WILDLIFE HEALTH COORDINATION AND ZOONOTIC DISEASE PREVENTION ACT S.4451 Chronic Wasting Disease CWD TSE Prion Singeltary Submission
WILDLIFE HEALTH COORDINATION AND ZOONOTIC DISEASE PREVENTION ACT S.4451 Chronic Wasting Disease CWD TSE Prion Singeltary Submission
My submission to;
WILDLIFE HEALTH COORDINATION AND ZOONOTIC DISEASE PREVENTION ACT
WILDLIFE HEALTH COORDINATION AND ZOONOTIC DISEASE PREVENTION ACT
Bills and resolutions
Enact (see S. 4451), S2170 [30AP]
https://www.congress.gov/congressional-record/congressional-record-index/119th-congress/2nd-session/wildlife-health-coordination-and-zoonotic-disease-prevention-act/2014435
S.4451 - A bill to support Federal, State, and Tribal coordination and management efforts relating to wildlife disease and zoonotic disease surveillance and ongoing and potential wildlife disease and zoonotic disease outbreaks, and for other purposes.119th Congress (2025-2026) | Get alerts
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Hide Overview| Sponsor: | Sen. Baldwin, Tammy [D-WI] (Introduced 04/30/2026) |
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| Committees: | Senate - Environment and Public Works |
| Latest Action: | Senate - 04/30/2026 Read twice and referred to the Committee on Environment and Public Works. (All Actions) |
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Summary: S.4451 — 119th Congress (2025-2026)All Information (Except Text)
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Text: S.4451 — 119th Congress (2025-2026)All Information (Except Text)
As of 05/07/2026 text has not been received for S.4451 - A bill to support Federal, State, and Tribal coordination and management efforts relating to wildlife disease and zoonotic disease surveillance and ongoing and potential wildlife disease and zoonotic disease outbreaks, and for other purposes.
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Baldwin bill to enhance animal disease outbreak coordination Measure would improve communication among agencies, states and tribes in managing wildlife and zoonotic disease outbreaks.
Release May 4, 2026 4 Min
Sen. Tammy Baldwin (D-Wis.) introduced legislation last week to prevent transmission of wildlife diseases like avian influenza, bovine tuberculosis, brucellosis and chronic wasting disease (CWD) between wildlife, livestock and humans.
The Wildlife Health Coordination and Zoonotic Disease Prevention Act increases interagency coordination, facilitates information sharing, improves coordination between states and furthers sharing of best practices for managing domestic wildlife and zoonotic disease outbreaks, according to a news release from Baldwin.
Since March 2022, Wisconsin has lost 11.6 million birds across 50 commercial and backyard flocks due to outbreaks of avian influenza. Between late February and March of this year, Wisconsin experienced three major avian flu outbreaks in commercial poultry flocks, affecting more than 4.3 million egg-laying hens. As a result, two Wisconsin farms were forced to temporarily lay off more than 80 employees.
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CWD also remains an increasing concern in Wisconsin. CWD has been detected in both captive and wild animals in most Wisconsin counties since its original incursion, and in 2025, it was detected in wild deer populations across 51 Wisconsin counties.
Addressing these outbreaks is not just important for protecting wildlife and agricultural industries but also public health. Three out of every four new or emerging infectious diseases in human populations originate from animals. In March 2024, the first reported cow-to-human case of highly pathogenic avian influenza was identified after the individual encountered herds believed to have been infected by wild birds.
“Wisconsin farmers have dealt with the devastating fallout of avian flu and chronic wasting disease for far too long,” said Baldwin. “These diseases don’t just threaten our deer herds and poultry flocks; they put our food supply, our rural economy and public health at risk. That’s why I am introducing this bill to ensure that our state has the tools it needs to monitor and manage outbreaks, support our farmers and protect our rural communities.”
The Wildlife Health Coordination and Zoonotic Disease Prevention Act would take a proactive approach to disease outbreaks, establishing the Wildlife Health Coordination and Zoonotic Disease Program.
The program will establish and support four Regional Wildlife Health Coordinators, one National Wildlife Health Coordinator and one Tribal Wildlife Health Coordinator to help increase communication between federal agencies, states and tribes and facilitate more comprehensive and effective responses to current and emerging wildlife disease outbreaks. More specifically, the coordinators will:
Establish relationships with relevant federal agencies, states and Indian tribes. Facilitate information sharing about existing and emerging zoonotic disease outbreaks between states, tribes and federal agencies (including the U.S. Department of Agriculture, U.S. Fish & Wildlife Service and Centers for Disease Control & Prevention). Assist states and tribes in applying for funding to work on wildlife disease issues. Coordinate between states, including state agencies that work on agriculture, environment, natural resources and public health. Share best management practices for zoonotic disease management and prevention. Report to Congress on necessary resources and response activities for preventing and mitigating wildlife diseases.
The bill is supported by the American Association of Veterinary Medical Colleges, Association of Fish & Wildlife Agencies, Backcountry Hunters & Anglers, Izaak Walton League, Midwest Dairy Coalition, National Cattleman’s Beef Association, National Deer Association, National Farmers Union, National Pork Producers Council (NPPC), National Turkey Federation, National Wildlife Federation, Organic Trade Association, University of Wisconsin-Madison School of Veterinary Medicine, Wisconsin Farm Bureau Federation, Wisconsin Farmers Union, Wisconsin Game Preserve Association, Wisconsin Pork Producers Association and Wisconsin Veterinary Medical Association.
re-WILDLIFE HEALTH COORDINATION AND ZOONOTIC DISEASE PREVENTION ACT S.4451 Chronic Wasting Disease CWD TSE Prion Singeltary Submission
Greetings Honorable Sen. Tammy Baldwin (D-Wis.), Senators, Everyone Involved on the WILDLIFE HEALTH COORDINATION AND ZOONOTIC DISEASE PREVENTION ACT, S.4451, specifically Chronic Wasting Disease CWD TSE Prion, and the Zoonotic and Environmental Factors and ramifications there from. Much science has come forth the past few years that should cause great concern from CWD TSE Prion in Cervid, and spillover there from.
WE already now have proven spillover of CWD to Pigs, and we now know CWD will transmit by ORAL routes to Cattle, Sheep, Pigs, Cervid, and Primates, and this should cause great concern with the FDA PART 589 SUBSTANCES PROHIBITED FROM USE IN ANIMAL FOOD OR FEED Regulations, because it fails to protect the livestock producing animals for human and animals from all this now, it’s a broke system, and has been.
Trucking CWD, is another huge factor, for the further spread of CWD TSE Prion, just look at Texas.
SEE TEXAS CWD DATA TOWARDS THE BOTTOM…TERRY
FeedARMOR emerges as the new standard in feed mitigation and operational biosecurity
Rapid industry adoption highlights the shift toward safer, lower-inclusion solutions for managing feed-borne pathogens in swine and poultry production.
re-WILDLIFE HEALTH COORDINATION AND ZOONOTIC DISEASE PREVENTION ACT S.4451 Chronic Wasting Disease CWD TSE Prion Singeltary Submission
I urge Everyone to read and understand the latest on Transmissible Spongiform Encephalopathy, Prion, Chronic Wasting Disease in Cervids, and oral transmission, there from, it’s a whole new game now, i call it TSE Prion poker, who’s all in$$$
IF/WHEN or has it already, CWD TSE Prion, mutates into anther strain, that transmits by contact, to other species, like cwd does with cervid, that would be the ultimate, OH SHIT. it’s always been wrote in stone CWD wouldn’t transmit by oral routes to these livestock species, of which we now know that was a wrong conclusion. yet were still feeding feed that could transmit CWD to all thes livestock species, BUT, if it really goes sideways, mutates, becomes transmissible by casual contact, and we already know TSE can transmit by air borne transmission, but CWD being a truly Contagious Disease would be the ultimate nail in the coffin, so what i’m trying to say is, if we don’t get serious and act, hit cwd at all fronts, it’s not going to end well. you just can’t keep kicking the cwd can down the road, or try to save the very industry, that still insists cwd isn’t a problem and continues to help spread CWD @ 50 MPH, or let captive cervid continue to escape, or continued Lacy act violations. and the industry rumor mill that keeps pushing cwd junk science, it’s a CWD conspiracy by the government, or the insurance companies are responsible for CWD, or it’s a CWD money grab by DNR et al, or my favorite, “deer don’t die from CWD”, or, “show me a picture of cwd under a microscope”, it’s utter insanity with some of the CWD junk science, and it helps spread CWD.
CWD Herd Management for all Captive, VOLUNTARY MUST become MANDATORY! you must remove the very industry helping to spread CWD and their Legislators, from the policy making decisions for CWD, it’s the very reason, imho, we’re in this mess now, at least for Texas, i know other States had the same problems. YOU can’t have different CWD regulations from state to state, based on legislative junk science, from different states. IT WILL NOT WORK!
Chronic Wasting Disease CWD TSE Prion Cervid
cwd transmits by oral routes to, cattle, pigs, sheep, cervid, primates, oh my!
***> cwd to cattle
Prion Conference 2023
Transmission of the chronic wasting disease agent from elk to cattle after oronasal exposure
Conclusions: Cattle with the E211K polymorphism are susceptible to the CWD agent after oronasal exposure of 0.2 g of infectious material.
Strain characterization of chronic wasting disease in bovine-PrP transgenic mice
Conclusions: Altogether, these results exhibit the diversity of CWD strains present in the panel of CWD isolates and the ability of at least some CWD isolates to infect bovine species. Cattle being one of the most important farming species, this ability represents a potential threat to both animal and human health, and consequently deserves further study.
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
Transmission of the chronic wasting disease agent from elk to cattle after oronasal exposure
Justin Greenlee, Jifeng Bian, Zoe Lambert, Alexis Frese, and Eric Cassmann Virus and Prion Research Unit, National Animal Disease Center, USDA-ARS, Ames, IA, USA
Aims: The purpose of this study was to determine the susceptibility of cattle to chronic wasting disease agent from elk.
Materials and Methods: Initial studies were conducted in bovinized mice using inoculum derived from elk with various genotypes at codon 132 (MM, LM, LL). Based upon attack rates, inoculum (10% w/v brain homogenate) from an LM132 elk was selected for transmission studies in cattle. At approximately 2 weeks of age, one wild type steer (EE211) and one steer with the E211K polymorphism (EK211) were fed 1 mL of brain homogenate in a quart of milk replacer while another 1 mL was instilled intranasally. The cattle were examined daily for clinical signs for the duration of the experiment. One steer is still under observation at 71 months post-inoculation (mpi).
Results: Inoculum derived from MM132 elk resulted in similar attack rates and incubation periods in mice expressing wild type or K211 bovine PRNP, 35% at 531 days post inoculation (dpi) and 27% at 448 dpi, respectively. Inoculum from LM132 elk had a slightly higher attack rates in mice: 45% (693 dpi) in wild type cattle PRNP and 33% (468) in K211 mice. Inoculum from LL132 elk resulted in the highest attack rate in wild type bovinized mice (53% at 625 dpi), but no K211 mice were affected at >700 days. At approximately 70 mpi, the EK211 genotype steer developed clinical signs suggestive of prion disease, depression, low head carriage, hypersalivation, and ataxia, and was necropsied. Enzyme immunoassay (IDEXX) was positive in brainstem (OD=4.00, but non-detect in retropharyngeal lymph nodes and palatine tonsil. Immunoreactivity was largely limited to the brainstem, midbrain, and cervical spinal cord with a pattern that was primarily glia-associated.
Conclusions: Cattle with the E211K polymorphism are susceptible to the CWD agent after oronasal exposure of 0.2 g of infectious material.
***> cwd to pigs
Chronic wasting disease prions in cervids and wild pigs in North America Preliminary Outbreak Assessment DEFRA 26 January 2026
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
Chronic wasting disease (CWD) is a fatal neurodegenerative disease of cervids, such as deer, elk, moose and reindeer. It is caused by prions – infectious proteins that cause normal cellular prion proteins to misfold (CIDRAP, 2025). The disease is widespread in captive and free-ranging cervids in North America (Figure 1). For the first time, CWD prions have also been detected in the tissues of wild pigs (Sus scrofa) caught in CWD-affected areas of the USA (Soto et al. 2025). This discovery emerged from a study designed to investigate potential interactions between wild pigs and CWD prions, as wild pigs often coexist with cervids, which can shed prions into the environment. The following assessment discusses the epidemiology of CWD in North America and the detection of CWD prions in wild pigs. It also considers the potential implications for Great Britain.
Figure 1. Distribution of CWD in cervids in North America as of 11 April 2025 (USGS, 2025).Department for Environment, Food and Rural Affairs
Situation assessment
CWD is considered one of the most important cervid diseases due to its capacity for infectious spread, high mortality rate and associated socio-economic impacts on cervid farming and hunting-related industries (Kincheloe et al., 2021, CFSPH, 2024). The disease is always fatal, with no cure or vaccine (CFSPH, 2024).
CWD was first reported among captive cervids in the USA in the 1960s (Kincheloe et al., 2021). It has since been detected in captive and or free-ranging cervids in 36 US states and 5 Canadian provinces, as well as South Korea, Norway, Finland and Sweden (Silva, 2022, USGS, 2025). While the South Korean strains are thought to have originated from North America, the European strains appear to have emerged independently (Silva, 2022).
Transmission between cervids occurs by direct contact with infected animals or indirectly, through contact with a contaminated environment, most likely via the oral route (Otero et al., 2021). The disease may also be vertically transmitted from doe to fawn (Nalls et al., 2013, Salariu et al., 2015). Environmental contamination occurs when infected animals shed infectious prions in various secretions and excretions, such as urine, faeces and saliva (Otero et al., 2021). It can also occur when infected carcasses decompose and release prions into the surrounding soil and vegetation (Miller et al., 2004). The minimum number of CWD prions required to cause infection in cervids is unknown but appears to be low (Denkers et al., 2020).
The disease is difficult to control, as infected animals can also be subclinical for months or years. During this time, they can shed CWD prions, which can remain infectious in the environment for at least 2 years (Miller et al., 2004, CFSPH, 2024). Diagnosis usually relies on post-mortem tests, which may fail to identify infected animals during the early stages of the disease (CFSPH, 2024, CIDRAP, 2025). Control efforts are further hampered by lack of evidence to inform effective CWD management and control strategies (Uehlinger et al., 2016, Mori et al., 2024).
CWD in North American cervids
CWD has been reported in a range of North American cervids, including white-tailed deer, mule deer, black-tailed deer, moose, wapiti, reindeer (captive) and red deer (captive) (EFSA BIOHAZ Panel, 2023). It was first reported in captive mule deer and black-tailed deer at research facilities in Colorado and Wyoming in the late 1960s (Otero et al., 2021). These animals were derived from wild populations. The disease was later identified in Rocky Mountain elk at these facilities and subsequently, in free-ranging populations of mule deer and elk in Wyoming and Colorado. The geographic expansion of CWD in North America is thought to reflect the commercial movement of subclinical animals and natural cervid migration (Otero et al., 2021). Epidemiological data suggest that the disease spread from the USA to Canada and then to South Korea through imports of infected cervids (Otero et al., 2021). A retrospective analysis revealed that, in 1978, a Colorado‑born mule deer at Toronto Zoo in Ontario, Canada, died of CWD (Dubé et al., 2006). In 1996, the disease was detected in captive elk in Saskatchewan (Williams and Miller, 2002).
The disease
Department for Environment, Food and Rural Affairs
has since been detected in captive cervids in Alberta and Quebec and free-ranging cervids in Alberta, British Columbia, Manitoba and Saskatchewan (USGS, 2025). The origin of the outbreak in free-ranging Canadian cervids is unknown (Otero et al., 2021).
While the spread of CWD across North America is often described as ‘rapid,’ it has been suggested that this may reflect widening disease surveillance, rather than a ‘real-time’ indication of geographic spread. CWD epidemics appear to develop relatively slowly compared with other wildlife diseases (EFSA BIOHAZ Panel, 2023). Field and modelling data from North America suggest that it may take 15 to 20 years for CWD prevalence to reach 1% in free-ranging cervid populations, although more rapid transmission may occur in captive populations. The surveillance sensitivity in North America means that the disease may have been present for 10 years or more in some areas before it was detected (Miller et al., 2000).
The prevalence of CWD in affected populations or species varies across North America. In captive herds, prevalence may reach 100% over time, while in affected free-ranging populations, reported prevalence ranges from <1% to >30%. Most clinical cases are observed in cervids 2 to 7 years old, especially males, which is believed to be due to behavioural differences rather than differences in susceptibility between sexes (EFSA BIOHAZ Panel, 2023). At least 13 different risk factors may contribute towards CWD spread in North America, such as host genetics, high deer density or inappropriate disposal of deer carcasses and slaughter by-products (EFSA BIOHAZ Panel, 2019).
Approaches towards CWD control and surveillance in captive and free-ranging deer vary widely across North America within and between jurisdictions (CIDRAP, 2025). A summary of the measures in place in each US state and Canadian province is available from the CWD Alliance (2026), a coalition of wildlife conservation agencies, dedicated to providing accurate information on CWD and supporting strategies to minimise its impact on free-ranging cervids. Wildlife agencies rely on voluntary testing of hunted deer carcasses as the main mechanism for CWD surveillance and management, usually using post-mortem ELISA or immunohistochemistry methods (CIDRAP, 2025).
