Missouri, Some CWD Regulations Paused, what next?
Missouri, Some CWD Regulations Paused, what next?
Missouri CWD Total as at the end 2025 was 815+ confirmed to date, in wild cervid.
key word is ‘wild’, But, what about Captive Cervid?
CWD Sampling Results IN THIS SECTION CWD Management Zone Regulations CWD Management Permit Program Mandatory CWD Sampling Voluntary CWD Sampling CWD Studies CWD Sampling Results CWD FAQs CWD vs. EHD Carcass Transportation and Disposal Human Health & CWD Test Results for Your Deer CWD Interactive Hub (NEW) Post-Season Targeted Removal Share the Harvest: CWD Testing Requirements CWD Hunter Harvest Initiative 2025 Fall Deer and Turkey Hunting Cover
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Each year, MDC tests a sample of the state’s deer population for CWD. CWD testing has two main goals: detect the disease as early as possible in new locations and monitor changes in disease occurrence over time.
Taxidermists throughout the state partner with MDC and collect CWD samples from hunter-harvested deer. Focusing testing on adult males increases the likelihood of finding CWD in new areas.
Within designated CWD Management Zone counties (counties within 10 miles of CWD detections), a greater number of samples are collected, due mostly to mandatory sampling on opening weekend of fall firearms season.
This important effort allows MDC scientists to better understand where the disease is on the landscape so that management actions can be applied (especially post-season targeted removal), learn about how the disease is spreading, and keep the public informed.
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2025-26 Sampling Results to Date
The table below shows MDC sampling efforts and test results so far for the current sampling season (July 1, 2025, through June 30, 2026). These numbers are subject to frequent change.
CWD Sampling Results
Area Positives Not Detected Pending Unsuitable Sample Total
Statewide 122 24069 1 93 24305
Title
CWD in Free-Ranging Deer
see CWD Dashboard
“Those new cases bring the total number of CWD positives found in the state to 815 over 46 counties since the first positive CWD case was found in wild deer by MDC in early 2012.”
what about captive cervid?
Open Letter from MDC Director Jason Sumners on CWD
By Jason Sumners Published Date 12/15/2025
As a young boy growing up in rural Missouri, many days were spent outdoors enjoying wild places and wild critters. At a young age, I became fascinated with the graceful ghost of our forest, the white-tailed deer. This fascination fueled a life-long pursuit to learn everything I could about this iconic species. After graduating high school, the decision to align this passion with career pursuits was natural. It turned from an outsized fascination to a professional pursuit that led me on a decades long journey studying and researching white-tailed deer management across the southern U.S., eventually leading to an opportunity to “come home” and serve as the private-lands deer biologist for the Missouri Department of Conservation. This was truly a dream come true for a small-town country kid with a passion for deer management and conservation of our natural resources.
The dream would turn to dread in February 2010 when chronic wasting disease (CWD) was first detected in our state. By that time, CWD had been known to occur in eastern Colorado and Wyoming since the 1960s and was slowly spreading east across the great plains. It had been detected in Wisconsin and Illinois eight years earlier. Long-term studies of CWD on mule deer populations in the west were beginning to show the destructive impacts on those herds. Research over the last 20 years has continued to demonstrate that, if left unmanaged, CWD will increase in prevalence and distribution leading to increased mortality in deer populations.
As with many diseases, early detection and aggressive management have the greatest impact on the future distribution of the disease. So we embarked on an aggressive strategy to minimize the likelihood of spreading the disease within Missouri (i.e., increased safeguards for the importation of captive deer from outside of Missouri and carcass movement restrictions). Using science to inform management actions, we liberalized local harvest opportunities, prohibited the use of feed and minerals that unnaturally concentrate deer, and implemented localized targeted removals in an effort to minimize the number of infected deer on the landscape (a strategy that Illinois had utilized with measurable success).
Aggressive management actions implemented by cooperating hunters, landowners, and agency staff over the last decade have been successful in slowing the number of infected deer on our state’s landscape. Unfortunately, CWD has continued to be introduced to new parts of the state and spread where it was previously detected.
Some will say CWD is simply a political disease that has not impacted deer populations, but this couldn’t be farther from the truth. Scientific studies have continued to demonstrate that CWD is a fatal disease that, if left unchecked, will increase in prevalence resulting in increased mortality on local populations that significantly alter buck age structure and the ability of the population to recover from other natural factors like extreme droughts and other disease outbreaks like EHD. Others recognize that CWD is a serious threat but disagree with the approach we have implemented to address the disease.
Regardless of where you stand on the issue of CWD, most share the same goal—a healthy sustainable population of deer in Missouri that can be appreciated and utilized by future generations. I certainly hope that my son (and hopefully grandchildren one day) will continue to have the opportunity to utilize and appreciate a healthy and thriving deer population into the future. The white-tailed deer is the heartbeat of Missouri’s wild places—familiar, resilient, and woven into our outdoor heritage. It is also a symbol of the success of wildlife conservation and restoration across North America.
The Missouri Conservation Commission, and subsequently the Missouri Department of Conservation, were created by the citizens of Missouri to restore and manage our valuable fish, forest, and wildlife resources. There is no species more emblematic of this conservation success than the white-tailed deer.
As CWD has spread in Missouri over the last decade, MDC’s objective has been and continues to be to keep CWD infection rates low to protect the long-term health of the deer herd. This extensive undertaking can only be accomplished by working collaboratively with hunters and landowners to achieve both surveillance and management goals. MDC has continued to work with hunters and landowners to adapt the management tools, including creating CWD management permits and simplifying regulations. Last year, we piloted the Hunter Harvest Initiative to encourage additional deer harvest during deer season to alleviate the need for post-season targeted removal.
We remain committed to keeping our deer herd heathy and working collaboratively with the hunters and landowners that are critical to our conservation mission. We cannot be successful in this work, and at the scale needed, without hunters’ and landowners’ support and participation.
At this time, MDC will be pausing our post-season targeted removal efforts to work with hunters and landowners to adapt and identify a more sustainable path forward.
Future generations of Missourians are counting on us to work together to sustain the future of one of our great state’s most important natural resources. Together, we can preserve the health of the herd and the future of hunting; divided, we may lose it.
We are committed to continuing our engagement with hunters, landowners, and Missourians on this hard work ahead. Feel free to send your thoughts to CWDFeedback@mdc.mo.gov.
In gratitude,
Jason Sumners Director, Missouri Department of Conservation
MDC reports 243 new cases of CWD found during past year
News from the region
Statewide
By Joe Jerek
Published Date 04/21/2025
JEFFERSON CITY, Mo. – The Missouri Department of Conservation (MDC) reports it has confirmed 243 new cases of chronic wasting disease (CWD) in Missouri deer in 35 counties. Seven of those counties had their first CWD-positive case: Audrain, Callaway, Lewis, Marion, Miller, Morgan, and Texas.
The CWD-positive cases were found through sampling and testing of more than 36,000 deer during the past deer-hunting season and post-season targeted-removal efforts with most cases being from hunter-harvested deer submitted for sampling.
Missouri has an estimated population of more than 1.5 million white-tailed deer in the state. CWD is a 100% fatal disease in white-tailed deer and other members of the deer family. The disease has been attributed to significant deer population declines in other states and threatens Missouri’s deer population, hunting culture, and economy.
Most of the new CWD positive cases were from the more than 276,000 deer harvested during the 2024-2025 deer-hunting season.
MDC confirmed an additional 70 cases of CWD found through its targeted-removal efforts of 4,768 deer after the close of the deer season in localized areas near where CWD has been found.
“The goal of targeted removal is to remove CWD-positive deer and reduce deer density in these localized areas to slow the spread of CWD and protect Missouri’s deer herd,” explained MDC Wildlife Health Program Supervisor Deb Hudman. “Targeted removal is a proven method to slow the spread of CWD and Missouri is one of several states that uses it to manage the disease.”
For more details on Post-Season Targeted Removal, visit mdc.mo.gov/cwd.
Those new cases bring the total number of CWD positives found in the state to 815 over 46 counties since the first positive CWD case was found in wild deer by MDC in early 2012.
Although the number of CWD-positive counties increased, Hudman noted that CWD management efforts have kept infection rates low.
“Less than 1% of samples tested positive for CWD,” said Hudman.
According to MDC, hunters and landowners are critical partners in the fight against CWD and can assist the Department by continuing to deer hunt, by participating in CWD sampling, by following regulations designed to slow CWD spread, and by cooperating with targeted removal efforts. Learn more about CWD at mdc.mo.gov/cwd.
mdc.mo.gov MDC reports 243 new cases of CWD found during past year MDC thanks hunters, landowners, taxidermists, and meat processors who participated in CWD sampling and management activities. mdc.mo.gov mdc.mo.gov
Chronic Wasting Disease: Missouri MDC reports 243 new cases of CWD found during past year
end
“Those new cases bring the total number of CWD positives found in the state to 815 over 46 counties since the first positive CWD case was found in wild deer by MDC in early 2012.”
So, Missouri CWD positives found in the state to 815 over 46 counties since the first positive CWD case was found in wild deer by MDC in early 2012.”
What about Captive CWD Positives in Missouri, Trace outs, Trace in, etc.???
Missouri Captive Cervid
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News Release Home News 2010 Chronic Wasting Disease Found in Captive Deer February 25, 2010 Chronic Wasting Disease Found in Captive Deer The Missouri Departments of Agriculture, Conservation and Health and Senior Services and the U.S. Department of Agriculture announced today that a captive white-tailed deer in Linn County, Missouri has tested positive for Chronic Wasting Disease (CWD). CWD is a neurological disease found in deer<...
well, looks like Missouri has caved to the captive cervid industry and the clowns that hunt them, imo. you know the ones, ie, car insurance causes cwd, it’s a money grab, deer don’t die from cwd, DNR money grab, show me a picture of cwd, some deer are resistant to cwd, or another good one, cwd does not effect cervid herds, herds are healthy, not declining, the list of industry fed bull**** is endless. crazy part, the cwd entitlement program…i mean the cwd indemnity program, is really where the real money grab is, but most folks don’t realize that i have a link to that. in Texas, where cwd can travel at 50 mph, seems the TAHC and TPWD , both have given up it looks like, caved to the very industry that helped spread cwd to hell and back, i don’t know what’s going on anymore, see for yourself below, but it ain’t good. the insanity of it all is really crazy imo, just throw in the cwd towel, it will take care of itself, that’s one of my favorite stupid comments. don’t get me wrong, i wish all that were true, but it’s not. time will tell, but at what cost$$$ with my thoughts out of the way, what does science show us, or does that even matter anymore$ (im very disgusted with all this, sorry if i sound angry, but i am).
Chronic Wasting Disease CWD TSE Prion, and the Zoonotic and Environmental Factors and ramifications there from. Much science has come forth the past few years that should cause great concern from CWD TSE Prion in Cervid, and spillover there from.
