USDA EXPLANATORY NOTES ANIMAL AND PLANT HEALTH INSPECTION SERVICE 2025-2014 CHRONIC WASTING DISEASE CWD TSE CERVID
USDA EXPLANATORY NOTES ANIMAL AND PLANT HEALTH INSPECTION SERVICE 2025-2014 CHRONIC WASTING DISEASE CWD TSE CERVID
2025 USDA EXPLANATORY NOTES – ANIMAL AND PLANT HEALTH INSPECTION SERVICE
Cervids
APHIS works with State agencies to encourage cervid owners to certify their herds by meeting the requirements in the CWD Herd Certification Program (HCP) Standards. APHIS’ voluntary national CWD HCP helps States, Tribes, and the cervid industry control CWD in farmed cervids by allowing the interstate movement only from certified herds. Currently, 28 States participate in the national CWD HCP.
In 2023, eight percent of the farmed cervids in the HCP were tested for CWD at APHIS and State laboratories.
Of the 303,242 farmed cervids tested in 2023, APHIS confirmed 22 new CWD positive farmed cervid herds.
APHIS provided Federal indemnity to depopulate one of the newly identified positive herds and approved an indemnity payment for a second positive herd which will be provided in 2024 once depopulation occurs. The remaining infected herds are under State quarantines.
APHIS determines the use of Federal indemnity payments within the CWD program on a case-by-case basis. In 2023, APHIS made approximately $12.3 million available for cooperative agreements with States and Tribal governments to further develop and implement CWD surveillance, testing, management, and response activities. This includes the further development and evaluation of techniques and strategies to prevent or control CWD in farmed and wild cervid populations. APHIS funded cooperative agreement with 22 States, 15 universities, and 11 Tribes and Tribal Organizations for CWD projects…
https://www.usda.gov/sites/default/files/documents/22-APHIS-2025-ExNotes.pdf
2024 USDA EXPLANATORY NOTES – ANIMAL AND PLANT HEALTH INSPECTION SERVICE
Cervids
APHIS works with State agencies to encourage cervid owners to certify their herds by meeting the requirements in the CWD Herd Certification Program (HCP) Standards. APHIS’ voluntary national CWD HCP helps States, Tribes, and the cervid industry control CWD in farmed cervids by allowing the interstate movement only from certified herds.
Currently, 28 States participate in the national CWD HCP.
In 2022, 7 percent of the 285,589 farmed cervids in the HCP participating states were tested for CWD at State and APHIS laboratories.
APHIS confirmed 23 new CWD positive farmed cervid herds.
APHIS provided Federal indemnity to depopulate nine of the newly identified positive herds in 2022. The remaining infected herds are under State quarantines. APHIS determines the use of Federal indemnity payments within the CWD program on a case-by-case basis. In 2022, APHIS made approximately $9.4 million available for cooperative agreements with States and Tribal governments to further develop and implement CWD surveillance, testing, management, and response activities. This includes the further development and evaluation of techniques and strategies to prevent or control CWD in farmed and wild cervid populations. APHIS funded 27 States and 5 Tribes, 1 Tribal Organization, and 1 State university. The State university agreement was to conduct wild cervid surveillance on Tribal lands…
https://www.usda.gov/sites/default/files/documents/23-2024-APHIS.pdf
2023 USDA EXPLANATORY NOTES – ANIMAL AND PLANT HEALTH INSPECTION SERVICE
Cervids
APHIS coordinates with State agencies to encourage cervid owners to certify their herds and comply with the CWD Herd Certification Program (HCP) Standards…
APHIS’ voluntary national CWD HCP helps States, Tribes, and the cervid industry control CWD in farmed cervids by allowing the interstate movement only from certified herds.
Currently, 28 States participate in the national CWD HCP. In FY 2021, more than 20,502 farmed cervids were tested for CWD at State and APHIS laboratories.
As a result, APHIS identified 35 new CWD positive farmed cervid herds.
APHIS provided Federal indemnity to depopulate nine of the newly identified deer herds in FY 2021. The remaining infected herds are under State quarantines. APHIS determines the use of Federal indemnity payments within the CWD program on a case-by-case basis. In 2021, APHIS made $5.6 million available in cooperative agreement funding to further develop and implement CWD surveillance, testing, management, and response activities, including the further development and evaluation of techniques and strategies to prevent or control CWD in farmed and wild cervid populations. APHIS funded awards to 39 entities: 20 to State Departments of Wildlife, 11 to State Departments of Agriculture, and 8 to Tribal Organizations.
https://www.usda.gov/sites/default/files/documents/23-2023-APHIS.pdf
2022 USDA EXPLANATORY NOTES – ANIMAL AND PLANT HEALTH INSPECTION SERVICE
Cervids
APHIS coordinates with State agencies to encourage cervid owners to certify their herds and comply with the CWD Herd Certification Program Standards…
APHIS’ voluntary national CWD Herd Certification Plan (HCP) helps States, Tribes, and the cervid industry control CWD in farmed cervids by allowing the interstate movement only from certified herds.
Currently, 28 States participate in the national CWD HCP. In FY 2020, more than 11,182 farmed cervids were tested for CWD at State and APHIS laboratories.
As a result, APHIS identified 22 new CWD positive farmed cervid herds.
APHIS provided Federal indemnity to depopulate 15 of the 22 newly identified deer herds in FY 2020.
Four additional farmed cervid herds that were identified as CWD positive herds in FY 2019, were indemnified in FY 2020.
The remaining infected herds are under State quarantines.
APHIS determines the use of Federal indemnity payments within the CWD program on a case- by-case basis. In FY 2020, APHIS and the Department of Interior held a virtual summit with representatives from State agriculture and wildlife agencies, Tribal Nations, conservation and hunting groups, and the cervid industry to identify and discuss stakeholder CWD management needs and information gaps that need to be addressed to effectively control CWD. The information from the summit helped APHIS establish priorities for proposals for competitive cooperative agreements dedicated to CWD control. These cooperative agreement opportunities allow for State departments of agriculture, State animal health agencies, State departments of wildlife or natural resources, and Tribal governments to further develop and implement CWD management and response activities in accordance with the following priorities:
• improving CWD management of affected farmed herds and free-ranging endemic populations;
• improving CWD management of affected areas or premises;
• conducting additional research on amplification assays;
• conducting additional research on predictive genetics; and,
• developing and/or delivering educational outreach materials or programs.
To execute projects based upon those priorities, APHIS funded awards to 25 entities:
19 to State Departments of Natural Resources, 5 to State Departments of Agriculture, and 1 to Tribal Nations.
https://www.usda.gov/sites/default/files/documents/22APHIS2022Notes.pdf
2021 USDA EXPLANATORY NOTES – ANIMAL AND PLANT HEALTH INSPECTION SERVICE
Cervids
In FY 2019, 10 mule deer were tested as part of the project and all 10 tested negative.
Currently, 28 States participate in APHIS’ voluntary national CWD Herd Certification Plan (HCP).
In FY 2019 APHIS tested more than 11,000 farmed cervids for CWD.
As a result, APHIS identified 17 new CWD positive farmed cervid herds.
APHIS provided Federal indemnity to depopulate 7 of the 17 newly identified deer herds in FY 2019. The remaining infected herds found in FY 2019 are under State quarantines.
https://www.usda.gov/sites/default/files/documents/20aphis2021notes.pdf
2020 USDA EXPLANATORY NOTES – ANIMAL AND PLANT HEALTH INSPECTION SERVICE
Cervids
APHIS’ voluntary national CWD Herd Certification Plan (HCP) helps States, Tribes, and the cervid industry control CWD in farmed cervids by allowing the interstate movement only from certified herds.
Currently, 28 States participate in the national CWD HCP and the program used an immunohistochemistry test method to test 21,584 farmed cervids for CWD.
In FY 2018, APHIS identified 15 new CWD positive farmed cervid herds (14 deer herds and 1 reindeer herd).
The reindeer herd in Illinois was the first confirmed case of CWD in a reindeer in North America.
APHIS provided Federal indemnity to depopulate seven of the 15 newly identified deer herds in FY 2018.
The Agency also provided funding for the test and removal of 161 high risk animals that were in close proximity to reactors.
The remaining herds in FY 2018 are under State quarantines.
The Agency determines the use of Federal indemnities within the CWD program on a case-by-case basis. 20-59
https://www.usda.gov/sites/default/files/documents/20aphis2020notes.pdf
2019 President’s Budget Animal and Plant Health Inspection Service
Cervids
APHIS’ voluntary national CWD Herd Certification Plan (HCP) helps States, Tribes, and the cervid industry control CWD in farmed cervids by allowing the interstate movement only from certified herds.
Currently, 28 States participate in the national CWD HCP and the program tested 23,053 farmed cervids for CWD.
In FY 2017, eight new CWD positive farmed cervid herds were identified– one white-tail deer in Iowa, one white-tail deer herd in Minnesota, one white-tail and mule deer herd in Minnesota, one white-tail and sika deer herd in Michigan, three white-tail deer herds in Pennsylvania, and one white-tail deer herd in Texas.
APHIS provided Federal indemnity to depopulate the Iowa herd, the white-tail deer herd in Minnesota, one herd in Pennsylvania and the Texas herd. The State depopulated the Michigan herd. The remaining herds are under State quarantines. One Texas herd used Federal indemnity to remove and test select, high-risk animals to inform the epidemiological investigation and to evaluate the performance of ante-mortem tests.
The Agency determines the use of Federal indemnities within the CWD program on a case-by-case basis. The CWD Program Standards provide guidance on how to meet CWD Herd Certification Program and interstate movement requirements. In July 2016, APHIS convened a working group of State and Federal animal health and wildlife officials and representatives from the farmed cervidae industry to review the CWD Program Standards. APHIS issued a summary of the working group’s discussions and recommended changes to the CWD Program Standards at the 2016 United States Animal Health Association meeting for public comment. APHIS evaluated public comments, and is currently reviewing revisions to the CWD Program. In FY 2017, APHIS published VS Guidance 8000: Requirements for Interstate Transport of Wild Caught Cervids. This guidance document establishes a recommended minimum standard for testing and a uniform process of disease risk assessment to help prevent the spread of cervid diseases such as chronic wasting disease (CWD), bovine tuberculosis (TB), and brucellosis when wild cervids are captured for interstate movement and release.
https://www.usda.gov/sites/default/files/documents/20aphis2019notes.pdf
2018 President’s Budget Animal and Plant Health Inspection Service
Cervids
APHIS’ voluntary national CWD Herd Certification Plan (HCP) helps States, Tribes, and the cervid industry control CWD in farmed cervids by allowing the interstate movement only from certified herds considered to be low risk.
Currently, 29 States participate in the national CWD HCP.
In FY 2016, the program tested 14,503 farmed cervids for CWD and identified seven new CWD positive farmed cervid herds – two white-tail deer herds in Texas, three white-tail deer herds in Wisconsin, one elk herd in Colorado and one elk herd in Iowa. The elk herd in Colorado was depopulated without Federal indemnity and the rest of the herds are under State quarantines. One Texas herd used Federal indemnity to remove and test select animals to inform the epidemiological investigation and to evaluate 20-72 the performance of ante-mortem tests.
The use of Federal indemnities within the CWD program is determined on a case-by-case basis. APHIS is also conducting several pilot projects related to new technologies. In FY 2016, the Agency sponsored a pilot project in Ohio to evaluate the use of a new method for ante-mortem testing in whitetail deer known as rectoanal mucosa associated lymphoid tissue or RAMALT testing. A proof-of-concept pilot project was also performed by APHIS’ National Veterinary Services Laboratories (NVSL) to evaluate ante-mortem biopsies of the medial retropharyngeal lymph node biopsy or MRPLN biopsy. APHIS anticipates implementing both types of ante- mortem testing in the future. Beginning early September 2014, APHIS, in cooperation with the National Agricultural Statistics Service, conducted the first national study of the U.S. farmed cervid industry. The study surveyed 3,000 producers from all States that have farmed cervids. The study provides baseline industry statistics, a description of current production practices and challenges, producer-reported disease occurrences, and an overview of health management and biosecurity practices. A report from the study is now available in electronic and printed formats at: http://www.aphis.usda.gov/nahms.
https://www.usda.gov/sites/default/files/documents/20aphisexnotes2018.pdf
2017 Explanatory Notes Animal and Plant Health Inspection Service
Cervids
APHIS’ voluntary national CWD Herd Certification Plan (HCP) helps States, Tribes, and the cervid industry control CWD in farmed cervids by allowing the interstate movement only from certified herds considered to be low risk.
Currently, 30 States participate in the national CWD HCP: 29 have Approved Status and 1 has Provisional Approved Status. States that meet the CWD HCP requirements have Approved Status and States that do not meet CWD HCP program requirements but have developed a work plan and time frame with APHIS to complete those requirements have Provisional Approved Status.
In FY 2015, the program tested approximately 20,000 farmed cervids for CWD and identified eight new CWD positive farmed white-tailed deer herds – one in Utah, one in Pennsylvania, two in Ohio, two in Wisconsin, and two in Texas.
APHIS depopulated five of these herds (Pennsylvania, Utah, and one each in Wisconsin, Texas, and Ohio). Six elk herds in Colorado, four elk herds in Nebraska, one white-tailed deer herd in Wisconsin and one white-tailed deer herd in Texas remained in quarantine at the end of FY 2015.
APHIS also provided indemnity for and was the lead agency for the depopulation and disposal of four large CWD infected farmed cervid herds in Pennsylvania, Ohio, Utah, and Texas. In cooperation with the National Agricultural Statistics Service, APHIS conducted the first national study of the U.S. farmed-cervid industry in FY 2015. The study provides baseline industry statistics, a description of production practices and challenges, producer-reported disease occurrences, and an overview of health management and biosecurity practices.
https://www.usda.gov/sites/default/files/documents/20aphis2017notes.pdf
2016 Explanatory Notes Animal and Plant Health Inspection Service
https://www.usda.gov/sites/default/files/documents/20aphis2016notes.pdf
2015 Explanatory Notes Animal and Plant Health Inspection Service
https://www.usda.gov/sites/default/files/documents/20aphis2015notes.pdf
2014 Explanatory Notes Animal and Plant Health Inspection Service
https://www.usda.gov/sites/default/files/documents/18aphis2014notes.pdf
Louisiana House of Representative Aug 27, 9:30 AM, HCR-6 CWD Arkansas
Louisiana House of Representative
Chronic Wasting Disease CWD
Arkansas
Snip…
40:35 “…and conversely, I was co-Principle Investigator in NW Arkansas, where prevalence is approaching 50 percent.”
Snip…
41:00 “Specific to the work in Arkansas, in 2020, the state agency was showing the Prevalence at 30 percent in the Northwest part of the State, so flip a coin, so, 1 out of every 3 deer had the disease. We started that research in 2020, and now, the prevalence rate is now exceeding 40% in both sexes, and 50% in males.”
43:00 “what we’re seeing Arkansas now is, that population is declining about 11% a year.”
https://house.louisiana.gov/H_Video/VideoArchivePlayer?v=house/2025/Aug/0827_25_NR_Joint
FRIDAY, SEPTEMBER 05, 2025
Louisiana CWD Task Force Update, Catahoula Parish positive brings total CWD detections for Louisiana to 40, September 2025
https://chronic-wasting-disease.blogspot.com/2025/09/louisiana-cwd-task-force-update.html
SATURDAY, SEPTEMBER 27, 2025
Illinois IDNR Report 539 CWD positive deer in 25 counties Between July 1, 2024, and June 30, 2025
https://chronic-wasting-disease.blogspot.com/2025/09/illinois-idnr-report-539-cwd-positive.html
WEDNESDAY, SEPTEMBER 24, 2025
Michigan CWD Update DNR reports Genesee County’s first Positive Wild Deer
https://chronic-wasting-disease.blogspot.com/2025/09/michigan-dnr-reports-genesee-countys.html
WEDNESDAY, SEPTEMBER 24, 2025
Alabama CWD Report 12 Cases Confirmed To Date
https://chronic-wasting-disease.blogspot.com/2025/09/alabama-cwd-report-12-cases-confirmed.html
WEDNESDAY, SEPTEMBER 24, 2025
Arkansas Total CWD FY16-FY25 Positive 2,036 Confirmed Cases to Date
https://chronic-wasting-disease.blogspot.com/2025/09/arkansas-total-cwd-fy16-fy25-positive.html
WEDNESDAY, SEPTEMBER 24, 2025
Georgia Chronic Wasting Disease CWD TSE Prion Update
https://chronic-wasting-disease.blogspot.com/2025/09/georgia-chronic-wasting-disease-cwd-tse.html
MONDAY, SEPTEMBER 08, 2025
Kentucky Confirmed Captive CWD Oct. 14, 2024, this month KDA confirmed eight new CWD positive deer at the same facility
https://chronic-wasting-disease.blogspot.com/2025/09/kentucky-confirmed-captive-cwd-oct-14.html
THURSDAY, SEPTEMBER 04, 2025
Montana Chronic Wasting Disease CWD TSE Prion May 2017 to Sept 2025 Confirmed 2,593 Cases
https://chronic-wasting-disease.blogspot.com/2025/09/montana-chronic-wasting-disease-cwd-tse.html
August 2025
Oklahoma Confirms Fourth Case CWD in Wild Deer
https://chronic-wasting-disease.blogspot.com/2025/08/oklahoma-confirms-fourth-case-chronic.html
WEDNESDAY, AUGUST 20, 2025
Pennsylvania CAPTIVE CHRONIC WASTING DISEASE CASES 2025 to date
https://chronic-wasting-disease.blogspot.com/2025/08/pennsylvania-captive-chronic-wasting.html
TUESDAY, JULY 29, 2025
Pennsylvania 2,424 confirmed cases CWD to date
https://prpsc.proboards.com/thread/169/pennsylvania-424-confirmed-cases-date
https://pagame.maps.arcgis.com/apps/dashboards/b3c0fd44cc5944ebbc2229ede897b2ae
https://chronic-wasting-disease.blogspot.com/2025/07/pennsylvania-2424-confirmed-cases-cwd_41.html
THURSDAY, JULY 10, 2025
Distribution of chronic wasting disease (CWD) prions in tissues from experimentally exposed coyotes (Canis latrans) Published: July 9, 2025
https://chronic-wasting-disease.blogspot.com/2025/07/distribution-of-chronic-wasting-disease.html
TUESDAY, JUNE 24, 2025
Maryland Department of Natural Resources’ Annual Survey Detects 62 Deer with Chronic Wasting Disease in 2024
https://chronic-wasting-disease.blogspot.com/2025/06/maryland-department-of-natural.html
TUESDAY, MAY 27, 2025
Iowa CWD Update May 2025 confirms 523 case to date
https://chronic-wasting-disease.blogspot.com/2025/05/iowa-cwd-update-may-2025-confirms-523.html
WEDNESDAY, MAY 14, 2025
Virginia DWR Reports 2024–2025 CWD Results 109 positive
https://dwr.virginia.gov/media/press-release/dwr-reports-2024-2025-chronic-wasting-disease-surveillance-results/
https://chronic-wasting-disease.blogspot.com/2025/05/virginia-dwr-reports-20242025-cwd.html
WEDNESDAY, MAY 14, 2025
North Dakota 2024 CWD Test Results Confirm 17 Positive
https://chronic-wasting-disease.blogspot.com/2025/05/north-dakota-2024-cwd-test-results.html
WEDNESDAY, MARCH 26, 2025
Ohio ODNR Confirm 24 WTD Positive For CWD 2024-25 Hunting Season
https://chronic-wasting-disease.blogspot.com/2025/03/ohio-odnr-confirm-24-wtd-positive-for.html
WEDNESDAY, MARCH 12, 2025
West Virginia DNR Expands Containment Area after detection of CWD in a Grant County deer
https://chronic-wasting-disease.blogspot.com/2025/03/west-virginia-dnr-expands-containment.html
2025 Colorado CWD TSE Prion prevalence increased in 14 herds, remained about the same in 16 herds, and decreased in 4 herds
Colorado 2022 2024 CWD prevalence increased in 14 herds, remained about the same in 16 herds, and decreased in 4 herds
Colorado CWD has gotten so bad, they can’t even give a Total To Date count. Best they can do is is give you Total Herds With CWD…
Jeff Davis, Director, Colorado Parks and Wildlife Parks and Wildlife Commission: Dallas May, Chair ∙ Richard Reading, Vice-Chair ∙ Karen Bailey, Secretary ∙ Jessica Beaulieu Marie Haskett ∙ Tai Jacober ∙ Jack Murphy ∙ Gabriel Otero ∙ Murphy Robinson ∙ James Jay Tutchton ∙ Eden Vardy
MEMORANDUM
April 25, 2025
TO: Colorado Parks and Wildlife Commissioners
FROM: Brian Dreher, Assistant Director, Terrestrial Branch
Subject: Chronic Wasting Disease Update for Parks and Wildlife Commission
Dear Commissioners,
This briefing summarizes CPW’s mandatory chronic wasting disease (CWD) findings from the 2022- 2024 hunting seasons. Results provide the first indication of whether CWD management actions taken for deer over the past 5-7 years have had an effect on CWD prevalence (estimated percent infected) in each herd. In summary, CWD prevalence decreased in 4 herds, increased in 14 herds, and remained about the same in 16 herds.
Background
Chronic wasting disease, a fatal neurological disease found in deer, elk, and moose, is well established in herds throughout much of Colorado. We have detected CWD in 42 of our 51 deer herds, 17 of 42 elk herds, and 2 of 13 moose herds. CWD prevalence is highest in deer and lowest in moose. This disease is always fatal and animals die from the disease within about 2-2.5 years of infection. CWD infection shortens the lifespan of infected animals. If infection rates become too high, CWD can affect a herd’s ability to sustain itself.
In response to increasing CWD prevalence, the Parks and Wildlife Commission approved a statewide CWD Response Plan in 2019. One element was a 15-year mandatory testing plan, which will include three 5-year rotations for deer. Pilot work in 2017 and 2018 had shown that the number of deer submitted for testing is much higher through mandatory testing than for voluntary submissions, which allows CPW to generate reliable estimates of CWD prevalence at the herd level.
In addition, the CWD Response Plan establishes a compulsory management threshold, which means when prevalence exceeds 5% in adult (>2 years) male deer then some form of management action will be taken to reduce prevalence until it falls below the 5% threshold. CPW identifies various management actions in the plan that are available to local managers to prescribe in herd management efforts, all of which have the potential to help reduce prevalence in deer herds.
CWD prevalence was assessed via mandatory testing in all deer herds from 2017-2020; mandatory testing focused on elk in 2021. In 2022, CPW restarted the 5-year testing rotation for deer. Thirty-four deer herds have been included in a second round of mandatory testing. Three herds, White River (D- 07, 2024) Middle Park (D-09, 2024), and Bears Ears (D-02, 2025) were already scheduled for a third round of mandatory testing to learn more about how prevalence is changing in these herds related to the 2022-2023 severe winter and exponential growth in CWD prevalence. CPW will conclude the second round of mandatory testing for deer in 2025 and for elk in 2026.
Mandatory Testing Results CWD prevalence estimates have decreased in 4 deer herds, increased in 14 deer herds, and remained about the same in 16 deer herds (Figure 1, Table 1).
Prevalence was expected to increase in many high-prevalence herds. However, prevalence stayed about the same between the two rounds of mandatory testing in many high- prevalence herds. This is an indication that prescribed management actions are preventing or slowing increases in CWD prevalence, even if we are not seeing a reduction in prevalence. Additional data and robust analyses are needed over the next 7 years of mandatory testing to guide CPW's interpretation of these results before we are in a position to show an association between prescribed management actions and CWD prevalence.
CPW prescribed various management actions in each of these 34 herds and the response in prevalence varies. Therefore, CPW will evaluate why prevalence increased in some herds and decreased in others. Overall, these preliminary data are encouraging for some herds and suggest harvest-based management actions could be a promising CWD control strategy.
Further Analyses
CPW will continue analyses of these CWD prevalence changes by comparing various factors between herds and the respective management actions prescribed. Comparing changes to license quotas by season, dates of harvest and prevalence estimates by season, post-hunt buck/doe ratios, abundance of bucks and does, and the percent change in buck licenses and buck harvest, etc., all in relation to changes in CWD prevalence, should improve our ability to evaluate relationships between various management actions and disease prevalence. CPW plans to complete these analyses as the 15-year mandatory testing period concludes, if not sooner.
In our more than 40-year history working with CWD, one of the most important lessons we have learned is that we rarely see immediate changes in CWD dynamics. This is a slow-moving disease and changes in prevalence (both increases and decreases) may not be readily apparent. Multiple repeated prevalence estimates over the long-term along with consistent management application will be necessary to evaluate patterns of change in relationship to management actions.
Lastly, severe winter conditions seen in Northwestern Colorado during the 2022-2023 winter generated many questions on potential implications for CWD dynamics in the region. Harsh winter conditions may cause more rapid mortality of infected deer in the clinical phase of disease and could reduce the number of infected animals on the landscape. Overall population reductions associated with harsh winter conditions may also affect deer/elk density on the landscape and reduce direct animal-to-animal transmission. On the other hand, prolonged concentrations of deer and elk on very limited winter ranges could facilitate increased contact as well as environmental accumulation of CWD prions (infectious agent) that could increase both direct and indirect transmission pathways. Preliminary, based on 2024 results, it does not appear that the severe winter of 2022-2023 resulted in reduced CWD prevalence. Ultimately, the interplay of weather conditions, changing population dynamics, and changes in habitat use associated with a severe winter limit our capacity to predict how CWD prevalence might change. As we proceed with analyses to evaluate factors influencing CWD prevalence in Colorado wildlife populations, incorporating changes associated with periodic severe winters will be an important consideration.
CC: J. Davis R. DeWalt Regional Managers M. Eckert Senior Biologists J. Runge A. Holland
https://cpw.widen.net/view/pdf/rozctppvvm/Item.11_2025-04-24_Chronic_Wasting_Disease_Update_for_PWC.pdf?u=xyuvvu
2022 Colorado detected CWD in 40 of our 54 deer herds, 17 of 42 elk herds, and 2 of 9 moose herds
MEMORANDUM
To: Members of the Colorado Parks and Wildlife Commission
From: Dan Prenzlow, Director
Date: April 22, 2022
Subject: Chronic Wasting Disease Update for Parks and Wildlife Commission
Dear Commissioners,
This briefing summarizes CPW’s mandatory chronic wasting disease (CWD) findings from the 2021-2022 hunting seasons and, more broadly, things we have learned over the first 5-year rotation of mandatory testing (2017-2021 hunting seasons). Overall, the decision to commit to annual mandatory testing has been resoundingly important to understanding the status of this disease in Colorado, acquiring and communicating reliable prevalence estimates, and laying a foundation to assess herd-specific management actions to combat CWD. It is my pleasure to present this current information to keep you apprised on the status of CWD in our big game herds.
Background
Chronic wasting disease, a fatal neurological disease found in deer, elk, and moose, is well established in herds throughout much of Colorado. We have detected CWD in 40 of our 54 deer herds, 17 of 42 elk herds, and 2 of 9 moose herds. Disease prevalence (percent infected) is highest in deer and lowest in moose. This disease is always fatal and animals die from the disease within about 2-2.5 years of infection. CWD infection shortens the lifespan of infected animals. If infection rates become too high, CWD can affect a herd’s ability to sustain itself.
Snip…
https://web.archive.org/web/20220513134346/https://cpw.state.co.us/Documents/Commission/2022/May/Item.11-PWC_Memo_CWD_Update_EckertMillerWood_April2022-Matthew_Eckert-DNR.pdf
Colorado As of July 2018, at least 31 of Colorado's 54 deer herds (57%), 16 of 43 elk herds (37%), and 2 of 9 moose herds (22%) are known to be infected with CWD. Four of Colorado's 5 largest deer herds and 2 of the state’s 5 largest elk herds are infected.
