattle with the EK211 PRNP polymorphism are susceptible to the H-type bovine spongiform encephalopathy agent from either E211K or wild type donors after oronasal inoculation.
Prion 2022 Conference abstracts: pushing the boundaries. 16(1):150. https://doi.org/10.1080/19336896.2022.2091286.
DOI: https://doi.org/10.1080/19336896.2022.2091286
Interpretive Summary:
Technical Abstract: In 2006, a case of H-type bovine spongiform encephalopathy (H-BSE) was reported in a cow with a previously unreported prion protein polymorphism (E211K). The E211K polymorphism is heritable and homologous to the E200K mutation in humans that is the most frequent PRNP mutation associated with familial Creutzfeldt-Jakob disease. Although the prevalence of the E211K polymorphism is low, cattle carrying the K211 allele develop H-type BSE with a rapid onset after experimental inoculation by the intracranial route. The purpose of this study was to investigate whether the agents of H-type BSE or H-type BSE associated with the E211K polymorphism transmit to wild type cattle or cattle with the K211 allele after oronasal exposure. Wild type (EE211) or heterozygous (EK211) cattle were oronasally inoculated with the H-BSE agent from either the US 2004 case (wild type donor; n=3) or from the US 2006 case with the E211K polymorphism (n=4). Cattle were observed daily throughout the course of the experiment for the development of clinical signs. When signs were noted, animals were euthanized and necropsied. Cattle were confirmed positive for abnormal BSE prions by enzyme immunoassay (EIA; Idexx HerdChek BSE Ag Test), anti-PrP immunohistochemistry (IHC) on brainstem, and microscopic examination for vacuolation. Three-out-of-four (75%) calves with the EK211 genotype developed clinical signs of H-BSE including inattentiveness, loss of body condition, weakness, ataxia, and muscle fasciculations and were euthanized. Two of the positive EK211 steers received H-BSE US 2004 inoculum (Incubation Period (IP): 59.3 and 72.3 months) while the other positive steer received the E211K H-BSE inoculum (IP: 49.7 months). EIA confirmed that abundant misfolded protein (O.D. 2.57-4.0) in the brainstem, and IHC demonstrated PrPSc throughout the brain. All cattle in the EE211 recipient group remain asymptomatic for the duration of the experiment (approximately 7 years post-inoculation).
This study demonstrates that the H-type BSE agent is transmissible by the oronasal route. Cattle with the EK211 genotype are oronasally susceptible to small doses of the H-BSE agent from either EK211 or EE211 (wild type) donors. Wild-type EE211 cattle remained asymptomatic for the duration of the experiment with this small dose (0.1g) of inoculum. These results reinforce the need for ongoing surveillance for classical and atypical BSE to minimize the risk of potentially infectious tissues entering the animal or human food chains.
https://www.ars.usda.gov/research/publications/publication/?seqNo115=395351
Highlights
This study demonstrates that the H-type BSE agent is transmissible by the oronasal route. Cattle with the EK211 genotype are oronasally susceptible to small doses of the H-BSE agent from either EK211 or EE211 (wild type) donors. Wild-type EE211 cattle remained asymptomatic for the duration of the experiment with this small dose (0.1g) of inoculum. These results reinforce the need for ongoing surveillance for classical and atypical BSE to minimize the risk of potentially infectious tissues entering the animal or human food chains.
https://www.ars.usda.gov/research/publications/publication/?seqNo115=395351
Title: A comparison of classical and H-type bovine spongiform encephalopathy associated with E211K prion protein polymorphism in wild type and EK211cattle following intracranial inoculation
Author item MOORE, S - Orise Fellow item WEST GREENLEE, M - Iowa State University item Smith, Jodi item Vrentas, Catherine item Nicholson, Eric item Greenlee, Justin
Submitted to: Frontiers in Veterinary Science Publication Type: Peer Reviewed Journal Publication Acceptance Date: 8/30/2016 Publication Date: 9/15/2016 Citation: 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 EK211cattle following intracranial inoculation.
Frontiers in Veterinary Science. 3:78. Interpretive
Summary: Cases of bovine spongiform encephalopathy (BSE) or mad cow disease can be subclassified into at least 3 distinct disease forms with the predominate form known as classical BSE and the others collectively referred to as atypical BSE. Atypical BSE can be further subdivided into H-type and L-type cases that are distinct from classical BSE and from each other. Both of the atypical BSE subtypes are believed to occur spontaneously, whereas classical BSE is spread through feeding contaminated meat and bone meal to cattle. Work by other research groups suggests that the stability of the distinguishing features of atypical BSE cases (phenotypical stability) can change to closely resemble classical BSE after experimental passage implicating atypical BSE as a possible origin of classical BSE. Interestingly, one case of H-type BSE in the US was associated with an inherited mutation in the prion protein gene referred to as E211K. The purpose of this work was to compare wild type and cattle with the E211K mutation after experimental inoculation with either classical BSE or H-BSE from the original E211K case. This study demonstrates that the disease features of E211K BSE-H remain stable when transmitted to cattle without the K211 polymorphism. In addition, passage of classical BSE to cattle with the K211 polymorphism results in disease with features consistent with classical BSE and not a switch to atypical BSE-H as a result of the K211 polymorphism. As the origin of classical, feedborne BSE remains unknown and low numbers of atypical BSE are diagnosed each year, parties with interest in the cattle and beef industries and regulatory officials responsible for safe feeding practices of cattle will be interested in this work.
Technical Abstract: In 2006, a case of H-type bovine spongiform encephalopathy (BSE-H) was diagnosed in a cow that was associated with a heritable polymorphism in the bovine prion protein gene (PRNP) resulting in a lysine for glutamine amino acid substitution at codon 211 (called E211K) of the prion protein. Although the prevalence of this polymorphism is low, cattle carrying the K211 allele may be predisposed to rapid onset of BSE-H when exposed or to the potential development of a genetic BSE. This study was conducted to better understand the relationship between the K211 polymorphism and its effect on BSE phenotype. BSE-H from the US 2006 case was inoculated intracranially (IC) in one PRNP wild type (EE211) calf and one EK211 calf. In addition, one wild type calf and one EK211 calf were inoculated IC with brain homogenate from a US 2003 classical BSE case. All cattle developed clinical disease. The survival times of the E211K BSE-H inoculated EK211 calf (10 months) was shorter than the wild type calf (18 months). This genotype effect was not observed in classical BSE inoculated cattle (both 26 months). Significant changes in retinal function were observed in H-type BSE challenged cattle only. Cattle challenged with the same inoculum showed similar severity and neuroanatomical distribution of vacuolation and disease-associated prion protein deposition in the brain, though differences in neuropathology were observed between E211K BSE-H and classical BSE inoculated animals. Western blot results for brain tissue from challenged animals were consistent with the inoculum strains. This study demonstrates that the phenotype of E211K BSE-H remains stable when transmitted to cattle without the K211 polymorphism, and exhibits a number of features that differ from classical BSE in both wild type and heterozygous EK211 animals.
https://www.ars.usda.gov/research/publications/publication/?seqNo115=326785
THURSDAY, JUNE 5, 2025
World Organisation for Animal Health (WOAH) downgrades UK’s BSE risk rating to negligible, what could go wrong?
https://bovineprp.blogspot.com/2025/06/world-organisation-for-animal-health.html
OIE Conclusions on transmissibility of atypical BSE among cattle
Given that cattle have been successfully infected by the oral route, at least for L-BSE, it is reasonable to conclude that atypical BSE is potentially capable of being recycled in a cattle population if cattle are exposed to contaminated feed. In addition, based on reports of atypical BSE from several countries that have not had C-BSE, it appears likely that atypical BSE would arise as a spontaneous disease in any country, albeit at a very low incidence in old cattle. In the presence of livestock industry practices that would allow it to be recycled in the cattle feed chain, it is likely that some level of exposure and transmission may occur. As a result, since atypical BSE can be reasonably considered to pose a potential background level of risk for any country with cattle, the recycling of both classical and atypical strains in the cattle and broader ruminant populations should be avoided.
https://www.oie.int/fileadmin/SST/adhocreports/Bovine%20spongiform%20encephalopathy/AN/A_AhG_BSEsurv_RiskAss_Mar2019.pdf
Annex 7 (contd) AHG on BSE risk assessment and surveillance/March 2019
34 Scientific Commission/September 2019
3. Atypical BSE
The Group discussed and endorsed with minor revisions an overview of relevant literature on the risk of atypical BSE being recycled in a cattle population and its zoonotic potential that had been prepared ahead of the meeting by one expert from the Group. This overview is provided as Appendix IV and its main conclusions are outlined below. With regard to the risk of recycling of atypical BSE, recently published research confirmed that the L-type BSE prion (a type of atypical BSE prion) may be orally transmitted to calves1 . In light of this evidence, and the likelihood that atypical BSE could arise as a spontaneous disease in any country, albeit at a very low incidence, the Group was of the opinion that it would be reasonable to conclude that atypical BSE is potentially capable of being recycled in a cattle population if cattle were to be exposed to contaminated feed. Therefore, the recycling of atypical strains in cattle and broader ruminant populations should be avoided.
4. Definitions of meat-and-bone meal (MBM) and greaves
http://web.oie.int/downld/PROC2020/A_SCAD_Sept2019.pdf
The L-type BSE prion is much more virulent in primates and in humanized mice than is the classical BSE prion, which suggests the possibility of zoonotic risk associated with the L-type BSE prion
https://wwwnc.cdc.gov/eid/article/16/7/09-1882_article
Consumption of L-BSE–contaminated feed may pose a risk for oral transmission of the disease agent to cattle.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5324790/
Thus, it is imperative to maintain measures that prevent the entry of tissues from cattle possibly infected with the agent of L-BSE into the food chain.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3310119/
Atypical L-type bovine spongiform encephalopathy (L-BSE) transmission to cynomolgus macaques, a non-human primate
Fumiko Ono 1, Naomi Tase, Asuka Kurosawa, Akio Hiyaoka, Atsushi Ohyama, Yukio Tezuka, Naomi Wada, Yuko Sato, Minoru Tobiume, Ken'ichi Hagiwara, Yoshio Yamakawa, Keiji Terao, Tetsutaro Sata
Affiliations expand
PMID: 21266763
Abstract
A low molecular weight type of atypical bovine spongiform encephalopathy (L-BSE) was transmitted to two cynomolgus macaques by intracerebral inoculation of a brain homogenate of cattle with atypical BSE detected in Japan. They developed neurological signs and symptoms at 19 or 20 months post-inoculation and were euthanized 6 months after the onset of total paralysis. Both the incubation period and duration of the disease were shorter than those for experimental transmission of classical BSE (C-BSE) into macaques. Although the clinical manifestations, such as tremor, myoclonic jerking, and paralysis, were similar to those induced upon C-BSE transmission, no premonitory symptoms, such as hyperekplexia and depression, were evident. Most of the abnormal prion protein (PrP(Sc)) was confined to the tissues of the central nervous system, as determined by immunohistochemistry and Western blotting. The PrP(Sc) glycoform that accumulated in the monkey brain showed a similar profile to that of L-BSE and consistent with that in the cattle brain used as the inoculant. PrP(Sc) staining in the cerebral cortex showed a diffuse synaptic pattern by immunohistochemistry, whereas it accumulated as fine and coarse granules and/or small plaques in the cerebellar cortex and brain stem. Severe spongiosis spread widely in the cerebral cortex, whereas florid plaques, a hallmark of variant Creutzfeldt-Jakob disease in humans, were observed in macaques inoculated with C-BSE but not in those inoculated with L-BSE.
https://pubmed.ncbi.nlm.nih.gov/21266763/
see full text;
https://www.niid.go.jp/niid/images/JJID/64/81.pdf
''H-TYPE BSE AGENT IS TRANSMISSIBLE BY THE ORONASAL ROUTE''
This study demonstrates that the H-type BSE agent is transmissible by the oronasal route. These results reinforce the need for ongoing surveillance for classical and atypical BSE to minimize the risk of potentially infectious tissues entering the animal or human food chains.
https://www.ars.usda.gov/research/publications/publication/?seqNo115=353094
'Spontaneous mutation'
***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.***
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.
https://www.nature.com/articles/srep11573
***> US Report, Scrapie, CWD, Cattle, Sheep, Pigs, Cervid, Humans, Zoonotic, 2026 <***
*** Grant Agreement number: 222887 ***
*** Project acronym: PRIORITY ***
*** Project title: Protecting the food chain from prions: shaping European priorities through basic and applied research Funding ***
Scheme: Large-scale integrating project Period covered: from Oct. 1, 2009 to Sept. 30, 2014
Name of the scientific representative of the project's co-ordinator1, Title and Organisation: Jesús R. Requena, Ph.D., Associate Professor, Department of medicine, University of Santiago de Compostela, Spàin. Tel: 34-881815464 Fax: 34-881815403 E-mail: jesus.requena@usc.es
Project website¡ Error! Marcador no definido. address: www.prionpriority.eu
PRIORITY, PROJECT FINAL REPORT
*** 14) Concluding that atypical scrapie can transmit to Humans and that its strain properties change as it transmits between species ***
snip...
http://cordis.europa.eu/docs/results/222/222887/final1-priority-final-report.pdf
see;
https://nor-98.blogspot.com/2016/09/goat-k222-prpc-polymorphic-variant-does.html
Block D: Prion epidemiology
Studies on atypical scrapie were identified as a key element of this block, given the potential risk associated to this agent. We studied the permeability of Human, bovine and porcine species barriers to atypical scrapie agent transmission. Experiments in transgenic mice expressing bovine, porcine or human PrPC suggest that this TSE agent has the intrinsic ability to propagate across these species barriers including the Human one. Upon species barrier passage the biological properties and phenotype of atypical scrapie seem to be altered. Further experiments are currently ongoing (in the framework of this project but also in other projects) in order to: (i) characterize the properties of the prion that emerged from the propagation of atypical scrapie in tg Hu; (ii) to confirm that the phenomena we observed are also true for atypical scrapie isolates other than the ones we have studied.
In parallel, studies in sheep have concluded that:
*** Atypical scrapie can be transmitted by both oral and intracerebral route in sheep with various PRP genotypes
*** Low but consistent amount of infectivity accumulates in peripheral tissue (mammary gland, lymph nodes, placenta, skeletal muscles, nerves) of sheep incubating atypical scrapie.
*** The combination of data from all our studies leads us to conclude that:
*** Atypical scrapie passage through species barriers can lead to the emergence of various prions including classical BSE (following propagation in porcine PRP transgenic mice).
*** Atypical scrapie can propagate, with a low efficacy, in human PrP expressing mice. This suggests the existence of a zoonotic potential for this TSE agent.
snip...
We advance our main conclusions and recommendations, in particular as they might affect public policy, including a detailed elaboration of the evidence that led to them. Our main recommendations are:
a. The issue of re-introducing ruminant protein into the food-chain The opinion of the members of Priority is that sustaining an absolute feed ban for ruminant protein to ruminants is the essential requirement, especially since the impact of non-classical forms of scrapie in sheep and goats is not fully understood and cannot be fully estimated. Therefore, the consortium strongly recommends prohibiting re-introduction of processed ruminant protein into the food-chain. Arguments in support of this opinion are:
• the large (and still uncharacterized) diversity of prion agents that circulate in animal populations;
• the uncertainties related to prion epidemiology in animal populations;
• the unknown efficacy of industrial processes applied to reduce microbiological risk during processed animal protein (PAP) production on most prion agents; • the intrinsic capacity of prions to cross interspecies transmission barriers; • the lack of sensitive methodology for identifying cross contamination in food.
• the evolution of natural food chains in nature (i.e. who eats whom or what) has generated an efficient barrier preventing, to some extent, novel prion epidemies and that this naturally evolved ecology should be respected.