WE already now have proven spillover of CWD to Pigs, and we now know CWD will transmit by ORAL routes to Cattle, Sheep, Pigs, Cervid, and Primates, and this should cause great concern with the FDA PART 589 SUBSTANCES PROHIBITED FROM USE IN ANIMAL FOOD OR FEED Regulations, because it fails to protect the livestock producing animals for human and animals from all this now, it’s a broke system, and has been.
Trucking CWD, is another huge factor, for the further spread of CWD TSE Prion, just look at Texas.
SEE TEXAS CWD DATA TOWARDS THE BOTTOM…TERRY
I urge Everyone to read and understand the latest on Transmissible Spongiform Encephalopathy, Prion, Chronic Wasting Disease in Cervids, and oral transmission, there from, it’s a whole new game now, i call it TSE Prion poker, who’s all in$$$
IF/WHEN or has it already, CWD TSE Prion, mutates into anther strain, that transmits by contact, to other species, like cwd does with cervid, that would be the ultimate, OH ****. it’s always been wrote in stone CWD wouldn’t transmit by oral routes to these livestock species, of which we now know that was a wrong conclusion. yet were still feeding feed that could transmit CWD to all thes livestock species, BUT, if it really goes sideways, mutates, becomes transmissible by casual contact, and we already know TSE can transmit by air borne transmission, but CWD being a truly Contagious Disease would be the ultimate nail in the coffin, so what i’m trying to say is, if we don’t get serious and act, hit cwd at all fronts, it’s not going to end well. you just can’t keep kicking the cwd can down the road, or try to save the very industry, that still insists cwd isn’t a problem and continues to help spread CWD @ 50 MPH, or let captive cervid continue to escape, or continued Lacy act violations. and the industry rumor mill that keeps pushing cwd junk science, it’s a CWD conspiracy by the government, or the insurance companies are responsible for CWD, or it’s a CWD money grab by DNR et al, or my favorite, “deer don’t die from CWD”, or, “show me a picture of cwd under a microscope”, it’s utter insanity with some of the CWD junk science, and it helps spread CWD.
CWD Herd Management for all Captive, VOLUNTARY MUST become MANDATORY! you must remove the very industry helping to spread CWD and their Legislators, from the policy making decisions for CWD, it’s the very reason, imho, we’re in this mess now, at least for Texas, i know other States had the same problems. YOU can’t have different CWD regulations from state to state, based on legislative junk science, from different states. IT WILL NOT WORK!..terry
Missouri CWD
Missouri 2025 Fall Deer Hunting CWD Information
Chronic Wasting Disease: Missouri MDC reports 243 new cases of CWD found during past year
MDC reports 243 new cases of CWD found during past year
2026 CWD
FRIDAY, MAY 08, 2026
WILDLIFE HEALTH COORDINATION AND ZOONOTIC DISEASE PREVENTION ACT S.4451 Chronic Wasting Disease CWD TSE Prion Singeltary Submission
Chronic Wasting Disease: WILDLIFE HEALTH COORDINATION AND ZOONOTIC DISEASE PREVENTION ACT S.4451 Chronic Wasting Disease CWD TSE Prion Singeltary Submission
Texas CWD Cases 1,310 Cases Detected To Date May, 9, 2026
Chronic Wasting Disease: Texas CWD Cases 1,310 Cases Detected To Date May, 9, 2026
Updated March 2026
Chronic Wasting Disease: APHIS USDA Captive CWD Herds Update by State March 2026 Update
Texas Chronic Wasting Disease CWD TSE Prion Dashboard Update August 2025
SEE NEW DASHBOARD FOR CWD POSITIVES!
Texas CWD total by calendar years
Counties where CWD Exposed Deer were Released
Number of CWD Exposed Deer Released by County
TEXAS CWD TSE PRION POSITIVE SAMPLES BY CALENDAR YEAR JANUARY 1 TO DECEMBER 31 2024 TOTAL TO DATE 1061 CASES CONFIRMED
Where does the madness end, i don’t make this stuff up?
JANUARY 22, 2026
snip…
COMMISSIONER GALO: Chairman, if I may.
I agree with you. There’s a lot of people that really do disagree with this plan. And I think that it does change a lot of what we have been doing in the past when we were with Texas Animal Health Commission.
And, as you know, at the last meeting I had some very big concerns. And I left that meeting and I’ve been thinking about a lot that was said there and a lot about this particular rule package.
And if you may favor me, Chairman, I actually put a statement together because I don’t want to… I felt like I left a lot of things unsaid at the last meeting.
So, if you don’t mind, I’m going to read, and maybe that will clarify some of the reasons that people disagree with this rule package.
Texas A&M studies put the total economic output of white-tailed deer hunting in Texas at around $9.6 billion– $4.6 billion for hunters and $5 billion from landowners, encompassing expenditures on licenses, lodging, feed, management, and more.
Additionally, it generates tens of thousands of jobs across the state. Chronic wasting disease is a threat to this vital cornerstone of Texas’ outdoor recreation and its economy. Unfortunately, CWD remains an incredibly difficult disease to manage due to the ease of transmission, the elusive detection in infected animals, its extended incubation period, and its tenacious persistence in the environment once it’s introduced.
Because we now know that there are two primary sources of exposure, one, CWD-infected deer, and two, a CWD-contaminated environment, the Texas Parks and Wildlife Department must continue a rigorous statewide surveillance program, follow effective protocol for action in the instance of detection, and especially prevent its spread pursuant to TWD [Sic]/CWD management plan.
While the TPWD plan to deal with CWD was meant to be dynamic and evolving, TPWD cannot accept the proposed rule which grants, quote– and I quote– “grants TPWD staff explicit authority to develop disease management plans for trace and positive facilities,” end quote; and especially that which relates to the movement of animals out of an infected location.
***>
The department has determined that allowing breeder deer to be moved from an exposed location represents an unacceptable risk of spreading CWD to native, free-ranging, and captive deer populations unless a determination based on the particulars of a given circumstance indicates the risk is neither nonexistent or acceptable.
The above proposed discretionary approach to management resulted in TWD [Sic] staff electing to release 13 bucks from a CWD-positive facility onto an immediately adjacent uninfected site, something which under the previous rule, and adhering to previous protocol, they would not have had the authority to do.
The release was done in mid-September of 2025. One month later, one of the bucks released under the disease management plan tested positive for CWD on the release site; and a second buck from the same group a month and a few days after that. There were 11 properties that were directly exposed to the department’s action… exposed by the department’s actions– 11 properties.
The recent documented disease spread due to deviation from the previous rule adopted during the period where the Texas Animal Health Commission was managing CWD with TPWD is incontrovertible evidence that we cannot deviate from those previously established safeguards. To date, CWD has persisted, spread, and increased in prevalence in nearly every area where it has been introduced.
Unfortunately, because currently there are no known management strategies to successfully mitigate the risk of indirect transmission once an environment has been contaminated with infectious prions, disease prevention is the only prudent recourse.
The best way to manage CWD is to prevent its introduction into new areas and limit its spread. Established safeguards cannot be abandoned. Discontinuation or deviation from prior proven protocol exposes the department to potential liability as CWD will certainly spread to neighboring properties unless established CWD containment procedures are followed.
<***
The department cannot revert to methods from the past which we know caused the spread of this ultimately fatal disease. We must recognize the need for full cooperation and partnership between the Texas Parks and Wildlife Commissioners and the department and its staff, and continue to implement the plans and procedures which were developed and incorporated as the epidemiology and management of this disease became better understood, and until science provides a new and a better plan.
snip…see;
TPW Commission Work Session Transcript January 21, 2026 TEXAS PARKS AND WILDLIFE COMMISSION
JANUARY 21, 2026
COMMISSION HEARING ROOM
4200 SMITH SCHOOL ROAD
AUSTIN, TEXAS 78744
COMMISSION WORK SESSION AND EXECUTIVE SESSION
TPWD: January 21-22, 2026 TPW Commission Work Session Transcript
Singeltary Submission
Chronic Wasting Disease: TPW Commission Meeting Transcript CWD TSE PrP January 22, 2026 TEXAS PARKS AND WILDLIFE COMMISSION
MONDAY, MAY 05, 2026
TEXAS ANIMAL HEALTH COMMISSION AGENCY STRATEGIC PLAN FISCAL YEARS 2025 - 2029 CWD TSE Prion
Chronic Wasting Disease: TEXAS ANIMAL HEALTH COMMISSION AGENCY STRATEGIC PLAN FISCAL YEARS 2025 - 2029 CWD TSE Prion
FRIDAY, MAY 01, 2026
Oklahoma House Bill 3270 FAILED, Great News for Hunters and Wildlife
Chronic Wasting Disease: Oklahoma House Bill 3270 FAILED, Great News for Hunters and Wildlife
***> USA Report, Scrapie, CWD, BSE, TSE, Cattle, Sheep, Pigs, Cervid, Humans, Zoonotic, 2026
April 2026
USA Report, Scrapie, CWD, BSE, TSE, Cattle, Sheep, Pigs, Cervid, Humans, Zoonotic, 2026
So, this is what we leave our children and grandchildren?
kind regards, terry
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Captive CWD Indemnity Program or Entitlement Program?
CWD, who’s getting paid?
USDA EXPLANATORY NOTES ANIMAL AND PLANT HEALTH INSPECTION SERVICE 2025-2014 CHRONIC WASTING DISEASE CWD TSE CERVID
2025 USDA EXPLANATORY NOTES – ANIMAL AND PLANT HEALTH INSPECTION SERVICE
In 2023, eight percent of the farmed cervids in the HCP were tested for CWD at APHIS and State laboratories.
Of the 303,242 farmed cervids tested in 2023, APHIS confirmed 22 new CWD positive farmed cervid herds.
APHIS provided Federal indemnity to depopulate one of the newly identified positive herds and approved an indemnity payment for a second positive herd which will be provided in 2024 once depopulation occurs. The remaining infected herds are under State quarantines.
2024 USDA EXPLANATORY NOTES – ANIMAL AND PLANT HEALTH INSPECTION SERVICE
Cervids
In 2022, 7 percent of the 285,589 farmed cervids in the HCP participating states were tested for CWD at State and APHIS laboratories.
APHIS confirmed 23 new CWD positive farmed cervid herds.
APHIS provided Federal indemnity to depopulate nine of the newly identified positive herds in 2022. The remaining infected herds are under State quarantines. APHIS determines the use of Federal indemnity payments within the CWD program on a case-by-case basis.
2023 USDA EXPLANATORY NOTES – ANIMAL AND PLANT HEALTH INSPECTION SERVICE
Cervids
Currently, 28 States participate in the national CWD HCP. In FY 2021, more than 20,502 farmed cervids were tested for CWD at State and APHIS laboratories.
As a result, APHIS identified 35 new CWD positive farmed cervid herds.