As of July 2018, at least 31 of Colorado's 54 deer herds (57%), 16 of 43 elk herds (37%), and 2 of 9 moose herds (22%) are known to be infected with CWD. Four of Colorado's 5 largest deer herds and 2 of the state’s 5 largest elk herds are infected. Deer herds tend to be more heavily infected than elk and moose herds living in the same geographic area. Not only are the number of infected herds increasing, the past 15 years of disease trends generally show an increase in the proportion of infected animals within herds as well. Of most concern, greater than a 10-fold increase in CWD prevalence has been estimated in some mule deer herds since the early 2000s; CWD is now adversely affecting the performance of these herds…
https://cpw.widen.net/s/d7b55k9dcm/colorado_chronic_wasting_disease_response_plan
https://cpw.state.co.us/hunting/chronic-wasting-disease
TUESDAY, SEPTEMBER 30, 2025
Colorado 2022 2024 CWD TSE Prion prevalence increased in 14 herds, remained about the same in 16 herds, and decreased in 4 herds
https://chronic-wasting-disease.blogspot.com/2025/09/colorado-2022-2024-cwd-tse-prion.html
MONDAY, MAY 09, 2022
Colorado CWD TSE Prion Detected in 40 of 54 deer herds, 17 of 42 elk herds, and 2 of 9 moose herds
https://chronic-wasting-disease.blogspot.com/2022/05/colorado-cwd-tse-prion-detected-in-40.html
THURSDAY, SEPTEMBER 11, 2025
CWD IS RAVAGING MY FAMILY’S LAND, BUT IT’S NOT TOO LATE FOR YOU
https://chronic-wasting-disease.blogspot.com/2025/09/cwd-is-ravaging-my-familys-land-but-its.html
MONDAY, APRIL 28, 2025
Wisconsin DNR 2024 CWD 1,786 samples testing positive
https://chronic-wasting-disease.blogspot.com/2025/04/wisconsin-dnr-2024-cwd-1786-samples.html
https://chronic-wasting-disease.blogspot.com/2025/05/wisconsin-rock-county-deer-farm.html
FRIDAY, APRIL 04, 2025
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
“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
Texas Chronic Wasting Disease CWD TSE Prion Dashboard Update August 2025
SEE NEW DASHBOARD FOR CWD POSITIVES!
https://experience.arcgis.com/experience/8f6c27330c444a19b4b57beb7ffabb8b/page/Dashboard#data_s=id%3AdataSource_3-1966d773e34-layer-10%3A29
Texas CWD total by calendar years
https://chronic-wasting-disease.blogspot.com/2024/12/texas-cwd-tse-prion-positive-samples-by.html
https://tpwd.texas.gov/huntwild/wild/diseases/cwd/positive-cases/listing-cwd-cases-texas.phtml#texasCWD
Counties where CWD Exposed Deer were Released
https://tpwd.texas.gov/documents/257/CWD-Trace-OutReleaseSites.pdf
Number of CWD Exposed Deer Released by County
https://tpwd.texas.gov/documents/258/CWD-Trace-OutReleaseSites-NbrDeer.pdf
CWD Status Captive Herds
https://www.aphis.usda.gov/sites/default/files/status-of-captive-herds.pdf
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
https://prpsc.proboards.com/thread/178/texas-game-wardens-conclusion-ghost
WEDNESDAY, MAY 14, 2025
Texas CWD TSE Prion Cases Rises to 1099 Confirmed Cases To Date
https://chronic-wasting-disease.blogspot.com/2025/05/texas-cwd-tse-prion-cases-rises-to-1099.html
TAHC 425th Commission Meeting CWD 1:45:00
* See CWD speakers expressing their concerns with changed regulations…
2:00 hr mark
https://m.youtube.com/watch?v=bWawHpdn_7I
TEXAS ANIMAL HEALTH COMMISSION 423rd Commission Meeting CWD Update February 25, 2025
https://chronic-wasting-disease.blogspot.com/2025/02/texas-animal-health-commission-423rd.html
THURSDAY, APRIL 24, 2025
***> US Captive CWD Positive Herds Update April 2025
https://chronic-wasting-disease.blogspot.com/2025/04/us-captive-cwd-positive-herds-update.html
Captive CHRONIC WASTING DISEASE CASES Update August 2025 Captive CHRONIC WASTING DISEASE CASES Update August 2025, Pennsylvania, Wisconsin, Utah, and Texas
https://www.aphis.usda.gov/sites/default/files/status-of-captive-herds.pdf
https://chronic-wasting-disease.blogspot.com/2025/08/texas-game-wardens-near-conclusion-of.html
MONDAY, SEPTEMBER 15, 2025
Chronic Wasting Disease CWD TSE Prion Environmental Factors Update
https://chronic-wasting-disease.blogspot.com/2025/09/chronic-wasting-disease-cwd-tse-prion.html
https://chronic-wasting-disease.blogspot.com/
Chronic Wasting Disease CWD TSE Prion Environmental & Zoonosis Factors Update September 2025
What does CDC say?
CDC CWD TSE Prion Update 2025
KEY POINTS
Chronic wasting disease affects deer, elk and similar animals in the United States and a few other countries.
The disease hasn't been shown to infect people.
However, it might be a risk to people if they have contact with or eat meat from animals infected with CWD.
https://www.cdc.gov/chronic-wasting/about/index.html
Prions in Muscles of Cervids with Chronic Wasting Disease, Norway
Volume 31, Number 2—February 2025
Research
Prions in Muscles of Cervids with Chronic Wasting Disease, Norway
Snip…
In summary, the results of our study indicate that prions are widely distributed in peripheral and edible tissues of cervids in Norway, including muscles. This finding highlights the risk of human exposure to small amounts of prions through handling and consuming infected cervids. Nevertheless, we note that this study did not investigate the zoonotic potential of the Norway CWD prions. In North America, humans have historically consumed meat from CWD-infected animals, which has been documented to harbor prions (35,44–47). Despite the potential exposure to prions, no epidemiologic evidence indicates a correlation between the occurrence of CWD cases in animals and the prevalence of human prion diseases (48). A recent bioassay study reported no transmissions from 3 Nordic isolates into transgenic mice expressing human PrP (49). Therefore, our findings should be interpreted with caution in terms of human health implications, and further research is required to determine the zoonotic potential of these CWD strains.
The presence of prions in peripheral tissues indicates that CWD may have a systemic nature in all Norwegian cervid species, challenging the view that prions are exclusively localized in the CNS in sporadic CWD of moose and red deer. Our findings expand the notion of just how widely distributed prions can be in cervids affected with CWD and call into question the capability of emerging CWD strains in terms of infectivity to other species, including humans.
Appendix
https://wwwnc.cdc.gov/eid/article/31/2/24-0903-app1.pdf
https://wwwnc.cdc.gov/eid/article/31/2/24-0903_article
Volume 31, Number 2—February 2025
Dispatch
Detection of Chronic Wasting Disease Prions in Raw, Processed, and Cooked Elk Meat, Texas, USA
Rebeca Benavente, Fraser Brydon, Francisca Bravo-Risi, Paulina Soto, J. Hunter Reed, Mitch Lockwood, Glenn Telling, Marcelo A. Barria, and Rodrigo MoralesComments to Author
Snip…
CWD prions have been detected in the muscle of both farmed and wild deer (10), and at concentrations relevant to sustain disease transmission (11). CWD prions have also been identified across several cervid species and in multiple tissues, including lymph nodes, spleen, tongue, intestines, adrenal gland, eyes, reproductive tissues, ears, lungs, and liver, among others (12–14). Those findings raise concerns about the safety of ingesting processed meats that contain tissues other than skeletal muscle (15) (Appendix). https://wwwnc.cdc.gov/eid/article/31/2/24-0906-app1.pdf .
In addition, those findings highlight the need for continued vigilance and research on the transmission risks of prion diseases and for development of new preventative and detection measures to ensure the safety of the human food supply.
Snip…
Overall, our study results confirm previous reports describing the presence of CWD prions in elk muscles (13). The data also demonstrated CWD prion persistence in food products even after processing through different procedures, including the addition of salts, spices, and other edible elements. 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
Volume 31, Number 1—January 2025
Dispatch
Detection of Prions in Wild Pigs (Sus scrofa) from Areas with Reported Chronic Wasting Disease Cases, United States
Abstract
Using a prion amplification assay, we identified prions in tissues from wild pigs (Sus scrofa) living in areas of the United States with variable chronic wasting disease (CWD) epidemiology. Our findings indicate that scavenging swine could play a role in disseminating CWD and could therefore influence its epidemiology, geographic distribution, and interspecies spread.
Snip…
Conclusions In summary, results from this study showed that wild pigs are exposed to cervid prions, although the pigs seem to display some resistance to infection via natural exposure. Future studies should address the susceptibility of this invasive animal species to the multiple prion strains circulating in the environment. Nonetheless, identification of CWD prions in wild pig tissues indicated the potential for pigs to move prions across the landscape, which may, in turn, influence the epidemiology and geographic spread of CWD.
https://wwwnc.cdc.gov/eid/article/%2031/1/24-0401_article
Although the current U.S. feed ban is based on keeping tissues from TSE infected cattle from contaminating animal feed, swine rations in the U.S. could contain animal derived components including materials from scrapie infected sheep and goats. These results indicating the susceptibility of pigs to sheep scrapie, coupled with the limitations of the current feed ban, indicates that a revision of the feed ban may be necessary to protect swine production and potentially human health.
2. Determined that pigs naturally exposed to chronic wasting disease (CWD) may act as a reservoir of CWD infectivity. Chronic wasting disease is a naturally occurring, fatal, neurodegenerative disease of cervids. The potential for swine to serve as a host for the agent of CWD disease is unknown. The purpose of this study was to investigate the susceptibility of swine to the CWD agent following experimental oral or intracranial inoculation. Pigs were assigned to 1 of 3 groups: intracranially inoculated; orally inoculated; or non-inoculated. At market weight age, half of the pigs in each group were tested ('market weight' groups). The remaining pigs ('aged' groups) were allowed to incubate for up to 73 months post inoculation (MPI). Tissues collected at necropsy were examined for disease-associated prion protein (PrPSc) by multiple diagnostic methods. Brain samples from selected pigs were bioassayed in mice expressing porcine prion protein. Some pigs from each inoculated group were positive by one or more tests. Bioassay was positive in 4 out of 5 pigs assayed. Although only small amounts of PrPSc were detected using sensitive methods, this study demonstrates that pigs can serve as hosts for CWD. Detection of infectivity in orally inoculated pigs using mouse bioassay raises the possibility that naturally exposed pigs could act as a reservoir of CWD infectivity. Currently, swine rations in the U.S. could contain animal derived components including materials from deer or elk. In addition, feral swine could be exposed to infected carcasses in areas where CWD is present in wildlife populations. The current feed ban in the U.S. is based exclusively on keeping tissues from TSE infected cattle from entering animal feeds. These results indicating the susceptibility of pigs to CWD, coupled with the limitations of the current feed ban, indicates that a revision of the feed ban may be necessary to protect swine production and potentially human health.
The agent of chronic wasting disease from pigs is infectious in transgenic mice expressing human PRNP
https://www.ars.usda.gov/research/publications/publication/?seqNo115=353091
Currently, swine rations in the U.S. could contain animal derived components including materials from deer or elk. In addition, feral swine could be exposed to infected carcasses in areas where CWD is present in wildlife populations. The current feed ban in the U.S. is based exclusively on keeping tissues from TSE infected cattle from entering animal feeds. These results indicating the susceptibility of pigs to CWD, coupled with the limitations of the current feed ban, indicates that a revision of the feed ban may be necessary to protect swine production and potentially human health.
https://www.ars.usda.gov/research/project/?accnNo=432011&fy=2017
Conclusions: This study demonstrates that PrPSc accumulates in lymphoid tissues from pigs challenged intracranially or orally with the CWD agent, and can be detected as early as 4 months after challenge. CWD-infected pigs rarely develop clinical disease and if they do, they do so after a long incubation period. This raises the possibility that CWD-infected pigs could shed prions into their environment long before they develop clinical disease. Furthermore, lymphoid tissues from CWD-infected pigs could present a potential source of CWD infectivity in the animal and human food chains.
https://www.ars.usda.gov/research/publications/publication/?seqNo115=337105
This study demonstrates that pigs can serve as potential hosts for CWD, although with low attack rates and scant PrPcwd accumulation. Detection of infectivity in orally challenged pigs using mouse bioassay raises the possibility that naturally exposed pigs act as a reservoir of CWD infectivity, even though affected pigs do not develop overt clinical signs or readily detectable PrPcwd.
https://www.ars.usda.gov/research/publications/publication/?seqNo115=326166
***> Price of TSE Prion Poker goes up substantially, all you cattle ranchers and such, better pay close attention here...terry <***
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.
Funded by: This research was funded in its entirety by congressionally appropriated funds to the United States Department of Agriculture, Agricultural Research Service. The funders of the work did not influence study design, data collection and analysis, decision to publish, or preparation of the manuscript.
*****>>> "Cattle with the E211K polymorphism are susceptible to the CWD agent after oronasal exposure of 0.2 g of infectious material." <<<*****
=====end
Strain characterization of chronic wasting disease in bovine-PrP transgenic mice
Nuria Jerez-Garrido1, Sara Canoyra1, Natalia Fernández-Borges1, Alba Marín Moreno1, Sylvie L. Benestad2, Olivier Andreoletti3, Gordon Mitchell4, Aru Balachandran4, Juan María Torres1 and Juan Carlos Espinosa1. 1 Centro de Investigación en Sanidad Animal, CISA-INIA-CSIC, Madrid, Spain. 2 Norwegian Veterinary Institute, Ås, Norway. 3 UMR Institut National de la Recherche Agronomique (INRA)/École Nationale Vétérinaire de Toulouse (ENVT), Interactions Hôtes Agents Pathogènes, Toulouse, France. 4 Canadian Food Inspection Agency, Ottawa, Canada.
Aims: Chronic wasting disease (CWD) is an infectious prion disease that affects cervids. Various CWD prion strains have been identified in different cervid species from North America and Europe. The properties of the infectious prion strains are influenced by amino acid changes and polymorphisms in the PrP sequences of different cervid species. This study, aimed to assess the ability of a panel of CWD prion isolates from diverse cervid species from North America and Europe to infect bovine species, as well as to investigate the properties of the prion strains following the adaptation to the bovine-PrP context.
Materials and Methods: BoPrP-Tg110 mice overexpressing the bovine-PrP sequence were inoculated by intracranial route with a panel of CWD prion isolates from both North America (two white-tailed deer and two elk) and Europe (one reindeer, one moose and one red deer).
Results: Our results show distinct behaviours in the transmission of the CWD isolates to the BoPrP-Tg110 mouse model. Some of these isolates did not transmit even after the second passage. Those able to transmit displayed differences in terms of attack rate, survival times, biochemical properties of brain PrPres, and histopathology.
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.
Funded by: MCIN/AEI /10.13039/501100011033 and by European Union NextGeneration EU/PRTR
Grant number: PCI2020-120680-2 ICRAD
"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."
=====end
https://prion2023.org/wp-content/uploads/2023/10/Meeting-book-final-version2.pdf
so, this is what we leave our children and grandchildren?
Redefining the zoonotic potential of chronic wasting disease
Project Number 5R01NS121016-04
Contact PI/Project Leader SCHATZL, HERMANN M
Other PIs
Awardee Organization
UNIVERSITY OF CALGARY
Description
Abstract Text
The rapid expansion of chronic wasting disease (CWD), a prion disease of free-ranging and farmed deer, elk and moose, is a major and ongoing threat in North America. Approximately 1 in 36 Americans hunt deer and elk and eat venison, and it is estimated that 7,000 – 15,000 CWD-infected cervids are consumed annually. This fuels growing concerns about the human health risks imposed by CWD. There are no documented cases of CWD transmission to humans, even though with the long incubation periods of all prion diseases and the unknown presentation of CWD in humans definite conclusions are not possible. The zoonotic potential of prion diseases has been exemplified by bovine spongiform encephalopathy (BSE, mad cow disease) which resulted in a new form of human prion disease (vCJD). BSE was transmissible to Cynomolgus macaques and transgenic mice expressing the human prion protein. Initial results of CWD transmission studies to the same non-human primate and mouse models of human prion disease were not successful, corroborating the conclusion that the zoonotic potential of CWD is low, if not absent. Our groups were part of a consortium that inoculated Cynomolgus macaques via different routes with CWD. Some animals exhibited subtle clinical signs reminiscent of prion disease, and upon euthanasia, weak signs of vacuolation, PrPSc deposition and astrocytosis in the brain were found, while no proteinase K (PK) resistant prion protein (PrP) was detectable. We have now demonstrated for the first time that CWD from macaques can transmit clinical prion disease to transgenic mouse models of CWD and human prion disease, albeit in the absence of detectable PK-resistant PrP. Bona fide PrPSc was only detected upon 3rd passage from mouse to bank vole models. Altogether, this is the first evidence that CWD very likely has zoonotic potential. The goal of the current proposal is to redefine the zoonotic potential of CWD by characterizing the biological properties of CWD prions emerging upon experimental transmission into macaques, for obtaining important information on how CWD could manifest in humans.
In Aim 1, we will study whether CWD from macaque (CWDmac) in bank voles represents a new prion strain, by comparing biochemical and biological properties to an array of known prion strains from different species.
Aim 2 addresses the question whether CWDmac represents an intermediate prion strain, adaptable to cervids or humans upon passage, and possessing an expanded host range. We will address this by in vivo passage in cervidized or humanized mouse models. In vitro, we will utilize serial PMCA and a newly generated PrP0/0 cell culture model for infection, upon reconstitution with PrP from different species.
In Aim 3, we will shed light on the observed dissociation between infectivity and the presence of bona fide PrPSc. We propose to identify atypical PrP fragments associated with CWDmac, and we will elucidate brain cell responses to CWDmac exposure by innovative single cell RNA sequencing. In summary, our studies will uncover the possible manifestation of CWD in humans, which is of critical importance for drawing definite conclusions about the zoonotic potential of CWD.
Public Health Relevance Statement
The zoonotic potential of chronic wasting disease (CWD) is unclear to date. We provide the first evidence by transmission experiments to different transgenic mouse models and bank voles that Cynomolgus macaques inoculated via different routes with CWD-positive cervid tissues harbor infectious prions that elicit clinical disease in rodents. Our proposed studies will unravel the properties of these prions, how they will adapt to humans and which pathways are activated in brain cells and associated with clinical disease. Results from these studies uncover the potential manifestation of CWD in humans, which is highly relevant for human health.
https://eventos.galoa.com.br/prion-2025/page/5178-home
Project 3A: CWD Prion Shedding and Environmental Contamination: Role in Transmission and Zoonotic
Parent Project Number 5P01AI077774-14
Sub-Project ID 5512
Contact PI/Project Leader HOOVER, EDWARD ARTHUR
Awardee Organization UNIVERSITY OF TEXAS HLTH SCI CTR HOUSTON
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/project-details/11056111#description
Project 3B: Pathogenesis Transmission and Detection of Zoonotic Prion Diseases
Parent Project Number 5P01AI077774-14
Sub-Project ID 5513
Contact PI/Project Leader BARTZ, JASON C
Awardee Organization UNIVERSITY OF TEXAS HLTH SCI CTR HOUSTON
Description Abstract Text
Project Summary: 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/project-details/11056115#description
Project 1: Modeling the Mechanisms of Prion Transmission, Strain Selection, Mutation and Species Barrier in Transgenic Mice
Parent Project Number 5P01AI077774-14
Sub-Project ID 5510
Contact PI/Project Leader TELLING, GLENN C
Awardee Organization UNIVERSITY OF TEXAS HLTH SCI CTR HOUSTON
Description Abstract Text
Our broad, long-term objectives are to are to decipher the mechanisms by which infectious prions replicate, encode strain information, and evolve to acquire new properties. We propose four Specific Aims to address our central hypothesis that incompletely adapted prion strains are comprised of poorly optimized ensembles of PrPSc quasi species conformers that evolve under selective pressure towards states of enhanced stability and pathogenicity. Our particular focus is chronic wasting disease (CWD), an uncontrollable contagious epidemic of cervids of uncertain zoonotic potential. Using genetically engineered CWD-susceptible mice, cultured cells, cell free amplification, and antibodies recognizing defined conformation-dependent PrP epitopes,
Aim I will address the mechanism of adaptation of unstable emergent CWD prions in response to physical and chemical constraints.
In Aim II we will address the hypothesis that that residue 226 and other cervid PrP polymorphisms influence selection of distinct portfolios of CWD strain conformers with different adaptive potentials. Using gene targeted mice expressing physiologically controlled levels of PrP variants and in vitro systems for prion replication, we will characterize the properties of strains propagated in these backgrounds and explore whether interference between them affects selection and adaptation of CWD.
In Aim III, we will assess the properties of emergent Norwegian moose and reindeer CWD strains experimentally propagated in deer and compare with established North American CWD.
Aim IV will address an unmet need in the field of significant importance, namely the paucity of model systems and tools for studying human prions. Using newly generated gene targeted mice expressing physiological levels of human PrP and novel approaches to derive susceptible human neuroblastoma cells, we will assess the zoonotic potential of emergent CWD strains and their adapted derivatives propagated in different cervid PrP backgrounds. Our ultimate goal is to assess and manage the risk posed to humans from continually evolving prions, specifically those causing CWD, by understanding the means by which they propagate and exist as heritable strains with protean host range properties that adapt and evolve under selective pressure.
https://reporter.nih.gov/project-details/11056096#description
Project 2
Parent Project Number 5P01AI077774-14
Sub-Project ID 5511
Contact PI/Project Leader SOTO, CLAUDIO
Awardee Organization UNIVERSITY OF TEXAS HLTH SCI CTR HOUSTON
Description Abstract Text
ABSTRACT Chronic wasting disease (CWD) affecting various species of cervids in North American and Northern Europe represents a serious problem, because it continues to propagate uncontrollably among wild and captive cervids. CWD appears to be very heterogeneous with multiple different strains and can be transmitted to other animal species. The risk of CWD transmission to humans is unknown which is a major concern because the number of sick animals and their geographical distribution is rapidly increasing. The mechanism by which CWD propagates so efficiently among cervids is also unknown. The main goal of this project is to utilize a set of highly innovative techniques to study the cellular, molecular and structural features of naturally occurring CWD strains and their potential for inter- species transmission, particularly focusing on the possibility that certain CWD strains may infect humans. We will also attempt to elucidate the atomic resolution structure of CWD prions using cryo-electron microscopy. The overarching hypothesis is that CWD exists as multiple strains in distinct individuals and even within the same individual in different brain cells and that inter- species transmission and zoonotic potential depend on the specific strain characteristics. The project is divided in the following specific aims:
(1) Study the structural and molecular diversity of natural CWD strains and the high resolution three-dimensional structure of CWD prions.
(2) Understand CWD prion strain diversity in single brain cells isolated by laser capture microdissection and subsequently amplified by PMCA.
(3) Evaluate CWD inter-species transmission spillover potential and its effect on zoonotic potential.
(4) Analyze the deer-human prion species barrier in vivo using chimeric mice harboring human and cervid neuronal cells.
The studies included in this projects will address some of the most pressing questions regarding CWD, including
(i) the CWD prion strain variability,
(ii) the zoonotic potential of different CWD prion strains,
(iii) the atomic resolution structure of infectious prions and the structural basis of prion strains,
(iv) the cellular distribution of CWD prion strains in the brain and its gene expression consequences,
(v) the spillover potential of CWD to other animal species,
(vi) the potential role of intermediate species in the transmission of CWD prions to humans.
The findings generated in this project will be essential to design measures to prevent further propagation of CWD, and to avoid the emergence of new diseases with potentially disastrous consequences.
https://reporter.nih.gov/search/fXQ8kEmVa0mNDk1JNnx3Cw/project-details/11056103#description
18. Zoonotic potential of moose-derived chronic wasting disease prions after adaptation in intermediate species
Tomás Barrioa, Jean-Yves Doueta, Alvina Huora, Séverine Lugana, Naïma Arona, Hervé Cassarda, Sylvie L. Benestadb, Juan Carlos Espinosac, Juan María Torresc, Olivier Andréolettia
aUnité Mixte de Recherche de l’Institut National de Recherche pour l’Agriculture, l’Alimentation et l’Environnement 1225 Interactions Hôtes-Agents Pathogènes, École Nationale Vétérinaire de Toulouse, 31076 Toulouse, France; bNorwegian Veterinary Institute, P.O. Box 64, NO-1431 Ås, Norway; cCentro de Investigación en Sanidad Animal (CISA-INIA), 28130, Valdeolmos, Madrid, Spain
Aims: Chronic wasting disease (CWD) is an emerging prion disease in Europe. To date, cases have been reported in three Nordic countries and in several species, including reindeer (Rangifer tarandus), moose (Alces alces) and red deer (Cervus elaphus). Cumulating data suggest that the prion strains responsible for the European cases are distinct from those circulating in North America. The biological properties of CWD prions are still poorly documented, in particular their spillover and zoonotic capacities. In this study, we aimed at characterizing the interspecies transmission potential of Norwegian moose CWD isolates.
Materials and Methods: For that purpose, we performed experimental transmissions in a panel of transgenic models expressing the PrPC sequence of various species.
Results: On first passage, one moose isolate propagated in the ovine PrPC-expressing model (Tg338). After adaptation in this host, moose CWD prions were able to transmit in mice expressing either bovine or human PrPC with high efficacy.
Conclusions: These results suggest that CWD prions can acquire enhanced zoonotic properties following adaptation in an intermediate species.
Funding
Grant number: AAPG2020 EU-CWD, ICRAD2020 TCWDE, NRC2022 NorCWD
Acknowledgement
https://www.tandfonline.com/doi/full/10.1080/19336896.2024.2424058
“ After adaptation in this host, moose CWD prions were able to transmit in mice expressing either bovine or human PrPC with high efficacy.”
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
Consumption of venison and veal was much less widespread among both cases and controls. For both of these meats there was evidence of a trend with increasing frequency of consumption being associated with increasing risk of CJD. (not nvCJD, but sporadic CJD...tss) These associations were largely unchanged when attention was restricted to pairs with data obtained from relatives. ...
Table 9 presents the results of an analysis of these data.
There is STRONG evidence of an association between ‘’regular’’ veal eating and risk of CJD (p = .0.01).
Individuals reported to eat veal on average at least once a year appear to be at 13 TIMES THE RISK of individuals who have never eaten veal.
There is, however, a very wide confidence interval around this estimate. There is no strong evidence that eating veal less than once per year is associated with increased risk of CJD (p = 0.51).
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).
There is some evidence that risk of CJD INCREASES WITH INCREASING FREQUENCY OF LAMB EATING (p = 0.02).
The evidence for such an association between beef eating and CJD is weaker (p = 0.14). When only controls for whom a relative was interviewed are included, this evidence becomes a little STRONGER (p = 0.08).
snip...
It was found that when veal was included in the model with another exposure, the association between veal and CJD remained statistically significant (p = < 0.05 for all exposures), while the other exposures ceased to be statistically significant (p = > 0.05).
snip...
In conclusion, an analysis of dietary histories revealed statistical associations between various meats/animal products and INCREASED RISK OF CJD. When some account was taken of possible confounding, the association between VEAL EATING AND RISK OF CJD EMERGED AS THE STRONGEST OF THESE ASSOCIATIONS STATISTICALLY. ...
snip...
In the study in the USA, a range of foodstuffs were associated with an increased risk of CJD, including liver consumption which was associated with an apparent SIX-FOLD INCREASE IN THE RISK OF CJD. By comparing the data from 3 studies in relation to this particular dietary factor, the risk of liver consumption became non-significant with an odds ratio of 1.2 (PERSONAL COMMUNICATION, PROFESSOR A. HOFMAN. ERASMUS UNIVERSITY, ROTTERDAM). (???...TSS)
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 ############
BSE INQUIRY
CJD9/10022
October 1994
Mr R.N. Elmhirst Chairman British Deer Farmers Association Holly Lodge Spencers Lane
BerksWell Coventry CV7 7BZ
Dear Mr Elmhirst,
CREUTZFELDT-JAKOB DISEASE (CJD) SURVEILLANCE UNIT REPORT
Thank you for your recent letter concerning the publication of the third annual report from the CJD Surveillance Unit. I am sorry that you are dissatisfied with the way in which this report was published.
The Surveillance Unit is a completely independant outside body and the Department of Health is committed to publishing their reports as soon as they become available. In the circumstances it is not the practice to circulate the report for comment since the findings of the report would not be amended.. In future we can ensure that the British Deer Farmers Association receives a copy of the report in advance of publication.
The Chief Medical Officer has undertaken to keep the public fully informed of the results of any research in respect of CJD. This report was entirely the work of the unit and was produced completely independantly of the the Department.
The statistical results reqarding the consumption of venison was put into perspective in the body of the report and was not mentioned at all in the press release. Media attention regarding this report was low key but gave a realistic presentation of the statistical findings of the Unit. This approach to publication was successful in that consumption of venison was highlighted only once by the media ie. in the News at one television proqramme.
I believe that a further statement about the report, or indeed statistical links between CJD and consumption of venison, would increase, and quite possibly give damaging credence, to the whole issue. From the low key media reports of which I am aware it seems unlikely that venison consumption will suffer adversely, if at all.
http://web.archive.org/web/20030511010117/http://www.bseinquiry.gov.uk/files/yb/1994/10/00003001.pdf
TSE in wild UK deer? The first case of BSE (as we now realise) was in a nyala in London zoo and the further zoo cases in ungulates were simply thought of as being interesting transmissions of scrapie initially. The big problem started to appear with animals in 1993-5 when it became clear that there was an increase in the CJD cases in people that had eaten deer although the statistics involved must have been questionable. The reason for this was that the CJD Surveillance was well funded to look into the diet of people dying of CJD. This effect is not clear with vCJD...if only because the numbers involved are much smaller and hence it is difficult to gain enough statistics. They found that many other foods did not appear to have much association at all but that deer certainly did and as years went by the association actually became clearer. The appearance of vCJD in 1996 made all this much more difficult in that it was suddenly clearer that the cases of sporadic CJD that they had been checking up until then probably had nothing to do with beef...and the study decreased. During the period there was an increasing worry that deer were involved with CJD..
see references:
DEER BRAIN SURVEY
https://web.archive.org/web/20090506025229/http://www.bseinquiry.gov.uk/files/yb/1991/11/20004001.pdf
CONFIDENTIAL AND IN CONFIDENCE TRANSMISSION TO CHIMPANZEES AND PIGS
IN CONFIDENCE
TRANSMISSION TO CHIMPANZEES
Kuru and CJD have been successfully transmitted to chimpanzees but scrapie and TME have not.
