Saturday, May 16, 2026

Captive CWD Indemnity Program or Entitlement Program?

 ***> Captive CWD Indemnity Program or Entitlement Program? <***

***> CWD money grab you say, who’s getting paid?
USDA EXPLANATORY NOTES ANIMAL AND PLANT HEALTH INSPECTION SERVICE 2025-2014 CHRONIC WASTING DISEASE CWD TSE CERVID
2025 USDA EXPLANATORY NOTES – ANIMAL AND PLANT HEALTH INSPECTION SERVICE
In 2023, eight percent of the farmed cervids in the HCP were tested for CWD at APHIS and State laboratories.
Of the 303,242 farmed cervids tested in 2023, APHIS confirmed 22 new CWD positive farmed cervid herds.
APHIS provided Federal indemnity to depopulate one of the newly identified positive herds and approved an indemnity payment for a second positive herd which will be provided in 2024 once depopulation occurs. The remaining infected herds are under State quarantines.
2024 USDA EXPLANATORY NOTES – ANIMAL AND PLANT HEALTH INSPECTION SERVICE
Cervids
In 2022, 7 percent of the 285,589 farmed cervids in the HCP participating states were tested for CWD at State and APHIS laboratories.
APHIS confirmed 23 new CWD positive farmed cervid herds.
APHIS provided Federal indemnity to depopulate nine of the newly identified positive herds in 2022. The remaining infected herds are under State quarantines. APHIS determines the use of Federal indemnity payments within the CWD program on a case-by-case basis.
2023 USDA EXPLANATORY NOTES – ANIMAL AND PLANT HEALTH INSPECTION SERVICE
Cervids
Currently, 28 States participate in the national CWD HCP. In FY 2021, more than 20,502 farmed cervids were tested for CWD at State and APHIS laboratories.
As a result, APHIS identified 35 new CWD positive farmed cervid herds.
APHIS provided Federal indemnity to depopulate nine of the newly identified deer herds in FY 2021. The remaining infected herds are under State quarantines. APHIS determines the use of Federal indemnity payments within the CWD program on a case-by-case basis.
2022 USDA EXPLANATORY NOTES – ANIMAL AND PLANT HEALTH INSPECTION SERVICE
Cervids
Currently, 28 States participate in the national CWD HCP. In FY 2020, more than 11,182 farmed cervids were tested for CWD at State and APHIS laboratories.
As a result, APHIS identified 22 new CWD positive farmed cervid herds.
APHIS provided Federal indemnity to depopulate 15 of the 22 newly identified deer herds in FY 2020.
Four additional farmed cervid herds that were identified as CWD positive herds in FY 2019, were indemnified in FY 2020.
The remaining infected herds are under State quarantines.
2021 USDA EXPLANATORY NOTES – ANIMAL AND PLANT HEALTH INSPECTION SERVICE
In FY 2019 APHIS tested more than 11,000 farmed cervids for CWD.
As a result, APHIS identified 17 new CWD positive farmed cervid herds.
APHIS provided Federal indemnity to depopulate 7 of the 17 newly identified deer herds in FY 2019. The remaining infected herds found in FY 2019 are under State quarantines.
2020 USDA EXPLANATORY NOTES – ANIMAL AND PLANT HEALTH INSPECTION SERVICE
Cervids
In FY 2018, APHIS identified 15 new CWD positive farmed cervid herds (14 deer herds and 1 reindeer herd).
The reindeer herd in Illinois was the first confirmed case of CWD in a reindeer in North America.
APHIS provided Federal indemnity to depopulate seven of the 15 newly identified deer herds in FY 2018.
The Agency also provided funding for the test and removal of 161 high risk animals that were in close proximity to reactors.
The remaining herds in FY 2018 are under State quarantines.
The Agency determines the use of Federal indemnities within the CWD program on a case-by-case basis. 20-59
2019 President’s Budget Animal and Plant Health Inspection Service
Cervids
APHIS’ voluntary national CWD Herd Certification Plan (HCP) helps States, Tribes, and the cervid industry control CWD in farmed cervids by allowing the interstate movement only from certified herds.
Currently, 28 States participate in the national CWD HCP and the program tested 23,053 farmed cervids for CWD.
In FY 2017, eight new CWD positive farmed corvid herds were identified– one white-tail deer in Iowa, one white-tail deer herd in Minnesota, one white-tail and mule deer herd in Minnesota, one white-tail and sika deer herd in Michigan, three white-tail deer herds in Pennsylvania, and one white-tail deer herd in Texas.
APHIS provided Federal indemnity to depopulate the Iowa herd, the white-tail deer herd in Minnesota, one herd in Pennsylvania and the Texas herd. The State depopulated the Michigan herd. The remaining herds are under State quarantines. One Texas herd used Federal indemnity to remove and test select, high-risk animals to inform the epidemiological investigation and to evaluate the performance of ante-mortem tests.
The Agency determines the use of Federal indemnities within the CWD program on a case-by-case basis.
2018 President’s Budget Animal and Plant Health Inspection Service
Cervids
APHIS’ voluntary national CWD Herd Certification Plan (HCP) helps States, Tribes, and the cervid industry control CWD in farmed cervids by allowing the interstate movement only from certified herds considered to be low risk.
Currently, 29 States participate in the national CWD HCP.
In FY 2016, the program tested 14,503 farmed cervids for CWD and identified seven new CWD positive farmed cervid herds – two white-tail deer herds in Texas, three white-tail deer herds in Wisconsin, one elk herd in Colorado and one elk herd in Iowa. The elk herd in Colorado was depopulated without Federal indemnity and the rest of the herds are under State quarantines. One Texas herd used Federal indemnity to remove and test select animals to inform the epidemiological investigation and to evaluate 20-72 the performance of ante-mortem tests.
The use of Federal indemnities within the CWD program is determined on a case-by-case basis. APHIS is also conducting several pilot projects related to new technologies. In FY 2016, the Agency…
2017 Explanatory Notes Animal and Plant Health Inspection Service
Cervids
APHIS’ voluntary national CWD Herd Certification Plan (HCP) helps States, Tribes, and the cervid industry control CWD in farmed cervids by allowing the interstate movement only from certified herds considered to be low risk.
Currently, 30 States participate in the national CWD HCP: 29 have Approved Status and 1 has Provisional Approved Status. States that meet the CWD HCP requirements have Approved Status and States that do not meet CWD HCP program requirements but have developed a work plan and time frame with APHIS to complete those requirements have Provisional Approved Status.
In FY 2015, the program tested approximately 20,000 farmed cervids for CWD and identified eight new CWD positive farmed white-tailed deer herds – one in Utah, one in Pennsylvania, two in Ohio, two in Wisconsin, and two in Texas.
APHIS depopulated five of these herds (Pennsylvania, Utah, and one each in Wisconsin, Texas, and Ohio). Six elk herds in Colorado, four elk herds in Nebraska, one white-tailed deer herd in Wisconsin and one white-tailed deer herd in Texas remained in quarantine at the end of FY 2015.
APHIS also provided indemnity for and was the lead agency for the depopulation and disposal of four large CWD infected farmed cervid herds in Pennsylvania, Ohio, Utah, and Texas. In cooperation with the National Agricultural Statistics Service, APHIS conducted the first national study of the U.S. farmed-cervid industry in FY 2015. The study provides baseline industry statistics, a description of production practices and challenges, producer-reported disease occurrences, and an overview of health management and biosecurity practices.
2016 Explanatory Notes Animal and Plant Health Inspection Service
In FY 2014, the program tested approximately 20,000 farmed cervids for CWD. 
Two new CWD positive farmed white-tailed deer herds were identified – one in Pennsylvania and one in Wisconsin. 
The program depopulated the PA herd and two additional CWD positive herds in quarantine since FY 2012 in Iowa (white-tailed deer herd) and Minnesota (red deer herd). 
Six elk herds in Colorado, four elk herds in Nebraska, and one white-tailed deer in Wisconsin remained in quarantine at the end of FY 2014. 
There also are numerous CWD exposed herds that are epidemiologically linked to CWD positive herds that remain in State quarantine pending completion of the epidemiology investigations.
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APHIS provided indemnity for and was the lead agency for the depopulation and disposal of two large CWD infected farmed cervid herds in Iowa and Minnesota. 
APHIS also provided indemnity for and assisted with the 20-80 appraisal and depopulation of a CWD infected farmed cervid herd in Pennsylvania. 
APHIS also provided assistance to States with outbreak investigation, assessment of risk posed by infected or exposed animals, development of herd plans and continues to develop strategies for the purpose of controlling and managing CWD in farmed cervids.
2015 Explanatory Notes Animal and Plant Health Inspection Service
In FY 2013, the program tested approximately 18,100 farmed cervids for CWD, a fatal, degenerative disease that affects the central nervous system and lymphoid system of cervids. Through this routine surveillance, no new CWD cases were reported in farmed cervids in FY 2013. The last CWD positive herd was reported in FY 2012 in an Iowa white tail deer herd. Twelve positive herds remain (seven elk herds in Colorado, three elk herds in Nebraska, one white tail deer herd in Iowa, and one red deer herd in Minnesota).
2014 Explanatory Notes Animal and Plant Health Inspection Service
In 2007, the cervid industry in the United States included 5,600 deer farms and 1,900 elk farms with an economic value of $894 million that supported nearly 30,000 jobs.
APHIS’ main cervid activities are testing approximately 15,000 captive cervids for tuberculosis each year and supporting the chronic wasting disease (CWD) herd certification program (HCP). The joint tuberculosis (TB) and brucellosis proposed rule will represent significant changes to TB activities in captive cervids when implemented; it proposes to bring cervids into the regulatory program for brucellosis, as requested by stakeholders. As a result, surveillance will be enhanced and the number of captive cervids that are tested for TB annually is expected to increase. In 2014, APHIS will implement a survey to evaluate the effectiveness and impact of new APHIS regulations on the industry. Additionally, approval for a new diagnostic test for TB in captive cervids is expected to occur by FY 2013. The CWD HCP allows participating States to enroll herd owners
18-26
to meet minimum Federal standards to achieve and maintain a herd certification status. APHIS approves State applications for the national voluntary CWD herd certification program, conducts periodic reviews to ensure compliance, and supports confirmatory testing of presumptive CWD cases. 
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Without continued program funding, there would be a reduced preparedness, surveillance, and response to equine/cervid health issues that could increase the likelihood of disease spread resulting in larger and more serious disease outbreaks, lack of national standards leading to a patchwork of State level requirements which diminish interstate commerce, and loss in international credibility regarding U.S. animal health status. 
Approximately 59 percent of the Equine and Cervid Health funding will be used for salaries and benefits, less than 1 percent for cooperative agreements and programmatic contracts, and the remaining supports normal operating costs such as travel, supplies, rent and utilities. 
Reduce lower priority program activities (-$1.295 million) APHIS will reduce lower priority equine and cervid program activities in 2014, including eliminating Federal contributions for addressing CWD. 
CWD is a degenerative neurological illness affecting elk and deer (cervids) in North America. 
***> APHIS has determined that continued efforts to manage CWD are not practical and therefore considers this to be a low priority for the Agency. 
***> On August 13, 2012, the rule that established uniform standards for a voluntary Federal-State cooperative CWD HCP and interstate movement requirements became effective. Implementation of the interstate movement of cervids was implemented in December 2012. 
***> Many States have herd certification programs in place, and the incidence of CWD detections in farmed cervids is decreasing. 
***> With the regulatory framework in place, continued APHIS activity, while useful, is no longer essential. 
Stakeholders can continue to carry on program activities. The success of the voluntary HCP is based upon cooperation and shared responsibility among the Federal government and State and local interests. However, since these are local or regional disease spread issues, State and local governments are better positioned to take a more active role and to better anticipate and plan for local or regional needs. APHIS will continue to conduct higher priority equine and cervid health activities and address concerns when identified. APHIS will reassign staff years to other Equine and Cervid Health activities as practical and reduce the overall staff years by eliminating the positions when vacancies arise. Reduction in Agency-level operating expenses (-$66,000) A reduction of $66,000 is requested for this line item related to Agency-level cost savings measures and operating efficiencies. Please refer to second paragraph on page 18-18.
18-27
Pay Increase (+$15,000)
An increase of $15,000 for pay costs which includes $3,000 for annualization of the FY 2013 pay raise and $12,000 for the anticipated FY 2014 pay raise.
***> APHIS has determined that continued efforts to manage CWD are not practical and therefore considers this to be a low priority for the Agency. 
***> On August 13, 2012, the rule that established uniform standards for a voluntary Federal-State cooperative CWD HCP and interstate movement requirements became effective. Implementation of the interstate movement of cervids was implemented in December 2012.
***> Many States have herd certification programs in place, and the incidence of CWD detections in farmed cervids is decreasing. 
***> With the regulatory framework in place, continued APHIS activity, while useful, is no longer essential. 
***> 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.
APHIS USDA Captive CWD Herds Update by State March 2026
Updated March 2026
***> CWD Transmission To, Cattle, Pigs, Sheep, Primates, oh my!
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.
Meeting-book-final-version prion 2023 Prion 2023 Congress Organizing Committee and the NeuroPrion Association, we invite you to join us for the International Conference Prion2023 from 16-20 October 2023 in Faro, Portugal.
https://prion2023.org/wp-content/uploads/2023/10/Meeting-book-final-version2.pdf
https://web.archive.org/web/20250828201533/https://prion2023.org/wp-content/uploads/2023/10/Meeting-book-final-version2.pdf
https://www.researchgate.net/profile/Syed-Zahid-Shah/publication/378314391_Meeting-book-final-version_prion_2023/links/65d44dad28b7720cecdca95f/Meeting-book-final-version-prion-2023.pdf
***> 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
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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, Glenn Telling, Claudio Soto, 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.
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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.
https://journals.asm.org/doi/10.1128/mbio.01800-25
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.
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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
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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.
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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.
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.
TSS