APHIS provided Federal indemnity to depopulate nine of the newly identified deer herds in FY 2021. The remaining infected herds are under State quarantines. APHIS determines the use of Federal indemnity payments within the CWD program on a case-by-case basis.
2022 USDA EXPLANATORY NOTES – ANIMAL AND PLANT HEALTH INSPECTION SERVICE
Cervids
Currently, 28 States participate in the national CWD HCP. In FY 2020, more than 11,182 farmed cervids were tested for CWD at State and APHIS laboratories.
As a result, APHIS identified 22 new CWD positive farmed cervid herds.
APHIS provided Federal indemnity to depopulate 15 of the 22 newly identified deer herds in FY 2020.
Four additional farmed cervid herds that were identified as CWD positive herds in FY 2019, were indemnified in FY 2020.
The remaining infected herds are under State quarantines.
2021 USDA EXPLANATORY NOTES – ANIMAL AND PLANT HEALTH INSPECTION SERVICE
In FY 2019 APHIS tested more than 11,000 farmed cervids for CWD.
As a result, APHIS identified 17 new CWD positive farmed cervid herds.
APHIS provided Federal indemnity to depopulate 7 of the 17 newly identified deer herds in FY 2019. The remaining infected herds found in FY 2019 are under State quarantines.
2020 USDA EXPLANATORY NOTES – ANIMAL AND PLANT HEALTH INSPECTION SERVICE
Cervids
In FY 2018, APHIS identified 15 new CWD positive farmed cervid herds (14 deer herds and 1 reindeer herd).
The reindeer herd in Illinois was the first confirmed case of CWD in a reindeer in North America.
APHIS provided Federal indemnity to depopulate seven of the 15 newly identified deer herds in FY 2018.
The Agency also provided funding for the test and removal of 161 high risk animals that were in close proximity to reactors.
The remaining herds in FY 2018 are under State quarantines.
The Agency determines the use of Federal indemnities within the CWD program on a case-by-case basis. 20-59
2019 President’s Budget Animal and Plant Health Inspection Service
Cervids
APHIS’ voluntary national CWD Herd Certification Plan (HCP) helps States, Tribes, and the cervid industry control CWD in farmed cervids by allowing the interstate movement only from certified herds.
Currently, 28 States participate in the national CWD HCP and the program tested 23,053 farmed cervids for CWD.
In FY 2017, eight new CWD positive farmed corvid herds were identified– one white-tail deer in Iowa, one white-tail deer herd in Minnesota, one white-tail and mule deer herd in Minnesota, one white-tail and sika deer herd in Michigan, three white-tail deer herds in Pennsylvania, and one white-tail deer herd in Texas.
APHIS provided Federal indemnity to depopulate the Iowa herd, the white-tail deer herd in Minnesota, one herd in Pennsylvania and the Texas herd. The State depopulated the Michigan herd. The remaining herds are under State quarantines. One Texas herd used Federal indemnity to remove and test select, high-risk animals to inform the epidemiological investigation and to evaluate the performance of ante-mortem tests.
The Agency determines the use of Federal indemnities within the CWD program on a case-by-case basis.
2018 President’s Budget Animal and Plant Health Inspection Service
Cervids
APHIS’ voluntary national CWD Herd Certification Plan (HCP) helps States, Tribes, and the cervid industry control CWD in farmed cervids by allowing the interstate movement only from certified herds considered to be low risk.
Currently, 29 States participate in the national CWD HCP.
In FY 2016, the program tested 14,503 farmed cervids for CWD and identified seven new CWD positive farmed cervid herds – two white-tail deer herds in Texas, three white-tail deer herds in Wisconsin, one elk herd in Colorado and one elk herd in Iowa. The elk herd in Colorado was depopulated without Federal indemnity and the rest of the herds are under State quarantines. One Texas herd used Federal indemnity to remove and test select animals to inform the epidemiological investigation and to evaluate 20-72 the performance of ante-mortem tests.
The use of Federal indemnities within the CWD program is determined on a case-by-case basis. APHIS is also conducting several pilot projects related to new technologies. In FY 2016, the Agency
2017 Explanatory Notes Animal and Plant Health Inspection Service
Cervids
APHIS’ voluntary national CWD Herd Certification Plan (HCP) helps States, Tribes, and the cervid industry control CWD in farmed cervids by allowing the interstate movement only from certified herds considered to be low risk.
Currently, 30 States participate in the national CWD HCP: 29 have Approved Status and 1 has Provisional Approved Status. States that meet the CWD HCP requirements have Approved Status and States that do not meet CWD HCP program requirements but have developed a work plan and time frame with APHIS to complete those requirements have Provisional Approved Status.
In FY 2015, the program tested approximately 20,000 farmed cervids for CWD and identified eight new CWD positive farmed white-tailed deer herds – one in Utah, one in Pennsylvania, two in Ohio, two in Wisconsin, and two in Texas.
APHIS depopulated five of these herds (Pennsylvania, Utah, and one each in Wisconsin, Texas, and Ohio). Six elk herds in Colorado, four elk herds in Nebraska, one white-tailed deer herd in Wisconsin and one white-tailed deer herd in Texas remained in quarantine at the end of FY 2015.
APHIS also provided indemnity for and was the lead agency for the depopulation and disposal of four large CWD infected farmed cervid herds in Pennsylvania, Ohio, Utah, and Texas. In cooperation with the National Agricultural Statistics Service, APHIS conducted the first national study of the U.S. farmed-cervid industry in FY 2015. The study provides baseline industry statistics, a description of production practices and challenges, producer-reported disease occurrences, and an overview of health management and biosecurity practices.
2016 Explanatory Notes Animal and Plant Health Inspection Service
2015 Explanatory Notes Animal and Plant Health Inspection Service
2014 Explanatory Notes Animal and Plant Health Inspection Service
APHIS USDA Captive CWD Herds Update by State March 2026
Updated March 2026
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***> Missouri Year by Year History of CWD TSE Prion my files
MONDAY, APRIL 10, 2023
Missouri MDC reports 117 new cases of CWD for 2022 surveillance year
MONDAY, JANUARY 30, 2023
Missouri CWD TSE PRION 2022-2023 Sampling Results to Date 74 Positive
WEDNESDAY, APRIL 27, 2022
Missouri MDC reports final CWD results for 2021 deer season with 86 testing positive for CWD
WEDNESDAY, DECEMBER 15, 2021
Missouri CWD TSE PrP 28 confirmed positive test results so far for the current sampling season (July 1, 2021 - June 30, 2022)
WEDNESDAY, MAY 06, 2020
Missouri 46 new cases Chronic Wasting Disease found, total to date at 162 documented CWD
TUESDAY, FEBRUARY 11, 2020
Missouri MDC 2019-2020 SAMPLING RESULTS CWD TSE PRION TO DATE 28 Positive
SUNDAY, JANUARY 19, 2020
Missouri CWD TSE Prion 2019-2020 SAMPLING RESULTS TO DATE 25 Positive
THURSDAY, JANUARY 02, 2020
Missouri MDC officially reports more than 20 new cases of Chronic Wasting Disease CWD TSE Prion
TUESDAY, DECEMBER 31, 2019
Missouri MDC TESTS SHOW SEVEN NEW CHRONIC WASTING DISEASE CASES IN SOUTHEAST
FRIDAY, DECEMBER 20, 2019
Missouri MDC Confirms 24 New Cases of Chronic Wasting Disease CWD TSE Prion
THURSDAY, JUNE 06, 2019
Missouri MDC proposes new efforts to limit spread of CWD TSE Prion To Date 116 Cases Confirmed
THURSDAY, APRIL 25, 2019
Missouri MDC reports 41 new positive test results for CWD have been confirmed following its sampling
FRIDAY, APRIL 22, 2016
Missouri MDC finds seven new cases of Chronic Wasting Disease CWD during past‐season testing
Saturday, September 05, 2015
Missouri Captive Cervid Industry, CWD TSE Prion, and Procrastinating for Money, while mad deer and elk disease silently spreads
Tuesday, June 16, 2015
Missouri MDC changes deer hunting regs to help slow CWD
Wednesday, March 11, 2015
MDC reports 11 new cases of Chronic Wasting Disease CWD in Missouri deer
Monday, January 26, 2015
Missouri MDC reports two new cases of CWD found in Adair and Macon counties
Tuesday, December 09, 2014
Missouri MDC reports one new case of CWD, found in Adair County
Friday, October 17, 2014
Missouri Final action on Orders of Rule making Breeders and Big Game Hunting Preserves
Thursday, September 11, 2014
Missouri Nixon's Veto Stands Overide Fails on Agriculture Legislation How they voted: attempt to override veto of ag bill fails in the House
Thursday, May 01, 2014
Missouri DNR CWD prevention and captive cervid farming Update
Friday, September 20, 2013
* Missouri State records show gaps in oversight of captive deer farms, ranches *
Tuesday, March 26, 2013
CWD Missouri remains confined to Linn-Macon-County Core Area with four new cases
Wednesday, January 23, 2013
Missouri sixth case CWD documented northwest Macon County
Tuesday, January 24, 2012
CWD found in two free-ranging deer from Macon County Missouri
Friday, February 26, 2010
Chronic wasting disease found in Missouri deer
Sunday, March 25, 2012
Three more cases of CWD found in free-ranging deer in Macon County
From: Terry S. Singeltary Sr. Sent: Thursday, March 29, 2012 6:26 PM
To: warhovert@missouri.edu
Cc: abbottjm@missouri.edu ; waltermr@missouri.edu; John.McLaughlin@missouri.edu ; connerek@missouri.edu ; contact@dnr.mo.gov ; Shelly.Witt@mda.mo.gov ; Animal.Health@mda.mo.gov ; acfa@mda.mo.gov ; animalid@mda.mo.gov ; Linda.Hickam@mda.mo.gov
Subject: re-Missouri officials seek states' advice on chronic wasting disease in deer
Thursday, May 31, 2012
Missouri MDC staff will provide information on five recently found cases of CWD in free-ranging deer in northwest Macon County June 2, 2012
Wednesday, September 05, 2012
Missouri MDC seeks hunters’ help when processing harvested deer and preventing CWD
Thursday, December 20, 2012
MISSOURI Initial CWD sampling test results available online from MDC so far one adult buck has tested positive for the disease
Friday, October 21, 2011
Chronic Wasting Disease Found in Captive Deer Missouri
The Missouri Department of Agriculture discovers the state's first case of CWD in a captive white-tailed deer.
Friday, February 26, 2010
Chronic wasting disease found in Missouri deer
February 25, 2010
Chronic Wasting Disease Found in Captive Deer The Missouri Departments of Agriculture, Conservation and Health and Senior Services and the U.S. Department of Agriculture announced today that a captive white-tailed deer in Linn County, Missouri has tested positive for Chronic Wasting Disease (CWD).
