APHIS Announces Plans To Modernize Chronic Wasting Disease Control in Farmed Cervids, Seeks Comment on Revised Herd Certification Program Standards October 23, 2026 Docket No. APHIS-2026-0563 Singeltary Submission
APHIS Announces Plans To Modernize Chronic Wasting Disease Control in Farmed Cervids, Seeks Comment on Revised Herd Certification Program Standards October 23, 2026 Docket No. APHIS-2026-0563 Singeltary Submission
https://www.regulations.gov/docket/APHIS-2026-0563
https://www.aphis.usda.gov/news/agency-announcements/aphis-announces-plans-modernize-chronic-wasting-disease-control-farmed
ACTION:
Notice of Availability.
SUMMARY:
We are advising the public that we are making available for review and comment a revised version of the Chronic Wasting Disease (CWD) Herd Certification Program Standards. The CWD Program Standards provide guidance on how to meet CWD Herd Certification Program and interstate movement requirements. We are taking this action to address concerns of State and industry participants regarding the existing standards.
DATES:
We will consider all comments that we receive on or before November 25, 2026.
ADDRESSES:
You may submit comments by either of the following methods:
• Federal eRulemaking Portal: Go to www.regulations.gov. Enter APHIS-2026-0563 in the Search field. Select the Documents tab, then select the Comment button in the list of documents.
• Postal Mail/Commercial Delivery: Send your comment to Docket No. APHIS-2026-0563, Regulatory Analysis and Development, PPD, APHIS, 5601 Sunnyside Ave., #AP760, Beltsville, MD 20705.
Supporting documents and any comments we receive on this docket may be viewed at www.regulations.gov or in our reading room, which is located in room 1620 of the USDA South Building, 14th Street and Independence Avenue SW, Washington, DC. Normal reading room hours are 8 a.m. to 4:30 p.m., Monday through Friday, except holidays. To be sure someone is there to help you, please call (202) 799-7039 before coming.
FOR FURTHER INFORMATION CONTACT:
Dr. Tracy Nichols, Molecular Biologist, Cervid Health Staff, Strategy and Policy, Veterinary Services, APHIS; 2150 Centre Ave, Bldg. B, Fort Collins, CO 80526; (970) 494-7380; Tracy.A.Nichols@usda.gov.
SUPPLEMENTARY INFORMATION:
Chronic wasting disease (CWD) is a transmissible spongiform encephalopathy of cervids (members of Cervidae, the deer family). Species currently known to be susceptible to CWD include elk, mule deer, moose, white-tail deer, sika deer, muntjac, axis, reindeer, and black-tail deer.
In 2014, the Animal and Plant Health Inspection Service (APHIS) implemented the National CWD Herd Certification Program (HCP), a voluntary Federal-State-industry cooperative program administered by APHIS and implemented by participating States. States and herd owners choosing to participate must comply with the provisions of 9 CFR part 55 and all producers must comply with part 81 (referred to below as the regulations), which include requirements for animal identification, interstate movement, fencing, recordkeeping, herd inspections and inventories, animal mortality testing, and response to any findings of CWD-exposed, -suspect, or -positive herds. APHIS monitors the approved State HCPs to ensure consistency with Federal standards by means of annual State reporting and state reviews. With each year of successful compliance with the requirements, participating herds will advance in status. After 5 years of compliance with no evidence of CWD, the State or APHIS will certify the herd as being low risk for CWD. Farmed cervids may only move interstate from enrolled herds certified as low risk for CWD.
The CWD Program Standards, last revised in 2019, provide detailed guidance on how to meet the regulatory requirements referred to above. The Program Standards are reviewed on an ongoing basis by APHIS in collaboration with State agencies and industry representatives.
We are advising the public that we have prepared revisions of the CWD Program Standards. The proposed revisions include the following:
Reducing the trace and quarantine period for white-tail and mule deer, and maintaining it for elk and other species.
Updating indemnity prioritization to include reducing CWD transmission risk, strategically removing high risk animals, and encouraging HCP participation and genetic strategies to lower herd susceptibility.
Making science-based updates and clarifications in areas that were open to interpretation. Including guidelines for use of predictive genetics to reduce herd CWD susceptibility and increase CWD prevention.
Adding a section on the indemnity appeal process and revising the prioritization guidelines for indemnity funds to include predictive genetics.
Allowance for moving cervids from a CWD positive herd to a terminal positive quarantined hunt facility in a wildlife endemic area in another State with concurrence of the State Animal Health Authorities in the origin and receiving States.
The revised Program Standards may be viewed on the Regulations.gov website or in our reading room. (Instructions for accessing Regulations.govand information on the location and hours of the reading room are provided under the heading ADDRESSES at the beginning of this notice.) The documents are also available by contacting the person listed under FOR FURTHER INFORMATION CONTACT .
We welcome public comment on this notice and the proposed revisions to the CWD Program Standards. After considering all comments, if no substantive changes to the proposed revisions to the CWD Program Standards are deemed necessary by the APHIS Administrator based on the comments received, the proposed revisions to the CWD Program Standards will be adopted as final without subsequent publication of another document in the Federal Register . If substantive changes to the proposed revisions are deemed necessary, we will publish an additional document in the Federal Register to discuss them and to make available a final version of the Program Standards that incorporates these substantive changes.
Authority: 7 U.S.C. 8301-8317; 7 CFR 2.22, 2.80, and 371.4.
Done in Washington, DC, this 21st day of October 2026. Kelly Moore, Administrator, Animal and Plant Health Inspection Service. [FR Doc. 2026-21745Filed 10-23-26; 8:45 am] BILLING CODE 3410-34-P
https://www.regulations.gov/document/APHIS-2026-0563-0001
[Federal Register Volume 91, Number 205 (Monday, October 26, 2026)] [Notices] [Page 67266] From the Federal Register Online via the Government Publishing Office [www.gpo.gov] [FR Doc No: 2026-21745]
[[Page 67266]]
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DEPARTMENT OF AGRICULTURE
Animal and Plant Health Inspection Service
[Docket No. APHIS-2026-0563]
Chronic Wasting Disease Herd Certification Program Standards
https://www.govinfo.gov/content/pkg/FR-2026-10-26/html/2026-21745.htm
Singeltary Submission Animal and Plant Health Inspection Service [Docket No. APHIS-2026-0563]
Greetings APHIS et al, i must comment on the proposal to deregulate Chronic Wasting Disease CWD TSE Prion regulations for the Captive Farm industry for cervids Docket No. APHIS-2026-0563.
You would have thought from past mistakes with this industry, we would have learned at least, that voluntary rules and regulations just do not work.
THIS is just the beginning of deregulation of cwd rules for cwd, and what we’re in for.
These are my comments and concerns, as follows;
“Allowance for moving cervids from a CWD positive herd to a terminal positive quarantined hunt facility in a wildlife endemic area in another State with concurrence of the State Animal Health Authorities in the origin and receiving States.”
stupid move, not science based…perfect example;
“The above proposed discretionary approach to management resulted in TWD [Sic] staff electing to release 13 bucks from a CWD-positive facility onto an immediately adjacent uninfected site, something which under the previous rule, and adhering to previous protocol, they would not have had the authority to do.”
“The release was done in mid-September of 2025. One month later, one of the bucks released under the disease management plan tested positive for CWD on the release site; and a second buck from the same group a month and a few days after that. There were 11 properties that were directly exposed to the department’s action… exposed by the department’s actions– 11 properties.”
see;
COMMISSIONER GALO: Chairman, if I may.
I agree with you. There’s a lot of people that really do disagree with this plan. And I think that it does change a lot of what we have been doing in the past when we were with Texas Animal Health Commission.
And, as you know, at the last meeting I had some very big concerns. And I left that meeting and I’ve been thinking about a lot that was said there and a lot about this particular rule package.
And if you may favor me, Chairman, I actually put a statement together because I don’t want to… I felt like I left a lot of things unsaid at the last meeting.
So, if you don’t mind, I’m going to read, and maybe that will clarify some of the reasons that people disagree with this rule package.
Texas A&M studies put the total economic output of white-tailed deer hunting in Texas at around $9.6 billion– $4.6 billion for hunters and $5 billion from landowners, encompassing expenditures on licenses, lodging, feed, management, and more.
Additionally, it generates tens of thousands of jobs across the state. Chronic wasting disease is a threat to this vital cornerstone of Texas’ outdoor recreation and its economy. Unfortunately, CWD remains an incredibly difficult disease to manage due to the ease of transmission, the elusive detection in infected animals, its extended incubation period, and its tenacious persistence in the environment once it’s introduced.
Because we now know that there are two primary sources of exposure, one, CWD-infected deer, and two, a CWD-contaminated environment, the Texas Parks and Wildlife Department must continue a rigorous statewide surveillance program, follow effective protocol for action in the instance of detection, and especially prevent its spread pursuant to TWD [Sic]/CWD management plan.
While the TPWD plan to deal with CWD was meant to be dynamic and evolving, TPWD cannot accept the proposed rule which grants, quote– and I quote– “grants TPWD staff explicit authority to develop disease management plans for trace and positive facilities,” end quote; and especially that which relates to the movement of animals out of an infected location.