The consortium is also hesitant to introduce processed ruminant proteins into fish food considering the paucity of data on prion infections in fishes and sea animals including those of mammalian origin, and the risk of establishing an environmental contamination of the oceans that cannot be controlled.
b. Atypical prion agents and surveillance
Atypical prion agents (see below) will probably continue to represent the dominant form of prion diseases in the near future, particularly in Europe.
*** Atypical L-type BSE has clear zoonotic potential, as demonstrated in experimental models.
*** Similarly, there are now some data that seem to indicate that the atypical scrapie agent can cross various species barriers.
*** Moreover, the current EU policy for eradicating scrapie (genetic selection in affected flocks) is ineffective for preventing atypical scrapie.
*** The recent identification of cell-to-cell propagation and the protein-encoded strain properties of human neurodegenerative diseases such as Alzheimer's disease and Parkinson's disease, suggest that they bear the potential to be transmissible even if not with the same efficiency as CJD. More epidemiological data from large cohorts are necessary to reach any conclusion on the impact of their transmissibility on public health. Re-evaluations of safety precautions may become necessary depending on the outcome of these studies. In that context it would appear valuable
• to develop knowledge related to the pathogenesis and inter-individual transmission of atypical prion agents in ruminants (both intra- and inter-species)
• to improve the sensitivity of detection assays that are applied in the field towards this type of agent
• to maintain a robust surveillance of both animal and human populations
c. The need for extended research on prions
Intensified searching for a molecular determinants of the species barrier is recommended, since this barrier is a key for many important policy areas - risk assessment, proportional policies, the need for screening of human products and food. In this respect, prion strain structural language also remains an important issue for public health for the foreseeable future. Understanding the structural basis for strains and the basis for adaptation of a strain to a new host will require continued fundamental research. Prions maintain a complex two-way relationship with the host cell and fundamental research is needed on mechanisms for their transmission, replication and cause of nervous system dysfunction and death.
Early detection of prion infection, ideally at preclinical stage, also remains crucial for development of effective treatment strategies in humans affected by the disease.
Position of the Priority consortium
Nearly 30 years ago, the appearance in the UK of Bovine Spongiform Encephalopathy (BSE) quickly brought the previously obscure “prion diseases” to the spotlight. The ensuing health and food crises that spread throughout Europe had devastating consequences. In the UK alone, there were more than 36,000 farms directly affected by BSE and the transmission of BSE prions to humans via the food chain has caused over 200 people in Europe to die from variant Creutzfeldt-Jakob disease (vCJD) (http://www.cjd.ed.ac.uk
Origins of prion epidemies
Classical BSE now appears to be under control, with 18 EU Member States having achieved the World Organisation for Animal Health (Office International Epizooties) „negligible risk‟ status (May 2014; http://www.oie.int/en/animal-health-in-the-world/official-disease-status/bse/list-of-bse-risk-status/), and the remaining MS assessed as „controlled‟ risk. Of note, research, including EU-funded research, has played a key role in this success: while the origin of the infection was never defined, the principle driver of the epidemic was identified as prions in Meat and Bone Meal (MBM). Tests based on prion protein-specific antibodies were developed, allowing detection of infected animals, and a better understanding of disease pathogenesis and the distribution of infectivity in edible tissues; experimental investigation of transmission barriers between different species allowed a rational estimation of risks, etc. All of this led to the implementation of rational and effective policies, such as the MBM ban to protect the animal feed chain, and the Specified Risk Material (SRM) regulations to protect the human food chain.
In spite of this progress, prions are still a threat. Epidemiological re-assessment indicates that the ∼10 year incubation period separating the peaks of the BSE and the vCJD epidemics is probably too short. In addition, results from a large number of human tonsil and appendix analyses in the UK suggest that there may be a high number of asymptomatic individuals who are positive for the disease-associated conformer prion protein PrPSc. While vCJD is the only form of human prion disease that has been consistently demonstrated to have lymphoreticular involvement, there has been no systematic investigation of lymphoid tissue in cases with other prion diseases.
The human prion problem
The clinical cases of vCJD identified to date have all shared a common PrP genotype (M129M), although one pre-clinical case was confirmed as an M129V heterozygote, and it has been mooted that perhaps only the M129M proportion of the population is susceptible. However, in the UK appendix study, PrP accumulation was described in samples representing every codon 129 genotype, raising the possibility that genotype does not confer resistance but instead modulates incubation period. Apart from the two UK studies, the lymphoid tissues of non-CJD patients have not been examined for the presence of PrPSc, so, these cases may not solely represent pre-clinical vCJD, but also other forms of prion disease.
Recent experiments in highly susceptible mouse models indicate the presence of infectivity in blood or blood components at late disease stages in sporadic CJD. The significance of this experimental finding for humans has to be explored in more detail and, at the present time, there is no evidence for the transmission of prions via blood in sporadic CJD. However a likely scenario is that all those with signs of infection or abnormal PrP accumulation in peripheral tissue could have infective blood, posing the risk for transmission via blood products, which has been clearly demonstrated in experimental models, and confirmed in several cases of vCJD in man. Altogether, these data clearly demonstrate the potential risk of a second wave of vCJD, particularly when the number people identified with lymphoid accumulation of PrPSc (16/32,411) gives a prevalence estimate in the UK of 493 per million, much higher than the number of clinical cases seen to date.
The animal prion problem
An increasing number of reports on cases of “atypical” BSE in cattle throughout the EU and beyond may lead to a new epidemic, particularly since we still do not understand all factors determining the species barrier. Ovine scrapie is another concern, because it could mask ovine BSE, presumably transmissible to humans. Scrapie is endemic and not likely to be eradicated soon, although current control measures are effective at greatly reducing disease incidence. Atypical forms, which may be spontaneous, are not affected by these control measures and these forms of disease will persist in the global animal population. The low prevalence of these disease forms makes effective surveillance very challenging. However, there is a clear risk attendant on ignoring these cases without an understanding of their possible zoonotic potential, particularly when most forms of human disease have no established aetiology. In summary, atypical cases of BSE and scrapie presently clearly outnumber classical cases in cattle and sheep in all member states.
We will highlight the state-of-the-art knowledge and point out scientific challenges and the major questions for research. Strategic objectives and priorities in Europe in the future for research that aims to control, eliminate or eradicate the threat posed by prions to our food and health are also indicated.
The Priority project has focused on 4 themes, namely the structure, function, conversion and toxicity of prions; detection of prions; mechanisms of prion transmission and spreading and epidemiology of prion diseases. This paper summarizes the opinions/positions reached within these themes at the end of the project.
http://cordis.europa.eu/docs/results/222/222887/final1-priority-final-report.pdf
see;
https://nor-98.blogspot.com/2016/09/goat-k222-prpc-polymorphic-variant-does.html
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
O.05: Transmission of prions to primates after extended silent incubation periods: Implications for BSE and scrapie risk assessment in human populations
*** 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.
==============
PRION 2015 CONFERENCE
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5019500/
PRION 2016 TOKYO
Saturday, April 23, 2016
SCRAPIE WS-01: Prion diseases in animals and zoonotic potential 2016
Prion. 10:S15-S21. 2016 ISSN: 1933-68961933-690X
WS-01: Prion diseases in animals and zoonotic potential
***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
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
Comparing the Distribution of Ovine Classical Scrapie and Sporadic Creutzfeldt-Jakob Disease in Italy: Spatial and Temporal Associations (2002-2014)
Ru G1 ., Pocchiari M2 ., Bertolini S. 1, Pite L.1 , Puopolo M.2 , Ladogana A.2 , Perrotta M.G.3 , Meloni D 1 . (1) National reference center for the study and research on animal encephalopathies and comparative neuropathologies (CEA). Experimental Zooprophylactic Institute of Piemonte, Liguria and Valle d'Aosta, Torino, Italy.
(2) Department of Cellular Biology and Neuroscience, Istituto Superiore di Sanità, Roma, Italy. (3) Office 3 National center for the fight and emergency against animal diseases. Ministry of Health, Roma, Italy.
Aim: This study aims to investigate potential spatial and temporal associations between Creutzfeldt-Jakob disease (CJD) in humans (2010-2014) and ovine classical scrapie (CS) (2002- 2006) in Italy, serving as a proxy for exposure.
Materials and Methods: National data from prion disease surveillance in humans (sporadic CJD) and small ruminants (CS) in Italy were utilized. A descriptive geographic analysis was conducted for each disease individually. Subsequently, an ecological study was performed to compare the occurrence of both diseases at the district and regional levels. Standardized incidence ratios (SIR), adjusted for confounders, were calculated for CJD and CS by district and region, respectively, representing the outcome and proxy of exposure. Considering a possible long incubation period of CJD, two study periods were analysed: 2010-2014 for CJD and 2002-2006 for CS. Eight alternative linear regression models were developed using SIR in humans as the dependent variable and SIR in sheep as the independent variable. These models varied in the scale of SIR data (continuous vs. categorical), geographical level (district vs. region), and the potential past exposure of sheep in specific areas to a known source of infection (via a contaminated vaccine).
Results: The analysis of data at the district level revealed no significant association. However, when considering aggregated regional data, all four models consistently indicated a statistically significant positive association, suggesting a higher incidence of the disease in humans as the regional incidence of sheep scrapie increased.
Conclusions: While the results are intriguing, it is important to acknowledge the inherent limitations of ecological studies. Nevertheless, these findings provide valuable evidence to formulate a hypothesis regarding the zoonotic potential of classical scrapie. Further investigations are necessary, employing specific designs such as analytical epidemiology studies, to test this hypothesis effectively.
Funded by: Italian Ministry of Health Grant number: Realizzazione del programma epidemiologico finalizzato a dare evidenza del potenziale zoonotico delle TSE animali diverse dalla BSE. Prot. N. 0018730-17/07/2015-DGSAFCOD_UO-P
''Nevertheless, these findings provide valuable evidence to formulate a hypothesis regarding the zoonotic potential of classical scrapie. Further investigations are necessary, employing specific designs such as analytical epidemiology studies, to test this hypothesis effectively.''
Meeting-book-final-version prion 2023 Prion 2023 Congress Organizing Committee and the NeuroPrion Association, we invite you to join us for the International Conference Prion2023 from 16-20 October 2023 in Faro, Portugal.
https://prion2023.org/wp-content/uploads/2023/10/Meeting-book-final-version2.pdf
https://web.archive.org/web/20250828201533/https://prion2023.org/wp-content/uploads/2023/10/Meeting-book-final-version2.pdf
https://www.researchgate.net/profile/Syed-Zahid-Shah/publication/378314391_Meeting-book-final-version_prion_2023/links/65d44dad28b7720cecdca95f/Meeting-book-final-version-prion-2023.pdf
Canadian 2021 H-type Bovine Spongiform Encephalopathy case associated with a novel E211K polymorphism in prion protein gene novel E211K polymorphism in prion protein gene
Waqas Tahir , Sandor Dudas , Renee Anderson , Jianmin Yang , Sarah Bogart , Kristina Santiago-Mateo, Yuanmu Fang & Roberta Quaghebeur
Pages 36-49 | Received 20 Feb 2025, Accepted 22 May 2025, Published online: 04 Aug 2025 Cite this article https://doi.org/10.1080/19336896.2025.2511933
ABSTRACT
Bovine Spongiform Encephalopathy (BSE) is a fatal neurodegenerative disease in cattle which can be either classical BSE (C-BSE) or atypical BSE (including H-BSE and L-BSE). Here, we report the results of our analyses of an H-BSE case found in Canada in 2021, indicating restriction of the pathological agent (PrPSc) mainly to the central nervous system with no or occasional weak involvement of peripheral tissues. Importantly, a non-synonymous mutation at codon 211 of the PRNP gene was detected and confirmed to be present as a germline mutation. This is the first case of BSE in Canada with a predisposing E211K mutation.
Snip…
Based on the results of this study, and the 2006 H-BSE case in the USA, there is an expanded spectrum of aetiologies for bovine prion diseases similar to what is observed in humans, including sporadic, genetic and acquired versions.
Supplemental material Canadian 2021 H-type Bovine Spongiform Encephalopathy case associated with a novel E211K polymorphism in prion protein gene
KEYWORDS:
Atypical BSE Bovine Spongiform Encephalopathycentral nervous systemE211K mutationprion diseasesprion protein genesynonymous mutation
https://www.tandfonline.com/doi/full/10.1080/19336896.2025.2511933#d1e1606
“Based on the results of this study, and the 2006 H-BSE case in the USA, there is an expanded spectrum of aetiologies for bovine prion diseases similar to what is observed in humans, including sporadic, genetic and acquired versions.”
see my full report here;
Saturday, April 25, 2026
***> USDA Statement BSE Surveillance Information Center Update 2026 <***
https://oieusdabseprp.blogspot.com/2026/04/usda-statement-bse-surveillance.html
Re-USA BSE Surveillance, BSE Testing, BSE Feed Regulation (21 CFR 589.2000), SRMs, and CWD
“Conclusion: These results demonstrate the oral transmission potential of atypical BSE in cattle. Surprisingly, regardless of which atypical type of BSE was used for P1 oral challenge, Prpsc in the P2 animals acquired biochemical characteristics similar to that of Prps in C-BSE, suggesting atypical BSE as a possible origin of C-BSE in UK.”
Abstract for Prion 2023
Title: Transmission of atypical BSE: a possible origin of Classical BSE in cattle
Abstract for Prion 2023
https://prion2023.org/wp-content/uploads/2023/10/Meeting-book-final-version2.pdf
https://web.archive.org/web/20250828201533/https://prion2023.org/wp-content/uploads/2023/10/Meeting-book-final-version2.pdf
https://www.researchgate.net/profile/Syed-Zahid-Shah/publication/378314391_Meeting-book-final-version_prion_2023/links/65d44dad28b7720cecdca95f/Meeting-book-final-version-prion-2023.pdf
***> 1. 01 Determined that white-tailed deer (WTD) infected with scrapie from sheep can transmit the disease to other deer under conditions mimicking natural exposure.
https://www.ars.usda.gov/research/project/?accnNo=440677&fy=202
https://www.ars.usda.gov/research/publications/publication/?seqNo115=336834
https://wwwnc.cdc.gov/eid/article/30/8/24-0007_article
see;
https://nor-98.blogspot.com/2016/09/goat-k222-prpc-polymorphic-variant-does.html
https://transmissiblespongiformencephalopathy.blogspot.com/2026/04/us-report-scrapie-cwd-cattle-sheep-pigs.html
***> USA Report, Scrapie, CWD, BSE, TSE, Cattle, Sheep, Pigs, Cervid, Humans, Zoonotic, 2026
April 2026
https://fdabse589.blogspot.com/2026/04/usa-report-scrapie-cwd-bse-tse-cattle.html
https://www.researchgate.net/publication/403956772_USA_Report_Scrapie_CWD_BSE_TSE_Cattle_Sheep_Pigs_Cervid_Humans_Zoonotic_2026
USA NEW SCRAPIE CASE 2026
United States of America - Scrapie - Immediate notification WAHIS
https://wahis.woah.org/#/in-review/7742
USDA APHIS statement
https://www.aphis.usda.gov/news/program-update/usda-confirms-detection-classical-scrapie-slaughtered-sheep
Oregon statement
https://apps.oregon.gov/oregon-newsroom/OR/ODA/Posts/Post/Classical-Scrapie-Confirmed-in-Oregon-Sheep-Through-Routine-Surveillance
Scrapie Update
https://scrapie-usa.blogspot.com/2026/08/usda-confirms-detection-of-classical.html
*** 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
O.05: Transmission of prions to primates after extended silent incubation periods: Implications for BSE and scrapie risk assessment in human populations
*** 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.
==============
PRION 2015 CONFERENCE
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5019500/
PRION 2016 TOKYO
Saturday, April 23, 2016
SCRAPIE WS-01: Prion diseases in animals and zoonotic potential 2016
Prion. 10:S15-S21. 2016 ISSN: 1933-68961933-690X
WS-01: Prion diseases in animals and zoonotic potential
***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
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
Comparing the Distribution of Ovine Classical Scrapie and Sporadic Creutzfeldt-Jakob Disease in Italy: Spatial and Temporal Associations (2002-2014)
Ru G1 ., Pocchiari M2 ., Bertolini S. 1, Pite L.1 , Puopolo M.2 , Ladogana A.2 , Perrotta M.G.3 , Meloni D 1 . (1) National reference center for the study and research on animal encephalopathies and comparative neuropathologies (CEA). Experimental Zooprophylactic Institute of Piemonte, Liguria and Valle d'Aosta, Torino, Italy.