CWD is a neurological disease found in deer, elk and moose. "There is no evidence that CWD poses a risk to domestic animals or humans," said State Veterinarian Dr. Taylor Woods. "We have protocols in place to quickly and effectively handle these situations."
The animal that tested positive for CWD was a white-tailed deer inspected as part of the State's CWD surveillance and testing program.
Preliminary tests were conducted by the USDA National Veterinary Services Laboratory in Ames, Iowa. Upon receiving the confirmed CWD positive, Missouri's departments of Agriculture, Conservation and Health and Senior Services initiated their CWD Contingency Plan. The plan was developed in 2002 by the Cervid Health Committee, a task force comprised of veterinarians, animal health officers and conservation officers from USDA, MDA, MDC and DHSS working together to mitigate challenges associated with CWD.
CWD is transmitted by live animal to animal contact or soil to animal contact.
The disease was first recognized in 1967 in captive mule deer in the Colorado Division of Wildlife captive wildlife research facility in Fort Collins, Colorado.
CWD has been documented in deer and/or elk in Colorado, Illinois, Kansas, Michigan, Minnesota, Montana, Nebraska, New Mexico, New York, Oklahoma, South Dakota, Utah, Virginia, West Virginia, Wisconsin, and the Canadian Provinces of Alberta and Saskatchewan.
There has been no evidence that the disease can be transmitted to humans.
"Missouri's proactive steps to put a testing protocol in place and create a contingency plan years ago is proving beneficial. We are in a solid position to follow pre-established steps to ensure Missouri's valuable whitetail deer resource remains healthy and strong," said Jason Sumners Missouri's Deer Biologist. For more information regarding CWD, please contact Dr. Taylor Woods at (573) 751-3377.
2026 ENVIRONMENTAL FACTORS FOR CHRONIC WASTING DISEASE CWD TSE Prion
Title: Horizontal transmission of chronic wasting disease in reindeer
Submitted to: Emerging Infectious Diseases Publication Type: Peer Reviewed Journal Publication Acceptance Date: 8/29/2016 Publication Date: 12/1/2016
Interpretive Summary: Chronic wasting disease (CWD) is a fatal neurodegenerative disease that occurs in farmed and wild cervids (deer and elk) of North America and was recently diagnosed in a single free-ranging reindeer (Rangifer tarandus tarandus) in Norway. CWD is a transmissible spongiform encephalopathy (TSE) that is caused by infectious proteins called prions that are resistant to various methods of decontamination and environmental degradation. Little is known about the susceptibility of or potential for transmission amongst reindeer. In this experiment, we tested the susceptibility of reindeer to CWD from various sources (elk, mule deer, or white-tailed deer) after intracranial inoculation and tested the potential for infected reindeer to transmit to non-inoculated animals by co-housing or housing in adjacent pens. Reindeer were susceptible to CWD from elk, mule deer, or white-tailed deer sources after experimental inoculation. Most importantly, non-inoculated reindeer that were co-housed with infected reindeer or housed in pens adjacent to infected reindeer but without the potential for nose-to-nose contact also developed evidence of CWD infection. This is a major new finding that may have a great impact on the recently diagnosed case of CWD in the only remaining free-ranging reindeer population in Europe as our findings imply that horizontal transmission to other reindeer within that herd has already occurred. Further, this information will help regulatory and wildlife officials developing plans to reduce or eliminate CWD and cervid farmers that want to ensure that their herd remains CWD-free, but were previously unsure of the potential for reindeer to transmit CWD.
https://www.ars.usda.gov/research/publications/publication/?seqNo115=328261
https://wwwnc.cdc.gov/eid/article/22/12/16-0635_article
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5189146/
Chronic wasting disease (CWD) prion detection in environmental and biological samples from a taxidermy site and nursing facility, and instruments used in surveillance activities
Available online 9 April 2025
Highlights
• CWD prions were identified in a taxidermy and deer nursing facility.
• Contaminated samples included waters, soils, dermestid beetles, domestic flies and a dumpster.
• Surgical instruments used to collect deer samples can get contaminated with CWD prions.
• Some of the infectious particles are readily released from surgical instruments when washed.
• Our results suggest that taxidermy practices actively contribute in the spreading of CWD.
Snip…
In summary, the information provided in this report demonstrate how anthropogenic activities, specifically taxidermy practices, animal processing, and rehabilitation of CWD susceptible species, may facilitate CWD transmission through the environmental dissemination of CWD prions. This study, along with future research efforts characterizing the overall level of infectivity, provides relevant information on managing CWD and to control its rapid geographic expansion. …
https://www.sciencedirect.com/science/article/abs/pii/S0048969725009544
Chronic wasting disease detection in environmental and biological samples from a taxidermy site
Results: The PMCA analysis demonstrated CWD seeding activity in some of the components of this facility, including insects involved in head processing, soils, and a trash dumpster.
Conclusions: Different areas of this property were used for various taxidermy procedures. We were able to detect the presence of prions in
i) soils that were in contact with the heads of dead animals, ii) insects involved in the cleaning of skulls, and iii) an empty dumpster where animal carcasses were previously placed.
This is the first report demonstrating that swabbing is a helpful method to screen for prion infectivity on surfaces potentially contaminated with CWD. These findings are relevant as this swabbing and amplification strategy may be used to evaluate the disease status of other free-ranging and captive settings where there is a concern for CWD transmissions, such as at feeders and water troughs with CWD-exposed properties. This approach could have substantial implications for free-ranging cervid surveillance as well as in epidemiological investigations of CWD.
Prion 2022 Conference abstracts: pushing the boundaries
https://www.tandfonline.com/doi/full/10.1080/19336896.2022.2091286
Artificial mineral sites that pre-date endemic chronic wasting disease become prion hotspots
The Ames Research and Educational Center property, centrally located within the CWD zone of southwest Tennessee, contains 49 historical mineral supplementation sites that were decommissioned in 2012. Here, we demonstrate that 32 of the 49 (65%) mineral sites within Ames established prior to the regional CWD outbreak, serve as foci of environmental PrPCWD contamination. Detection of PrPCWD in soils from these artificial mineral sites was dependent on site-specific management efforts. Soil physical properties were very similar across sites and no correlation between PrPCWD detection and soil physical properties was found. The detection of PrPCWD in soils at attractant sites within an endemic CWD zone significantly advances our understanding of environmental PrPCWD accumulation dynamics, providing valuable information for advancing adaptive CWD management approaches.
https://intcwdsympo.files.wordpress.com/2023/06/final-agenda-with-abstracts.pdf
Shedding of Chronic Wasting Disease Prions in Multiple Excreta Throughout Disease Course in White-tailed Deer
Conclusions: These studies demonstrate: (a) CWD prion excretion occurs throughout infection; (2) PRNP genotype (GG≫GS/NT) influences the excreta shedding; and (3) detection sensitivity in excreta can vary with different RT-QuIC protocols. These results provide a more complete perspective of prion shedding in deer during the course of CWD infection.
Prion 2022 Conference abstracts: pushing the boundaries
https://www.tandfonline.com/doi/full/10.1080/19336896.2022.2091286
"Additionally, we have determined that prion seeding activity is retained for at least fifteen years at a contaminated site following attempted remediation."
***> 15 YEARS!!!
Detection of prions in soils contaminated by multiple routes
Results: We are able to detect prion seeding activity at multiple types of environmental hotspots, including carcass sites, contaminated captive facilities, and scrapes (i.e. urine and saliva). Differences in relative prion concentration vary depending on the nature and source of the contamination. Additionally, we have determined that prion seeding activity is retained for at least fifteen years at a contaminated site following attempted remediation.
Conclusions: Detection of prions in the environment is of the utmost importance for controlling chronic wasting disease spread. Here, we have demonstrated a viable method for detection of prions in complex environmental matrices. However, it is quite likely that this method underestimates the total infectious prion load in a contaminated sample, due to incomplete recovery of infectious prions. Further refinements are necessary for accurate quantification of prions in such samples, and to account for the intrinsic heterogeneities found in the broader environment.
Funded by: Wisconsin Department of Natural Resources
Meeting-book-final-version prion 2023 Prion 2023 Congress Organizing Committee and the NeuroPrion Association, we invite you to join us for the International Conference Prion2023 from 16-20 October 2023 in Faro, Portugal.
https://prion2023.org/wp-content/uploads/2023/10/Meeting-book-final-version2.pdf
https://web.archive.org/web/20250828201533/https://prion2023.org/wp-content/uploads/2023/10/Meeting-book-final-version2.pdf
https://www.researchgate.net/profile/Syed-Zahid-Shah/publication/378314391_Meeting-book-final-version_prion_2023/links/65d44dad28b7720cecdca95f/Meeting-book-final-version-prion-2023.pdf
***> 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/
I remember what “deep throat” told me about Scrapie back around 2001, during early days of my BSE investigation, after my Mom died from hvCJD, I never forgot, and it seems it’s come to pass;
***> Confidential!!!!
***> As early as 1992-3 there had been long studies conducted on small pastures containing scrapie infected sheep at the sheep research station associated with the Neuropathogenesis Unit in Edinburgh, Scotland. Whether these are documented...I don't know. But personal recounts both heard and recorded in a daily journal indicate that leaving the pastures free and replacing the topsoil completely at least 2 feet of thickness each year for SEVEN years....and then when very clean (proven scrapie free) sheep were placed on these small pastures.... the new sheep also broke out with scrapie and passed it to offspring. I am not sure that TSE contaminated ground could ever be free of the agent!! A very frightening revelation!!!
---end personal email---end...tss
and so it seems…
Chronic Wasting Disease CWD TSE Prion
THE CWD TSE Prion aka mad cow type disease is not your normal pathogen.
The TSE prion disease survives ashing to 600 degrees celsius, that’s around 1112 degrees farenheit.
You cannot cook the TSE prion disease out of meat. In fact new data now shows that exposure to high temperatures used to cook the meat increased the availability of prions for in vitro amplification.
you can take the ash and mix it with saline and inject that ash into a mouse, and the mouse will go down with TSE.
Prion Infected Meat-and-Bone Meal Is Still Infectious after Biodiesel Production as well.
the TSE prion agent also survives Simulated Wastewater Treatment Processes.
IN fact, you should also know that the TSE Prion agent will survive in the environment for years, if not decades.
you can bury it and it will not go away.
The TSE agent is capable of infected your water table i.e. Detection of protease-resistant cervid prion protein in water from a CWD-endemic area.
it’s not your ordinary pathogen you can just cook it out and be done
New studies on the heat resistance of hamster-adapted scrapie agent: Threshold survival after ashing at 600°C suggests an inorganic template of replication
http://www.pnas.org/content/97/7/3418.full
Prion Infected Meat-and-Bone Meal Is Still Infectious after Biodiesel Production
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2493038/
Rapid assessment of bovine spongiform encephalopathy prion inactivation by heat treatment in yellow grease produced in the industrial manufacturing process of meat and bone meals
https://bmcvetres.biomedcentral.com/track/pdf/10.1186/1746-6148-9-134.pdf
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
Chronic wasting disease prions on deer feeders and wildlife visitation to deer feeding areas
First published: 10 February 2025
Snip…
Finally, we swabbed 19 feeders in 2 areas where CWD was newly detected, finding prion contamination on swabs from 4 feeders. We show that deer feeders in free-ranging populations with high CWD prevalence become contaminated with CWD prions quickly, becoming a potential site of exposure of deer to CWD prions. Our results also demonstrate the ability to find evidence of prion contamination on deer feeders, even in areas where CWD is newly detected.