posted by Terry S. Singeltary Sr. at 4:25 PM 0 Comments

Thursday, May 14, 2026

New Mexico CWD TSE Prion Confirmed Total To Date May 2026, Wild and Captive Cervid, Anyone’s Guess

 New Mexico CWD TSE Prion Confirmed Total To Date May 2026, Wild and Captive Cervid, Anyone’s Guess 

AS i have said countless times, about the great state of New Mexico, and the New Mexico Department of Game and Fish NMDGF, and NMDA et al, and the information about Chronic Wasting Disease CWD TSE Prion, that they put out to the public about CWD Surveillance, or the lack there from, Testing, sample sizes, confirmed positives to date, confirmed positives annually, locatons, info on animal, in a CWD Dashboard someone can read, in both free range and captive cervid is absolutely horrible, imho. it’s been that way. it’s like the NMDGF and NMDA don’t want the public to have easy access to this CWD TSE prion information, and that’s dangerous imo, you must educate the public about this CWD with all the facts and data, that is easily accessible…so, with that, i submit the following for the public from my files.

terry


As of March 2026, the New Mexico Department of Game and Fish (NMDGF) reported a cumulative total of 26 confirmed cases of Chronic Wasting Disease (CWD) in the state. Out of these, four cases were found in harvested elk.


https://wildlife.dgf.nm.gov/conservation/invasive-species-and-diseases/chronic-wasting-disease/


CWD Results


https://wildlife.dgf.nm.gov/download/cwd-results/?wpdmdl=48316


AI Overview

Based on reports from the New Mexico Department of Game and Fish (NMDGF) and wildlife experts, approximately 59 to 65 cumulative cases of Chronic Wasting Disease (CWD) have been identified in free-ranging deer and elk in New Mexico since it was first discovered in 2002. [1, 2]

https://wildlife.dgf.nm.gov/conservation/invasive-species-and-diseases/chronic-wasting-disease/


DEER MANAGEMENT NEW MEXICO DEPARTMENT OF GAME AND FISH


Prepared by Orrin Duvuvuei, Deer program Manager Updated May 2025


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Chronic Wasting Disease (CWD) is the biggest disease concern for New Mexico’s deer populations. CWD is a fatal neurological disease that affects deer, elk, and other members of the deer family (Family Cervidae). Because CWD is always fatal, it can negatively impact population growth when prevalence rates are high. CWD has been detected in GMUs 19, 28, 29, and 34, special restrictions apply for deer and elk harvested in these units. The Department continues to expand CWD testing throughout the state. For more information see this fact sheet on CWD developed by the WAFWA Mule Deer Working Group.


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Diseases and Parasites In most cases, disease by itself does not generally determine deer abundance, but stressors such as drought can exacerbate the impact of diseases in a population. When diseases are present in a population, they rarely cause large-scale deer die-offs; mortality events are typically smaller scale or productivity is reduced.


Chronic Wasting Disease (CWD) is the biggest disease concern for New Mexico’s deer populations. CWD is a fatal neurological disease that affects deer, elk, and other members of the deer family (Family Cervidae). Because CWD is always fatal, it can negatively impact population growth when prevalence rates are high. CWD has been detected in GMUs 19, 28, 29, and 34, special restrictions apply for deer and elk harvested in these units. The Department continues to expand CWD testing throughout the state. For more information see this fact sheet on CWD developed by the WAFWA Mule Deer Working Group.


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BIOLOGY – Deer in this DMZ are largely resident; they may make short seasonal movements in response to weather patterns or water and food distributions. If deer make seasonal movements, they will return to their home ranges when conditions become favorable. Aerial surveys are not conducted regularly in this DMZ. Thus, population trajectories are monitored using hunter harvest data. The Black Hills deer herd is considered stable. CWD has been detected a few miles from GMU 41 in Texas.


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BIOLOGY – Deer in the Guadalupe Mountains are year-round residents, but they might make short movements to take advantage of favorable conditions in this arid landscape. Hunter harvest data provides an index of population productivity. Deer densities and the resulting population size in the Guadalupe Mountains are considered low. CWD has been detected in GMUs 28 and 29.


BIOLOGY – Deer in the Sacramento Mountains DMZ are partially migratory. They will migrate out of high elevations during periods of high snowpack and return as the snow melts. In lower elevations, deer do not tend to migrate and are year-round residents. Overall, the Sacramento Mountains have good deer numbers, and densities can be higher in some pockets. The deer population is considered stable. CWD has been detected in GMU 34.