(2) Department of Cellular Biology and Neuroscience, Istituto Superiore di Sanità, Roma, Italy. (3) Office 3 National center for the fight and emergency against animal diseases. Ministry of Health, Roma, Italy.
Aim: This study aims to investigate potential spatial and temporal associations between Creutzfeldt-Jakob disease (CJD) in humans (2010-2014) and ovine classical scrapie (CS) (2002- 2006) in Italy, serving as a proxy for exposure.
Materials and Methods: National data from prion disease surveillance in humans (sporadic CJD) and small ruminants (CS) in Italy were utilized. A descriptive geographic analysis was conducted for each disease individually. Subsequently, an ecological study was performed to compare the occurrence of both diseases at the district and regional levels. Standardized incidence ratios (SIR), adjusted for confounders, were calculated for CJD and CS by district and region, respectively, representing the outcome and proxy of exposure. Considering a possible long incubation period of CJD, two study periods were analysed: 2010-2014 for CJD and 2002-2006 for CS. Eight alternative linear regression models were developed using SIR in humans as the dependent variable and SIR in sheep as the independent variable. These models varied in the scale of SIR data (continuous vs. categorical), geographical level (district vs. region), and the potential past exposure of sheep in specific areas to a known source of infection (via a contaminated vaccine).
Results: The analysis of data at the district level revealed no significant association. However, when considering aggregated regional data, all four models consistently indicated a statistically significant positive association, suggesting a higher incidence of the disease in humans as the regional incidence of sheep scrapie increased.
Conclusions: While the results are intriguing, it is important to acknowledge the inherent limitations of ecological studies. Nevertheless, these findings provide valuable evidence to formulate a hypothesis regarding the zoonotic potential of classical scrapie. Further investigations are necessary, employing specific designs such as analytical epidemiology studies, to test this hypothesis effectively.
Funded by: Italian Ministry of Health Grant number: Realizzazione del programma epidemiologico finalizzato a dare evidenza del potenziale zoonotico delle TSE animali diverse dalla BSE. Prot. N. 0018730-17/07/2015-DGSAFCOD_UO-P
''Nevertheless, these findings provide valuable evidence to formulate a hypothesis regarding the zoonotic potential of classical scrapie. Further investigations are necessary, employing specific designs such as analytical epidemiology studies, to test this hypothesis effectively.''
Meeting-book-final-version prion 2023 Prion 2023 Congress Organizing Committee and the NeuroPrion Association, we invite you to join us for the International Conference Prion2023 from 16-20 October 2023 in Faro, Portugal.
https://prion2023.org/wp-content/uploads/2023/10/Meeting-book-final-version2.pdf
https://web.archive.org/web/20250828201533/https://prion2023.org/wp-content/uploads/2023/10/Meeting-book-final-version2.pdf
https://www.researchgate.net/profile/Syed-Zahid-Shah/publication/378314391_Meeting-book-final-version_prion_2023/links/65d44dad28b7720cecdca95f/Meeting-book-final-version-prion-2023.pdf
Canadian 2021 H-type Bovine Spongiform Encephalopathy case associated with a novel E211K polymorphism in prion protein gene novel E211K polymorphism in prion protein gene
Waqas Tahir , Sandor Dudas , Renee Anderson , Jianmin Yang , Sarah Bogart , Kristina Santiago-Mateo, Yuanmu Fang & Roberta Quaghebeur
Pages 36-49 | Received 20 Feb 2025, Accepted 22 May 2025, Published online: 04 Aug 2025 Cite this article https://doi.org/10.1080/19336896.2025.2511933
ABSTRACT
Bovine Spongiform Encephalopathy (BSE) is a fatal neurodegenerative disease in cattle which can be either classical BSE (C-BSE) or atypical BSE (including H-BSE and L-BSE). Here, we report the results of our analyses of an H-BSE case found in Canada in 2021, indicating restriction of the pathological agent (PrPSc) mainly to the central nervous system with no or occasional weak involvement of peripheral tissues. Importantly, a non-synonymous mutation at codon 211 of the PRNP gene was detected and confirmed to be present as a germline mutation. This is the first case of BSE in Canada with a predisposing E211K mutation.
Snip…
Based on the results of this study, and the 2006 H-BSE case in the USA, there is an expanded spectrum of aetiologies for bovine prion diseases similar to what is observed in humans, including sporadic, genetic and acquired versions.
Supplemental material Canadian 2021 H-type Bovine Spongiform Encephalopathy case associated with a novel E211K polymorphism in prion protein gene
KEYWORDS:
Atypical BSE Bovine Spongiform Encephalopathycentral nervous systemE211K mutationprion diseasesprion protein genesynonymous mutation
https://www.tandfonline.com/doi/full/10.1080/19336896.2025.2511933#d1e1606
“Based on the results of this study, and the 2006 H-BSE case in the USA, there is an expanded spectrum of aetiologies for bovine prion diseases similar to what is observed in humans, including sporadic, genetic and acquired versions.”
see my full report here;
Saturday, April 25, 2026
***> USDA Statement BSE Surveillance Information Center Update 2026 <***
https://oieusdabseprp.blogspot.com/2026/04/usda-statement-bse-surveillance.html
***> see also, Texas mad cow attempted BSE cover-up files, with receipts!
Re-USA BSE Surveillance, BSE Testing, BSE Feed Regulation (21 CFR 589.2000), SRMs, and CWD
“Conclusion: These results demonstrate the oral transmission potential of atypical BSE in cattle. Surprisingly, regardless of which atypical type of BSE was used for P1 oral challenge, Prpsc in the P2 animals acquired biochemical characteristics similar to that of Prps in C-BSE, suggesting atypical BSE as a possible origin of C-BSE in UK.”
Abstract for Prion 2023
Title: Transmission of atypical BSE: a possible origin of Classical BSE in cattle
Abstract for Prion 2023
https://prion2023.org/wp-content/uploads/2023/10/Meeting-book-final-version2.pdf
https://web.archive.org/web/20250828201533/https://prion2023.org/wp-content/uploads/2023/10/Meeting-book-final-version2.pdf
https://www.researchgate.net/profile/Syed-Zahid-Shah/publication/378314391_Meeting-book-final-version_prion_2023/links/65d44dad28b7720cecdca95f/Meeting-book-final-version-prion-2023.pdf
***> 1. 01 Determined that white-tailed deer (WTD) infected with scrapie from sheep can transmit the disease to other deer under conditions mimicking natural exposure.
https://www.ars.usda.gov/research/project/?accnNo=440677&fy=202
https://www.ars.usda.gov/research/publications/publication/?seqNo115=336834
https://wwwnc.cdc.gov/eid/article/30/8/24-0007_article
see;
https://nor-98.blogspot.com/2016/09/goat-k222-prpc-polymorphic-variant-does.html
https://transmissiblespongiformencephalopathy.blogspot.com/2026/04/us-report-scrapie-cwd-cattle-sheep-pigs.html
***> USA Report, Scrapie, CWD, BSE, TSE, Cattle, Sheep, Pigs, Cervid, Humans, Zoonotic, 2026
April 2026
https://fdabse589.blogspot.com/2026/04/usa-report-scrapie-cwd-bse-tse-cattle.html
https://www.researchgate.net/publication/403956772_USA_Report_Scrapie_CWD_BSE_TSE_Cattle_Sheep_Pigs_Cervid_Humans_Zoonotic_2026
USA NEW SCRAPIE CASE 2026
United States of America - Scrapie - Immediate notification WAHIS
https://wahis.woah.org/#/in-review/7742
USDA APHIS statement
https://www.aphis.usda.gov/news/program-update/usda-confirms-detection-classical-scrapie-slaughtered-sheep
Oregon statement
https://apps.oregon.gov/oregon-newsroom/OR/ODA/Posts/Post/Classical-Scrapie-Confirmed-in-Oregon-Sheep-Through-Routine-Surveillance
Scrapie Update
https://scrapie-usa.blogspot.com/2026/08/usda-confirms-detection-of-classical.html
https://scrapie-usa.blogspot.com/
Chronic Wasting Disease CWD TSE Prion
Arkansas, Texas, CWD TSE Prion Update Cervid and Pigs, and CJD Humans
Arkansas CWD
White-tailed deer population declines in a high-prevalence chronic wasting disease region of Arkansas, USA
Heather E. Gaya , Marcelo H. Jorge, Lisa A. Jorge, Mark G. Ruder, Gino J. D’Angelo, Richard B. Chandler, Michael J. Chamberlain
Published: January 7, 2026
https://doi.org/10.1371/journal.pone.0340070
Abstract
Chronic wasting disease (CWD) is a fatal transmissible spongiform encephalopathy affecting cervids worldwide. CWD was first detected in Arkansas in 2015 and as of August 2025 has been detected in 24 counties across the state. Within the Tier 1 CWD management zone of northern Arkansas, average apparent CWD prevalence exceeded 25% at the onset of our study in 2021. We tested the hypothesis that high prevalence of CWD negatively affects white-tailed deer population viability. We collected data from 243 camera traps and deployed GPS-collars on 131 adult deer to monitor population dynamics. Using spatial mark-resight models, we estimated density of adult deer from 2021 to 2024 at three sites across a presumed CWD gradient to assess the impacts of high CWD prevalence on deer abundance. Deer densities declined at all three study sites, at an average 17% (95% CI: 8% − 24%) decline per year. Male densities declined by an average 23% (95% CI: 5% − 31%) per year compared to 15% (95% CI: 2% − 23%) yearly declines for females. These findings suggest that CWD can negatively impact deer populations through direct reductions in density, but additional research is needed to determine if additional factors contributed to these declines. Furthermore, our findings suggest the populations we studied are not sustainable under current harvest regulations.
snip…
Conclusion
Our findings add to a growing body of evidence that CWD can greatly alter deer populations. Given that previous research has demonstrated reductions in survival due to CWD [5], the high prevalence in our study area likely contributed to the observed population declines. However, it is possible that factors other than CWD contributed to the observed trends in deer densities. Future work in this region should document the direct effects of CWD on vital rates such as survival and fecundity to confirm the role of CWD in population declines. At present, few management tools are available to control CWD once established on the landscape. We therefore suggest that wildlife managers focus on slowing or preventing the spread of CWD to uninfected populations, taking actions that aim to stabilize or lower CWD prevalence, and collect accurate data on deer abundance to monitor when harvest limits become unsustainable.
Supporting information
Estimates of encounter rate and spatial scale parameters. Showing 1/3: pone.0340070.s001.docx
S1 Table. Estimates of encounter rate and spatial scale parameters. https://doi.org/10.1371/journal.pone.0340070.s001 (DOCX) S1 Fig. Estimated sex ratio of adult white-tailed deer. https://doi.org/10.1371/journal.pone.0340070.s002
(DOCX) S2 Fig. CWD sample prevalence and hunter harvest in Newton County, Searcy County and Arkansas’s Zone 2 harvest area. https://doi.org/10.1371/journal.pone.0340070.s003
(DOCX)
https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0340070
AGFC CWD-positive deer found in Grant, Sevier counties, 2,278 Confirmed Cases To Date
CWD-positive deer found in Grant, Sevier counties
BY Randy Zellers ON 12-19-2025 LAB DATA
AGFC CWD-positive deer found in Grant, Sevier counties, 2,278 Confirmed Cases To Date
https://www.agfc.com/news/cwd-positive-deer-found-in-grant-sevier-counties/
SATURDAY, JULY 25, 2026
White-tailed deer population declines in a high-prevalence chronic wasting disease region of Arkansas, USA
https://chronic-wasting-disease.blogspot.com/2026/07/white-tailed-deer-population-declines.html
https://prpsc.proboards.com/thread/227/deer-population-declines-prevalence-region
Texas CWD
SUNDAY, JULY 19, 2026
Texas Chronic Wasting Disease CWD TSE Prion 1,393 Confirmed Cases To Date July 2026
https://chronic-wasting-disease.blogspot.com/2026/07/texas-chronic-wasting-disease-cwd-tse.html
https://prpsc.proboards.com/thread/225/texas-cwd-prion-confirmed-date
Disease report
“They analysed over 300 brain and lymph node samples from 178 wild pigs living across Arkansas and Texas, USA…the researchers identified CWD prions in up to 37% of the lymph node samples and 15% of brain samples. The lowest detection rates were in the Texas samples (below 16%), matching the lower CWD prevalence in the state’s cervid population.”
Chronic wasting disease prions in cervids and wild pigs in North America Preliminary Outbreak Assessment DEFRA 26 January 2026 Department for Environment, Food and Rural Affairs
Preliminary Outbreak Assessment
Chronic wasting disease prions in cervids and wild pigs in North America
26 January 2026
Disease report
“They analysed over 300 brain and lymph node samples from 178 wild pigs living across Arkansas and Texas, USA…the researchers identified CWD prions in up to 37% of the lymph node samples and 15% of brain samples. The lowest detection rates were in the Texas samples (below 16%), matching the lower CWD prevalence in the state’s cervid population.”