The department has determined that allowing breeder deer to be moved from an exposed location represents an unacceptable risk of spreading CWD to native, free-ranging, and captive deer populations unless a determination based on the particulars of a given circumstance indicates the risk is neither nonexistent or acceptable.
The above proposed discretionary approach to management resulted in TWD [Sic] staff electing to release 13 bucks from a CWD-positive facility onto an immediately adjacent uninfected site, something which under the previous rule, and adhering to previous protocol, they would not have had the authority to do.
The release was done in mid-September of 2025. One month later, one of the bucks released under the disease management plan tested positive for CWD on the release site; and a second buck from the same group a month and a few days after that. There were 11 properties that were directly exposed to the department’s action… exposed by the department’s actions– 11 properties.
The recent documented disease spread due to deviation from the previous rule adopted during the period where the Texas Animal Health Commission was managing CWD with TPWD is incontrovertible evidence that we cannot deviate from those previously established safeguards. To date, CWD has persisted, spread, and increased in prevalence in nearly every area where it has been introduced.
Unfortunately, because currently there are no known management strategies to successfully mitigate the risk of indirect transmission once an environment has been contaminated with infectious prions, disease prevention is the only prudent recourse.
The best way to manage CWD is to prevent its introduction into new areas and limit its spread. Established safeguards cannot be abandoned. Discontinuation or deviation from prior proven protocol exposes the department to potential liability as CWD will certainly spread to neighboring properties unless established CWD containment procedures are followed.
The department cannot revert to methods from the past which we know caused the spread of this ultimately fatal disease. We must recognize the need for full cooperation and partnership between the Texas Parks and Wildlife Commissioners and the department and its staff, and continue to implement the plans and procedures which were developed and incorporated as the epidemiology and management of this disease became better understood, and until science provides a new and a better plan.
Those are my comments.
CHAIRMAN FOSTER: That’s impressive, first of all, and I appreciate you doing that.
It does… it’s kind of a wake-up call to us to make sure that we keep our eye on the ball. It causes me to ask the question, gentlemen, that I know we’re being forced to implement new rules because of the Texas Animal Health Commission’s withdrawal from this area.
And I want to make sure that what we’re doing doesn’t dilute our efforts to manage this disease, and that we, by trying to step in and replace Animal Health Commission’s role, that we don’t change our mission.
And I think that’s a lot of what Commissioner Galo was talking about. And so, I just would ask you to comment, first of all, on her statement because that was quite a statement.
https://tpwd.texas.gov/business/feedback/meetings/2026/0326/agenda/prev_worksession_transcript.phtml
Mar 17, 2026 at 11:33am Post by Terry S. Singeltary Sr. on Mar 17, 2026 at 11:33am
Texas Chronic Wasting Disease CWD TSE Prion Science Update 2026 Update
Greetings again Honorable Texas Wildlife and Government Officials,
i am writing you all today with great concern about CWD.
Besides of my concerns with the zoonotic and environmental risk factors of cwd tse prp, i am extremely concerned with the disconnect showing now between TPWD and TAHC with Concerns with CWD management, attempted containment or eradication of CWD. This is terrible. you all must get on the same page, and you all cannot let the captive cervid industry dictate their junk science to you, (which appears what TPWD is doing) and then legislate cwd regulations there from. that’s absolutely why Texas is in this mess with CWD (i have those receipts)…imho!
the last time i updated you all on cwd was;
From: Terry Singeltary <flounder9@verizon.net> Date: January 17, 2024 at 3:25:26 PM CST To: "TERRY SINGELTARY Sr." <flounder9@verizon.net> Cc: execdir@tahc.texas.gov, … Subject: TPWD Action CWD Detection and Response Rules Containment and Surveillance Zone Boundaries Recommended Adoption of Proposed Changes January 25, 2024
WEDNESDAY, JANUARY 17, 2024
TPWD Action CWD Detection and Response Rules Containment and Surveillance Zone Boundaries Recommended Adoption of Proposed Changes January 25, 2024
2026
COMMISSIONER GALO: Chairman, if I may.
snip…
***> the movement of captive cervid is why Texas have so many cases of CWD TSE Prion to date…
***> now, for the worse part, recent cwd transmission studies, to cattle, pigs, sheep, cervid, and 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.”
Strain characterization of chronic wasting disease in bovine-PrP transgenic mice
Conclusions: Altogether, these results exhibit the diversity of CWD strains present in the panel of CWD isolates and the ability of at least some CWD isolates to infect bovine species. Cattle being one of the most important farming species, this ability represents a potential threat to both animal and human health, and consequently deserves further study.
Prion 2023 Congress Organizing Committee and the NeuroPrion Association, we invite you to join us for the International Conference Prion2023 from 16-20 October 2023 in Faro, Portugal.
https://prion2023.org/wp-content/uploads/2023/10/Meeting-book-final-version2.pdf
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
don’t forget the pigs, outbreak of cwd in pigs in Texas and Arkansas;
Chronic wasting disease prions in cervids and wild pigs in North America Preliminary Outbreak Assessment DEFRA 26 January 2026 Department for Environment, Food and Rural Affairs
Preliminary Outbreak Assessment
Chronic wasting disease prions in cervids and wild pigs in North America
26 January 2026
Disease report
“They analysed over 300 brain and lymph node samples from 178 wild pigs living across Arkansas and Texas, USA…the researchers identified CWD prions in up to 37% of the lymph node samples and 15% of brain samples. The lowest detection rates were in the Texas samples (below 16%), matching the lower CWD prevalence in the state’s cervid population.”
https://assets.publishing.service.gov.uk/media/697a3b013c71d838df6bd413/CWD_Prions_in_Cervids_and_Wild_Pigs_in_North_America.pdf
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
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.
https://www.ars.usda.gov/research/project/?accnNo=440677&fy=202
***> Very low oral exposure to prions of brain or saliva origin can transmit chronic wasting disease
Nathaniel D. Denkers , Clare E. Hoover , Kristen A. Davenport, Davin M. Henderson, Erin E. McNulty, Amy V. Nalls, Candace K. Mathiason, Edward A. Hoover
Published: August 20, 2020
https://doi.org/10.1371/journal.pone.0237410
Abstract
The minimum infectious dose required to induce CWD infection in cervids remains unknown, as does whether peripherally shed prions and/or multiple low dose exposures are important factors in CWD transmission. With the goal of better understand CWD infection in nature, we studied oral exposures of deer to very low doses of CWD prions and also examined whether the frequency of exposure or prion source may influence infection and pathogenesis. We orally inoculated white-tailed deer with either single or multiple divided doses of prions of brain or saliva origin and monitored infection by serial longitudinal tissue biopsies spanning over two years. We report that oral exposure to as little as 300 nanograms (ng) of CWD-positive brain or to saliva containing seeding activity equivalent to 300 ng of CWD-positive brain, were sufficient to transmit CWD disease. This was true whether the inoculum was administered as a single bolus or divided as three weekly 100 ng exposures. However, when the 300 ng total dose was apportioned as 10, 30 ng doses delivered over 12 weeks, no infection occurred. While low-dose exposures to prions of brain or saliva origin prolonged the time from inoculation to first detection of infection, once infection was established, we observed no differences in disease pathogenesis. These studies suggest that the CWD minimum infectious dose approximates 100 to 300 ng CWD-positive brain (or saliva equivalent), and that CWD infection appears to conform more with a threshold than a cumulative dose dynamic.
https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0237410
Tuesday, June 9, 2026
Hazard identification for the risks to terrestrial animal health from the import of hay and straw, BSE, CWD, Scrapie, TSE, Prion
https://www.gov.uk/government/publications/hazard-identification-for-the-risks-to-terrestrial-animal-health-from-the-import-of-hay-and-straw/hazard-identification-for-the-risks-to-terrestrial-animal-health-from-the-import-of-hay-and-straw
https://defrauktseprp.blogspot.com/2026/06/hazard-identification-for-risks-to.html
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
ALREADY, the captive industry and it’s participants of fenced-in hunting, are jumping for joy. this just out. looks to me, they just don’t care about nothing but their bottom dollar, and those gmo deer and their morphed racks…imho…see post from;
Stephen Ziegler Outdoor writer | Rack Junkies Podcast
The federal government is backing off CWD regulations. As more research comes out and decades of doomsday predictions fail to play out as promised, we’re watching states rethink their approach to CWD. Indiana has already decided to not go down the ridiculous road of killing deer to save them. Now the federal government is getting on board.
The USDA and APHIS just announced proposed changes to CWD regulations for captive deer. Instead of what we’ve watched happen in Texas, where entire healthy uninfected herds have been slaughtered over CWD, they’re moving away from needlessly slaughtering healthy deer that never tested positive. I don’t care where you stand on high-fence hunting. Killing entire herds in the name of saving deer is one of the dumbest things I’ve seen in this industry. That goes for any animal. The new approach focuses on targeted removal, genetics, and using money saved to fund more research.
I called this over the summer. I said this was going to be the year things started changing and this is just one more example. High fence, low fence, no fence, it doesn’t matter. After decades of CWD research, it’s about time government agencies stopped these ridiculous kill-all-the-deer-to-save-them policies. Genetics is a huge part of the way forward, and we’ve known that for years. Things are changing, and it’s about damn time.