In the USA, Animal and Plant Health Inspection Service (APHIS) operates the CWD Herd Certification Programme (HCP) in collaboration with state and wildlife agencies. This is a voluntary scheme which aims to provide a consistent, national approach to controlling CWD in farmed cervids and preventing interstate spread by establishing control measures such as fencing, detailed record keeping and CWD testing of all cervids over 12 months old that die for any reason. The Canadian Food Inspection Agency (CFIA) operates a similar programme, the CWD Herd Certification Programme. As of December 2025, 28 states were participating in the USA’s CWD HCP and 5 Canadian provinces and one Canadian territory were participating in the Canadian programme (USDA, 2025b, CFIA, 2025).
Control methods fall within three general categories: prevention, containment, and control and suppression. Prevention and containment aim to prevent CWDDepartment for Environment, Food and Rural Affairs introduction into areas where it has not previously been reported and to limit its geographical spread once it has been introduced, respectively. Both tend to include regulatory measures such as bans on the movement of live cervids, cervid carcasses or specified risk materials. Control and suppression aim to stabilise or reduce infection rates within a herd or population through measures such as selective or random culling (EFSA BIOHAZ Panel, 2017).
Despite control efforts, CWD has continued to spread among captive and free- ranging cervids in North America, with increasing prevalence in affected areas (Uehlinger et al., 2016, CFSPH, 2024). Eradicating CWD from North America appears infeasible due to its extent of geographic spread and epidemiological characteristics, such as environmental persistence (EFSA BIOHAZ Panel, 2017).
CWD in wild pigs in the USA
Wild pigs are an invasive population in the USA, especially in the south (Figure 2). They comprise escaped domestic swine, Eurasian wild boar and hybrids of the two (Smyser et al., 2020). Wild pigs frequently coexist with cervids in areas where CWD is endemic and may be exposed to CWD prions through rooting in contaminated soil, scavenging deer carcasses and predation on fawns. These ecological interactions provide multiple routes by which wild pigs could encounter prions from infected deer (Soto et al. 2025).
Under experimental conditions, domestic pigs can become infected with CWD by oral and intracerebral routes, suggesting that wild pigs might also be susceptible. Domestic pigs rarely develop clinical signs of CWD but accumulate prions in the lymphoid tissues in their heads and gut, suggesting that, like cervids, they could shed the prions in saliva and faeces (Moore et al., 2017).
Against this background, Soto et al. (2025) investigated potential interactions between wild pigs and CWD prions. They analysed over 300 brain and lymph node samples from 178 wild pigs living across Arkansas and Texas, USA. The animals were captured by the United States Department of Agriculture (USDA) between 2020 and 2021. None of the pigs included in the study were reported to be displaying clinical signs of disease.
Using an ultra-sensitive laboratory method (protein misfolding cyclic amplification (PMCA)), 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. These findings indicate that wild pigs are naturally exposed to CWD prions in areas where the disease is present (Soto et al., 2025).
When intracerebrally inoculated with tissues from wild pigs, a small proportion of mice expressing deer prion protein developed subclinical prion infection. No transmission was detected in mice expressing pig prion protein. This suggests that wild pig tissues only contain low levels of infectious prions and that wild pigs are relatively resistant to natural infection. However, they could still contribute to CWD transmission, influencing its epidemiology, geographic distribution and interspecies spread (Soto et al., 2025).Department for Environment, Food and Rural Affairs While their exact role and importance in CWD transmission is unclear, wild pigs have considerable home ranges in North America (1.1 to 5.32 km on average), which may increase when food is scarce. This mobility could complicate efforts to control the disease if they play a role in its transmission (Soto et al., 2025).
The USDA’s APHIS does not currently conduct active surveillance for CWD in wild pigs (USDA, 2025a).
Figure 2. Geographic distribution of wild pigs (purple) in the USA as of 27 January 2025, comprising escaped domestic pigs, Eurasian wild boar and hybrids of the two (adapted from USDA, 2026). Yellow (Texas) and green (Arkansas) circles indicate the states where CWD prions were detected in wild pig tissues.
Department for Environment, Food and Rural Affairs
Implications for Great Britain
CWD is a notifiable animal disease in Great Britain, but no cases have ever been reported (Defra and APHA, 2018, CIDRAP, 2025).
The introduction of CWD into Great Britain’s cervid population could have devastating socio-economic and animal welfare impacts, resulting in marked population declines, as seen in the USA (Miller et al., 2008). There could also be significant losses to cervid farming, hunting and rural tourism industries, as well as significant costs associated with controlling the spread of the disease. The UK venison market alone is worth an estimated £100 million (Scotland Food and Drink, 2018).
There are several discrete wild pig populations in Great Britain, including wild boar and feral pigs. The largest known population is in the Forest of Dean in Gloucestershire, with an estimated 583 wild boar as of 2025/2026, although Forestry England (2025) aims to reduce the number to 400 to protect other species, such as plants and insects. Pockets of wild boar and feral pigs exist in other parts of the country, but their exact numbers are unknown (Mathews et al., 2018). The potential impact of CWD introduction into Great Britain’s wild pig population is uncertain because their role in disease transmission remains unclear. While they appear to be relatively resistant to natural CWD infection and disease, they could potentially contribute towards the maintenance and spread of CWD in Great Britain’s cervid population (Soto et al., 2025).
To reduce the risk of CWD introduction, Great Britain suspended the import of live cervids and high-risk cervid products in June 2023, including urine hunting lures, from all countries where CWD has been reported. Fresh cervid meat, excluding offal and spinal cord, can only be imported into Great Britain from CWD-affected countries if it has tested negative for CWD using an approved diagnostic method, such as immunohistochemistry, and originates from an area where CWD has not been reported or officially suspected in the last 3 years (Defra and APHA, 2026).
The current risk of CWD prions being introduced into Great Britain’s wild pig or cervid population ranges from very low (event is very rare but cannot be excluded) to negligible (event is so rare it does not merit consideration). This is based on the risk of incursion tool, developed by Roberts et al., (2011). It is also supported by a recent Defra and APHA (2025) risk assessment. While this assessment identified a few theoretical entry pathways, such as contaminated equipment, that could not be fully assessed due to limited data, there is no definitive evidence that they have ever resulted in the introduction of CWD into a new area.
Detection of CWD prions in wild pigs in the USA is unlikely to affect Great Britain’s CWD risk level, as the USA is not approved to export live wild pigs to Great Britain (Defra, 2025). Import of infected wild pig meat or wild pig by-products from the USA could theoretically introduce CWD prions into Great Britain, but the risk of this is also very low. To date, CWD prions have only been reported in lymph node and brain tissue samples in wild pigs, at levels too low to cause disease in mouse models
Department for Environment, Food and Rural Affairs
(Soto et al., 2025). However, their presence in other tissues cannot be excluded. The USA is approved to export wild pig meat and certain wild pig by-products to Great Britain, excluding offal, minced meat and germplasm (Defra, 2025), but there appears to be limited trade in these commodities.
It is difficult to quantify the exact amount of wild pig meat exported to Great Britain, as available trade data does not always distinguish between meat of wild and domestic pigs. However, based on HMRC data, the last known export of non- domestic pig meat from the USA to Great Britain was in 2013 (4,881 kg).
Conclusion
CWD has continued to spread among captive and free-ranging cervids in North America since it was first detected in the 1960s. The finding of CWD prions in wild pigs in the USA suggests they could contribute towards transmission of the disease, influencing its epidemiology, geographic distribution and interspecies spread. However, further research is needed to confirm this. CWD has never been reported in Great Britain and the current risk of CWD prions being introduced into Great Britain’s wild pig or cervid population ranges from very low to negligible.
Readers are reminded to be vigilant for signs of CWD. Information on how to spot the disease can be found here. Suspected cases must be reported immediately to the Defra Rural Services Helpline on 03000 200 301. In Wales, call 0300 303 8268. In Scotland, contact your local Field Services Office. Failure to do so is an offence. We will continue to monitor the situation.
Authors • Lawrence Finn • Dr. Lauren Perrin • John Spiropoulos • Dr. Helen RobertsDepartment for Environment, Food and Rural Affairs
References
snip…see;
Shedding, retention and spreading of chronic wasting disease prions in the environment
Project Number 2R01AI132695-06A1 Former Number 2R01AI132695-06 Contact PI/Project Leader MORALES, RODRIGO
Abstract Text
ABSTRACT
Chronic Wasting Disease (CWD) is a prion disease affecting natural and captive cervid populations. This disease is progressively spreading across the United States and new foci of infectivity are constantly being reported. Despite decades of research, there are still several unanswered questions concerning CWD.
Compelling evidence suggest that CWD prions enter the environment through carcasses from diseased animals or by the progressive accumulation of prions shed in excreta. Unfortunately, the role that plants, parasites, predators, and scavengers play in CWD spreading has been poorly studied. During the past funding cycle, our group made important technical and conceptual contributions in this field.
Data from our group and others (in collaboration) demonstrate that plants can bind prions into their surfaces as well as transport them from soils to leaves. This is relevant, considering that prions are shown to progressively accumulate in soils and strongly suggests plants as potential vectors for CWD transmission. Unfortunately, the previously mentioned evidence has been collected using proof-of-concept conditions, including the exposure of high titers of rodent (laboratory generated) adapted prions, and grass plants only.
We have generated preliminary data showing that carrots grown in CWD infected soil carry prions in their roots and leaves as evaluated by bioassays. In contrast, tomato plants do not share these features. The significance of these findings cannot be ignored considering the interaction of CWD prions with a human and animal edible vegetable. Considering the use of carrots roots and leaves in human and animal nutrition, and the still unknown zoonotic potential of CWD, future research involving edible plants is urgently needed.
Another relevant (published) finding from our laboratory involves the high CWD infectivity titers found in nasal bots, a common cervid parasite that develops in the nasal cavity (a hotspot of prion infectivity). These parasites are found in large quantities in CWD pre- clinical and clinical deer, and may importantly contribute to environmental CWD transmission. Our research also identified CWD prions in naturally exposed flies, ticks, and dermestid beetles. However, the prion infectivity titers in these parasites have not been evaluated.
Finally, animals other than cervids, including hunters and scavengers, are expected to be exposed to CWD prions. Interestingly, we identified CWD prions and de novo generated porcine prions in tissues from wild pigs living in areas with variable CWD epidemiology. We plan to further investigate all these events and their relevance in natural prion transmission using a complementary set of techniques, including in vitro and in vivo systems. Emphasis will be made in analyzing the strain properties and zoonotic potentials of the prion agents under investigation. For this purpose, we gathered a unique group of collaborators able to supply us with the samples and expertise required to execute this project. Outcomes from this research are expected to deliver new insights on this animal prionopathy and provide regulatory agencies with useful information to control its continuous spread.
Public Health Relevance Statement
PROJECT NARRATIVE Despite decades of research, several questions remain unanswered for the Chronic Wasting Disease (CWD) epidemic affecting several deer species in the United States. Continuing with our previous R01 project, we will explore novel factors mediating the spread of CWD prions, including different plant types, invertebrate parasites (e.g., ticks, nasal bots) and scavengers (wild boars). These potential disease vectors will be studied for their ability to transmit disease within and across species, including humans.
Infectious prions in brains and muscles of domestic pigs experimentally challenged with the BSE, scrapie, and CWD agents
Authors: Francisca Bravo-Risi, Fraser Brydon, Angela Chong, Kane Spicker, Justin J. Greenlee https://orcid.org/0000-0003-2202-3054, Glenn Telling, Claudio Soto https://orcid.org/0000-0002-3412-0524, Sandra Pritzkow, Marcelo A. Barria, Rodrigo Morales
ABSTRACT
Experimental studies suggest that animal species not previously described as naturally infected by prions are susceptible to prion diseases affecting sheep, cattle, and deer. These interspecies transmissions may generate prions with unknown host ranges. Pigs are susceptible to prions from different origins, including deer chronic wasting disease (CWD), sheep scrapie, and bovine spongiform encephalopathy (BSE). Here, we studied prions in brains and muscles from pigs previously infected with these different prion sources. Specifically, we measured the total prion protein (PrP) and PK-resistant PrP by western blot. Seeding activity in these tissues was evaluated using the protein misfolding cyclic amplification (PMCA) technique. We found that BSE-infected pigs contained substantially more seeding competent prions compared with those infected with CWD and scrapie. Moreover, the zoonotic potential of porcine-BSE prions seems to be relevant, as both brains and muscles from BSE-infected pigs induced the misfolding of the human prion protein in vitro. This study helps to understand the potential fate of naturally existing prion strains in a relevant host and calls for caution considering the co-existence between feral swine and other prion-susceptible animal species.
IMPORTANCE
Prions (PrPSc) are proteinaceous, infectious pathogens responsible for prion diseases. Some livestock are highly susceptible to prion diseases. These include cattle (bovine spongiform encephalopathy, BSE), sheep and goat (scrapie), and cervids (chronic wasting disease, CWD). Unfortunately, BSE has been reported to be naturally transmitted to humans and other animal species. Domestic pigs, a relevant livestock animal, have not been reported to be naturally affected by prions; however, they are susceptible to the experimental exposure to BSE, scrapie, and CWD prions. Given the widespread consumption of porcine food products by humans, we aimed to evaluate the levels of pig-derived BSE, scrapie, and CWD prions from experimentally challenged domestic pigs in brain and meat cuts (leg, cheek meat, skirt meat, and tenderloin). We detected pig-adapted prions in the brains and some muscles of these animals. Additionally, we evaluated the in vitro compatibility between pig prions and the human prion protein (as a surrogate of zoonosis). Our results show that only pig-derived BSE prions were able to induce the misfolding of the cellular human prion protein. This data highlights the consequences of prion spillovers to other animal species and their potential availability to humans.
Snip…
In summary, our data shows the dynamic of animal prions when exposed to infectious pigs, as well as their distributions and zoonotic potentials. The data presented here may be relevant to understanding the fate of naturally existing prions in a sympatric animal species relevant for human consumption. This acquires importance considering a recent report describing the interaction between CWD and wild pigs in natural settings.
Volume 31, Number 1—January 2025
Dispatch
Detection of Prions in Wild Pigs (Sus scrofa) from Areas with Reported Chronic Wasting Disease Cases, United States
Paulina Soto, Francisca Bravo-Risi, Rebeca Benavente, Tucker H. Stimming, Michael J. Bodenchuk, Patrick Whitley, Clint Turnage, Terry R. Spraker, Justin Greenlee, Glenn Telling, Jennifer Malmberg, Thomas Gidlewski, Tracy Nichols, Vienna R. Brown, and Rodrigo Morales Author affiliation: The University of Texas Health Science Center at Houston, Texas, USA (P. Soto, F. Bravo-Risi, R. Benavente, T.H. Stimming, R. Morales); Centro Integrativo de Biologia y Quimica Aplicada, Universidad Bernardo O’Higgins, Santiago, Chile (P. Soto, F. Bravo-Risi, R. Morales); US Department of Agriculture, Fort Collins, Colorado, USA (M.J. Bodenchuk, P. Whitley, C. Turnage, J. Malmberg, T. Gidlewski, T. Nichols, V.R. Brown); Colorado State University, Fort Collins, Colorado, USA (T.R. Spraker, G. Telling); US Department of Agriculture, Ames, Iowa, USA (J. Greenlee)
Abstract
Using a prion amplification assay, we identified prions in tissues from wild pigs (Sus scrofa) living in areas of the United States with variable chronic wasting disease (CWD) epidemiology. Our findings indicate that scavenging swine could play a role in disseminating CWD and could therefore influence its epidemiology, geographic distribution, and interspecies spread.
Chronic wasting disease (CWD) is a prion disease of particular concern because of its uncontrolled contagious spread among various cervid species in North America
its recent discovery in Nordic countries (1), and its increasingly uncertain zoonotic potential (2). CWD is the only animal prion disease affecting captive as well as wild animals. Persistent shedding of prions by CWD-affected animals and resulting environmental contamination is considered a major route of transmission contributing to spread of the disease. Carcasses of CWD-affected animals represent relevant sources of prion infectivity to multiple animal species that can develop disease or act as vectors to spread infection to new locations.
Free-ranging deer are sympatric with multiple animal species, including some that act as predators, scavengers, or both. Experimental transmissions to study the potential for interspecies CWD transmissions have been attempted in raccoons, ferrets, cattle, sheep, and North American rodents (3–7). Potential interspecies CWD transmission has also been addressed using transgenic (Tg) mice expressing prion proteins (PrP) from relevant animal species (8). Although no reports of natural interspecies CWD transmissions have been documented, experimental studies strongly suggest the possibility for interspecies transmission in nature exists (3–7). Inoculation and serial passage studies reveal the potential of CWD prions to adapt to noncervid species, resulting in emergence of novel prion strains with unpredicted features (9–11).