https://assets.publishing.service.gov.uk/media/697a3b013c71d838df6bd413/CWD_Prions_in_Cervids_and_Wild_Pigs_in_North_America.pdf
Detection of Prions in Wild Pigs (Sus scrofa) from Areas with Reported Chronic Wasting Disease Cases, United State Volume 31, Number 1—January 2025
https://wwwnc.cdc.gov/eid/article/31/1/24-0401_article
Chronic Wasting Disease CWD TSE Prion, Economical, Environmental, Zoonotic, Risk Factors 2026
https://transmissiblespongiformencephalopathy.blogspot.com/2026/02/chronic-wasting-disease-cwd-tse-prion.html
SUNDAY, AUGUST 09, 2026
Chronic Wasting Disease CWD and Population Declines of Cervid
https://chronic-wasting-disease.blogspot.com/2026/08/chronic-wasting-disease-cwd-and.html
https://prpsc.proboards.com/thread/229/cwd-prion-population-declines-cervid
Chronic Wasting Disease CWD TSE Prion June 2026
WEDNESDAY, MAY 27, 2026
Limited transmission of cervid prions to nonhuman primates provides insights into the zoonotic potential of chronic wasting disease
https://www.science.org/doi/10.1126/sciadv.aeb7613
https://chronic-wasting-disease.blogspot.com/2026/05/limited-transmission-of-cervid-prions.html
https://prpsc.proboards.com/thread/220/limited-transmission-cervid-nonhuman-primates
FRIDAY, MAY 08, 2026
WILDLIFE HEALTH COORDINATION AND ZOONOTIC DISEASE PREVENTION ACT S.4451 Chronic Wasting Disease CWD TSE Prion Singeltary Submission
https://chronic-wasting-disease.blogspot.com/2026/05/wildlife-health-coordination-and.html
https://prpsc.proboards.com/thread/217/wildlife-health-coordination-zoonotic-disease
https://fdabse589.blogspot.com/2026/04/usa-report-scrapie-cwd-bse-tse-cattle.html
https://transmissiblespongiformencephalopathy.blogspot.com/2026/04/us-report-scrapie-cwd-cattle-sheep-pigs.html
https://www.researchgate.net/publication/403956772_USA_Report_Scrapie_CWD_BSE_TSE_Cattle_Sheep_Pigs_Cervid_Humans_Zoonotic_2026
***> Cervid CWD TSE PrP Transmission to Humans, has it already happened and being masked as sporadic CJD, What if? July 2026 Review
https://chronic-wasting-disease.blogspot.com/2026/07/cervid-cwd-tse-prp-transmission-to.html
https://prpsc.proboards.com/thread/224/cervid-transmission-humans-july-review
TUESDAY, APRIL 07, 2026
APHIS USDA Captive CWD Herds Update by State March 2026
https://chronic-wasting-disease.blogspot.com/2026/04/aphis-usda-captive-cwd-herds-update-by.html
***> USA Report, Scrapie, CWD, BSE, TSE, Cattle, Sheep, Pigs, Cervid, Humans, Zoonotic, 2026
April 2026
https://fdabse589.blogspot.com/2026/04/usa-report-scrapie-cwd-bse-tse-cattle.html
https://www.researchgate.net/publication/403956772_USA_Report_Scrapie_CWD_BSE_TSE_Cattle_Sheep_Pigs_Cervid_Humans_Zoonotic_2026
Tuesday, June 9, 2026
Hazard identification for the risks to terrestrial animal health from the import of hay and straw, BSE, CWD, Scrapie, TSE, Prion
https://www.gov.uk/government/publications/hazard-identification-for-the-risks-to-terrestrial-animal-health-from-the-import-of-hay-and-straw/hazard-identification-for-the-risks-to-terrestrial-animal-health-from-the-import-of-hay-and-straw
https://defrauktseprp.blogspot.com/2026/06/hazard-identification-for-risks-to.html
CAMEL PRION DISEASE
Thursday, July 16, 2026
Camel Prion Disease, Tataouine, Tunisia, 2019–2021 CDC Dispatch August 2026
https://camelusprp.blogspot.com/2026/07/camel-prion-disease-tataouine-tunisia.html
Chronic Wasting Disease CWD TSE Prion
Arkansas, Texas, CWD TSE Prion Update Cervid and Pigs, and CJD Humans
Arkansas CWD
White-tailed deer population declines in a high-prevalence chronic wasting disease region of Arkansas, USA
Heather E. Gaya , Marcelo H. Jorge, Lisa A. Jorge, Mark G. Ruder, Gino J. D’Angelo, Richard B. Chandler, Michael J. Chamberlain
Published: January 7, 2026
https://doi.org/10.1371/journal.pone.0340070
Abstract
Chronic wasting disease (CWD) is a fatal transmissible spongiform encephalopathy affecting cervids worldwide. CWD was first detected in Arkansas in 2015 and as of August 2025 has been detected in 24 counties across the state. Within the Tier 1 CWD management zone of northern Arkansas, average apparent CWD prevalence exceeded 25% at the onset of our study in 2021. We tested the hypothesis that high prevalence of CWD negatively affects white-tailed deer population viability. We collected data from 243 camera traps and deployed GPS-collars on 131 adult deer to monitor population dynamics. Using spatial mark-resight models, we estimated density of adult deer from 2021 to 2024 at three sites across a presumed CWD gradient to assess the impacts of high CWD prevalence on deer abundance. Deer densities declined at all three study sites, at an average 17% (95% CI: 8% − 24%) decline per year. Male densities declined by an average 23% (95% CI: 5% − 31%) per year compared to 15% (95% CI: 2% − 23%) yearly declines for females. These findings suggest that CWD can negatively impact deer populations through direct reductions in density, but additional research is needed to determine if additional factors contributed to these declines. Furthermore, our findings suggest the populations we studied are not sustainable under current harvest regulations.
snip…
Conclusion
Our findings add to a growing body of evidence that CWD can greatly alter deer populations. Given that previous research has demonstrated reductions in survival due to CWD [5], the high prevalence in our study area likely contributed to the observed population declines. However, it is possible that factors other than CWD contributed to the observed trends in deer densities. Future work in this region should document the direct effects of CWD on vital rates such as survival and fecundity to confirm the role of CWD in population declines. At present, few management tools are available to control CWD once established on the landscape. We therefore suggest that wildlife managers focus on slowing or preventing the spread of CWD to uninfected populations, taking actions that aim to stabilize or lower CWD prevalence, and collect accurate data on deer abundance to monitor when harvest limits become unsustainable.
Supporting information
Estimates of encounter rate and spatial scale parameters. Showing 1/3: pone.0340070.s001.docx
S1 Table. Estimates of encounter rate and spatial scale parameters. https://doi.org/10.1371/journal.pone.0340070.s001 (DOCX) S1 Fig. Estimated sex ratio of adult white-tailed deer. https://doi.org/10.1371/journal.pone.0340070.s002
(DOCX) S2 Fig. CWD sample prevalence and hunter harvest in Newton County, Searcy County and Arkansas’s Zone 2 harvest area. https://doi.org/10.1371/journal.pone.0340070.s003
(DOCX)
https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0340070
AGFC CWD-positive deer found in Grant, Sevier counties, 2,278 Confirmed Cases To Date
CWD-positive deer found in Grant, Sevier counties
BY Randy Zellers ON 12-19-2025 LAB DATA
AGFC CWD-positive deer found in Grant, Sevier counties, 2,278 Confirmed Cases To Date
https://www.agfc.com/news/cwd-positive-deer-found-in-grant-sevier-counties/
SATURDAY, JULY 25, 2026
White-tailed deer population declines in a high-prevalence chronic wasting disease region of Arkansas, USA
https://chronic-wasting-disease.blogspot.com/2026/07/white-tailed-deer-population-declines.html
https://prpsc.proboards.com/thread/227/deer-population-declines-prevalence-region
Texas CWD
SUNDAY, JULY 19, 2026
Texas Chronic Wasting Disease CWD TSE Prion 1,393 Confirmed Cases To Date July 2026
https://chronic-wasting-disease.blogspot.com/2026/07/texas-chronic-wasting-disease-cwd-tse.html
https://prpsc.proboards.com/thread/225/texas-cwd-prion-confirmed-date
Disease report
“They analysed over 300 brain and lymph node samples from 178 wild pigs living across Arkansas and Texas, USA…the researchers identified CWD prions in up to 37% of the lymph node samples and 15% of brain samples. The lowest detection rates were in the Texas samples (below 16%), matching the lower CWD prevalence in the state’s cervid population.”
Chronic wasting disease prions in cervids and wild pigs in North America Preliminary Outbreak Assessment DEFRA 26 January 2026 Department for Environment, Food and Rural Affairs
Preliminary Outbreak Assessment
Chronic wasting disease prions in cervids and wild pigs in North America
26 January 2026
Disease report
“They analysed over 300 brain and lymph node samples from 178 wild pigs living across Arkansas and Texas, USA…the researchers identified CWD prions in up to 37% of the lymph node samples and 15% of brain samples. The lowest detection rates were in the Texas samples (below 16%), matching the lower CWD prevalence in the state’s cervid population.”
https://assets.publishing.service.gov.uk/media/697a3b013c71d838df6bd413/CWD_Prions_in_Cervids_and_Wild_Pigs_in_North_America.pdf
Detection of Prions in Wild Pigs (Sus scrofa) from Areas with Reported Chronic Wasting Disease Cases, United State Volume 31, Number 1—January 2025
https://wwwnc.cdc.gov/eid/article/31/1/24-0401_article
Chronic Wasting Disease CWD TSE Prion, Economical, Environmental, Zoonotic, Risk Factors 2026
https://transmissiblespongiformencephalopathy.blogspot.com/2026/02/chronic-wasting-disease-cwd-tse-prion.html
SUNDAY, AUGUST 09, 2026
Chronic Wasting Disease CWD and Population Declines of Cervid
https://chronic-wasting-disease.blogspot.com/2026/08/chronic-wasting-disease-cwd-and.html
https://prpsc.proboards.com/thread/229/cwd-prion-population-declines-cervid
Chronic Wasting Disease CWD TSE Prion June 2026
WEDNESDAY, MAY 27, 2026
Limited transmission of cervid prions to nonhuman primates provides insights into the zoonotic potential of chronic wasting disease
https://www.science.org/doi/10.1126/sciadv.aeb7613
https://chronic-wasting-disease.blogspot.com/2026/05/limited-transmission-of-cervid-prions.html
https://prpsc.proboards.com/thread/220/limited-transmission-cervid-nonhuman-primates
FRIDAY, MAY 08, 2026
WILDLIFE HEALTH COORDINATION AND ZOONOTIC DISEASE PREVENTION ACT S.4451 Chronic Wasting Disease CWD TSE Prion Singeltary Submission
https://chronic-wasting-disease.blogspot.com/2026/05/wildlife-health-coordination-and.html
https://prpsc.proboards.com/thread/217/wildlife-health-coordination-zoonotic-disease
https://fdabse589.blogspot.com/2026/04/usa-report-scrapie-cwd-bse-tse-cattle.html
https://transmissiblespongiformencephalopathy.blogspot.com/2026/04/us-report-scrapie-cwd-cattle-sheep-pigs.html
https://www.researchgate.net/publication/403956772_USA_Report_Scrapie_CWD_BSE_TSE_Cattle_Sheep_Pigs_Cervid_Humans_Zoonotic_2026
***> Cervid CWD TSE PrP Transmission to Humans, has it already happened and being masked as sporadic CJD, What if? July 2026 Review
https://chronic-wasting-disease.blogspot.com/2026/07/cervid-cwd-tse-prp-transmission-to.html
https://prpsc.proboards.com/thread/224/cervid-transmission-humans-july-review
TUESDAY, APRIL 07, 2026
APHIS USDA Captive CWD Herds Update by State March 2026
https://chronic-wasting-disease.blogspot.com/2026/04/aphis-usda-captive-cwd-herds-update-by.html
***> USA Report, Scrapie, CWD, BSE, TSE, Cattle, Sheep, Pigs, Cervid, Humans, Zoonotic, 2026
April 2026
https://fdabse589.blogspot.com/2026/04/usa-report-scrapie-cwd-bse-tse-cattle.html
https://www.researchgate.net/publication/403956772_USA_Report_Scrapie_CWD_BSE_TSE_Cattle_Sheep_Pigs_Cervid_Humans_Zoonotic_2026
Tuesday, June 9, 2026
Hazard identification for the risks to terrestrial animal health from the import of hay and straw, BSE, CWD, Scrapie, TSE, Prion
https://www.gov.uk/government/publications/hazard-identification-for-the-risks-to-terrestrial-animal-health-from-the-import-of-hay-and-straw/hazard-identification-for-the-risks-to-terrestrial-animal-health-from-the-import-of-hay-and-straw
https://defrauktseprp.blogspot.com/2026/06/hazard-identification-for-risks-to.html
CAMEL PRION DISEASE
Thursday, July 16, 2026
Camel Prion Disease, Tataouine, Tunisia, 2019–2021 CDC Dispatch August 2026
https://camelusprp.blogspot.com/2026/07/camel-prion-disease-tataouine-tunisia.html
https://camelusprp.blogspot.com/
Arkansas CJD Surveillance
Creutzfeldt-Jakob disease (CJD) is a reportable condition under the Arkansas Department of Health Rules and Regulations for Reportable Diseases, but specific public health surveillance case totals or localized CJD outbreak data for 2025 are not published as an independent, open-access dataset by the state. National surveillance data compiled by the National Prion Disease Pathology Surveillance Center track aggregated national case examinations rather than breaking down explicit annual counts by individual state public health reports...
Texas Creutzfeldt Jakob Disease CJD TSE Prion Disease 2025
Update as of 10/15/25, NO REPORT TO UPDATE…
https://www.dshs.texas.gov/creutzfeldt-jakob-disease-cjd/creutzfeldt-jakob-disease-cjd-data
US NATIONAL PRION DISEASE PATHOLOGY SURVEILLANCE CENTER CJD TSE REPORT SEPTEMBER 2025
From the first full year of reporting CJD TSE in the US in 2000, where 90 cases of CJD was reported that year, to today, where in September 2025, the number of CJD cases reported in the last full year reporting, which would have been 2024, the number of CJD cases for 2024 was 249 cases. So, from the first full year 2000 CJD cases were 90 cases confirmed in that year, to 2024, where 2024 CJD statistics rose to 249 confirmed CJD cases in a single year. A dramatic increase in deaths, from figures that don’t seem to be dramatic. But thes figures today, they are not from “better surveillance”, that dog don’t hunt no more. They have been saying this for over 25 years, year after year, well it’s time to call it for what it is, Human Transmissible Spongiform Encephalopathy TSE Prion cases are rising, and it’s NOT because of better surveillance, or just a “happenstance of bad luck, that 85%+ of all human cases, sporadic CJD, including VPSPr, just happen spontaneously, no, it’s because of unknown environmental factors, and or iatrogenic factors, imho…terry
US NATIONAL PRION DISEASE PATHOLOGY SURVEILLANCE CENTER CJD TSE REPORT SEPTEMBER 2025
https://prionunitusaupdate.blogspot.com/2025/10/us-national-prion-disease-pathology.html
So, this is what we leave our children and grandchildren?
Mad Cow Scaremongers , The Center For Consumer Freedom Team Terry Singletary — A retired machinist and high school dropout, Terry Singletary suffered the tragic loss of his mother to “sporadic” Creutzfeldt-Jakob disease (CJD) in 1997. Desperate to find an explanation for his mother’s death, he has devoted himself to the sad and fruitless task of connecting her death to her diet. Various reports confirm that Mrs. Singletary’s life was claimed by the most common sub-type of CJD (one that accounts for 70 percent of “sporadic” cases). Sporadic CJD, unlike its newer “variant,” is not linked to meat.
Mad Cow Scaremongers , The Center For Consumer Freedom Team As the self-appointed international coordinator of CJD Watch, an organization he co-founded with social worker Deborah Oney, Singletary is cited in media reports as an apparent expert on tracking mad cow disease. This despite his lack of formal education and the absence for support from any credible academic, medical or scientific authority. His sensationalist allegations about the safety of U.S. beef have found their way into hundreds of newspapers and broadcasts. Singletary moderates a mad-cow discussion forum run by a vegetarian activist group; his contributions account for more than half the traffic on the “BSE-L” mailing list, which is generally read by real scientists. Animal rights activists and other food-scare artists frequently refer to him as “Dr. Terry Singletary,” apparently an honorary degree as he has yet to finish high school.
Mad Cow Scaremongers , The Center For Consumer Freedom Team Like many activists, Singletary ignores overwhelming epidemiological and laboratory evidence that rules out a connection between sporadic CJD and beef. Relying entirely on shallow circumstantial evidence and frequent repetition of claims which have been publicly refuted as false, he also blindly insists upon a mad-cow with Alzheimer’s, Parkinson’s, and Lou Gehrig’s disease. His specific allegations have been clearly refuted by Centers for Disease Countrol and Prevention scientists in the journal Neurology.
https://consumerfreedom.com/articles/138-mad-cow-scaremongers/
***> Mad Cow Scaremongers , The Center For Consumer Freedom Team Terry Singletary “he also blindly insists upon a mad-cow with Alzheimer’s, Parkinson’s, and Lou Gehrig’s disease. His specific allegations have been clearly refuted by Centers for Disease Countrol and Prevention scientists in the journal Neurology.”
2024, iatrogenic AD, what if?
Price of TSE prion poker goes up drastically…Terry
Alzheimer’s disease acquired from historic medical treatments
30 January 2024
“However, the recognition of transmission of amyloid-beta pathology in these rare situations should lead us to review measures to prevent accidental transmission via other medical or surgical procedures, in order to prevent such cases occurring in future.