— Stephen Ziegler Outdoor writer | Rack Junkies Podcast
https://m.facebook.com/story.php?story_fbid=pfbid0x9kWar6afageXjx869GXLp1y2HKwft78XxKDU1Cf353areNx34xdrfhRhwLhhUiBl&id=100044148474161
Listing of CWD Cases in Texas
Positive Number CWD Positive Confirmation Date Free Range Captive County Facility Species Sex Age
1420 10/21/2026 Breeder Deer Zavala 23 WTD F 7.2
1419 10/21/2026 Breeder Deer Zavala 23 WTD F 3.2
1418 10/21/2026 Breeder Deer Zavala 23 WTD F 4.2
1417 10/21/2026 Breeder Deer Zavala 23 WTD F 4.2
1416 10/21/2026 Breeder Deer Zavala 23 WTD F 5.2
1415 10/21/2026 Breeder Deer Zavala 23 WTD F 5.2
1414 10/21/2026 Breeder Deer Zavala 23 WTD F 5.2
1413 10/21/2026 Breeder Deer Zavala 23 WTD F 4.2
1412 10/21/2026 Breeder Deer Zavala 23 WTD F 6.2
1411 10/21/2026 Breeder Deer Zavala 23 WTD F 6.2
1410 10/21/2026 Breeder Deer Zavala 23 WTD F 6.2
1409 10/21/2026 Breeder Deer Zavala 23 WTD F 6.2
1408 10/21/2026 Breeder Deer Zavala 23 WTD F 6.2
1407 10/21/2026 Breeder Deer Zavala 23 WTD F 6.2
1406 9/23/2026 Breeder Deer Navarro 38 WTD M 2.1
1405 9/23/2026 Breeder Deer Navarro 38 WTD M 7.1
1404 9/23/2026 Breeder Deer Navarro 38 WTD M 2.1
1403 9/23/2026 Breeder Deer Navarro 38 WTD M 1.1
1402 10/5/2026 Free Range Oldham N/A Mule Deer M 5.5
1401 9/29/2026 Breeder Deer Gonzales 47 WTD M 3.1
1400 9/29/2026 Breeder Deer Gonzales 47 WTD M 3.1
1399 10/5/2026 Free Range Hartley N/A Mule Deer F 5.5
1398 8/10/26 Breeder Deer Cherokee 44 WTD M 1
1397 8/10/26 Breeder Deer Cherokee 44 WTD M 1
Showing 1 to 24 of 1,420 entries
1398 8/10/26 Breeder Deer Cherokee 44 WTD M 1
1397 8/10/26 Breeder Deer Cherokee 44 WTD M 1
1396 8/10/26 Breeder Deer Cherokee 44 WTD F 1
1395 8/10/26 Breeder Deer Cherokee 44 WTD F 2
1394 7/23/26 Breeder Deer Callahan 46 WTD F 13
1393 7/2/26 Breeder Deer Duval 37 WTD F 2.9
1392 7/2/26 Breeder Deer Duval 37 WTD M 2
1391 7/2/26 Breeder Deer Duval 37 WTD M 3.9
1390 7/2/206 Breeder Deer Zavala 45 WTD F 2
1389 7/2/26 Breeder Deer Zavala 45 WTD M 2.9
1388 7/15/26 Breeder Deer Gillespie 15 WTD F 2.9
1387 7/2/26 Breeder Deer Navarro 38 WTD F 2.9
1386 6/25/26 Breeder Deer Navarro 38 WTD F 2.8
1385 6/24/26 Breeder Deer Navarro 38 WTD F 5.8
1384 5/27/26 Breeder Deer Mason 42 WTD M 1.8
1383 5/27/26 Breeder Deer Mason 42 WTD M 3.8
1382 6/25/26 Free Range El Paso N/A Mule Deer M 3.5
1381 6/25/26 Free Range El Paso N/A Mule Deer F 3.5
1380 6/25/26 Free Range El Paso N/A Mule Deer M 2.5
1379 5/27/26 Breeder Deer Duval 37 WTD M 3.8
1378 5/12/26 Breeder Deer Gillespie 15 WTD M 3.7
1377 4/27/26 Breeder Release Site Zavala N/A WTD F 7.5
1376 4/27/26 Breeder Deer Gillespie 15 WTD M 2.7
1375 4/27/26 Free Range Hartley N/A WTD M 3.
Showing 1 to 24 of 1,398 entries
*CWD Positive Confirmation Dates marked with * are dates confirmed by Texas A&M Veterinary Diagnostic Laboratory rather than the National Veterinary Diagnostic Laboratory
https://tpwd.texas.gov/huntwild/wild/diseases/cwd/positive-cases/listing-cwd-cases-texas.phtml
you cannot let the very industry that is responsible for helping spread chronic wasting disease cwd tse prion, across a large portion of Texas, (and other States have had the same problem, see Wisconsin) dictate rules for CWD TSE Prion, it just will not work, and the ‘voluntary’ aspect of any cwd regulations must be removed. it’s painfully obvious, voluntarily means nothing but a green light to most, imho. NO, the captive cervid industry is not the only reason CWD is spreading, but they have exacerbated the CWD situation, and that’s painfully obvious, just look at the ‘ghost deer’ spread of CWD in Texas…terry
Trucking CWD TSE Prion
Chronic Wasting Disease CWD TSE Prion of Cervid
“CWD spreads among wild populations at a relatively slow rate, limited by the natural home range and dispersed nature of wild animals.”
NOW HOLD YOUR HORSES, Chronic Wasting Disease CWD of Cervid can spread rather swiftly, traveling around 50 MPH, from the back of truck and trailer, and Here in Texas, we call it ‘Trucking CWD’…
Preventive Veterinary Medicine Volume 234, January 2025, 106385
Use of biosecurity practices to prevent chronic wasting disease in Minnesota cervid herds
Vehicles or trailers that entered the farm were used to transport other live cervids, cervid carcasses, or cervid body parts in past 3 years in 64.3 % (95 % CI 46.3–82.3) of larger elk/reindeer herds compared to 13.6 % (95 % CI 4.7–22.4) of smaller deer herds.
Snip…
Identifying the exact pathway of initial CWD transmission to cervid herds is often not possible, in part due to many potential pathways of transmission for the infection, including both direct and indirect contact with infected farmed or wild cervids (Kincheloe et al., 2021). That study identified that transmissions from infected farmed cervids may occur from direct contact with the movement of cervids from one herd to another and from indirect contact with the sharing of equipment, vehicles, clothing, reproductive equipment, and potentially through semen or embryos.
https://www.sciencedirect.com/science/article/abs/pii/S016758772400271X
“That study identified that transmissions from infected farmed cervids may occur from direct contact with the movement of cervids from one herd to another and from indirect contact with the sharing of equipment, vehicles, clothing, reproductive equipment, and potentially through semen or embryos.”
remember that…terry
Texas Game Wardens Near Conclusion of ‘Ghost Deer’ Case with 24 Suspects, 1,400 Charges Filed Statewide
Aug. 14, 2025
AUSTIN – The Texas Game Warden investigation known as "Ghost Deer" has reached a possible conclusion after two additional suspects turned themselves in on felony charges. This brings the total number of individuals implicated in the case to 24, with approximately 1,400 charges filed across 11 Texas counties.
Ken Schlaudt, 64, of San Antonio, the owner of four deer breeding facilities and one release site, along with facility manager Bill Bowers, 55, of San Angelo, surrendered to the Travis County District Attorney’s Office on charges of felony tampering with a governmental record. Both men allegedly entered false information into the Texas Wildlife Information Management System (TWIMS) to facilitate illegal smuggling of white-tailed breeder deer. They also face more than 100 misdemeanor charges related to unlawful breeder deer activities in Tom Green County.
The "Ghost Deer" investigation has uncovered widespread, coordinated deer breeding violations including, but not limited to: smuggling captive breeder deer and free-range whitetail deer between breeder facilities and ranches, Chronic Wasting Disease (CWD) testing violations, license violations and misdemeanor and felony drug charges relating to the possession and mishandling of prescribed sedation drugs classified as controlled substances.
The suspects charged in the case include:
Evan Bircher, 59, San Antonio Vernon Carr, 55, Corpus Christi Jarrod Croaker, 47, Corpus Christi Terry Edwards, 54, Angleton Joshua Jurecek, 41, Alice Justin Leinneweber, 36, Orange Grove James Mann, 53, Odem Gage McKinzie, 28, Normanna Herbert “Tim” McKinzie, 47, Normanna Eric Olivares, 47, Corpus Christi Bruce Pipkin, 57, Beaumont Dustin Reynolds, 38, Robstown Kevin Soto, 55, Hockley Jared Utter, 52, Pipe Creek Reed Vollmering, 32, Orange Grove Clint West, 56, Beaumont James Whaley, 49, Sevierville, Tenn. Ryder Whitstine, 19, Rockport Ryker Whitstine, 21, Rockport Claude Wilhelm, 52, Orange Cases are pending adjudication in Bandera, Bee, Brazoria, Duval, Edwards, Jim Wells, Live Oak, Montgomery, Tom Green, Travis and Webb counties.