Wild pigs (Sus scrofa), also called feral swine, are an invasive population comprising domestic swine, Eurasian wild boar, and hybrids of the 2 species (12). Wild pig populations have become established in the United States (Appendix Figure 1, panel A), enabled by their high rates of fecundity; omnivorous and opportunistic diet; and widespread, often human-mediated movement (13). Wild pigs scavenge carcasses on the landscape and have an intimate relationship with the soil because of their routine rooting and wallowing behaviors (14). CWD prions have been experimentally transmitted to domestic pigs by intracerebral and oral exposure routes (15), which is relevant because wild pigs coexist with cervids in CWD endemic areas and reportedly prey on fawns and scavenge deer carcasses. Considering the species overlap in many parts of the United States (Appendix Figure 1, panel 😎, we studied potential interactions between wild pigs and CWD prions.
Snip…
Conclusions
In summary, results from this study showed that wild pigs are exposed to cervid prions, although the pigs seem to display some resistance to infection via natural exposure. Future studies should address the susceptibility of this invasive animal species to the multiple prion strains circulating in the environment. Nonetheless, identification of CWD prions in wild pig tissues indicated the potential for pigs to move prions across the landscape, which may, in turn, influence the epidemiology and geographic spread of CWD.
THURSDAY, JANUARY 08, 2026
Confucius Ponders, what about Wild Pigs (Sus scrofa) and CWD TSE Prion, and the Environment, what if?
Confucius Ponders, what about Wild Pigs (Sus scrofa), they can cover some distance rather quickly, what about Wild Pigs (Sus scrofa) digging up the terrain, and as they do it, what if these Wild Pigs (Sus scrofa) were exposed to CWD TSE Prion, and then they go on exposing and saturating the land with CWD TSE Prion, then the soil becomes contaminated with CWD TSE Prion, then what about the plants that grow from that soil for the decades to come, what if???
WEDNESDAY, JANUARY 28, 2026
Chronic wasting disease prions in cervids and wild pigs in North America Preliminary Outbreak
***> CWD to sheep, Scrapie to Cervid
Chronic Wasting Disease CWD vs Scrapie TSE Prion
Detection of infectivity in orally inoculated pigs using mouse bioassay raises the possibility that naturally exposed pigs could act as a reservoir of CWD infectivity. Currently, swine rations in the U.S. could contain animal derived components including materials from deer or elk. In addition, feral swine could be exposed to infected carcasses in areas where CWD is present in wildlife populations. The current feed ban in the U.S. is based exclusively on keeping tissues from TSE infected cattle from entering animal feeds. These results indicating the susceptibility of pigs to CWD, coupled with the limitations of the current feed ban, indicates that a revision of the feed ban may be necessary to protect swine production and potentially human health.
***> However, at 51 months of incubation or greater, 5 animals were positive by one or more diagnostic methods. Furthermore, positive bioassay results were obtained from all inoculated groups (oral and intracranial; market weight and end of study) suggesting that swine are potential hosts for the agent of scrapie. <***
*** Although the current U.S. feed ban is based on keeping tissues from TSE infected cattle from contaminating animal feed, swine rations in the U.S. could contain animal derived components including materials from scrapie infected sheep and goats. These results indicating the susceptibility of pigs to sheep scrapie, coupled with the limitations of the current feed ban, indicates that a revision of the feed ban may be necessary to protect swine production and potentially human health. <***
***> Results: PrPSc was not detected by EIA and IHC in any RPLNs. All tonsils and MLNs were negative by IHC, though the MLN from one pig in the oral <6 month group was positive by EIA. PrPSc was detected by QuIC in at least one of the lymphoid tissues examined in 5/6 pigs in the intracranial <6 months group, 6/7 intracranial >6 months group, 5/6 pigs in the oral <6 months group, and 4/6 oral >6 months group. Overall, the MLN was positive in 14/19 (74%) of samples examined, the RPLN in 8/18 (44%), and the tonsil in 10/25 (40%).
***> Conclusions: This study demonstrates that PrPSc accumulates in lymphoid tissues from pigs challenged intracranially or orally with the CWD agent, and can be detected as early as 4 months after challenge. CWD-infected pigs rarely develop clinical disease and if they do, they do so after a long incubation period. This raises the possibility that CWD-infected pigs could shed prions into their environment long before they develop clinical disease. Furthermore, lymphoid tissues from CWD-infected pigs could present a potential source of CWD infectivity in the animal and human food chains.
Conclusions: This study demonstrates that PrPSc accumulates in lymphoid tissues from pigs challenged intracranially or orally with the CWD agent, and can be detected as early as 4 months after challenge. CWD-infected pigs rarely develop clinical disease and if they do, they do so after a long incubation period. This raises the possibility that CWD-infected pigs could shed prions into their environment long before they develop clinical disease. Furthermore, lymphoid tissues from CWD-infected pigs could present a potential source of CWD infectivity in the animal and human food chains.
Research Project: Elucidating the Pathobiology and Transmission of Transmissible Spongiform Encephalopathies
Location: Virus and Prion Research
Title: Differentiation of scrapie from chronic wasting disease in white-tailed deer
snip…
Accomplishments
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. It has long been suggested that prion disease in deer (chronic wasting disease (CWD)) was caused by the prion agent from sheep. The prion disease that affects sheep, scrapie, has been recognized for hundreds of years. However, chronic wasting disease, a similar disease found in WTD, has only been recognized since the 1960s. ARS researchers in Ames, Iowa, showed that white-tailed deer sick with scrapie from sheep can infect other deer under conditions mimicking natural exposure. Furthermore, this work shows that CWD is difficult to differentiate from WTD infected with scrapie. WTD scrapie prions accumulate in the lymphoreticular system in a manner similar to CWD, meaning that environmental contamination may occur through feces, saliva, and other body fluids of scrapie affected WTD as has been shown for CWD. The presence of WTD infected with scrapie could confound mitigation efforts for chronic wasting disease. This information informs regulatory officials, the farmed cervid industry, and officials tasked with protecting animal health such as state Departments of Agriculture, Natural Resources, or Parks and Wildlife with regard to a disease similar to CWD but arising from sheep scrapie that could be present in WTD that have contact with scrapie affected sheep and/or goats.
Chronic Wasting Disease CWD vs Scrapie TSE Prion
Volume 30, Number 8—August 2024
Research
Scrapie Versus Chronic Wasting Disease in White-Tailed Deer
Zoe J. Lambert1, Jifeng Bian, Eric D. Cassmann, M. Heather West Greenlee, and Justin J. Greenlee
Author affiliations: Oak Ridge Institute for Science and Education, Oak Ridge, Tennessee, USA (Z.J. Lambert); US Department of Agriculture, Ames, Iowa, USA (Z.J. Lambert, J. Bian, E.D. Cassmann, J.J. Greenlee); Iowa State University, Ames (Z.J. Lambert, M.H. West Greenlee) Suggested citation for this article
Abstract
White-tailed deer are susceptible to scrapie (WTD scrapie) after oronasal inoculation with the classical scrapie agent from sheep. Deer affected by WTD scrapie are difficult to differentiate from deer infected with chronic wasting disease (CWD). To assess the transmissibility of the WTD scrapie agent and tissue phenotypes when further passaged in white-tailed deer, we oronasally inoculated wild-type white-tailed deer with WTD scrapie agent. We found that WTD scrapie and CWD agents were generally similar, although some differences were noted. The greatest differences were seen in bioassays of cervidized mice that exhibited significantly longer survival periods when inoculated with WTD scrapie agent than those inoculated with CWD agent. Our findings establish that white-tailed deer are susceptible to WTD scrapie and that the presence of WTD scrapie agent in the lymphoreticular system suggests the handling of suspected cases should be consistent with current CWD guidelines because environmental shedding may occur.
snip…
The potential for zoonoses of cervid-derived PrPSc is still not well understood (6,18,45–47); however, interspecies transmission can increase host range and zoonotic potential (48–50). Therefore, to protect herds and the food supply, suspected cases of WTD scrapie should be handled the same as cases of CWD.
Western blots done on samples from the brainstem, cerebellum, and lymph nodes of scrapie-infected WTD have a molecular profile similar to CWD and distinct from western blots of samples from the cerebral cortex, retina, or the original sheep scrapie inoculum. WTD are susceptible to the agent of scrapie from sheep and differentiation from CWD may be difficult.
Component 6: Transmissible Spongiform Encephalopathies
Sheep scrapie agent can infect white-tailed deer after oronasal exposure.
The origin of chronic wasting disease (CWD) is not known, but it has many similarities to the sheep prion disease called scrapie. It has long been hypothesized that CWD arose through transmission of sheep scrapie to deer. ARS researchers in Ames, Iowa, conducted research to determine if scrapie derived from sheep could be transmitted to white-tailed deer. The deer inoculated with sheep scrapie developed clinical signs and the abnormal prion protein could be detected in a wide range of tissues. These results indicate that deer may be susceptible to sheep scrapie if exposed to the disease in natural or agricultural settings. In addition, several strong similarities between CWD in white-tailed deer and the experimental cases of scrapie in white-tailed deer suggests that it would be difficult to distinguish scrapie from CWD in deer or identify scrapie if a case occurs. This information should be considered by deer farmers for keeping their herds free from prion diseases.
https://www.ars.usda.gov/ARSUserFiles/np103/AnnualReports/NP103%20FY2023%20Annual%20Report_Final.pdf
It has long been hypothesized that CWD arose through transmission of sheep scrapie to deer. ARS researchers in Ames, Iowa, conducted research to determine if scrapie derived from sheep could be transmitted to white-tailed deer. The deer inoculated with sheep scrapie developed clinical signs and the abnormal prion protein could be detected in a wide range of tissues. These results indicate that deer may be susceptible to sheep scrapie if exposed to the disease in natural or agricultural settings. In addition, several strong similarities between CWD in white-tailed deer and the experimental cases of scrapie in white-tailed deer suggests that it would be difficult to distinguish scrapie from CWD in deer or identify scrapie if a case occurs. This information should be considered by deer farmers for keeping their herds free from prion diseases.
https://www.ars.usda.gov/ARSUserFiles/np103/AnnualReports/NP103%20FY2023%20Annual%20Report_Final.pdf
ORIGIN OF CHRONIC WASTING DISEASE TSE PRION?COLORADO THE ORIGIN OF CHRONIC WASTING DISEASE CWD TSE PRION?
*** Spraker suggested an interesting explanation for the occurrence of CWD. The deer pens at the Foot Hills Campus were built some 30-40 years ago by a Dr. Bob Davis. At or abut that time, allegedly, some scrapie work was conducted at this site. When deer were introduced to the pens they occupied ground that had previously been occupied by sheep.
IN CONFIDENCE, REPORT OF AN UNCONVENTIONAL SLOW VIRUS DISEASE IN ANIMALS IN THE USA 1989
The occurrence of CWD must be viewed against the contest of the locations in which it occurred. It was an incidental and unwelcome complication of the respective wildlife research programmes. Despite its subsequent recognition as a new disease of cervids, therefore justifying direct investigation, no specific research funding was forthcoming. The USDA viewed it as a wildlife problem and consequently not their province!” page 26.
***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.
***> ”Our data suggest that the phenotype of CWD in sheep is indistinguishable from some strains of scrapie in sheep. Given our results, current detection techniques would be unlikely to distinguish CWD in sheep from scrapie in sheep if cross-species transmission occurred naturally.” https://pubmed.ncbi.nlm.nih.gov/34047228/
Additional studies in WTD established a minimum oral CWD infectious dose equivalent to 100–300 ng CWD-positive brain tissue (10)…
We report that oral exposure to as little as 300 nanograms (ng) of CWD-positive brain or to saliva containing seeding activity equivalent to 300 ng of CWD-positive brain, were sufficient to transmit CWD disease.
***> CWD TSE cervid, oral dose
“We report that oral exposure to as little as 300 nanograms (ng) of CWD-positive brain or to saliva containing seeding activity equivalent to 300 ng of CWD-positive brain, were sufficient to transmit CWD disease.”
PLoS One. 2020 Aug 20;15(8):e0237410. doi: 10.1371/journal.pone.0237410. eCollection 2020.
Very low oral exposure to prions of brain or saliva origin can transmit chronic wasting disease
Nathaniel D Denkers 1 , Clare E Hoover 2 , Kristen A Davenport 3 , Davin M Henderson 1 , Erin E McNulty 1 , Amy V Nalls 1 , Candace K Mathiason 1 , Edward A Hoover 1
PMID: 32817706 PMCID: PMC7446902 DOI: 10.1371/journal.pone.0237410
Abstract
The minimum infectious dose required to induce CWD infection in cervids remains unknown, as does whether peripherally shed prions and/or multiple low dose exposures are important factors in CWD transmission. With the goal of better understand CWD infection in nature, we studied oral exposures of deer to very low doses of CWD prions and also examined whether the frequency of exposure or prion source may influence infection and pathogenesis. We orally inoculated white-tailed deer with either single or multiple divided doses of prions of brain or saliva origin and monitored infection by serial longitudinal tissue biopsies spanning over two years. We report that oral exposure to as little as 300 nanograms (ng) of CWD-positive brain or to saliva containing seeding activity equivalent to 300 ng of CWD-positive brain, were sufficient to transmit CWD disease. This was true whether the inoculum was administered as a single bolus or divided as three weekly 100 ng exposures. However, when the 300 ng total dose was apportioned as 10, 30 ng doses delivered over 12 weeks, no infection occurred. While low-dose exposures to prions of brain or saliva origin prolonged the time from inoculation to first detection of infection, once infection was established, we observed no differences in disease pathogenesis. These studies suggest that the CWD minimum infectious dose approximates 100 to 300 ng CWD-positive brain (or saliva equivalent), and that CWD infection appears to conform more with a threshold than a cumulative dose dynamic.
Snip…
Discussion
As CWD expands across North America and Scandinavia, how this disease is transmitted so efficiently remains unclear, given the low concentrations of prions shed in secretions and excretions [13, 14]. The present studies demonstrated that a single oral exposure to as little as 300nmg of CWD-positive brain or equivalent saliva can initiate infection in 100% of exposed white-tailed deer. However, distributing this dose as 10, 30 ng exposures failed to induce infection. Overall, these results suggest that the minimum oral infectious exposure approaches 100 to 300 ng of CWD-positive brain equivalent. These dynamics also invite speculation as to whether potential infection co-factors, such as particle binding [46, 47] or compromises in mucosal integrity may influence infection susceptibility, as suggested from two studies in rodent models [48, 49].
Prion 2023 Experimental Oronasal Inoculation of the Chronic Wasting Disease Agent into White Tailed Deer
Author list: Sarah Zurbuchena,b , S. Jo Moorea,b , Jifeng Biana , Eric D. Cassmanna , and Justin J. Greenleea . a. Virus and Prion Research Unit, National Animal Disease Center, ARS, United States Department of Agriculture, Ames, IA, US b. Oak Ridge Institute for Science and Education (ORISE), U.S. Department of Energy, Oak Ridge, TN, United States
Aims: The purpose of this experiment was to determine whether white-tailed deer (WTD) are susceptible to inoculation of chronic wasting disease (CWD) via oronasal exposure.
Materials and methods: Six male, neutered WTD were oronasally inoculated with brainstem material (10% w/v) from a CWD-positive wild-type WTD. The genotypes of five inoculated deer were Q95/G96 (wild-type). One inoculated deer was homozygous S at codon 96 (96SS). Cervidized (Tg12; M132 elk PrP) mice were inoculated with 1% w/v brainstem homogenate from either a 96GG WTD (n=10) or the 96SS WTD (n=10).
Results: All deer developed characteristic clinical signs of CWD including weight loss, regurgitation, and ataxia. The 96SS individual had a prolonged disease course and incubation period compared to the other deer. Western blots of the brainstem on all deer yielded similar molecular profiles. All deer had widespread lymphoid distribution of PrPCWD and neuropathologic lesions associated with transmissible spongiform encephalopathies. Both groups of mice had a 100% attack rate and developed clinical signs, including loss of body condition, ataxia, and loss of righting reflex. Mice inoculated with material from the 96SS deer had a significantly shorter incubation period than mice inoculated with material from 96GG deer (Welch two sample T-test, P<0.05). Serial dilutions of each inocula suggests that differences in incubation period were not due to a greater concentration of PrPCWD in the 96SS inoculum. Molecular profiles from western blot of brain homogenates from mice appeared similar regardless of inoculum and appear similar to those of deer used for inoculum.
Conclusions: This study characterizes the lesions and clinical course of CWD in WTD inoculated in a similar manner to natural conditions. It supports previous findings that 96SS deer have a prolonged disease course. Further, it describes a first pass of inoculum from a 96SS deer in cervidized mice which shortened the incubation period.
Funded by: This research was funded in its entirety by congressionally appropriated funds to the United States Department of Agriculture, Agricultural Research Service. The funders of the work did not influence study design, data collection, analysis, decision to publish, or preparation of the manuscript.
Acknowledgement: We thank Ami Frank and Kevin Hassall for their technical contributions to this project.