“Importantly, our findings also suggest that Alzheimer's and some other neurological conditions share similar disease processes to CJD, and this may have important implications for understanding and treating Alzheimer’s disease in the future.”
https://www.ucl.ac.uk/prion/news/2024/jan/alzheimers-disease-acquired-historic-medical-treatments
not that it matters, but i started telling them from 2001, that Alzheimer’s and other neurological disorders were a TSE prion disease, and were capable of transmitting by iatrogenic routes…kind regards, Terry
Singeltary 2001 Alzheimer's disease
Singeltary 2001
Subject: CJD or Alzheimer's or the same ???
Date: Sun, 29 Apr 2001 12:45:28 -0700
From: "Terry S. Singeltary Sr."
Reply-To: Bovine Spongiform Encephalopathy
To: BSE-L@uni-karlsruhe.de
Bovine Spongiform Encephalopathy
Greetings List,
thought some might be interested in this. I have always wondered if CJD and or all TSEs and Alzheimer's could be linked. i have been of the opinion that Alzheimer's is a TSE for a long time, just at the low end of the titre of infectivity scale. i also believe in the accumulation theory. by dose, you could be killed by one sitting, or one injection, or one whatever, depending on the titre of infectivity of that whatever. on the other hand, if the dose is not a lethal dose, over a period of time, the accumulation will become lethal (if consumption continued), and i believe the route/source/titre of infectivity, will be a key roll to the incubation period, and symptoms.
just my opinion...snip…end
Singeltary Alzheimer’s 2014
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...
Self-Propagative Replication of Aβ Oligomers Suggests Potential Transmissibility in Alzheimer Disease
Amit Kumar, Kayla M. Pate, Melissa A. Moss, Dexter N. Dean, Vijayaraghavan Rangachari
Published: November 3, 2014
https://doi.org/10.1371/journal.pone.0111492
Reader Comments
Posted by flounder on 05 Nov 2014 at 21:27 GMT
Alzheimer’s disease and Transmissible Spongiform Encephalopathy prion disease, Iatrogenic, what if ?
Background
Alzheimer’s disease and Transmissible Spongiform Encephalopathy disease have both been around a long time, and was discovered in or around the same time frame, early 1900’s. Both diseases are incurable and debilitating brain disease, that are in the end, 100% fatal, with the incubation/clinical period of the Alzheimer’s disease being longer (most of the time) than the TSE prion disease. Symptoms are very similar, and pathology is very similar.
Methods
Through years of research, as a layperson, of peer review journals, transmission studies, and observations of loved ones and friends that have died from both Alzheimer’s and the TSE prion disease i.e. Heidenhain Variant Creutzfelt Jakob Disease CJD.
Results
I propose that Alzheimer’s is a TSE disease of low dose, slow, and long incubation disease, and that Alzheimer’s is Transmissible, and is a threat to the public via the many Iatrogenic routes and sources. It was said long ago that the only thing that disputes this, is Alzheimer’s disease transmissibility, or the lack of. The likelihood of many victims of Alzheimer’s disease from the many different Iatrogenic routes and modes of transmission as with the TSE prion disease.
Conclusions
There should be a Global Congressional Science round table event set up immediately to address these concerns from the many potential routes and sources of the TSE prion disease, including Alzheimer’s disease, and a emergency global doctrine put into effect to help combat the spread of Alzheimer’s disease via the medical, surgical, dental, tissue, and blood arena’s. All human and animal TSE prion disease, including Alzheimer’s should be made reportable in every state, and Internationally, WITH NO age restrictions. Until a proven method of decontamination and autoclaving is proven, and put forth in use universally, in all hospitals and medical, surgical arena’s, or the TSE prion agent will continue to spread. IF we wait until science and corporate politicians wait until politics lets science _prove_ this once and for all, and set forth regulations there from, we will all be exposed to the TSE Prion agents, if that has not happened already.
end...tss
Alzheimer’s disease and Transmissible Spongiform Encephalopathy prion disease, Iatrogenic, what if ?
Posted by flounder on 05 Nov 2014 at 21:27 GMT
https://journals.plos.org/plosone/article/comment?id=10.1371/annotation/933cc83a-a384-45c3-b3b2-336882c30f9d
Ann N Y Acad Sci. 1982;396:131-43.
Alzheimer's disease and transmissible virus dementia (Creutzfeldt-Jakob disease).
Brown P, Salazar AM, Gibbs CJ Jr, Gajdusek DC.
Abstract
Ample justification exists on clinical, pathologic, and biologic grounds for considering a similar pathogenesis for AD and the spongiform virus encephalopathies. However, the crux of the comparison rests squarely on results of attempts to transmit AD to experimental animals, and these results have not as yet validated a common etiology. Investigations of the biologic similarities between AD and the spongiform virus encephalopathies proceed in several laboratories, and our own observation of inoculated animals will be continued in the hope that incubation periods for AD may be even longer than those of CJD.
https://pubmed.ncbi.nlm.nih.gov/6758661/
CJD1/9 0185 Ref: 1M51A
IN STRICT CONFIDENCE
Dr McGovern From: Dr A Wight Date: 5 January 1993 Copies: Dr Metters Dr Skinner Dr Pickles Dr Morris Mr Murray
TRANSMISSION OF ALZHEIMER-TYPE PLAQUES TO PRIMATES
1. CMO will wish to be aware that a meeting was held at DH yesterday, 4 January, to discuss the above findings. It was chaired by Professor Murray (Chairman of the MRC Co-ordinating Committee on Research in the Spongiform Encephalopathies in Man), and attended by relevant experts in the fields of Neurology, Neuropathology, molecular biology, amyloid biochemistry, and the spongiform encephalopathies, and by representatives of the MRC and AFRC. 2. Briefly, the meeting agreed that:
i) Dr Ridley et als findings of experimental induction of p amyloid in primates were valid, interesting and a significant advance in the understanding of neurodegenerative disorders;
ii) there were no immediate implications for the public health, and no further safeguards were thought to be necessary at present; and
iii) additional research was desirable, both epidemiological and at the molecular level. Possible avenues are being followed up by DH and the MRC, but the details will require further discussion. 93/01.05/4.1
http://web.archive.org/web/20090506012455/http://www.bseinquiry.gov.uk/files/yb/1993/01/05004001.pdf
BSE101/1 0136
IN CONFIDENCE
5 NOV 1992 CMO From: Dr J S Metters DCMO 4 November 1992
TRANSMISSION OF ALZHEIMER TYPE PLAQUES TO PRIMATES
1. Thank you for showing me Diana Dunstan's letter. I am glad that MRC have recognized the public sensitivity of these findings and intend to report them in their proper context. This hopefully will avoid misunderstanding and possible distortion by the media to portray the results as having more greater significance than the findings so far justify.
2. Using a highly unusual route of transmission (intra-cerebral injection) the researchers have demonstrated the transmission of a pathological process from two cases one of severe Alzheimer's disease the other of Gerstmann-Straussler disease to marmosets. However they have not demonstrated the transmission of either clinical condition as the "animals were behaving normally when killed'. As the report emphasizes the unanswered question is whether the disease condition would have revealed itself if the marmosets had lived longer. They are planning further research to see if the conditions, as opposed to the partial pathological process, is transmissible. What are the implications for public health?
3. The route of transmission is very specific and in the natural state of things highly unusual. However it could be argued that the results reveal a potential risk, in that brain tissue from these two patients has been shown to transmit a pathological process. Should therefore brain tissue from such cases be regarded as potentially infective? Pathologists, morticians, neuro surgeons and those assisting at neuro surgical procedures and others coming into contact with "raw" human brain tissue could in theory be at risk. However, on a priori grounds given the highly specific route of transmission in these experiments that risk must be negligible if the usual precautions for handling brain tissue are observed.
92/11.4/1-1 BSE101/1 0137
4. The other dimension to consider is the public reaction. To some extent the GSS case demonstrates little more than the transmission of BSE to a pig by intra-cerebral injection. If other prion diseases can be transmitted in this way it is little surprise that some pathological findings observed in GSS were also transmissible to a marmoset. But the transmission of features of Alzheimer's pathology is a different matter, given the much greater frequency of this disease and raises the unanswered question whether some cases are the result of a transmissible prion. The only tenable public line will be that "more research is required" before that hypothesis could be evaluated. The possibility on a transmissible prion remains open. In the meantime MRC needs carefully to consider the range and sequence of studies needed to follow through from the preliminary observations in these two cases. Not a particularly comfortable message, but until we know more about the causation of Alzheimer's disease the total reassurance is not practical.
JS METTERS Room 509 Richmond House Pager No: 081-884 3344 Callsign: DOH 832 121/YdeS 92/11.4/1.2
https://web.archive.org/web/20170126060344/http://collections.europarchive.org/tna/20080102232842/http://www.bseinquiry.gov.uk/files/yb/1992/11/04001001.pdf
CJD1/9 0185
Ref: 1M51A
IN STRICT CONFIDENCE
From: Dr. A Wight Date: 5 January 1993
Copies:
Dr Metters Dr Skinner Dr Pickles Dr Morris Mr Murray
TRANSMISSION OF ALZHEIMER-TYPE PLAQUES TO PRIMATES
http://collections.europarchive.org/tna/20080102191246/http://www.bseinquiry.gov.uk/files/yb/1993/01/05004001.pdf
archived URL
https://web.archive.org/web/20090506012455/http://www.bseinquiry.gov.uk/files/yb/1993/01/05004001.pdf
''on the possible transmissibility of Alzheimer's''
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. There are also results to be made available shortly
(1) concerning a farmer with CJD who had BSE animals,
(2) on the possible transmissibility of Alzheimer's and
(3) a CMO letter on prevention of iatrogenic CJD transmission in neurosurgery, all of which will serve to increase media interest.
https://web.archive.org/web/20090506012455/http://www.bseinquiry.gov.uk/files/yb/1993/01/05004001.pdf
https://web.archive.org/web/20040315075058/http://www.bseinquiry.gov.uk/files/yb/1992/12/16005001.pdf
Alzheimer’s disease and Transmissible Spongiform Encephalopathy prion disease, Iatrogenic, what if ?
Posted by flounder on 05 Nov 2014 at 21:27 GMT
https://journals.plos.org/plosone/article/comment?id=10.1371/annotation/933cc83a-a384-45c3-b3b2-336882c30f9d
http://journals.plos.org/plosone/article/comments?id=10.1371/journal.pone.0111492
https://www.frontiersin.org/articles/10.3389/fnagi.2016.00005/full
FRIDAY, JANUARY 10, 2014
vpspr, sgss, sffi, TSE, an iatrogenic by-product of gss, ffi, familial type prion disease, what it ???
Greetings Friends, Neighbors, and Colleagues,
vpspr, sgss, sffi, TSE, an iatrogenic by-product of gss, ffi, familial type prion disease, what it ???
Confucius is confused again.
I was just sitting and thinking about why there is no genetic link to some of these TSE prion sGSS, sFFi, and it’s really been working on my brain, and then it hit me today.
what if, vpspr, sgss, sffi, TSE prion disease, was a by-product from iatrogenic gss, ffi, familial type prion disease ???
it could explain the cases of no genetic link to the gss, ffi, familial type prion disease, to the family.
sporadic and familial is a red herring, in my opinion, and underestimation is spot on, due to the crude prehistoric diagnostic procedures and criteria and definition of a prion disease.
I say again, what if, iatrogenic, what if, with all these neurological disorders, with a common denominator that is increasingly showing up in the picture, called the prion.
I urge all scientist to come together here, with this as the utmost of importance about all these neurological disease that are increasingly showing up as a prion mechanism, to put on the front burners, the IATROGENIC aspect and the potential of transmission there from, with diseases/disease??? in question.
by definition, could they be a Transmissible Spongiform Encephalopathy TSE prion type disease, and if so, what are the iatrogenic chances of transmission?
this is very important, and should be at the forefront of research, and if proven, could be a monumental breakthrough in science and battle against the spreading of these disease/diseases.
the US National Library of Medicine National Institutes of Health pub-med site, a quick search of the word SPORADIC will give you a hit of 40,747. of those, there are a plethora of disease listed under sporadic. sporadic simply means (UNKNOWN).
http://www.ncbi.nlm.nih.gov/pubmed/?term=sporadic
the US National Library of Medicine National Institutes of Health pub-med site, a quick search of the word FAMILIAL will give you a hit of 921,815. of those, there are a plethora of disease listed under familial.
http://www.ncbi.nlm.nih.gov/pubmed/?term=familial
again, sporadic and familial is a red herring, in my opinion.
also, in my opinion, when you start have disease such as sporadic Fatal Familial Insomnia, (and or sporadic GSS, or the VPSPr type prion disease), and there is NO familial genetic linkage to the family of the diseased, I have serious questions there as to a familial type disease, and thus, being defined as such.
snip...see full text;
Friday, January 10, 2014
vpspr, sgss, sffi, TSE, an iatrogenic by-product of gss, ffi, familial type prion disease, what it ???
http://transmissiblespongiformencephalopathy.blogspot.com/2014/01/vpspr-sgss-sffi-tse-iatrogenic-by.html
Singeltary Alzheimer’s 2015
re-Evidence for human transmission of amyloid-? pathology and cerebral amyloid angiopathy
Nature 525, 247?250 (10 September 2015)
Terry S. Singeltary Sr. 7 December 2015, 14:27
re-Evidence for human transmission of amyloid-? pathology and cerebral amyloid angiopathy
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)
I would kindly like to comment on the Nature Paper, the Lancet reply, and the newspaper articles.
First, I applaud Nature, the Scientist and Authors of the Nature paper, for bringing this important finding to the attention of the public domain, and the media for printing said findings.
Secondly, it seems once again, politics is getting in the way possibly of more important Transmissible Spongiform Encephalopathy TSE Prion scientific findings. findings that could have great implications for human health, and great implications for the medical surgical arena. but apparently, the government peer review process, of the peer review science, tries to intervene again to water down said disturbing findings.
where have we all heard this before? it?s been well documented via the BSE Inquiry. have they not learned a lesson from the last time?
we have seen this time and time again in England (and other Country?s) with the BSE mad cow TSE Prion debacle.
That ?anonymous' Lancet editorial was disgraceful. The editor, Dick Horton is not a scientist.
The pituitary cadavers were very likely elderly and among them some were on their way to CJD or Alzheimer's. Not a bit unusual. Then the recipients ? who got pooled extracts injected from thousands of cadavers ? were 100% certain to have been injected with both seeds. No surprise that they got both diseases going after thirty year incubations.
That the UK has a "system in place to assist science journalists" to squash embargoed science reports they find ?alarming? is pathetic.
Sounds like the journalists had it right in the first place: ?Alzheimer?s may be a transmissible infection? in The Independent to ?You can catch Alzheimer?s? in The Daily Mirror or ?Alzheimer?s bombshell" in The Daily Express
if not for the journalist, the layperson would not know about these important findings.
where would we be today with sound science, from where we were 30 years ago, if not for the cloak of secrecy and save the industry at all cost mentality?
when you have a peer review system for science, from which a government constantly circumvents, then you have a problem with science, and humans die.
to date, as far as documented body bag count, with all TSE prion named to date, that count is still relatively low (one was too many in my case, Mom hvCJD), however that changes drastically once the TSE Prion link is made with Alzheimer?s, the price of poker goes up drastically.
so, who makes that final decision, and how many more decades do we have to wait?
the iatrogenic mode of transmission of TSE prion, the many routes there from, load factor, threshold from said load factor to sub-clinical disease, to clinical disease, to death, much time is there to spread a TSE Prion to anywhere, but whom, by whom, and when, do we make that final decision to do something about it globally? how many documented body bags does it take? how many more decades do we wait? how many names can we make up for one disease, TSE prion?
Professor Collinge et al, and others, have had troubles in the past with the Government meddling in scientific findings, that might in some way involve industry, never mind human and or animal health.