The investigation began in March 2024 when game wardens discovered the first violations during a traffic stop.
https://tpwd.texas.gov/newsmedia/releases/?req=20250206a
That incident led wardens to the much larger network of violations,
https://tpwd.texas.gov/newsmedia/releases/?req=20250227b
Texas is a fine example, see; “Chronic Wasting Disease (CWD) is a fatal neurological disease and can devastate deer populations by silently spreading through direct animal contact and contaminated environments. Without close monitoring, illegal movement of captive deer increases the risk of introducing CWD to areas it is not known to exist, potentially leading to widespread outbreaks which will impact more than just the health of Texas deer.”
https://tpwd.texas.gov/newsmedia/releases/?req=20250227b
resulting in one of the largest deer smuggling operations in Texas history.
About Texas Game Wardens
Texas Game Wardens, within the Law Enforcement Division of Texas Parks and Wildlife Department, are responsible for enforcing laws related to the conservation and management of natural resources and public safety through community-based law enforcement. Their mission is to provide hunting, fishing and outdoor recreation opportunities for the use and enjoyment of present and future generations. Additionally, they play a crucial role in search and rescue operations during natural disasters, exemplifying their commitment to protecting both the environment and the people of Texas.
If you witness a fishing, wildlife or boating violation in progress, please call 1-800-792-GAME(4263) immediately and report it to Operation Game Thief (OGT), Texas’ Wildlife Crime-Stoppers Program. You can also text your tip by sending the keyword TXOGT plus your tip to 847411 or through the Texas OGT App, available for iOS and Android devices. Dispatchers are available 24/7.
https://tpwd.texas.gov/newsmedia/releases/?req=20250814c
THURSDAY, AUGUST 14, 2025
Texas Game Wardens Near Conclusion of ‘Ghost Deer’ Case with 24 Suspects, 1,400 Charges Filed Statewide
https://chronic-wasting-disease.blogspot.com/2025/08/texas-game-wardens-near-conclusion-of.html
MONDAY, MAY 05, 2026
TEXAS ANIMAL HEALTH COMMISSION AGENCY STRATEGIC PLAN FISCAL YEARS 2025 - 2029 CWD TSE Prion
https://chronic-wasting-disease.blogspot.com/2026/05/texas-animal-health-commission-agency.html
Texas CWD TSE Prion Cases Climb To 1,420 Detected To Date and TPWC Meeting November 2026 Singeltary Submission
https://prpsc.proboards.com/thread/262/texas-prion-cases-climb-detected
https://chronic-wasting-disease.blogspot.com/2026/10/texas-cwd-tse-prion-cases-climb-to-1420.html
https://www.researchgate.net/publication/416770173_Texas_CWD_TSE_Prion_Cases_Climb_To_1420_Detected_To_Date_and_TPWC_Meeting_November_2026_Singeltary_Submission
SATURDAY, SEPTEMBER 19, 2026
Texas 5th Captive Herd Depopulated This Year Due To Positive CWD TSE Prion
https://chronic-wasting-disease.blogspot.com/2026/09/texas-5th-captive-herd-depopulated-this.html
https://prpsc.proboards.com/thread/242/texas-captive-deer-herd-depopulated
Texas Kimble County Farm Chronic Wasting Disease CWD TSE Prion Approximate Herd Prevalence 12%
SUMMARY MINUTES OF THE 407th COMMISSION MEETING Texas Animal Health Commission
September 22, 2020
http://web.archive.org/web/20201017124040/https://www.tahc.texas.gov/agency/meetings/minutes/SummaryMinutes_CommMtg_2020-09-22.pdf
Thursday, October 2, 2014
TEST RESULTS FROM CAPTIVE DEER HERD WITH CHRONIC WASTING DISEASE RELEASED 79.8 percent of the deer tested positive for the disease
DES MOINES – The Iowa Department of Agriculture and Land Stewardship today announced that the test results from the depopulation of a quarantined captive deer herd in north-central Iowa showed that 284 of the 356 deer, or 79.8% of the herd, tested positive for Chronic Wasting Disease (CWD).
http://web.archive.org/web/20141006172620/https://www.iowaagriculture.gov/press/2014press/press10022014.asp
Wisconsin Buckhorn Flats CWD
SUBJECT: Almond Deer Farm Update
Sixty of the 76 animals tested positive for CWD. The 76 deer constituted the breeding herd in the breeding facility on the farm. The property also had a hunting preserve until 2005. Four deer, two does and two fawns, the only deer remaining in the former preserve, were killed and tested as well. CWD was not detected in those animals.
The total number of deer to test positive from this farm from the initial discovery to final depopulation is 82. The nearly 80% prevalence rate discovered on Buckhorn Flats is the highest prevalence recorded in any captive cervid operation in North America.
http://web.archive.org/web/20140831060348/http://dnr.wi.gov/about/nrb/2011/december/12-11-2b2.pdf
Colorado CWD TSE Prion
“The overall incidence of clinical CWD in white-tailed deer was 82% “
Epidemiology of Chronic Wasting Disease in Captive White-Tailed and Mule Deer
http://web.archive.org/web/20150908134715/https://cpw.state.co.us/Documents/Hunting/BigGame/CWD/PDF/ResearchArticles/JWDEpiCWD.pdf
Wisconsin CWD TSE Prion
In total, 17,759 deer were sampled throughout the state during the 2025 hunting seasons with 2,006 samples testing positive. Most (87%) of these detections were in the Southern Farmland Zone.
https://dnr.wisconsin.gov/newsroom/release/118496
MONDAY, MARCH 09, 2026
Wisconsin Confirms 2,006 Cases CWD TSE Prion During 2025 Hunting Season
https://chronic-wasting-disease.blogspot.com/2026/03/wisconsin-confirms-2006-cases-cwd-tse.html
https://prpsc.proboards.com/thread/210/wisconsin-confirms-cases-prion-2025
Lacey Act Violations and CWD?
https://search.justice.gov/search?affiliate=justice&query=lacey+act+deer+illegal+hunting%2C+transport%2C+cwd
https://search.justice.gov/search?affiliate=justice&query=lacey+act+cwd+captive+illegal
https://search.justice.gov/search?affiliate=justice&query=lacey+act+illegal+hunting%2C+transport%2C+cwd
CWD and ENVIRONMENTAL FACTORS
Environmental Factors for CWD TSE Prion, and why these regulations have been in place…terry
So, this is what we leave our children and grandchildren , and what about land values?
Project 3A: CWD Prion Shedding and Environmental Contamination: Role in Transmission and Zoonotic
Parent Project Number 5P01AI077774-15
Sub-Project ID 5512
Contact PI/Project Leader HOOVER, EDWARD ARTHUR
Awardee Organization
Description
Abstract Text
Chronic wasting disease (CWD) is an emergent, highly transmissible, geographically expanding, prion disease of both wild and captive cervids. CWD is unique among prion diseases in its facile contagion and environmental persistence. Its expanding geographical range, combined with the increasing transport of animals and animal products, portend its continued expansion and diversification. The zoonotic potential of CWD remains poorly understood. CWD endemic areas interface cervids with livestock species and humans, posing obvious zoonotic risks that over time will increase. While it is known that strains of CWD exist, nothing is known about the zoonotic potential of these strains. Work from our applicant group has shown that CWD infected cervids continually shed prions into the environment and that previously unrecognized environmental factors can influence the emergence of a dominant strain from a mixture. The ability to recognize the zoonotic potential of CWD strains is central to mitigating CWD transmission risk. The central hypothesis for work described here is that CWD strains evolve continuously due to a combination of both host and environmental factors. We will test this hypothesis by: i) determining the evolution and zoonotic impact of CWD strains in the native cervid species; ii) leveraging our unique animal resources, expertise, and in vivo & in vitro methodologies to assess environmental factors that alter CWD strain selection and evolution and iii) evaluate zoonotic potential of CWD strains by a complementary combination of in vitro amplification assays and animal transmission studies. The results will provide new information about this emergent transmissible prion disease and the risk it poses to humans and other species.
https://reporter.nih.gov/search/E5DbPm-6OkG4kGjqIW6jgw/project-details/11317179#description
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.
https://reporter.nih.gov/search/VYlhnadNtUiur19eYeRPog/project-details/11227445#description
Shedding, retention and spreading of chronic wasting disease prions in the environment
Project Number 5R01AI132695-07 Former Number 2R01AI132695-06
Contact PI/Project Leader MORALES, RODRIGO
Awardee Organization Description
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.
https://reporter.nih.gov/search/E5DbPm-6OkG4kGjqIW6jgw/project-details/11401093#description
"Additionally, we have determined that prion seeding activity is retained for at least fifteen years at a contaminated site following attempted remediation."
Detection of prions in soils contaminated by multiple routes
snip…
Results: We are able to detect prion seeding activity at multiple types of environmental hotspots, including carcass sites, contaminated captive facilities, and scrapes (i.e. urine and saliva). Differences in relative prion concentration vary depending on the nature and source of the contamination. Additionally, we have determined that prion seeding activity is retained for at least fifteen years at a contaminated site following attempted remediation.