Snip…
We found that supplemental feeding increased the risk of exposure to CWD prions due to contamination of feeders, increased deer visitation, and increased deer-to-deer contact.
The 12-fold increase in deer visitation to feeders compared to mast trees and 2-fold increase compared to food plots demonstrates increased risk for direct disease spread.
https://wildlife.onlinelibrary.wiley.com/doi/10.1002/jwmg.70000
Chronic Wasting Disease in Texas A Real Disease with Proven Impacts
Produced by a coalition of concerned hunters, landowners, & conservationists (last update 1/2025)
storymaps.arcgis.com/stories/b93f528938ac48e9b56dcc79953cbec0
Aug 18, 2021
Oh, Deer
Heading Off a Wildlife Epidemic
CWD poses a significant threat to the future of hunting in Texas. Deer population declines of 45 and 50 percent have been documented in Colorado and Wyoming. A broad infection of Texas deer populations resulting in similar population impacts would inflict severe economic damage to rural communities and could negatively impact land markets. Specifically, those landowners seeking to establish a thriving herd of deer could avoid buying in areas with confirmed CWD infections. As they do with anthrax-susceptible properties, land brokers may find it advisable to inquire about the status of CWD infections on properties that they present for sale. Prospective buyers should also investigate the status of the wildlife on prospective properties. In addition, existing landowners should monitor developments as TPWD crafts management strategies to identify and contain this deadly disease.
Dr. Gilliland (c-gilliland@tamu.edu) is a research economist with the Texas Real Estate Research Center at Texas A&M University.
www.recenter.tamu.edu/articles/tierra-grande/oh-d
***> CWD Transmission To, Cattle, Pigs, Sheep, Primates, oh my!
Transmission of the chronic wasting disease agent from elk to cattle after oronasal exposure
Justin Greenlee, Jifeng Bian, Zoe Lambert, Alexis Frese, and Eric Cassmann Virus and Prion Research Unit, National Animal Disease Center, USDA-ARS, Ames, IA, USA
Aims: The purpose of this study was to determine the susceptibility of cattle to chronic wasting disease agent from elk.
Materials and Methods: Initial studies were conducted in bovinized mice using inoculum derived from elk with various genotypes at codon 132 (MM, LM, LL). Based upon attack rates, inoculum (10% w/v brain homogenate) from an LM132 elk was selected for transmission studies in cattle. At approximately 2 weeks of age, one wild type steer (EE211) and one steer with the E211K polymorphism (EK211) were fed 1 mL of brain homogenate in a quart of milk replacer while another 1 mL was instilled intranasally. The cattle were examined daily for clinical signs for the duration of the experiment. One steer is still under observation at 71 months post-inoculation (mpi).
Results: Inoculum derived from MM132 elk resulted in similar attack rates and incubation periods in mice expressing wild type or K211 bovine PRNP, 35% at 531 days post inoculation (dpi) and 27% at 448 dpi, respectively. Inoculum from LM132 elk had a slightly higher attack rates in mice: 45% (693 dpi) in wild type cattle PRNP and 33% (468) in K211 mice. Inoculum from LL132 elk resulted in the highest attack rate in wild type bovinized mice (53% at 625 dpi), but no K211 mice were affected at >700 days. At approximately 70 mpi, the EK211 genotype steer developed clinical signs suggestive of prion disease, depression, low head carriage, hypersalivation, and ataxia, and was necropsied. Enzyme immunoassay (IDEXX) was positive in brainstem (OD=4.00, but non-detect in retropharyngeal lymph nodes and palatine tonsil. Immunoreactivity was largely limited to the brainstem, midbrain, and cervical spinal cord with a pattern that was primarily glia-associated.
Conclusions: Cattle with the E211K polymorphism are susceptible to the CWD agent after oronasal exposure of 0.2 g of infectious material.
***> cwd to pigs
Chronic wasting disease prions in cervids and wild pigs in North America Preliminary Outbreak Assessment DEFRA 26 January 2026
DEFRA 26 January 2026 Department for Environment, Food and Rural Affairs
Preliminary Outbreak Assessment
Chronic wasting disease prions in cervids and wild pigs in North America
26 January 2026
Disease report
Chronic wasting disease (CWD) is a fatal neurodegenerative disease of cervids, such as deer, elk, moose and reindeer. It is caused by prions – infectious proteins that cause normal cellular prion proteins to misfold (CIDRAP, 2025). The disease is widespread in captive and free-ranging cervids in North America (Figure 1). For the first time, CWD prions have also been detected in the tissues of wild pigs (Sus scrofa) caught in CWD-affected areas of the USA (Soto et al. 2025). This discovery emerged from a study designed to investigate potential interactions between wild pigs and CWD prions, as wild pigs often coexist with cervids, which can shed prions into the environment. The following assessment discusses the epidemiology of CWD in North America and the detection of CWD prions in wild pigs. It also considers the potential implications for Great Britain.
Figure 1. Distribution of CWD in cervids in North America as of 11 April 2025 (USGS, 2025).Department for Environment, Food and Rural Affairs
Situation assessment
CWD is considered one of the most important cervid diseases due to its capacity for infectious spread, high mortality rate and associated socio-economic impacts on cervid farming and hunting-related industries (Kincheloe et al., 2021, CFSPH, 2024). The disease is always fatal, with no cure or vaccine (CFSPH, 2024).
CWD was first reported among captive cervids in the USA in the 1960s (Kincheloe et al., 2021). It has since been detected in captive and or free-ranging cervids in 36 US states and 5 Canadian provinces, as well as South Korea, Norway, Finland and Sweden (Silva, 2022, USGS, 2025). While the South Korean strains are thought to have originated from North America, the European strains appear to have emerged independently (Silva, 2022).
Transmission between cervids occurs by direct contact with infected animals or indirectly, through contact with a contaminated environment, most likely via the oral route (Otero et al., 2021). The disease may also be vertically transmitted from doe to fawn (Nalls et al., 2013, Salariu et al., 2015). Environmental contamination occurs when infected animals shed infectious prions in various secretions and excretions, such as urine, faeces and saliva (Otero et al., 2021). It can also occur when infected carcasses decompose and release prions into the surrounding soil and vegetation (Miller et al., 2004). The minimum number of CWD prions required to cause infection in cervids is unknown but appears to be low (Denkers et al., 2020).
The disease is difficult to control, as infected animals can also be subclinical for months or years. During this time, they can shed CWD prions, which can remain infectious in the environment for at least 2 years (Miller et al., 2004, CFSPH, 2024). Diagnosis usually relies on post-mortem tests, which may fail to identify infected animals during the early stages of the disease (CFSPH, 2024, CIDRAP, 2025). Control efforts are further hampered by lack of evidence to inform effective CWD management and control strategies (Uehlinger et al., 2016, Mori et al., 2024).
CWD in North American cervids
CWD has been reported in a range of North American cervids, including white-tailed deer, mule deer, black-tailed deer, moose, wapiti, reindeer (captive) and red deer (captive) (EFSA BIOHAZ Panel, 2023). It was first reported in captive mule deer and black-tailed deer at research facilities in Colorado and Wyoming in the late 1960s (Otero et al., 2021). These animals were derived from wild populations. The disease was later identified in Rocky Mountain elk at these facilities and subsequently, in free-ranging populations of mule deer and elk in Wyoming and Colorado. The geographic expansion of CWD in North America is thought to reflect the commercial movement of subclinical animals and natural cervid migration (Otero et al., 2021). Epidemiological data suggest that the disease spread from the USA to Canada and then to South Korea through imports of infected cervids (Otero et al., 2021). A retrospective analysis revealed that, in 1978, a Colorado‑born mule deer at Toronto Zoo in Ontario, Canada, died of CWD (Dubé et al., 2006). In 1996, the disease was detected in captive elk in Saskatchewan (Williams and Miller, 2002).
The disease
Department for Environment, Food and Rural Affairs
has since been detected in captive cervids in Alberta and Quebec and free-ranging cervids in Alberta, British Columbia, Manitoba and Saskatchewan (USGS, 2025). The origin of the outbreak in free-ranging Canadian cervids is unknown (Otero et al., 2021).
While the spread of CWD across North America is often described as ‘rapid,’ it has been suggested that this may reflect widening disease surveillance, rather than a ‘real-time’ indication of geographic spread. CWD epidemics appear to develop relatively slowly compared with other wildlife diseases (EFSA BIOHAZ Panel, 2023). Field and modelling data from North America suggest that it may take 15 to 20 years for CWD prevalence to reach 1% in free-ranging cervid populations, although more rapid transmission may occur in captive populations. The surveillance sensitivity in North America means that the disease may have been present for 10 years or more in some areas before it was detected (Miller et al., 2000).
The prevalence of CWD in affected populations or species varies across North America. In captive herds, prevalence may reach 100% over time, while in affected free-ranging populations, reported prevalence ranges from <1% to >30%. Most clinical cases are observed in cervids 2 to 7 years old, especially males, which is believed to be due to behavioural differences rather than differences in susceptibility between sexes (EFSA BIOHAZ Panel, 2023). At least 13 different risk factors may contribute towards CWD spread in North America, such as host genetics, high deer density or inappropriate disposal of deer carcasses and slaughter by-products (EFSA BIOHAZ Panel, 2019).
Approaches towards CWD control and surveillance in captive and free-ranging deer vary widely across North America within and between jurisdictions (CIDRAP, 2025). A summary of the measures in place in each US state and Canadian province is available from the CWD Alliance (2026), a coalition of wildlife conservation agencies, dedicated to providing accurate information on CWD and supporting strategies to minimise its impact on free-ranging cervids. Wildlife agencies rely on voluntary testing of hunted deer carcasses as the main mechanism for CWD surveillance and management, usually using post-mortem ELISA or immunohistochemistry methods (CIDRAP, 2025).
In the USA, Animal and Plant Health Inspection Service (APHIS) operates the CWD Herd Certification Programme (HCP) in collaboration with state and wildlife agencies. This is a voluntary scheme which aims to provide a consistent, national approach to controlling CWD in farmed cervids and preventing interstate spread by establishing control measures such as fencing, detailed record keeping and CWD testing of all cervids over 12 months old that die for any reason. The Canadian Food Inspection Agency (CFIA) operates a similar programme, the CWD Herd Certification Programme. As of December 2025, 28 states were participating in the USA’s CWD HCP and 5 Canadian provinces and one Canadian territory were participating in the Canadian programme (USDA, 2025b, CFIA, 2025).