=====end
PRION 2023 CONTINUED;
https://prion2023.org/wp-content/uploads/2023/10/Meeting-book-final-version2.pdf
USA FDA PART 589 SUBSTANCES PROHIBITED FROM USE IN ANIMAL FOOD OR FEED, CWD, Scrapie, BSE, Oh My, 2026
***> ENVIRONMENTAL FACTORS FROM CHRONIC WASTING DISEASE CWD TSE Prion
***> CWD TSE PrP Environmental Factors <***
DEFRA
In summary, in endemic areas, there is a medium probability that the soil and surrounding environment is contaminated with CWD prions and in a bioavailable form. In rural areas where CWD has not been reported and deer are present, there is a greater than negligible risk the soil is contaminated with CWD prion.
snip…
In summary, given the volume of tourists, hunters and servicemen moving between GB and North America, the probability of at least one person travelling to/from a CWD affected area and, in doing so, contaminating their clothing, footwear and/or equipment prior to arriving in GB is greater than negligible... For deer hunters, specifically, the risk is likely to be greater given the increased contact with deer and their environment. However, there is significant uncertainty associated with these estimates.
Friday, December 14, 2012
DEFRA U.K. What is the risk of Chronic Wasting Disease CWD being introduced into Great Britain? A Qualitative Risk Assessment October 2012
Title: Horizontal transmission of chronic wasting disease in reindeer
Submitted to: Emerging Infectious Diseases Publication Type: Peer Reviewed Journal Publication Acceptance Date: 8/29/2016 Publication Date: 12/1/2016
Interpretive Summary: Chronic wasting disease (CWD) is a fatal neurodegenerative disease that occurs in farmed and wild cervids (deer and elk) of North America and was recently diagnosed in a single free-ranging reindeer (Rangifer tarandus tarandus) in Norway. CWD is a transmissible spongiform encephalopathy (TSE) that is caused by infectious proteins called prions that are resistant to various methods of decontamination and environmental degradation. Little is known about the susceptibility of or potential for transmission amongst reindeer. In this experiment, we tested the susceptibility of reindeer to CWD from various sources (elk, mule deer, or white-tailed deer) after intracranial inoculation and tested the potential for infected reindeer to transmit to non-inoculated animals by co-housing or housing in adjacent pens. Reindeer were susceptible to CWD from elk, mule deer, or white-tailed deer sources after experimental inoculation. Most importantly, non-inoculated reindeer that were co-housed with infected reindeer or housed in pens adjacent to infected reindeer but without the potential for nose-to-nose contact also developed evidence of CWD infection. This is a major new finding that may have a great impact on the recently diagnosed case of CWD in the only remaining free-ranging reindeer population in Europe as our findings imply that horizontal transmission to other reindeer within that herd has already occurred. Further, this information will help regulatory and wildlife officials developing plans to reduce or eliminate CWD and cervid farmers that want to ensure that their herd remains CWD-free, but were previously unsure of the potential for reindeer to transmit CWD.
Chronic wasting disease (CWD) prion detection in environmental and biological samples from a taxidermy site and nursing facility, and instruments used in surveillance activities
Available online 9 April 2025
Highlights
• CWD prions were identified in a taxidermy and deer nursing facility.
• Contaminated samples included waters, soils, dermestid beetles, domestic flies and a dumpster.
• Surgical instruments used to collect deer samples can get contaminated with CWD prions.
• Some of the infectious particles are readily released from surgical instruments when washed.
• Our results suggest that taxidermy practices actively contribute in the spreading of CWD.
Snip…
In summary, the information provided in this report demonstrate how anthropogenic activities, specifically taxidermy practices, animal processing, and rehabilitation of CWD susceptible species, may facilitate CWD transmission through the environmental dissemination of CWD prions. This study, along with future research efforts characterizing the overall level of infectivity, provides relevant information on managing CWD and to control its rapid geographic expansion. …
Chronic wasting disease detection in environmental and biological samples from a taxidermy site
Results: The PMCA analysis demonstrated CWD seeding activity in some of the components of this facility, including insects involved in head processing, soils, and a trash dumpster.
Conclusions: Different areas of this property were used for various taxidermy procedures. We were able to detect the presence of prions in
i) soils that were in contact with the heads of dead animals, ii) insects involved in the cleaning of skulls, and iii) an empty dumpster where animal carcasses were previously placed.
This is the first report demonstrating that swabbing is a helpful method to screen for prion infectivity on surfaces potentially contaminated with CWD. These findings are relevant as this swabbing and amplification strategy may be used to evaluate the disease status of other free-ranging and captive settings where there is a concern for CWD transmissions, such as at feeders and water troughs with CWD-exposed properties. This approach could have substantial implications for free-ranging cervid surveillance as well as in epidemiological investigations of CWD.
Prion 2022 Conference abstracts: pushing the boundaries
Artificial mineral sites that pre-date endemic chronic wasting disease become prion hotspots
The Ames Research and Educational Center property, centrally located within the CWD zone of southwest Tennessee, contains 49 historical mineral supplementation sites that were decommissioned in 2012. Here, we demonstrate that 32 of the 49 (65%) mineral sites within Ames established prior to the regional CWD outbreak, serve as foci of environmental PrPCWD contamination. Detection of PrPCWD in soils from these artificial mineral sites was dependent on site-specific management efforts. Soil physical properties were very similar across sites and no correlation between PrPCWD detection and soil physical properties was found. The detection of PrPCWD in soils at attractant sites within an endemic CWD zone significantly advances our understanding of environmental PrPCWD accumulation dynamics, providing valuable information for advancing adaptive CWD management approaches.
Shedding of Chronic Wasting Disease Prions in Multiple Excreta Throughout Disease Course in White-tailed Deer
Conclusions: These studies demonstrate: (a) CWD prion excretion occurs throughout infection; (2) PRNP genotype (GG≫GS/NT) influences the excreta shedding; and (3) detection sensitivity in excreta can vary with different RT-QuIC protocols. These results provide a more complete perspective of prion shedding in deer during the course of CWD infection.
Prion 2022 Conference abstracts: pushing the boundaries
"Additionally, we have determined that prion seeding activity is retained for at least fifteen years at a contaminated site following attempted remediation."
***> 15 YEARS!!!
Detection of prions in soils contaminated by multiple routes
Results: We are able to detect prion seeding activity at multiple types of environmental hotspots, including carcass sites, contaminated captive facilities, and scrapes (i.e. urine and saliva). Differences in relative prion concentration vary depending on the nature and source of the contamination. Additionally, we have determined that prion seeding activity is retained for at least fifteen years at a contaminated site following attempted remediation.
Conclusions: Detection of prions in the environment is of the utmost importance for controlling chronic wasting disease spread. Here, we have demonstrated a viable method for detection of prions in complex environmental matrices. However, it is quite likely that this method underestimates the total infectious prion load in a contaminated sample, due to incomplete recovery of infectious prions. Further refinements are necessary for accurate quantification of prions in such samples, and to account for the intrinsic heterogeneities found in the broader environment.
Funded by: Wisconsin Department of Natural Resources
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
***> Infectious agent of sheep scrapie may persist in the environment for at least 16 years
***> Nine of these recurrences occurred 14–21 years after culling, apparently as the result of environmental contamination, but outside entry could not always be absolutely excluded.
JOURNAL OF GENERAL VIROLOGY Volume 87, Issue 12
Infectious agent of sheep scrapie may persist in the environment for at least 16 years Free
Rapid recontamination of a farm building occurs after attempted prion removal
First published: 19 January 2019 https://doi.org/10.1136/vr.105054
The data illustrates the difficulty in decontaminating farm buildings from scrapie, and demonstrates the likely contribution of farm dust to the recontamination of these environments to levels that are capable of causing disease. snip...
This study clearly demonstrates the difficulty in removing scrapie infectivity from the farm environment. Practical and effective prion decontamination methods are still urgently required for decontamination of scrapie infectivity from farms that have had cases of scrapie and this is particularly relevant for scrapie positive goatherds, which currently have limited genetic resistance to scrapie within commercial breeds.24 This is very likely to have parallels with control efforts for CWD in cervids.
***>This is very likely to have parallels with control efforts for CWD in cervids.
I remember what “deep throat” told me about Scrapie back around 2001, during early days of my BSE investigation, after my Mom died from hvCJD, I never forgot, and it seems it’s come to pass;
***> Confidential!!!!
***> As early as 1992-3 there had been long studies conducted on small pastures containing scrapie infected sheep at the sheep research station associated with the Neuropathogenesis Unit in Edinburgh, Scotland. Whether these are documented...I don't know. But personal recounts both heard and recorded in a daily journal indicate that leaving the pastures free and replacing the topsoil completely at least 2 feet of thickness each year for SEVEN years....and then when very clean (proven scrapie free) sheep were placed on these small pastures.... the new sheep also broke out with scrapie and passed it to offspring. I am not sure that TSE contaminated ground could ever be free of the agent!! A very frightening revelation!!!
---end personal email---end...tss
and so it seems…
Chronic Wasting Disease CWD TSE Prion
THE CWD TSE Prion aka mad cow type disease is not your normal pathogen.
The TSE prion disease survives ashing to 600 degrees celsius, that’s around 1112 degrees farenheit.
You cannot cook the TSE prion disease out of meat. In fact new data now shows that exposure to high temperatures used to cook the meat increased the availability of prions for in vitro amplification.
you can take the ash and mix it with saline and inject that ash into a mouse, and the mouse will go down with TSE.
Prion Infected Meat-and-Bone Meal Is Still Infectious after Biodiesel Production as well.
the TSE prion agent also survives Simulated Wastewater Treatment Processes.
IN fact, you should also know that the TSE Prion agent will survive in the environment for years, if not decades.
you can bury it and it will not go away.
The TSE agent is capable of infected your water table i.e. Detection of protease-resistant cervid prion protein in water from a CWD-endemic area.
it’s not your ordinary pathogen you can just cook it out and be done
New studies on the heat resistance of hamster-adapted scrapie agent: Threshold survival after ashing at 600°C suggests an inorganic template of replication
Prion Infected Meat-and-Bone Meal Is Still Infectious after Biodiesel Production
Rapid assessment of bovine spongiform encephalopathy prion inactivation by heat treatment in yellow grease produced in the industrial manufacturing process of meat and bone meals
THURSDAY, FEBRUARY 28, 2019
BSE infectivity survives burial for five years with only limited spread
Chronic wasting disease prions on deer feeders and wildlife visitation to deer feeding areas
First published: 10 February 2025
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Finally, we swabbed 19 feeders in 2 areas where CWD was newly detected, finding prion contamination on swabs from 4 feeders. We show that deer feeders in free-ranging populations with high CWD prevalence become contaminated with CWD prions quickly, becoming a potential site of exposure of deer to CWD prions. Our results also demonstrate the ability to find evidence of prion contamination on deer feeders, even in areas where CWD is newly detected.
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We found that supplemental feeding increased the risk of exposure to CWD prions due to contamination of feeders, increased deer visitation, and increased deer-to-deer contact.
The 12-fold increase in deer visitation to feeders compared to mast trees and 2-fold increase compared to food plots demonstrates increased risk for direct disease spread.
Chronic Wasting Disease in Texas A Real Disease with Proven Impacts
Produced by a coalition of concerned hunters, landowners, & conservationists (last update 1/2025)
Aug 18, 2021
Oh, Deer
Heading Off a Wildlife Epidemic
CWD poses a significant threat to the future of hunting in Texas. Deer population declines of 45 and 50 percent have been documented in Colorado and Wyoming. A broad infection of Texas deer populations resulting in similar population impacts would inflict severe economic damage to rural communities and could negatively impact land markets. Specifically, those landowners seeking to establish a thriving herd of deer could avoid buying in areas with confirmed CWD infections. As they do with anthrax-susceptible properties, land brokers may find it advisable to inquire about the status of CWD infections on properties that they present for sale. Prospective buyers should also investigate the status of the wildlife on prospective properties. In addition, existing landowners should monitor developments as TPWD crafts management strategies to identify and contain this deadly disease.
Dr. Gilliland (c-gilliland@tamu.edu) is a research economist with the Texas Real Estate Research Center at Texas A&M University.
***> TEXAS TRUCKING CWD TSE PRION
“CWD spreads among wild populations at a relatively slow rate, limited by the natural home range and dispersed nature of wild animals.”
***> NOW HOLD YOUR HORSES, Chronic Wasting Disease CWD of Cervid can spread rather swiftly, traveling around 50 MPH, from the back of truck and trailer, and Here in Texas, we call it ‘Trucking CWD’…
Preventive Veterinary Medicine Volume 234, January 2025, 106385
Use of biosecurity practices to prevent chronic wasting disease in Minnesota cervid herds
Vehicles or trailers that entered the farm were used to transport other live cervids, cervid carcasses, or cervid body parts in past 3 years in 64.3 % (95 % CI 46.3–82.3) of larger elk/reindeer herds compared to 13.6 % (95 % CI 4.7–22.4) of smaller deer herds.
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Identifying the exact pathway of initial CWD transmission to cervid herds is often not possible, in part due to many potential pathways of transmission for the infection, including both direct and indirect contact with infected farmed or wild cervids (Kincheloe et al., 2021). That study identified that transmissions from infected farmed cervids may occur from direct contact with the movement of cervids from one herd to another and from indirect contact with the sharing of equipment, vehicles, clothing, reproductive equipment, and potentially through semen or embryos.
“Chronic Wasting Disease (CWD) is a fatal neurological disease and can devastate deer populations by silently spreading through direct animal contact and contaminated environments. Without close monitoring, illegal movement of captive deer increases the risk of introducing CWD to areas it is not known to exist, potentially leading to widespread outbreaks which will impact more than just the health of Texas deer.”
Texas Chronic Wasting Disease CWD TSE Prion Dashboard Update August 2025
SEE NEW DASHBOARD FOR CWD POSITIVES!
Texas CWD total by calendar years
Counties where CWD Exposed Deer were Released
Number of CWD Exposed Deer Released by County
CWD Status Captive Herds
THURSDAY, MARCH 26, 2026
Texas Chronic Wasting Disease CWD TSE Prion Progression 2012 to 2026, Positives to date 1282 confirmed
THURSDAY, AUGUST 14, 2025
Texas Game Wardens Near Conclusion of ‘Ghost Deer’ Case with 24 Suspects, 1,400 Charges Filed Statewide
WEDNESDAY, MAY 14, 2025
Texas CWD TSE Prion Cases Rises to 1099 Confirmed Cases To Date
TAHC 425th Commission Meeting CWD 1:45:00
* See CWD speakers expressing their concerns with changed regulations…
2:00 hr mark
TEXAS ANIMAL HEALTH COMMISSION 423rd Commission Meeting CWD Update February 25, 2025
TEXAS ANIMAL HEALTH COMMISSION AGENCY STRATEGIC PLAN FISCAL YEARS 2025 - 2029 CWD TSE Prion
Texas Chronic Wasting Disease CWD TSE Prion Progression 2012 to 2026, Positives to date 1282 confirmed
So, this is what we leave our children and grandchildren?
***> CWD TSE Prion Zoonotic Zoonosis Humans, What if? <***
CDC CWD TSE Prion Update 2025
KEY POINTS
Chronic wasting disease affects deer, elk and similar animals in the United States and a few other countries.
The disease hasn't been shown to infect people.
However, it might be a risk to people if they have contact with or eat meat from animals infected with CWD.
https://www.cdc.gov/chronic-wasting/about/index.html
Prions in Muscles of Cervids with Chronic Wasting Disease, Norway
Volume 31, Number 2—February 2025
Research
Prions in Muscles of Cervids with Chronic Wasting Disease, Norway
Snip…
In summary, the results of our study indicate that prions are widely distributed in peripheral and edible tissues of cervids in Norway, including muscles. This finding highlights the risk of human exposure to small amounts of prions through handling and consuming infected cervids.
Appendix
Volume 31, Number 2—February 2025
Dispatch
Detection of Chronic Wasting Disease Prions in Raw, Processed, and Cooked Elk Meat, Texas, USA
Snip…
Of note, our data show that exposure to high temperatures used to cook the meat increased the availability of prions for in vitro amplification. Considering the potential implications in food safety and public health, we believe that the findings described in this study warrant further research. Our results suggest that although the elk meat used in this study resisted different manipulations involved in subsequent consumption by humans, their zoonotic potential was limited. Nevertheless, even though no cases of CWD transmission to human have been reported, the potential for human infection is still unclear and continued monitoring for zoonotic potential is warranted.
Detection of chronic wasting disease prions in processed meats
Results: Our results show positive prion detection in all the samples analyzed using deer and elk substrates. Surprisingly, cooked meats displayed increased seeding activities. This data suggests that CWD-prions are available to people even after meats are processed and cooked.
Conclusions: These results suggest CWD prions are accessible to humans through meats, even after processing and cooking. Considering the fact that these samples were collected from already processed specimens, the availability of CWD prions to humans is probably underestimated.
"Our results show positive prion detection in all the samples analyzed using deer and elk substrates. Surprisingly, cooked meats displayed increased seeding activities."
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
DETECTION OF CHRONIC WASTING DISEASE PRIONS IN PROCESSED MEATS.