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BIOLOGY – The deer in the San Juan Basin DMZ are a mix of migratory, partially migratory, and resident deer. Deer in GMU 2B are predominately migratory; these deer migrate 40-70 miles from their high elevation summer range in Colorado to winter west of Jicarilla Apache tribal lands in GMU 2B. Migration starts in the middle of October each year regardless of snowpack, 46and the deer arrive on the winter range within ~14 days. Deer in GMU 9 are partially migratory; some of these deer will summer on Mount Taylor and move to lower elevations when snowpack is high. Deer in GMUs 2A, 2C, 7, and 10 are considered year-round residents. Although considered stable, the deer population in this DMZ is lower than historically reported. CWD has been detected in…


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BIOLOGY – Deer in the Southern Desert DMZ are year-round residents. However, they may make seasonal movements in response to monsoonal rain patterns, livestock use, or breeding behavior. Some of these movements might be substantial to escape unfavorable conditions, such as when water sources dry up. They typically return to their known ranges when conditions become favorable. Deer numbers in this area are largely influenced by the timing and amount of rainfall. As such, deer densities can be sporadic in these desert habitats, but good numbers can be found in pockets. The deer population in this DMZ is low but stable. CWD has been detected in GMU 19.


https://wildlife.dgf.nm.gov/download/new-mexico-deer-hunting-prospects/?wpdmdl=45001&refresh=699f46e7a03421772046055


NEW MEXICO EXPERT TO DISCUSS CHRONIC WASTING AND OTHER WILDLIFE DISEASES

By BEN NEARY

NMWF Conservation Director

ALBUQUERQUE -- A scientist who tracks chronic wasting and other animal diseases around the state will be the featured speaker at the New Mexico Wildlife Federation's Wildlife Wednesday event in July.

Dr. Kerry Mower, animal health specialist with the New Mexico Department of Game and Fish, has been tracking chronic wasting disease since it first turned up in some southern New Mexico herds in 2002.

These days, Mower also has been tracking the recent outbreak of rabbit hemorrhagic fever and serves on a state/federal task force on the lookout for signs that the coronavirus now sweeping the world as a global pandemic is spreading to wildlife populations.

Mower's Wildlife Wednesday presentation about his work on animal diseases will be livestreamed on Zoom starting at 5:30 p.m., July 8. To join the meeting, use this LINK. Meeting ID: 924 3162 5461.

Mower, who started working with the game department as a contract employee 30 years ago, holds a Ph.D. from Ohio State in animal science. In addition to tracking wildlife diseases, he typically gets involved when the department captures wildlife for transplanting or other reasons.

Chronic wasting, a contagious neurological disease that affects deer, elk and moose, was first discovered in New Mexico in the foothills of the Organ Mountains, near Las Cruces. Since then, it's spread to some areas of the Sacramento Mountains.

“Most of the cases right now are in Unit 28, which is the McGregor Range, the southern foothills of the Sacramento Mountains,” Mower said. “So it doesn’t seem to be spreading quickly, but the presence seems to be remaining fairly high, and consistently high on the McGregor Range.”

In New Mexico, CWD primarily turns up in free-ranging mule deer, Mower said. He said it also occurs in elk, but said the state has never detected it among animals in any of the roughly 25 private game farms in the state.

Scientists believe that the most common mode of transmission of chronic wasting among animals is nose-to-nose contact.

“And in some areas, if we have a high density, they can pick it up from the ground,” Mower said. “They can pick it up with contact from urine and fecal matter on the ground. There’s some evidence that it might be uptaken in plants, and that the infective agent may bind to the soil, and they can pick it up from the soil. But probably most common is nose-to-nose contact and ingestion of the agents that way.”

Most scientists think it’s unlikely hunters could contract CWD through handling, field dressing and processing an infected animal and eating its meat, Mower said.

“They say that based on the fact that there’s no known human case of transmission with this disease to humans. And we do know that large numbers of these infected animals have been consumed by humans probably since the 1960s,” Mower said. “Furthermore, there’s a disease in domestic sheep that is very similar, and there’s no known transmission of that disease to humans, with humans in contact with and eating sheep for over 400 years."

It probably would be possible to infect a human with CWD experimentally through a radical procedure such as injecting it into the person’s brain, Mower said. “And experimentally with this disease, they can move it from one species to another by injecting either the agent directly, or sometimes other forms of the infected agent. But it seems unlikely given the history that it could happen through casual contact. But then, like most things in biology and science, I’m never going to say never.”

To keep CWD from spreading, the game department has implemented carcass removal restrictions in areas where the disease occurs. Hunters are required to leave high-risk tissues such as the brain and spinal cord and bones in the field.

“So, when they leave, we’d like them to take the meat, but leave behind the tissues that are most likely to be contaminants in a new area,” Mower said. “We ask them really just to take skeletal muscle, the meat, out with them. They can take the skin, they can take antlers they can take the ivories out of elk. But if they take the skull cap, we’d like it cleaned out so that they’re removing just the antlers with the skull cap, leaving behind the rest of the skull and the brain.”

The prevalence of CWD doesn’t seem to be high enough anywhere in New Mexico to merit the removal of whole animal herd, Mower said. “On the McGregor Range, that might be an exception, but it would require probably removal of a large portion of those deer and it seems to be one of the more sought-after places to hunt," he said.

Especially when an animal is in the early stages of suffering from CWD, it’s not obvious to hunters that they have the disease.

“It will look just like the next one,” Mower said of an infected animal. “And most of the cases that we’ve dealt with that have come from hunters have been exactly that: no critical manifestations at all. But then we do make it a practice in our management that whenever we find a sick deer or elk, and we euthanize it, we test every one of them. So occasionally we do pick up an animal with the disease and it is obviously sick.”

During rifle hunting seasons, the NMGF keeps collection stations in the field in areas where the disease is known to occur.

“Hunters can take a head, where the brainstem is not damaged, and we’ll take those tissues and we’ll test all of them for hunters,” Mower said. “Alternatively, any hunter can take a head and present it at one of our area offices. We’ll take the head and test it. Beyond that, hunters can contact laboratory officials or their veterinarian, and have it done completely privately if they’d rather do that.”

The field test stations are only in game management units 34, 28 and 19, Mower said. “And I get a total number of tests every year that numbers around 400, and those are primarily voluntary. Out of all the tests I run, I get between two and four positive cases in any given year.”

Over all of the years of testing, Mower said the game department has found about 65 cases of the disease, of which all were in deer except for about seven or eight in elk.

The federal Centers for Disease Control CDC offers hunters tips to avoid CWD exposure. It advises that hunters shouldn’t shoot, handle or eat meat from an animal that looks sick or is acting strangely, or that’s found dead such as a roadkill.

When field-dressing an animal and handling the meat, the CDC advises hunters to wear latex or rubber gloves and to minimize handling the organs of the animal, particularly the brain or spinal cord tissues. It advises not to use household knives or other kitchen utensils for field dressing.

In addition to discussing CWD, Mower’s talk will address the recent occurrence of Rabbit Hemorrhagic Disease, which was discovered for the first time in wild rabbit populations this spring when wild rabbits started turning up dead in New Mexico.

People previously believed that the disease only occurred in domestic rabbits, Mower said. Since its discovery in New Mexico, it’s been discovered in Arizona, California, Colorado, Nevada and Texas, he said.

Mower also serves on a group of state and federal officials that focuses on the risk of COVID-19 spreading to wildlife. Other agencies involved in tracking the disease behind the ongoing worldwide pandemic include the federal Centers for Disease Control, the U.S. Geological Survey and U.S. Department of Agricultural, as well as livestock and wildlife agencies from New Mexico and other states.

The group is particularly concerned that COVD-19 could spread to bats in North America, Mower said. “We don't know that it has, but it would be bad if, all of a sudden, we had our North American bats serving as our reservoir for the virus to reinfect humans at a later time,” he said.

So far, COVID-19 has been found in various places to have infected domestic cats, as well as in a lion and tiger in a zoo, Mower said. “There are cases in the Netherlands of the virus moving into mink on mink ranches,” he said.

“The single thing that we have done here in New Mexico is we have declared a halt on all research and wildlife rehabilitation involving bats,” Mower said. “So we have tried from a regulatory standpoint to prevent human contact with bats, all except for one research project that was proposed and funded and that was to capture bats and monitor specifically for the sign of COVID virus in New Mexico populations.”

The New Mexico Wildlife Federation has staged its Wildlife Wednesday events at Marble Brewery's Northeast Heights location before the pandemic forced it to go to online presentations earlier this year.