Conclusions: Detection of prions in the environment is of the utmost importance for controlling chronic wasting disease spread. Here, we have demonstrated a viable method for detection of prions in complex environmental matrices. However, it is quite likely that this method underestimates the total infectious prion load in a contaminated sample, due to incomplete recovery of infectious prions. Further refinements are necessary for accurate quantification of prions in such samples, and to account for the intrinsic heterogeneities found in the broader environment.
=====end
Prion 2023 Abstracts
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
JOURNAL OF GENERAL VIROLOGY Volume 87, Issue 12
Infectious agent of sheep scrapie may persist in the environment for at least 16 years
***> Infectious agent of sheep scrapie may persist in the environment for at least 16 years
***> Nine of these recurrences occurred 14–21 years after culling, apparently as the result of environmental contamination, but outside entry could not always be absolutely excluded.
https://www.microbiologyresearch.org/content/journal/jgv/10.1099/vir.0.82011-0
Rapid recontamination of a farm building occurs after attempted prion removal
First published: 19 January 2019 https://doi.org/10.1136/vr.105054
The data illustrates the difficulty in decontaminating farm buildings from scrapie, and demonstrates the likely contribution of farm dust to the recontamination of these environments to levels that are capable of causing disease. snip...
This study clearly demonstrates the difficulty in removing scrapie infectivity from the farm environment. Practical and effective prion decontamination methods are still urgently required for decontamination of scrapie infectivity from farms that have had cases of scrapie and this is particularly relevant for scrapie positive goatherds, which currently have limited genetic resistance to scrapie within commercial breeds.24 This is very likely to have parallels with control efforts for CWD in cervids.
https://bvajournals.onlinelibrary.wiley.com/doi/abs/10.1136/vr.105054
***>This is very likely to have parallels with control efforts for CWD in cervids.
https://pubmed.ncbi.nlm.nih.gov/30602491/
I remember what “deep throat” told me about Scrapie back around 2001, during early days of my BSE investigation, after my Mom died from hvCJD, I never forgot, and it seems it’s come to pass;
***> Confidential!!!!
***> As early as 1992-3 there had been long studies conducted on small pastures containing scrapie infected sheep at the sheep research station associated with the Neuropathogenesis Unit in Edinburgh, Scotland. Whether these are documented...I don't know. But personal recounts both heard and recorded in a daily journal indicate that leaving the pastures free and replacing the topsoil completely at least 2 feet of thickness each year for SEVEN years....and then when very clean (proven scrapie free) sheep were placed on these small pastures.... the new sheep also broke out with scrapie and passed it to offspring. I am not sure that TSE contaminated ground could ever be free of the agent!! A very frightening revelation!!!
---end personal email---end...tss
and so it seems…
Chronic Wasting Disease CWD TSE Prion
THE CWD TSE Prion aka mad cow type disease is not your normal pathogen.
The TSE prion disease survives ashing to 600 degrees celsius, that’s around 1112 degrees farenheit.
You cannot cook the TSE prion disease out of meat. In fact new data now shows that exposure to high temperatures used to cook the meat increased the availability of prions for in vitro amplification.
you can take the ash and mix it with saline and inject that ash into a mouse, and the mouse will go down with TSE.
Prion Infected Meat-and-Bone Meal Is Still Infectious after Biodiesel Production as well.
the TSE prion agent also survives Simulated Wastewater Treatment Processes.
IN fact, you should also know that the TSE Prion agent will survive in the environment for years, if not decades.
you can bury it and it will not go away.
The TSE agent is capable of infected your water table i.e. Detection of protease-resistant cervid prion protein in water from a CWD-endemic area.
it’s not your ordinary pathogen you can just cook it out and be done
New studies on the heat resistance of hamster-adapted scrapie agent: Threshold survival after ashing at 600°C suggests an inorganic template of replication
http://www.pnas.org/content/97/7/3418.full
Prion Infected Meat-and-Bone Meal Is Still Infectious after Biodiesel Production
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2493038/
Rapid assessment of bovine spongiform encephalopathy prion inactivation by heat treatment in yellow grease produced in the industrial manufacturing process of meat and bone meals
https://bmcvetres.biomedcentral.com/track/pdf/10.1186/1746-6148-9-134.pdf
Chronic wasting disease (CWD) prion detection in environmental and biological samples from a taxidermy site and nursing facility, and instruments used in surveillance activities
Available online 9 April 2025
Highlights
• CWD prions were identified in a taxidermy and deer nursing facility.
• Contaminated samples included waters, soils, dermestid beetles, domestic flies and a dumpster.
• Surgical instruments used to collect deer samples can get contaminated with CWD prions.
• Some of the infectious particles are readily released from surgical instruments when washed.
• Our results suggest that taxidermy practices actively contribute in the spreading of CWD.
Snip…
In summary, the information provided in this report demonstrate how anthropogenic activities, specifically taxidermy practices, animal processing, and rehabilitation of CWD susceptible species, may facilitate CWD transmission through the environmental dissemination of CWD prions. This study, along with future research efforts characterizing the overall level of infectivity, provides relevant information on managing CWD and to control its rapid geographic expansion. …
https://www.sciencedirect.com/science/article/abs/pii/S0048969725009544
Chronic wasting disease detection in environmental and biological samples from a taxidermy site
Results: The PMCA analysis demonstrated CWD seeding activity in some of the components of this facility, including insects involved in head processing, soils, and a trash dumpster.
Conclusions: Different areas of this property were used for various taxidermy procedures. We were able to detect the presence of prions in
i) soils that were in contact with the heads of dead animals, ii) insects involved in the cleaning of skulls, and iii) an empty dumpster where animal carcasses were previously placed.
This is the first report demonstrating that swabbing is a helpful method to screen for prion infectivity on surfaces potentially contaminated with CWD. These findings are relevant as this swabbing and amplification strategy may be used to evaluate the disease status of other free-ranging and captive settings where there is a concern for CWD transmissions, such as at feeders and water troughs with CWD-exposed properties. This approach could have substantial implications for free-ranging cervid surveillance as well as in epidemiological investigations of CWD.
Prion 2022 Conference abstracts: pushing the boundaries
https://www.tandfonline.com/doi/full/10.1080/19336896.2022.2091286
Chronic wasting disease prions on deer feeders and wildlife visitation to deer feeding areas
First published: 10 February 2025
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
Mineral licks as environmental reservoirs of chronic wasting disease prions
Ian H. Plummer,Chad J. Johnson,Alexandra R. Chesney,Joel A. Pedersen ,Michael D. Samuel
Abstract
Chronic wasting disease (CWD) is a fatal neurodegenerative disease of deer, elk, moose, and reindeer (cervids) caused by misfolded prion proteins. The disease has been reported across North America and recently discovered in northern Europe. Transmission of CWD in wild cervid populations can occur through environmental routes, but limited ability to detect prions in environmental samples has prevented the identification of potential transmission “hot spots”. We establish widespread CWD prion contamination of mineral licks used by free-ranging cervids in an enzootic area in Wisconsin, USA. We show mineral licks can serve as reservoirs of CWD prions and thus facilitate disease transmission. Furthermore, mineral licks attract livestock and other wildlife that also obtain mineral nutrients via soil and water consumption. Exposure to CWD prions at mineral licks provides potential for cross-species transmission to wildlife, domestic animals, and humans. Managing deer use of mineral licks warrants further consideration to help control outbreaks of CWD.
Snip...
Recent laboratory research indicates plants grown in prion-contaminated soil can accumulate prions [53]. Our data suggest that plants growing near contaminated mineral licks may warrant investigation as a source of prions for foraging animals. Areas where cervids congregate for mineral consumption, feeding and baiting sites, winter yarding, wallows [54] or other activities where CWD prions are deposited in the environment may also provide potential long-term reservoirs for transmission to cervid and non-cervid species.
CONCLUSIONS
We used mb-PMCA to detect CWD in soil and water from mineral licks naturally contaminated with prions and used by free-ranging deer, livestock, and non-cervid wildlife species. Detection of prions in environmental reservoirs represents an important first step in understanding the contribution of environmental transmission to CWD epizootics and potential for cross-species transmission. The present study characterized an environmental prion reservoir by (1) identifying an apparent “hot spot” of deposition and potential exposure to both cervid and non-cervid species; (2) indicating CWD prions shed by free-ranging cervids are present in areas of frequent use leading to environmental contamination and potentially plant uptake; and (3) motivating investigation of the exposure and susceptibility of non-cervid species to CWD contaminated soil, water, and plant materials. Future research should be directed at quantifying CWD prion concentrations at mineral licks and other areas where cervids congregate, determining the persistence of prion infectivity at these sites, delineating spatial-temporal patterns of environmental prion deposition and accumulation, and assessing consumption by susceptible animals. Identifying additional environmental reservoirs of CWD prions and determining the contributions of direct and indirect transmission over the course of CWD outbreaks represent key aims in advancing understanding of long-term CWD infection dynamics.
http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0196745#sec008
December 2014, Volume 36, Issue 6, pp 1049–1061
Mineral licks: motivational factors for visitation and accompanying disease risk at communal use sites of elk and deer
Authors Authors and affiliations Michael J. LavelleEmail authorGregory E. PhillipsJustin W. FischerPatrick W. BurkeNathan W. SewardRandal S. StahlTracy A. NicholsBruce A. WunderKurt C. VerCauteren 1. 2. 3. 4.