Control methods fall within three general categories: prevention, containment, and control and suppression. Prevention and containment aim to prevent CWDDepartment for Environment, Food and Rural Affairs introduction into areas where it has not previously been reported and to limit its geographical spread once it has been introduced, respectively. Both tend to include regulatory measures such as bans on the movement of live cervids, cervid carcasses or specified risk materials. Control and suppression aim to stabilise or reduce infection rates within a herd or population through measures such as selective or random culling (EFSA BIOHAZ Panel, 2017).
Despite control efforts, CWD has continued to spread among captive and free- ranging cervids in North America, with increasing prevalence in affected areas (Uehlinger et al., 2016, CFSPH, 2024). Eradicating CWD from North America appears infeasible due to its extent of geographic spread and epidemiological characteristics, such as environmental persistence (EFSA BIOHAZ Panel, 2017).
CWD in wild pigs in the USA
Wild pigs are an invasive population in the USA, especially in the south (Figure 2). They comprise escaped domestic swine, Eurasian wild boar and hybrids of the two (Smyser et al., 2020). Wild pigs frequently coexist with cervids in areas where CWD is endemic and may be exposed to CWD prions through rooting in contaminated soil, scavenging deer carcasses and predation on fawns. These ecological interactions provide multiple routes by which wild pigs could encounter prions from infected deer (Soto et al. 2025).
Under experimental conditions, domestic pigs can become infected with CWD by oral and intracerebral routes, suggesting that wild pigs might also be susceptible. Domestic pigs rarely develop clinical signs of CWD but accumulate prions in the lymphoid tissues in their heads and gut, suggesting that, like cervids, they could shed the prions in saliva and faeces (Moore et al., 2017).
Against this background, Soto et al. (2025) investigated potential interactions between wild pigs and CWD prions. They analysed over 300 brain and lymph node samples from 178 wild pigs living across Arkansas and Texas, USA. The animals were captured by the United States Department of Agriculture (USDA) between 2020 and 2021. None of the pigs included in the study were reported to be displaying clinical signs of disease.
Using an ultra-sensitive laboratory method (protein misfolding cyclic amplification (PMCA)), the researchers identified CWD prions in up to 37% of the lymph node samples and 15% of brain samples. The lowest detection rates were in the Texas samples (below 16%), matching the lower CWD prevalence in the state’s cervid population. These findings indicate that wild pigs are naturally exposed to CWD prions in areas where the disease is present (Soto et al., 2025).
When intracerebrally inoculated with tissues from wild pigs, a small proportion of mice expressing deer prion protein developed subclinical prion infection. No transmission was detected in mice expressing pig prion protein. This suggests that wild pig tissues only contain low levels of infectious prions and that wild pigs are relatively resistant to natural infection. However, they could still contribute to CWD transmission, influencing its epidemiology, geographic distribution and interspecies spread (Soto et al., 2025).Department for Environment, Food and Rural Affairs While their exact role and importance in CWD transmission is unclear, wild pigs have considerable home ranges in North America (1.1 to 5.32 km on average), which may increase when food is scarce. This mobility could complicate efforts to control the disease if they play a role in its transmission (Soto et al., 2025).
The USDA’s APHIS does not currently conduct active surveillance for CWD in wild pigs (USDA, 2025a).
Figure 2. Geographic distribution of wild pigs (purple) in the USA as of 27 January 2025, comprising escaped domestic pigs, Eurasian wild boar and hybrids of the two (adapted from USDA, 2026). Yellow (Texas) and green (Arkansas) circles indicate the states where CWD prions were detected in wild pig tissues.
Department for Environment, Food and Rural Affairs
Implications for Great Britain
CWD is a notifiable animal disease in Great Britain, but no cases have ever been reported (Defra and APHA, 2018, CIDRAP, 2025).
The introduction of CWD into Great Britain’s cervid population could have devastating socio-economic and animal welfare impacts, resulting in marked population declines, as seen in the USA (Miller et al., 2008). There could also be significant losses to cervid farming, hunting and rural tourism industries, as well as significant costs associated with controlling the spread of the disease. The UK venison market alone is worth an estimated £100 million (Scotland Food and Drink, 2018).
There are several discrete wild pig populations in Great Britain, including wild boar and feral pigs. The largest known population is in the Forest of Dean in Gloucestershire, with an estimated 583 wild boar as of 2025/2026, although Forestry England (2025) aims to reduce the number to 400 to protect other species, such as plants and insects. Pockets of wild boar and feral pigs exist in other parts of the country, but their exact numbers are unknown (Mathews et al., 2018). The potential impact of CWD introduction into Great Britain’s wild pig population is uncertain because their role in disease transmission remains unclear. While they appear to be relatively resistant to natural CWD infection and disease, they could potentially contribute towards the maintenance and spread of CWD in Great Britain’s cervid population (Soto et al., 2025).
To reduce the risk of CWD introduction, Great Britain suspended the import of live cervids and high-risk cervid products in June 2023, including urine hunting lures, from all countries where CWD has been reported. Fresh cervid meat, excluding offal and spinal cord, can only be imported into Great Britain from CWD-affected countries if it has tested negative for CWD using an approved diagnostic method, such as immunohistochemistry, and originates from an area where CWD has not been reported or officially suspected in the last 3 years (Defra and APHA, 2026).
The current risk of CWD prions being introduced into Great Britain’s wild pig or cervid population ranges from very low (event is very rare but cannot be excluded) to negligible (event is so rare it does not merit consideration). This is based on the risk of incursion tool, developed by Roberts et al., (2011). It is also supported by a recent Defra and APHA (2025) risk assessment. While this assessment identified a few theoretical entry pathways, such as contaminated equipment, that could not be fully assessed due to limited data, there is no definitive evidence that they have ever resulted in the introduction of CWD into a new area.
Detection of CWD prions in wild pigs in the USA is unlikely to affect Great Britain’s CWD risk level, as the USA is not approved to export live wild pigs to Great Britain (Defra, 2025). Import of infected wild pig meat or wild pig by-products from the USA could theoretically introduce CWD prions into Great Britain, but the risk of this is also very low. To date, CWD prions have only been reported in lymph node and brain tissue samples in wild pigs, at levels too low to cause disease in mouse models
Department for Environment, Food and Rural Affairs
(Soto et al., 2025). However, their presence in other tissues cannot be excluded. The USA is approved to export wild pig meat and certain wild pig by-products to Great Britain, excluding offal, minced meat and germplasm (Defra, 2025), but there appears to be limited trade in these commodities.
It is difficult to quantify the exact amount of wild pig meat exported to Great Britain, as available trade data does not always distinguish between meat of wild and domestic pigs. However, based on HMRC data, the last known export of non- domestic pig meat from the USA to Great Britain was in 2013 (4,881 kg).
Conclusion
CWD has continued to spread among captive and free-ranging cervids in North America since it was first detected in the 1960s. The finding of CWD prions in wild pigs in the USA suggests they could contribute towards transmission of the disease, influencing its epidemiology, geographic distribution and interspecies spread. However, further research is needed to confirm this. CWD has never been reported in Great Britain and the current risk of CWD prions being introduced into Great Britain’s wild pig or cervid population ranges from very low to negligible.
Readers are reminded to be vigilant for signs of CWD. Information on how to spot the disease can be found here. Suspected cases must be reported immediately to the Defra Rural Services Helpline on 03000 200 301. In Wales, call 0300 303 8268. In Scotland, contact your local Field Services Office. Failure to do so is an offence. We will continue to monitor the situation.
Authors • Lawrence Finn • Dr. Lauren Perrin • John Spiropoulos • Dr. Helen RobertsDepartment for Environment, Food and Rural Affairs
References
snip…see;
https://assets.publishing.service.gov.uk/media/697a3b013c71d838df6bd413/CWD_Prions_in_Cervids_and_Wild_Pigs_in_North_America.pdf
Shedding, retention and spreading of chronic wasting disease prions in the environment
Project Number 2R01AI132695-06A1 Former Number 2R01AI132695-06 Contact PI/Project Leader MORALES, RODRIGO
Abstract Text
ABSTRACT
Chronic Wasting Disease (CWD) is a prion disease affecting natural and captive cervid populations. This disease is progressively spreading across the United States and new foci of infectivity are constantly being reported. Despite decades of research, there are still several unanswered questions concerning CWD.
Compelling evidence suggest that CWD prions enter the environment through carcasses from diseased animals or by the progressive accumulation of prions shed in excreta. Unfortunately, the role that plants, parasites, predators, and scavengers play in CWD spreading has been poorly studied. During the past funding cycle, our group made important technical and conceptual contributions in this field.
Data from our group and others (in collaboration) demonstrate that plants can bind prions into their surfaces as well as transport them from soils to leaves. This is relevant, considering that prions are shown to progressively accumulate in soils and strongly suggests plants as potential vectors for CWD transmission. Unfortunately, the previously mentioned evidence has been collected using proof-of-concept conditions, including the exposure of high titers of rodent (laboratory generated) adapted prions, and grass plants only.
We have generated preliminary data showing that carrots grown in CWD infected soil carry prions in their roots and leaves as evaluated by bioassays. In contrast, tomato plants do not share these features. The significance of these findings cannot be ignored considering the interaction of CWD prions with a human and animal edible vegetable. Considering the use of carrots roots and leaves in human and animal nutrition, and the still unknown zoonotic potential of CWD, future research involving edible plants is urgently needed.
Another relevant (published) finding from our laboratory involves the high CWD infectivity titers found in nasal bots, a common cervid parasite that develops in the nasal cavity (a hotspot of prion infectivity). These parasites are found in large quantities in CWD pre- clinical and clinical deer, and may importantly contribute to environmental CWD transmission. Our research also identified CWD prions in naturally exposed flies, ticks, and dermestid beetles. However, the prion infectivity titers in these parasites have not been evaluated.
Finally, animals other than cervids, including hunters and scavengers, are expected to be exposed to CWD prions. Interestingly, we identified CWD prions and de novo generated porcine prions in tissues from wild pigs living in areas with variable CWD epidemiology. We plan to further investigate all these events and their relevance in natural prion transmission using a complementary set of techniques, including in vitro and in vivo systems. Emphasis will be made in analyzing the strain properties and zoonotic potentials of the prion agents under investigation. For this purpose, we gathered a unique group of collaborators able to supply us with the samples and expertise required to execute this project. Outcomes from this research are expected to deliver new insights on this animal prionopathy and provide regulatory agencies with useful information to control its continuous spread.