We cannot say that scrapie will not transmit to chimpanzees. There are several scrapie strains and I am not aware that all have been tried (that would have to be from mouse passaged material). Nor has a wide enough range of field isolates subsequently strain typed in mice been inoculated by the appropriate routes (i/c, i/p and i/v).
I believe the proposed experiment to determine transmissibility, if conducted, would only show the susceptibility or resistance of the chimpanzee to infection/disease by the routes used and the result could not be interpreted for the predictability of the susceptibility for man. proposals for prolonged oral exposure of chimpanzees to milk from cattle were suggested a long while ago and rejected.
In view of Dr Gibbs' probable use of chimpazees Mr Wells' comments (enclosed) are pertinent. I have yet to receive a direct communication from Dr Schellekers but before any collaboration or provision of material we should identify the Gibbs' proposals and objectives.
A positive result from a chimpanzee challenged severely would likely create alarm in some circles even if the result could not be interpreted for man. I have a view that all these agents could be transmitted provided a large enough dose by appropriate routes was given and the animals kept long enough. Until the mechanisms of the species barrier are more clearly understood it might be best to retain that hypothesis.
A negative result would take a lifetime to determine but that would be a shorter period than might be available for human exposure and it would still not answer the question regarding mans ‘susceptibility. In the meantime no doubt the negativity would be used defensively. It would however be counterproductive if the experiment finally became positive. We may learn more about public reactions following next Monday's meeting.
R Bradley
CVO (+ Mr Wells’ commenters 23 September 1990 Dr T W A Little Dr B J Shreeve
90/9.23/1.1
https://web.archive.org/web/20090506041740/http://www.bseinquiry.gov.uk/files/yb/1990/09/23001001.pdf
*** now, let’s see what the authors said about this casual link, personal communications years ago, and then the latest on the zoonotic potential from CWD to humans from the TOKYO PRION 2016 CONFERENCE.
see where it is stated NO STRONG evidence. so, does this mean there IS casual evidence ????
“Our conclusion stating that we found no strong evidence of CWD transmission to humans”
From: TSS Subject: CWD aka MAD DEER/ELK TO HUMANS ???
Date: September 30, 2002 at 7:06 am PST
From: "Belay, Ermias"
To: Cc: "Race, Richard (NIH)" ; ; "Belay, Ermias"
Sent: Monday, September 30, 2002 9:22 AM
Subject: RE: TO CDC AND NIH - PUB MED- 3 MORE DEATHS - CWD - YOUNG HUNTERS
Dear Sir/Madam, In the Archives of Neurology you quoted (the abstract of which was attached to your email), we did not say CWD in humans will present like variant CJD.. That assumption would be wrong. I encourage you to read the whole article and call me if you have questions or need more clarification (phone: 404-639-3091).
Also, we do not claim that "no-one has ever been infected with prion disease from eating venison." Our conclusion stating that we found no strong evidence of CWD transmission to humans in the article you quoted or in any other forum is limited to the patients we investigated.
Ermias Belay, M.D. Centers for Disease Control and Prevention
Subject: TO CDC AND NIH - PUB MED- 3 MORE DEATHS - CWD - YOUNG HUNTERS
Sunday, November 10, 2002 6:26 PM .......snip........end..............TSS
Thursday, April 03, 2008
A prion disease of cervids: Chronic wasting disease 2008 1: Vet Res. 2008 Apr 3;39(4):41 A prion disease of cervids: Chronic wasting disease Sigurdson CJ.
snip... *** twenty-seven CJD patients who regularly consumed venison were reported to the Surveillance Center***,
snip... full text ;
http://chronic-wasting-disease.blogspot.com/2008/04/prion-disease-of-cervids-chronic.html
However, to date, no CWD infections have been reported in people.
sporadic, spontaneous CJD, 85%+ of all human TSE, did not just happen. never in scientific literature has this been proven. if one looks up the word sporadic or spontaneous at pubmed, you will get a laundry list of disease that are classified in such a way;
sporadic = 54,983 hits
https://www.ncbi.nlm.nih.gov/pubmed/?term=sporadic
spontaneous = 325,650 hits
https://www.ncbi.nlm.nih.gov/pubmed/?term=spontaneous
key word here is 'reported'. science has shown that CWD in humans will look like sporadic CJD.
SO, how can one assume that CWD has not already transmitted to humans? they can't, and it's as simple as that. from all recorded science to date, CWD has already transmitted to humans, and it's being misdiagnosed as sporadic CJD. ...terry
*** LOOKING FOR CWD IN HUMANS AS nvCJD or as an ATYPICAL CJD, LOOKING IN ALL THE WRONG PLACES $$$ ***
However, to date, no CWD infections have been reported in people. key word here is ‘reported’. science has shown that CWD in humans will look like sporadic CJD. SO, how can one assume that CWD has not already transmitted to humans? they can’t, and it’s as simple as that. from all recorded science to date, CWD has already transmitted to humans, and it’s being misdiagnosed as sporadic CJD. …terry
*** LOOKING FOR CWD IN HUMANS AS nvCJD or as an ATYPICAL CJD, LOOKING IN ALL THE WRONG PLACES $$$ ***
*** These results would seem to suggest that CWD does indeed have zoonotic potential, at least as judged by the compatibility of CWD prions and their human PrPC target. Furthermore, extrapolation from this simple in vitro assay suggests that if zoonotic CWD occurred, it would most likely effect those of the PRNP codon 129-MM genotype and that the PrPres type would be similar to that found in the most common subtype of sCJD (MM1).***
http://www.tandfonline.com/doi/full/10.4161/pri.28124?src=recsys
http://www.tandfonline.com/doi/pdf/10.4161/pri.28124?needAccess=true
https://wwwnc.cdc.gov/eid/article/20/1/13-0858_article
So, this is what we leave our children and grandchildren?
CDC CWD TSE Prion Update 2025
KEY POINTS
Chronic wasting disease affects deer, elk and similar animals in the United States and a few other countries.
The disease hasn't been shown to infect people.
However, it might be a risk to people if they have contact with or eat meat from animals infected with CWD.
https://www.cdc.gov/chronic-wasting/about/index.html
Volume 31, Number 4—April 2025
Research
Detection and Decontamination of Chronic Wasting Disease Prions during Venison Processing
https://wwwnc.cdc.gov/eid/article/31/4/24-1176_article
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
Transmission of prion infectivity from CWD-infected 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
***> 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
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 Tg12mice became infected and their brain tissues were further examined by Western blot as well as serial passages in humanized or cervidized mice.
Results: Passage of sCJDMM1 in transgenic mice expressing elk PrP (Tg12) resulted in a “cervidized” CJD strain that we termed CJDElkPrP. We observed 100% transmission of the original CJDElkPrP in transgenic mice expressing human PrP. We passaged CJDElkPrP two more times in the Tg12mice. We found that such second and third passage CJDElkPrP prions retained 100% transmission rate in the humanized mice, despite that the natural elk CWD isolates and CJDElkPrP share the same elk PrP sequence. In contrast, we and others found zero or poor transmission of natural elk CWD isolates in humanized mice.
Conclusions: Our data indicate that highly zoonotic cervid prion strains are not only possible but also can retain zoonotic potential after serial passages in cervids, suggesting a very significant and serious long-term risk of CWD zoonosis given that the broad and continuing spread of CWD prions will provide fertile grounds for the emergence of zoonotic CWD strains over time.
https://prion2023.org/wp-content/uploads/2023/10/Meeting-book-final-version2.pdf
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
Transmission of cervid prions to humanized mice demonstrates the zoonotic potential of CWD
Samia Hannaoui1 · Irina Zemlyankina1 · Sheng Chun Chang1 · Maria Immaculata Arifn1 · Vincent Béringue2 · Debbie McKenzie3 · Hermann M. Schatzl1 · Sabine Gilch1
Received: 24 May 2022 / Revised: 5 August 2022 / Accepted: 7 August 2022
© The Author(s) 2022
Abstract
Prions cause infectious and fatal neurodegenerative diseases in mammals. Chronic wasting disease (CWD), a prion disease of cervids, spreads efficiently among wild and farmed animals. Potential transmission to humans of CWD is a growing concern due to its increasing prevalence. Here, we provide evidence for a zoonotic potential of CWD prions, and its probable signature using mice expressing human prion protein (PrP) as an infection model. Inoculation of these mice with deer CWD isolates resulted in atypical clinical manifestation with prion seeding activity and efficient transmissible infectivity in the brain and, remarkably, in feces, but without classical neuropathological or Western blot appearances of prion diseases. Intriguingly, the protease-resistant PrP in the brain resembled that found in a familial human prion disease and was transmissible upon second passage. Our results suggest that CWD might infect humans, although the transmission barrier is likely higher compared to zoonotic transmission of cattle prions. Notably, our data suggest a different clinical presentation, prion signature, and tissue tropism, which causes challenges for detection by current diagnostic assays. Furthermore, the presence of infectious prions in feces is concerning because if this occurs in humans, it is a source for human-to-human transmission. These findings have strong implications for public health and CWD management.
Keywords Chronic wasting disease · CWD · Zoonotic potential · Prion strains · Zoonotic prions
HIGHLIGHTS OF THIS STUDY
================================
Our results suggest that CWD might infect humans, although the transmission barrier is likely higher compared to zoonotic transmission of cattle prions. Notably, our data suggest a different clinical presentation, prion signature, and tissue tropism, which causes challenges for detection by current diagnostic assays. Furthermore, the presence of infectious prions in feces is concerning because if this occurs in humans, it is a source for human-to-human transmission. These findings have strong implications for public health and CWD management.
In this study, we evaluated the zoonotic potential of CWD using a transgenic mouse model overexpressing human M129-PrPC (tg650 [12]). We inoculated tg650 mice intracerebrally with two deer CWD isolates, Wisc-1 and 116AG [22, 23, 27, 29]. We demonstrate that this transgenic line was susceptible to infection with CWD prions and displayed a distinct leading clinical sign, an atypical PrPSc signature and unusual fecal shedding of infectious prions. Importantly, these prions generated by the human PrP transgenic mice were transmissible upon passage. Our results are the first evidence of a zoonotic risk of CWD when using one of the most common CWD strains, Wisc-1/CWD1 for infection. We demonstrated in a human transgenic mouse model that the species barrier for transmission of CWD to humans is not absolute. The fact that its signature was not typical raises the questions whether CWD would manifest in humans as a subclinical infection, whether it would arise through direct or indirect transmission including an intermediate host, or a silent to uncovered human-to-human transmission, and whether current detection techniques will be suffcient to unveil its presence.
Our findings strongly suggest that CWD should be regarded as an actual public health risk. Here, we use humanized mice to show that CWD prions can cross the species barrier to humans, and remarkably, infectious prions can be excreted in feces.
Our results indicate that if CWD crosses the species-barrier to humans, it is unlikely to resemble the most common forms of human prion diseases with respect to clinical signs, tissue tropism and PrPSc signature. For instance, PrPSc in variable protease-sensitive prionopathy (VPSPr), a sporadic form of human prion disease, and in the genetic form Gerstmann-Sträussler-Scheinker syndrome (GSS) is defined by an atypical PK-resistant PrPSc fragment that is non-glycosylated and truncated at both C- and N-termini, with a molecular weight between 6 and 8 kDa [24, 44–46]. These biochemical features are unique and distinctive from PrPSc (PrP27-30) found in most other human or animal prion disease. The atypical PrPSc signature detected in brain homogenate of tg650 mice #321 (1st passage) and #3063 (2nd passage), and the 7–8 kDa fragment (Figs. 2, 4) are very similar to that of GSS, both in terms of migration profile and the N-terminal cleavage site.
CWD in humans might remain subclinical but with PrPSc deposits in the brain with an unusual morphology that does not resemble the patterns usually seen in different prion diseases (e.g., mouse #328; Fig. 3), clinical with untraceable abnormal PrP (e.g., mouse #327) but still transmissible and uncovered upon subsequent passage (e.g., mouse #3063; Fig. 4), or prions have other reservoirs than the usual ones, hence the presence of infectivity in feces (e.g., mouse #327) suggesting a potential for human-to-human transmission and a real iatrogenic risk that might be unrecognizable.
“suggesting a potential for human-to-human transmission and a real iatrogenic risk that might be unrecognizable.”
=================================
Supplementary Information The online version contains supplementary material available at
https://doi.org/10.1007/s00401-022-02482-9
snip...see full text;
https://link.springer.com/article/10.1007/s00401-022-02482-9
https://link.springer.com/content/pdf/10.1007/s00401-022-02482-9.pdf
EFSA Panel on Biological Hazards (BIOHAZ) Antonia Ricci Ana Allende Declan Bolton Marianne Chemaly Robert Davies Pablo Salvador Fernández Escámez ...
First published: 17 January 2018 https://doi.org/10.2903/j.efsa.2018.5132
also, see;
8. Even though human TSE‐exposure risk through consumption of game from European cervids can be assumed to be minor, if at all existing, no final conclusion can be drawn due to the overall lack of scientific data.
***> In particular the US data do not clearly exclude the possibility of human (sporadic or familial) TSE development due to consumption of venison.
The Working Group thus recognizes a potential risk to consumers if a TSE would be present in European cervids. It might be prudent considering appropriate measures to reduce such a risk, e.g. excluding tissues such as CNS and lymphoid tissues from the human food chain, which would greatly reduce any potential risk for consumers.. However, it is stressed that currently, no data regarding a risk of TSE infections from cervid products are available.
https://efsa.onlinelibrary.wiley.com/doi/full/10.2903/j.efsa.2018.5132
2004
Jeff Swann and his Mom, cwd link... sporadic CJD?, CBC NEWS Jeff Schwan sCJD, CWD, and Professor Aguzzi on BSE and sporadic CJD
????: CBCnews
https://histodb15.usz.ch/pages/Images/videos/video-004/video-004.html
2004
April 22, 2004, 10:30 AM CDT Guests: Patrick Singh, Terry Schwan, Janet Skarbek, Bill Fielding (BEGIN VIDEOTAPE) ANNOUNCER: DEBORAH NORVILLE TONIGHT.
https://www.nbcnews.com/id/wbna4806886
1997-11-10: Panorama - The British disease
https://histodb15.usz.ch/pages/Images/videos/video-009/video-009.html
TUESDAY, MAY 11, 2021
A Unique Presentation of Creutzfeldt-Jakob Disease in a Patient Consuming Deer Antler Velvet <
Conclusion
We believe that our patient’s case of CJD is highly suspicious for cervid etiology given the circumstances of the case as well as the strong evidence of plausibility reported in published literature. This is the first known case of CJD in a patient who had consumed deer antler velvet. Despite the confirmed diagnosis of CJD, a causal relationship between the patient’s disease and his consumption of deer antler velvet cannot be definitively concluded.
Supplemental data including molecular tissue sample analysis and autopsy findings could yield further supporting evidence. Given this patient’s clinical resemblance to CBD and the known histological similarities of CBD with CJD, clinicians should consider both diseases in the differential diagnosis of patients with a similarly esoteric presentation. Regardless of the origin of this patient’s disease, it is clear that the potential for prion transmission from cervids to humans should be further investigated by the academic community with considerable urgency.
https://thescipub.com/pdf/ajidsp.2021.43.48.pdf
''We believe that our patient’s case of CJD is highly suspicious for cervid etiology given the circumstances of the case as well as the strong evidence of plausibility reported in published literature. This is the first known case of CJD in a patient who had consumed deer antler velvet. Despite the confirmed diagnosis of CJD, a causal relationship between the patient’s disease and his consumption of deer antler velvet cannot be definitively concluded.''
https://thescipub.com/pdf/ajidsp.2021.43.48.pdf
CREUTZFELDT JAKOB DISEASE: A Unique Presentation of Creutzfeldt-Jakob Disease in a Patient Consuming Deer Antler Velvet
i was warning England and the BSE Inquiry about just this, way back in 1998, and was ask to supply information to the BSE Inquiry. for anyone that might be interested, see;
Singeltary submission to the BSE Inquiry on CJD and Nutritional Supplements 1998
ABOUT that deer antler spray and CWD TSE PRION... I have been screaming this since my neighbors mom died from cjd, and she had been taking a supplement that contained bovine brain, bovine eyeball, and other SRMs specified risk materials, the most high risk for mad cow disease. just saying...
I made a submission to the BSE Inquiry long ago during the BSE Inquiry days, and they seemed pretty interested.
Sender: "Patricia Cantos"
To: "Terry S Singeltary Sr. (E-mail)"
Subject: Your submission to the Inquiry
Date: Fri, 3 Jul 1998 10:10:05 +0100 3 July 1998
Mr Terry S Singeltary Sr. E-Mail: Flounder at wt.netRef: E2979
Dear Mr Singeltary, Thank you for your E-mail message of the 30th of June 1998 providing the Inquiry with your further comments. Thank you for offering to provide the Inquiry with any test results on the nutritional supplements your mother was taking before she died. As requested I am sending you our general Information Pack and a copy of the Chairman's letter. Please contact me if your system cannot read the attachments. Regarding your question, the Inquiry is looking into many aspects of the scientific evidence on BSE and nvCJD.
I would refer you to the transcripts of evidence we have already heard which are found on our internet site at ;
http://www.bse.org.uk.
Could you please provide the Inquiry with a copy of the press article you refer to in your e-mail? If not an approximate date for the article so that we can locate it? In the meantime, thank you for you comments. Please do not hesitate to contact me on... snip...end...tss
everyone I tell this too gets it screwed up...MY MOTHER WAS NOT TAKING THOSE SUPPLEMENTS IPLEX (that I ever knew of). this was my neighbors mother that died exactly one year previously and to the day of sporadic CJD that was diagnosed as Alzheimer’s at first. my mother died exactly a year later from the Heidenhain Variant of Creutzfeldt Jakob Disease hvCJD, and exceedingly rare strains of the ever growing sporadic CJD’s. both cases confirmed. ...
kind regards, terry
TSEs i.e. mad cow disease's BSE/BASE and NUTRITIONAL SUPPLEMENTS IPLEX, mad by standard process; vacuum dried bovine BRAIN, bone meal, bovine EYE, veal Bone, bovine liver powder, bovine adrenal, vacuum dried bovine kidney, and vacuum dried porcine stomach. also; what about potential mad cow candy bars ? see their potential mad cow candy bar list too... THESE are just a few of MANY of just this ONE COMPANY...TSS
https://wwwnc.cdc.gov/eid/article/15/5/08-1458_article
http://www.spiegel.de/spiegel/print/d-18578755.html
http://chronic-wasting-disease.blogspot.com/2009/03/chronic-wasting-disease-prions-in-elk.html
http://creutzfeldt-jakob-disease.blogspot.com/2013/11/large-cjd-tse-prion-potential-case.html
http://tseac.blogspot.com/2011/02/usa-50-state-bse-mad-cow-conference.html
Two Hunters from the Same Lodge Afflicted with Sporadic CJD: Is Chronic Wasting Disease to Blame?
(P7-13.002) Jonathan Trout, Matthew Roberts, Michel Tabet, Eithan Kotkowski, and Sarah HornAUTHORS INFO & AFFILIATIONS April 9, 2024 issue 102 (17_supplement_1) https://doi.org/10.1212/WNL.0000000000204407
Abstract Publication History Information & Authors Metrics & Citations Share Abstract
Objective:
This study presents a cluster of Creutzfeldt-Jakob disease (CJD) cases after exposure to chronic wasting disease (CWD)-infected deer, suggestive of potential prion transmission from CWD-infected deer to humans.
Background:
CJD is a rapidly progressive central nervous system disorder caused by misfolded prion proteins. CWD, a prion disease prevalent in North American deer, has raised concerns due to its possible link to CJD. Although no conclusive evidence of cross-species prion transmission exists, vigilance for such cases is crucial for public health.
Design/Methods:
Not applicable.
Results:
In 2022, a 72-year-old man with a history of consuming meat from a CWD-infected deer population presented with rapid-onset confusion and aggression. His friend, who had also eaten venison from the same deer population, recently died of CJD, raising concerns about a potential link between CWD and human prion disease. Despite aggressive symptomatic treatment of seizures and agitation, the patient’s condition deteriorated and he died within a month of initial presentation. The diagnosis was confirmed postmortem as sporadic CJD with homozygous methionine at codon 129 (sCJDMM1). The patient’s history, including a similar case in his social group, suggests a possible novel animal-to-human transmission of CWD. Based on non-human primate and mouse models, cross-species transmission of CJD is plausible. Due to the challenge of distinguishing sCJDMM1 from CWD without detailed prion protein characterization, it is not possible to definitively rule out CWD in these cases. Although causation remains unproven, this cluster emphasizes the need for further investigation into the potential risks of consuming CWD-infected deer and its implications for public health.
Conclusions:
Clusters of sporadic CJD cases may occur in regions with CWD-confirmed deer populations, hinting at potential cross-species prion transmission. Surveillance and further research are essential to better understand this possible association.
Disclosure: Mr. Trout has nothing to disclose. Dr. Roberts has nothing to disclose. Dr. Tabet has nothing to disclose. Dr. Kotkowski has nothing to disclose. Dr. Horn has received personal compensation in the range of $500-$4,999 for serving as a Consultant for Cala Trio. The institution of Dr. Horn has received research support from Alzheimer's Association.
https://www.neurology.org/doi/abs/10.1212/WNL.0000000000204407
***> Creutzfeldt Jakob Disease CJD TSE Prion Cases Increasing March 2025
https://creutzfeldt-jakob-disease.blogspot.com/2025/03/creutzfeldt-jakob-disease-tse-prion.html
***> Creutzfeldt Jakob Disease CJD, BSE, CWD, TSE, Prion, December 14, 2024 Annual Update
https://creutzfeldt-jakob-disease.blogspot.com/2024/12/creutzfeldt-jacob-disease-cjd-bse-cwd.html
https://creutzfeldt-jakob-disease.blogspot.com/
Iatrogenic Transmissible Spongiform Encephalopathy TSE Prion, CWD, our worst nightmare, what if?
https://itseprion.blogspot.com/
So, this is what we leave our children and grandchildren?
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
Characterizing the hydrological spread of prion diseases through interdisciplinary science
September 11, 2025
Anu Li, Water Resources Science graduate student and WINS recipient Characterizing the hydrological spread of prion diseases through interdisciplinary science
Chronic wasting disease (CWD) is a 100% fatal disease found in cervids, which include deer, elk, and moose. CWD has been spreading more rapidly across Minnesota and much of North America in the past few years, causing people to come into contact with the disease more frequently through hunting, hide tanning, and consuming contaminated venison. This has raised concerns from epidemiologists that CWD, which has no cure, could evolve to infect humans sooner rather than later. Worries about CWD exposure and spread go beyond wildlife because the pathogens that cause CWD, called infectious prions, can contaminate the environment. Infectious prions are misfolded proteins with a highly stable structure, making them more difficult to degrade than viruses or bacteria. Their unique structure allows them to remain infectious for years in environmental materials, including soil and water. This means that areas with CWD outbreaks could remain an infection risk long after infected animals have been removed. Prions can also be carried by water, and if they reach a stream or river, they can travel over greater distances than deer, further spreading the disease across the landscape. In order to contain the disease and prevent it from infecting humans, we must understand how it moves through the environment.
Exploring this unique intersection of wildlife disease and environmental science requires an interdisciplinary approach. That’s why researchers from multiple fields came together several years ago to establish the Minnesota Center for Prion Research and Outreach (MNPRO), a group devoted to studying prion diseases in order to protect human, wildlife, environmental, and cultural health. Since 2022, I have collaborated with fellow MNPRO scientists to determine how, how far, and how quickly infectious prions are traveling through rivers, streams, and watersheds in Minnesota.
Researching hydrological prion movement is challenging because they are too dangerous to add to the environment for direct observation, and there is no good proxy to replicate their dynamics. There is little prior research about how these mysterious pathogens travel in the environment, so we developed creative methods to predict their movement without traditional experimental methods. One key finding laid the groundwork for our ongoing research: infectious prions preferentially attach to fine particles in surface waters. This means that prions are likely carried by sediments in rivers and streams, rather than free-floating in the water. Thus, in order to predict the how far and how quickly prions are moving through a watershed, we can focus on characterizing sediment movement.
This summer, I have been conducting sediment transport experiments in a flume at the St. Anthony Falls Laboratory. I packed the flume with sediment mixtures of different median particle sizes to represent diverse streambeds in Minnesota. Then, I adjusted the water flow rate, water depth, and slope of the flume until sediment particles on the bed began to move. The conditions which initiate sediment motion are called critical conditions; the stress exerted on the streambed must be greater than or equal to critical stress in order for sediments to move. I am comparing these critical flow measurements to streamflow data recorded in CWD-contaminated watersheds in order to determine how often sediments are mobile in contaminated streams, and thus how often prions are mobile. With these estimates, we can predict how far prions may have been transported from contaminated sites and how quickly they will reach downstream locations.
This method allows us to estimate prion transport without directly tracing them in streams. Hydrological transport predictions will aid in better assessing risk to the public downstream of detected CWD cases, guiding further CWD testing in previously unmonitored areas, and developing more comprehensive containment strategies to protect human and environmental health.
footer - 4 column Water Resources Center 173 McNeal Hall 1985 Buford Avenue St. Paul, MN 55108
612-624-9282 water@umn.edu
https://wrc.umn.edu/news/hydrological-spread-prion-diseases
Chronic wasting disease (CWD) prion detection in environmental and biological samples from a taxidermy site and nursing facility, and instruments used in surveillance activities
Author links open overlay panel Paulina Soto a b , Nancy Ho a , Mitch Lockwood c , Austin Stolte c , J. Hunter Reed c , Rodrigo Morales a b
Cite https://doi.org/10.1016/j.scitotenv.2025.179318Get rights and content 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.
https://www.sciencedirect.com/science/article/abs/pii/S0048969725009544
March 13, 2025
Prion Partitioning and Persistence in Environmental Waters
E. Anu Li,* Diana L. Karwan, Stuart Siegfried Lichtenberg, Gage R. Rowden, Marc D. Schwabenlander, Peter A. Larsen, and Tiffany M. Wolf Cite This: Environ. Sci. Technol. 2025, 59, 5715−5725 Read Online Downloaded via 76.143.208.142 on September 14, 2025 at 21:46:11 (UTC).
ABSTRACT: Chronic wasting disease (CWD) is a fatal neurodegenerative disease affecting cervids. CWD is caused by infectious prions, which can enter the environment through bodily fluids or the carcasses of infected animals. Prions can be stored, remain infectious in both soil and water for many years, and transported hydrologically, possibly expanding the geographic range of CWD transmission. In order to better predict hydrological prion transport, we investigated how CWD prion protein (PrPCWD) partitions and persists in environmental waters. We performed PrPCWD spike experiments with water samples containing fine sediments from two locations within a CWD-contaminated site, at which contamination sources were removed one year prior. Samples were filtered after spiking, and filtrates and sediments were tested separately for PrPCWD using real- time quaking-induced conversion (RT-QuIC). Unspiked filtrates tested negative for PrPCWD , while unspiked sediments were positive, indicating PrPCWD persistence in environmental sediments for at least one year. Spiked sediments were positive immediately after spiking and throughout 28 days of incubation. Spiked filtrates were largely negative immediately after spiking and remained negative for 28 days, with some inconsistent positives from one sampling location. Our results indicate that PrPCWD readily partitions to the sediment fraction of environmental waters, suggesting that hydrological prion transport is sediment-facilitated.
KEYWORDS: chronic wasting disease, sediment, aquatic sediment, hydrology, prion disease, environmental contamination, facilitated transport
https://pubs.acs.org/doi/epdf/10.1021/acs.est.4c11497?ref=article_openPDF
Detection of protease-resistant cervid prion protein in water from a CWD-endemic area
Prions in MN Waterways: Discovery Helps Water Managers Plan
September 03, 2024 This article is part of the Forest Scene newsletter, Issue 31.
Two white-tail deer with antlers lie nestled in grass. Chronic wasting disease (CWD) is a form of prion disease that affects white-tail deer and other cervids (deer family). “People in Minnesota value their water,” observes hydrologist Dr. Diana Karwan, Associate Professor with the Department of Forest Resources. So when the Minnesota Center for Prion Research and Outreach (MNPRO) received a state mandate to investigate chronic wasting disease (CWD), many questions from the public and legislators kept returning to the subject of our lakes, wells, marshes, and streams. In response, the team agreed to learn how prions move in waterways, recruiting Dr. Karwan to lead the effort. A 2024 report to the Minnesota Clean Water Council delivered on that promise.