WildlifeWildlife Disease


New Mexico Chronic Wasting Disease CWD  TSE Prion Confirmed CWD Results 2-15-2024

New Mexico Chronic Wasting Disease CWD TSE Prion Confirmed

CWD Results 2-15-2024

LICENSE # Results Obex Results Lymph Node

4807917 Detected Detected


2024*** PLEASE NOTE, New Mexico updated CWD results and information there from, to date, are extremely difficult to get out of New Mexico Wildlife et al. even more difficult from NM department of agriculture. IN fact, New Mexico wildlife.state.nm CWD page is terrible. woefully outdated. AS WELL, THE CWD confirmed cases to date is questionable imo., and their page is extremely outdate i.e. 2018, still holding at 59 confirmed cwd cases. IT'S 2024! i question that figure! SO, until otherwise, i don't believe there is a true cwd total count to date, in wild and captive cervid, that is available for the public. not one that i can find anyway. i believe that New Mexico and it's CWD surveillance to date is woefully lacking, and, there is no real accurate cwd data coming out of New Mexico, to date, imo...terry

Some Facts about CWD in New Mexico

CWD is the acronym for Chronic Wasting Disease

New Mexico Department of Game and Fish began testing suspect deer for CWD in the 1990’s

The first case of CWD in New Mexico was confirmed in 2002. This was a deer from Main Post on White Sands Missile Range

Since 2002, CWD has been detected in both free-ranging deer and elk

Found in Units 19, 28, and 34

In New Mexico, CWD has not been found in any Class A Game Park

Cumulative positive animals found with CWD in New Mexico since 2002 is 59 as of 1 January 2018 and includes:


New Mexico Chronic Wasting Disease CWD TSE Prion Cases Update May 2022

New Mexico Chronic Wasting Disease CWD TSE Prion Cases Update

New Mexico Most recent CWD results: CWD Results 03-22-2022

NM530 28 1541x22, 3927798 Detected

NM528 28 x552857 Detected

https://www.wildlife.state.nm.us/download/conservation/invasives-diseases/CWD-Results-03_22_2022.pdf

see archived link;


archived url ;


SUNDAY, AUGUST 15, 2021

New Mexico CWD TEST RESULTS: 1/19/2021 update

NM18-290 28 3418801 Detected

NM18-293 28 3446090 Detected

NM475 29 3460171 Detected

NM518 28 3464748 Detected

NM515 28 3500214 Detected

NM778 34 3510401 Detected


archived url;



Confirmed Cases of Chronic Wasting Disease in New Mexico 2002 to 2016

Confirmed Cases of Chronic Wasting Disease in New Mexico

GMU Collection Date Kill Date Location Tissue Species

19 June 1, 2002 June 1, 2002 WSMR main post (first CWD Positive in NM) CWD Area Deer

19 November 4, 2002 November 4, 2002 WSMR Main Post CWD Area Deer

19 November 12, 2002 November 12, 2002 WSMR Main Post CWD Area Deer

19 December 17, 2002 December 17, 2002 WSMR Main Post Tonsil Biopsy Deer

19 January 1, 2003 January 1, 2003 Organ Mtns. Hunter Harvest Deer

19 January 4, 2003 January 4, 2003 Dripping Springs Hunter Harvest Deer

19 November 14, 2003 November 14, 2003 WSMR MAIN POST CWD Area Deer

34 January 13, 2004 January 13, 2005 15 miles NE of Pinon CWD Suspect Deer

19 December 14, 2004 December 14, 2004 West Organs, W of Massey Tank Tonsil Biopsy Deer

19 December 14, 2004 December 14, 2004 West Organs, W of Dripping Spring Visitor Center Tonsil Biopsy Deer

19 April 5, 2005 April 5, 2005 WSMR - Tag # 482 Tonsil Biopsy Deer

19 April 11, 2005 WSMR, SW of Antelope Hill CWD Area Deer

19 April 15, 2005 April 15, 2005 SW of Dripping springs CWD Area Deer

34 June 6, 2005 June 5, 2005 Timberon CWD Suspect Deer

34 October 1, 2005 October 1, 2005 Hughes Canyon CWD Suspect Elk

34 October 3, 2005 October 3, 2005 Wayland Canyon Hunter Harvest Elk

19 December 10, 2005 Antelope Hill Tonsil Biopsy Deer

34 March 24, 2006 March 24, 2006 Timberon CWD Suspect Deer

19 April 21, 2006 April 21, 2006 N of sewage plant (Bishops Cap) CWD Area Deer

19 June 2, 2006 June 2, 2006 WSMR SW of Red Butte, Stallion range Found Dead Deer

34 August 12, 2006 August 12, 2006 Timberon CWD Area Deer

34 October 27, 2006 October 27, 2006 West of Pinon Hunter Harvest Deer

19 July 13, 2007 July 13, 2007 South of Bishop's Cap CWD Suspect Deer

28 October 14, 2007 October 14, 2007 Mc Gregor Hunter Harvest Deer

34 October 30, 2007 October 28, 2007 Unit 34 private land Hunter Harvest Deer

19 December 13, 2007 December 13, 2007 WSMR Main Post CWD Area Deer

28 October 12, 2008 October 12, 2008 McGregor Range Hunter Harvest Deer

28 October 13, 2008 October 12, 2008 McGregor Hunter Harvest Deer

34 October 29, 2008 October 25, 2008 Private land Hunter Harvest Deer

34 March 2, 2009 March 1, 2009 Rio Penasco CWD Suspect Elk

34 December 6, 2009 December 6, 2009 Wills Canyon CWD Suspect Elk

28 May 9, 2010 CWD Area Deer

28 October 10, 2010 October 10, 2010 McGregor Range Hunter Harvest Deer

28 November 17, 2010 November 17, 2010 McGregor CWD Area Deer

34 November 27, 2010 November 27, 2010 Lookout Station Hunter Harvest Elk

28 March 12, 2011 March 12, 2011 McGregor CWD Area Deer

28 March 13, 2011 March 13, 2011 McGregor CWD Area Deer

28 March 13, 2011 March 13, 2011 McGregor CWD Area Deer

28 October 9, 2011 October 9, 2011 McGregor Range Hunter Harvest Deer

28 October 9, 2011 October 9, 2011 McGregor Range South Hunter Harvest Deer

28 October 10, 2011 October 9, 2011 McGregor Range Hunter Harvest Deer

28 February 17, 2012 February 17, 2012 McGregor Rectal Biopsy Deer

28 February 18, 2012 February 18, 2012 McGregor Rectal Biopsy Deer

34 October 27, 2012 October 27, 2012 Timberon Hunter Harvest Deer

28 October 5, 2013 October 5, 2013 McGregor Hunter Harvest Deer

28 December 11, 2013 December 9, 2013 McGregor Hunter Harvest Elk

28 December 11, 2013 December 11, 2013 McGregor Hunter Harvest Elk

28 December 11, 2013 December 11, 2013 McGregor Hunter Harvest Elk

19 February 12, 2014 February 12, 2014 NASA CWD Suspect Deer

19 April 6, 2014 April 5, 2014 East of Las Cruces CWD Suspect Deer

28 November 21, 2015 November 21, 2015 McGregor Range Deer

28 November 21, 2015 November 21, 2015 McGregor Range Hunter Harvest Deer

28 November 21, 2015 December 21, 2015 McGregor Range Hunter Harvest Deer

28 November 22, 2015 November 21, 2015 McGregor Range Hunter Harvest Deer

28 November 22, 2015 November 22, 2015 McGregor Range Hunter Harvest Deer

28 November 27, 2016 November 26, 2016 McGregor Range Hunter Harvest Deer

28 November 27, 2016 November 27, 2016 McGregor Range Hunter Harvest Deer

28 December 12, 2016 December 12, 2016 McGregor Range Hunter Harvest Elk

Showing 1 to 58 of 58 entries



here's one i can't even find on NM web site from 2023;

2023

New Mexico Confirms CWD In Mule Deer

The New Mexico Department of Game and Fish (NMDGF) has informed Texas officials that three mule deer harvested a few miles from the Texas border last hunting season have tested positive for Chronic Wasting Disease (CWD).

The deer were harvested in the Hueco Mountains, which extend into Texas northeast of El Paso in Hudspeth County. New Mexico has been monitoring annually for CWD since it was first discovered 10 years ago and this event is the closest to Texas that the disease has been detected.

Texas also has had an active CWD-surveillance program for the past decade, and CWD has not yet been detected in the state. However, state wildlife officials have been preparing for the possibility since 2002. 

“While this finding is not a big surprise, we’re not going to ignore it,” said Mitch Lockwood, Big Game Program Director for the Texas Parks and Wildlife Department. “We are working with TPWD’s Wildlife Health Working Group to develop a more intensive strategy for sampling, and to determine the geographical extent of the disease if it is detected in Texas.”

The Wildlife Health Working Group is comprised of wildlife biologists, veterinarians and other animal-health experts from TPWD, Texas Animal Health Commission, Department of State Health Services, Texas A&M College of Veterinary Medicine, and USDA. NMDGF is also involved in the discussion.

While several thousand deer have been tested for CWD in Texas, wildlife officials express concern that the Trans Pecos region is underrepresented because of the very low number of deer and the relatively low deer harvest in that region. Samples are obtained from hunter-harvested deer, deer found dead on public roadways, and deer showing clinical symptoms.

TPWD is determining how many more deer need to be sampled and deer hunters in the region could be asked for their assistance during the next hunting season. “We are using disease models to determine the intensity of sampling that would be required to detect CWD in that deer population if it is present with a prevalence of at least two percent,” said Ryan Schoeneberg, Big Game Program Specialist with TPWD.