Public Health Relevance Statement
PROJECT NARRATIVE Despite decades of research, several questions remain unanswered for the Chronic Wasting Disease (CWD) epidemic affecting several deer species in the United States. Continuing with our previous R01 project, we will explore novel factors mediating the spread of CWD prions, including different plant types, invertebrate parasites (e.g., ticks, nasal bots) and scavengers (wild boars). These potential disease vectors will be studied for their ability to transmit disease within and across species, including humans.
https://reporter.nih.gov/search/VYlhnadNtUiur19eYeRPog/project-details/11227445#description
Infectious prions in brains and muscles of domestic pigs experimentally challenged with the BSE, scrapie, and CWD agents
Authors: Francisca Bravo-Risi, Fraser Brydon, Angela Chong, Kane Spicker, Justin J. Greenlee https://orcid.org/0000-0003-2202-3054, Glenn Telling, Claudio Soto https://orcid.org/0000-0002-3412-0524, Sandra Pritzkow, Marcelo A. Barria, Rodrigo Morales
ABSTRACT
Experimental studies suggest that animal species not previously described as naturally infected by prions are susceptible to prion diseases affecting sheep, cattle, and deer. These interspecies transmissions may generate prions with unknown host ranges. Pigs are susceptible to prions from different origins, including deer chronic wasting disease (CWD), sheep scrapie, and bovine spongiform encephalopathy (BSE). Here, we studied prions in brains and muscles from pigs previously infected with these different prion sources. Specifically, we measured the total prion protein (PrP) and PK-resistant PrP by western blot. Seeding activity in these tissues was evaluated using the protein misfolding cyclic amplification (PMCA) technique. We found that BSE-infected pigs contained substantially more seeding competent prions compared with those infected with CWD and scrapie. Moreover, the zoonotic potential of porcine-BSE prions seems to be relevant, as both brains and muscles from BSE-infected pigs induced the misfolding of the human prion protein in vitro. This study helps to understand the potential fate of naturally existing prion strains in a relevant host and calls for caution considering the co-existence between feral swine and other prion-susceptible animal species.
IMPORTANCE
Prions (PrPSc) are proteinaceous, infectious pathogens responsible for prion diseases. Some livestock are highly susceptible to prion diseases. These include cattle (bovine spongiform encephalopathy, BSE), sheep and goat (scrapie), and cervids (chronic wasting disease, CWD). Unfortunately, BSE has been reported to be naturally transmitted to humans and other animal species. Domestic pigs, a relevant livestock animal, have not been reported to be naturally affected by prions; however, they are susceptible to the experimental exposure to BSE, scrapie, and CWD prions. Given the widespread consumption of porcine food products by humans, we aimed to evaluate the levels of pig-derived BSE, scrapie, and CWD prions from experimentally challenged domestic pigs in brain and meat cuts (leg, cheek meat, skirt meat, and tenderloin). We detected pig-adapted prions in the brains and some muscles of these animals. Additionally, we evaluated the in vitro compatibility between pig prions and the human prion protein (as a surrogate of zoonosis). Our results show that only pig-derived BSE prions were able to induce the misfolding of the cellular human prion protein. This data highlights the consequences of prion spillovers to other animal species and their potential availability to humans.
Snip…
In summary, our data shows the dynamic of animal prions when exposed to infectious pigs, as well as their distributions and zoonotic potentials. The data presented here may be relevant to understanding the fate of naturally existing prions in a sympatric animal species relevant for human consumption. This acquires importance considering a recent report describing the interaction between CWD and wild pigs in natural settings.
https://journals.asm.org/doi/10.1128/mbio.01800-25
Volume 31, Number 1—January 2025
Dispatch
Detection of Prions in Wild Pigs (Sus scrofa) from Areas with Reported Chronic Wasting Disease Cases, United States
Paulina Soto, Francisca Bravo-Risi, Rebeca Benavente, Tucker H. Stimming, Michael J. Bodenchuk, Patrick Whitley, Clint Turnage, Terry R. Spraker, Justin Greenlee, Glenn Telling, Jennifer Malmberg, Thomas Gidlewski, Tracy Nichols, Vienna R. Brown, and Rodrigo Morales Author affiliation: The University of Texas Health Science Center at Houston, Texas, USA (P. Soto, F. Bravo-Risi, R. Benavente, T.H. Stimming, R. Morales); Centro Integrativo de Biologia y Quimica Aplicada, Universidad Bernardo O’Higgins, Santiago, Chile (P. Soto, F. Bravo-Risi, R. Morales); US Department of Agriculture, Fort Collins, Colorado, USA (M.J. Bodenchuk, P. Whitley, C. Turnage, J. Malmberg, T. Gidlewski, T. Nichols, V.R. Brown); Colorado State University, Fort Collins, Colorado, USA (T.R. Spraker, G. Telling); US Department of Agriculture, Ames, Iowa, USA (J. Greenlee)
Abstract
Using a prion amplification assay, we identified prions in tissues from wild pigs (Sus scrofa) living in areas of the United States with variable chronic wasting disease (CWD) epidemiology. Our findings indicate that scavenging swine could play a role in disseminating CWD and could therefore influence its epidemiology, geographic distribution, and interspecies spread.
Chronic wasting disease (CWD) is a prion disease of particular concern because of its uncontrolled contagious spread among various cervid species in North America
https://www.usgs.gov/media/images/distribution-chronic-wasting-disease-north-america
its recent discovery in Nordic countries (1), and its increasingly uncertain zoonotic potential (2). CWD is the only animal prion disease affecting captive as well as wild animals. Persistent shedding of prions by CWD-affected animals and resulting environmental contamination is considered a major route of transmission contributing to spread of the disease. Carcasses of CWD-affected animals represent relevant sources of prion infectivity to multiple animal species that can develop disease or act as vectors to spread infection to new locations.
Free-ranging deer are sympatric with multiple animal species, including some that act as predators, scavengers, or both. Experimental transmissions to study the potential for interspecies CWD transmissions have been attempted in raccoons, ferrets, cattle, sheep, and North American rodents (3–7). Potential interspecies CWD transmission has also been addressed using transgenic (Tg) mice expressing prion proteins (PrP) from relevant animal species (8). Although no reports of natural interspecies CWD transmissions have been documented, experimental studies strongly suggest the possibility for interspecies transmission in nature exists (3–7). Inoculation and serial passage studies reveal the potential of CWD prions to adapt to noncervid species, resulting in emergence of novel prion strains with unpredicted features (9–11).
Wild pigs (Sus scrofa), also called feral swine, are an invasive population comprising domestic swine, Eurasian wild boar, and hybrids of the 2 species (12). Wild pig populations have become established in the United States (Appendix Figure 1, panel A), enabled by their high rates of fecundity; omnivorous and opportunistic diet; and widespread, often human-mediated movement (13). Wild pigs scavenge carcasses on the landscape and have an intimate relationship with the soil because of their routine rooting and wallowing behaviors (14). CWD prions have been experimentally transmitted to domestic pigs by intracerebral and oral exposure routes (15), which is relevant because wild pigs coexist with cervids in CWD endemic areas and reportedly prey on fawns and scavenge deer carcasses. Considering the species overlap in many parts of the United States (Appendix Figure 1, panel 😎, we studied potential interactions between wild pigs and CWD prions.
Snip…
Conclusions
In summary, results from this study showed that wild pigs are exposed to cervid prions, although the pigs seem to display some resistance to infection via natural exposure. Future studies should address the susceptibility of this invasive animal species to the multiple prion strains circulating in the environment. Nonetheless, identification of CWD prions in wild pig tissues indicated the potential for pigs to move prions across the landscape, which may, in turn, influence the epidemiology and geographic spread of CWD.
https://wwwnc.cdc.gov/eid/article/31/1/24-0401_article
THURSDAY, JANUARY 08, 2026
Confucius Ponders, what about Wild Pigs (Sus scrofa) and CWD TSE Prion, and the Environment, what if?
Confucius Ponders, what about Wild Pigs (Sus scrofa), they can cover some distance rather quickly, what about Wild Pigs (Sus scrofa) digging up the terrain, and as they do it, what if these Wild Pigs (Sus scrofa) were exposed to CWD TSE Prion, and then they go on exposing and saturating the land with CWD TSE Prion, then the soil becomes contaminated with CWD TSE Prion, then what about the plants that grow from that soil for the decades to come, what if???
https://prpsc.proboards.com/thread/190/confucius-ponders-wild-pigs-scrofa
https://chronic-wasting-disease.blogspot.com/2026/01/confucius-ponders-what-about-wild-pigs.html
WEDNESDAY, JANUARY 28, 2026
Chronic wasting disease prions in cervids and wild pigs in North America Preliminary Outbreak
https://journals.asm.org/doi/10.1128/mbio.01800-25
https://wwwnc.cdc.gov/eid/article/31/1/24-0401_article
https://media.ark.org/agri/Moore_2017_Swine_CWD.pdf
https://transmissiblespongiformencephalopathy.blogspot.com/2026/01/chronic-wasting-disease-prions-in.html
***> CWD to sheep, Scrapie to Cervid
Chronic Wasting Disease CWD vs Scrapie TSE Prion
https://www.ars.usda.gov/research/publications/publication/?seqNo115=410511
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.
https://www.ars.usda.gov/research/publications/publication/?seqNo115=353091
https://www.ars.usda.gov/research/project/?accnNo=432011&fy=2017
https://www.ars.usda.gov/research/publications/publication/?seqNo115=337105
https://www.ars.usda.gov/research/publications/publication/?seqNo115=326166
***> However, at 51 months of incubation or greater, 5 animals were positive by one or more diagnostic methods. Furthermore, positive bioassay results were obtained from all inoculated groups (oral and intracranial; market weight and end of study) suggesting that swine are potential hosts for the agent of scrapie. <***
*** Although the current U.S. feed ban is based on keeping tissues from TSE infected cattle from contaminating animal feed, swine rations in the U.S. could contain animal derived components including materials from scrapie infected sheep and goats. These results indicating the susceptibility of pigs to sheep scrapie, coupled with the limitations of the current feed ban, indicates that a revision of the feed ban may be necessary to protect swine production and potentially human health. <***
***> Results: PrPSc was not detected by EIA and IHC in any RPLNs. All tonsils and MLNs were negative by IHC, though the MLN from one pig in the oral <6 month group was positive by EIA. PrPSc was detected by QuIC in at least one of the lymphoid tissues examined in 5/6 pigs in the intracranial <6 months group, 6/7 intracranial >6 months group, 5/6 pigs in the oral <6 months group, and 4/6 oral >6 months group. Overall, the MLN was positive in 14/19 (74%) of samples examined, the RPLN in 8/18 (44%), and the tonsil in 10/25 (40%).