What is a prion? And why should we care about chronic wasting disease?
A prion is "an abnormal form of a normally harmless protein found in the brain that is responsible for a variety of fatal neurodegenerative diseases of animals," per Encyclopedia Britannica.
Chronic wasting disease (CWD) is a form of prion disease that affects members of the deer family (cervids), and thus forested ecosystems. The disease is fatal and progressive, affecting the brain, spinal cord, and other tissues.
CWD can be transmitted both directly (via animal-to-animal contact) and indirectly (via objects or environmental contamination). Currently, there is no cure or treatment for it yet scientists are continuing to search for solutions. Land that has seen CWD can store that risk for a long time, but that doesn’t mean it isn’t going anywhere. Besides through animal movement, researchers hypothesized that prions could be transported by water, potentially increasing their threat across the landscape. Borne by water, prions might travel to places where CWD had previously been undetected or concentrate in an area where it makes infection more likely. At the end of a two-year study, MNPRO scientists gained clarity about how prions behave in water. One critical insight emerged: prions travel with a partner.
The report revealed how prions in water stick to soil particles they encounter. The outcome is that when snowmelt introduces sediment to Minnesota waterways, it may also carry CWD. The discovery does have some positive implications, however. Knowledge that prions tend to bind with particles can guide water resource managers as they assess ways to mitigate the risk. It helps them know how to sample waterways for protein-misfolding disease, for example, and establishes the first steps toward informing accurate models of where water may move CWD throughout the landscape.
This study is an example of timely science. While the report was in preparation for release, another county was added to the list for CWD detections in wild deer.
“Now we need to start integrating what we know about CWD behavior with what we know about water behavior. Models allow us to put these knowledge bases together,” says Dr. Karwan. “I feel like what we've done is come up with very important first-point findings. I'm excited to take the next steps with this research.”
Watch Prions in Our Waterways, a short video by the research team, to learn more.
~Story by Thomas Seiler, MNPRO. This article originally appeared in the March 2024 MNPRO newsletter and has been adapted for this publication.
https://forestry.umn.edu/news/prions-mn-waterways-forest-scene-31
Prions in Waterways
https://vimeo.com/898941380?fbclid=IwAR3Di7tLuU-iagCetdt4-CVPrOPQQrv037QS1Uxz0tX3z7BuvPeYlwIp7IY
Prion. 2009 Jul-Sep;3(3):171–183. doi: 10.4161/pri.3.3.9819
Detection of protease-resistant cervid prion protein in water from a CWD-endemic area
TA Nichols 1,2, Bruce Pulford 1, A Christy Wyckoff 1,2, Crystal Meyerett 1, Brady Michel 1, Kevin Gertig 3, Edward A Hoover 1, Jean E Jewell 4, Glenn C Telling 5, Mark D Zabel 1,
Abstract
Chronic wasting disease (CWD) is the only known transmissible spongiform encephalopathy affecting free-ranging wildlife. Although the exact mode of natural transmission remains unknown, substantial evidence suggests that prions can persist in the environment, implicating components thereof as potential prion reservoirs and transmission vehicles.1–4 CWD-positive animals may contribute to environmental prion load via decomposing carcasses and biological materials including saliva, blood, urine and feces.5–7 Sensitivity limitations of conventional assays hamper evaluation of environmental prion loads in soil and water. Here we show the ability of serial protein misfolding cyclic amplification (sPMCA) to amplify a 1.3 × 10−7 dilution of CWD-infected brain homogenate spiked into water samples, equivalent to approximately 5 × 107 protease resistant cervid prion protein (PrPCWD) monomers. We also detected PrPCWD in one of two environmental water samples from a CWD endemic area collected at a time of increased water runoff from melting winter snow pack, as well as in water samples obtained concurrently from the flocculation stage of water processing by the municipal water treatment facility. Bioassays indicated that the PrPCWD detected was below infectious levels. These data demonstrate detection of very low levels of PrPCWD in the environment by sPMCA and suggest persistence and accumulation of prions in the environment that may promote CWD transmission.
Snip…
The data presented here demonstrate that sPMCA can detect low levels of PrPCWD in the environment, corroborate previous biological and experimental data suggesting long term persistence of prions in the environment2,3 and imply that PrPCWD accumulation over time may contribute to transmission of CWD in areas where it has been endemic for decades. This work demonstrates the utility of sPMCA to evaluate other environmental water sources for PrPCWD, including smaller bodies of water such as vernal pools and wallows, where large numbers of cervids congregate and into which prions from infected animals may be shed and concentrated to infectious levels.
Key words: prions, chronic wasting disease, water, environment, serial protein misfolding cyclic amplification
https://pmc.ncbi.nlm.nih.gov/articles/PMC2802782/
Detection of chronic wasting disease prions in soil at an illegal white-tailed deer carcass disposal site
Published online: 06 Jun 2025
Abstract
Chronic wasting disease (CWD) is a contagious prion disorder affecting cervids such as deer, elk, caribou, and moose, causing progressive and severe neurological degeneration followed by eventual death. As CWD prions (PrPSc) accumulate in the body, they are shed through excreta and secreta, as well as through decomposing carcasses. Prions can persist in the environment for years, posing significant concerns for ongoing transmission to susceptible cervids and pose an unknown risk to sympatric species. We used a validated protocol for real-time quaking-induced conversion (RT-QuIC) in vitro prion amplification assay to detect prions in soil collected within and around an illegal white-tailed deer (Odocoileus virginianus, WTD) carcass disposal site and associated captive WTD farm in Beltrami County, Minnesota. We detected PrPSc in 26 of 201 soil samples across 15 locations within the illegal disposal site and one on the farm that housed the cervids. Importantly, a subset of RT-QuIC positive soil samples was collected from soils where carcasses were recovered, providing direct evidence that environmental contamination resulted from this illegal activity. These findings reveal that improper cervid carcass disposal practices may have important implications for ongoing CWD transmission through the environment.
Snip…
Conclusions
Using RT-QuIC, we detected PrPSc in 26 of 201 soil samples collected across 16 locations on public land where WTD carcasses had been disposed and the captive facility from where they originated. Within the disposal site, 25 out of 124 soil samples (20%) tested positive for PrPSc. Among those positive detections, 17, or 68%, were collected from locations where CWD-positive WTD remains had been previously recovered. This environmental investigation demonstrates how improper cervid carcass disposal practices can result in persistent environmental contamination, posing a potential risk to wildlife health. Given that disposal of livestock on the landscape is a common practice among producers [Citation54–56], these findings underscore the need for improved disposal practices and further investigation of environmental impacts. Expanding on this area of environmental research is crucial as the geographic range of CWD continues to expand [Citation57]. The use of RT-QuIC for prion detection in environmental samples offers an exciting advancement to environmental surveillance for prions, though as we demonstrate here and in Grunklee et al. [Citation41], assay optimization and validation for use with different environmental samples, including new soil types, is still necessary. Further enhancements to RT-QuIC and other methodologies for prion detection will facilitate more opportunities to explore the persistence, degradation, transport, and remediation of environmental prions.
https://www.tandfonline.com/doi/full/10.1080/19336896.2025.2514947
While the disease control measures effectively eliminated prion seeding activity in CWD-affected farms, CWD recurred at two of the 18 remediated farms 4 to 5 years after restocking animals. It remains unclear whether the recurrence of CWD at the two farms was due to residual prions in the environment after the control measures, or the introduction of the infected animals from other farms. This uncertainty is heightened by the annual occurrence of CWD at multiple farms and the absence of a traceability system for farmed cervids.
Keywords: Chronic wasting disease (CWD); NaOH; Protein-misfolding cyclic amplification (PMCA); Republic of Korea; farm; prions; remediation; topsoil.
https://www.tandfonline.com/doi/full/10.1080/19336896.2025.2527588
“While the disease control measures effectively eliminated prion seeding activity in CWD-affected farms, CWD recurred at two of the 18 remediated farms 4 to 5 years after restocking animals.”
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…
so, this is what we leave our children and grandchildren?
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/
Front. Vet. Sci., 14 September 2015 | https://doi.org/10.3389/fvets.2015.00032
Objects in contact with classical scrapie sheep act as a reservoir for scrapie transmission
In conclusion, the results in the current study indicate that removal of furniture that had been in contact with scrapie-infected animals should be recommended, particularly since cleaning and decontamination may not effectively remove scrapie infectivity (31), even though infectivity declines considerably if the pasture and the field furniture have not been in contact with scrapie-infected sheep for several months. As sPMCA failed to detect PrPSc in furniture that was subjected to weathering, even though exposure led to infection in sheep, this method may not always be reliable in predicting the risk of scrapie infection through environmental contamination.
http://journal.frontiersin.org/article/10.3389/fvets.2015.00032/full
"Additionally, we have determined that prion seeding activity is retained for at least fifteen years at a contaminated site following attempted remediation."
15 YEARS!
Detection of prions in soils contaminated by multiple routes
Results: We are able to detect prion seeding activity at multiple types of environmental hotspots, including carcass sites, contaminated captive facilities, and scrapes (i.e. urine and saliva). Differences in relative prion concentration vary depending on the nature and source of the contamination. Additionally, we have determined that prion seeding activity is retained for at least fifteen years at a contaminated site following attempted remediation.
Conclusions: Detection of prions in the environment is of the utmost importance for controlling chronic wasting disease spread. Here, we have demonstrated a viable method for detection of prions in complex environmental matrices. However, it is quite likely that this method underestimates the total infectious prion load in a contaminated sample, due to incomplete recovery of infectious prions. Further refinements are necessary for accurate quantification of prions in such samples, and to account for the intrinsic heterogeneities found in the broader environment.
Funded by: Wisconsin Department of Natural Resources
Prion 2023 Abstracts
https://prion2023.org/wp-content/uploads/2023/10/Meeting-book-final-version2.pdf
SUNDAY, APRIL 06, 2025
Failure to prevent classical scrapie after repeated decontamination of a barn
https://scrapie-usa.blogspot.com/2025/04/failure-to-prevent-classical-scrapie.html
https://prpsc.proboards.com/thread/165/failure-prevent-scrapie-repeated-decontamination
CWD, So, this is what we leave our children and grandchildren?
Detection of chronic wasting disease prions in the farm soil of the Republic of Korea
Here, we show that prion seeding activity was detected in extracts from farm soil following 4 years of incubation with CWD-infected brain homogenate.
https://journals.asm.org/doi/10.1128/msphere.00866-24
=====***>
"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
Results: We are able to detect prion seeding activity at multiple types of environmental hotspots, including carcass sites, contaminated captive facilities, and scrapes (i.e. urine and saliva). Differences in relative prion concentration vary depending on the nature and source of the contamination. Additionally, we have determined that prion seeding activity is retained for at least fifteen years at a contaminated site following attempted remediation.
Conclusions: Detection of prions in the environment is of the utmost importance for controlling chronic wasting disease spread. Here, we have demonstrated a viable method for detection of prions in complex environmental matrices. However, it is quite likely that this method underestimates the total infectious prion load in a contaminated sample, due to incomplete recovery of infectious prions. Further refinements are necessary for accurate quantification of prions in such samples, and to account for the intrinsic heterogeneities found in the broader environment.
Funded by: Wisconsin Department of Natural Resources
Prion 2023 Abstracts
https://prion2023.org/wp-content/uploads/2023/10/Meeting-book-final-version2.pdf
Artificial mineral sites that pre-date endemic chronic wasting disease become prion hotspots
The detection of PrPCWD in soils at attractant sites within an endemic CWD zone significantly advances our understanding of environmental PrPCWD accumulation dynamics, providing valuable information for advancing adaptive CWD management approaches.
https://int-cwd-sympo.org/wp-content/uploads/2023/06/final-agenda-with-abstracts.pdf
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
https://intcwdsympo.files.wordpress.com/2023/06/final-agenda-with-abstracts.pdf?force_download=true
***> Infectious agent of sheep scrapie may persist in the environment for at least 16 years
***> Nine of these recurrences occurred 14–21 years after culling, apparently as the result of environmental contamination, but outside entry could not always be absolutely excluded.
JOURNAL OF GENERAL VIROLOGY Volume 87, Issue 12
Infectious agent of sheep scrapie may persist in the environment for at least 16 years Free
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/
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.
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
THURSDAY, FEBRUARY 28, 2019
BSE infectivity survives burial for five years with only limited spread
https://link.springer.com/content/pdf/10.1007%2Fs00705-019-04154-8.pdf
CWD IS RAVAGING MY FAMILY’S LAND, BUT IT’S NOT TOO LATE FOR YOU
September 9, 2025 By: Paul Annear
My first season deer hunting in Wisconsin was 2001, the same season that produced Wisconsin’s first deer to test positive for chronic wasting disease. CWD has always been at the forefront of deer hunting discussions in my time as a hunter, and I’ve watched the disease slowly spread and worsen. Since 2019, eight of 11 deer I’ve taken on my family’s property in Richland County in Southwest Wisconsin have tested positive for CWD – including the buck in the photo above.
Aside from harvesting otherwise perfectly healthy-looking deer that test positive for CWD, we are now seeing live deer walking around in the awful final stages of this disease. Research has now confirmed what I’ve seen occurring on our hunting land in the last five to six years: CWD is beginning to reduce deer populations in high-prevalence areas like mine.
It didn’t have to reach this point. Hunters in areas with low CWD prevalence can keep infection rates low and deer populations healthy overall by accepting and implementing certain strategies. Some of the strategies I will lay out will challenge you as a hunter to play the “long game,” but there are ways to slow the spread of CWD in areas where it is newly discovered and infection rates are still low.
If you’re rolling your eyes at another guy talking about CWD, I get it, but I urge you to keep reading. Hear my personal story, how it has affected my hunting experiences, and what can happen if hunters ignore CWD.
“Where Are the Deer?”
Up until about seven years ago, I was still trying to figure out this CWD thing and what I thought of it all. I hadn’t yet seen or felt the effects. I was trying to improve my hunting in a variety of different ways like everyone else.
In Iowa County, hunters killed only 916 bucks during the 2024 nine-day firearms season. The last time Iowa County recorded less than 1,000 bucks killed during the nine-day firearms season was in 1971.
We began testing every deer taken on our farm in 2019, and with 72% of them testing positive, it’s safe to say we’re in the thick of it. I’m not alone. I speak to countless hunters in Southwest Wisconsin at trade shows and other events, and many of them are saying the same thing: “What is happening? Where are the deer?”
Since 2019, eight of 11 deer taken on Paul’s family land in southwest Wisconsin tested positive for CWD. This wall of bucks includes deer taken since 2006, and six of the more recent bucks added to this wall were CWD-positive.
In Iowa County, hunters killed only 916 bucks during the 2024 nine-day firearms season. The last time Iowa County recorded less than 1,000 bucks killed during the nine-day firearms season was in 1971. Iowa County tested 694 deer during the 2024 deer season, and 25% of deer tested were positive. Richland and Sauk counties both had a 33% positive CWD rate and together tested 2,193 deer. In 2004, a few years after the initial surge of testing occurred in Wisconsin, Richland County tested 1,691 deer and no deer tested positive for CWD. So, we haven’t been finding CWD just because we’re testing more. It arrived and has spread significantly.
The first time I saw what I believed to be CWD up close and personal was in spring 2023 when my dad and I were marching up a steep ridge for an afternoon turkey hunt. Just a short distance into the walk, I spotted a buck with velvet sprouts. “Dad,” I said. “Deer.”
We both thought it was unusual this deer wasn’t bounding off since we were within 40 yards. Springtime bucks are certainly not the paranoid creatures they become in fall, though. So, we closed the distance since we were headed that way and wanted a closer look.
The buck was very clearly sick. The hair on the back of my neck stood up instantly. A better view revealed his shaking, emaciated body and drool spilling from his mouth (see the photo below). His spine, shoulder blades, and scars up and down his legs told me this deer was in the final stage of CWD but had just enough energy to escape a few predators in the days prior. I had begun to wonder why so many of my 3½-year-old bucks never returned, and this moment convinced me CWD is playing a role in bucks constantly disappearing. This buck was days away from dying of holes eaten in his brain. We were able to put him out of his misery with permission from the Wisconsin DNR.
Though CWD has been in his area for more than 20 years, it wasn’t until 2023 that Paul Annear encountered a visibly sick deer. By the time hunters are seeing sick deer in the woods, the infection rate is usually too high to do anything about it.
I travel 200 miles one way to hunt this property in Southwest Wisconsin. The disease has in a way disrupted my motivation to keep traveling here, knowing full well there is a high likelihood of any deer we kill testing positive, resulting in us throwing out the meat. If you don’t hunt in a CWD zone, your routine following a successful hunt is probably simple and relatively careless. The presence of CWD changes that real quick. Shooting a deer means we could be in for a few frustrating weeks to follow as we wait for CWD test results. I’ve wasted countless hours butchering deer only to throw out the venison.
My friend and fellow Wisconsin deer hunter Bradie Ewing follows the same recommended protocols I do regarding CWD-positive venison.
“We have made the decision that we will not eat or feed a CWD positive deer to our kids or family, so this has caused some logistical headaches,” said Bradie. “The investment of time up front in butchering a deer is significant only to later throw it away if its positive.”
In 2020, I had nearly 30 bucks on trail-camera I estimated to be 3½ years old or older. In 2024, I felt confident we had only seven or eight deer in that age class. A stark decrease. I also ran about 20 more trail cameras on this 115-acre property in 2024 than I did in 2020, so fewer photos are not playing a role in my estimation of fewer mature deer. There are simply fewer mature deer, and DNR harvest data shows it’s not because hunters killed more older bucks in recent seasons. It’s because of CWD.
Why do I keep making the drive back to Richland County? My parents have lived on this land since 1987. This is the land where I was born and raised, where I grew up exploring the woods and learning to hunt squirrels and deer. It’s where I feel I belong, and I know that strong emotional attachment will keep me coming back to hunt deer with my family every fall.
Common Sense
Chronic Wasting Disease prions can be shed via saliva at mineral sites. CWD prions can exist in the soil below licking branches in a scrape. We’re never going to eliminate deer-to-deer contact in the wild. But if you’re in a low CWD prevalence area, there are some common-sense practices you should follow. You can learn from a few of my mistakes.
In the last few years, I’ve wondered if we can truly do anything to curb the spread of CWD in extremely high prevalence areas. One day I would feel the CWD battle is worth fighting, then just days later I’d harvest a CWD positive deer and be discouraged to the point of thinking “this is a bridge too far.”
With 33% of deer in Paul’s county now testing positive for CWD, he has begun to see visibly sick deer in the last two years. Paul’s trail-camera captured the photos above and below in fall 2024. Paul found the remains of the buck above three months after this photo was taken. Note: Deer with EHD die within 5 to 10 days of infection, which isn’t enough time for this kind of drastic weight loss.
I told myself I just wanted to get back to hunting. In the midst of these internal battles, I set out a tank-style waterhole on a Southwest Wisconsin property I hunt. While baiting or feeding is illegal in every Southwest Wisconsin county to help slow the spread of disease, the Wisconsin DNR has not banned the creation of artificial water sources. There are limited water resources on this property, and I thought a waterhole would be a unique way to attract deer near a stand site.
I had an abundance of deer visiting the water tank in the few months it was set up. Despite all the trail-camera photos, a famous Aldo Leopold quote would occasionally run through my mind: “A thing is right when it tends to preserve the integrity, stability, and the beauty of the biotic community – it is wrong if it tends otherwise.”
During the short time I had the waterhole out, I emptied and re-filled it many times since I still wanted to be cognizant of disease transmission. But I have to be honest with myself and admit that if I care about wild deer and the places they live, setting out a small, non-flowing waterhole in a CWD zone was a mistake. Not long after killing a visibly sick, CWD-positive doe that came to drink from the waterhole, we removed it.
In certain regions of the U.S., baiting is just a way of life and how it’s always been done. So, I get the enjoyment and desire to feed or provide artificial water sources for deer. I know hunters in states like Texas and Kansas who would hardly have a deer pass through their land if they didn’t run a feeder.
Are we going to stop the spread of CWD by banning waterholes or baiting? No. But common sense would say those things don’t help an infected herd. Artificially inflating your local deer population in a high CWD prevalence zone by feeding is dangerous because deer that may not otherwise come in contact with one another could share infectious prions at a bait or water site.
Does the presence of CWD mean you should never hang a mock licking branch or plant food plots to improve your hunting opportunities? I believe that’s an unreasonable way of thinking. I am still going to create food plots and mock scrapes. However, I strongly believe we need to practice common sense and realize there are matters we can take into our own hands when it comes to mitigating the spread of CWD. It begins with pulling triggers and landowners making strong, individual decisions regarding their deer herd and holding to them.
Sound Management and Testing
“Earn-A-Buck” was a tool some states used intermittently to effectively manage high deer herds. Wisconsin had implemented EAB off and on beginning in 1996, until it was signed out of law by Wisconsin Governor Scott Walker. I believe EAB is an effective tool for managing deer herds in some places, and I believe it’s no coincidence CWD rates have steadily increased in Wisconsin since Gov. Walker got rid of the law with pressure from other politicians and interest groups. There are few better incentives to take a doe than requiring it before you can take a buck. The only incentive that worked is now gone.
Earn-A-Buck cannot be signed back into law without the Wisconsin legislature doing so. Wisconsin hunters are left with a distinct choice that Wisconsin hunter Doug Duren is often heard saying. “Where CWD is established or taking hold, we have one of two choices,” Doug says. “We are going to manage the herd and the disease, or CWD is going to do it for us.” Wisconsin has had no effective deer management plan since the elimination of EAB in 2011.
In talking with countless hunters in my region, it appears CWD can be somewhat pocketed even within high prevalence counties like mine. The variability of CWD prevalence within a county could be due to availability of better habitat, people not illegally baiting in certain areas, or for unknown reasons. But we do know that high deer density helps CWD spread faster, so simply continuing to harvest deer – especially does – works. Doe harvest helps keep deer density in balance with the habitat and reduces deer-to-deer spread of CWD, which means healthier deer in all respects. But it’s not just about doe harvest.
Bucks test positive at a higher rate than does because of behaviors like traveling farther during the rut. I would encourage you to be less picky about harvesting bucks if CWD has just been discovered and you’re trying to keep prevalence rates low. NDA’s advice for hunters in CWD zones is to continue managing for older bucks if you wish but apply increased harvest pressure on all bucks 2½ years of age or older.
Do I wish we could go back to those days of low prevalence and undergo targeted removal missions on my family’s land to see if it would prevent or delay the problem we have today? Yes. Sustained harvest on all deer, bucks and does, means a better chance of removing infected deer from the landscape sooner. If hunters back off deer harvest because of CWD, infected deer enjoy greater protection, and they can spread more CWD prions into the environment and to other deer. In fact, every time you harvest a deer that tests positive for CWD, you should look at this as a win in the fight against this disease.
Jason Sumners is the Director of the Missouri Department of Conservation and has guided Missouri through a proactive approach to CWD.
“If all you are doing is testing to show you are doing something, it’s a complete waste of critical agency resources,” said Jason. “Short of documenting the demise of deer and giving some hunters a little more comfort when consuming deer harvested in CWD areas, it’s not doing anything to help the herd.”
What is Missouri doing? A lot of testing but also Targeted harvesting in select zones with landowner approval. In 2025, they’ve killed 4,793 deer with 68 (1.4%) of those being positive. While the CWD positive rate of these targeted removals is still low, that’s the point. This is a relatively small number of deer removed statewide, but because they are removed with precision from sites where deer previously tested positive, sick deer are removed sooner. Missouri is keeping CWD prevalence rates in check throughout these surveillance zones.
Would I have been hesitant to allow targeted deer removal or “sharpshooting”’on my property back when CWD had just been discovered? Yes. Do I wish we could go back to those days of low prevalence and undergo targeted removal missions on my family’s land to see if it would prevent or delay the problem we have today? Yes.
The early stage of CWD is the only stage when intervention and management can hope to hold infection rates low. If you wait until you are seeing sick deer in the woods, which is a sign you are in “late-stage” CWD, it’s too late to do anything about it.
If CWD isn’t in your woods yet, you should still make it a point to submit deer for testing anytime an opportunity is presented. Early detection of a new outbreak is critical. Early detection gives hunters and the state wildlife agency the opportunity to respond. CWD testing isn’t a proclamation of any political views or ideologies. However, it is absolutely a pledge that you care about deer and their future.
Paul Annear grew up hunting with his dad on family land in southwest Wisconsin and is now teaching his son Hudson how to hunt. We Are Not Doomed
I believe there will always be white-tailed deer in my area of Wisconsin. However, within 20 to 25 years, I believe fewer bucks will reach maturity than today, and a lot fewer than when I began hunting over 20 years ago.
This is despite more people than ever before passing younger deer and managing for older deer. I think in some areas like mine with high CWD prevalence, the average age of bucks has already dropped significantly from where it was just a few years ago – at a time when NDA’s Deer Report shows more bucks aged 3½ years old or older being harvested nationally than ever before.
If CWD has been found in your woods, ignoring it will take your hunting down the wrong path. Private landowners especially will play a critical role in properly managing whitetails in America in the next 30 years. I’m reminded of this Aldo Leopold quote: “Conservation will ultimately boil down to rewarding the private landowner who conserves the public interest.”
In this case, public interest is healthy deer. In most of whitetail country, unlike Southwest Wisconsin, it’s not too late to do something. Common-sense practices might seem like a burden to you now, but it’s nothing compared to what I’m experiencing. Ignoring those practices might help your short-term hunting opportunities, but remember you are in the position I wish I could go back to. Ask yourself if the choices you are making now will help conserve a better future for all.
Categories: Hunting
Tags: Chronic Wasting Disease, Cwd
About Paul Annear:
Paul Annear is an avid deer hunter, freelance writer and NDA member from the Driftless Region of southwest Wisconsin.
https://deerassociation.com/cwd-is-ravaging-my-familys-land-but-its-not-too-late-for-you/
MONDAY, APRIL 28, 2025
Wisconsin DNR 2024 CWD 1,786 samples testing positive
https://chronic-wasting-disease.blogspot.com/2025/04/wisconsin-dnr-2024-cwd-1786-samples.html
Captive CHRONIC WASTING DISEASE CASES Update August 2025 Captive CHRONIC WASTING DISEASE CASES Update August 2025, Pennsylvania, Wisconsin, Utah, and Texas
https://www.aphis.usda.gov/sites/default/files/status-of-captive-herds.pdf
https://chronic-wasting-disease.blogspot.com/2025/08/texas-game-wardens-near-conclusion-of.html
Published: 05 August 2025
Vertical transmission of chronic wasting disease in free-ranging white-tailed deer populations
Snip…
Our detection of CWD-positive fawns ≤ 10-month-old by ELISA testing provides indirect evidence of gestational infection, although direct or indirect CWD transmission after birth cannot be ruled out in these fawns (Table 5). The detection of CWD infection in ≤ 6-month-old fawns in the Arkansas and Tennessee study sites by ELISA test, which is not as sensitive as amplification assays37, was particularly suggestive of vertical transmission. Fawns less than 6 months of age are not routinely incorporated into statewide CWD surveillance programs because of the low likelihood of detectable infection using traditional assays (i.e., ELISA, IHC), yet have been previously identified17. Future studies should investigate the potential role of in utero transmission in local CWD transmission cycles. Considering the strong relationship between CWD infection probability and female white-tailed deer relatedness, in utero CWD transmission may serve as a small yet important route of transmission in addition to social interactions and indirect exposures53.