CWD was first recognized in 1967 in captive mule deer in Colorado and has also been documented in captive and/or free-ranging deer in nearly two dozen states and Canadian provinces, including New Mexico. Although fatal in deer, there is no evidence that CWD poses a risk to humans or livestock in the natural environment.

CWD is a member of the group of diseases called transmissible spongiform encephalopathies (TSEs). Other diseases in this group include scrapie in sheep and goats, bovine spongiform encephalopathy (BSE or mad cow disease) in cattle, and Cruetzfeldt-Jakob disease in people. CWD is a progressive, fatal disease that affects deer, elk, moose, and other cervid species and there is no vaccine or other biological method that prevents it. “It would be almost impossible to eradicate the disease once it becomes established in a population,” said Lockwood. “But, what we can do is manage the disease and minimize the risk of it spreading.”


From: TSS

Subject: CWD TWO NEW CASES NEAR WHITE SANDS MISSLE RANGE NEW MEXICO

Date: June 27, 2005 at 4:43 pm PST

New Mexico Department of Game and Fish

Contact: Dan Williams, (505) 476-8004

dan.williams@state.nm.us

FOR IMMEDIATE RELEASE, JUNE 24, 2005:

TWO MULE DEER TEST POSITIVE FOR CHRONIC WASTING DISEASE

ANGLER LANDS STATE RECORD BLUE CATFISH AT ELEPHANT BUTTE LAKE

TWO MULE DEER TEST POSITIVE FOR CHRONIC WASTING DISEASE

SANTA FE – Two mule deer captured in the Organ Mountains as part of an ongoing research project near White Sands Missile Range have tested positive for chronic wasting disease (CWD), a fatal neurological disease that attacks the brains of infected deer and elk, the Department of Game and Fish announced.

The number of confirmed CWD cases in New Mexico now stands at 11 since 2002, when the disease was first confirmed in a deer found near the eastern foothills of the Organ Mountains.

All 11 CWD-infected deer were found in the same general area of southern New Mexico.

The origin of the disease in New Mexico remains unknown.

The carcasses of the infected deer will be incinerated, said Kerry Mower, the Department’s lead wildlife disease biologist.

Chronic wasting disease causes animals to become emaciated, display abnormal behavior, lose bodily functions and die.

The disease has been found in wild deer and elk, and in captive deer and elk, in eight states and two Canadian provinces.

There currently is no evidence of CWD being transmitted to humans or livestock.

Mower said the most recent CWD-positive deer showed no obvious physical signs of having the disease.

They were captured in April 2005 and tested as part of a 3-year-old research project studying deer population dynamics in southern New Mexico.

More than 140 deer have been captured alive and tested for the study, in which researchers hope to find the cause of a 10-year decline in the area deer population.

Study participants include the Department of Game and Fish, the U.S. Army at White Sands Missile Range and Fort Bliss, Bureau of Land Management, U.S. Geological Survey at New Mexico State University, and San Andres National Wildlife Refuge.

Hunters can assist the Department in its CWD research and prevention efforts by bringing their fresh, legally harvested deer or elk head to an area office, where officers will remove the brain stem for testing. Participants will be eligible for drawings for an oryx hunt on White Sands Missile Range and a trophy elk hunt on the Valle Vidal. For more information about the drawing and chronic wasting disease, visit the Department web site at www.wildlife.state.nm.us.


archived url;


SEE MAP ;


archived url;


New Mexico Captive Deer


Greetings list members,

I am deeply concerned with these CWD mad deer so close to the Texas border. WHAT keeps them from crossing the border to Texas ??? IF these illegal aliens can so easily cross our borders, why not these infected deer? maybe we should get these minute men to start watching for mad deer coming in to Texas from New Mexico.

I mentioned my concerns several other times before;

-------- Original Message --------

Subject: Current status of CWD testing in Texas

Date: Tue, 10 May 2005 09:09:47 -0500

From: "kschwaus"

To:

Mr. Singeltary,

I was asked to provide you with the following information. If you have any other questions regarding CWD sampling in Texas, please do not hesitate to give me a call. My office number is below.

Below I have included a chart showing CWD samples that have been tested since the fall of 2002 through the present at the eco-region level. The second chart shows the totals on a given year. The unknown location samples come from private individuals sending in samples directly to the Texas Veterinary Medical Diagnostic Lab (TVMDL). Due to the confidentiality laws that the TVMDL operates under, they are unable to provide TPWD with the location of those samples.

Region Population Estimate

Sampling from Fall 2002 to Present

snip...

===============================

I would like to thank Kevin and TPWD for there prompt reply with updated data.

I am still concerned about the Texas, New Mexico border and New Mexico's apparent lack of CWD testing updates. Makes one wonder about there CWD testing program. NO report/reply back from New Mexico about there CWD testing update yet. ...

TSS

===================

MONDAY, MARCH 21, 2022

New Mexico Chronic Wasting Disease CWD TSE PrP Confirmed February 2022


SUNDAY, AUGUST 15, 2021

New Mexico CWD TEST RESULTS 1/19/2021 update


FRIDAY, FEBRUARY 08, 2019

New Mexico Chronic Wasting Disease CWD TSE Prion Update 2018-2019?


WEDNESDAY, FEBRUARY 07, 2018

New Mexico Bans All Live Cervid Importation Due To CWD TSE Prion still NO Final 2017 Positives Update for N.M.


THURSDAY, NOVEMBER 02, 2017

New Mexico Chronic Wasting Disease CWD Figures 2016 - 2017 Update ???

The great state of New Mexico has been notorious for keeping information about Chronic Wasting Disease CWD TSE prion aka Mad Deer Disease outdated and pretty much to themselves. urls to map links on cwd zones and such are not working anymore, that i can find. seems they are being mum again. so, i must give an outdated update as well, but here is what i have to date...


THURSDAY, SEPTEMBER 22, 2016

New Mexico CWD confirmed in 5 McGregor Range deer during the 2015-16 hunting season


WEDNESDAY, MARCH 25, 2015

Chronic Wasting Disease CWD Cases Confirmed In New Mexico 2013 and 2014 UPDATE 2015


MONDAY, SEPTEMBER 17, 2012

New Mexico DGF EXPANDS CHRONIC WASTING DISEASE CONTROL AREAS, while Texas flounder


Monday, March 26, 2012

3 CASES OF CWD FOUND NEW MEXICO MULE DEER SEVERAL MILES FROM TEXAS BORDER


SUNDAY, OCTOBER 04, 2009

CWD NEW MEXICO SPREADING SOUTH TO TEXAS 2009


MONDAY, FEBRUARY 11, 2013

TEXAS CHRONIC WASTING DISEASE CWD Four New Positives Found in Trans Pecos


Tuesday, July 10, 2012

Chronic Wasting Disease Detected in Far West Texas



***> TEXAS HISTORY OF CWD <***

Singeltary telling TAHC, that CWD was waltzing into Texas from WSMR around Trans Pecos region, starting around 2001, 2002, and every year, there after, until New Mexico finally shamed TAHC et al to test where i had been telling them to test for a decade. 2012 cwd was detected first right there where i had been trying to tell TAHC for 10 years. 

***> Singeltary on Texas Chronic Wasting Disease CWD TSE Prion History <***



***> CWD Transmission To, Cattle, Pigs, Sheep, Primates, oh my! <***

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.

Meeting-book-final-version prion 2023 Prion 2023 Congress Organizing Committee and the NeuroPrion Association, we invite you to join us for the International Conference Prion2023 from 16-20 October 2023 in Faro, Portugal.

https://prion2023.org/wp-content/uploads/2023/10/Meeting-book-final-version2.pdf

https://web.archive.org/web/20250828201533/https://prion2023.org/wp-content/uploads/2023/10/Meeting-book-final-version2.pdf

https://www.researchgate.net/profile/Syed-Zahid-Shah/publication/378314391_Meeting-book-final-version_prion_2023/links/65d44dad28b7720cecdca95f/Meeting-book-final-version-prion-2023.pdf

***> 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

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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.


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.



***> ENVIRONMENTAL FACTORS AND CHRONIC WASTING DISEASE CWD AND OR SCRAPIE <***

Chronic wasting disease prions on deer feeders and wildlife visitation to deer feeding areas

Miranda H. J. Huang, Steve Demarais, Marc D. Schwabenlander, Bronson K. Strickland, Kurt C. VerCauteren, William T. McKinley, Gage Rowden, Corina C. Valencia Tibbitts … See all authors

First published: 10 February 2025

https://doi.org/10.1002/jwmg.70000

Snip…

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.

Snip…

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.

https://wildlife.onlinelibrary.wiley.com/doi/10.1002/jwmg.70000

Chronic wasting disease (CWD) prion detection in environmental and biological samples from a taxidermy site and nursing facility, and instruments used in surveillance activities

Paulina Soto a b , Nancy Ho a , Mitch Lockwood c , Austin Stolte c , J. Hunter Reed c , Rodrigo Morales a b

Received 20 September 2024, Revised 27 February 2025, Accepted 31 March 2025, Available online 9 April 2025, Version of Record 9 April 2025.