In this study, we analyzed different processed meats derived from a pre-clinical, CWD-positive free-ranging elk. Products tested included filets, sausages, boneless steaks, burgers, ham steaks, seasoned chili meats, and spiced meats. CWD-prion presence in these products were assessed by PMCA using deer and elk substrates. Our results show positive prion detection in all products. To confirm the resilience of CWD-prions to traditional cooking methods, we grilled and boiled the meat products and evaluated them for any remnant PMCA seeding activity. Results confirmed the presence of CWD-prions in these meat products suggesting that infectious particles may still be available to people even after cooking. Our results strongly suggest ongoing human exposure to CWD-prions and raise significant concerns of zoonotic transmission through ingestion of CWD contaminated meat products.
Products tested included filets, sausages, boneless steaks, burgers, ham steaks, seasoned chili meats, and spiced meats.
CWD-prion presence in these products were assessed by PMCA using deer and elk substrates.
Our results show positive prion detection in all products.
Results confirmed the presence of CWD-prions in these meat products suggesting that infectious particles may still be available to people even after cooking.
Our results strongly suggest ongoing human exposure to CWD-prions and raise significant concerns of zoonotic transmission through ingestion of CWD contaminated meat products.
Transmission of prion infectivity from CWD-infected macaque tissues to rodent models demonstrates the zoonotic potential of chronic wasting disease.
Further passage to cervidized mice revealed transmission with a 100% attack rate.
Our findings demonstrate that macaques, considered the best model for the zoonotic potential of prions, were infected upon CWD challenge, including the oral one.
The disease manifested as atypical in macaques and initial transgenic mouse transmissions, but with infectivity present at all times, as unveiled in the bank vole model with an unusual tissue tropism.
Epidemiologic surveillance of prion disease among cervid hunters and people likely to have consumed venison contaminated with chronic wasting disease
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Fortuitous generation of a zoonotic cervid prion strain
Aims: Whether CWD prions can infect humans remains unclear despite the very substantial scale and long history of human exposure of CWD in many states or provinces of USA and Canada. Multiple in vitro conversion experiments and in vivo animal studies indicate that the CWD-to-human transmission barrier is not unbreakable. A major long-term public health concern on CWD zoonosis is the emergence of highly zoonotic CWD strains. We aim to address the question of whether highly zoonotic CWD strains are possible.
Materials and Methods: We inoculated several sCJD brain samples into cervidized transgenic mice (Tg12), which were intended as negative controls for bioassays of brain tissues from sCJD cases who had potentially been exposed to CWD. Some of the Tg12mice became infected and their brain tissues were further examined by Western blot as well as serial passages in humanized or cervidized mice.
Results: Passage of sCJDMM1 in transgenic mice expressing elk PrP (Tg12) resulted in a “cervidized” CJD strain that we termed CJDElkPrP. We observed 100% transmission of the original CJDElkPrP in transgenic mice expressing human PrP. We passaged CJDElkPrP two more times in the Tg12mice. We found that such second and third passage CJDElkPrP prions retained 100% transmission rate in the humanized mice, despite that the natural elk CWD isolates and CJDElkPrP share the same elk PrP sequence. In contrast, we and others found zero or poor transmission of natural elk CWD isolates in humanized mice.
Conclusions: Our data indicate that highly zoonotic cervid prion strains are not only possible but also can retain zoonotic potential after serial passages in cervids, suggesting a very significant and serious long-term risk of CWD zoonosis given that the broad and continuing spread of CWD prions will provide fertile grounds for the emergence of zoonotic CWD strains over time.
https://prion2023.org/wp-content/uploads/2023/10/Meeting-book-final-version2.pdf
Transmission of cervid prions to humanized mice demonstrates the zoonotic potential of CWD
Samia Hannaoui1 · Irina Zemlyankina1 · Sheng Chun Chang1 · Maria Immaculata Arifn1 · Vincent Béringue2 · Debbie McKenzie3 · Hermann M. Schatzl1 · Sabine Gilch1
Received: 24 May 2022 / Revised: 5 August 2022 / Accepted: 7 August 2022
© The Author(s) 2022
Abstract
Prions cause infectious and fatal neurodegenerative diseases in mammals. Chronic wasting disease (CWD), a prion disease of cervids, spreads efficiently among wild and farmed animals. Potential transmission to humans of CWD is a growing concern due to its increasing prevalence. Here, we provide evidence for a zoonotic potential of CWD prions, and its probable signature using mice expressing human prion protein (PrP) as an infection model. Inoculation of these mice with deer CWD isolates resulted in atypical clinical manifestation with prion seeding activity and efficient transmissible infectivity in the brain and, remarkably, in feces, but without classical neuropathological or Western blot appearances of prion diseases. Intriguingly, the protease-resistant PrP in the brain resembled that found in a familial human prion disease and was transmissible upon second passage. Our results suggest that CWD might infect humans, although the transmission barrier is likely higher compared to zoonotic transmission of cattle prions. Notably, our data suggest a different clinical presentation, prion signature, and tissue tropism, which causes challenges for detection by current diagnostic assays. Furthermore, the presence of infectious prions in feces is concerning because if this occurs in humans, it is a source for human-to-human transmission. These findings have strong implications for public health and CWD management.
Keywords Chronic wasting disease · CWD · Zoonotic potential · Prion strains · Zoonotic prions
HIGHLIGHTS OF THIS STUDY
================================
Our results suggest that CWD might infect humans, although the transmission barrier is likely higher compared to zoonotic transmission of cattle prions. Notably, our data suggest a different clinical presentation, prion signature, and tissue tropism, which causes challenges for detection by current diagnostic assays. Furthermore, the presence of infectious prions in feces is concerning because if this occurs in humans, it is a source for human-to-human transmission. These findings have strong implications for public health and CWD management.
In this study, we evaluated the zoonotic potential of CWD using a transgenic mouse model overexpressing human M129-PrPC (tg650 [12]). We inoculated tg650mice intracerebrally with two deer CWD isolates, Wisc-1 and 116AG [22, 23, 27, 29]. We demonstrate that this transgenic line was susceptible to infection with CWD prions and displayed a distinct leading clinical sign, an atypical PrPSc signature and unusual fecal shedding of infectious prions. Importantly, these prions generated by the human PrP transgenic mice were transmissible upon passage. Our results are the first evidence of a zoonotic risk of CWD when using one of the most common CWD strains, Wisc-1/CWD1 for infection. We demonstrated in a human transgenic mouse model that the species barrier for transmission of CWD to humans is not absolute. The fact that its signature was not typical raises the questions whether CWD would manifest in humans as a subclinical infection, whether it would arise through direct or indirect transmission including an intermediate host, or a silent to uncovered human-to-human transmission, and whether current detection techniques will be suffcient to unveil its presence.
Our findings strongly suggest that CWD should be regarded as an actual public health risk. Here, we use humanized mice to show that CWD prions can cross the species barrier to humans, and remarkably, infectious prions can be excreted in feces.
Our results indicate that if CWD crosses the species-barrier to humans, it is unlikely to resemble the most common forms of human prion diseases with respect to clinical signs, tissue tropism and PrPSc signature. For instance, PrPSc in variable protease-sensitive prionopathy (VPSPr), a sporadic form of human prion disease, and in the genetic form Gerstmann-Sträussler-Scheinker syndrome (GSS) is defined by an atypical PK-resistant PrPSc fragment that is non-glycosylated and truncated at both C- and N-termini, with a molecular weight between 6 and 8 kDa [24, 44–46]. These biochemical features are unique and distinctive from PrPSc (PrP27-30) found in most other human or animal prion disease. The atypical PrPSc signature detected in brain homogenate of tg650 mice #321 (1st passage) and #3063 (2nd passage), and the 7–8 kDa fragment (Figs. 2, 4) are very similar to that of GSS, both in terms of migration profile and the N-terminal cleavage site.
CWD in humans might remain subclinical but with PrPSc deposits in the brain with an unusual morphology that does not resemble the patterns usually seen in different prion diseases (e.g., mouse #328; Fig. 3), clinical with untraceable abnormal PrP (e.g., mouse #327) but still transmissible and uncovered upon subsequent passage (e.g., mouse #3063; Fig. 4), or prions have other reservoirs than the usual ones, hence the presence of infectivity in feces (e.g., mouse #327) suggesting a potential for human-to-human transmission and a real iatrogenic risk that might be unrecognizable.
“suggesting a potential for human-to-human transmission and a real iatrogenic risk that might be unrecognizable.”
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Supplementary Information The online version contains supplementary material available at
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Transmission of Cervid Prions to Humanized Mice Demonstrates the Zoonotic Potential of CWD
Samia Hannaouia, Irina Zemlyankinaa, Sheng Chun Changa, Maria Immaculata Arifina, Vincent Béringueb, Debbie McKenziec, Hermann M. Schatzla, and Sabine Gilcha
Results: Here, we provide the strongest evidence supporting the zoonotic potential of CWD prions, and their possible phenotype in humans. Inoculation of mice expressing human PrPCwith deer CWD isolates (strains Wisc-1 and 116AG) resulted in atypical clinical manifestations in > 75% of the mice, with myoclonus as leading clinical sign. Most of tg650brain homogenates were positive for seeding activity in RT-QuIC. Clinical disease and presentation was transmissible to tg650mice and bank voles. Intriguingly, protease-resistant PrP in the brain of tg650 mice resembled that found in a familial human prion disease and was transmissible upon passage. Abnormal PrP aggregates upon infection with Wisc-1 were detectable in thalamus, hypothalamus, and midbrain/pons regions.
Unprecedented in human prion disease, feces of CWD-inoculated tg650 mice harbored prion seeding activity and infectious prions, as shown by inoculation of bank voles and tg650 with fecal homogenates.
Conclusions: This is the first evidence that CWD can infect humans and cause disease with a distinctive clinical presentation, signature, and tropism, which might be transmissible between humans while current diagnostic assays might fail to detect it. These findings have major implications for public health and CWD-management.
Macaque tissues to rodent models demonstrates the zoonotic potential of chronic wasting disease.
Samia Hannaoui1,2, Ginny Cheng1,2, Wiebke Wemheuer3, Walter Schulz-Schaeffer3, Sabine Gilch1,2, Hermann Schatzl1,2 1University of Calgary, Calgary, Canada. 2Calgary Prion Research Unit, Calgary, Canada. 3Institute of Neuropathology, Medical Faculty, Saarland University, Homburg/Saar, Germany
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***> Further passage to cervidized mice revealed transmission with a 100% attack rate.
***> Our findings demonstrate that macaques, considered the best model for the zoonotic potential of prions, were infected upon CWD challenge, including the oral one.
****> The disease manifested as atypical in macaques and initial transgenic mouse transmissions, but with infectivity present at all times, as unveiled in the bank vole model with an unusual tissue tropism.
***> Epidemiologic surveillance of prion disease among cervid hunters and people likely to have consumed venison contaminated with chronic wasting disease
=====
18. Zoonotic potential of moose-derived chronic wasting disease prions after adaptation in intermediate species
Tomás Barrioa, Jean-Yves Doueta, Alvina Huora, Séverine Lugana, Naïma Arona, Hervé Cassarda, Sylvie L. Benestadb, Juan Carlos Espinosac, Juan María Torresc, Olivier Andréolettia
aUnité Mixte de Recherche de l’Institut National de Recherche pour l’Agriculture, l’Alimentation et l’Environnement 1225 Interactions Hôtes-Agents Pathogènes, École Nationale Vétérinaire de Toulouse, 31076 Toulouse, France; bNorwegian Veterinary Institute, P.O. Box 64, NO-1431 Ås, Norway; cCentro de Investigación en Sanidad Animal (CISA-INIA), 28130, Valdeolmos, Madrid, Spain
Aims: Chronic wasting disease (CWD) is an emerging prion disease in Europe. To date, cases have been reported in three Nordic countries and in several species, including reindeer (Rangifer tarandus), moose (Alces alces) and red deer (Cervus elaphus). Cumulating data suggest that the prion strains responsible for the European cases are distinct from those circulating in North America. The biological properties of CWD prions are still poorly documented, in particular their spillover and zoonotic capacities. In this study, we aimed at characterizing the interspecies transmission potential of Norwegian moose CWD isolates.
Materials and Methods: For that purpose, we performed experimental transmissions in a panel of transgenic models expressing the PrPC sequence of various species.
Results: On first passage, one moose isolate propagated in the ovine PrPC-expressing model (Tg338). After adaptation in this host, moose CWD prions were able to transmit in mice expressing either bovine or human PrPC with high efficacy.
Conclusions: These results suggest that CWD prions can acquire enhanced zoonotic properties following adaptation in an intermediate species.
Funding
Grant number: AAPG2020 EU-CWD, ICRAD2020 TCWDE, NRC2022 NorCWD
Acknowledgement
“ After adaptation in this host, moose CWD prions were able to transmit in mice expressing either bovine or human PrPC with high efficacy.”
***> CWD HERD DECLINES
Arkansas CWD Deer Study Final 2025
4. Objective 4 and 6 - Infection rates and population modeling
a. In 2024, CWD sample prevalence was 40% across the study area, with higher rates seen in males (65%) than in females (34%).
b. Approximately 50% of males tested positive for CWD by the age of 2.5.
c. White-tailed deer abundance in the study area declined, driven by reduced lifespans and lower lifetime reproduction.
d. If survival does not increase, this population is expected to continue to decline.
Louisiana House of Representative Aug 27, 9:30 AM, HCR-6 CWD
Louisiana House of Representative
Chronic Wasting Disease CWD
(A letter written from a Mississippi farmer who’s farm has been in his family for more than 100 years, and submitted it in this video presentation, 28 minute mark, another wake up call for sure, of what some have been warning for years, about CWD, but sadly will go by the wayside by the conspiracy theorists spreading fake news…terry)
Alston Ross
Marshall County, Mississippi
My family owns a 2,000 acre farm in Marshall County, which is in North Mississippi. CWD has plagued my farm since 2018 and has become progressively worse over time. We no longer have mature deer over the age of 3 years old on our property. Every buck harvested on our land has tested positive this year. The owners of our neighboring properties have continued to feed deer and ignore MDWFP regulations, which has exacerbated the spread of the disease throughout our area. This farm has been in my family for over 100 years, and due to the rapid spread of CWD, we are concerned about the future of our deer herd and the value of our hunting land…end
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Arkansas
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40:35 “…and conversely, I was co-Principle Investigator in NW Arkansas, where prevalence is approaching 50 percent.”
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41:00 “Specific to the work in Arkansas, in 2020, the state agency was showing the Prevalence at 30 percent in the Northwest part of the State, so flip a coin, so, 1 out of every 3 deer had the disease. We started that research in 2020, and now, the prevalence rate is now exceeding 40% in both sexes, and 50% in males.”
43:00 “what we’re seeing Arkansas now is, that population is declining about 11% a year.”
Snip…see full video presentation;
FOR IMMEDIATE RELEASE: 2025-01-22 Contact: DNR Office of Communications DNRPress@wisconsin.gov
DNR ANNOUNCES PRIMARY RESULTS OF SOUTHWEST WISCONSIN CWD, DEER AND PREDATOR STUDY A deer fitted with a tracking collar walks through a wooded area during winter. The purpose of this study was to determine how CWD impacts deer populations. Photo credit: Wisconsin DNR MADISON, Wis. – The Wisconsin Department of Natural Resources (DNR) today presented the primary results of the Southwest Wisconsin Chronic Wasting Disease (CWD), Deer and Predator Study to the Natural Resources Board (NRB). A recording of the NRB meeting, including this presentation, is available on the DNR's YouTube channel.
The purpose of this study was to determine how CWD impacts deer populations. This involved estimating deer survival rates and how they were influenced by CWD.
Fieldwork for this project took place in northern Iowa, Dane and Grant counties. This area was selected for study as it is the region where CWD was first detected in Wisconsin in 2002 and has maintained a high CWD prevalence in the years since.
As part of this study, over 1,200 animals (adult deer, fawns, coyotes and bobcats) were captured, 766 GPS collars were deployed on adult deer and 323 radio tracking collars were placed on deer fawns.
Results
Scientists analyzed data from the sample of collared adult white-tailed deer in order to estimate the differences in annual survival (the probability of surviving from one year to the next) between CWD-infected and uninfected deer. Annual survival estimates are listed in the table below.
Annual Survival Probability
Uninfected CWD-Infected Females 83% 41% Males 69% 17% These figures indicate that CWD is substantially reducing the annual survival probability of both male and female white-tailed deer. Reduced female survival lowers the growth rate of the population, and when sufficiently suppressed, may result in population decline.
Specifically, results from this study indicate that when the CWD prevalence rates of females surpasses about 29%, deer populations are expected to begin declining.
Implications
The key takeaways from these results are:
CWD substantially reduces deer survival rates and suppresses population growth. Where CWD prevalence is high, deer populations are likely declining. CWD will eventually impact deer populations elsewhere if it continues to spread and increase in prevalence. If CWD continues to spread and its prevalence continues to increase, populations will likely face further declines. The exact degree of these declines, however, will depend on local harvest and recruitment rates. It is important to note here that researchers do not expect CWD-affected deer herds to become extirpated (completely eliminated in a given area), as deer populations have a strong ability to increase reproduction when deer abundance is lower, due to less competition for food, space and other resources.