Overall, this study describes the dissemination of CWD prions throughout tissues and birthing fluids of the pregnancy microenvironment demonstrating that offspring are routinely exposed to the infectious prion in-utero prior to parturition. We report infectious prions in the reproductive and fetal tissue of naturally exposed free-ranging white-tailed deer suggesting that in utero maternal transmission is likely an underappreciated mode of CWD transmission. Our study shows that vertical transmission is indeed a viable route of infection within the southeastern U.S. and is another potential factor contributing to the relentless spread of chronic wasting disease.
https://www.nature.com/articles/s41598-025-12727-8
WISCONSIN 16 MONTH AGE LIMIT ON TESTING DEAD DEER GAME FARM CWD TESTING PROTOCOL NEEDS TO BE REVISED SINGELTARY ET AL
ENVT.18: MOTHER TO OFFSPRING TRANSMISSION OF CHRONIC WASTING DISEASE
Candace K. Mathiason,† Amy Nalls, Kelly Anderson, Jeanette Hayes-Klug, Jenny G. Powers, Nicholas J. Haley and Edward A. Hoover
"PrPCWD has been detected in one fawn as early as 40 days of age. Moreover, sPMCA performed on rectal lymphoid tissue has yield positive results on another fawn at 10 days of age"
https://www.tandfonline.com/doi/pdf/10.4161/pri.15899
Oral transmission and early lymphoid tropism of chronic wasting disease PrPres in mule deer fawns (Odocoileus hemionus)
The rapid infection of deer fawns following exposure by the most plausible natural route is consistent with the efficient horizontal transmission of CWD in nature and enables accelerated studies of transmission and pathogenesis in the native species. Introduction
https://www.microbiologyresearch.org/content/journal/jgv/10.1099/0022-1317-80-10-2757#tab2
Demographic Patterns and Harvest Vulnerability of Chronic Wasting Disease Infected White-Tailed Deer in Wisconsin
Six fawns tested positive for CWD, five fawns from the core study area, including the youngest (5 months) free-ranging cervid to test positive.
http://forestandwildlifeecology.wisc.edu/facstaff/samuel/2006_grear_et_al_demographic_patterns.pdf
http://web.archive.org/web/20100613124552/http://forestandwildlifeecology.wisc.edu/facstaff/samuel/2006_grear_et_al_demographic_patterns.pdf
Chronic Wasting Disease in a Wisconsin White-Tailed Deer Farm
and 15 of 22 fawns aged 6 to 9 months (68.2%) were positive.
http://vdi.sagepub.com/content/20/5/698.full
https://digitalcommons.unl.edu/cgi/viewcontent.cgi?article=1143&context=zoonoticspub
Wisconsin : Six White-Tailed Deer Fawns Test Positive for CWD
Date: May 13, 2003 Source: Wisconsin Department of Natural Resources
Approximately 4,200 fawns, defined as deer under 1 year of age, were sampled from the eradication zone over the last year. The majority of fawns sampled were between the ages of 5 to 9 months, though some were as young as 1 month. Two of the six fawns with CWD detected were 5 to 6 months old. All six of the positive fawns were taken from the core area of the CWD eradication zone where the highest numbers of positive deer have been identified.
http://www.cwd-info.org/index.php/fuseaction/news.detail/ID/a4b4e5e8749d729af242e253ac742084
http://web.archive.org/web/20071012001856/http://www.cwd-info.org/index.php/fuseaction/news.detail/ID/a4b4e5e8749d729af242e253ac742084
Age specific susceptibility? 194. It is probable, based on age-class specific prevalence data from wild cervids and epidemiological evidence from captive cervids in affected research centres, that both adults and fawns may become infected with CWD (Miller, Wild & Williams, 1998; Miller et al., 2000). 198. In Odocoileus virginianus – white tailed deer, out of 179 white-tailed deer which had become enclosed by an elk farm fence, in Sioux County, northwestern Nebraska, four fawns only eight months old were among the 50% of CWD-positive animals; these fawns were not showing any clinical signs of CWD (Davidson, 2002).
http://wildpro.twycrosszoo.org/s/00ref/miscellaneouscontents/D161_CWDReview_Seac/08_Susceptibility_Nat_Hosts.htm
http://web.archive.org/web/20160312230103/http://wildpro.twycrosszoo.org/s/00ref/miscellaneouscontents/D161_CWDReview_Seac/08_Susceptibility_Nat_Hosts.htm
SCWDS BRIEFS
Volume 17 January 2002 Number 4
CWD News from Nebraska and Kansas
Infection with the chronic wasting disease (CWD) agent recently was found in 28 of 58 formerly wild white-tailed deer in a high-fenced enclosure adjacent to a pen containing CWD affected captive elk in northern Sioux County, Nebraska.
Four of the positive deer were fawns approximately 8 months old, which is unusually young for animals testing positive for CWD.
https://digitalcommons.unl.edu/cgi/viewcontent.cgi?article=1017&context=secwdspubs
CWD in adult deer and fawns
A hundred and thirty-three white-tailed deer in the study were killed after CWD was diagnosed in the deer within the fenced area. Paired samples of formalin-fixed tissue for CWD diagnosis and frozen tissue for DNA sequence analysis were collected. Fifty per cent (67/133) of deer were diagnosed with CWD (Table 2) using an immunohistochemical assay for PrPd in formalin-fixed, paraffinembedded brain and lymphoid tissues.
Five of the CWD-positive deer were fawns, less than 1 year of age.
http://digitalcommons.unl.edu/cgi/viewcontent.cgi?article=1125&context=zoonoticspub
Illinois CWD, see where there 2003 sampling showed 2. % of fawns tested had CWD i.e. 1 positive out of 51 samples.
2003
Boone-Winnebago Unit Fawn 51 1 2.0%
http://dnr.state.il.us/cwd/Sampling_Summary_2003.pdf
http://web.archive.org/web/20041106203740/http://dnr.state.il.us/cwd/Sampling_Summary_2003.pdf
2011 FAWN CWD POSITIVE ILLINOIS
1/26/11 WINNEBAGO 344N 2E S36 F FAWN SHARPSHOOTING
2/10/11 OGLE 341N 1E S7 F FAWN SHARPSHOOTING
3/9/11 OGLE 341N 1E S7 M FAWN SHARPSHOOTING
http://dnr.state.il.us/CWD/2010-2011_Illinois_CWD_Report.pdf
https://ngrrec-hunt-illinois-wordpress-images.s3.amazonaws.com/wp-content/uploads/2023/04/13110846/cwdannualreport20102011.pdf
So, this is what we leave our children and grandchildren?
TUESDAY, JULY 08, 2025
Addressing chronic wasting disease in Korean farms: topsoil removal and 2N NaOH treatment before cervid restocking
https://chronic-wasting-disease.blogspot.com/2025/07/addressing-chronic-wasting-disease-in.html
THURSDAY, JULY 10, 2025
Distribution of chronic wasting disease (CWD) prions in tissues from experimentally exposed coyotes (Canis latrans) Published: July 9, 2025
https://chronic-wasting-disease.blogspot.com/2025/07/distribution-of-chronic-wasting-disease.html
THURSDAY, JULY 10, 2025
Modelling the effect of genotype (PRNP) linked to susceptibility, infection duration and prion shedding on chronic wasting disease dynamics of cervids
https://chronic-wasting-disease.blogspot.com/2025/07/modelling-effect-of-genotype-prnp.html
WEDNESDAY, MAY 14, 2025
Texas CWD TSE Prion Cases Rises to 1099 Confirmed Cases To Date
https://tpwd.texas.gov/huntwild/wild/diseases/cwd/positive-cases/listing-cwd-cases-texas.phtml
https://chronic-wasting-disease.blogspot.com/2025/05/texas-cwd-tse-prion-cases-rises-to-1099.html
FRIDAY, APRIL 04, 2025
Trucking CWD TSE Prion
“CWD spreads among wild populations at a relatively slow rate, limited by the natural home range and dispersed nature of wild animals.”
NOW HOLD YOUR HORSES, Chronic Wasting Disease CWD of Cervid can spread rather swiftly, traveling around 50 MPH, from the back of truck and trailer, and Here in Texas, we call it ‘Trucking CWD’…
https://chronic-wasting-disease.blogspot.com/2025/04/trucking-cwd-tse-prion.html
SUNDAY, MAY 04, 2025
Texas Senate Bill 2649 creation of a statewide Chronic Wasting Disease plan
https://chronic-wasting-disease.blogspot.com/2025/05/texas-senate-bill-2649-creation-of.html
SUNDAY, MAY 04, 2025
Texas Senate Bill 2651 establishment of a pilot program to breed deer resistant to CWD TSE Prion, what could go wrong?
https://chronic-wasting-disease.blogspot.com/2025/05/texas-senate-bill-2651-establishment-of_4.html
Texas S.B. 2843 Directs TPWD to conduct a comprehensive study of current measures to control chronic wasting disease (CWD) in deer
https://chronic-wasting-disease.blogspot.com/2025/04/texas-sb-2843-directs-tpwd-to-conduct.html
Friday, February 21, 2025
Deer don’t die from CWD, it’s the insurance companies, or it's a Government conspiracy?
https://chronic-wasting-disease.blogspot.com/2025/02/deer-dont-die-from-cwd-its-insurance.html
Friday, February 21, 2025
CWD, BAITING, AND MINERAL LICKS, WHAT IF?
https://chronic-wasting-disease.blogspot.com/2025/02/cwd-baiting-and-mineral-licks-what-if.html
SUNDAY, MAY 05, 2024
Chronic Wasting Disease, Cervid Captive Herd CWD Infection rates, Zoonosis, and Environmental Risk Factors
https://chronic-wasting-disease.blogspot.com/2024/05/chronic-wasting-disease-cervid-captive.html
Texas Game Wardens Bust Illegal Deer Operations Across the State Feb. 27, 2025
https://chronic-wasting-disease.blogspot.com/2025/02/texas-game-wardens-bust-illegal-deer.html
TUESDAY, AUGUST 26, 2025
Transmissible Spongiform Encephalopathy TSE Prion Disease UPDATE AUGUST 2025
https://transmissiblespongiformencephalopathy.blogspot.com/2025/08/transmissible-spongiform-encephalopathy.html
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
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
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
Terry S. Singeltary Sr.
https://pagame.maps.arcgis.com/apps/dashboards/b3c0fd44cc5944ebbc2229ede897b2ae
https://chronic-wasting-disease.blogspot.com/2025/07/pennsylvania-2424-confirmed-cases-cwd_41.html
THURSDAY, JULY 10, 2025
Distribution of chronic wasting disease (CWD) prions in tissues from experimentally exposed coyotes (Canis latrans) Published: July 9, 2025
https://chronic-wasting-disease.blogspot.com/2025/07/distribution-of-chronic-wasting-disease.html
TUESDAY, JUNE 24, 2025
Maryland Department of Natural Resources’ Annual Survey Detects 62 Deer with Chronic Wasting Disease in 2024
https://chronic-wasting-disease.blogspot.com/2025/06/maryland-department-of-natural.html
TUESDAY, MAY 27, 2025
Iowa CWD Update May 2025 confirms 523 case to date
https://chronic-wasting-disease.blogspot.com/2025/05/iowa-cwd-update-may-2025-confirms-523.html
WEDNESDAY, MAY 14, 2025
Virginia DWR Reports 2024–2025 CWD Results 109 positive
https://dwr.virginia.gov/media/press-release/dwr-reports-2024-2025-chronic-wasting-disease-surveillance-results/
https://chronic-wasting-disease.blogspot.com/2025/05/virginia-dwr-reports-20242025-cwd.html
WEDNESDAY, MAY 14, 2025
North Dakota 2024 CWD Test Results Confirm 17 Positive
https://chronic-wasting-disease.blogspot.com/2025/05/north-dakota-2024-cwd-test-results.html
WEDNESDAY, MARCH 26, 2025
Ohio ODNR Confirm 24 WTD Positive For CWD 2024-25 Hunting Season
https://chronic-wasting-disease.blogspot.com/2025/03/ohio-odnr-confirm-24-wtd-positive-for.html
WEDNESDAY, MARCH 12, 2025
West Virginia DNR Expands Containment Area after detection of CWD in a Grant County deer
https://chronic-wasting-disease.blogspot.com/2025/03/west-virginia-dnr-expands-containment.html
2025 Colorado CWD TSE Prion prevalence increased in 14 herds, remained about the same in 16 herds, and decreased in 4 herds
Colorado 2022 2024 CWD prevalence increased in 14 herds, remained about the same in 16 herds, and decreased in 4 herds
Colorado CWD has gotten so bad, they can’t even give a Total To Date count. Best they can do is is give you Total Herds With CWD…
Jeff Davis, Director, Colorado Parks and Wildlife Parks and Wildlife Commission: Dallas May, Chair ∙ Richard Reading, Vice-Chair ∙ Karen Bailey, Secretary ∙ Jessica Beaulieu Marie Haskett ∙ Tai Jacober ∙ Jack Murphy ∙ Gabriel Otero ∙ Murphy Robinson ∙ James Jay Tutchton ∙ Eden Vardy
MEMORANDUM
April 25, 2025
TO: Colorado Parks and Wildlife Commissioners
FROM: Brian Dreher, Assistant Director, Terrestrial Branch
Subject: Chronic Wasting Disease Update for Parks and Wildlife Commission
Dear Commissioners,
This briefing summarizes CPW’s mandatory chronic wasting disease (CWD) findings from the 2022- 2024 hunting seasons. Results provide the first indication of whether CWD management actions taken for deer over the past 5-7 years have had an effect on CWD prevalence (estimated percent infected) in each herd. In summary, CWD prevalence decreased in 4 herds, increased in 14 herds, and remained about the same in 16 herds.
Background
Chronic wasting disease, a fatal neurological disease found in deer, elk, and moose, is well established in herds throughout much of Colorado. We have detected CWD in 42 of our 51 deer herds, 17 of 42 elk herds, and 2 of 13 moose herds. CWD prevalence is highest in deer and lowest in moose. This disease is always fatal and animals die from the disease within about 2-2.5 years of infection. CWD infection shortens the lifespan of infected animals. If infection rates become too high, CWD can affect a herd’s ability to sustain itself.
In response to increasing CWD prevalence, the Parks and Wildlife Commission approved a statewide CWD Response Plan in 2019. One element was a 15-year mandatory testing plan, which will include three 5-year rotations for deer. Pilot work in 2017 and 2018 had shown that the number of deer submitted for testing is much higher through mandatory testing than for voluntary submissions, which allows CPW to generate reliable estimates of CWD prevalence at the herd level.
In addition, the CWD Response Plan establishes a compulsory management threshold, which means when prevalence exceeds 5% in adult (>2 years) male deer then some form of management action will be taken to reduce prevalence until it falls below the 5% threshold. CPW identifies various management actions in the plan that are available to local managers to prescribe in herd management efforts, all of which have the potential to help reduce prevalence in deer herds.
CWD prevalence was assessed via mandatory testing in all deer herds from 2017-2020; mandatory testing focused on elk in 2021. In 2022, CPW restarted the 5-year testing rotation for deer. Thirty-four deer herds have been included in a second round of mandatory testing. Three herds, White River (D- 07, 2024) Middle Park (D-09, 2024), and Bears Ears (D-02, 2025) were already scheduled for a third round of mandatory testing to learn more about how prevalence is changing in these herds related to the 2022-2023 severe winter and exponential growth in CWD prevalence. CPW will conclude the second round of mandatory testing for deer in 2025 and for elk in 2026.
Mandatory Testing Results CWD prevalence estimates have decreased in 4 deer herds, increased in 14 deer herds, and remained about the same in 16 deer herds (Figure 1, Table 1).
Prevalence was expected to increase in many high-prevalence herds. However, prevalence stayed about the same between the two rounds of mandatory testing in many high- prevalence herds. This is an indication that prescribed management actions are preventing or slowing increases in CWD prevalence, even if we are not seeing a reduction in prevalence. Additional data and robust analyses are needed over the next 7 years of mandatory testing to guide CPW's interpretation of these results before we are in a position to show an association between prescribed management actions and CWD prevalence.
CPW prescribed various management actions in each of these 34 herds and the response in prevalence varies. Therefore, CPW will evaluate why prevalence increased in some herds and decreased in others. Overall, these preliminary data are encouraging for some herds and suggest harvest-based management actions could be a promising CWD control strategy.
Further Analyses
CPW will continue analyses of these CWD prevalence changes by comparing various factors between herds and the respective management actions prescribed. Comparing changes to license quotas by season, dates of harvest and prevalence estimates by season, post-hunt buck/doe ratios, abundance of bucks and does, and the percent change in buck licenses and buck harvest, etc., all in relation to changes in CWD prevalence, should improve our ability to evaluate relationships between various management actions and disease prevalence. CPW plans to complete these analyses as the 15-year mandatory testing period concludes, if not sooner.
In our more than 40-year history working with CWD, one of the most important lessons we have learned is that we rarely see immediate changes in CWD dynamics. This is a slow-moving disease and changes in prevalence (both increases and decreases) may not be readily apparent. Multiple repeated prevalence estimates over the long-term along with consistent management application will be necessary to evaluate patterns of change in relationship to management actions.
Lastly, severe winter conditions seen in Northwestern Colorado during the 2022-2023 winter generated many questions on potential implications for CWD dynamics in the region. Harsh winter conditions may cause more rapid mortality of infected deer in the clinical phase of disease and could reduce the number of infected animals on the landscape. Overall population reductions associated with harsh winter conditions may also affect deer/elk density on the landscape and reduce direct animal-to-animal transmission. On the other hand, prolonged concentrations of deer and elk on very limited winter ranges could facilitate increased contact as well as environmental accumulation of CWD prions (infectious agent) that could increase both direct and indirect transmission pathways. Preliminary, based on 2024 results, it does not appear that the severe winter of 2022-2023 resulted in reduced CWD prevalence. Ultimately, the interplay of weather conditions, changing population dynamics, and changes in habitat use associated with a severe winter limit our capacity to predict how CWD prevalence might change. As we proceed with analyses to evaluate factors influencing CWD prevalence in Colorado wildlife populations, incorporating changes associated with periodic severe winters will be an important consideration.
CC: J. Davis R. DeWalt Regional Managers M. Eckert Senior Biologists J. Runge A. Holland
https://cpw.widen.net/view/pdf/rozctppvvm/Item.11_2025-04-24_Chronic_Wasting_Disease_Update_for_PWC.pdf?u=xyuvvu
2022 Colorado detected CWD in 40 of our 54 deer herds, 17 of 42 elk herds, and 2 of 9 moose herds
MEMORANDUM
To: Members of the Colorado Parks and Wildlife Commission
From: Dan Prenzlow, Director
Date: April 22, 2022
Subject: Chronic Wasting Disease Update for Parks and Wildlife Commission
Dear Commissioners,
This briefing summarizes CPW’s mandatory chronic wasting disease (CWD) findings from the 2021-2022 hunting seasons and, more broadly, things we have learned over the first 5-year rotation of mandatory testing (2017-2021 hunting seasons). Overall, the decision to commit to annual mandatory testing has been resoundingly important to understanding the status of this disease in Colorado, acquiring and communicating reliable prevalence estimates, and laying a foundation to assess herd-specific management actions to combat CWD. It is my pleasure to present this current information to keep you apprised on the status of CWD in our big game herds.
Background
Chronic wasting disease, a fatal neurological disease found in deer, elk, and moose, is well established in herds throughout much of Colorado. We have detected CWD in 40 of our 54 deer herds, 17 of 42 elk herds, and 2 of 9 moose herds. Disease prevalence (percent infected) is highest in deer and lowest in moose. This disease is always fatal and animals die from the disease within about 2-2.5 years of infection. CWD infection shortens the lifespan of infected animals. If infection rates become too high, CWD can affect a herd’s ability to sustain itself.
Snip…
https://web.archive.org/web/20220513134346/https://cpw.state.co.us/Documents/Commission/2022/May/Item.11-PWC_Memo_CWD_Update_EckertMillerWood_April2022-Matthew_Eckert-DNR.pdf
Colorado As of July 2018, at least 31 of Colorado's 54 deer herds (57%), 16 of 43 elk herds (37%), and 2 of 9 moose herds (22%) are known to be infected with CWD. Four of Colorado's 5 largest deer herds and 2 of the state’s 5 largest elk herds are infected.
As of July 2018, at least 31 of Colorado's 54 deer herds (57%), 16 of 43 elk herds (37%), and 2 of 9 moose herds (22%) are known to be infected with CWD. Four of Colorado's 5 largest deer herds and 2 of the state’s 5 largest elk herds are infected. Deer herds tend to be more heavily infected than elk and moose herds living in the same geographic area. Not only are the number of infected herds increasing, the past 15 years of disease trends generally show an increase in the proportion of infected animals within herds as well. Of most concern, greater than a 10-fold increase in CWD prevalence has been estimated in some mule deer herds since the early 2000s; CWD is now adversely affecting the performance of these herds…
https://cpw.widen.net/s/d7b55k9dcm/colorado_chronic_wasting_disease_response_plan
https://cpw.state.co.us/hunting/chronic-wasting-disease
TUESDAY, SEPTEMBER 30, 2025
Colorado 2022 2024 CWD TSE Prion prevalence increased in 14 herds, remained about the same in 16 herds, and decreased in 4 herds
https://chronic-wasting-disease.blogspot.com/2025/09/colorado-2022-2024-cwd-tse-prion.html
MONDAY, MAY 09, 2022
Colorado CWD TSE Prion Detected in 40 of 54 deer herds, 17 of 42 elk herds, and 2 of 9 moose herds
https://chronic-wasting-disease.blogspot.com/2022/05/colorado-cwd-tse-prion-detected-in-40.html
THURSDAY, SEPTEMBER 11, 2025
CWD IS RAVAGING MY FAMILY’S LAND, BUT IT’S NOT TOO LATE FOR YOU
https://chronic-wasting-disease.blogspot.com/2025/09/cwd-is-ravaging-my-familys-land-but-its.html
MONDAY, APRIL 28, 2025
Wisconsin DNR 2024 CWD 1,786 samples testing positive
https://chronic-wasting-disease.blogspot.com/2025/04/wisconsin-dnr-2024-cwd-1786-samples.html
https://chronic-wasting-disease.blogspot.com/2025/05/wisconsin-rock-county-deer-farm.html
FRIDAY, APRIL 04, 2025
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
“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
Texas Chronic Wasting Disease CWD TSE Prion Dashboard Update August 2025
SEE NEW DASHBOARD FOR CWD POSITIVES!
https://experience.arcgis.com/experience/8f6c27330c444a19b4b57beb7ffabb8b/page/Dashboard#data_s=id%3AdataSource_3-1966d773e34-layer-10%3A29
Texas CWD total by calendar years
https://chronic-wasting-disease.blogspot.com/2024/12/texas-cwd-tse-prion-positive-samples-by.html
https://tpwd.texas.gov/huntwild/wild/diseases/cwd/positive-cases/listing-cwd-cases-texas.phtml#texasCWD
Counties where CWD Exposed Deer were Released
https://tpwd.texas.gov/documents/257/CWD-Trace-OutReleaseSites.pdf
Number of CWD Exposed Deer Released by County
https://tpwd.texas.gov/documents/258/CWD-Trace-OutReleaseSites-NbrDeer.pdf
CWD Status Captive Herds
https://www.aphis.usda.gov/sites/default/files/status-of-captive-herds.pdf
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
https://prpsc.proboards.com/thread/178/texas-game-wardens-conclusion-ghost
WEDNESDAY, MAY 14, 2025
Texas CWD TSE Prion Cases Rises to 1099 Confirmed Cases To Date
https://chronic-wasting-disease.blogspot.com/2025/05/texas-cwd-tse-prion-cases-rises-to-1099.html
TAHC 425th Commission Meeting CWD 1:45:00
* See CWD speakers expressing their concerns with changed regulations…
2:00 hr mark
https://m.youtube.com/watch?v=bWawHpdn_7I
TEXAS ANIMAL HEALTH COMMISSION 423rd Commission Meeting CWD Update February 25, 2025
https://chronic-wasting-disease.blogspot.com/2025/02/texas-animal-health-commission-423rd.html
THURSDAY, APRIL 24, 2025
***> US Captive CWD Positive Herds Update April 2025
https://chronic-wasting-disease.blogspot.com/2025/04/us-captive-cwd-positive-herds-update.html
Captive CHRONIC WASTING DISEASE CASES Update August 2025 Captive CHRONIC WASTING DISEASE CASES Update August 2025, Pennsylvania, Wisconsin, Utah, and Texas
https://www.aphis.usda.gov/sites/default/files/status-of-captive-herds.pdf
https://chronic-wasting-disease.blogspot.com/2025/08/texas-game-wardens-near-conclusion-of.html
MONDAY, SEPTEMBER 15, 2025
Chronic Wasting Disease CWD TSE Prion Environmental Factors Update
https://chronic-wasting-disease.blogspot.com/2025/09/chronic-wasting-disease-cwd-tse-prion.html
https://chronic-wasting-disease.blogspot.com/
Chronic Wasting Disease CWD TSE Prion Environmental & Zoonosis Factors Update September 2025
What does CDC say?
CDC CWD TSE Prion Update 2025
KEY POINTS
Chronic wasting disease affects deer, elk and similar animals in the United States and a few other countries.
The disease hasn't been shown to infect people.
However, it might be a risk to people if they have contact with or eat meat from animals infected with CWD.
https://www.cdc.gov/chronic-wasting/about/index.html
Prions in Muscles of Cervids with Chronic Wasting Disease, Norway
Volume 31, Number 2—February 2025
Research
Prions in Muscles of Cervids with Chronic Wasting Disease, Norway
Snip…
In summary, the results of our study indicate that prions are widely distributed in peripheral and edible tissues of cervids in Norway, including muscles. This finding highlights the risk of human exposure to small amounts of prions through handling and consuming infected cervids. Nevertheless, we note that this study did not investigate the zoonotic potential of the Norway CWD prions. In North America, humans have historically consumed meat from CWD-infected animals, which has been documented to harbor prions (35,44–47). Despite the potential exposure to prions, no epidemiologic evidence indicates a correlation between the occurrence of CWD cases in animals and the prevalence of human prion diseases (48). A recent bioassay study reported no transmissions from 3 Nordic isolates into transgenic mice expressing human PrP (49). Therefore, our findings should be interpreted with caution in terms of human health implications, and further research is required to determine the zoonotic potential of these CWD strains.
The presence of prions in peripheral tissues indicates that CWD may have a systemic nature in all Norwegian cervid species, challenging the view that prions are exclusively localized in the CNS in sporadic CWD of moose and red deer. Our findings expand the notion of just how widely distributed prions can be in cervids affected with CWD and call into question the capability of emerging CWD strains in terms of infectivity to other species, including humans.
Appendix
https://wwwnc.cdc.gov/eid/article/31/2/24-0903-app1.pdf
https://wwwnc.cdc.gov/eid/article/31/2/24-0903_article
Volume 31, Number 2—February 2025
Dispatch
Detection of Chronic Wasting Disease Prions in Raw, Processed, and Cooked Elk Meat, Texas, USA
Rebeca Benavente, Fraser Brydon, Francisca Bravo-Risi, Paulina Soto, J. Hunter Reed, Mitch Lockwood, Glenn Telling, Marcelo A. Barria, and Rodrigo MoralesComments to Author
Snip…
CWD prions have been detected in the muscle of both farmed and wild deer (10), and at concentrations relevant to sustain disease transmission (11). CWD prions have also been identified across several cervid species and in multiple tissues, including lymph nodes, spleen, tongue, intestines, adrenal gland, eyes, reproductive tissues, ears, lungs, and liver, among others (12–14). Those findings raise concerns about the safety of ingesting processed meats that contain tissues other than skeletal muscle (15) (Appendix). https://wwwnc.cdc.gov/eid/article/31/2/24-0906-app1.pdf .
In addition, those findings highlight the need for continued vigilance and research on the transmission risks of prion diseases and for development of new preventative and detection measures to ensure the safety of the human food supply.
Snip…
Overall, our study results confirm previous reports describing the presence of CWD prions in elk muscles (13). The data also demonstrated CWD prion persistence in food products even after processing through different procedures, including the addition of salts, spices, and other edible elements. 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
Volume 31, Number 1—January 2025
Dispatch
Detection of Prions in Wild Pigs (Sus scrofa) from Areas with Reported Chronic Wasting Disease Cases, United States
Abstract
Using a prion amplification assay, we identified prions in tissues from wild pigs (Sus scrofa) living in areas of the United States with variable chronic wasting disease (CWD) epidemiology. Our findings indicate that scavenging swine could play a role in disseminating CWD and could therefore influence its epidemiology, geographic distribution, and interspecies spread.
Snip…
Conclusions In summary, results from this study showed that wild pigs are exposed to cervid prions, although the pigs seem to display some resistance to infection via natural exposure. Future studies should address the susceptibility of this invasive animal species to the multiple prion strains circulating in the environment. Nonetheless, identification of CWD prions in wild pig tissues indicated the potential for pigs to move prions across the landscape, which may, in turn, influence the epidemiology and geographic spread of CWD.
https://wwwnc.cdc.gov/eid/article/%2031/1/24-0401_article
Although the current U.S. feed ban is based on keeping tissues from TSE infected cattle from contaminating animal feed, swine rations in the U.S. could contain animal derived components including materials from scrapie infected sheep and goats. These results indicating the susceptibility of pigs to sheep scrapie, coupled with the limitations of the current feed ban, indicates that a revision of the feed ban may be necessary to protect swine production and potentially human health.