Cite https://doi.org/10.1016/j.scitotenv.2025.179318

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 this study, we evaluated the presence of CWD prions in a taxidermy facility where deer heads are processed to prepare skull mounts. Analyses were made using the protein misfolding cyclic amplification (PMCA) technique in various biological and environmental samples. In addition, we also tested the persistence of CWD prions in surgical materials used in surveillance procedures. Our results show, for the first time, CWD-prion detection in a potentially exposed taxidermy facility. In addition, we also tested the persistence of CWD prions in surgical materials used in surveillance procedures. This information has important implications on several fronts of CWD research including environmental spreading, human-related practices, and exposure of humans to infectious animal prions.

Section snippets

Samples

The samples were collected from a taxidermy and free-ranging deer rehabilitation facility located on the same property in Val Verde County, Texas. Texas Parks and Wildlife Department (TPWD) staff were initially notified of a CWD clinical suspect on this property; this animal was ultimately euthanized and confirmed positive for CWD by the National Veterinary Services Laboratory on January 5th, 2020. Samples were collected from different areas on this property where deer heads were processed to Screening of CWD prions in environmental and processing elements from a taxidermy facility

The European mount technique is a widely utilized taxidermy practice aiming to produce a skull of an animal that is free of tissue. The first critical step in making a European mount is removing the flesh from the animal's head. This is achieved by removing the majority of the external flesh, eyeballs, ears, and the brain. Then, the de-meated skull is subjected to a maceration process using bacteria. The purpose of this step is to soften and degrade any remaining tissue on the skull. This Discussion

CWD continues expanding in distribution and prevalence in North America. Hence, an essential factor in limiting the spread of this disease is to monitor and contain infectivity foci. This has proven to be difficult considering the limited diagnostic tools available to effectively identify the CWD infectious agent (prions). Identifying and mitigating the negative role that anthropogenic activities have in promoting CWD transmission is an essential step in developing a prevention strategy. The Conclusion

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. …

https://www.sciencedirect.com/science/article/abs/pii/S0048969725009544

Chronic wasting disease detection in environmental and biological samples from a taxidermy site

Paulina Sotoa,b, J. Hunter Reedc, Mitch Lockwoodc, and Rodrigo Moralesa,b aDepartment of Neurology, McGovern Medical School, University of Texas Health Science Center at Houston, Texas, USA; bUniversidad Bernardo O’Higgins, Santiago, Chile; cTexas Parks and Wildlife Department, Texas, USA

Chronic wasting disease (CWD) is a transmissible spongiform encephalopathy affecting captive and free-ranging cervids (e.g., mule deer, white-tailed deer, elk, reindeer, and moose). Nowadays, CWD is widely distributed in North America. It is suggested that CWD spreads due to direct animal contact or through exposure to contaminated environments previously inhabited by infected animals. CWD may also be spread through the movement of infected animals and carcasses. Taxidermy practices involve processing deer tissues (or whole animal carcasses). In many cases, the CWD status of processed animals is unknown. This can generate risks of disease spread and transmission. Taxidermy practices include different steps involving physical, chemical, and biological procedures. Without proper tissue handling or disposal practices, taxidermist facilities may become a focus of prion infectivity.

Aims: In this study, we evaluated the presence of infectious prions in a taxidermy facility believed to be exposed to CWD. Detection was performed using the Protein Misfolding Cyclic Amplification (PMCA) technique in biological and inert environmental samples.

Methods: We collected biological and environmental samples (plants, soils, insects, excreta, and others) from a taxidermy facility, and we tested these samples using the PMCA technique. In addition, we swabbed different surfaces possibly exposed to CWD-infected animals. For the PMCA reaction, we directly used a swab piece or 10 µL of 20% w/v homogenized samples.

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.

Funded by: USDA Grant number: AP20VSSPRS00C143

PRION 2022 ABSTRACTS, AND A BIG THANK YOU TO On behalf of the Prion2020/2022 Congress Organizing Committee and the NeuroPrion Association, we heartily invite you to join us for the International Conference Prion2020/2022 from 13.-16. September 2022 in Göttingen.

Prion 2022 Conference abstracts: pushing the boundaries

https://www.tandfonline.com/doi/full/10.1080/19336896.2022.2091286

Artificial mineral sites that pre-date endemic chronic wasting disease become prion hotspots

Heather N'te Inzalaco1,1, Marie L. Gilbertson1, Stephanie J. Katircioglu1, Kenny Lepard2, Jordan McEarl2, Austin Bibb2, Jeremy Dennison2, Dan Grove3, Allen Houston4, Dan J. Storm5, Dan P. Walsh6, Wendy C. Turner7, Stuart S. Lichtenberg8 1Wisconsin Cooperative Wildlife Research Unit, Department of Forest and Wildlife Ecology, University of Wisconsin, Madison, Madison, USA. 2Tennessee Wildlife Resources Agency, Jackson, USA. 3University of Tennessee Extension, Nashville, USA. 4University of Tennessee -Knoxville, School of Forest, Wildlife, and Fisheries, Ames Research and Education Center, Grand Junction, USA. 5Wisconsin Department of Natural Resources, Eau Claire, USA. 6U.S. Geological Survey, Montana Cooperative Wildlife Research Unit, Department of Ecosystem and Conservation Sciences, University of Montana, Missoula, USA. 7U.S. Geological Survey, Wisconsin Cooperative Wildlife Research Unit, Department of Forest and Wildlife Ecology, University of Wisconsin – Madison, Madison, USA. 8Department of Veterinary and Biomedical Sciences, University of Minnesota, Minnesota, USA

Abstract

Chronic wasting disease (CWD) is a highly contagious, fatal neurodegenerative disease caused by infectious prions (PrPCWD) affecting wild and captive cervids. As CWD continues to spread broadly over North America, factors influencing geographic expansion remain poorly understood. CWD-infected cervids shed infectious prions in urine, feces, and saliva. Activities that result in cervids aggregating and shedding PrPCWD may result in ‘hot spots’ of environmental PrPCWD deposition, however empirical data regarding the impact of deer attractants on environmental PrPCWD deposition is lacking. Filling this knowledge gap could inform deer and disease management. In 2018, the southwest region of Tennessee, U.S.A. experienced a CWD outbreak. 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.

https://intcwdsympo.files.wordpress.com/2023/06/final-agenda-with-abstracts.pdf

Shedding of Chronic Wasting Disease Prions in Multiple Excreta Throughout Disease Course in White-tailed Deer

Nathaniel D. Denkersa, Erin E. McNultya, Caitlyn N. Krafta, Amy V. Nallsa, Joseph A. Westricha, Wilfred Goldmannb, Candace K. Mathiasona, and Edward A. Hoovera

aPrion Research Center, College of Veterinary Medicine and Biological Sciences, Department of Microbiology, Immunology, and Pathology; Colorado State University, Fort Collins, CO, USA; bDivision of Infection and Immunity, The Roslin Institute and the Royal Dick School of Veterinary Studies, University of Edinburgh, Midlothian, UK

Aims: Chronic wasting disease (CWD) now infects cervids in South Korea, North America, and Scandinavia. CWD is unique in its efficient transmission and shedding of prions in body fluids throughout long course infections. Questions remain as to the magnitude of shedding and the route of prion acquisition. As CWD continues to expand, the need to better understand these facets of disease becomes more pertinent. The purpose of the studies described was to define the longitudinal shedding profile of CWD prions in urine, saliva, and feces throughout the course of infection in white-tailed deer.

Material and Methods: Twelve (12) white-tailed deer were inoculated with either 1 mg or 300ng of CWD. Urine, saliva, and feces were collected every 3-month post-inoculation (MPI) throughout the study duration. Cohorts were established based on PNRP genotype: codon 96 GG (n = 6) and alternate codons 96 GS (n = 5) & 103NT (n = 1). Urine and saliva were analyzed using iron-oxide magnetic extraction (IOME) and real-time quaking induced conversion (RT-QuIC)(IQ). Feces were subjected to IOME, followed by 4 rounds protein misfolding cyclic amplification (PMCA) with products analyzed by RT-QuIC (IPQ). To determine whether IPQ may be superior to IQ, a subset of urine and saliva were also tested by IPQ. Results were compared with clinical disease status.

Results: Within the 96 GG cohort, positive seeding activity was detected in feces from all deer (100%), in saliva from 5 of 6 (83%), and in urine from 4 of 6 (66%). Shedding in all excreta occurred at, or just after, the first positive tonsil biopsy result. In the 96 GS/103NT cohort, positive seeding activity could be detected in feces from 3 of 6 (50%) deer, saliva in 2 of 6 (33%), and urine in 1 of 6 (16%). Shedding in excreta was detected >5 months after the first tonsil positive result. Four of six 96 GG deer developed clinical signs of CWD, whereas only 2 of the 96 GS/103NT did. Shedding was more frequently detected in deer with clinical disease. The IPQ protocol did not significantly improve detection in saliva or urine samples, however, it significantly augmented detection in feces by eliminating non-specific background commonly experienced with IQ. Negative control samples remained negative in samples tested.

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.