The public can learn more about these results by visiting the study’s results webpage.
Looking Forward
It should be noted that the results presented here are the primary findings of the Southwest Wisconsin CWD Deer And Predator Study. Although the scope of this study provides us with a rich dataset from which we can continue to learn about our deer herd and CWD’s impact, there are sure to be more results to come as analysis continues. Additional findings will continue to be released to the public as completed.
To stay informed about these announcements and results from additional analyses on topics like movement, habitat use and predator survival rates, subscribe to the Field Notes Newsletter.
WISCONSIN CWD IS RAVAGING MY FAMILY’S LAND, BUT IT’S NOT TOO LATE FOR YOU
September 9, 2025 By: Paul Annear
My first season deer hunting in Wisconsin was 2001, the same season that produced Wisconsin’s first deer to test positive for chronic wasting disease. CWD has always been at the forefront of deer hunting discussions in my time as a hunter, and I’ve watched the disease slowly spread and worsen. Since 2019, eight of 11 deer I’ve taken on my family’s property in Richland County in Southwest Wisconsin have tested positive for CWD – including the buck in the photo above.
Aside from harvesting otherwise perfectly healthy-looking deer that test positive for CWD, we are now seeing live deer walking around in the awful final stages of this disease. Research has now confirmed what I’ve seen occurring on our hunting land in the last five to six years: CWD is beginning to reduce deer populations in high-prevalence areas like mine.
It didn’t have to reach this point. Hunters in areas with low CWD prevalence can keep infection rates low and deer populations healthy overall by accepting and implementing certain strategies. Some of the strategies I will lay out will challenge you as a hunter to play the “long game,” but there are ways to slow the spread of CWD in areas where it is newly discovered and infection rates are still low.
If you’re rolling your eyes at another guy talking about CWD, I get it, but I urge you to keep reading. Hear my personal story, how it has affected my hunting experiences, and what can happen if hunters ignore CWD.
“Where Are the Deer?”
…snip…see full text;
This CWD Study Could Change Deer Hunting FOREVER | The Check Station October 8, 2025 NW Arkansas
NW Arkansas CWD 11:25 minutes;
50% of all deer positive for CWD.
35% of Does are Positive for CWD.
68% Bucks are Positive for CWD.
Most Bucks NW Arkansas that where Tested, are Positive for CWD.
MEMORANDUM
To: Members of the Colorado Parks and Wildlife Commission
From: Dan Prenzlow, Director
Date: April 22, 2022
Subject: Chronic Wasting Disease Update for Parks and Wildlife Commission Chronic wasting disease, a fatal neurological disease found in deer, elk, and moose, is well established in herds throughout much of Colorado. We have detected CWD in 40 of our 54 deer herds, 17 of 42 elk herds, and 2 of 9 moose herds. Disease prevalence (percent infected) is highest in deer and lowest in moose. This disease is always fatal and animals die from the disease within about 2-2.5 years of infection. CWD infection shortens the lifespan of infected animals. If infection rates become too high, CWD can affect a herd’s ability to sustain itself.
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Montana Chronic Wasting Disease CWD MANAGEMENT Announcements for 2025
HOW COULD CWD IMPACT MONTANA'S DEER AND ELK HERDS? If CWD infects enough animals, it could reduce herd numbers in the long term. Other states have seen deer population declines correlated with CWD prevalences above 20 to 40 percent. In Wyoming, some heavily infected herds of mule deer declined 21 percent per year, and white-tailed deer declined 10 percent per year. Colorado saw a 45 percent decline in mule deer in CWD-positive areas over 20 years...
“Wyoming, We estimated λ= 0.79, indicating an annual population decline of 21% under current CWD prevalence levels.”
Endemic chronic wasting disease causes mule deer population decline in Wyoming
PLoS ONE
By: Melia DeVivo, David R. Edmunds, Matthew J. Kauffman, Brant A. Schumaker, Justin Binfet, Terry J. Kreeger, Bryan J. Richards, Hermann M. Schatzl, and Todd Cornish
Abstract
Chronic wasting disease (CWD) is a fatal transmissible spongiform encephalopathy affecting white-tailed deer (Odocoileus virginianus), mule deer (Odocoileus hemionus), Rocky Mountain elk (Cervus elaphus nelsoni), and moose (Alces alces shirasi) in North America. In southeastern Wyoming average annual CWD prevalence in mule deer exceeds 20% and appears to contribute to regional population declines. We determined the effect of CWD on mule deer demography using age-specific, female-only, CWD transition matrix models to estimate the population growth rate (λ). Mule deer were captured from 2010–2014 in southern Converse County Wyoming, USA. Captured adult (≥ 1.5 years old) deer were tested ante-mortem for CWD using tonsil biopsies and monitored using radio telemetry. Mean annual survival rates of CWD-negative and CWD-positive deer were 0.76 and 0.32, respectively. Pregnancy and fawn recruitment were not observed to be influenced by CWD. We estimated λ= 0.79, indicating an annual population decline of 21% under current CWD prevalence levels. A model derived from the demography of only CWD-negative individuals yielded; λ = 1.00, indicating a stable population if CWD were absent. These findings support CWD as a significant contributor to mule deer population decline. Chronic wasting disease is difficult or impossible to eradicate with current tools, given significant environmental contamination, and at present our best recommendation for control of this disease is to minimize spread to new areas and naïve cervid populations.
PLoS One. 2016 Aug 30;11(8):e0161127. doi: 10.1371/journal.pone.0161127. eCollection 2016.
Chronic Wasting Disease Drives Population Decline of White-Tailed Deer
We show that a chronic disease that becomes endemic in wildlife populations has the potential to be population-limiting and the strong population-level effects of CWD suggest affected populations are not sustainable at high disease prevalence under current harvest levels.
The effectiveness of harvest for limiting wildlife disease: Insights from 20 years of chronic wasting disease in Wyoming
First published: 21 January 2025
https://doi.org/10.1002/eap.3089
How does CWD impact deer, elk, and moose populations?
Recent research in Wyoming has demonstrated declines in both mule and white-tailed deer populations in deer hunt area 65 due to CWD (see below for citations). These declines are in the core endemic area where prevalence is highest. In areas with lower prevalence, effects of CWD are poorly understood but are considered additive along with other factors that can negatively affect deer populations in Wyoming (i.e. habitat loss, predation, other diseases). The distribution and prevalence of CWD in Wyoming elk is less than that of deer. Currently there are no documented direct population impacts in Wyoming elk from CWD; however, research from Rocky Mountain National Park suggests that CWD could impact elk populations at higher prevalence (13%). While CWD has been found in free ranging moose, there have been few detections, and there is no evidence that CWD is currently having an impact on moose populations.
Friday, December 14, 2012
DEFRA U.K. What is the risk of Chronic Wasting Disease CWD being introduced into Great Britain? A Qualitative Risk Assessment October 2012
snip.....
36% in 2007 (Almberg et al., 2011). In such areas, population declines of deer of up to 30 to 50% have been observed (Almberg et al., 2011). In areas of Colorado, the prevalence can be as high as 30% (EFSA, 2011).
snip.....
The rate of transmission of CWD has been reported to be as high as 30% and can approach 100% among captive animals in endemic areas (Safar et al., 2008). snip.....
Chronic Wasting Disease in Texas A Real Disease with Proven Impacts
Produced by a coalition of concerned hunters, landowners, & conservationists (last update 1/2025)
Aug 18, 2021
Oh, Deer
Heading Off a Wildlife Epidemic
CWD poses a significant threat to the future of hunting in Texas. Deer population declines of 45 and 50 percent have been documented in Colorado and Wyoming. A broad infection of Texas deer populations resulting in similar population impacts would inflict severe economic damage to rural communities and could negatively impact land markets. Specifically, those landowners seeking to establish a thriving herd of deer could avoid buying in areas with confirmed CWD infections. As they do with anthrax-susceptible properties, land brokers may find it advisable to inquire about the status of CWD infections on properties that they present for sale. Prospective buyers should also investigate the status of the wildlife on prospective properties. In addition, existing landowners should monitor developments as TPWD crafts management strategies to identify and contain this deadly disease.
Dr. Gilliland (c-gilliland@tamu.edu) is a research economist with the Texas Real Estate Research Center at Texas A&M University.
Texas Kimble County Farm Chronic Wasting Disease CWD TSE Prion Approximate Herd Prevalence 12%
SUMMARY MINUTES OF THE 407th COMMISSION MEETING Texas Animal Health Commission
September 22, 2020
Thursday, October 2, 2014
TEST RESULTS FROM CAPTIVE DEER HERD WITH CHRONIC WASTING DISEASE RELEASED 79.8 percent of the deer tested positive for the disease
DES MOINES – The Iowa Department of Agriculture and Land Stewardship today announced that the test results from the depopulation of a quarantined captive deer herd in north-central Iowa showed that 284 of the 356 deer, or 79.8% of the herd, tested positive for Chronic Wasting Disease (CWD).
Wisconsin Buckhorn Flats CWD
SUBJECT: Almond Deer Farm Update
Sixty of the 76 animals tested positive for CWD. The 76 deer constituted the breeding herd in the breeding facility on the farm. The property also had a hunting preserve until 2005. Four deer, two does and two fawns, the only deer remaining in the former preserve, were killed and tested as well. CWD was not detected in those animals.
The total number of deer to test positive from this farm from the initial discovery to final depopulation is 82. The nearly 80% prevalence rate discovered on Buckhorn Flats is the highest prevalence recorded in any captive cervid operation in North America.
Colorado CWD TSE Prion
“The overall incidence of clinical CWD in white-tailed deer was 82% “
Epidemiology of Chronic Wasting Disease in Captive White-Tailed and Mule Deer
Farmed, Wild, Tribal, Cervid Chronic Wasting Disease Management and Response Activities 2023 Cooperative Agreements 2023 Spending Plan
Farmed Cervid Chronic Wasting Disease Management and Response Activities 2023 Cooperative Agreements 2023 Spending Plan
USAHA 129th Annual Meeting CWD TSE PrP 2025 and a Decade Review
USAHA 129th Annual Meeting CWD TSE PrP 2025 and a Decade Review of Progress, or not so much, of the attempts to try and eradicate, or at least control the spread of Chronic Wasting Disease CWD TSE PrP. i put that in AI Google, too see what would come up… terry
to AI trials and tribulations and failures of science of CWD Transmissible Spongiform Encephalopathy
AI answer; The scientific pursuit to understand, detect, and control Chronic Wasting Disease (CWD)—a Transmissible Spongiform Encephalopathy (TSE) affecting cervids—has been characterized by significant, long-term challenges, slow progress, and frustrating management failures. CWD is a 100% fatal, infectious, and resilient prion disease that has spread to 24 U.S. states, 3 Canadian provinces, South Korea, and Norway, defying many traditional wildlife management strategies.
Here is an overview of the trials, tribulations, and failures of CWD science:
1. Scientific Tribulations and Challenges Insidious Nature of Prions: Unlike bacteria or viruses, prions are misfolded proteins that are extremely resilient. They resist traditional disinfection, freezing, incineration below 1100°F, radiation, and desiccation. They persist in the environment for years, making containment nearly impossible.
Long Incubation Periods: CWD has a long pre-clinical phase where animals look healthy but shed prions, with incubation ranging from 15 to over 34 months. This makes early detection in wild populations exceptionally difficult.
Environmental Reservoirs: Research has struggled to map how prions bind to soil and minerals, which creates long-lasting "hotspots" of infection.
Diagnostic Limitations: While post-mortem testing of lymph nodes or brain tissue is accurate, it is not practical for massive, live wild populations. Live-animal testing (e.g., rectal biopsy) is less sensitive and cannot effectively monitor the scale of the spread.
2. Scientific Failures and Unresolved Questions Inconclusive Zoonotic Risk: A major failure of scientific communication and research has been the inability to definitively rule out whether CWD can infect humans. While no cases have been reported, laboratory studies on transgenic mice and macaques have yielded mixed results, leading to a "high level of uncertainty".
Failed Containment: Management strategies, including population reduction and, in some cases, eradication of infected herds, have largely failed to halt the spread in the wild. The disease continues to spread geographically and increase in prevalence.
Inconsistent Data: Studies on management, such as culling, have produced conflicting results, with some showing effectiveness and others showing no difference.
3. Management and Policy Failures Captive Herd Industry: A major, ongoing failure is the inability to strictly regulate the captive deer industry, which has acted as a primary driver of long-distance, artificial spread of the disease.
Inconsistent Governance: State wildlife agencies have often failed to apply consistent, science-based regulations, bowing to pressure from the captive deer industry, leading to loopholes in testing and, in some cases, the spread of the disease through the movement of contaminated, farmed deer.
Human Activity Drivers: Failure to curb human-caused concentration of animals, such as baiting and feeding, has worsened the spread.
4. Recent Scientific Advancements (The Path Forward) Ultrasensitive Detection (RT-QuIC): The development of Real-Time Quaking-Induced Conversion (RT-QuIC) and Serial Protein Misfolding Amplification (PMCA) has allowed scientists to detect very low levels of prions, improving the ability to identify prions in soil, water, and even in live animals (e.g., in feces or saliva).
Better Environmental Sampling: Techniques to sample contaminated, environmentally relevant surfaces like metal fences or water sources are now being developed.
The science of CWD has moved from a lack of understanding to a state of high alarm, driven by the realization that this disease is not just a localized issue but a persistent, growing threat to wildlife, ecosystems, and potentially human health. end…TSS
not bad.
please let me elaborate on the dire consequences we face with CWD TSE PrP, if we fail to act swiftly, with sound science, and NOT let the industry continue to legislate junk science, and regulations there from, by trucking CWD to hell and back, no better example is Texas…
USAHA 129th Annual Meeting CWD TSE PrP 2025 and a Decade Review
USAHA 129th Annual Meeting CWD TSE PrP 2025 and a Decade Review
2025 AAVLD/USAHA 129th Annual Meeting CWD TSE PrP October 30, 2025 - November 5, 2025
***> CWD Genetics GM Cervid, what could go wrong???
***> CWD genetic resistance
Research Project: Elucidating the Pathobiology and Transmission of Transmissible Spongiform Encephalopathies
Location: Virus and Prion Research
Title: Update: CWD genetic resistance project at NADC
Author item Cassmann, Eric item Greenlee, Justin Submitted to: North American Deer Farmer Publication Type: Trade Journal Publication Acceptance Date: 11/5/2023 Publication Date: 11/15/2023 Citation: Cassmann, E.D., Greenlee, J.J. 2023.
Update: CWD genetic resistance project at NADC. North American Deer Farmer. P. 83.
Interpretive Summary: Technical Abstract:
In March of 2020, we began a study to examine the susceptibility of whitetail deer with rare prion protein genotypes to chronic wasting disease (CWD). In the sequence of amino acids that make up the deer prion protein, there are several locations that are variable. These variations are sometimes called polymorphisms. In the data collected from depopulations, whitetail deer with certain prion gene polymorphisms were not positive for CWD. In 2019, Dr. Nick Haley published a paper that showed H95/S96, HH95, and S96/K226 deer from depopulated herds in the US were not CWD positive. Based on the overall low number of deer with these genotypes () we’re unable to determine if they were resistant to CWD or if there were too few deer with these genotypes to be statistically represented in the positive cases. It’s also possible that they could be partially susceptible with longer incubation times than deer with generic (wild type) prion genotypes. Samples gathered at depopulation represent a snapshot of the herd. It is possible these rare genotypes were exposed, but had not yet accumulated abnormal prion protein to a level detectable by the detection methods used. The NADC susceptibility study was initiated to help answer these questions.
We studied deer with polymorphisms at 3 amino acid locations (codons): 95, 96, and 226. Wild type deer are QQ95GG96QQ226. Whitetail deer with wild type prion genotypes were inoculated with CWD and co-housed with other whitetail deer (contact deer) that had rare prion protein genotypes. The genotypes of contact deer included QH95GS96QQ226, QH95GG96QK226, QQ95GS96QQ226, QQ95SS96QQ226, Q95GS96QK226, and QQ95GG96KK226 (bolded text indicates a prion gene polymorphism). During the first year, we collected feces, saliva, nasal swabs, skin, blood, and rectal biopsies from the inoculated and contact deer to determine if deer are CWD positive and the period of CWD shedding. After the first year, we started collecting rectal biopsies annually on the contact deer, but all other samples are still collected every three months.
Eight out of ten (8/10) inoculated deer developed clinical signs for CWD and tested positive after necropsy (Figure 1). The average time from inoculation to euthanasia of these eight inoculated deer was 23 months. Two inoculated deer are still on-study; one of these deer has tested positive for CWD on rectal biopsy IHC.
To date, two deer from the contact group have developed CWD clinical signs and tested positive (Figure 2). The positive deer from the contact group had the GS96QK226 and KK226 genotypes.
We have detected CWD prions in rectal biopsies with IHC in three other contact deer as of October 2023. Their prion genotypes are GS96, QH95GS96, and GS96QK226.
As the experiment continues, we hope to answer 2 main questions. (
1) Are there any prion protein polymorphisms that make deer resistant to CWD, and
(2) what are the CWD shedding dynamics in deer with detectable CWD.