2. Determined that pigs naturally exposed to chronic wasting disease (CWD) may act as a reservoir of CWD infectivity. Chronic wasting disease is a naturally occurring, fatal, neurodegenerative disease of cervids. The potential for swine to serve as a host for the agent of CWD disease is unknown. The purpose of this study was to investigate the susceptibility of swine to the CWD agent following experimental oral or intracranial inoculation. Pigs were assigned to 1 of 3 groups: intracranially inoculated; orally inoculated; or non-inoculated. At market weight age, half of the pigs in each group were tested ('market weight' groups). The remaining pigs ('aged' groups) were allowed to incubate for up to 73 months post inoculation (MPI). Tissues collected at necropsy were examined for disease-associated prion protein (PrPSc) by multiple diagnostic methods. Brain samples from selected pigs were bioassayed in mice expressing porcine prion protein. Some pigs from each inoculated group were positive by one or more tests. Bioassay was positive in 4 out of 5 pigs assayed. Although only small amounts of PrPSc were detected using sensitive methods, this study demonstrates that pigs can serve as hosts for CWD. Detection of infectivity in orally inoculated pigs using mouse bioassay raises the possibility that naturally exposed pigs could act as a reservoir of CWD infectivity. Currently, swine rations in the U.S. could contain animal derived components including materials from deer or elk. In addition, feral swine could be exposed to infected carcasses in areas where CWD is present in wildlife populations. The current feed ban in the U.S. is based exclusively on keeping tissues from TSE infected cattle from entering animal feeds. These results indicating the susceptibility of pigs to CWD, coupled with the limitations of the current feed ban, indicates that a revision of the feed ban may be necessary to protect swine production and potentially human health.
The agent of chronic wasting disease from pigs is infectious in transgenic mice expressing human PRNP
https://www.ars.usda.gov/research/publications/publication/?seqNo115=353091
Currently, swine rations in the U.S. could contain animal derived components including materials from deer or elk. In addition, feral swine could be exposed to infected carcasses in areas where CWD is present in wildlife populations. The current feed ban in the U.S. is based exclusively on keeping tissues from TSE infected cattle from entering animal feeds. These results indicating the susceptibility of pigs to CWD, coupled with the limitations of the current feed ban, indicates that a revision of the feed ban may be necessary to protect swine production and potentially human health.
https://www.ars.usda.gov/research/project/?accnNo=432011&fy=2017
Conclusions: This study demonstrates that PrPSc accumulates in lymphoid tissues from pigs challenged intracranially or orally with the CWD agent, and can be detected as early as 4 months after challenge. CWD-infected pigs rarely develop clinical disease and if they do, they do so after a long incubation period. This raises the possibility that CWD-infected pigs could shed prions into their environment long before they develop clinical disease. Furthermore, lymphoid tissues from CWD-infected pigs could present a potential source of CWD infectivity in the animal and human food chains.
https://www.ars.usda.gov/research/publications/publication/?seqNo115=337105
This study demonstrates that pigs can serve as potential hosts for CWD, although with low attack rates and scant PrPcwd accumulation. Detection of infectivity in orally challenged pigs using mouse bioassay raises the possibility that naturally exposed pigs act as a reservoir of CWD infectivity, even though affected pigs do not develop overt clinical signs or readily detectable PrPcwd.
https://www.ars.usda.gov/research/publications/publication/?seqNo115=326166
***> Price of TSE Prion Poker goes up substantially, all you cattle ranchers and such, better pay close attention here...terry <***
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.
Funded by: This research was funded in its entirety by congressionally appropriated funds to the United States Department of Agriculture, Agricultural Research Service. The funders of the work did not influence study design, data collection and analysis, decision to publish, or preparation of the manuscript.
*****>>> "Cattle with the E211K polymorphism are susceptible to the CWD agent after oronasal exposure of 0.2 g of infectious material." <<<*****
=====end
Strain characterization of chronic wasting disease in bovine-PrP transgenic mice
Nuria Jerez-Garrido1, Sara Canoyra1, Natalia Fernández-Borges1, Alba Marín Moreno1, Sylvie L. Benestad2, Olivier Andreoletti3, Gordon Mitchell4, Aru Balachandran4, Juan María Torres1 and Juan Carlos Espinosa1. 1 Centro de Investigación en Sanidad Animal, CISA-INIA-CSIC, Madrid, Spain. 2 Norwegian Veterinary Institute, Ås, Norway. 3 UMR Institut National de la Recherche Agronomique (INRA)/École Nationale Vétérinaire de Toulouse (ENVT), Interactions Hôtes Agents Pathogènes, Toulouse, France. 4 Canadian Food Inspection Agency, Ottawa, Canada.
Aims: Chronic wasting disease (CWD) is an infectious prion disease that affects cervids. Various CWD prion strains have been identified in different cervid species from North America and Europe. The properties of the infectious prion strains are influenced by amino acid changes and polymorphisms in the PrP sequences of different cervid species. This study, aimed to assess the ability of a panel of CWD prion isolates from diverse cervid species from North America and Europe to infect bovine species, as well as to investigate the properties of the prion strains following the adaptation to the bovine-PrP context.
Materials and Methods: BoPrP-Tg110 mice overexpressing the bovine-PrP sequence were inoculated by intracranial route with a panel of CWD prion isolates from both North America (two white-tailed deer and two elk) and Europe (one reindeer, one moose and one red deer).
Results: Our results show distinct behaviours in the transmission of the CWD isolates to the BoPrP-Tg110 mouse model. Some of these isolates did not transmit even after the second passage. Those able to transmit displayed differences in terms of attack rate, survival times, biochemical properties of brain PrPres, and histopathology.
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.
Funded by: MCIN/AEI /10.13039/501100011033 and by European Union NextGeneration EU/PRTR
Grant number: PCI2020-120680-2 ICRAD
"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."
=====end
https://prion2023.org/wp-content/uploads/2023/10/Meeting-book-final-version2.pdf
so, this is what we leave our children and grandchildren?
Redefining the zoonotic potential of chronic wasting disease
Project Number 5R01NS121016-04
Contact PI/Project Leader SCHATZL, HERMANN M
Other PIs
Awardee Organization
UNIVERSITY OF CALGARY
Description
Abstract Text
The rapid expansion of chronic wasting disease (CWD), a prion disease of free-ranging and farmed deer, elk and moose, is a major and ongoing threat in North America. Approximately 1 in 36 Americans hunt deer and elk and eat venison, and it is estimated that 7,000 – 15,000 CWD-infected cervids are consumed annually. This fuels growing concerns about the human health risks imposed by CWD. There are no documented cases of CWD transmission to humans, even though with the long incubation periods of all prion diseases and the unknown presentation of CWD in humans definite conclusions are not possible. The zoonotic potential of prion diseases has been exemplified by bovine spongiform encephalopathy (BSE, mad cow disease) which resulted in a new form of human prion disease (vCJD). BSE was transmissible to Cynomolgus macaques and transgenic mice expressing the human prion protein. Initial results of CWD transmission studies to the same non-human primate and mouse models of human prion disease were not successful, corroborating the conclusion that the zoonotic potential of CWD is low, if not absent. Our groups were part of a consortium that inoculated Cynomolgus macaques via different routes with CWD. Some animals exhibited subtle clinical signs reminiscent of prion disease, and upon euthanasia, weak signs of vacuolation, PrPSc deposition and astrocytosis in the brain were found, while no proteinase K (PK) resistant prion protein (PrP) was detectable. We have now demonstrated for the first time that CWD from macaques can transmit clinical prion disease to transgenic mouse models of CWD and human prion disease, albeit in the absence of detectable PK-resistant PrP. Bona fide PrPSc was only detected upon 3rd passage from mouse to bank vole models. Altogether, this is the first evidence that CWD very likely has zoonotic potential. The goal of the current proposal is to redefine the zoonotic potential of CWD by characterizing the biological properties of CWD prions emerging upon experimental transmission into macaques, for obtaining important information on how CWD could manifest in humans.
In Aim 1, we will study whether CWD from macaque (CWDmac) in bank voles represents a new prion strain, by comparing biochemical and biological properties to an array of known prion strains from different species.
Aim 2 addresses the question whether CWDmac represents an intermediate prion strain, adaptable to cervids or humans upon passage, and possessing an expanded host range. We will address this by in vivo passage in cervidized or humanized mouse models. In vitro, we will utilize serial PMCA and a newly generated PrP0/0 cell culture model for infection, upon reconstitution with PrP from different species.
In Aim 3, we will shed light on the observed dissociation between infectivity and the presence of bona fide PrPSc. We propose to identify atypical PrP fragments associated with CWDmac, and we will elucidate brain cell responses to CWDmac exposure by innovative single cell RNA sequencing. In summary, our studies will uncover the possible manifestation of CWD in humans, which is of critical importance for drawing definite conclusions about the zoonotic potential of CWD.
Public Health Relevance Statement
The zoonotic potential of chronic wasting disease (CWD) is unclear to date. We provide the first evidence by transmission experiments to different transgenic mouse models and bank voles that Cynomolgus macaques inoculated via different routes with CWD-positive cervid tissues harbor infectious prions that elicit clinical disease in rodents. Our proposed studies will unravel the properties of these prions, how they will adapt to humans and which pathways are activated in brain cells and associated with clinical disease. Results from these studies uncover the potential manifestation of CWD in humans, which is highly relevant for human health.
https://eventos.galoa.com.br/prion-2025/page/5178-home
Project 3A: CWD Prion Shedding and Environmental Contamination: Role in Transmission and Zoonotic
Parent Project Number 5P01AI077774-14
Sub-Project ID 5512
Contact PI/Project Leader HOOVER, EDWARD ARTHUR
Awardee Organization UNIVERSITY OF TEXAS HLTH SCI CTR HOUSTON
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/project-details/11056111#description
Project 3B: Pathogenesis Transmission and Detection of Zoonotic Prion Diseases
Parent Project Number 5P01AI077774-14
Sub-Project ID 5513
Contact PI/Project Leader BARTZ, JASON C
Awardee Organization UNIVERSITY OF TEXAS HLTH SCI CTR HOUSTON
Description Abstract Text
Project Summary: 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/project-details/11056115#description
Project 1: Modeling the Mechanisms of Prion Transmission, Strain Selection, Mutation and Species Barrier in Transgenic Mice
Parent Project Number 5P01AI077774-14
Sub-Project ID 5510
Contact PI/Project Leader TELLING, GLENN C
Awardee Organization UNIVERSITY OF TEXAS HLTH SCI CTR HOUSTON
Description Abstract Text
Our broad, long-term objectives are to are to decipher the mechanisms by which infectious prions replicate, encode strain information, and evolve to acquire new properties. We propose four Specific Aims to address our central hypothesis that incompletely adapted prion strains are comprised of poorly optimized ensembles of PrPSc quasi species conformers that evolve under selective pressure towards states of enhanced stability and pathogenicity. Our particular focus is chronic wasting disease (CWD), an uncontrollable contagious epidemic of cervids of uncertain zoonotic potential. Using genetically engineered CWD-susceptible mice, cultured cells, cell free amplification, and antibodies recognizing defined conformation-dependent PrP epitopes,
Aim I will address the mechanism of adaptation of unstable emergent CWD prions in response to physical and chemical constraints.
In Aim II we will address the hypothesis that that residue 226 and other cervid PrP polymorphisms influence selection of distinct portfolios of CWD strain conformers with different adaptive potentials. Using gene targeted mice expressing physiologically controlled levels of PrP variants and in vitro systems for prion replication, we will characterize the properties of strains propagated in these backgrounds and explore whether interference between them affects selection and adaptation of CWD.
In Aim III, we will assess the properties of emergent Norwegian moose and reindeer CWD strains experimentally propagated in deer and compare with established North American CWD.
Aim IV will address an unmet need in the field of significant importance, namely the paucity of model systems and tools for studying human prions. Using newly generated gene targeted mice expressing physiological levels of human PrP and novel approaches to derive susceptible human neuroblastoma cells, we will assess the zoonotic potential of emergent CWD strains and their adapted derivatives propagated in different cervid PrP backgrounds. Our ultimate goal is to assess and manage the risk posed to humans from continually evolving prions, specifically those causing CWD, by understanding the means by which they propagate and exist as heritable strains with protean host range properties that adapt and evolve under selective pressure.
https://reporter.nih.gov/project-details/11056096#description
Project 2
Parent Project Number 5P01AI077774-14
Sub-Project ID 5511
Contact PI/Project Leader SOTO, CLAUDIO
Awardee Organization UNIVERSITY OF TEXAS HLTH SCI CTR HOUSTON
Description Abstract Text
ABSTRACT Chronic wasting disease (CWD) affecting various species of cervids in North American and Northern Europe represents a serious problem, because it continues to propagate uncontrollably among wild and captive cervids. CWD appears to be very heterogeneous with multiple different strains and can be transmitted to other animal species. The risk of CWD transmission to humans is unknown which is a major concern because the number of sick animals and their geographical distribution is rapidly increasing. The mechanism by which CWD propagates so efficiently among cervids is also unknown. The main goal of this project is to utilize a set of highly innovative techniques to study the cellular, molecular and structural features of naturally occurring CWD strains and their potential for inter- species transmission, particularly focusing on the possibility that certain CWD strains may infect humans. We will also attempt to elucidate the atomic resolution structure of CWD prions using cryo-electron microscopy. The overarching hypothesis is that CWD exists as multiple strains in distinct individuals and even within the same individual in different brain cells and that inter- species transmission and zoonotic potential depend on the specific strain characteristics. The project is divided in the following specific aims:
(1) Study the structural and molecular diversity of natural CWD strains and the high resolution three-dimensional structure of CWD prions.
(2) Understand CWD prion strain diversity in single brain cells isolated by laser capture microdissection and subsequently amplified by PMCA.
(3) Evaluate CWD inter-species transmission spillover potential and its effect on zoonotic potential.
(4) Analyze the deer-human prion species barrier in vivo using chimeric mice harboring human and cervid neuronal cells.
The studies included in this projects will address some of the most pressing questions regarding CWD, including
(i) the CWD prion strain variability,
(ii) the zoonotic potential of different CWD prion strains,
(iii) the atomic resolution structure of infectious prions and the structural basis of prion strains,
(iv) the cellular distribution of CWD prion strains in the brain and its gene expression consequences,
(v) the spillover potential of CWD to other animal species,
(vi) the potential role of intermediate species in the transmission of CWD prions to humans.
The findings generated in this project will be essential to design measures to prevent further propagation of CWD, and to avoid the emergence of new diseases with potentially disastrous consequences.
https://reporter.nih.gov/search/fXQ8kEmVa0mNDk1JNnx3Cw/project-details/11056103#description
18. Zoonotic potential of moose-derived chronic wasting disease prions after adaptation in intermediate species
Tomás Barrioa, Jean-Yves Doueta, Alvina Huora, Séverine Lugana, Naïma Arona, Hervé Cassarda, Sylvie L. Benestadb, Juan Carlos Espinosac, Juan María Torresc, Olivier Andréolettia
aUnité Mixte de Recherche de l’Institut National de Recherche pour l’Agriculture, l’Alimentation et l’Environnement 1225 Interactions Hôtes-Agents Pathogènes, École Nationale Vétérinaire de Toulouse, 31076 Toulouse, France; bNorwegian Veterinary Institute, P.O. Box 64, NO-1431 Ås, Norway; cCentro de Investigación en Sanidad Animal (CISA-INIA), 28130, Valdeolmos, Madrid, Spain
Aims: Chronic wasting disease (CWD) is an emerging prion disease in Europe. To date, cases have been reported in three Nordic countries and in several species, including reindeer (Rangifer tarandus), moose (Alces alces) and red deer (Cervus elaphus). Cumulating data suggest that the prion strains responsible for the European cases are distinct from those circulating in North America. The biological properties of CWD prions are still poorly documented, in particular their spillover and zoonotic capacities. In this study, we aimed at characterizing the interspecies transmission potential of Norwegian moose CWD isolates.
Materials and Methods: For that purpose, we performed experimental transmissions in a panel of transgenic models expressing the PrPC sequence of various species.
Results: On first passage, one moose isolate propagated in the ovine PrPC-expressing model (Tg338). After adaptation in this host, moose CWD prions were able to transmit in mice expressing either bovine or human PrPC with high efficacy.
Conclusions: These results suggest that CWD prions can acquire enhanced zoonotic properties following adaptation in an intermediate species.
Funding
Grant number: AAPG2020 EU-CWD, ICRAD2020 TCWDE, NRC2022 NorCWD
Acknowledgement
https://www.tandfonline.com/doi/full/10.1080/19336896.2024.2424058
“ After adaptation in this host, moose CWD prions were able to transmit in mice expressing either bovine or human PrPC with high efficacy.”
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
Consumption of venison and veal was much less widespread among both cases and controls. For both of these meats there was evidence of a trend with increasing frequency of consumption being associated with increasing risk of CJD. (not nvCJD, but sporadic CJD...tss) These associations were largely unchanged when attention was restricted to pairs with data obtained from relatives. ...
Table 9 presents the results of an analysis of these data.
There is STRONG evidence of an association between ‘’regular’’ veal eating and risk of CJD (p = .0.01).
Individuals reported to eat veal on average at least once a year appear to be at 13 TIMES THE RISK of individuals who have never eaten veal.
There is, however, a very wide confidence interval around this estimate. There is no strong evidence that eating veal less than once per year is associated with increased risk of CJD (p = 0.51).
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).
There is some evidence that risk of CJD INCREASES WITH INCREASING FREQUENCY OF LAMB EATING (p = 0.02).
The evidence for such an association between beef eating and CJD is weaker (p = 0.14). When only controls for whom a relative was interviewed are included, this evidence becomes a little STRONGER (p = 0.08).
snip...
It was found that when veal was included in the model with another exposure, the association between veal and CJD remained statistically significant (p = < 0.05 for all exposures), while the other exposures ceased to be statistically significant (p = > 0.05).
snip...
In conclusion, an analysis of dietary histories revealed statistical associations between various meats/animal products and INCREASED RISK OF CJD. When some account was taken of possible confounding, the association between VEAL EATING AND RISK OF CJD EMERGED AS THE STRONGEST OF THESE ASSOCIATIONS STATISTICALLY. ...
snip...
In the study in the USA, a range of foodstuffs were associated with an increased risk of CJD, including liver consumption which was associated with an apparent SIX-FOLD INCREASE IN THE RISK OF CJD. By comparing the data from 3 studies in relation to this particular dietary factor, the risk of liver consumption became non-significant with an odds ratio of 1.2 (PERSONAL COMMUNICATION, PROFESSOR A. HOFMAN. ERASMUS UNIVERSITY, ROTTERDAM). (???...TSS)
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 ############
BSE INQUIRY
CJD9/10022
October 1994
Mr R.N. Elmhirst Chairman British Deer Farmers Association Holly Lodge Spencers Lane
BerksWell Coventry CV7 7BZ
Dear Mr Elmhirst,
CREUTZFELDT-JAKOB DISEASE (CJD) SURVEILLANCE UNIT REPORT
Thank you for your recent letter concerning the publication of the third annual report from the CJD Surveillance Unit. I am sorry that you are dissatisfied with the way in which this report was published.
The Surveillance Unit is a completely independant outside body and the Department of Health is committed to publishing their reports as soon as they become available. In the circumstances it is not the practice to circulate the report for comment since the findings of the report would not be amended.. In future we can ensure that the British Deer Farmers Association receives a copy of the report in advance of publication.
The Chief Medical Officer has undertaken to keep the public fully informed of the results of any research in respect of CJD. This report was entirely the work of the unit and was produced completely independantly of the the Department.
The statistical results reqarding the consumption of venison was put into perspective in the body of the report and was not mentioned at all in the press release. Media attention regarding this report was low key but gave a realistic presentation of the statistical findings of the Unit. This approach to publication was successful in that consumption of venison was highlighted only once by the media ie. in the News at one television proqramme.
I believe that a further statement about the report, or indeed statistical links between CJD and consumption of venison, would increase, and quite possibly give damaging credence, to the whole issue. From the low key media reports of which I am aware it seems unlikely that venison consumption will suffer adversely, if at all.
http://web.archive.org/web/20030511010117/http://www.bseinquiry.gov.uk/files/yb/1994/10/00003001.pdf
TSE in wild UK deer? The first case of BSE (as we now realise) was in a nyala in London zoo and the further zoo cases in ungulates were simply thought of as being interesting transmissions of scrapie initially. The big problem started to appear with animals in 1993-5 when it became clear that there was an increase in the CJD cases in people that had eaten deer although the statistics involved must have been questionable. The reason for this was that the CJD Surveillance was well funded to look into the diet of people dying of CJD. This effect is not clear with vCJD...if only because the numbers involved are much smaller and hence it is difficult to gain enough statistics. They found that many other foods did not appear to have much association at all but that deer certainly did and as years went by the association actually became clearer. The appearance of vCJD in 1996 made all this much more difficult in that it was suddenly clearer that the cases of sporadic CJD that they had been checking up until then probably had nothing to do with beef...and the study decreased. During the period there was an increasing worry that deer were involved with CJD..
see references:
DEER BRAIN SURVEY
https://web.archive.org/web/20090506025229/http://www.bseinquiry.gov.uk/files/yb/1991/11/20004001.pdf
CONFIDENTIAL AND IN CONFIDENCE TRANSMISSION TO CHIMPANZEES AND PIGS
IN CONFIDENCE
TRANSMISSION TO CHIMPANZEES
Kuru and CJD have been successfully transmitted to chimpanzees but scrapie and TME have not.
We cannot say that scrapie will not transmit to chimpanzees. There are several scrapie strains and I am not aware that all have been tried (that would have to be from mouse passaged material). Nor has a wide enough range of field isolates subsequently strain typed in mice been inoculated by the appropriate routes (i/c, i/p and i/v).
I believe the proposed experiment to determine transmissibility, if conducted, would only show the susceptibility or resistance of the chimpanzee to infection/disease by the routes used and the result could not be interpreted for the predictability of the susceptibility for man. proposals for prolonged oral exposure of chimpanzees to milk from cattle were suggested a long while ago and rejected.
In view of Dr Gibbs' probable use of chimpazees Mr Wells' comments (enclosed) are pertinent. I have yet to receive a direct communication from Dr Schellekers but before any collaboration or provision of material we should identify the Gibbs' proposals and objectives.
A positive result from a chimpanzee challenged severely would likely create alarm in some circles even if the result could not be interpreted for man. I have a view that all these agents could be transmitted provided a large enough dose by appropriate routes was given and the animals kept long enough. Until the mechanisms of the species barrier are more clearly understood it might be best to retain that hypothesis.
A negative result would take a lifetime to determine but that would be a shorter period than might be available for human exposure and it would still not answer the question regarding mans ‘susceptibility. In the meantime no doubt the negativity would be used defensively. It would however be counterproductive if the experiment finally became positive. We may learn more about public reactions following next Monday's meeting.
R Bradley
CVO (+ Mr Wells’ commenters 23 September 1990 Dr T W A Little Dr B J Shreeve
90/9.23/1.1
https://web.archive.org/web/20090506041740/http://www.bseinquiry.gov.uk/files/yb/1990/09/23001001.pdf
*** now, let’s see what the authors said about this casual link, personal communications years ago, and then the latest on the zoonotic potential from CWD to humans from the TOKYO PRION 2016 CONFERENCE.
see where it is stated NO STRONG evidence. so, does this mean there IS casual evidence ????
“Our conclusion stating that we found no strong evidence of CWD transmission to humans”
From: TSS Subject: CWD aka MAD DEER/ELK TO HUMANS ???
Date: September 30, 2002 at 7:06 am PST
From: "Belay, Ermias"
To: Cc: "Race, Richard (NIH)" ; ; "Belay, Ermias"
Sent: Monday, September 30, 2002 9:22 AM
Subject: RE: TO CDC AND NIH - PUB MED- 3 MORE DEATHS - CWD - YOUNG HUNTERS
Dear Sir/Madam, In the Archives of Neurology you quoted (the abstract of which was attached to your email), we did not say CWD in humans will present like variant CJD.. That assumption would be wrong. I encourage you to read the whole article and call me if you have questions or need more clarification (phone: 404-639-3091).
Also, we do not claim that "no-one has ever been infected with prion disease from eating venison." Our conclusion stating that we found no strong evidence of CWD transmission to humans in the article you quoted or in any other forum is limited to the patients we investigated.
Ermias Belay, M.D. Centers for Disease Control and Prevention
Subject: TO CDC AND NIH - PUB MED- 3 MORE DEATHS - CWD - YOUNG HUNTERS
Sunday, November 10, 2002 6:26 PM .......snip........end..............TSS
Thursday, April 03, 2008
A prion disease of cervids: Chronic wasting disease 2008 1: Vet Res. 2008 Apr 3;39(4):41 A prion disease of cervids: Chronic wasting disease Sigurdson CJ.
snip... *** twenty-seven CJD patients who regularly consumed venison were reported to the Surveillance Center***,
snip... full text ;
http://chronic-wasting-disease.blogspot.com/2008/04/prion-disease-of-cervids-chronic.html
However, to date, no CWD infections have been reported in people.
sporadic, spontaneous CJD, 85%+ of all human TSE, did not just happen. never in scientific literature has this been proven. if one looks up the word sporadic or spontaneous at pubmed, you will get a laundry list of disease that are classified in such a way;
sporadic = 54,983 hits
https://www.ncbi.nlm.nih.gov/pubmed/?term=sporadic
spontaneous = 325,650 hits
https://www.ncbi.nlm.nih.gov/pubmed/?term=spontaneous
key word here is 'reported'. science has shown that CWD in humans will look like sporadic CJD.
SO, how can one assume that CWD has not already transmitted to humans? they can't, and it's as simple as that. from all recorded science to date, CWD has already transmitted to humans, and it's being misdiagnosed as sporadic CJD. ...terry
*** LOOKING FOR CWD IN HUMANS AS nvCJD or as an ATYPICAL CJD, LOOKING IN ALL THE WRONG PLACES $$$ ***
However, to date, no CWD infections have been reported in people. key word here is ‘reported’. science has shown that CWD in humans will look like sporadic CJD. SO, how can one assume that CWD has not already transmitted to humans? they can’t, and it’s as simple as that. from all recorded science to date, CWD has already transmitted to humans, and it’s being misdiagnosed as sporadic CJD. …terry
*** LOOKING FOR CWD IN HUMANS AS nvCJD or as an ATYPICAL CJD, LOOKING IN ALL THE WRONG PLACES $$$ ***
*** These results would seem to suggest that CWD does indeed have zoonotic potential, at least as judged by the compatibility of CWD prions and their human PrPC target. Furthermore, extrapolation from this simple in vitro assay suggests that if zoonotic CWD occurred, it would most likely effect those of the PRNP codon 129-MM genotype and that the PrPres type would be similar to that found in the most common subtype of sCJD (MM1).***
http://www.tandfonline.com/doi/full/10.4161/pri.28124?src=recsys
http://www.tandfonline.com/doi/pdf/10.4161/pri.28124?needAccess=true
https://wwwnc.cdc.gov/eid/article/20/1/13-0858_article
So, this is what we leave our children and grandchildren?
CDC CWD TSE Prion Update 2025
KEY POINTS
Chronic wasting disease affects deer, elk and similar animals in the United States and a few other countries.
The disease hasn't been shown to infect people.
However, it might be a risk to people if they have contact with or eat meat from animals infected with CWD.
https://www.cdc.gov/chronic-wasting/about/index.html
Volume 31, Number 4—April 2025
Research
Detection and Decontamination of Chronic Wasting Disease Prions during Venison Processing
https://wwwnc.cdc.gov/eid/article/31/4/24-1176_article
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
Transmission of prion infectivity from CWD-infected 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
***> 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
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 Tg12mice became infected and their brain tissues were further examined by Western blot as well as serial passages in humanized or cervidized mice.
Results: Passage of sCJDMM1 in transgenic mice expressing elk PrP (Tg12) resulted in a “cervidized” CJD strain that we termed CJDElkPrP. We observed 100% transmission of the original CJDElkPrP in transgenic mice expressing human PrP. We passaged CJDElkPrP two more times in the Tg12mice. We found that such second and third passage CJDElkPrP prions retained 100% transmission rate in the humanized mice, despite that the natural elk CWD isolates and CJDElkPrP share the same elk PrP sequence. In contrast, we and others found zero or poor transmission of natural elk CWD isolates in humanized mice.
Conclusions: Our data indicate that highly zoonotic cervid prion strains are not only possible but also can retain zoonotic potential after serial passages in cervids, suggesting a very significant and serious long-term risk of CWD zoonosis given that the broad and continuing spread of CWD prions will provide fertile grounds for the emergence of zoonotic CWD strains over time.
https://prion2023.org/wp-content/uploads/2023/10/Meeting-book-final-version2.pdf
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
Transmission of cervid prions to humanized mice demonstrates the zoonotic potential of CWD
Samia Hannaoui1 · Irina Zemlyankina1 · Sheng Chun Chang1 · Maria Immaculata Arifn1 · Vincent Béringue2 · Debbie McKenzie3 · Hermann M. Schatzl1 · Sabine Gilch1
Received: 24 May 2022 / Revised: 5 August 2022 / Accepted: 7 August 2022
© The Author(s) 2022
Abstract
Prions cause infectious and fatal neurodegenerative diseases in mammals. Chronic wasting disease (CWD), a prion disease of cervids, spreads efficiently among wild and farmed animals. Potential transmission to humans of CWD is a growing concern due to its increasing prevalence. Here, we provide evidence for a zoonotic potential of CWD prions, and its probable signature using mice expressing human prion protein (PrP) as an infection model. Inoculation of these mice with deer CWD isolates resulted in atypical clinical manifestation with prion seeding activity and efficient transmissible infectivity in the brain and, remarkably, in feces, but without classical neuropathological or Western blot appearances of prion diseases. Intriguingly, the protease-resistant PrP in the brain resembled that found in a familial human prion disease and was transmissible upon second passage. Our results suggest that CWD might infect humans, although the transmission barrier is likely higher compared to zoonotic transmission of cattle prions. Notably, our data suggest a different clinical presentation, prion signature, and tissue tropism, which causes challenges for detection by current diagnostic assays. Furthermore, the presence of infectious prions in feces is concerning because if this occurs in humans, it is a source for human-to-human transmission. These findings have strong implications for public health and CWD management.