Funded by: National Institutes of Health (NIH)

Grant number: RO1-NS061902-09 R to EAH, PO1-AI077774 to EAH, and R01-AI112956-06 to CKM

Acknowledgement: We abundantly thank Sallie Dahmes at WASCO and David Osborn and Gino D’Angelo at the University of Georgia Warnell School of Forestry and Natural Resources for their long-standing support of this work through provision of the hand-raised, CWD-free, white-tailed deer used in these studies…snip

End

PRION 2022 ABSTRACTS, AND A BIG THANK YOU TO On behalf of the Prion2020/2022 Congress Organizing Committee and the NeuroPrion Association, we heartily invite you to join us for the International Conference Prion2020/2022 from 13.-16. September 2022 in Göttingen.

Prion 2022 Conference abstracts: pushing the boundaries

https://www.tandfonline.com/doi/full/10.1080/19336896.2022.2091286

Research Paper Prion forensics: a multidisciplinary approach to investigate CWD at an illegal deer carcass disposal site​

Pages 72-86 | Received 15 Jan 2024, Accepted 10 Apr 2024, Published online: 26 Apr 2024

https://www.tandfonline.com/doi/full/10.1080/19336896.2024.2343298#d1e740

Characterizing Hydrological Transport Pathways of Chronic Wasting Disease in the Environment

Authors Anu Wille, Diana L Karwan, Stuart Siegfried Lichtenberg, Madeline Grunklee, Gage Rowden, Victoria Ferguson-Kramer, Marc D Schwabenlander, Tiffany M Wolf, Peter A Larsen Publication date 2024/6 Journal Water Science Conference (WaterSciCon24 Pages 110-04

Description Chronic wasting disease (CWD) is a fatal neurodegenerative prion disease found in deer, moose, and elk. Cases of CWD in Minnesota have risen considerably over the last few years, raising wildlife, environmental, and public health concerns.

Infectious prions, such as those causing CWD, enter the environment through bodily fluids or decomposing carcasses of infected individuals and can persist for at least fifteen years in soil and water.

Previous studies have shown strong prion sorption to various mineral particles in soils.

Through field observation and laboratory experimentation, we observed that prions readily partition to the particulate fraction of environmental waters, suggesting that hydrological transport of prions is likely sediment-facilitated.

To effectively contain the spread of CWD through the environment, it is imperative to predict prion transport times and pathways in the context of specific landscape and … 

Scholar articles Characterizing Hydrological Transport Pathways of Chronic Wasting Disease in the Environment

A Wille, DL Karwan, SS Lichtenberg, M Grunklee… - Water Science Conference (WaterSciCon24, 2024 Related articles

https://scholar.google.com/citations?view_op=view_citation&hl=en&user=cVqWACIAAAAJ&cstart=20&pagesize=80&citation_for_view=cVqWACIAAAAJ:0EnyYjriUFMC

Characterizing Hydrological Transport Pathways of Chronic Wasting Disease in the Environment

Wille, Anu search by orcid.svg ; Karwan, Diana L. search by orcid.svg ; Lichtenberg, Stuart Siegfried ;Grunklee, Madeline ; Rowden, Gage ; Ferguson-Kramer, Victoria ;Schwabenlander, Marc D. ; Wolf, Tiffany M. ; Larsen, Peter A.

https://ui.adsabs.harvard.edu/abs/2024wsc..conf11004W/abstract

https://agu.confex.com/agu/hydrology24/meetingapp.cgi/Paper/1502243

Characterizing Hydrological Transport Pathways of Chronic Wasting Disease in the Environment

Wille, Anu search by orcid ; Karwan, Diana L. search by orcid ; Lichtenberg, Stuart Siegfried ; Grunklee, Madeline ; Rowden, Gage ; Ferguson-Kramer, Victoria ; Schwabenlander, Marc D. ; Wolf, Tiffany M. ; Larsen, Peter A.

Abstract Chronic wasting disease (CWD) is a fatal neurodegenerative prion disease found in deer, moose, and elk. Cases of CWD in Minnesota have risen considerably over the last few years, raising wildlife, environmental, and public health concerns. Infectious prions, such as those causing CWD, enter the environment through bodily fluids or decomposing carcasses of infected individuals and can persist for at least fifteen years in soil and water. Previous studies have shown strong prion sorption to various mineral particles in soils. Through field observation and laboratory experimentation, we observed that prions readily partition to the particulate fraction of environmental waters, suggesting that hydrological transport of prions is likely sediment-facilitated. To effectively contain the spread of CWD through the environment, it is imperative to predict prion transport times and pathways in the context of specific landscape and watershed conditions. Our purpose is to characterize the hydrological transport of prions through watersheds at multiple scales. Through spatial analysis, we mapped surface flow pathways from CWD hotspots in Minnesota to identify how they overlap with major rivers and regions of high soil erosion. Based on in-stream measurements and sediment characterization, we used empirical equations to predict sediment mobilization conditions and transport rates in CWD-contaminated regions with diverse flow regimes. In order to model subsurface prion transport, we began conducting flow-through column experiments testing various flow rates and soil matrices.

Publication: Water Science Conference (WaterSciCon24), held in St. Paul, Minnesota, 24-27 June 2024, Session: Learning from observations / Catchment and Critical Zone Science - Understanding Ecosystems through Monitoring, Analysis, and Experimentation III Oral (Coupled Workshop: 231), id. 110-04. Pub Date: June 2024

https://ui.adsabs.harvard.edu/abs/2024wsc..conf11004W/abstract

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.

2024 archived link


2026 new link with new wording, based on same science, see cwd zoonosis risk factors below…terry

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

https://wwwnc.cdc.gov/eid/article/31/2/24-0903-app1.pdf

https://wwwnc.cdc.gov/eid/article/31/2/24-0903_article

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.

https://wwwnc.cdc.gov/eid/article/31/2/24-0906_article

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

https://web.archive.org/web/20250828201533/https://prion2023.org/wp-content/uploads/2023/10/Meeting-book-final-version2.pdf

https://www.researchgate.net/profile/Syed-Zahid-Shah/publication/378314391_Meeting-book-final-version_prion_2023/links/65d44dad28b7720cecdca95f/Meeting-book-final-version-prion-2023.pdf

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.

https://intcwdsympo.files.wordpress.com/2023/06/final-agenda-with-abstracts.pdf?force_download=true

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

=====

https://intcwdsympo.files.wordpress.com/2023/06/final-agenda-with-abstracts.pdf?force_download=true

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

https://web.archive.org/web/20250828201533/https://prion2023.org/wp-content/uploads/2023/10/Meeting-book-final-version2.pdf

https://www.researchgate.net/profile/Syed-Zahid-Shah/publication/378314391_Meeting-book-final-version_prion_2023/links/65d44dad28b7720cecdca95f/Meeting-book-final-version-prion-2023.pdf

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.”

=================================

Supplementary Information The online version contains supplementary material available at

https://doi.org/10.1007/s00401-022-02482-9

snip...see full text;

https://link.springer.com/article/10.1007/s00401-022-02482-9

https://link.springer.com/content/pdf/10.1007/s00401-022-02482-9.pdf

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.

https://www.tandfonline.com/doi/full/10.1080/19336896.2022.2091286

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

Snip…

***> 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

=====

https://intcwdsympo.files.wordpress.com/2023/06/final-agenda-with-abstracts.pdf?force_download=true

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

https://www.tandfonline.com/doi/full/10.1080/19336896.2024.2424058

“ After adaptation in this host, moose CWD prions were able to transmit in mice expressing either bovine or human PrPC with high efficacy.”

“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

Thursday, April 03, 2008

A prion disease of cervids: Chronic wasting disease 2008 1: Vet Res. 2008 Apr 3;39(4):41 A prion disease of cervids: Chronic wasting disease Sigurdson CJ.

snip...

*** twenty-seven CJD patients who regularly consumed venison were reported to the Surveillance Center, however there have been no unusual or novel prion subtypes that might indicate the appearance of a new prion strain [7, 41].

snip... full text ;

https://www.vetres.org/articles/vetres/abs/2008/04/v08092/v08092.html

https://chronic-wasting-disease.blogspot.com/2008/04/prion-disease-of-cervids-chronic.html

“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 ############

*** These results would seem to suggest that CWD does indeed have zoonotic potential, at least as judged by the compatibility of CWD prions and their human PrPC target. Furthermore, extrapolation from this simple in vitro assay suggests that if zoonotic CWD occurred, it would most likely effect those of the PRNP codon 129-MM genotype and that the PrPres type would be similar to that found in the most common subtype of sCJD (MM1).***

http://www.tandfonline.com/doi/full/10.4161/pri.28124?src=recsys

http://www.tandfonline.com/doi/pdf/10.4161/pri.28124?needAccess=true

https://wwwnc.cdc.gov/eid/article/20/1/13-0858_article

Two Hunters from the Same Lodge Afflicted with Sporadic CJD: Is Chronic Wasting Disease to Blame?