Article First Online: 08 April 2014 258 Downloads 1 Citations
Abstract
Free-ranging cervids acquire most of their essential minerals through forage consumption, though occasionally seek other sources to account for seasonal mineral deficiencies. Mineral sources occur as natural geological deposits (i.e., licks) or as anthropogenic mineral supplements. In both scenarios, these sources commonly serve as focal sites for visitation. We monitored 11 licks in Rocky Mountain National Park, north-central Colorado, using trail cameras to quantify daily visitation indices (DVI) and soil consumption indices (SCI) for Rocky Mountain elk (Cervus elaphus) and mule deer (Odocoileus hemionus) during summer 2006 and documented elk, mule deer, and moose (Alces alces) visiting licks. Additionally, soil samples were collected, and mineral concentrations were compared to discern levels that explain rates of visitation. Relationships between response variables; DVI and SCI, and explanatory variables; elevation class, moisture class, period of study, and concentrations of minerals were examined. We found that DVI and SCI were greatest at two wet, low-elevation licks exhibiting relatively high concentrations of manganese and sodium. Because cervids are known to seek Na from soils, we suggest our observed association of Mn with DVI and SCI was a likely consequence of deer and elk seeking supplemental dietary Na. Additionally, highly utilized licks such as these provide an area of concentrated cervid occupation and interaction, thus increasing risk for environmental transmission of infectious pathogens such as chronic wasting disease, which has been shown to be shed in the saliva, urine, and feces of infected cervids.
Keywords Cervus elaphus Chronic wasting disease Elk Geophagy Mineral lick Mule deer Odocoileus hemionus
https://rd.springer.com/article/10.1007/s10653-014-9600-0
Elk and Deer Use of Mineral Licks: Implications for Disease Transmission
Kurt C. VerCauteren1*, Michael J. Lavelle1, Gregory E. Phillips1, Justin W.. Fischer1, and Randal S. Stahl1 1United States Department of Agriculture, Animal and Plant Health Inspection Service, Wildlife Services, National Wildlife Research Center, 4101 LaPorte Avenue, Fort Collins, CO 80521-2154, USA *Cooresponding author e-mail: kurt.c.vercauteren@aphis.usda.gov
North American cervids require and actively seek out minerals to satisfy physiological requirements. Minerals required by free-ranging cervids exist within natural and artificial mineral licks that commonly serve as focal sites for cervids. Ingestion of soils contaminated with the agent that causes chronic wasting disease (CWD) may result in risk of contracting CWD. Our objective was to evaluate the extent and nature of use of mineral licks by CWD-susceptible cervid species. We used animal-activated cameras to monitor use of 18 mineral licks between 1 June and 16 October 2006 in Rocky Mountain National Park, north-central Colorado.. We also assessed mineral concentrations at mineral licks to evaluate correlations between visitation rates and site-specific characteristics. We collected > 400,000 images of which 991 included elk, 293 included deer, and 6 included moose. We documented elk and deer participating in a variety of potentially risky behaviors (e.g., ingesting soil, ingesting water, defecating, urinating) while at mineral licks. Results from the mineral analyses combined with camera data revealed that visitation was highest at sodium-rich mineral licks. Mineral licks may play a role in disease transmission by acting as sites of increased interaction as well as reservoirs for deposition, accumulation, and ingestion of disease agents.
https://int-cwd-sympo.org/wp-content/uploads/2023/06/final-agenda-with-abstracts.pdf
Chronic Wasting Disease in Texas A Real Disease with Proven Impacts
Produced by a coalition of concerned hunters, landowners, & conservationists (last update 1/2025)
storymaps.arcgis.com/stories/b93f528938ac48e9b56dcc79953cbec0
Aug 18, 2021
Oh, Deer
Heading Off a Wildlife Epidemic
CWD poses a significant threat to the future of hunting in Texas. Deer population declines of 45 and 50 percent have been documented in Colorado and Wyoming. A broad infection of Texas deer populations resulting in similar population impacts would inflict severe economic damage to rural communities and could negatively impact land markets. Specifically, those landowners seeking to establish a thriving herd of deer could avoid buying in areas with confirmed CWD infections. As they do with anthrax-susceptible properties, land brokers may find it advisable to inquire about the status of CWD infections on properties that they present for sale. Prospective buyers should also investigate the status of the wildlife on prospective properties. In addition, existing landowners should monitor developments as TPWD crafts management strategies to identify and contain this deadly disease.
Dr. Gilliland (c-gilliland@tamu.edu) is a research economist with the Texas Real Estate Research Center at Texas A&M University.
www.recenter.tamu.edu/articles/tierra-grande/oh-d
Chronic Wasting Disease CWD TSE Prion Zoonotic, Zoonosis, Risk Factors Humans
CWD infectivity MEATS
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
Transmission of Cervid Prions to Humanized Mice Demonstrates the Zoonotic Potential of CWD
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
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 tg650 mice 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
The finding that infectious PrPSc was shed in fecal material of CWD-infected humanized mice and induced clinical disease, different tropism, and typical three banding pattern-PrPres in bank voles that is transmissible upon second passage is highly concerning for public health. The fact that this biochemical signature in bank voles resembles that of the Wisc-1 original deer isolate and is different from that of bvWisc-1, in the migration profile and the glyco-form-ratio, is valid evidence that these results are not a product of contamination in our study. If CWD in humans is found to be contagious and transmissible among humans, as it is in cervids [57], the spread of the disease within humans might become endemic.
Transmission of cervid prions to humanized mice demonstrates the zoonotic potential of CWD
Acta Neuropathol 144, 767–784 (2022). https://doi.org/10.1007/s00401-022-02482-9
Published
22 August 2022
https://link.springer.com/article/10.1007/s00401-022-02482-9
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 Tg12 mice 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 Tg12 mice. 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
“However, epidemiologic and laboratory investigations of these case-patients indicated no strong evidence for a causal link between CWD and their CJD illness (33).” ???
“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
U.S. Army Prion Disease
HUMAN TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES: A CRITICAL SCIENTIFIC INVESTMENT
Final Report
National Prion Research Program
US Army Medical Research and Materiel Command Congressionally Directed Medical Research Programs
Fort Detrick, Maryland 2007
*** The potential impact of prion diseases on human health was greatly magnified by the recognition that interspecies transfer of BSE to humans by beef ingestion resulted in vCJD. While changes in animal feed constituents and slaughter practices appear to have curtailed vCJD, there is concern that CWD of free-ranging deer and elk in the U.S. might also cross the species barrier. Thus, consuming venison could be a source of human prion disease. Whether BSE and CWD represent interspecies scrapie transfer or are newly arisen prion diseases is unknown. Therefore, the possibility of transmission of prion disease through other food animals cannot be ruled out. There is evidence that vCJD can be transmitted through blood transfusion. There is likely a pool of unknown size of asymptomatic individuals infected with vCJD, and there may be asymptomatic individuals infected with the CWD equivalent. These circumstances represent a potential threat to blood, blood products, and plasma supplies.
http://cdmrp.army.mil/prevfunded/nprp/NPRP_Summit_Final_Report.pdf
archived url;
https://web.archive.org/web/20120928015709/http://cdmrp.army.mil/prevfunded/nprp/NPRP_Summit_Final_Report.pdf
Limited transmission of cervid prions to nonhuman primates provides insights into the zoonotic potential of chronic wasting disease
SAMIA HANNAOUI, SANDRA PRITZKOW, WIEBKE M. JÜRGENS-WEMHEUER, DIRK MOTZKUS, [...] , AND HERMANN M. SCHÄTZL +12 authors Authors Info & Affiliations
SCIENCE ADVANCES
27 May 2026 Vol 12, Issue 22 DOI: 10.1126/sciadv.aeb7613
Abstract
Chronic wasting disease (CWD) is an expanding prion disease of cervids. CWD prions persist in the environment, are shed in excreta, and accumulate in tissues of infected cervids, raising concerns about its zoonotic potential. Using cynomolgus macaques, we explored the zoonotic potential of CWD. Although most inoculated macaques remained asymptomatic, sensitive in vitro prion amplification assays revealed low levels of prions in macaque tissues. Inoculation of transgenic mice and bank voles with macaque tissues induced prion disease, achieving 100% transmission rates upon serial passage. One interpretation of these findings is that CWD prions retain infectivity across species and that primate infection may manifest atypically while still enabling transmission. Our results challenge earlier conclusions that minimize the zoonotic risk of CWD and underscore the need for continued surveillance.
snip…
These findings suggest that cynomolgus macaques, often considered the most relevant model for assessing prion zoonotic potential, can support CWD infection under experimental conditions, although disease manifestation is atypical and only became evident through transmission to highly susceptible rodent models with unusual tissue tropism. While these results do not demonstrate efficient transmission of CWD to macaques, they indicate that this cross-species transmission cannot be excluded and warrants continued attention. These observations provide critical insights into how prion disease might present in the event of a spillover, reinforcing the need for sustained vigilance and further research into prion adaptation and zoonotic potential.