Keywords Chronic wasting disease · CWD · Zoonotic potential · Prion strains · Zoonotic prions
HIGHLIGHTS OF THIS STUDY
================================
Our results suggest that CWD might infect humans, although the transmission barrier is likely higher compared to zoonotic transmission of cattle prions. Notably, our data suggest a different clinical presentation, prion signature, and tissue tropism, which causes challenges for detection by current diagnostic assays. Furthermore, the presence of infectious prions in feces is concerning because if this occurs in humans, it is a source for human-to-human transmission. These findings have strong implications for public health and CWD management.
In this study, we evaluated the zoonotic potential of CWD using a transgenic mouse model overexpressing human M129-PrPC (tg650 [12]). We inoculated tg650 mice intracerebrally with two deer CWD isolates, Wisc-1 and 116AG [22, 23, 27, 29]. We demonstrate that this transgenic line was susceptible to infection with CWD prions and displayed a distinct leading clinical sign, an atypical PrPSc signature and unusual fecal shedding of infectious prions. Importantly, these prions generated by the human PrP transgenic mice were transmissible upon passage. Our results are the first evidence of a zoonotic risk of CWD when using one of the most common CWD strains, Wisc-1/CWD1 for infection. We demonstrated in a human transgenic mouse model that the species barrier for transmission of CWD to humans is not absolute. The fact that its signature was not typical raises the questions whether CWD would manifest in humans as a subclinical infection, whether it would arise through direct or indirect transmission including an intermediate host, or a silent to uncovered human-to-human transmission, and whether current detection techniques will be suffcient to unveil its presence.
Our findings strongly suggest that CWD should be regarded as an actual public health risk. Here, we use humanized mice to show that CWD prions can cross the species barrier to humans, and remarkably, infectious prions can be excreted in feces.
Our results indicate that if CWD crosses the species-barrier to humans, it is unlikely to resemble the most common forms of human prion diseases with respect to clinical signs, tissue tropism and PrPSc signature. For instance, PrPSc in variable protease-sensitive prionopathy (VPSPr), a sporadic form of human prion disease, and in the genetic form Gerstmann-Sträussler-Scheinker syndrome (GSS) is defined by an atypical PK-resistant PrPSc fragment that is non-glycosylated and truncated at both C- and N-termini, with a molecular weight between 6 and 8 kDa [24, 44–46]. These biochemical features are unique and distinctive from PrPSc (PrP27-30) found in most other human or animal prion disease. The atypical PrPSc signature detected in brain homogenate of tg650 mice #321 (1st passage) and #3063 (2nd passage), and the 7–8 kDa fragment (Figs. 2, 4) are very similar to that of GSS, both in terms of migration profile and the N-terminal cleavage site.
CWD in humans might remain subclinical but with PrPSc deposits in the brain with an unusual morphology that does not resemble the patterns usually seen in different prion diseases (e.g., mouse #328; Fig. 3), clinical with untraceable abnormal PrP (e.g., mouse #327) but still transmissible and uncovered upon subsequent passage (e.g., mouse #3063; Fig. 4), or prions have other reservoirs than the usual ones, hence the presence of infectivity in feces (e.g., mouse #327) suggesting a potential for human-to-human transmission and a real iatrogenic risk that might be unrecognizable.
“suggesting a potential for human-to-human transmission and a real iatrogenic risk that might be unrecognizable.”
=================================
Supplementary Information The online version contains supplementary material available at
https://doi.org/10.1007/s00401-022-02482-9
snip...see full text;
https://link.springer.com/article/10.1007/s00401-022-02482-9
https://link.springer.com/content/pdf/10.1007/s00401-022-02482-9.pdf
EFSA Panel on Biological Hazards (BIOHAZ) Antonia Ricci Ana Allende Declan Bolton Marianne Chemaly Robert Davies Pablo Salvador Fernández Escámez ...
First published: 17 January 2018 https://doi.org/10.2903/j.efsa.2018.5132
also, see;
8. Even though human TSE‐exposure risk through consumption of game from European cervids can be assumed to be minor, if at all existing, no final conclusion can be drawn due to the overall lack of scientific data.
***> In particular the US data do not clearly exclude the possibility of human (sporadic or familial) TSE development due to consumption of venison.
The Working Group thus recognizes a potential risk to consumers if a TSE would be present in European cervids. It might be prudent considering appropriate measures to reduce such a risk, e.g. excluding tissues such as CNS and lymphoid tissues from the human food chain, which would greatly reduce any potential risk for consumers.. However, it is stressed that currently, no data regarding a risk of TSE infections from cervid products are available.
https://efsa.onlinelibrary.wiley.com/doi/full/10.2903/j.efsa.2018.5132
2004
Jeff Swann and his Mom, cwd link... sporadic CJD?, CBC NEWS Jeff Schwan sCJD, CWD, and Professor Aguzzi on BSE and sporadic CJD
????: CBCnews
https://histodb15.usz.ch/pages/Images/videos/video-004/video-004.html
2004
April 22, 2004, 10:30 AM CDT Guests: Patrick Singh, Terry Schwan, Janet Skarbek, Bill Fielding (BEGIN VIDEOTAPE) ANNOUNCER: DEBORAH NORVILLE TONIGHT.
https://www.nbcnews.com/id/wbna4806886
1997-11-10: Panorama - The British disease
https://histodb15.usz.ch/pages/Images/videos/video-009/video-009.html
TUESDAY, MAY 11, 2021
A Unique Presentation of Creutzfeldt-Jakob Disease in a Patient Consuming Deer Antler Velvet <
Conclusion
We believe that our patient’s case of CJD is highly suspicious for cervid etiology given the circumstances of the case as well as the strong evidence of plausibility reported in published literature. This is the first known case of CJD in a patient who had consumed deer antler velvet. Despite the confirmed diagnosis of CJD, a causal relationship between the patient’s disease and his consumption of deer antler velvet cannot be definitively concluded.
Supplemental data including molecular tissue sample analysis and autopsy findings could yield further supporting evidence. Given this patient’s clinical resemblance to CBD and the known histological similarities of CBD with CJD, clinicians should consider both diseases in the differential diagnosis of patients with a similarly esoteric presentation. Regardless of the origin of this patient’s disease, it is clear that the potential for prion transmission from cervids to humans should be further investigated by the academic community with considerable urgency.
https://thescipub.com/pdf/ajidsp.2021.43.48.pdf
''We believe that our patient’s case of CJD is highly suspicious for cervid etiology given the circumstances of the case as well as the strong evidence of plausibility reported in published literature. This is the first known case of CJD in a patient who had consumed deer antler velvet. Despite the confirmed diagnosis of CJD, a causal relationship between the patient’s disease and his consumption of deer antler velvet cannot be definitively concluded.''
https://thescipub.com/pdf/ajidsp.2021.43.48.pdf
CREUTZFELDT JAKOB DISEASE: A Unique Presentation of Creutzfeldt-Jakob Disease in a Patient Consuming Deer Antler Velvet
i was warning England and the BSE Inquiry about just this, way back in 1998, and was ask to supply information to the BSE Inquiry. for anyone that might be interested, see;
Singeltary submission to the BSE Inquiry on CJD and Nutritional Supplements 1998
ABOUT that deer antler spray and CWD TSE PRION... I have been screaming this since my neighbors mom died from cjd, and she had been taking a supplement that contained bovine brain, bovine eyeball, and other SRMs specified risk materials, the most high risk for mad cow disease. just saying...
I made a submission to the BSE Inquiry long ago during the BSE Inquiry days, and they seemed pretty interested.
Sender: "Patricia Cantos"
To: "Terry S Singeltary Sr. (E-mail)"
Subject: Your submission to the Inquiry
Date: Fri, 3 Jul 1998 10:10:05 +0100 3 July 1998
Mr Terry S Singeltary Sr. E-Mail: Flounder at wt.netRef: E2979
Dear Mr Singeltary, Thank you for your E-mail message of the 30th of June 1998 providing the Inquiry with your further comments. Thank you for offering to provide the Inquiry with any test results on the nutritional supplements your mother was taking before she died. As requested I am sending you our general Information Pack and a copy of the Chairman's letter. Please contact me if your system cannot read the attachments. Regarding your question, the Inquiry is looking into many aspects of the scientific evidence on BSE and nvCJD.
I would refer you to the transcripts of evidence we have already heard which are found on our internet site at ;
http://www.bse.org.uk.
Could you please provide the Inquiry with a copy of the press article you refer to in your e-mail? If not an approximate date for the article so that we can locate it? In the meantime, thank you for you comments. Please do not hesitate to contact me on... snip...end...tss
everyone I tell this too gets it screwed up...MY MOTHER WAS NOT TAKING THOSE SUPPLEMENTS IPLEX (that I ever knew of). this was my neighbors mother that died exactly one year previously and to the day of sporadic CJD that was diagnosed as Alzheimer’s at first. my mother died exactly a year later from the Heidenhain Variant of Creutzfeldt Jakob Disease hvCJD, and exceedingly rare strains of the ever growing sporadic CJD’s. both cases confirmed. ...
kind regards, terry
TSEs i.e. mad cow disease's BSE/BASE and NUTRITIONAL SUPPLEMENTS IPLEX, mad by standard process; vacuum dried bovine BRAIN, bone meal, bovine EYE, veal Bone, bovine liver powder, bovine adrenal, vacuum dried bovine kidney, and vacuum dried porcine stomach. also; what about potential mad cow candy bars ? see their potential mad cow candy bar list too... THESE are just a few of MANY of just this ONE COMPANY...TSS
https://wwwnc.cdc.gov/eid/article/15/5/08-1458_article
http://www.spiegel.de/spiegel/print/d-18578755.html
http://chronic-wasting-disease.blogspot.com/2009/03/chronic-wasting-disease-prions-in-elk.html
http://creutzfeldt-jakob-disease.blogspot.com/2013/11/large-cjd-tse-prion-potential-case.html
http://tseac.blogspot.com/2011/02/usa-50-state-bse-mad-cow-conference.html
Two Hunters from the Same Lodge Afflicted with Sporadic CJD: Is Chronic Wasting Disease to Blame?
(P7-13.002) Jonathan Trout, Matthew Roberts, Michel Tabet, Eithan Kotkowski, and Sarah HornAUTHORS INFO & AFFILIATIONS April 9, 2024 issue 102 (17_supplement_1) https://doi.org/10.1212/WNL.0000000000204407
Abstract Publication History Information & Authors Metrics & Citations Share Abstract
Objective:
This study presents a cluster of Creutzfeldt-Jakob disease (CJD) cases after exposure to chronic wasting disease (CWD)-infected deer, suggestive of potential prion transmission from CWD-infected deer to humans.
Background:
CJD is a rapidly progressive central nervous system disorder caused by misfolded prion proteins. CWD, a prion disease prevalent in North American deer, has raised concerns due to its possible link to CJD. Although no conclusive evidence of cross-species prion transmission exists, vigilance for such cases is crucial for public health.
Design/Methods:
Not applicable.
Results:
In 2022, a 72-year-old man with a history of consuming meat from a CWD-infected deer population presented with rapid-onset confusion and aggression. His friend, who had also eaten venison from the same deer population, recently died of CJD, raising concerns about a potential link between CWD and human prion disease. Despite aggressive symptomatic treatment of seizures and agitation, the patient’s condition deteriorated and he died within a month of initial presentation. The diagnosis was confirmed postmortem as sporadic CJD with homozygous methionine at codon 129 (sCJDMM1). The patient’s history, including a similar case in his social group, suggests a possible novel animal-to-human transmission of CWD. Based on non-human primate and mouse models, cross-species transmission of CJD is plausible. Due to the challenge of distinguishing sCJDMM1 from CWD without detailed prion protein characterization, it is not possible to definitively rule out CWD in these cases. Although causation remains unproven, this cluster emphasizes the need for further investigation into the potential risks of consuming CWD-infected deer and its implications for public health.
Conclusions:
Clusters of sporadic CJD cases may occur in regions with CWD-confirmed deer populations, hinting at potential cross-species prion transmission. Surveillance and further research are essential to better understand this possible association.
Disclosure: Mr. Trout has nothing to disclose. Dr. Roberts has nothing to disclose. Dr. Tabet has nothing to disclose. Dr. Kotkowski has nothing to disclose. Dr. Horn has received personal compensation in the range of $500-$4,999 for serving as a Consultant for Cala Trio. The institution of Dr. Horn has received research support from Alzheimer's Association.
https://www.neurology.org/doi/abs/10.1212/WNL.0000000000204407
***> Creutzfeldt Jakob Disease CJD TSE Prion Cases Increasing March 2025
https://creutzfeldt-jakob-disease.blogspot.com/2025/03/creutzfeldt-jakob-disease-tse-prion.html
***> Creutzfeldt Jakob Disease CJD, BSE, CWD, TSE, Prion, December 14, 2024 Annual Update
https://creutzfeldt-jakob-disease.blogspot.com/2024/12/creutzfeldt-jacob-disease-cjd-bse-cwd.html
https://creutzfeldt-jakob-disease.blogspot.com/
Iatrogenic Transmissible Spongiform Encephalopathy TSE Prion, CWD, our worst nightmare, what if?
https://itseprion.blogspot.com/
So, this is what we leave our children and grandchildren?
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
Characterizing the hydrological spread of prion diseases through interdisciplinary science
September 11, 2025
Anu Li, Water Resources Science graduate student and WINS recipient Characterizing the hydrological spread of prion diseases through interdisciplinary science
Chronic wasting disease (CWD) is a 100% fatal disease found in cervids, which include deer, elk, and moose. CWD has been spreading more rapidly across Minnesota and much of North America in the past few years, causing people to come into contact with the disease more frequently through hunting, hide tanning, and consuming contaminated venison. This has raised concerns from epidemiologists that CWD, which has no cure, could evolve to infect humans sooner rather than later. Worries about CWD exposure and spread go beyond wildlife because the pathogens that cause CWD, called infectious prions, can contaminate the environment. Infectious prions are misfolded proteins with a highly stable structure, making them more difficult to degrade than viruses or bacteria. Their unique structure allows them to remain infectious for years in environmental materials, including soil and water. This means that areas with CWD outbreaks could remain an infection risk long after infected animals have been removed. Prions can also be carried by water, and if they reach a stream or river, they can travel over greater distances than deer, further spreading the disease across the landscape. In order to contain the disease and prevent it from infecting humans, we must understand how it moves through the environment.
Exploring this unique intersection of wildlife disease and environmental science requires an interdisciplinary approach. That’s why researchers from multiple fields came together several years ago to establish the Minnesota Center for Prion Research and Outreach (MNPRO), a group devoted to studying prion diseases in order to protect human, wildlife, environmental, and cultural health. Since 2022, I have collaborated with fellow MNPRO scientists to determine how, how far, and how quickly infectious prions are traveling through rivers, streams, and watersheds in Minnesota.
Researching hydrological prion movement is challenging because they are too dangerous to add to the environment for direct observation, and there is no good proxy to replicate their dynamics. There is little prior research about how these mysterious pathogens travel in the environment, so we developed creative methods to predict their movement without traditional experimental methods. One key finding laid the groundwork for our ongoing research: infectious prions preferentially attach to fine particles in surface waters. This means that prions are likely carried by sediments in rivers and streams, rather than free-floating in the water. Thus, in order to predict the how far and how quickly prions are moving through a watershed, we can focus on characterizing sediment movement.
This summer, I have been conducting sediment transport experiments in a flume at the St. Anthony Falls Laboratory. I packed the flume with sediment mixtures of different median particle sizes to represent diverse streambeds in Minnesota. Then, I adjusted the water flow rate, water depth, and slope of the flume until sediment particles on the bed began to move. The conditions which initiate sediment motion are called critical conditions; the stress exerted on the streambed must be greater than or equal to critical stress in order for sediments to move. I am comparing these critical flow measurements to streamflow data recorded in CWD-contaminated watersheds in order to determine how often sediments are mobile in contaminated streams, and thus how often prions are mobile. With these estimates, we can predict how far prions may have been transported from contaminated sites and how quickly they will reach downstream locations.
This method allows us to estimate prion transport without directly tracing them in streams. Hydrological transport predictions will aid in better assessing risk to the public downstream of detected CWD cases, guiding further CWD testing in previously unmonitored areas, and developing more comprehensive containment strategies to protect human and environmental health.
footer - 4 column Water Resources Center 173 McNeal Hall 1985 Buford Avenue St. Paul, MN 55108
612-624-9282 water@umn.edu
https://wrc.umn.edu/news/hydrological-spread-prion-diseases
Chronic wasting disease (CWD) prion detection in environmental and biological samples from a taxidermy site and nursing facility, and instruments used in surveillance activities
Author links open overlay panel Paulina Soto a b , Nancy Ho a , Mitch Lockwood c , Austin Stolte c , J. Hunter Reed c , Rodrigo Morales a b
Cite https://doi.org/10.1016/j.scitotenv.2025.179318Get rights and content 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.
https://www.sciencedirect.com/science/article/abs/pii/S0048969725009544
March 13, 2025
Prion Partitioning and Persistence in Environmental Waters
E. Anu Li,* Diana L. Karwan, Stuart Siegfried Lichtenberg, Gage R. Rowden, Marc D. Schwabenlander, Peter A. Larsen, and Tiffany M. Wolf Cite This: Environ. Sci. Technol. 2025, 59, 5715−5725 Read Online Downloaded via 76.143.208.142 on September 14, 2025 at 21:46:11 (UTC).
ABSTRACT: Chronic wasting disease (CWD) is a fatal neurodegenerative disease affecting cervids. CWD is caused by infectious prions, which can enter the environment through bodily fluids or the carcasses of infected animals. Prions can be stored, remain infectious in both soil and water for many years, and transported hydrologically, possibly expanding the geographic range of CWD transmission. In order to better predict hydrological prion transport, we investigated how CWD prion protein (PrPCWD) partitions and persists in environmental waters. We performed PrPCWD spike experiments with water samples containing fine sediments from two locations within a CWD-contaminated site, at which contamination sources were removed one year prior. Samples were filtered after spiking, and filtrates and sediments were tested separately for PrPCWD using real- time quaking-induced conversion (RT-QuIC). Unspiked filtrates tested negative for PrPCWD , while unspiked sediments were positive, indicating PrPCWD persistence in environmental sediments for at least one year. Spiked sediments were positive immediately after spiking and throughout 28 days of incubation. Spiked filtrates were largely negative immediately after spiking and remained negative for 28 days, with some inconsistent positives from one sampling location. Our results indicate that PrPCWD readily partitions to the sediment fraction of environmental waters, suggesting that hydrological prion transport is sediment-facilitated.
KEYWORDS: chronic wasting disease, sediment, aquatic sediment, hydrology, prion disease, environmental contamination, facilitated transport
https://pubs.acs.org/doi/epdf/10.1021/acs.est.4c11497?ref=article_openPDF
Detection of protease-resistant cervid prion protein in water from a CWD-endemic area
Prions in MN Waterways: Discovery Helps Water Managers Plan
September 03, 2024 This article is part of the Forest Scene newsletter, Issue 31.
Two white-tail deer with antlers lie nestled in grass. Chronic wasting disease (CWD) is a form of prion disease that affects white-tail deer and other cervids (deer family). “People in Minnesota value their water,” observes hydrologist Dr. Diana Karwan, Associate Professor with the Department of Forest Resources. So when the Minnesota Center for Prion Research and Outreach (MNPRO) received a state mandate to investigate chronic wasting disease (CWD), many questions from the public and legislators kept returning to the subject of our lakes, wells, marshes, and streams. In response, the team agreed to learn how prions move in waterways, recruiting Dr. Karwan to lead the effort. A 2024 report to the Minnesota Clean Water Council delivered on that promise.
What is a prion? And why should we care about chronic wasting disease?
A prion is "an abnormal form of a normally harmless protein found in the brain that is responsible for a variety of fatal neurodegenerative diseases of animals," per Encyclopedia Britannica.
Chronic wasting disease (CWD) is a form of prion disease that affects members of the deer family (cervids), and thus forested ecosystems. The disease is fatal and progressive, affecting the brain, spinal cord, and other tissues.
CWD can be transmitted both directly (via animal-to-animal contact) and indirectly (via objects or environmental contamination). Currently, there is no cure or treatment for it yet scientists are continuing to search for solutions. Land that has seen CWD can store that risk for a long time, but that doesn’t mean it isn’t going anywhere. Besides through animal movement, researchers hypothesized that prions could be transported by water, potentially increasing their threat across the landscape. Borne by water, prions might travel to places where CWD had previously been undetected or concentrate in an area where it makes infection more likely. At the end of a two-year study, MNPRO scientists gained clarity about how prions behave in water. One critical insight emerged: prions travel with a partner.
The report revealed how prions in water stick to soil particles they encounter. The outcome is that when snowmelt introduces sediment to Minnesota waterways, it may also carry CWD. The discovery does have some positive implications, however. Knowledge that prions tend to bind with particles can guide water resource managers as they assess ways to mitigate the risk. It helps them know how to sample waterways for protein-misfolding disease, for example, and establishes the first steps toward informing accurate models of where water may move CWD throughout the landscape.
This study is an example of timely science. While the report was in preparation for release, another county was added to the list for CWD detections in wild deer.
“Now we need to start integrating what we know about CWD behavior with what we know about water behavior. Models allow us to put these knowledge bases together,” says Dr. Karwan. “I feel like what we've done is come up with very important first-point findings. I'm excited to take the next steps with this research.”
Watch Prions in Our Waterways, a short video by the research team, to learn more.
~Story by Thomas Seiler, MNPRO. This article originally appeared in the March 2024 MNPRO newsletter and has been adapted for this publication.
https://forestry.umn.edu/news/prions-mn-waterways-forest-scene-31
Prions in Waterways
https://vimeo.com/898941380?fbclid=IwAR3Di7tLuU-iagCetdt4-CVPrOPQQrv037QS1Uxz0tX3z7BuvPeYlwIp7IY
Prion. 2009 Jul-Sep;3(3):171–183. doi: 10.4161/pri.3.3.9819
Detection of protease-resistant cervid prion protein in water from a CWD-endemic area
TA Nichols 1,2, Bruce Pulford 1, A Christy Wyckoff 1,2, Crystal Meyerett 1, Brady Michel 1, Kevin Gertig 3, Edward A Hoover 1, Jean E Jewell 4, Glenn C Telling 5, Mark D Zabel 1,
Abstract
Chronic wasting disease (CWD) is the only known transmissible spongiform encephalopathy affecting free-ranging wildlife. Although the exact mode of natural transmission remains unknown, substantial evidence suggests that prions can persist in the environment, implicating components thereof as potential prion reservoirs and transmission vehicles.1–4 CWD-positive animals may contribute to environmental prion load via decomposing carcasses and biological materials including saliva, blood, urine and feces.5–7 Sensitivity limitations of conventional assays hamper evaluation of environmental prion loads in soil and water. Here we show the ability of serial protein misfolding cyclic amplification (sPMCA) to amplify a 1.3 × 10−7 dilution of CWD-infected brain homogenate spiked into water samples, equivalent to approximately 5 × 107 protease resistant cervid prion protein (PrPCWD) monomers. We also detected PrPCWD in one of two environmental water samples from a CWD endemic area collected at a time of increased water runoff from melting winter snow pack, as well as in water samples obtained concurrently from the flocculation stage of water processing by the municipal water treatment facility. Bioassays indicated that the PrPCWD detected was below infectious levels. These data demonstrate detection of very low levels of PrPCWD in the environment by sPMCA and suggest persistence and accumulation of prions in the environment that may promote CWD transmission.
Snip…
The data presented here demonstrate that sPMCA can detect low levels of PrPCWD in the environment, corroborate previous biological and experimental data suggesting long term persistence of prions in the environment2,3 and imply that PrPCWD accumulation over time may contribute to transmission of CWD in areas where it has been endemic for decades. This work demonstrates the utility of sPMCA to evaluate other environmental water sources for PrPCWD, including smaller bodies of water such as vernal pools and wallows, where large numbers of cervids congregate and into which prions from infected animals may be shed and concentrated to infectious levels.
Key words: prions, chronic wasting disease, water, environment, serial protein misfolding cyclic amplification
https://pmc.ncbi.nlm.nih.gov/articles/PMC2802782/
Detection of chronic wasting disease prions in soil at an illegal white-tailed deer carcass disposal site
Published online: 06 Jun 2025
Abstract
Chronic wasting disease (CWD) is a contagious prion disorder affecting cervids such as deer, elk, caribou, and moose, causing progressive and severe neurological degeneration followed by eventual death. As CWD prions (PrPSc) accumulate in the body, they are shed through excreta and secreta, as well as through decomposing carcasses. Prions can persist in the environment for years, posing significant concerns for ongoing transmission to susceptible cervids and pose an unknown risk to sympatric species. We used a validated protocol for real-time quaking-induced conversion (RT-QuIC) in vitro prion amplification assay to detect prions in soil collected within and around an illegal white-tailed deer (Odocoileus virginianus, WTD) carcass disposal site and associated captive WTD farm in Beltrami County, Minnesota. We detected PrPSc in 26 of 201 soil samples across 15 locations within the illegal disposal site and one on the farm that housed the cervids. Importantly, a subset of RT-QuIC positive soil samples was collected from soils where carcasses were recovered, providing direct evidence that environmental contamination resulted from this illegal activity. These findings reveal that improper cervid carcass disposal practices may have important implications for ongoing CWD transmission through the environment.
Snip…
Conclusions
Using RT-QuIC, we detected PrPSc in 26 of 201 soil samples collected across 16 locations on public land where WTD carcasses had been disposed and the captive facility from where they originated. Within the disposal site, 25 out of 124 soil samples (20%) tested positive for PrPSc. Among those positive detections, 17, or 68%, were collected from locations where CWD-positive WTD remains had been previously recovered. This environmental investigation demonstrates how improper cervid carcass disposal practices can result in persistent environmental contamination, posing a potential risk to wildlife health. Given that disposal of livestock on the landscape is a common practice among producers [Citation54–56], these findings underscore the need for improved disposal practices and further investigation of environmental impacts. Expanding on this area of environmental research is crucial as the geographic range of CWD continues to expand [Citation57]. The use of RT-QuIC for prion detection in environmental samples offers an exciting advancement to environmental surveillance for prions, though as we demonstrate here and in Grunklee et al. [Citation41], assay optimization and validation for use with different environmental samples, including new soil types, is still necessary. Further enhancements to RT-QuIC and other methodologies for prion detection will facilitate more opportunities to explore the persistence, degradation, transport, and remediation of environmental prions.
https://www.tandfonline.com/doi/full/10.1080/19336896.2025.2514947
While the disease control measures effectively eliminated prion seeding activity in CWD-affected farms, CWD recurred at two of the 18 remediated farms 4 to 5 years after restocking animals. It remains unclear whether the recurrence of CWD at the two farms was due to residual prions in the environment after the control measures, or the introduction of the infected animals from other farms. This uncertainty is heightened by the annual occurrence of CWD at multiple farms and the absence of a traceability system for farmed cervids.
Keywords: Chronic wasting disease (CWD); NaOH; Protein-misfolding cyclic amplification (PMCA); Republic of Korea; farm; prions; remediation; topsoil.
https://www.tandfonline.com/doi/full/10.1080/19336896.2025.2527588
“While the disease control measures effectively eliminated prion seeding activity in CWD-affected farms, CWD recurred at two of the 18 remediated farms 4 to 5 years after restocking animals.”
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…
so, this is what we leave our children and grandchildren?
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/
Front. Vet. Sci., 14 September 2015 | https://doi.org/10.3389/fvets.2015.00032
Objects in contact with classical scrapie sheep act as a reservoir for scrapie transmission
In conclusion, the results in the current study indicate that removal of furniture that had been in contact with scrapie-infected animals should be recommended, particularly since cleaning and decontamination may not effectively remove scrapie infectivity (31), even though infectivity declines considerably if the pasture and the field furniture have not been in contact with scrapie-infected sheep for several months. As sPMCA failed to detect PrPSc in furniture that was subjected to weathering, even though exposure led to infection in sheep, this method may not always be reliable in predicting the risk of scrapie infection through environmental contamination.
http://journal.frontiersin.org/article/10.3389/fvets.2015.00032/full
"Additionally, we have determined that prion seeding activity is retained for at least fifteen years at a contaminated site following attempted remediation."