(P7-13.002) Jonathan Trout, Matthew Roberts, Michel Tabet, Eithan Kotkowski, and Sarah HornAUTHORS INFO & AFFILIATIONS April 9, 2024 issue 102 (17_supplement_1) https://doi.org/10.1212/WNL.0000000000204407

Abstract Publication History Information & Authors Metrics & Citations Share Abstract

Objective:

This study presents a cluster of Creutzfeldt-Jakob disease (CJD) cases after exposure to chronic wasting disease (CWD)-infected deer, suggestive of potential prion transmission from CWD-infected deer to humans.

Background:

CJD is a rapidly progressive central nervous system disorder caused by misfolded prion proteins. CWD, a prion disease prevalent in North American deer, has raised concerns due to its possible link to CJD. Although no conclusive evidence of cross-species prion transmission exists, vigilance for such cases is crucial for public health.

Design/Methods:

Not applicable.

Results:

In 2022, a 72-year-old man with a history of consuming meat from a CWD-infected deer population presented with rapid-onset confusion and aggression. His friend, who had also eaten venison from the same deer population, recently died of CJD, raising concerns about a potential link between CWD and human prion disease. Despite aggressive symptomatic treatment of seizures and agitation, the patient’s condition deteriorated and he died within a month of initial presentation. The diagnosis was confirmed postmortem as sporadic CJD with homozygous methionine at codon 129 (sCJDMM1). The patient’s history, including a similar case in his social group, suggests a possible novel animal-to-human transmission of CWD. Based on non-human primate and mouse models, cross-species transmission of CJD is plausible. Due to the challenge of distinguishing sCJDMM1 from CWD without detailed prion protein characterization, it is not possible to definitively rule out CWD in these cases. Although causation remains unproven, this cluster emphasizes the need for further investigation into the potential risks of consuming CWD-infected deer and its implications for public health.

Conclusions:

Clusters of sporadic CJD cases may occur in regions with CWD-confirmed deer populations, hinting at potential cross-species prion transmission. Surveillance and further research are essential to better understand this possible association.

Disclosure: Mr. Trout has nothing to disclose. Dr. Roberts has nothing to disclose. Dr. Tabet has nothing to disclose. Dr. Kotkowski has nothing to disclose. Dr. Horn has received personal compensation in the range of $500-$4,999 for serving as a Consultant for Cala Trio. The institution of Dr. Horn has received research support from Alzheimer's Association.

https://www.neurology.org/doi/abs/10.1212/WNL.0000000000204407

TUESDAY, MAY 11, 2021

A Unique Presentation of Creutzfeldt-Jakob Disease in a Patient Consuming Deer Antler Velvet

Conclusion

We believe that our patient’s case of CJD is highly suspicious for cervid etiology given the circumstances of the case as well as the strong evidence of plausibility reported in published literature. This is the first known case of CJD in a patient who had consumed deer antler velvet. Despite the confirmed diagnosis of CJD, a causal relationship between the patient’s disease and his consumption of deer antler velvet cannot be definitively concluded.

Supplemental data including molecular tissue sample analysis and autopsy findings could yield further supporting evidence. Given this patient’s clinical resemblance to CBD and the known histological similarities of CBD with CJD, clinicians should consider both diseases in the differential diagnosis of patients with a similarly esoteric presentation. Regardless of the origin of this patient’s disease, it is clear that the potential for prion transmission from cervids to humans should be further investigated by the academic community with considerable urgency.

https://thescipub.com/pdf/ajidsp.2021.43.48.pdf

''We believe that our patient’s case of CJD is highly suspicious for cervid etiology given the circumstances of the case as well as the strong evidence of plausibility reported in published literature. This is the first known case of CJD in a patient who had consumed deer antler velvet. Despite the confirmed diagnosis of CJD, a causal relationship between the patient’s disease and his consumption of deer antler velvet cannot be definitively concluded.''

https://thescipub.com/pdf/ajidsp.2021.43.48.pdf

CREUTZFELDT JAKOB DISEASE: A Unique Presentation of Creutzfeldt-Jakob Disease in a Patient Consuming Deer Antler Velvet

i was warning England and the BSE Inquiry about just this, way back in 1998, and was ask to supply information to the BSE Inquiry. for anyone that might be interested, see;

Singeltary submission to the BSE Inquiry on CJD and Nutritional Supplements 1998

ABOUT that deer antler spray and CWD TSE PRION... I have been screaming this since my neighbors mom died from cjd, and she had been taking a supplement that contained bovine brain, bovine eyeball, and other SRMs specified risk materials, the most high risk for mad cow disease. just saying...

I made a submission to the BSE Inquiry long ago during the BSE Inquiry days, and they seemed pretty interested.

Sender: "Patricia Cantos"

To: "Terry S Singeltary Sr. (E-mail)"

Subject: Your submission to the Inquiry

Date: Fri, 3 Jul 1998 10:10:05 +0100 3 July 1998

Mr Terry S Singeltary Sr. E-Mail: Flounder at wt.netRef: E2979

Dear Mr Singeltary, Thank you for your E-mail message of the 30th of June 1998 providing the Inquiry with your further comments. Thank you for offering to provide the Inquiry with any test results on the nutritional supplements your mother was taking before she died. As requested I am sending you our general Information Pack and a copy of the Chairman's letter. Please contact me if your system cannot read the attachments. Regarding your question, the Inquiry is looking into many aspects of the scientific evidence on BSE and nvCJD.

I would refer you to the transcripts of evidence we have already heard which are found on our internet site at ;

http://www.bse.org.uk.

Could you please provide the Inquiry with a copy of the press article you refer to in your e-mail? If not an approximate date for the article so that we can locate it? In the meantime, thank you for you comments. Please do not hesitate to contact me on... snip...end...tss

everyone I tell this too gets it screwed up...MY MOTHER WAS NOT TAKING THOSE SUPPLEMENTS IPLEX (that I ever knew of). this was my neighbors mother that died exactly one year previously and to the day of sporadic CJD that was diagnosed as Alzheimer’s at first. my mother died exactly a year later from the Heidenhain Variant of Creutzfeldt Jakob Disease hvCJD, and exceedingly rare strains of the ever growing sporadic CJD’s. both cases confirmed. ...kind regards, terry

2001 Singeltary on CJD, Journal of American Medical Association

February 14, 2001

Diagnosis and Reporting of Creutzfeldt-Jakob Disease

Terry S. Singeltary, Sr

Author Affiliations

JAMA. 2001;285(6):733-734. doi:10-1001/pubs.JAMA-ISSN-0098-7484-285-6-jlt0214

To the Editor: In their Research Letter, Dr Gibbons and colleagues1 reported that the annual US death rate due to Creutzfeldt-Jakob disease (CJD) has been stable since 1985. These estimates, however, are based only on reported cases, and do not include misdiagnosed or preclinical cases. It seems to me that misdiagnosis alone would drastically change these figures. An unknown number of persons with a diagnosis of Alzheimer disease in fact may have CJD, although only a small number of these patients receive the postmortem examination necessary to make this diagnosis. Furthermore, only a few states have made CJD reportable. Human and animal transmissible spongiform encephalopathies should be reportable nationwide and internationally.

February 14, 2001

Diagnosis and Reporting of Creutzfeldt-Jakob Disease

Terry S. Singeltary, Sr

Author Affiliations

JAMA. 2001;285(6):733-734. doi:10-1001/pubs.JAMA-ISSN-0098-7484-285-6-jlt0214

https://jamanetwork.com/journals/jama/article-abstract/1031186

RE-Monitoring the occurrence of emerging forms of Creutzfeldt-Jakob disease in the United States 2003 Singeltary Journal of Neurology

26 MARCH 2003

RE-Monitoring the occurrence of emerging forms of Creutzfeldt-Jakob disease in the United States

Terry S. Singeltary, retired (medically)

I lost my mother to hvCJD (Heidenhain Variant CJD). I would like to comment on the CDC's attempts to monitor the occurrence of emerging forms of CJD. Asante, Collinge et al [1] have reported that BSE transmission to the 129-methionine genotype can lead to an alternate phenotype that is indistinguishable from type 2 PrPSc, the commonest sporadic CJD. However, CJD and all human TSEs are not reportable nationally. CJD and all human TSEs must be made reportable in every state and internationally. I hope that the CDC does not continue to expect us to still believe that the 85%+ of all CJD cases which are sporadic are all spontaneous, without route/source. We have many TSEs in the USA in both animal and man. CWD in deer/elk is spreading rapidly and CWD does transmit to mink, ferret, cattle, and squirrel monkey by intracerebral inoculation. With the known incubation periods in other TSEs, oral transmission studies of CWD may take much longer. Every victim/family of CJD/TSEs should be asked about route and source of this agent. To prolong this will only spread the agent and needlessly expose others. In light of the findings of Asante and Collinge et al, there should be drastic measures to safeguard the medical and surgical arena from sporadic CJDs and all human TSEs. I only ponder how many sporadic CJDs in the USA are type 2 PrPSc?

https://www.neurology.org/doi/10.1212/01.WNL.0000036913.87823.D6

2023

https://creutzfeldt-jakob-disease.blogspot.com/2023/09/professor-john-collinge-on-tackling.html

Good Luck!

Terry S. Singeltary Sr.

posted by Terry S. Singeltary Sr. at 3:34 PM 0 Comments