FOR any government to continue to circumvent science for monetary gain, fear factor, or any reason, shame, shame on you.
in my opinion, it?s one of the reasons we are at where we are at to date, with regards to the TSE Prion disease science i.e. money, industry, politics, then comes science, in that order.
greed, corporate, lobbyist there from, and government, must be removed from the peer review process of sound science, it?s bad enough having them in the pharmaceutical aspect of healthcare policy making, in my opinion.
my mother died from confirmed hvCJD, and her brother (my uncle) Alzheimer?s of some type (no autopsy?). just made a promise, never forget, and never let them forget, before I do.
I kindly wish to remind the public of the past, and a possible future we all hopes never happens again. ...end
references
[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. There are also results to be made available shortly (1) concerning a farmer with CJD who had BSE animals, (2) on the possible transmissibility of Alzheimer?s and (3) a CMO letter on prevention of iatrogenic CJD transmission in neurosurgery, all of which will serve to increase media interest.]
http://web.archive.org/web/20030714222309/www.bseinquiry.gov.uk/files/yb/1992/12/16005001.pdf
http://collections.europarchive.org/tna/20080102232842/http://www.bseinquiry.gov.uk/files/yb/1992/11/04001001.pdf
http://www.plosone.org/annotation/listThread.action?root=82860
please see more of this history and references there from (these blogs are for educational use, I do not advertise or make money from this. just made a promise to mom dod 12/14/97 hvCJD, never forget, and never let them forget.)
human transmission of amyloid-? pathology and cerebral amyloid angiopathy, Singeltary Submission to Nature
http://betaamyloidcjd.blogspot.com/2015/10/alzheimergate-re-evidence-for-human.html
http://betaamyloidcjd.blogspot.com/
***> Singeltary comment scroll down after article in comments…
https://www.nature.com/articles/nature15369#article-comments
Singeltary TSE Prion 2009
Monitoring the occurrence of emerging forms of Creutzfeldt-Jakob disease in the United States 2003 revisited 2009 Plos Singeltary August 10, 2009
Monitoring the occurrence of emerging forms of Creutzfeldt-Jakob disease in the United States 2003 revisited 2009
August 10, 2009
Greetings,
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. North America seems to have the most species with documented Transmissible Spongiform Encephalopathy's, most all of which have been rendered and fed back to food producing animals and to humans for years. If you look at the statistics, sporadic CJD seems to be rising in the USA, and has been, with atypical cases of the sCJD. I find deeply disturbing in the year of 2009, that Human Transmissible Spongiform Encephalopathy of any strain and or phenotype, of all age groups, and I stress all age groups, because human TSE's do not know age, and they do not know borders. someone 56 years old, that has a human TSE, that has surgery, can pass this TSE agent on i.e. friendly fire, and or passing it forward, and there have been documented nvCJD in a 74 year old. Remembering also that only sporadic CJD has been documented to transmit via iatrogenic routes, until recently with the 4 cases of blood related transmission, of which the origin is thought to be nvCJD donors. However most Iatrogenic CJD cases are nothing more than sporadic CJD, until the source is proven, then it becomes Iatrogenic. An oxymoron of sorts, because all sporadic CJD is, are multiple forms, or strains, or phenotypes of Creutzfeldt Jakob Disease, that the route and source and species have not been confirmed and or documented. When will the myth of the UKBSEnvCJD only theory be put to bed for good. This theory in my opinion, and the following there from, as the GOLD STANDARD, has done nothing more than help spread this agent around the globe. Politics and money have caused the terrible consequences to date, and the fact that TSEs are a slow incubating death, but a death that is 100% certain for those that are exposed and live long enough to go clinical. once clinical, there is no recourse, to date.
But, while sub-clinical, how many can one exposed human infect?
Can humans exposed to CWD and scrapie strains pass it forward as some form of sporadic CJD in the surgical and medical arenas?
why must we wait decades and decades to prove this point, only to expose millions needlessly, only for the sake of the industries involved?
would it not have been prudent from the beginning to just include all TSE's, and rule them out from there with transmission studies and change policies there from, as opposed to doing just the opposite?
The science of TSE's have been nothing more than a political circus since the beginning, and for anyone to still believe in this one strain, one group of bovines, in one geographical location, with only one age group of human TSE i.e. nvCJD myth, for anyone to believe this today only enhances to spreading of these human and animal TSE's. This is exactly why we have been in this quagmire.
The ones that believe that there is a spontaneous CJD in 85%+ of all cases of human TSE, and the ones that do not believe that cattle can have this same phenomenon, are two of the same, the industry, and so goes the political science aspect of this tobacco and or asbestos scenario i.e. follow the money. I could go into all angles of this man made nightmare, the real facts and science, for instance, the continuing rendering technology and slow cooking with low temps that brewed this stew up, and the fact that THE USA HAD THIS TECHNOLOGY FIRST AND SHIPPED IT TO THE U.K. SOME 5 YEARS BEFORE THE U.S. STARTED USING THE SAME TECHNOLOGY, to save on fuel cost. This is what supposedly amplified the TSE agent via sheep scrapie, and spread via feed in the U.K. bovine, and other countries exporting the tainted product. BUT most everyone ignores this fact, and the fact that the U.S. has been recycling more TSE, from more species with TSEs, than any other country documented, but yet, it's all spontaneous, and the rise in sporadic CJD in the U.S. is a happenstance of bad luck ??? I respectfully disagree. To top that all off, the infamous BSE-FIREWALL that the USDA always brags about was nothing more than ink on paper, and I can prove this. YOU can ignore it, but this is FACT (see source, as late as 2007, in one recall alone, some 10,000,000 MILLION POUNDS OF BANNED MAD COW FEED WENT OUT INTO COMMERCE TO BE FED OUT, and most was never recovered. This was banned blood laced, meat and bone meal. 2006 was a banner year for banned mad cow protein going into commerce in the U.S. (see source of FDA feed ban warning letter below). I stress that the August 4, 1997 USA mad cow feed ban and this infamous BSE firewall, was nothing more than ink on paper, it was never enforceable.
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.
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. This would further have to be broken down to strain of species and then the route of transmission would further have to be broken down. Accumulation and Transmission are key to the threshold from sub- clinical to clinical disease, and key to all this, is to stop the amplification and transmission of this agent, the spreading of, no matter what strain. In my opinion, to continue with this myth that the U.K. strain of BSE one strain TSE in cows, and the nv/v CJD one strain TSE humans, and the one geographical location source i.e. U.K., and that all the rest of human TSE are just one single strain i.e. sporadic CJD, a happenstance of bad luck that just happens due to a twisted protein that just twisted the wrong way, IN 85%+ OF ALL HUMAN TSEs, when to date there are 6 different phenotypes of sCJD, and growing per Gambetti et al, and that no other animal TSE transmits to humans ??? With all due respect to all Scientist that believe this, I beg to differ. To continue with this masquerade will only continue to spread, expose, and kill, who knows how many more in the years and decades to come. ONE was enough for me, My Mom, hvCJD i.e. Heidenhain Variant CJD, DOD 12/14/97 confirmed, which is nothing more than another mans name added to CJD, like CJD itself, Jakob and Creutzfeldt, or Gerstmann-Straussler-Scheinker syndrome, just another CJD or human TSE, named after another human. WE are only kidding ourselves with the current diagnostic criteria for human and animal TSE, especially differentiating between the nvCJD vs the sporadic CJD strains and then the GSS strains and also the FFI fatal familial insomnia strains or the ones that mimics one or the other of those TSE? Tissue infectivity and strain typing of the many variants of the human and animal TSEs are paramount in all variants of all TSE. There must be a proper classification that will differentiate between all these human TSE in order to do this. With the CDI and other more sensitive testing coming about, I only hope that my proposal will some day be taken seriously. ...
please see history, and the ever evolving TSE science to date ;
Saturday, June 13, 2009
Monitoring the occurrence of emerging forms of Creutzfeldt-Jakob disease in the United States 2003 revisited 2009
https://journals.plos.org/plosone/article/comment?id=10.1371/annotation/04ce2b24-613d-46e6-9802-4131e2bfa6fd
Singeltary Submission SEAC 2007
SEAC SPONGIFORM ENCEPHALOPATHY ADVISORY COMMITTEE Minutes of the 99th meeting held on 14th December 2007 Singeltary Submission
This was 22 years to the day Mom died from the Heidenhain Variant of Creutzfeldt Jakob Disease i.e. hvCJD, when i made this submission to SEAC and this was their reply to my questions of concern about cjd in the USA, my how things have changed...terry
SEAC SPONGIFORM ENCEPHALOPATHY ADVISORY COMMITTEE Minutes of the 99th meeting held on 14th December 2007
ITEM 8 – PUBLIC QUESTION AND ANSWER SESSION 40. The Chair explained that the purpose of the question and answer session was to give members of the public an opportunity to ask questions related to the work of SEAC. Mr Terry Singeltary (Texas, USA) had submitted a question prior to the meeting, asking: “With the Nor-98 now documented in five different states so far in the USA in 2007, and with the two atypical BSE H-base cases in Texas and Alabama, with both scrapie and chronic wasting disease (CWD) running rampant in the USA, is there any concern from SEAC with the rise of sporadic CJD in the USA from ''unknown phenotype'', and what concerns if any, in relations to blood donations, surgery, optical, and dental treatment, do you have with these unknown atypical phenotypes in both humans and animals in the USA? Does it concern SEAC, or is it of no concern to SEAC? Should it concern USA animal and human health officials?”
41. A member considered that this question appeared to be primarily related to possible links between animal and human TSEs in the USA. There is no evidence that sCJD is increasing in the USA and no evidence of any direct link between TSEs and CJD in the USA. Current evidence does not suggest that CWD is a significant risk to human health. There are unpublished data from a case of human TSE in the USA that are suggestive of an apparently novel form of prion disease with distinct molecular characteristics. However, it is unclear whether the case had been further characterised, if it could be linked to animal TSEs or if other similar cases had been found in the USA or elsewhere. In relation to the possible public health implications of atypical scrapie, H-type BSE and CWD, research was being conducted to investigate possible links and surveillance was in place to detect any changes in human TSEs. Although possible links between these diseases and human TSEs are of concern and require research, there is no evidence to suggest immediate public health action is warranted. The possible human health risks from classical scrapie had been discussed earlier in the meeting. Members noted that there are effective channels of discussion and collaboration on research between USA and European groups. Members agreed it is important to keep a watching brief on new developments on TSEs.
http://web.archive.org/web/20091010132933/http://www.seac.gov.uk/minutes/99.pdf
14th ICID International Scientific Exchange Brochure -
Final Abstract Number: ISE.114
Session: International Scientific Exchange
Transmissible Spongiform encephalopathy (TSE) animal and human TSE in North America
update October 2009
T. Singeltary
Bacliff, TX, USA
Background:
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.
Methods:
12 years independent research of available data
Results:
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.
Conclusion:
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. 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.
International Society for Infectious Diseases Web: http://www.isid.org
http://ww2.isid.org/Downloads/14th_ICID_ISE_Abstracts.pdf
https://web.archive.org/web/20101116225529/http://ww2.isid.org/Downloads/14th_ICID_ISE_Abstracts.pdf
2001 Singeltary on CJD, Journal of American Medical Association
February 14, 2001
Diagnosis and Reporting of Creutzfeldt-Jakob Disease
Terry S. Singeltary, Sr
Author Affiliations
JAMA. 2001;285(6):733-734. doi:10-1001/pubs.JAMA-ISSN-0098-7484-285-6-jlt0214
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.
February 14, 2001
Diagnosis and Reporting of Creutzfeldt-Jakob Disease
Terry S. Singeltary, Sr
Author Affiliations
JAMA. 2001;285(6):733-734. doi:10-1001/pubs.JAMA-ISSN-0098-7484-285-6-jlt0214
https://jamanetwork.com/journals/jama/article-abstract/1031186
RE-Monitoring the occurrence of emerging forms of Creutzfeldt-Jakob disease in the United States 2003 Singeltary Journal of Neurology
26 MARCH 2003
RE-Monitoring the occurrence of emerging forms of Creutzfeldt-Jakob disease in the United States
Terry S. Singeltary, retired (medically)
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?
https://www.neurology.org/doi/10.1212/01.WNL.0000036913.87823.D6
Prion Scientific Advisors and Consultants Staff Meeting Singeltary Submission Freas Monday, January 08,2001 3:03 PM
Scientific Advisors and Consultants Staff 2001 Advisory Committee TSE PRION Singeltary Submission Freas
Monday, January 08,2001 3:03 PM
FDA Singeltary submission 2001
Greetings again Dr. Freas and Committee Members,
I wish to submit the following information to the Scientific Advisors and Consultants Staff 2001 Advisory Committee (short version). I understand the reason of having to shorten my submission, but only hope that you add it to a copy of the long version, for members to take and read at their pleasure, (if cost is problem, bill me, address below). So when they realize some time in the near future of the 'real' risks i speak of from human/animal TSEs and blood/surgical products. I cannot explain the 'real' risk of this in 5 or 10 minutes at some meeting, or on 2 or 3 pages, but will attempt here: fda link is dead in the water;
http://web.archive.org/web/20041212232925/http://www.fda.gov/ohrms/dockets/ac/01/slides/3681s2_09.pdf
https://tseac.blogspot.com/2009/05/meeting-of-transmissible-spongiform.html
wasted days and wasted nights…Freddy Fender
Terry S. Singeltary Sr., Bacliff, Texas USA 77518
Arkansas CJD Surveillance
Creutzfeldt-Jakob disease (CJD) is a reportable condition under the Arkansas Department of Health Rules and Regulations for Reportable Diseases, but specific public health surveillance case totals or localized CJD outbreak data for 2025 are not published as an independent, open-access dataset by the state. National surveillance data compiled by the National Prion Disease Pathology Surveillance Center track aggregated national case examinations rather than breaking down explicit annual counts by individual state public health reports...
Texas Creutzfeldt Jakob Disease CJD TSE Prion Disease 2025
Update as of 10/15/25, NO REPORT TO UPDATE…
https://www.dshs.texas.gov/creutzfeldt-jakob-disease-cjd/creutzfeldt-jakob-disease-cjd-data
US NATIONAL PRION DISEASE PATHOLOGY SURVEILLANCE CENTER CJD TSE REPORT SEPTEMBER 2025
From the first full year of reporting CJD TSE in the US in 2000, where 90 cases of CJD was reported that year, to today, where in September 2025, the number of CJD cases reported in the last full year reporting, which would have been 2024, the number of CJD cases for 2024 was 249 cases. So, from the first full year 2000 CJD cases were 90 cases confirmed in that year, to 2024, where 2024 CJD statistics rose to 249 confirmed CJD cases in a single year. A dramatic increase in deaths, from figures that don’t seem to be dramatic. But thes figures today, they are not from “better surveillance”, that dog don’t hunt no more. They have been saying this for over 25 years, year after year, well it’s time to call it for what it is, Human Transmissible Spongiform Encephalopathy TSE Prion cases are rising, and it’s NOT because of better surveillance, or just a “happenstance of bad luck, that 85%+ of all human cases, sporadic CJD, including VPSPr, just happen spontaneously, no, it’s because of unknown environmental factors, and or iatrogenic factors, imho…terry
US NATIONAL PRION DISEASE PATHOLOGY SURVEILLANCE CENTER CJD TSE REPORT SEPTEMBER 2025
https://prionunitusaupdate.blogspot.com/2025/10/us-national-prion-disease-pathology.html
So, this is what we leave our children and grandchildren?