snip…
Together, these results underscore the potential zoonotic threat that may manifest subtly in primates while maintaining infectivity and transmissibility, opening the potential to adapt to humans. These findings prompt critical questions about the broader zoonotic landscape of CWD and emphasize the need for vigilant monitoring as CWD continues to spread through diverse ecosystems, broadening the potential for human exposure.
snip…
In summary, macaques infected orally (AU501 and AU467), intracerebrally (AU408 and AU469), or by intracerebrally steel wire implantation (AU519 and AU389) exhibited no detectable PrPSc signals on immunoblots and minimal prion detection via immunohistochemistry (IHC); however, prion seeding activity in brains and spleens of some animals were confirmed using highly sensitive prion conversion assays.
snip…
Our group (25) and others highlighted the importance of sensitive prion detection methods on interspecies prion transmission, where RT-QuIC and PMCA proved more reliable in detecting and identifying subclinical prion infections than traditional techniques, e.g., IHC and immunoblot that showed a higher detection threshold than the amplification assays. These findings suggest that standard diagnostic tools may underestimate prion infectivity in early or subclinical stages, raising concerns about undetected transmission risks. In addition, it is worth mentioning that while several prion-positive materials were passaged into bank voles, not all successfully adapted, reinforcing the specificity of the observed results. The selective propagation of certain materials indicates a requirement for specific strain compatibility or adaptation to the bank vole model. The persistence of prion seeding activity in both symptomatic and asymptomatic animals further suggests that subclinical infections may pose a long-term zoonotic risk, especially with repeated or prolonged exposure to CWD prions, including new CWD strains with different potential to cross the species barrier to humans (18, 21, 23, 73). Previous research has established the presence of distinct CWD prion types that result in different CWD strains in a new host (41, 74, 75), which could further complicate efforts to assess human model susceptibility to CWD. CWD prions have potential for strain adaptation/evolution in different hosts with relative resistance, suggesting that certain CWD isolates may pose a risk of crossing into new species, including intermediate hosts (76–79). Together, these observations highlight a scenario in which CWD transmission to primates may be inefficient, clinically atypical, and largely subclinical yet biologically capable of generating infectious prions with zoonotic relevance.
Previous reports demonstrated that prions can silently replicate in hosts, often going undetected by traditional diagnostic tools, while still being capable of transmission and eventual disease progression (80–82). In a previous study assessing the zoonotic potential of CWD using a transgenic humanized mouse model (25), we reported the involvement of gastrointestinal tissues, but we did not evaluate the transmissibility of these prions. In the present study, we demonstrated the infectivity and transmissibility of prions in gastrointestinal tissues in bank voles, where inoculation with small intestine homogenate, positive only in RT-QuIC for prion seeding activity, led to a 100% attack rate. The presence of subclinical prion carriers underscores the need for advanced diagnostic techniques to better understand prion infection’s dormant phase and to identify potential reservoirs currently overlooked in prion human diagnostics. This approach is essential to prevent transmission from asymptomatic carriers or those with atypical clinical symptoms. As the geographic range and prevalence of CWD-infected animals continue to expand, the risk of exposure to humans may escalate. As with any pathogen, an increase in CWD prevalence and prion replication provides more opportunities for adaptations, mutations, and potential zoonotic transmission; hence, our results and the growing concern for this question (83) warrant serious consideration.
We stress that our results do not imply efficient transmission to primates; rather, they reveal that exposure under certain conditions can lead to sustained prion infectivity that remains undetectable by classical diagnostic tools.
https://www.science.org/doi/10.1126/sciadv.aeb7613
“ Highly endemic states had a higher rate of prion disease mortality compared to non-CWD states”
Prion Conference 2018
P190 Human prion disease mortality rates by occurrence of chronic wasting disease in free ranging cervids, United States
Abrams JY (1), Maddox RA (1), Schonberger LB (1), Person MK (1), Appleby BS (2), Belay ED (1)
(1) Centers for Disease Control and Prevention (CDC), National Center for Emerging and Zoonotic Infectious Diseases, Atlanta, GA, USA (2) Case Western Reserve University, National Prion Disease Pathology Surveillance Center (NPDPSC), Cleveland, OH, USA.
Background
Chronic wasting disease (CWD) is a prion disease of deer and elk that has been identified in free ranging cervids in 23 US states. While there is currently no epidemiological evidence for zoonotic transmission through the consumption of contaminated venison, studies suggest the CWD agent can cross the species barrier in experimental models designed to closely mimic humans. We compared rates of human prion disease in states with and without CWD to examine the possibility of undetermined zoonotic transmission.
Methods
Death records from the National Center for Health Statistics, case records from the National Prion Disease Pathology Surveillance Center, and additional state case reports were combined to create a database of human prion disease cases from 2003-2015. Identification of CWD in each state was determined through reports of positive CWD tests by state wildlife agencies. Age- and race-adjusted mortality rates for human prion disease, excluding cases with known etiology, were determined for four categories of states based on CWD occurrence: highly endemic (>16 counties with CWD identified in free-ranging cervids); moderately endemic (3-10 counties with CWD); low endemic (1-2 counties with CWD); and no CWD states. States were counted as having no CWD until the year CWD was first identified. Analyses stratified by age, sex, and time period were also conducted to focus on subgroups for which zoonotic transmission would be more likely to be detected: cases <55 years old, male sex, and the latter half of the study (2010-2015).
Results
Highly endemic states had a higher rate of prion disease mortality compared to non-CWD states (rate ratio [RR]: 1.12, 95% confidence interval [CI] = 1.01 - 1.23), as did low endemic states (RR: 1.15, 95% CI = 1.04 - 1.27). Moderately endemic states did not have an elevated mortality rate (RR: 1.05, 95% CI = 0.93 - 1.17). In age-stratified analyses, prion disease mortality rates among the <55 year old population were elevated for moderately endemic states (RR: 1.57, 95% CI = 1.10 – 2.24) while mortality rates were elevated among those ≥55 for highly endemic states (RR: 1.13, 95% CI = 1.02 - 1.26) and low endemic states (RR: 1.16, 95% CI = 1.04 - 1.29). In other stratified analyses, prion disease mortality rates for males were only elevated for low endemic states (RR: 1.27, 95% CI = 1.10 - 1.48), and none of the categories of CWD-endemic states had elevated mortality rates for the latter time period (2010-2015).
Conclusions
While higher prion disease mortality rates in certain categories of states with CWD in free-ranging cervids were noted, additional stratified analyses did not reveal markedly elevated rates for potentially sensitive subgroups that would be suggestive of zoonotic transmission. Unknown confounding factors or other biases may explain state-by-state differences in prion disease mortality.
“ Highly endemic states had a higher rate of prion disease mortality compared to non-CWD states”
=====
P172 Peripheral Neuropathy in Patients with Prion Disease
Wang H(1), Cohen M(1), Appleby BS(1,2)
(1) University Hospitals Cleveland Medical Center, Cleveland, Ohio (2) National Prion Disease Pathology Surveillance Center, Cleveland, Ohio.
Prion disease is a fatal progressive neurodegenerative disease due to deposition of an abnormal protease-resistant isoform of prion protein. Typical symptoms include rapidly progressive dementia, myoclonus, visual disturbance and hallucinations. Interestingly, in patients with prion disease, the abnormal protein canould also be found in the peripheral nervous system. Case reports of prion deposition in peripheral nerves have been reported. Peripheral nerve involvement is thought to be uncommon; however, little is known about the exact prevalence and features of peripheral neuropathy in patients with prion disease.
We reviewed autopsy-proven prion cases from the National Prion Disease Pathology Surveillance Center that were diagnosed between September 2016 to March 2017. We collected information regarding prion protein diagnosis, demographics, comorbidities, clinical symptoms, physical exam, neuropathology, molecular subtype, genetics lab, brain MRI, image and EMG reports. Our study included 104 patients. Thirteen (12.5%) patients had either subjective symptoms or objective signs of peripheral neuropathy. Among these 13 patients, 3 had other known potential etiologies of peripheral neuropathy such as vitamin B12 deficiency or prior chemotherapy. Among 10 patients that had no other clear etiology, 3 (30%) had familial CJD. The most common sCJD subtype was MV1-2 (30%), followed by MM1-2 (20%). The Majority of cases wasere male (60%). Half of them had exposure to wild game. The most common subjective symptoms were tingling and/or numbness of distal extremities. The most common objective finding was diminished vibratory sensation in the feet. Half of them had an EMG with the findings ranging from fasciculations to axonal polyneuropathy or demyelinating polyneuropathy.
Our study provides an overview of the pattern of peripheral neuropathy in patients with prion disease. Among patients with peripheral neuropathy symptoms or signs, majority has polyneuropathy. It is important to document the baseline frequency of peripheral neuropathy in prion diseases as these symptoms may become important when conducting surveillance for potential novel zoonotic prion diseases.