One potential outcome of the study would be identifying genotypes with very long incubation periods that, while susceptible to CWD, still could be used to manage CWD.
Update: CWD genetic resistance project at NADC 1) Are there any prion protein polymorphisms that make deer resistant to CWD, and (2) what are the CWD shedding dynamics in deer with detectable CWD. One potential outcome of the study would be identifying genotypes with very long incubation periods that, while susceptible to CWD, still could be used to manage CWD.
''There are no known familial or genetic TSEs of animals, although polymorphisms in the PRNP gene of some species (sheep for example) may influence the length of the incubation period and occurrence of disease.''
c) The commonest form of CJD occurs as a sporadic disease, the cause of which is unknown, although genetic factors (particularly the codon 129 polymorphism in the prion protein gene (PRNP)) influence disease susceptibility. The familial forms of human TSEs (see Box 1) appear to have a solely genetic origin and are closely associated with mutations or insertions in the PRNP gene. Most, but not all, of the familial forms of human TSEs have been transmitted experimentally to animals. There are no known familial or genetic TSEs of animals, although polymorphisms in the PRNP gene of some species (sheep for example) may influence the length of the incubation period and occurrence of disease.
P-145 Estimating chronic wasting disease resistance in cervids using real time quaking- induced conversion
Nicholas J Haley1, Rachel Rielinqer2, Kristen A Davenport3, W. David Walter4, Katherine I O'Rourke5, Gordon Mitchell6, Juergen A Richt2 1
Our studies demonstrate that in vitro amplification metrics predict in vivo susceptibility, and that alleles with multiple codons, each influencing resistance independently, do not necessarily contribute additively to resistance. Importantly, we found that the white-tailed deer 226K substrate exhibited the slowest amplification rate among those evaluated, suggesting that further investigation of this allele and its resistance in vivo are warranted to determine if absolute resistance to CWD is possible. ***at present, no cervid PrP allele conferring absolute resistance to prion infection has been identified.
PRION 2016 CONFERENCE TOKYO
***> at present, no PrPC allele conferring absolute resistance in cervids has been identified.
J Gen Virol. 2017 Nov; 98(11): 2882–2892.
Published online 2017 Oct 23. doi: 10.1099/jgv.0.000952
Estimating chronic wasting disease susceptibility in cervids using real-time quaking-induced conversion
Chronic wasting disease (CWD) resistance in cervids is often characterized as decreased prevalence and/or protracted disease progression in individuals with specific alleles; at present, no PrPC allele conferring absolute resistance in cervids has been identified.
Another potential and likely outcome of this study, imo, is that genotypes developed with very long incubation, could therefore, if released into the wild, could help spread cwd even further, exposing even more wild species, and surrounding environments, for even longer periods of time, due to the longer incubation, a terrible potential outcome, one that must be avoided at all cost, imo…terry
FRIDAY, MAY 01, 2026
Oklahoma House Bill 3270 FAILED, Great News for Hunters and Wildlife
***> Singeltary Submission to Federal Dockets on CWD TSE Prions
Monday, November 13, 2023
Food and Drug Administration's BSE Feed Regulation (21 CFR 589.2000) Singeltary Another Request for Update 2023 Food and Drug Administration's BSE Feed Regulation (21 CFR 589.2000) Singeltary Another Request for Update 2023
The infamous 1997 mad cow feed ban i.e. Food and Drug Administration's BSE Feed Regulation (21 CFR 589.2000) most material (exceptions include milk, tallow, and gelatin) from deer and elk is prohibited for use in feed for ruminant animals. With regards to feed for non-ruminant animals, under FDA law, CWD positive deer may not be used for any animal feed or feed ingredients. For elk and deer considered at high risk for CWD, the FDA recommends that these animals do not enter the animal feed system. However, this recommendation is guidance and not a requirement by law.
***>However, this recommendation is guidance and not a requirement by law.
WITH GREAT URGENCY, THE Food and Drug Administration's BSE Feed Regulation (21 CFR 589.2000) MUST BE ENHANCED AND UPDATED TO INCLUDE CERVID, PIGS, AND SHEEP, SINCE RECENT SCIENCE AND TRANSMISSION STUDIES ALL, INCLUDING CATTLE, HAVE SHOWN ORAL TSE PrP TRANSMISSIONS BETWEEN THE SPECIES, AND THIS SHOULD BE DONE WITH THE UTMOST URGENCY, REASONS AS FOLLOW.
snip…end
Monday, November 13, 2023
Food and Drug Administration's BSE Feed Regulation (21 CFR 589.2000) Singeltary Another Request for Update 2023
Automatic reply: America BSE 589.2001 FEED REGULATIONS, BSE SURVEILLANCE, BSE TESTING, and CJD TSE Prion [SEC=UNCLASSIFIED]
Thank you for your email. Your query has been directed to the plant import risk analyses stakeholder engagement team and will be responded to as soon as possible. For importing enquiries, please contact imports@agriculture.gov.au or phone 1800 900 090. Kind regards, Plant Stakeholders Plant Systems and Strategies | Biosecurity Plant Division Phone: 02 6272 5094 | Email: plantstakeholders@agriculture.gov.au
For importing enquiries please phone 1800 900 090 (when prompted press 1 and then 1 again) or emailimports@agriculture.gov.au. Department of Agriculture and Water Resources 7 London Circuit, Canberra ACT 2601 Australia GPO Box 858, Canberra ACT 2601 Australia www.agriculture.gov.au end…TSS
Control of Chronic Wasting Disease OMB Control Number: 0579-0189APHIS-2021-0004 Singeltary Submission
Control of Chronic Wasting Disease OMB Control Number: 0579-0189 APHIS-2021-0004 Singeltary Submission
Greetings APHIS et al, i would kindly like to comment on Control of Chronic Wasting Disease OMB Control Number: 0579-0189 APHIS-2021-0004.
Greetings APHIS et al, i would kindly like to comment on Control of Chronic Wasting Disease OMB Control Number: 0579-0189 APHIS-2021-0004.
***> 1st and foremost your biggest problem is 'VOLUNTARY'! AS with the BSE 589.2001 FEED REGULATIONS, especially since it is still voluntary with cervid, knowing full well that cwd and scrapie will transmit to pigs by oral route. VOLUNTARY DOES NOT WORK! all animal products should be banned and be made mandatory, and the herd certification program should be mandatory, or you don't move cervid. IF THE CWD HERD CERTIFICATION IS NOT MANDATORY, it will be another colossal tse prion failure from the start.
***> 2nd USA should declare a Declaration of Extraordinary Emergency due to CWD, and all exports of cervid and cervid products must be stopped internationally, and there should be a ban of interstate movement of cervid, until a live cwd test is available.
***> 3rd Captive Farmed cervid ESCAPEES should be made mandatory to report immediately, and strict regulations for those suspect cwd deer that just happen to disappear. IF a cervid escapes and is not found, that farm should be indefinitely shut down, all movement, until aid MIA cervid is found, and if not ever found, that farm shut down permanently.
***> 4th Captive Farmed Cervid, INDEMNITY, NO MORE Federal indemnity program, or what i call, ENTITLEMENT PROGRAM for game farm industry. NO MORE BAIL OUTS FROM TAX PAYERS. if the captive industry can't buy insurance to protect not only themselves, but also their customers, and especially the STATE, from Chronic Wasting Disease CWD TSE Prion or what some call mad deer disease and harm therefrom, IF they can't afford to buy that insurance that will cover all of it, then they DO NOT GET A PERMIT to have a game farm for anything. This CWD TSE Prion can/could/has caused property values to fall from some reports in some places. roll the dice, how much is a state willing to lose?
***> 5th QUARANTINE OF ALL FARMED CAPTIVE, BREEDERS, URINE, ANTLER, VELVET, SPERM, OR ANY FACILITY, AND THEIR PRODUCTS, that has been confirmed to have Chronic Wasting Disease CWD TSE Prion, the QUARANTINE should be for 21 years due to science showing what scrapie can do. 5 years is NOT near long enough. see; Infectious agent of sheep scrapie may persist in the environment for at least 16 to 21 years.
***> 6th America BSE 589.2001 FEED REGULATIONS CWD TSE Prion
***> 7TH TRUCKING TRANSPORTING CERVID CHRONIC WASTING DISEASE TSE PRION VIOLATING THE LACEY ACT
***> 8TH ALL CAPTIVE FARMING CERVID OPERATIONS MUST BE INSURED TO PAY FOR ANY CLEAN UP OF CWD AND QUARANTINE THERE FROM FOR THE STATE, NO MORE ENTITLEMENT PROGRAM FOR CERVID GAME FARMING PAY TO PLAY FOR CWD TSE PRION OFF THE TAX PAYERS BACK.
***> 9TH ANY STATE WITH DOCUMENTED CWD, INTERSTATE, NATIONAL, AND INTERNATIONAL MOVEMENT OF ALL CERVID, AND ALL CERVID PRODUCTS MUST BE HALTED!
***> 10TH BAN THE SALE OF STRAW BRED BUCKS AND ALL CERVID SEMEN AND URINE PRODUCTS
***> 11th ALL CAPTIVE FARMED CERVID AND THEIR PRODUCTS MUST BE CWD TSE PRION TESTED ANNUALLY AND BEFORE SALE FOR CWD TSE PRION
SEE FULL SCIENCE REFERENCES AND REASONINGS ;
***> 1st and foremost your biggest problem is 'VOLUNTARY'!
''APHIS created a cooperative, voluntary Federal-State-private sector CWD Herd Certification Program designed to identify farmed or captive herds infected with CWD.''
key word failure is 'voluntary'.
WE know for a fact now that voluntary does NOT WORK!
AS with the BSE 589.2001 FEED REGULATIONS (see , another colossal failure, and proven to be a sham, especially since it is still voluntary with cervid, knowing full well that cwd and scrapie will transmit to pigs by oral route. VOLUNTARY DOES NOT WORK! all animal products should be banned and be made mandatory, and the herd certification program should be mandatory, or you don't move cervid. IF THE CWD HERD CERTIFICATION IS NOT MANDATORY, it will be another colossal tse prion failure from the start.
***> 2nd USA should declare a Declaration of Extraordinary Emergency due to CWD, and all exports of cervid and cervid products must be stopped internationally, and there should be a ban of interstate movement of cervid, until a live cwd test is available.
***> 3rd Captive Farmed cervid ESCAPEES should be made mandatory to report immediately, and strict regulations for those suspect cwd deer that just happen to disappear. IF a cervid escapes and is not found, that farm should be indefinitely shut down, all movement, until aid MIA cervid is found, and if not ever found, that farm shut down permanently. ...snip...see full text submission with science references...TSS
Docket No. APHIS-2018-0011 Chronic Wasting Disease Herd Certification Program Standards Singeltary Submission March 30, 2018
Greetings APHIS, USDA, Dr. Tracy Nichols, et al,
I wish to kindly submit my comments on the Docket No. APHIS-2018-0011 Chronic Wasting Disease Herd Certification Program Standards please. i have submitted online and sent a hard copy to Dr. Nichols via email. i know that my concern may not be the same concern as others, but ramifications from cwd tse prion can be long lasting, and science is still emerging. however, the science today warrants immediate and further actions be taken, especially about zoonosis potential for cwd tse prion, if it has not happened already. my comments, with reference materials, are as follows, and will be formatted in such a way, i will address issues by numbers 1-10, and under each one of my comments by each number, i will reference my comments with science to back up what i am stating/asking...thank you kindly, terry
1. I believe that immediately, there should be a 'DECLARATION OF EXTRAORDINARY EMERGENCY FOR FOREIGN ANIMAL DISEASE OF THE United States of America USA' due to Chronic Wasting Disease CWD Transmissible Spongiform Encephalopathy TSE Prion disease. All Intercontinental, International, Interstate movements of cervid should be banned immediately from the USA, and documented CWD TSE Prion Countries. ...snip...see full text Singeltary Submission for references.
2. Voluntary Chronic Wasting Disease Herd Certification Program should be made MANDATORY immediately, OR NO PERMIT TO FARM DEER OR ELK, PERIOD! you don't want to join, then fine, you don't farm cervid and or any product there from...see full text Singeltary Submission for references.
3. INDEMNITY, NO MORE Federal indemnity program, or what i call, ENTITLEMENT PROGRAM for game farm industry. NO MORE BAIL OUTS FROM TAX PAYERS. if the captive industry can't buy insurance to protect not only themselves, but also their customers, and especially the STATE, from Chronic Wasting Disease CWD TSE Prion or what some call mad deer disease and harm therefrom, IF they can't afford to buy that insurance that will cover all of it, then they DO NOT GET A PERMIT to have a game farm for anything. This CWD TSE Prion can/could/has caused property values to fall from some reports in some places. roll the dice, how much is a state willing to lose?...see full text Singeltary Submission for references.
4. QUARANTINE OF ALL CAPTIVE, BREEDERS, URINE, ANTLER, VELVET, SPERM, OR ANY FACILITY that has been confirmed to have Chronic Wasting Disease CWD TSE Prion, the QUARANTINE should be for 21 years due to science showing what scrapie can do. 5 years is NOT enough. see; Infectious agent of sheep scrapie may persist in the environment for at least 16 years...snip...see full text Singeltary Submission for references.
PLEASE SEE Singeltary 5 - 10 comoments, and full text file DOWNLOAD ON GOVERNMENT SITE, OR GO TO THIS URL LINK FOR FULL TEXT OF SINGELTARY SUBMISSION TO Docket No. APHIS-2018-0011 Chronic Wasting Disease Herd Certification Program Standards Singeltary Submission March 30, 2018, PLEASE SEE;
Docket No. FDA-2003-D-0432 (formerly 03D-0186) Use of Material from Deer and Elk in Animal Feed
PUBLIC SUBMISSION
Comment from Terry Singeltary Sr.
Posted by the Food and Drug Administration on May 17, 2016 Comment
Docket No. FDA-2003-D-0432 (formerly 03D-0186) Use of Material from Deer and Elk in Animal Feed Singeltary Submission
ARS Research Elucidating the Pathobiology and Transmission of Transmissible Spongiform Encephalopathies 2025 Annual Report
Price of TSE Prion Poker Goes Up Again…terry
TUESDAY, SEPTEMBER 30, 2025
USDA National Scrapie Program History and Bovine Spongiform Encephalopathy BSE TSE Update 2025
SCRAPIE TSE Prion USA RAPID RESPONSE URGENT UPDATES DECEMBER 25, 2025
USA FDA PART 589 SUBSTANCES PROHIBITED FROM USE IN ANIMAL FOOD OR FEED, CWD, Scrapie, BSE, Oh My, 2026
TUESDAY, APRIL 07, 2026 APHIS USDA Captive CWD Herds Update by State March 2026 Update
APHIS USDA Captive CWD Herds Update by State March 2026 Update
CHRONIC WASTING DISEASE CASES
Date of Index Case Confirmation Index Case State County Species Herd Type HCP Enrolled HCP Certified Number of Animals Herd Status
3/5/2026 2 YR Male PA Huntingdon WTD Elk Sika Hunt No No 100+ Quarantine
3/5/2026 1.5 YR Male TX Mason WTD Breeder No No 73 Quarantine
3/5/2026 2.5 YR Female TX Medina WTD Breeder No No 90 Quarantine
2/20/2026 2.75 YR Male MI Calhoun WTD Breeder Yes Yes 24 Quarantine
2/17/2026 2.5 YR Male KS Osage Axis Breeder No No 21 Quarantine
2/12/2026 3.5 YR TX Duval WTD Hunt No No ukn Quarantine
1/22/2026 3 YR Male PA Butler Elk Breeding Yes Yes 30 Quarantine
12/16/2025 Adults Male PA Indiana WTD elk Red deer Fallow Hunt No No ukn Quarantine
12/15/2025 3 YR Male PA Warren WTD Breeder No No >100 Quarantine
12/15/2025 4.5 YR Male PA Lycoming WTD ELK Hunt No No >100 Quarantine
12/15/2025 2.5 YR Male PA Juniata WTD Hobby No No 4 Quarantine
Updated March 2026
APHIS USDA Captive CWD Herds Update by State December 2025 Update
Action Plan National Program 103 Animal Health 2022-2027
Animal Health (NP103) Annual Report for 2024
Component 6: Transmissible Spongiform Encephalopathies (TSEs)
Problem Statement 6A: Determine pathobiology of prion strains.
TUESDAY, JANUARY 20, 2026
Pathogenesis, Transmission and Detection of Zoonotic Prion Diseases Project Number 5P01AI077774-14 2025
FRIDAY, OCTOBER 31, 2025
Captive Cervid and the Economic Burden of Chronic Wasting Disease CWD TSE Prion?
The economic burden of ignoring CWD would be far greater, imo, with time, if no cervid were left, or just a select few, if the environment/property was so exposed and saturated with CWD, that you couldn’t sell it, you couldn’t grow crops because of the soil saturation of the CWD, water tables saturated with CWD, saturation of hay, grains, from crops uptake on said property, cervid meat saturated from Cervid CWD, remember, You cannot cook the TSE prion disease out of meat, In fact new data now shows that exposure to high temperatures used to cook the meat increased the availability of prions for in vitro amplification. So, what Do we do, how many humans and animals do we continue to expose, continue to saturate with the CWD TSE Prion, …
***> USA BSE TSE PrP
Six of the seven cases of BSE identified in the United States have been diagnosed as atypical BSE. In most cases, the animals were 10 years of age or older. Two of the six detections of atypical BSE involved animals aged approximately 5 years or older.