Mad Cow Scaremongers , The Center For Consumer Freedom Team Terry Singletary — A retired machinist and high school dropout, Terry Singletary suffered the tragic loss of his mother to “sporadic” Creutzfeldt-Jakob disease (CJD) in 1997. Desperate to find an explanation for his mother’s death, he has devoted himself to the sad and fruitless task of connecting her death to her diet. Various reports confirm that Mrs. Singletary’s life was claimed by the most common sub-type of CJD (one that accounts for 70 percent of “sporadic” cases). Sporadic CJD, unlike its newer “variant,” is not linked to meat.
Mad Cow Scaremongers , The Center For Consumer Freedom Team As the self-appointed international coordinator of CJD Watch, an organization he co-founded with social worker Deborah Oney, Singletary is cited in media reports as an apparent expert on tracking mad cow disease. This despite his lack of formal education and the absence for support from any credible academic, medical or scientific authority. His sensationalist allegations about the safety of U.S. beef have found their way into hundreds of newspapers and broadcasts. Singletary moderates a mad-cow discussion forum run by a vegetarian activist group; his contributions account for more than half the traffic on the “BSE-L” mailing list, which is generally read by real scientists. Animal rights activists and other food-scare artists frequently refer to him as “Dr. Terry Singletary,” apparently an honorary degree as he has yet to finish high school.
Mad Cow Scaremongers , The Center For Consumer Freedom Team Like many activists, Singletary ignores overwhelming epidemiological and laboratory evidence that rules out a connection between sporadic CJD and beef. Relying entirely on shallow circumstantial evidence and frequent repetition of claims which have been publicly refuted as false, he also blindly insists upon a mad-cow with Alzheimer’s, Parkinson’s, and Lou Gehrig’s disease. His specific allegations have been clearly refuted by Centers for Disease Countrol and Prevention scientists in the journal Neurology.
https://consumerfreedom.com/articles/138-mad-cow-scaremongers/
***> Mad Cow Scaremongers , The Center For Consumer Freedom Team Terry Singletary “he also blindly insists upon a mad-cow with Alzheimer’s, Parkinson’s, and Lou Gehrig’s disease. His specific allegations have been clearly refuted by Centers for Disease Countrol and Prevention scientists in the journal Neurology.”
2024, iatrogenic AD, what if?
Price of TSE prion poker goes up drastically…Terry
Alzheimer’s disease acquired from historic medical treatments
30 January 2024
“However, the recognition of transmission of amyloid-beta pathology in these rare situations should lead us to review measures to prevent accidental transmission via other medical or surgical procedures, in order to prevent such cases occurring in future.
“Importantly, our findings also suggest that Alzheimer's and some other neurological conditions share similar disease processes to CJD, and this may have important implications for understanding and treating Alzheimer’s disease in the future.”
https://www.ucl.ac.uk/prion/news/2024/jan/alzheimers-disease-acquired-historic-medical-treatments
not that it matters, but i started telling them from 2001, that Alzheimer’s and other neurological disorders were a TSE prion disease, and were capable of transmitting by iatrogenic routes…kind regards, Terry
Singeltary 2001 Alzheimer's disease
Singeltary 2001
Subject: CJD or Alzheimer's or the same ???
Date: Sun, 29 Apr 2001 12:45:28 -0700
From: "Terry S. Singeltary Sr."
Reply-To: Bovine Spongiform Encephalopathy
To: BSE-L@uni-karlsruhe.de
Bovine Spongiform Encephalopathy
Greetings List,
thought some might be interested in this. I have always wondered if CJD and or all TSEs and Alzheimer's could be linked. i have been of the opinion that Alzheimer's is a TSE for a long time, just at the low end of the titre of infectivity scale. i also believe in the accumulation theory. by dose, you could be killed by one sitting, or one injection, or one whatever, depending on the titre of infectivity of that whatever. on the other hand, if the dose is not a lethal dose, over a period of time, the accumulation will become lethal (if consumption continued), and i believe the route/source/titre of infectivity, will be a key roll to the incubation period, and symptoms.
just my opinion...snip…end
Singeltary Alzheimer’s 2014
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...
Self-Propagative Replication of Aβ Oligomers Suggests Potential Transmissibility in Alzheimer Disease
Amit Kumar, Kayla M. Pate, Melissa A. Moss, Dexter N. Dean, Vijayaraghavan Rangachari
Published: November 3, 2014
https://doi.org/10.1371/journal.pone.0111492
Reader Comments
Posted by flounder on 05 Nov 2014 at 21:27 GMT
Alzheimer’s disease and Transmissible Spongiform Encephalopathy prion disease, Iatrogenic, what if ?
Background
Alzheimer’s disease and Transmissible Spongiform Encephalopathy disease have both been around a long time, and was discovered in or around the same time frame, early 1900’s. Both diseases are incurable and debilitating brain disease, that are in the end, 100% fatal, with the incubation/clinical period of the Alzheimer’s disease being longer (most of the time) than the TSE prion disease. Symptoms are very similar, and pathology is very similar.
Methods
Through years of research, as a layperson, of peer review journals, transmission studies, and observations of loved ones and friends that have died from both Alzheimer’s and the TSE prion disease i.e. Heidenhain Variant Creutzfelt Jakob Disease CJD.
Results
I propose that Alzheimer’s is a TSE disease of low dose, slow, and long incubation disease, and that Alzheimer’s is Transmissible, and is a threat to the public via the many Iatrogenic routes and sources. It was said long ago that the only thing that disputes this, is Alzheimer’s disease transmissibility, or the lack of. The likelihood of many victims of Alzheimer’s disease from the many different Iatrogenic routes and modes of transmission as with the TSE prion disease.
Conclusions
There should be a Global Congressional Science round table event set up immediately to address these concerns from the many potential routes and sources of the TSE prion disease, including Alzheimer’s disease, and a emergency global doctrine put into effect to help combat the spread of Alzheimer’s disease via the medical, surgical, dental, tissue, and blood arena’s. All human and animal TSE prion disease, including Alzheimer’s should be made reportable in every state, and Internationally, WITH NO age restrictions. Until a proven method of decontamination and autoclaving is proven, and put forth in use universally, in all hospitals and medical, surgical arena’s, or the TSE prion agent will continue to spread. IF we wait until science and corporate politicians wait until politics lets science _prove_ this once and for all, and set forth regulations there from, we will all be exposed to the TSE Prion agents, if that has not happened already.
end...tss
Alzheimer’s disease and Transmissible Spongiform Encephalopathy prion disease, Iatrogenic, what if ?
Posted by flounder on 05 Nov 2014 at 21:27 GMT
https://journals.plos.org/plosone/article/comment?id=10.1371/annotation/933cc83a-a384-45c3-b3b2-336882c30f9d
Ann N Y Acad Sci. 1982;396:131-43.
Alzheimer's disease and transmissible virus dementia (Creutzfeldt-Jakob disease).
Brown P, Salazar AM, Gibbs CJ Jr, Gajdusek DC.
Abstract
Ample justification exists on clinical, pathologic, and biologic grounds for considering a similar pathogenesis for AD and the spongiform virus encephalopathies. However, the crux of the comparison rests squarely on results of attempts to transmit AD to experimental animals, and these results have not as yet validated a common etiology. Investigations of the biologic similarities between AD and the spongiform virus encephalopathies proceed in several laboratories, and our own observation of inoculated animals will be continued in the hope that incubation periods for AD may be even longer than those of CJD.
https://pubmed.ncbi.nlm.nih.gov/6758661/
CJD1/9 0185 Ref: 1M51A
IN STRICT CONFIDENCE
Dr McGovern From: Dr A Wight Date: 5 January 1993 Copies: Dr Metters Dr Skinner Dr Pickles Dr Morris Mr Murray
TRANSMISSION OF ALZHEIMER-TYPE PLAQUES TO PRIMATES
1. CMO will wish to be aware that a meeting was held at DH yesterday, 4 January, to discuss the above findings. It was chaired by Professor Murray (Chairman of the MRC Co-ordinating Committee on Research in the Spongiform Encephalopathies in Man), and attended by relevant experts in the fields of Neurology, Neuropathology, molecular biology, amyloid biochemistry, and the spongiform encephalopathies, and by representatives of the MRC and AFRC. 2. Briefly, the meeting agreed that:
i) Dr Ridley et als findings of experimental induction of p amyloid in primates were valid, interesting and a significant advance in the understanding of neurodegenerative disorders;
ii) there were no immediate implications for the public health, and no further safeguards were thought to be necessary at present; and
iii) additional research was desirable, both epidemiological and at the molecular level. Possible avenues are being followed up by DH and the MRC, but the details will require further discussion. 93/01.05/4.1
http://web.archive.org/web/20090506012455/http://www.bseinquiry.gov.uk/files/yb/1993/01/05004001.pdf
BSE101/1 0136
IN CONFIDENCE
5 NOV 1992 CMO From: Dr J S Metters DCMO 4 November 1992
TRANSMISSION OF ALZHEIMER TYPE PLAQUES TO PRIMATES
1. Thank you for showing me Diana Dunstan's letter. I am glad that MRC have recognized the public sensitivity of these findings and intend to report them in their proper context. This hopefully will avoid misunderstanding and possible distortion by the media to portray the results as having more greater significance than the findings so far justify.
2. Using a highly unusual route of transmission (intra-cerebral injection) the researchers have demonstrated the transmission of a pathological process from two cases one of severe Alzheimer's disease the other of Gerstmann-Straussler disease to marmosets. However they have not demonstrated the transmission of either clinical condition as the "animals were behaving normally when killed'. As the report emphasizes the unanswered question is whether the disease condition would have revealed itself if the marmosets had lived longer. They are planning further research to see if the conditions, as opposed to the partial pathological process, is transmissible. What are the implications for public health?
3. The route of transmission is very specific and in the natural state of things highly unusual. However it could be argued that the results reveal a potential risk, in that brain tissue from these two patients has been shown to transmit a pathological process. Should therefore brain tissue from such cases be regarded as potentially infective? Pathologists, morticians, neuro surgeons and those assisting at neuro surgical procedures and others coming into contact with "raw" human brain tissue could in theory be at risk. However, on a priori grounds given the highly specific route of transmission in these experiments that risk must be negligible if the usual precautions for handling brain tissue are observed.
92/11.4/1-1 BSE101/1 0137
4. The other dimension to consider is the public reaction. To some extent the GSS case demonstrates little more than the transmission of BSE to a pig by intra-cerebral injection. If other prion diseases can be transmitted in this way it is little surprise that some pathological findings observed in GSS were also transmissible to a marmoset. But the transmission of features of Alzheimer's pathology is a different matter, given the much greater frequency of this disease and raises the unanswered question whether some cases are the result of a transmissible prion. The only tenable public line will be that "more research is required" before that hypothesis could be evaluated. The possibility on a transmissible prion remains open. In the meantime MRC needs carefully to consider the range and sequence of studies needed to follow through from the preliminary observations in these two cases. Not a particularly comfortable message, but until we know more about the causation of Alzheimer's disease the total reassurance is not practical.
JS METTERS Room 509 Richmond House Pager No: 081-884 3344 Callsign: DOH 832 121/YdeS 92/11.4/1.2
https://web.archive.org/web/20170126060344/http://collections.europarchive.org/tna/20080102232842/http://www.bseinquiry.gov.uk/files/yb/1992/11/04001001.pdf
CJD1/9 0185
Ref: 1M51A
IN STRICT CONFIDENCE
From: Dr. A Wight Date: 5 January 1993
Copies:
Dr Metters Dr Skinner Dr Pickles Dr Morris Mr Murray
TRANSMISSION OF ALZHEIMER-TYPE PLAQUES TO PRIMATES
http://collections.europarchive.org/tna/20080102191246/http://www.bseinquiry.gov.uk/files/yb/1993/01/05004001.pdf
archived URL
https://web.archive.org/web/20090506012455/http://www.bseinquiry.gov.uk/files/yb/1993/01/05004001.pdf
''on the possible transmissibility of Alzheimer's''
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. There are also results to be made available shortly
(1) concerning a farmer with CJD who had BSE animals,
(2) on the possible transmissibility of Alzheimer's and
(3) a CMO letter on prevention of iatrogenic CJD transmission in neurosurgery, all of which will serve to increase media interest.
https://web.archive.org/web/20090506012455/http://www.bseinquiry.gov.uk/files/yb/1993/01/05004001.pdf
https://web.archive.org/web/20040315075058/http://www.bseinquiry.gov.uk/files/yb/1992/12/16005001.pdf
Alzheimer’s disease and Transmissible Spongiform Encephalopathy prion disease, Iatrogenic, what if ?
Posted by flounder on 05 Nov 2014 at 21:27 GMT
https://journals.plos.org/plosone/article/comment?id=10.1371/annotation/933cc83a-a384-45c3-b3b2-336882c30f9d
http://journals.plos.org/plosone/article/comments?id=10.1371/journal.pone.0111492
https://www.frontiersin.org/articles/10.3389/fnagi.2016.00005/full
FRIDAY, JANUARY 10, 2014
vpspr, sgss, sffi, TSE, an iatrogenic by-product of gss, ffi, familial type prion disease, what it ???
Greetings Friends, Neighbors, and Colleagues,
vpspr, sgss, sffi, TSE, an iatrogenic by-product of gss, ffi, familial type prion disease, what it ???
Confucius is confused again.
I was just sitting and thinking about why there is no genetic link to some of these TSE prion sGSS, sFFi, and it’s really been working on my brain, and then it hit me today.
what if, vpspr, sgss, sffi, TSE prion disease, was a by-product from iatrogenic gss, ffi, familial type prion disease ???
it could explain the cases of no genetic link to the gss, ffi, familial type prion disease, to the family.
sporadic and familial is a red herring, in my opinion, and underestimation is spot on, due to the crude prehistoric diagnostic procedures and criteria and definition of a prion disease.
I say again, what if, iatrogenic, what if, with all these neurological disorders, with a common denominator that is increasingly showing up in the picture, called the prion.
I urge all scientist to come together here, with this as the utmost of importance about all these neurological disease that are increasingly showing up as a prion mechanism, to put on the front burners, the IATROGENIC aspect and the potential of transmission there from, with diseases/disease??? in question.
by definition, could they be a Transmissible Spongiform Encephalopathy TSE prion type disease, and if so, what are the iatrogenic chances of transmission?
this is very important, and should be at the forefront of research, and if proven, could be a monumental breakthrough in science and battle against the spreading of these disease/diseases.
the US National Library of Medicine National Institutes of Health pub-med site, a quick search of the word SPORADIC will give you a hit of 40,747. of those, there are a plethora of disease listed under sporadic. sporadic simply means (UNKNOWN).
http://www.ncbi.nlm.nih.gov/pubmed/?term=sporadic
the US National Library of Medicine National Institutes of Health pub-med site, a quick search of the word FAMILIAL will give you a hit of 921,815. of those, there are a plethora of disease listed under familial.
http://www.ncbi.nlm.nih.gov/pubmed/?term=familial
again, sporadic and familial is a red herring, in my opinion.
also, in my opinion, when you start have disease such as sporadic Fatal Familial Insomnia, (and or sporadic GSS, or the VPSPr type prion disease), and there is NO familial genetic linkage to the family of the diseased, I have serious questions there as to a familial type disease, and thus, being defined as such.
snip...see full text;
Friday, January 10, 2014
vpspr, sgss, sffi, TSE, an iatrogenic by-product of gss, ffi, familial type prion disease, what it ???
http://transmissiblespongiformencephalopathy.blogspot.com/2014/01/vpspr-sgss-sffi-tse-iatrogenic-by.html
Singeltary Alzheimer’s 2015
re-Evidence for human transmission of amyloid-? pathology and cerebral amyloid angiopathy
Nature 525, 247?250 (10 September 2015)
Terry S. Singeltary Sr. 7 December 2015, 14:27
re-Evidence for human transmission of amyloid-? pathology and cerebral amyloid angiopathy
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)
I would kindly like to comment on the Nature Paper, the Lancet reply, and the newspaper articles.