“The most common sCJD subtype was MV1-2 (30%), followed by MM1-2 (20%). The Majority of cases wasere male (60%). Half of them had exposure to wild game.”
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WA2 Oral transmission of CWD into Cynomolgus macaques: signs of atypical disease, prion conversion and infectivity in macaques and bio-assayed transgenic mice
Schatzl HM (1, 2), Hannaoui S (1, 2), Cheng Y-C (1, 2), Gilch S (1, 2), Beekes M (3), SchulzSchaeffer W (4), Stahl-Hennig C (5) and Czub S (2, 6)
(1) University of Calgary, Calgary Prion Research Unit, Calgary, Canada (2) University of Calgary, Faculty of Veterinary Medicine, Calgary, Canada, (3) Robert Koch Institute, Berlin, Germany, (4) University of Homburg/Saar, Homburg, Germany, (5) German Primate Center, Goettingen, Germany, (6) Canadian Food Inspection Agency (CFIA), Lethbridge, Canada.
To date, BSE is the only example of interspecies transmission of an animal prion disease into humans. The potential zoonotic transmission of CWD is an alarming issue and was addressed by many groups using a variety of in vitro and in vivo experimental systems. Evidence from these studies indicated a substantial, if not absolute, species barrier, aligning with the absence of epidemiological evidence suggesting transmission into humans. Studies in non-human primates were not conclusive so far, with oral transmission into new-world monkeys and no transmission into old-world monkeys. Our consortium has challenged 18 Cynomolgus macaques with characterized CWD material, focusing on oral transmission with muscle tissue. Some macaques have orally received a total of 5 kg of muscle material over a period of 2 years. After 5-7 years of incubation time some animals showed clinical symptoms indicative of prion disease, and prion neuropathology and PrPSc deposition were found in spinal cord and brain of euthanized animals. PrPSc in immunoblot was weakly detected in some spinal cord materials and various tissues tested positive in RT-QuIC, including lymph node and spleen homogenates. To prove prion infectivity in the macaque tissues, we have intracerebrally inoculated 2 lines of transgenic mice, expressing either elk or human PrP. At least 3 TgElk mice, receiving tissues from 2 different macaques, showed clinical signs of a progressive prion disease and brains were positive in immunoblot and RT-QuIC. Tissues (brain, spinal cord and spleen) from these and preclinical mice are currently tested using various read-outs and by second passage in mice. Transgenic mice expressing human PrP were so far negative for clear clinical prion disease (some mice >300 days p.i.). In parallel, the same macaque materials are inoculated into bank voles.
Taken together, there is strong evidence of transmissibility of CWD orally into macaques and from macaque tissues into transgenic mouse models, although with an incomplete attack rate. The clinical and pathological presentation in macaques was mostly atypical, with a strong emphasis on spinal cord pathology. Our ongoing studies will show whether the transmission of CWD into macaques and passage in transgenic mice represents a form of non-adaptive prion amplification, and whether macaque-adapted prions have the potential to infect mice expressing human PrP.
The notion that CWD can be transmitted orally into both new-world and old-world non-human primates asks for a careful reevaluation of the zoonotic risk of CWD.
See also poster P103
***> The notion that CWD can be transmitted orally into both new-world and old-world non-human primates asks for a careful reevaluation of the zoonotic risk of CWD.
====
Source Prion Conference 2018 Abstracts
https://hal.science/hal-04236401v1/file/Prion%202018%20book%20of%20abstracts%20180516.pdf
http://transmissiblespongiformencephalopathy.blogspot.com/2018/05/prion-2018-may-22-25-2018-santiago-de.html
http://chronic-wasting-disease.blogspot.com/2018/07/oral-transmission-of-cwd-into.html
http://prionconference.blogspot.com/2018/
So, this is what we leave our children and grandchildren?
***> CWD TSE Prion Zoonotic Zoonosis Humans, What if? <***
CDC CWD TSE Prion Update 2024
KEY POINTS
Chronic wasting disease affects deer, elk and similar animals in the United States and a few other countries.
The disease hasn't been shown to infect people.
However, it might be a risk to people if they have contact with or eat meat from animals infected with CWD.
https://www.cdc.gov/chronic-wasting/about/index.html
see archived url link;
https://web.archive.org/web/20240617224730/https://www.cdc.gov/chronic-wasting/about/index.html
THURSDAY, SEPTEMBER 24, 2026
Looming Crisis U. S. Transmissible Spongiform Encephalopathy TSE Prion, in Cattle, Cervid, Sheep, Pigs, and Humans
https://transmissiblespongiformencephalopathy.blogspot.com/2026/09/looming-crisis-u-s-transmissible.html
https://prpsc.proboards.com/thread/246/looming-crisis-prion-cattle-cervid
CWD, So, this is what we leave our children and grandchildren?
Control of Chronic Wasting Disease OMB Control Number: 0579-0189APHIS-2021-0004 Singeltary Submission
https://www.regulations.gov/comment/APHIS-2021-0004-0002
https://downloads.regulations.gov/APHIS-2021-0004-0002/attachment_1.pdf
Docket No. APHIS-2018-0011 Chronic Wasting Disease Herd Certification
https://www.regulations.gov/document/APHIS-2018-0011-0003
https://downloads.regulations.gov/APHIS-2018-0011-0003/attachment_1.pdf
APHIS Indemnity Regulations [Docket No. APHIS-2021-0010] RIN 0579-AE65 Singeltary Comment Submission
Comment from Singeltary Sr., Terry
Posted by the Animal and Plant Health Inspection Service on Sep 8, 2022
https://www.regulations.gov/comment/APHIS-2021-0010-0003
https://downloads.regulations.gov/APHIS-2021-0010-0003/attachment_1.pdf
Docket No. FDA-2003-D-0432 (formerly 03D-0186) Use of Material from Deer and Elk in Animal Feed
PUBLIC SUBMISSION
Comment from Terry Singeltary Sr.
Posted by the Food and Drug Administration on May 17, 2016 Comment
Docket No. FDA-2003-D-0432 (formerly 03D-0186) Use of Material from Deer and Elk in Animal Feed Singeltary Submission
https://www.regulations.gov/comment/FDA-2003-D-0432-0011
https://www.regulations.gov/docket/FDA-2003-D-0432
MONDAY, OCTOBER 12, 2026
Chronic Wasting Disease CWD TSE Prion Strains and Potential Zoonotic Ramifications
https://chronic-wasting-disease.blogspot.com/2026/10/chronic-wasting-disease-cwd-tse-prion.html
https://prpsc.proboards.com/thread/255/prion-strains-potential-zoonotic-ramifications
THURSDAY, JUNE 12, 2025
***> Redefining the zoonotic potential of chronic wasting disease Singeltary Review
https://chronic-wasting-disease.blogspot.com/2025/06/redefining-zoonotic-potential-of.html
***> Cervid CWD TSE PrP Transmission to Humans, has it already happened and being masked as sporadic CJD, What if? July 2026 Review <***
https://chronic-wasting-disease.blogspot.com/2026/07/cervid-cwd-tse-prp-transmission-to.html
https://prpsc.proboards.com/thread/224/cervid-transmission-humans-july-review
MONDAY, JUNE 1, 2026
NATIONAL PRION DISEASE PATHOLOGY SURVEILLANCE CENTER CJD SURVEILLANCE TABLES OF CASES EXAMINED NPDPSC Last updated March 31st, 2026
https://prionunitusaupdate.blogspot.com/2026/06/national-prion-disease-pathology.html
US NATIONAL PRION DISEASE PATHOLOGY SURVEILLANCE CENTER CJD TSE REPORT SEPTEMBER 2025
From the first full year of reporting CJD TSE in the US in 2000, where 90 cases of CJD was reported that year, to today, where in September 2025, the number of CJD cases reported in the last full year reporting, which would have been 2024, the number of CJD cases for 2024 was 249 cases. So, from the first full year 2000 CJD cases were 90 cases confirmed in that year, to 2024, where 2024 CJD statistics rose to 249 confirmed CJD cases in a single year. A dramatic increase in deaths, from figures that don’t seem to be dramatic. But thes figures today, they are not from “better surveillance”, that dog don’t hunt no more. They have been saying this for over 25 years, year after year, well it’s time to call it for what it is, Human Transmissible Spongiform Encephalopathy TSE Prion cases are rising, and it’s NOT because of better surveillance, or just a “happenstance of bad luck, that 85%+ of all human cases, sporadic CJD, including VPSPr, just happen spontaneously, no, it’s because of unknown environmental factors, and or iatrogenic factors, imho…terry
US NATIONAL PRION DISEASE PATHOLOGY SURVEILLANCE CENTER CJD TSE REPORT SEPTEMBER 2025
https://prionunitusaupdate.blogspot.com/2025/10/us-national-prion-disease-pathology.html
WEDNESDAY, SEPTEMBER 2, 2026
A new chapter for CWRU’s Prion Center
https://prionunitusaupdate.blogspot.com/2026/09/a-new-chapter-for-cwrus-prion-center.html
https://prpsc.proboards.com/thread/239/new-chapter-cwru-prion-center
Terry S. Singeltary Sr.
posted by Terry S. Singeltary Sr. at
3:29 PM
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