USA BSE Testing and Surveillance?
Bottom line, USA is testing so few cows for BSE (<25k tested annually)
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$$$
Wednesday, May 24, 2023
***> WAHIS, WOAH, OIE, United States of America Bovine spongiform encephalopathy Immediate notification
SATURDAY, MAY 20, 2023
***> Tennessee State Veterinarian Alerts Cattle Owners to Disease Detection Mad Cow atypical L-Type BSE
MAY 19, 2023
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''...
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.
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.
***>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...
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
SATURDAY, JANUARY 10, 2026
***> Neuropsychiatric symptoms in sporadic Creutzfeldt-Jakob disease, a review
WEDNESDAY, OCTOBER 15, 2025
US NATIONAL PRION DISEASE PATHOLOGY SURVEILLANCE CENTER CJD TSE REPORT 2025
FRIDAY, NOVEMBER 21, 2025
While no one was watching: Tenuous status of CDC prion unit, risk of CWD to people worry scientists
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
2023
iatrogenic Transmissible Spongiform Encephalopathy, Friendly Fire, Pass It Forward, Unforeseen Circumstances
Chronic Wasting Disease CWD TSE PrP transmission to, Cattle, Sheep, Pigs, Cervid, Primates, oh my!
so, this is what we leave our children and grandchildren???
***> CWD TSE primates and humans
***> Human CWD TSE PrP, what if?
the problem is, to date, there is NO diagnostic criteria set in stone that would confirm a case of human Cwd, like there was with nvCJD (my Mom died from confirmed hvCJD a rare strain of the infamous sporadic CJDs with new strains mounting, sporadic CJD simply means ‘unknown’, IT DOES NOT MEAN 85%+ SPORADIC CJD IS ALL SPONTANEOUS, that’s all iatrogenic CJD is sporadic CJD, until the iatrogenic event is detected, confirmed, traced back, confirmed, put I to the academic domain, and finally, if your lucky, finally published to the media, and finally the public domain.) sorry, I got off course…but let me perfectly clear here, all science to date shows, Human CWD will not look like New Variant Creutzfeldt Jakob disease nvCJD. CWD to humans will look like some variant of sporadic Creutzfeldt Jakob Disease. And here me out very clearly, and this is from the to TSE Prion Gods themselves, old correspondence from way back during my investigations early BSE nvCJD days…2002
“Also, we do not claim that "no-one has ever been infected with prion disease from eating venison." Our conclusion stating that we found no strong evidence of CWD transmission to humans in the article you quoted or in any other forum is limited to the patients we investigated.”
*** now, let’s see what the authors said about this casual link, personal communications years ago, and then the latest on the zoonotic potential from CWD to humans from the TOKYO PRION 2016 CONFERENCE.
see where it is stated NO STRONG evidence. so, does this mean there IS casual evidence ????
“Our conclusion stating that we found no strong evidence of CWD transmission to humans”
Subject: CWD aka MAD DEER/ELK TO HUMANS ???
Date: September 30, 2002 at 7:06 am PST
From: "Belay, Ermias"
To: Cc: "Race, Richard (NIH)" ; ; "Belay, Ermias"
Sent: Monday, September 30, 2002 9:22 AM
Subject: RE: TO CDC AND NIH - PUB MED- 3 MORE DEATHS - CWD - YOUNG HUNTERS
Dear Sir/Madam, In the Archives of Neurology you quoted (the abstract of which was attached to your email), we did not say CWD in humans will present like variant CJD.. That assumption would be wrong. I encourage you to read the whole article and call me if you have questions or need more clarification (phone: 404-639-3091).
Also, we do not claim that "no-one has ever been infected with prion disease from eating venison." Our conclusion stating that we found no strong evidence of CWD transmission to humans in the article you quoted or in any other forum is limited to the patients we investigated.
Ermias Belay, M.D. Centers for Disease Control and Prevention
Subject: TO CDC AND NIH - PUB MED- 3 MORE DEATHS - CWD - YOUNG HUNTERS
Sunday, November 10, 2002 6:26 PM .......snip........end..............TSS
-----Original Message-----
From:
Sent: Sunday, September 29, 2002 10:15 AM
To: rr26k@nih.gov; rrace@niaid.nih.gov; ebb8@CDC.GOV
Subject: TO CDC AND NIH - PUB MED- 3 MORE DEATHS - CWD - YOUNG HUNTERS
Sunday, November 10, 2002 6:26 PM .......snip........end..............TSS
“regular venison eating associated with a 9 FOLD INCREASE IN RISK OF CJD”
Subject: Re: DEER SPONGIFORM ENCEPHALOPATHY SURVEY & HOUND STUDY
Date: Fri, 18 Oct 2002 23:12:22 +0100
From: Steve Dealler Reply-To: Bovine Spongiform Encephalopathy Organization: Netscape Online member
To: BSE-L@ …
######## Bovine Spongiform Encephalopathy <BSE-L@UNI-KARLSRUHE.DE> #########
Dear Terry,
An excellent piece of review as this literature is desparately difficult to get back from Government sites. What happened with the deer was that an association between deer meat eating and sporadic CJD was found in about 1993. The evidence was not great but did not disappear after several years of asking CJD cases what they had eaten. I think that the work into deer disease largely stopped because it was not helpful to the UK industry...and no specific cases were reported.
Well, if you dont look adequately like they are in USA currenly then you wont find any!
Steve Dealler
########### http://mailhost.rz.uni-karlsruhe.de/warc/bse-l.html ############
Subject: DEER SPONGIFORM ENCEPHALOPATHY SURVEY & HOUND STUDY
From: "Terry S. Singeltary Sr." <flounder@WT.NET>
Reply To: Bovine Spongiform Encephalopathy <BSE-L@UNI-KARLSRUHE.DE>
Date: Thu, 17 Oct 2002 17:04:51 -0700
snip...
''The association between venison eating and risk of CJD shows similar pattern, with regular venison eating associated with a 9 FOLD INCREASE IN RISK OF CJD (p = 0.04).''
CREUTZFELDT JAKOB DISEASE SURVEILLANCE IN THE UNITED KINGDOM THIRD ANNUAL REPORT AUGUST 1994
snip...see full report ;
http://web.archive.org/web/20090506050043/http://www.bseinquiry.gov.uk/files/yb/1994/08/00004001.pdf
http://web.archive.org/web/20090506050007/http://www.bseinquiry.gov.uk/files/yb/1994/10/00003001.pdf
http://web.archive.org/web/20090506050244/http://www.bseinquiry.gov.uk/files/yb/1994/07/00001001.pdf
Stephen Dealler is a consultant medical microbiologist deal@airtime.co.uk BSE Inquiry Steve Dealler Management In Confidence BSE: Private Submission of Bovine Brain Dealler
snip...end
########### http://mailhost.rz.uni-karlsruhe.de/warc/bse-l.html ############
***> ''The association between venison eating and risk of CJD shows similar pattern, with regular venison eating associated with a 9 FOLD INCREASE IN RISK OF CJD (p = 0.04).''
GAME FARM INDUSTRY WANTS TO COVER UP FINDINGS OF INCREASE RISK TO CJD FROM CERVID
BSE INQUIRY
CJD9/10022
October 1994
Mr R.N. Elmhirst Chairman British Deer Farmers Association Holly Lodge Spencers Lane
BerksWell Coventry CV7 7BZ
Dear Mr Elmhirst,
CREUTZFELDT-JAKOB DISEASE (CJD) SURVEILLANCE UNIT REPORT
Thank you for your recent letter concerning the publication of the third annual report from the CJD Surveillance Unit. I am sorry that you are dissatisfied with the way in which this report was published.
The Surveillance Unit is a completely independant outside body and the Department of Health is committed to publishing their reports as soon as they become available. In the circumstances it is not the practice to circulate the report for comment since the findings of the report would not be amended.. In future we can ensure that the British Deer Farmers Association receives a copy of the report in advance of publication.
The Chief Medical Officer has undertaken to keep the public fully informed of the results of any research in respect of CJD. This report was entirely the work of the unit and was produced completely independantly of the the Department.
The statistical results regarding the consumption of venison was put into perspective in the body of the report and was not mentioned at all in the press release. Media attention regarding this report was low key but gave a realistic presentation of the statistical findings of the Unit. This approach to publication was successful in that consumption of venison was highlighted only once by the media ie. in the News at one television proqramme.
I believe that a further statement about the report, or indeed statistical links between CJD and consumption of venison, would increase, and quite possibly give damaging credence, to the whole issue. From the low key media reports of which I am aware it seems unlikely that venison consumption will suffer adversely, if at all.
http://web.archive.org/web/20030511010117/http://www.bseinquiry.gov.uk/files/yb/1994/10/00003001.pdf
MONDAY, FEBRUARY 25, 2019
***> MAD DOGS AND ENGLISHMEN BSE, SCRAPIE, CWD, CJD, TSE PRION A REVIEW 2019
***> Camel Prion Disease PrP
Thursday, February 19, 2026
Identification of Camel Prion Disease in Tunisia: evidence of an emerging prion disease in North Africa
https://camelusprp.blogspot.com/2026/02/identification-of-camel-prion-disease.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, 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
https://www.aphis.usda.gov/sites/default/files/status-of-captive-herds.pdf
SATURDAY, APRIL 11, 2026
Chronic Wasting Disease CWD TSE PrP, Cervid, Genetic Manipulation, Unforeseen Circumstances
https://chronic-wasting-disease.blogspot.com/2026/04/chronic-wasting-disease-cwd-tse-prp.html
***> USDA Statement BSE Surveillance Information Center Update 2026 <***
https://oieusdabseprp.blogspot.com/2026/04/usda-statement-bse-surveillance.html
TUESDAY, APRIL 28, 2026
Possible alignment of the EU BSE surveillance with the new WOAH provisions
https://woahoie.blogspot.com/2026/04/possible-alignment-of-eu-bse.html
https://efsaopinionbseanimalprotein.blogspot.com/2026/04/possible-alignment-of-eu-bse.html
SATURDAY, JANUARY 10, 2026
Neuropsychiatric symptoms in sporadic Creutzfeldt-Jakob disease, a review
https://creutzfeldt-jakob-disease.blogspot.com/2026/01/neuropsychiatric-symptoms-in-sporadic.html
https://prpsc.proboards.com/thread/191/neuropsychiatric-symptoms-sporadic-cjd-review
SUNDAY, MARCH 8, 2026
Texas Creutzfeldt-Jakob Disease Deaths and Death Rates per Year (2013-2022) More Than Tripled, and case reporting has ceased since then
https://cjdtexas.blogspot.com/2026/03/texas-creutzfeldt-jakob-disease-deaths.html
https://prpsc.proboards.com/thread/209/texas-cases-more-triples-2013
FRIDAY, NOVEMBER 21, 2025
While no one was watching: Tenuous status of CDC prion unit, risk of CWD to people worry scientists
https://chronic-wasting-disease.blogspot.com/2025/11/while-no-one-was-watching-tenuous.html
WEDNESDAY, OCTOBER 15, 2025
US NATIONAL PRION DISEASE PATHOLOGY SURVEILLANCE CENTER CJD TSE REPORT 2025
https://prionunitusaupdate.blogspot.com/2025/10/us-national-prion-disease-pathology.html
SUNDAY, MARCH 23, 2025
Creutzfeldt Jakob Disease TSE Prion Increasing 2025 Update
https://creutzfeldt-jakob-disease.blogspot.com/2025/03/creutzfeldt-jakob-disease-tse-prion.html
FRIDAY, DECEMBER 13, 2024
Creutzfeldt Jacob Disease CJD, BSE, CWD, TSE Prion, December 14, 2024 Annual Update
https://creutzfeldt-jakob-disease.blogspot.com/2024/12/creutzfeldt-jacob-disease-cjd-bse-cwd.html
Senator Cornyn helped me long ago when the NIH et al were threatening to destroy our loved ones brains we had donated for research, Senator Cornyn helped us stop that, and we graciously thank him for that. But I don’t think John Cornyn can save us this time, for obvious reasons…
https://www.upi.com/NIH-may-destroy-human-brain-collection/84811111671758/
https://www.upi.com/Groups-seek-to-save-NIH-brain-collection/72961112392131/
https://www.upi.com/NIH-says-it-will-preserve-CJD-brains/67711117574761/
http://creutzfeldt-jakob-disease.blogspot.com/2009/08/cjdstraight-talk-withjames.html
https://www.upi.com/Science_News/2003/12/30/Mad-Cow-Linked-to-thousands-of-CJD-cases/47861072816318/
https://www.upi.com/Health_News/2005/10/21/Questions-linger-in-US-CJD-cases/65761129945790/
FRIDAY, NOVEMBER 21, 2025
While no one was watching: Tenuous status of CDC prion unit, risk of CWD to people worry scientists
https://chronic-wasting-disease.blogspot.com/2025/11/while-no-one-was-watching-tenuous.html
JOHN CORNYN TEXAS UNITED STATES SENATE WASHINGTON, DC 20510-4305 April 26,2005
Mr. Terry Singeltary
P.O. Box
Bacliff, Texas 77518
Dear Mr. Singeltary:
In response to your recent request for my assistance, I have contacted the National Institutes ofHealth. I will write you again as soon as I receive a reply. I appreciate having the opportunity to represent you in the United States Senate and to be ofservice in this matter.
Sincerely,
JOHN CORNYN United States Senator JC:djl
===============
JOHN CORNYN TEXAS UNITED STATES SENATE WASHINGTON, DC 20510-4305
May 18,2005
Mr. Terry Singeltary
P.O. Box
Bacliff, Texas 77518
Dear Mr. Singeltary:
Enclosed is the reply I received from the Department of Health and Human Services in response to my earlier inquiry on your behalf. I hope this will be useful to you. I appreciate having the opportunity to represent you in the United States Senate. Thank you for taking time to contact me. Sincerely,
JOHN CORNYN United States Senate JC:djl Enclosure
DEPARTMENT OF HEALTH & HUMAN SERVICES National Institutes of HealthNational Institute of NeurologicalDisorders and Stroke NINDS Building 31, Room 8A52 31 Center Dr., MSC 2540 Bethesda, Maryland 20892-2540 Phone: 301-496-9746 Fax: 301-496-0296 Email: [log in to unmask]
May 10, 2005
The Honorable John CornynUnited States SenatorOccidental Tower5005 LBJ Freeway, Suite 1150Dallas, Texas 75244-6199
Dear Senator Cornyn:
Your letter to the National Institutes of Health (NIH) forwarding correspondence from Mr. Terry S. Singeltary, Sr., has been forwarded to me for reply. Mr. Singeltary is concerned about thepreservation of Creutzfeldt-Jakob disease (CJD) brain samples that have been maintained by theNational Institute of Neurological Disorders and Stroke (NINDS) Intramural Research programfor many years. I am sorry to learn that Mr. Singeltary's mother died of CJD and can certainly understand hisdesire that any tissues that could help investigators unravel the puzzle of this deadly disease arepreserved. I hope he will be pleased to learn that all the brains and other tissues with potential tohelp scientists learn about CJD are, and will continue to be, conserved. (The tissues that arediscarded are those that have either decayed to an extent that renders them no longer appropriatefor research or those for which we do not have sufficient identification.) The purpose of gathering these brains and tissues is to help scientists learn about CJD. To that end, some of the NINDS-held samples are distributed to investigators who can demonstrate thatthey have a compelling research or public health need for such materials. For example, sampleshave been transferred to NIH grantee Dr. Pierluigi Gambetti, who heads the National PrionDiseases Pathology Surveillance Center at Case Western Reserve University in Ohio and workswith the Centers for Disease Control and Prevention to monitor all cases of CJD in the UnitedStates. Dr. Gambetti studies the tissues to learn about the formation, physical and chemicalproperties, and pathogenic mechanisms of prion proteins, which are believed to be involved inthe cause of CJD. Samples have also been transferred to Dr. David Asher, at the U.S. Food andDrug Administration, for use in assessing a potential diagnostic test for CJD.
Page 2 - The Honorable John Cornyn
in closing, we know that donating organs and tissue from loved ones is a very difficult andpersonal choice that must often be made at the most stressful of times. We at the NINDS aregrateful to those stalwart family members who make this choice in the selfless hope that it willhelp others afflicted with CJD. We also know the invaluable contribution such donations maketo the advancement of medical science, and we are dedicated to the preservation of all of thetissue samples that can help in our efforts to overcome CJD.
I hope this information is helpful to you in responding to Mr. Singeltary. Sincerely,
Story C. Landis, Ph.D. Director, National Institute ofNeurological Disorders and Stroke
==================================...end...tss
Terry S. Singeltary Sr. flounder9@verizon.net
posted by Terry S. Singeltary Sr. at
4:25 PM
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