15 YEARS!
Detection of prions in soils contaminated by multiple routes
Results: We are able to detect prion seeding activity at multiple types of environmental hotspots, including carcass sites, contaminated captive facilities, and scrapes (i.e. urine and saliva). Differences in relative prion concentration vary depending on the nature and source of the contamination. Additionally, we have determined that prion seeding activity is retained for at least fifteen years at a contaminated site following attempted remediation.
Conclusions: Detection of prions in the environment is of the utmost importance for controlling chronic wasting disease spread. Here, we have demonstrated a viable method for detection of prions in complex environmental matrices. However, it is quite likely that this method underestimates the total infectious prion load in a contaminated sample, due to incomplete recovery of infectious prions. Further refinements are necessary for accurate quantification of prions in such samples, and to account for the intrinsic heterogeneities found in the broader environment.
Funded by: Wisconsin Department of Natural Resources
Prion 2023 Abstracts
https://prion2023.org/wp-content/uploads/2023/10/Meeting-book-final-version2.pdf
SUNDAY, APRIL 06, 2025
Failure to prevent classical scrapie after repeated decontamination of a barn
https://scrapie-usa.blogspot.com/2025/04/failure-to-prevent-classical-scrapie.html
https://prpsc.proboards.com/thread/165/failure-prevent-scrapie-repeated-decontamination
CWD, So, this is what we leave our children and grandchildren?
Detection of chronic wasting disease prions in the farm soil of the Republic of Korea
Here, we show that prion seeding activity was detected in extracts from farm soil following 4 years of incubation with CWD-infected brain homogenate.
https://journals.asm.org/doi/10.1128/msphere.00866-24
=====***>
"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
Results: We are able to detect prion seeding activity at multiple types of environmental hotspots, including carcass sites, contaminated captive facilities, and scrapes (i.e. urine and saliva). Differences in relative prion concentration vary depending on the nature and source of the contamination. Additionally, we have determined that prion seeding activity is retained for at least fifteen years at a contaminated site following attempted remediation.
Conclusions: Detection of prions in the environment is of the utmost importance for controlling chronic wasting disease spread. Here, we have demonstrated a viable method for detection of prions in complex environmental matrices. However, it is quite likely that this method underestimates the total infectious prion load in a contaminated sample, due to incomplete recovery of infectious prions. Further refinements are necessary for accurate quantification of prions in such samples, and to account for the intrinsic heterogeneities found in the broader environment.
Funded by: Wisconsin Department of Natural Resources
Prion 2023 Abstracts
https://prion2023.org/wp-content/uploads/2023/10/Meeting-book-final-version2.pdf
Artificial mineral sites that pre-date endemic chronic wasting disease become prion hotspots
The detection of PrPCWD in soils at attractant sites within an endemic CWD zone significantly advances our understanding of environmental PrPCWD accumulation dynamics, providing valuable information for advancing adaptive CWD management approaches.
https://int-cwd-sympo.org/wp-content/uploads/2023/06/final-agenda-with-abstracts.pdf
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
https://intcwdsympo.files.wordpress.com/2023/06/final-agenda-with-abstracts.pdf?force_download=true
***> Infectious agent of sheep scrapie may persist in the environment for at least 16 years
***> Nine of these recurrences occurred 14–21 years after culling, apparently as the result of environmental contamination, but outside entry could not always be absolutely excluded.
JOURNAL OF GENERAL VIROLOGY Volume 87, Issue 12
Infectious agent of sheep scrapie may persist in the environment for at least 16 years Free
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/
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.
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
THURSDAY, FEBRUARY 28, 2019
BSE infectivity survives burial for five years with only limited spread
https://link.springer.com/content/pdf/10.1007%2Fs00705-019-04154-8.pdf
CWD IS RAVAGING MY FAMILY’S LAND, BUT IT’S NOT TOO LATE FOR YOU
September 9, 2025 By: Paul Annear
My first season deer hunting in Wisconsin was 2001, the same season that produced Wisconsin’s first deer to test positive for chronic wasting disease. CWD has always been at the forefront of deer hunting discussions in my time as a hunter, and I’ve watched the disease slowly spread and worsen. Since 2019, eight of 11 deer I’ve taken on my family’s property in Richland County in Southwest Wisconsin have tested positive for CWD – including the buck in the photo above.
Aside from harvesting otherwise perfectly healthy-looking deer that test positive for CWD, we are now seeing live deer walking around in the awful final stages of this disease. Research has now confirmed what I’ve seen occurring on our hunting land in the last five to six years: CWD is beginning to reduce deer populations in high-prevalence areas like mine.
It didn’t have to reach this point. Hunters in areas with low CWD prevalence can keep infection rates low and deer populations healthy overall by accepting and implementing certain strategies. Some of the strategies I will lay out will challenge you as a hunter to play the “long game,” but there are ways to slow the spread of CWD in areas where it is newly discovered and infection rates are still low.
If you’re rolling your eyes at another guy talking about CWD, I get it, but I urge you to keep reading. Hear my personal story, how it has affected my hunting experiences, and what can happen if hunters ignore CWD.
“Where Are the Deer?”
Up until about seven years ago, I was still trying to figure out this CWD thing and what I thought of it all. I hadn’t yet seen or felt the effects. I was trying to improve my hunting in a variety of different ways like everyone else.
In Iowa County, hunters killed only 916 bucks during the 2024 nine-day firearms season. The last time Iowa County recorded less than 1,000 bucks killed during the nine-day firearms season was in 1971.
We began testing every deer taken on our farm in 2019, and with 72% of them testing positive, it’s safe to say we’re in the thick of it. I’m not alone. I speak to countless hunters in Southwest Wisconsin at trade shows and other events, and many of them are saying the same thing: “What is happening? Where are the deer?”
Since 2019, eight of 11 deer taken on Paul’s family land in southwest Wisconsin tested positive for CWD. This wall of bucks includes deer taken since 2006, and six of the more recent bucks added to this wall were CWD-positive.
In Iowa County, hunters killed only 916 bucks during the 2024 nine-day firearms season. The last time Iowa County recorded less than 1,000 bucks killed during the nine-day firearms season was in 1971. Iowa County tested 694 deer during the 2024 deer season, and 25% of deer tested were positive. Richland and Sauk counties both had a 33% positive CWD rate and together tested 2,193 deer. In 2004, a few years after the initial surge of testing occurred in Wisconsin, Richland County tested 1,691 deer and no deer tested positive for CWD. So, we haven’t been finding CWD just because we’re testing more. It arrived and has spread significantly.
The first time I saw what I believed to be CWD up close and personal was in spring 2023 when my dad and I were marching up a steep ridge for an afternoon turkey hunt. Just a short distance into the walk, I spotted a buck with velvet sprouts. “Dad,” I said. “Deer.”
We both thought it was unusual this deer wasn’t bounding off since we were within 40 yards. Springtime bucks are certainly not the paranoid creatures they become in fall, though. So, we closed the distance since we were headed that way and wanted a closer look.
The buck was very clearly sick. The hair on the back of my neck stood up instantly. A better view revealed his shaking, emaciated body and drool spilling from his mouth (see the photo below). His spine, shoulder blades, and scars up and down his legs told me this deer was in the final stage of CWD but had just enough energy to escape a few predators in the days prior. I had begun to wonder why so many of my 3½-year-old bucks never returned, and this moment convinced me CWD is playing a role in bucks constantly disappearing. This buck was days away from dying of holes eaten in his brain. We were able to put him out of his misery with permission from the Wisconsin DNR.
Though CWD has been in his area for more than 20 years, it wasn’t until 2023 that Paul Annear encountered a visibly sick deer. By the time hunters are seeing sick deer in the woods, the infection rate is usually too high to do anything about it.
I travel 200 miles one way to hunt this property in Southwest Wisconsin. The disease has in a way disrupted my motivation to keep traveling here, knowing full well there is a high likelihood of any deer we kill testing positive, resulting in us throwing out the meat. If you don’t hunt in a CWD zone, your routine following a successful hunt is probably simple and relatively careless. The presence of CWD changes that real quick. Shooting a deer means we could be in for a few frustrating weeks to follow as we wait for CWD test results. I’ve wasted countless hours butchering deer only to throw out the venison.
My friend and fellow Wisconsin deer hunter Bradie Ewing follows the same recommended protocols I do regarding CWD-positive venison.
“We have made the decision that we will not eat or feed a CWD positive deer to our kids or family, so this has caused some logistical headaches,” said Bradie. “The investment of time up front in butchering a deer is significant only to later throw it away if its positive.”
In 2020, I had nearly 30 bucks on trail-camera I estimated to be 3½ years old or older. In 2024, I felt confident we had only seven or eight deer in that age class. A stark decrease. I also ran about 20 more trail cameras on this 115-acre property in 2024 than I did in 2020, so fewer photos are not playing a role in my estimation of fewer mature deer. There are simply fewer mature deer, and DNR harvest data shows it’s not because hunters killed more older bucks in recent seasons. It’s because of CWD.
Why do I keep making the drive back to Richland County? My parents have lived on this land since 1987. This is the land where I was born and raised, where I grew up exploring the woods and learning to hunt squirrels and deer. It’s where I feel I belong, and I know that strong emotional attachment will keep me coming back to hunt deer with my family every fall.
Common Sense
Chronic Wasting Disease prions can be shed via saliva at mineral sites. CWD prions can exist in the soil below licking branches in a scrape. We’re never going to eliminate deer-to-deer contact in the wild. But if you’re in a low CWD prevalence area, there are some common-sense practices you should follow. You can learn from a few of my mistakes.
In the last few years, I’ve wondered if we can truly do anything to curb the spread of CWD in extremely high prevalence areas. One day I would feel the CWD battle is worth fighting, then just days later I’d harvest a CWD positive deer and be discouraged to the point of thinking “this is a bridge too far.”
With 33% of deer in Paul’s county now testing positive for CWD, he has begun to see visibly sick deer in the last two years. Paul’s trail-camera captured the photos above and below in fall 2024. Paul found the remains of the buck above three months after this photo was taken. Note: Deer with EHD die within 5 to 10 days of infection, which isn’t enough time for this kind of drastic weight loss.
I told myself I just wanted to get back to hunting. In the midst of these internal battles, I set out a tank-style waterhole on a Southwest Wisconsin property I hunt. While baiting or feeding is illegal in every Southwest Wisconsin county to help slow the spread of disease, the Wisconsin DNR has not banned the creation of artificial water sources. There are limited water resources on this property, and I thought a waterhole would be a unique way to attract deer near a stand site.
I had an abundance of deer visiting the water tank in the few months it was set up. Despite all the trail-camera photos, a famous Aldo Leopold quote would occasionally run through my mind: “A thing is right when it tends to preserve the integrity, stability, and the beauty of the biotic community – it is wrong if it tends otherwise.”
During the short time I had the waterhole out, I emptied and re-filled it many times since I still wanted to be cognizant of disease transmission. But I have to be honest with myself and admit that if I care about wild deer and the places they live, setting out a small, non-flowing waterhole in a CWD zone was a mistake. Not long after killing a visibly sick, CWD-positive doe that came to drink from the waterhole, we removed it.
In certain regions of the U.S., baiting is just a way of life and how it’s always been done. So, I get the enjoyment and desire to feed or provide artificial water sources for deer. I know hunters in states like Texas and Kansas who would hardly have a deer pass through their land if they didn’t run a feeder.
Are we going to stop the spread of CWD by banning waterholes or baiting? No. But common sense would say those things don’t help an infected herd. Artificially inflating your local deer population in a high CWD prevalence zone by feeding is dangerous because deer that may not otherwise come in contact with one another could share infectious prions at a bait or water site.
Does the presence of CWD mean you should never hang a mock licking branch or plant food plots to improve your hunting opportunities? I believe that’s an unreasonable way of thinking. I am still going to create food plots and mock scrapes. However, I strongly believe we need to practice common sense and realize there are matters we can take into our own hands when it comes to mitigating the spread of CWD. It begins with pulling triggers and landowners making strong, individual decisions regarding their deer herd and holding to them.
Sound Management and Testing
“Earn-A-Buck” was a tool some states used intermittently to effectively manage high deer herds. Wisconsin had implemented EAB off and on beginning in 1996, until it was signed out of law by Wisconsin Governor Scott Walker. I believe EAB is an effective tool for managing deer herds in some places, and I believe it’s no coincidence CWD rates have steadily increased in Wisconsin since Gov. Walker got rid of the law with pressure from other politicians and interest groups. There are few better incentives to take a doe than requiring it before you can take a buck. The only incentive that worked is now gone.
Earn-A-Buck cannot be signed back into law without the Wisconsin legislature doing so. Wisconsin hunters are left with a distinct choice that Wisconsin hunter Doug Duren is often heard saying. “Where CWD is established or taking hold, we have one of two choices,” Doug says. “We are going to manage the herd and the disease, or CWD is going to do it for us.” Wisconsin has had no effective deer management plan since the elimination of EAB in 2011.
In talking with countless hunters in my region, it appears CWD can be somewhat pocketed even within high prevalence counties like mine. The variability of CWD prevalence within a county could be due to availability of better habitat, people not illegally baiting in certain areas, or for unknown reasons. But we do know that high deer density helps CWD spread faster, so simply continuing to harvest deer – especially does – works. Doe harvest helps keep deer density in balance with the habitat and reduces deer-to-deer spread of CWD, which means healthier deer in all respects. But it’s not just about doe harvest.
Bucks test positive at a higher rate than does because of behaviors like traveling farther during the rut. I would encourage you to be less picky about harvesting bucks if CWD has just been discovered and you’re trying to keep prevalence rates low. NDA’s advice for hunters in CWD zones is to continue managing for older bucks if you wish but apply increased harvest pressure on all bucks 2½ years of age or older.
Do I wish we could go back to those days of low prevalence and undergo targeted removal missions on my family’s land to see if it would prevent or delay the problem we have today? Yes. Sustained harvest on all deer, bucks and does, means a better chance of removing infected deer from the landscape sooner. If hunters back off deer harvest because of CWD, infected deer enjoy greater protection, and they can spread more CWD prions into the environment and to other deer. In fact, every time you harvest a deer that tests positive for CWD, you should look at this as a win in the fight against this disease.
Jason Sumners is the Director of the Missouri Department of Conservation and has guided Missouri through a proactive approach to CWD.
“If all you are doing is testing to show you are doing something, it’s a complete waste of critical agency resources,” said Jason. “Short of documenting the demise of deer and giving some hunters a little more comfort when consuming deer harvested in CWD areas, it’s not doing anything to help the herd.”
What is Missouri doing? A lot of testing but also Targeted harvesting in select zones with landowner approval. In 2025, they’ve killed 4,793 deer with 68 (1.4%) of those being positive. While the CWD positive rate of these targeted removals is still low, that’s the point. This is a relatively small number of deer removed statewide, but because they are removed with precision from sites where deer previously tested positive, sick deer are removed sooner. Missouri is keeping CWD prevalence rates in check throughout these surveillance zones.
Would I have been hesitant to allow targeted deer removal or “sharpshooting”’on my property back when CWD had just been discovered? Yes. Do I wish we could go back to those days of low prevalence and undergo targeted removal missions on my family’s land to see if it would prevent or delay the problem we have today? Yes.
The early stage of CWD is the only stage when intervention and management can hope to hold infection rates low. If you wait until you are seeing sick deer in the woods, which is a sign you are in “late-stage” CWD, it’s too late to do anything about it.
If CWD isn’t in your woods yet, you should still make it a point to submit deer for testing anytime an opportunity is presented. Early detection of a new outbreak is critical. Early detection gives hunters and the state wildlife agency the opportunity to respond. CWD testing isn’t a proclamation of any political views or ideologies. However, it is absolutely a pledge that you care about deer and their future.
Paul Annear grew up hunting with his dad on family land in southwest Wisconsin and is now teaching his son Hudson how to hunt. We Are Not Doomed
I believe there will always be white-tailed deer in my area of Wisconsin. However, within 20 to 25 years, I believe fewer bucks will reach maturity than today, and a lot fewer than when I began hunting over 20 years ago.
This is despite more people than ever before passing younger deer and managing for older deer. I think in some areas like mine with high CWD prevalence, the average age of bucks has already dropped significantly from where it was just a few years ago – at a time when NDA’s Deer Report shows more bucks aged 3½ years old or older being harvested nationally than ever before.
If CWD has been found in your woods, ignoring it will take your hunting down the wrong path. Private landowners especially will play a critical role in properly managing whitetails in America in the next 30 years. I’m reminded of this Aldo Leopold quote: “Conservation will ultimately boil down to rewarding the private landowner who conserves the public interest.”
In this case, public interest is healthy deer. In most of whitetail country, unlike Southwest Wisconsin, it’s not too late to do something. Common-sense practices might seem like a burden to you now, but it’s nothing compared to what I’m experiencing. Ignoring those practices might help your short-term hunting opportunities, but remember you are in the position I wish I could go back to. Ask yourself if the choices you are making now will help conserve a better future for all.
Categories: Hunting
Tags: Chronic Wasting Disease, Cwd
About Paul Annear:
Paul Annear is an avid deer hunter, freelance writer and NDA member from the Driftless Region of southwest Wisconsin.
https://deerassociation.com/cwd-is-ravaging-my-familys-land-but-its-not-too-late-for-you/
MONDAY, APRIL 28, 2025
Wisconsin DNR 2024 CWD 1,786 samples testing positive
https://chronic-wasting-disease.blogspot.com/2025/04/wisconsin-dnr-2024-cwd-1786-samples.html
Captive CHRONIC WASTING DISEASE CASES Update August 2025 Captive CHRONIC WASTING DISEASE CASES Update August 2025, Pennsylvania, Wisconsin, Utah, and Texas
https://www.aphis.usda.gov/sites/default/files/status-of-captive-herds.pdf
https://chronic-wasting-disease.blogspot.com/2025/08/texas-game-wardens-near-conclusion-of.html
Published: 05 August 2025
Vertical transmission of chronic wasting disease in free-ranging white-tailed deer populations
Snip…
Our detection of CWD-positive fawns ≤ 10-month-old by ELISA testing provides indirect evidence of gestational infection, although direct or indirect CWD transmission after birth cannot be ruled out in these fawns (Table 5). The detection of CWD infection in ≤ 6-month-old fawns in the Arkansas and Tennessee study sites by ELISA test, which is not as sensitive as amplification assays37, was particularly suggestive of vertical transmission. Fawns less than 6 months of age are not routinely incorporated into statewide CWD surveillance programs because of the low likelihood of detectable infection using traditional assays (i.e., ELISA, IHC), yet have been previously identified17. Future studies should investigate the potential role of in utero transmission in local CWD transmission cycles. Considering the strong relationship between CWD infection probability and female white-tailed deer relatedness, in utero CWD transmission may serve as a small yet important route of transmission in addition to social interactions and indirect exposures53.
Overall, this study describes the dissemination of CWD prions throughout tissues and birthing fluids of the pregnancy microenvironment demonstrating that offspring are routinely exposed to the infectious prion in-utero prior to parturition. We report infectious prions in the reproductive and fetal tissue of naturally exposed free-ranging white-tailed deer suggesting that in utero maternal transmission is likely an underappreciated mode of CWD transmission. Our study shows that vertical transmission is indeed a viable route of infection within the southeastern U.S. and is another potential factor contributing to the relentless spread of chronic wasting disease.
https://www.nature.com/articles/s41598-025-12727-8
WISCONSIN 16 MONTH AGE LIMIT ON TESTING DEAD DEER GAME FARM CWD TESTING PROTOCOL NEEDS TO BE REVISED SINGELTARY ET AL
ENVT.18: MOTHER TO OFFSPRING TRANSMISSION OF CHRONIC WASTING DISEASE
Candace K. Mathiason,† Amy Nalls, Kelly Anderson, Jeanette Hayes-Klug, Jenny G. Powers, Nicholas J. Haley and Edward A. Hoover
"PrPCWD has been detected in one fawn as early as 40 days of age. Moreover, sPMCA performed on rectal lymphoid tissue has yield positive results on another fawn at 10 days of age"
https://www.tandfonline.com/doi/pdf/10.4161/pri.15899
Oral transmission and early lymphoid tropism of chronic wasting disease PrPres in mule deer fawns (Odocoileus hemionus)
The rapid infection of deer fawns following exposure by the most plausible natural route is consistent with the efficient horizontal transmission of CWD in nature and enables accelerated studies of transmission and pathogenesis in the native species. Introduction
https://www.microbiologyresearch.org/content/journal/jgv/10.1099/0022-1317-80-10-2757#tab2
Demographic Patterns and Harvest Vulnerability of Chronic Wasting Disease Infected White-Tailed Deer in Wisconsin
Six fawns tested positive for CWD, five fawns from the core study area, including the youngest (5 months) free-ranging cervid to test positive.
http://forestandwildlifeecology.wisc.edu/facstaff/samuel/2006_grear_et_al_demographic_patterns.pdf
http://web.archive.org/web/20100613124552/http://forestandwildlifeecology.wisc.edu/facstaff/samuel/2006_grear_et_al_demographic_patterns.pdf
Chronic Wasting Disease in a Wisconsin White-Tailed Deer Farm
and 15 of 22 fawns aged 6 to 9 months (68.2%) were positive.
http://vdi.sagepub.com/content/20/5/698.full
https://digitalcommons.unl.edu/cgi/viewcontent.cgi?article=1143&context=zoonoticspub
Wisconsin : Six White-Tailed Deer Fawns Test Positive for CWD
Date: May 13, 2003 Source: Wisconsin Department of Natural Resources
Approximately 4,200 fawns, defined as deer under 1 year of age, were sampled from the eradication zone over the last year. The majority of fawns sampled were between the ages of 5 to 9 months, though some were as young as 1 month. Two of the six fawns with CWD detected were 5 to 6 months old. All six of the positive fawns were taken from the core area of the CWD eradication zone where the highest numbers of positive deer have been identified.
http://www.cwd-info.org/index.php/fuseaction/news.detail/ID/a4b4e5e8749d729af242e253ac742084
http://web.archive.org/web/20071012001856/http://www.cwd-info.org/index.php/fuseaction/news.detail/ID/a4b4e5e8749d729af242e253ac742084
Age specific susceptibility? 194. It is probable, based on age-class specific prevalence data from wild cervids and epidemiological evidence from captive cervids in affected research centres, that both adults and fawns may become infected with CWD (Miller, Wild & Williams, 1998; Miller et al., 2000). 198. In Odocoileus virginianus – white tailed deer, out of 179 white-tailed deer which had become enclosed by an elk farm fence, in Sioux County, northwestern Nebraska, four fawns only eight months old were among the 50% of CWD-positive animals; these fawns were not showing any clinical signs of CWD (Davidson, 2002).
http://wildpro.twycrosszoo.org/s/00ref/miscellaneouscontents/D161_CWDReview_Seac/08_Susceptibility_Nat_Hosts.htm
http://web.archive.org/web/20160312230103/http://wildpro.twycrosszoo.org/s/00ref/miscellaneouscontents/D161_CWDReview_Seac/08_Susceptibility_Nat_Hosts.htm
SCWDS BRIEFS
Volume 17 January 2002 Number 4
CWD News from Nebraska and Kansas
Infection with the chronic wasting disease (CWD) agent recently was found in 28 of 58 formerly wild white-tailed deer in a high-fenced enclosure adjacent to a pen containing CWD affected captive elk in northern Sioux County, Nebraska.
Four of the positive deer were fawns approximately 8 months old, which is unusually young for animals testing positive for CWD.
https://digitalcommons.unl.edu/cgi/viewcontent.cgi?article=1017&context=secwdspubs
CWD in adult deer and fawns
A hundred and thirty-three white-tailed deer in the study were killed after CWD was diagnosed in the deer within the fenced area. Paired samples of formalin-fixed tissue for CWD diagnosis and frozen tissue for DNA sequence analysis were collected. Fifty per cent (67/133) of deer were diagnosed with CWD (Table 2) using an immunohistochemical assay for PrPd in formalin-fixed, paraffinembedded brain and lymphoid tissues.
Five of the CWD-positive deer were fawns, less than 1 year of age.
http://digitalcommons.unl.edu/cgi/viewcontent.cgi?article=1125&context=zoonoticspub
Illinois CWD, see where there 2003 sampling showed 2. % of fawns tested had CWD i.e. 1 positive out of 51 samples.
2003
Boone-Winnebago Unit Fawn 51 1 2.0%
http://dnr.state.il.us/cwd/Sampling_Summary_2003.pdf
http://web.archive.org/web/20041106203740/http://dnr.state.il.us/cwd/Sampling_Summary_2003.pdf
2011 FAWN CWD POSITIVE ILLINOIS
1/26/11 WINNEBAGO 344N 2E S36 F FAWN SHARPSHOOTING
2/10/11 OGLE 341N 1E S7 F FAWN SHARPSHOOTING
3/9/11 OGLE 341N 1E S7 M FAWN SHARPSHOOTING
http://dnr.state.il.us/CWD/2010-2011_Illinois_CWD_Report.pdf
https://ngrrec-hunt-illinois-wordpress-images.s3.amazonaws.com/wp-content/uploads/2023/04/13110846/cwdannualreport20102011.pdf
So, this is what we leave our children and grandchildren?
TUESDAY, JULY 08, 2025
Addressing chronic wasting disease in Korean farms: topsoil removal and 2N NaOH treatment before cervid restocking
https://chronic-wasting-disease.blogspot.com/2025/07/addressing-chronic-wasting-disease-in.html
THURSDAY, JULY 10, 2025
Distribution of chronic wasting disease (CWD) prions in tissues from experimentally exposed coyotes (Canis latrans) Published: July 9, 2025
https://chronic-wasting-disease.blogspot.com/2025/07/distribution-of-chronic-wasting-disease.html
THURSDAY, JULY 10, 2025
Modelling the effect of genotype (PRNP) linked to susceptibility, infection duration and prion shedding on chronic wasting disease dynamics of cervids
https://chronic-wasting-disease.blogspot.com/2025/07/modelling-effect-of-genotype-prnp.html
WEDNESDAY, MAY 14, 2025
Texas CWD TSE Prion Cases Rises to 1099 Confirmed Cases To Date
https://tpwd.texas.gov/huntwild/wild/diseases/cwd/positive-cases/listing-cwd-cases-texas.phtml
https://chronic-wasting-disease.blogspot.com/2025/05/texas-cwd-tse-prion-cases-rises-to-1099.html
FRIDAY, APRIL 04, 2025
Trucking CWD TSE Prion
“CWD spreads among wild populations at a relatively slow rate, limited by the natural home range and dispersed nature of wild animals.”
NOW HOLD YOUR HORSES, Chronic Wasting Disease CWD of Cervid can spread rather swiftly, traveling around 50 MPH, from the back of truck and trailer, and Here in Texas, we call it ‘Trucking CWD’…
https://chronic-wasting-disease.blogspot.com/2025/04/trucking-cwd-tse-prion.html
SUNDAY, MAY 04, 2025
Texas Senate Bill 2649 creation of a statewide Chronic Wasting Disease plan
https://chronic-wasting-disease.blogspot.com/2025/05/texas-senate-bill-2649-creation-of.html
SUNDAY, MAY 04, 2025
Texas Senate Bill 2651 establishment of a pilot program to breed deer resistant to CWD TSE Prion, what could go wrong?
https://chronic-wasting-disease.blogspot.com/2025/05/texas-senate-bill-2651-establishment-of_4.html
Texas S.B. 2843 Directs TPWD to conduct a comprehensive study of current measures to control chronic wasting disease (CWD) in deer
https://chronic-wasting-disease.blogspot.com/2025/04/texas-sb-2843-directs-tpwd-to-conduct.html
Friday, February 21, 2025
Deer don’t die from CWD, it’s the insurance companies, or it's a Government conspiracy?
https://chronic-wasting-disease.blogspot.com/2025/02/deer-dont-die-from-cwd-its-insurance.html
Friday, February 21, 2025
CWD, BAITING, AND MINERAL LICKS, WHAT IF?
https://chronic-wasting-disease.blogspot.com/2025/02/cwd-baiting-and-mineral-licks-what-if.html
SUNDAY, MAY 05, 2024
Chronic Wasting Disease, Cervid Captive Herd CWD Infection rates, Zoonosis, and Environmental Risk Factors
https://chronic-wasting-disease.blogspot.com/2024/05/chronic-wasting-disease-cervid-captive.html
Texas Game Wardens Bust Illegal Deer Operations Across the State Feb. 27, 2025
https://chronic-wasting-disease.blogspot.com/2025/02/texas-game-wardens-bust-illegal-deer.html
TUESDAY, AUGUST 26, 2025
Transmissible Spongiform Encephalopathy TSE Prion Disease UPDATE AUGUST 2025
https://transmissiblespongiformencephalopathy.blogspot.com/2025/08/transmissible-spongiform-encephalopathy.html
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
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
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
Terry S. Singeltary Sr.
posted by Terry S. Singeltary Sr. at
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