First, I applaud Nature, the Scientist and Authors of the Nature paper, for bringing this important finding to the attention of the public domain, and the media for printing said findings.
Secondly, it seems once again, politics is getting in the way possibly of more important Transmissible Spongiform Encephalopathy TSE Prion scientific findings. findings that could have great implications for human health, and great implications for the medical surgical arena. but apparently, the government peer review process, of the peer review science, tries to intervene again to water down said disturbing findings.
where have we all heard this before? it?s been well documented via the BSE Inquiry. have they not learned a lesson from the last time?
we have seen this time and time again in England (and other Country?s) with the BSE mad cow TSE Prion debacle.
That ?anonymous' Lancet editorial was disgraceful. The editor, Dick Horton is not a scientist.
The pituitary cadavers were very likely elderly and among them some were on their way to CJD or Alzheimer's. Not a bit unusual. Then the recipients ? who got pooled extracts injected from thousands of cadavers ? were 100% certain to have been injected with both seeds. No surprise that they got both diseases going after thirty year incubations.
That the UK has a "system in place to assist science journalists" to squash embargoed science reports they find ?alarming? is pathetic.
Sounds like the journalists had it right in the first place: ?Alzheimer?s may be a transmissible infection? in The Independent to ?You can catch Alzheimer?s? in The Daily Mirror or ?Alzheimer?s bombshell" in The Daily Express
if not for the journalist, the layperson would not know about these important findings.
where would we be today with sound science, from where we were 30 years ago, if not for the cloak of secrecy and save the industry at all cost mentality?
when you have a peer review system for science, from which a government constantly circumvents, then you have a problem with science, and humans die.
to date, as far as documented body bag count, with all TSE prion named to date, that count is still relatively low (one was too many in my case, Mom hvCJD), however that changes drastically once the TSE Prion link is made with Alzheimer?s, the price of poker goes up drastically.
so, who makes that final decision, and how many more decades do we have to wait?
the iatrogenic mode of transmission of TSE prion, the many routes there from, load factor, threshold from said load factor to sub-clinical disease, to clinical disease, to death, much time is there to spread a TSE Prion to anywhere, but whom, by whom, and when, do we make that final decision to do something about it globally? how many documented body bags does it take? how many more decades do we wait? how many names can we make up for one disease, TSE prion?
Professor Collinge et al, and others, have had troubles in the past with the Government meddling in scientific findings, that might in some way involve industry, never mind human and or animal health.
FOR any government to continue to circumvent science for monetary gain, fear factor, or any reason, shame, shame on you.
in my opinion, it?s one of the reasons we are at where we are at to date, with regards to the TSE Prion disease science i.e. money, industry, politics, then comes science, in that order.
greed, corporate, lobbyist there from, and government, must be removed from the peer review process of sound science, it?s bad enough having them in the pharmaceutical aspect of healthcare policy making, in my opinion.
my mother died from confirmed hvCJD, and her brother (my uncle) Alzheimer?s of some type (no autopsy?). just made a promise, never forget, and never let them forget, before I do.
I kindly wish to remind the public of the past, and a possible future we all hopes never happens again. ...end
references
[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. There are also results to be made available shortly (1) concerning a farmer with CJD who had BSE animals, (2) on the possible transmissibility of Alzheimer?s and (3) a CMO letter on prevention of iatrogenic CJD transmission in neurosurgery, all of which will serve to increase media interest.]
http://web.archive.org/web/20030714222309/www.bseinquiry.gov.uk/files/yb/1992/12/16005001.pdf
http://collections.europarchive.org/tna/20080102232842/http://www.bseinquiry.gov.uk/files/yb/1992/11/04001001.pdf
http://www.plosone.org/annotation/listThread.action?root=82860
please see more of this history and references there from (these blogs are for educational use, I do not advertise or make money from this. just made a promise to mom dod 12/14/97 hvCJD, never forget, and never let them forget.)
human transmission of amyloid-? pathology and cerebral amyloid angiopathy, Singeltary Submission to Nature
http://betaamyloidcjd.blogspot.com/2015/10/alzheimergate-re-evidence-for-human.html
http://betaamyloidcjd.blogspot.com/
***> Singeltary comment scroll down after article in comments…
https://www.nature.com/articles/nature15369#article-comments
Singeltary TSE Prion 2009
Monitoring the occurrence of emerging forms of Creutzfeldt-Jakob disease in the United States 2003 revisited 2009 Plos Singeltary August 10, 2009
Monitoring the occurrence of emerging forms of Creutzfeldt-Jakob disease in the United States 2003 revisited 2009
August 10, 2009
Greetings,
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. North America seems to have the most species with documented Transmissible Spongiform Encephalopathy's, most all of which have been rendered and fed back to food producing animals and to humans for years. If you look at the statistics, sporadic CJD seems to be rising in the USA, and has been, with atypical cases of the sCJD. I find deeply disturbing in the year of 2009, that Human Transmissible Spongiform Encephalopathy of any strain and or phenotype, of all age groups, and I stress all age groups, because human TSE's do not know age, and they do not know borders. someone 56 years old, that has a human TSE, that has surgery, can pass this TSE agent on i.e. friendly fire, and or passing it forward, and there have been documented nvCJD in a 74 year old. Remembering also that only sporadic CJD has been documented to transmit via iatrogenic routes, until recently with the 4 cases of blood related transmission, of which the origin is thought to be nvCJD donors. However most Iatrogenic CJD cases are nothing more than sporadic CJD, until the source is proven, then it becomes Iatrogenic. An oxymoron of sorts, because all sporadic CJD is, are multiple forms, or strains, or phenotypes of Creutzfeldt Jakob Disease, that the route and source and species have not been confirmed and or documented. When will the myth of the UKBSEnvCJD only theory be put to bed for good. This theory in my opinion, and the following there from, as the GOLD STANDARD, has done nothing more than help spread this agent around the globe. Politics and money have caused the terrible consequences to date, and the fact that TSEs are a slow incubating death, but a death that is 100% certain for those that are exposed and live long enough to go clinical. once clinical, there is no recourse, to date.
But, while sub-clinical, how many can one exposed human infect?
Can humans exposed to CWD and scrapie strains pass it forward as some form of sporadic CJD in the surgical and medical arenas?
why must we wait decades and decades to prove this point, only to expose millions needlessly, only for the sake of the industries involved?
would it not have been prudent from the beginning to just include all TSE's, and rule them out from there with transmission studies and change policies there from, as opposed to doing just the opposite?
The science of TSE's have been nothing more than a political circus since the beginning, and for anyone to still believe in this one strain, one group of bovines, in one geographical location, with only one age group of human TSE i.e. nvCJD myth, for anyone to believe this today only enhances to spreading of these human and animal TSE's. This is exactly why we have been in this quagmire.
The ones that believe that there is a spontaneous CJD in 85%+ of all cases of human TSE, and the ones that do not believe that cattle can have this same phenomenon, are two of the same, the industry, and so goes the political science aspect of this tobacco and or asbestos scenario i.e. follow the money. I could go into all angles of this man made nightmare, the real facts and science, for instance, the continuing rendering technology and slow cooking with low temps that brewed this stew up, and the fact that THE USA HAD THIS TECHNOLOGY FIRST AND SHIPPED IT TO THE U.K. SOME 5 YEARS BEFORE THE U.S. STARTED USING THE SAME TECHNOLOGY, to save on fuel cost. This is what supposedly amplified the TSE agent via sheep scrapie, and spread via feed in the U.K. bovine, and other countries exporting the tainted product. BUT most everyone ignores this fact, and the fact that the U.S. has been recycling more TSE, from more species with TSEs, than any other country documented, but yet, it's all spontaneous, and the rise in sporadic CJD in the U.S. is a happenstance of bad luck ??? I respectfully disagree. To top that all off, the infamous BSE-FIREWALL that the USDA always brags about was nothing more than ink on paper, and I can prove this. YOU can ignore it, but this is FACT (see source, as late as 2007, in one recall alone, some 10,000,000 MILLION POUNDS OF BANNED MAD COW FEED WENT OUT INTO COMMERCE TO BE FED OUT, and most was never recovered. This was banned blood laced, meat and bone meal. 2006 was a banner year for banned mad cow protein going into commerce in the U.S. (see source of FDA feed ban warning letter below). I stress that the August 4, 1997 USA mad cow feed ban and this infamous BSE firewall, was nothing more than ink on paper, it was never enforceable.
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.
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. This would further have to be broken down to strain of species and then the route of transmission would further have to be broken down. Accumulation and Transmission are key to the threshold from sub- clinical to clinical disease, and key to all this, is to stop the amplification and transmission of this agent, the spreading of, no matter what strain. In my opinion, to continue with this myth that the U.K. strain of BSE one strain TSE in cows, and the nv/v CJD one strain TSE humans, and the one geographical location source i.e. U.K., and that all the rest of human TSE are just one single strain i.e. sporadic CJD, a happenstance of bad luck that just happens due to a twisted protein that just twisted the wrong way, IN 85%+ OF ALL HUMAN TSEs, when to date there are 6 different phenotypes of sCJD, and growing per Gambetti et al, and that no other animal TSE transmits to humans ??? With all due respect to all Scientist that believe this, I beg to differ. To continue with this masquerade will only continue to spread, expose, and kill, who knows how many more in the years and decades to come. ONE was enough for me, My Mom, hvCJD i.e. Heidenhain Variant CJD, DOD 12/14/97 confirmed, which is nothing more than another mans name added to CJD, like CJD itself, Jakob and Creutzfeldt, or Gerstmann-Straussler-Scheinker syndrome, just another CJD or human TSE, named after another human. WE are only kidding ourselves with the current diagnostic criteria for human and animal TSE, especially differentiating between the nvCJD vs the sporadic CJD strains and then the GSS strains and also the FFI fatal familial insomnia strains or the ones that mimics one or the other of those TSE? Tissue infectivity and strain typing of the many variants of the human and animal TSEs are paramount in all variants of all TSE. There must be a proper classification that will differentiate between all these human TSE in order to do this. With the CDI and other more sensitive testing coming about, I only hope that my proposal will some day be taken seriously. ...
please see history, and the ever evolving TSE science to date ;
Saturday, June 13, 2009
Monitoring the occurrence of emerging forms of Creutzfeldt-Jakob disease in the United States 2003 revisited 2009
https://journals.plos.org/plosone/article/comment?id=10.1371/annotation/04ce2b24-613d-46e6-9802-4131e2bfa6fd
Singeltary Submission SEAC 2007
SEAC SPONGIFORM ENCEPHALOPATHY ADVISORY COMMITTEE Minutes of the 99th meeting held on 14th December 2007 Singeltary Submission
This was 22 years to the day Mom died from the Heidenhain Variant of Creutzfeldt Jakob Disease i.e. hvCJD, when i made this submission to SEAC and this was their reply to my questions of concern about cjd in the USA, my how things have changed...terry
SEAC SPONGIFORM ENCEPHALOPATHY ADVISORY COMMITTEE Minutes of the 99th meeting held on 14th December 2007
ITEM 8 – PUBLIC QUESTION AND ANSWER SESSION 40. The Chair explained that the purpose of the question and answer session was to give members of the public an opportunity to ask questions related to the work of SEAC. Mr Terry Singeltary (Texas, USA) had submitted a question prior to the meeting, asking: “With the Nor-98 now documented in five different states so far in the USA in 2007, and with the two atypical BSE H-base cases in Texas and Alabama, with both scrapie and chronic wasting disease (CWD) running rampant in the USA, is there any concern from SEAC with the rise of sporadic CJD in the USA from ''unknown phenotype'', and what concerns if any, in relations to blood donations, surgery, optical, and dental treatment, do you have with these unknown atypical phenotypes in both humans and animals in the USA? Does it concern SEAC, or is it of no concern to SEAC? Should it concern USA animal and human health officials?”
41. A member considered that this question appeared to be primarily related to possible links between animal and human TSEs in the USA. There is no evidence that sCJD is increasing in the USA and no evidence of any direct link between TSEs and CJD in the USA. Current evidence does not suggest that CWD is a significant risk to human health. There are unpublished data from a case of human TSE in the USA that are suggestive of an apparently novel form of prion disease with distinct molecular characteristics. However, it is unclear whether the case had been further characterised, if it could be linked to animal TSEs or if other similar cases had been found in the USA or elsewhere. In relation to the possible public health implications of atypical scrapie, H-type BSE and CWD, research was being conducted to investigate possible links and surveillance was in place to detect any changes in human TSEs. Although possible links between these diseases and human TSEs are of concern and require research, there is no evidence to suggest immediate public health action is warranted. The possible human health risks from classical scrapie had been discussed earlier in the meeting. Members noted that there are effective channels of discussion and collaboration on research between USA and European groups. Members agreed it is important to keep a watching brief on new developments on TSEs.
http://web.archive.org/web/20091010132933/http://www.seac.gov.uk/minutes/99.pdf
14th ICID International Scientific Exchange Brochure -
Final Abstract Number: ISE.114
Session: International Scientific Exchange
Transmissible Spongiform encephalopathy (TSE) animal and human TSE in North America
update October 2009
T. Singeltary
Bacliff, TX, USA
Background:
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.
Methods:
12 years independent research of available data
Results:
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.
Conclusion:
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. 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.
International Society for Infectious Diseases Web: http://www.isid.org
http://ww2.isid.org/Downloads/14th_ICID_ISE_Abstracts.pdf
https://web.archive.org/web/20101116225529/http://ww2.isid.org/Downloads/14th_ICID_ISE_Abstracts.pdf
2001 Singeltary on CJD, Journal of American Medical Association
February 14, 2001
Diagnosis and Reporting of Creutzfeldt-Jakob Disease
Terry S. Singeltary, Sr
Author Affiliations
JAMA. 2001;285(6):733-734. doi:10-1001/pubs.JAMA-ISSN-0098-7484-285-6-jlt0214
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.
February 14, 2001
Diagnosis and Reporting of Creutzfeldt-Jakob Disease
Terry S. Singeltary, Sr
Author Affiliations
JAMA. 2001;285(6):733-734. doi:10-1001/pubs.JAMA-ISSN-0098-7484-285-6-jlt0214
https://jamanetwork.com/journals/jama/article-abstract/1031186
RE-Monitoring the occurrence of emerging forms of Creutzfeldt-Jakob disease in the United States 2003 Singeltary Journal of Neurology
26 MARCH 2003
RE-Monitoring the occurrence of emerging forms of Creutzfeldt-Jakob disease in the United States
Terry S. Singeltary, retired (medically)
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?
https://www.neurology.org/doi/10.1212/01.WNL.0000036913.87823.D6
Prion Scientific Advisors and Consultants Staff Meeting Singeltary Submission Freas Monday, January 08,2001 3:03 PM
Scientific Advisors and Consultants Staff 2001 Advisory Committee TSE PRION Singeltary Submission Freas
Monday, January 08,2001 3:03 PM
FDA Singeltary submission 2001
Greetings again Dr. Freas and Committee Members,
I wish to submit the following information to the Scientific Advisors and Consultants Staff 2001 Advisory Committee (short version). I understand the reason of having to shorten my submission, but only hope that you add it to a copy of the long version, for members to take and read at their pleasure, (if cost is problem, bill me, address below). So when they realize some time in the near future of the 'real' risks i speak of from human/animal TSEs and blood/surgical products. I cannot explain the 'real' risk of this in 5 or 10 minutes at some meeting, or on 2 or 3 pages, but will attempt here: fda link is dead in the water;
http://web.archive.org/web/20041212232925/http://www.fda.gov/ohrms/dockets/ac/01/slides/3681s2_09.pdf
https://tseac.blogspot.com/2009/05/meeting-of-transmissible-spongiform.html
wasted days and wasted nights…Freddy Fender
Terry S. Singeltary Sr., Bacliff, Texas USA 77518
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