***> Conclusions: This study demonstrates that PrPSc accumulates in lymphoid tissues from pigs challenged intracranially or orally with the CWD agent, and can be detected as early as 4 months after challenge. CWD-infected pigs rarely develop clinical disease and if they do, they do so after a long incubation period. This raises the possibility that CWD-infected pigs could shed prions into their environment long before they develop clinical disease. Furthermore, lymphoid tissues from CWD-infected pigs could present a potential source of CWD infectivity in the animal and human food chains.
https://www.ars.usda.gov/research/publications/publication/?seqNo115=353091
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
Research Project: Elucidating the Pathobiology and Transmission of Transmissible Spongiform Encephalopathies
Location: Virus and Prion Research
Title: Differentiation of scrapie from chronic wasting disease in white-tailed deer
snip…
Accomplishments
1. 01 Determined that white-tailed deer (WTD) infected with scrapie from sheep can transmit the disease to other deer under conditions mimicking natural exposure. It has long been suggested that prion disease in deer (chronic wasting disease (CWD)) was caused by the prion agent from sheep. The prion disease that affects sheep, scrapie, has been recognized for hundreds of years. However, chronic wasting disease, a similar disease found in WTD, has only been recognized since the 1960s. ARS researchers in Ames, Iowa, showed that white-tailed deer sick with scrapie from sheep can infect other deer under conditions mimicking natural exposure. Furthermore, this work shows that CWD is difficult to differentiate from WTD infected with scrapie. WTD scrapie prions accumulate in the lymphoreticular system in a manner similar to CWD, meaning that environmental contamination may occur through feces, saliva, and other body fluids of scrapie affected WTD as has been shown for CWD. The presence of WTD infected with scrapie could confound mitigation efforts for chronic wasting disease. This information informs regulatory officials, the farmed cervid industry, and officials tasked with protecting animal health such as state Departments of Agriculture, Natural Resources, or Parks and Wildlife with regard to a disease similar to CWD but arising from sheep scrapie that could be present in WTD that have contact with scrapie affected sheep and/or goats.
https://www.ars.usda.gov/research/project/?accnNo=440677&fy=202
Chronic Wasting Disease CWD vs Scrapie TSE Prion
Volume 30, Number 8—August 2024
Research
Scrapie Versus Chronic Wasting Disease in White-Tailed Deer
Zoe J. Lambert1, Jifeng Bian, Eric D. Cassmann, M. Heather West Greenlee, and Justin J. Greenlee
Author affiliations: Oak Ridge Institute for Science and Education, Oak Ridge, Tennessee, USA (Z.J. Lambert); US Department of Agriculture, Ames, Iowa, USA (Z.J. Lambert, J. Bian, E.D. Cassmann, J.J. Greenlee); Iowa State University, Ames (Z.J. Lambert, M.H. West Greenlee) Suggested citation for this article
Abstract
White-tailed deer are susceptible to scrapie (WTD scrapie) after oronasal inoculation with the classical scrapie agent from sheep. Deer affected by WTD scrapie are difficult to differentiate from deer infected with chronic wasting disease (CWD). To assess the transmissibility of the WTD scrapie agent and tissue phenotypes when further passaged in white-tailed deer, we oronasally inoculated wild-type white-tailed deer with WTD scrapie agent. We found that WTD scrapie and CWD agents were generally similar, although some differences were noted. The greatest differences were seen in bioassays of cervidized mice that exhibited significantly longer survival periods when inoculated with WTD scrapie agent than those inoculated with CWD agent. Our findings establish that white-tailed deer are susceptible to WTD scrapie and that the presence of WTD scrapie agent in the lymphoreticular system suggests the handling of suspected cases should be consistent with current CWD guidelines because environmental shedding may occur.
snip…
The potential for zoonoses of cervid-derived PrPSc is still not well understood (6,18,45–47); however, interspecies transmission can increase host range and zoonotic potential (48–50). Therefore, to protect herds and the food supply, suspected cases of WTD scrapie should be handled the same as cases of CWD.
https://wwwnc.cdc.gov/eid/article/30/8/24-0007_article
Western blots done on samples from the brainstem, cerebellum, and lymph nodes of scrapie-infected WTD have a molecular profile similar to CWD and distinct from western blots of samples from the cerebral cortex, retina, or the original sheep scrapie inoculum. WTD are susceptible to the agent of scrapie from sheep and differentiation from CWD may be difficult.
https://www.ars.usda.gov/research/publications/publication/?seqNo115=336834 Component 6: Transmissible Spongiform Encephalopathies
Sheep scrapie agent can infect white-tailed deer after oronasal exposure.
The origin of chronic wasting disease (CWD) is not known, but it has many similarities to the sheep prion disease called scrapie. It has long been hypothesized that CWD arose through transmission of sheep scrapie to deer. ARS researchers in Ames, Iowa, conducted research to determine if scrapie derived from sheep could be transmitted to white-tailed deer. The deer inoculated with sheep scrapie developed clinical signs and the abnormal prion protein could be detected in a wide range of tissues. These results indicate that deer may be susceptible to sheep scrapie if exposed to the disease in natural or agricultural settings. In addition, several strong similarities between CWD in white-tailed deer and the experimental cases of scrapie in white-tailed deer suggests that it would be difficult to distinguish scrapie from CWD in deer or identify scrapie if a case occurs. This information should be considered by deer farmers for keeping their herds free from prion diseases.
https://www.ars.usda.gov/ARSUserFiles/np103/AnnualReports/NP103%20FY2023%20Annual%20Report_Final.pdf
It has long been hypothesized that CWD arose through transmission of sheep scrapie to deer. ARS researchers in Ames, Iowa, conducted research to determine if scrapie derived from sheep could be transmitted to white-tailed deer. The deer inoculated with sheep scrapie developed clinical signs and the abnormal prion protein could be detected in a wide range of tissues. These results indicate that deer may be susceptible to sheep scrapie if exposed to the disease in natural or agricultural settings. In addition, several strong similarities between CWD in white-tailed deer and the experimental cases of scrapie in white-tailed deer suggests that it would be difficult to distinguish scrapie from CWD in deer or identify scrapie if a case occurs. This information should be considered by deer farmers for keeping their herds free from prion diseases.
https://www.ars.usda.gov/ARSUserFiles/np103/AnnualReports/NP103%20FY2023%20Annual%20Report_Final.pdf
***> CWD to Primates and Humans, what if?
So, this is what we leave our children and grandchildren?
***> CWD TSE Prion Zoonotic Zoonosis Humans, What if? <***
CDC CWD TSE Prion Update 2025
KEY POINTS
Chronic wasting disease affects deer, elk and similar animals in the United States and a few other countries.
The disease hasn't been shown to infect people.
However, it might be a risk to people if they have contact with or eat meat from animals infected with CWD.
https://www.cdc.gov/chronic-wasting/about/index.html
Prions in Muscles of Cervids with Chronic Wasting Disease, Norway
Volume 31, Number 2—February 2025
Research
Prions in Muscles of Cervids with Chronic Wasting Disease, Norway
Snip…
In summary, the results of our study indicate that prions are widely distributed in peripheral and edible tissues of cervids in Norway, including muscles. This finding highlights the risk of human exposure to small amounts of prions through handling and consuming infected cervids.
Appendix
https://wwwnc.cdc.gov/eid/article/31/2/24-0903-app1.pdf
https://wwwnc.cdc.gov/eid/article/31/2/24-0903_article
Volume 31, Number 2—February 2025
Dispatch
Detection of Chronic Wasting Disease Prions in Raw, Processed, and Cooked Elk Meat, Texas, USA
Snip…
Of note, our data show that exposure to high temperatures used to cook the meat increased the availability of prions for in vitro amplification. Considering the potential implications in food safety and public health, we believe that the findings described in this study warrant further research. Our results suggest that although the elk meat used in this study resisted different manipulations involved in subsequent consumption by humans, their zoonotic potential was limited. Nevertheless, even though no cases of CWD transmission to human have been reported, the potential for human infection is still unclear and continued monitoring for zoonotic potential is warranted.
https://wwwnc.cdc.gov/eid/article/31/2/24-0906_article
Detection of chronic wasting disease prions in processed meats
Results: Our results show positive prion detection in all the samples analyzed using deer and elk substrates. Surprisingly, cooked meats displayed increased seeding activities. This data suggests that CWD-prions are available to people even after meats are processed and cooked.
Conclusions: These results suggest CWD prions are accessible to humans through meats, even after processing and cooking. Considering the fact that these samples were collected from already processed specimens, the availability of CWD prions to humans is probably underestimated.
"Our results show positive prion detection in all the samples analyzed using deer and elk substrates. Surprisingly, cooked meats displayed increased seeding activities."
Meeting-book-final-version prion 2023 Prion 2023 Congress Organizing Committee and the NeuroPrion Association, we invite you to join us for the International Conference Prion2023 from 16-20 October 2023 in Faro, Portugal.
https://prion2023.org/wp-content/uploads/2023/10/Meeting-book-final-version2.pdf
https://web.archive.org/web/20250828201533/https://prion2023.org/wp-content/uploads/2023/10/Meeting-book-final-version2.pdf
https://www.researchgate.net/profile/Syed-Zahid-Shah/publication/378314391_Meeting-book-final-version_prion_2023/links/65d44dad28b7720cecdca95f/Meeting-book-final-version-prion-2023.pdf
DETECTION OF CHRONIC WASTING DISEASE PRIONS IN PROCESSED MEATS.
In this study, we analyzed different processed meats derived from a pre-clinical, CWD-positive free-ranging elk. Products tested included filets, sausages, boneless steaks, burgers, ham steaks, seasoned chili meats, and spiced meats. CWD-prion presence in these products were assessed by PMCA using deer and elk substrates. Our results show positive prion detection in all products. To confirm the resilience of CWD-prions to traditional cooking methods, we grilled and boiled the meat products and evaluated them for any remnant PMCA seeding activity. Results confirmed the presence of CWD-prions in these meat products suggesting that infectious particles may still be available to people even after cooking. Our results strongly suggest ongoing human exposure to CWD-prions and raise significant concerns of zoonotic transmission through ingestion of CWD contaminated meat products.
Products tested included filets, sausages, boneless steaks, burgers, ham steaks, seasoned chili meats, and spiced meats.
CWD-prion presence in these products were assessed by PMCA using deer and elk substrates.
Our results show positive prion detection in all products.
Results confirmed the presence of CWD-prions in these meat products suggesting that infectious particles may still be available to people even after cooking.
Our results strongly suggest ongoing human exposure to CWD-prions and raise significant concerns of zoonotic transmission through ingestion of CWD contaminated meat products.
https://intcwdsympo.files.wordpress.com/2023/06/final-agenda-with-abstracts.pdf?force_download=true
Transmission of prion infectivity from CWD-infected macaque tissues to rodent models demonstrates the zoonotic potential of chronic wasting disease.
Further passage to cervidized mice revealed transmission with a 100% attack rate.
Our findings demonstrate that macaques, considered the best model for the zoonotic potential of prions, were infected upon CWD challenge, including the oral one.
The disease manifested as atypical in macaques and initial transgenic mouse transmissions, but with infectivity present at all times, as unveiled in the bank vole model with an unusual tissue tropism.
Epidemiologic surveillance of prion disease among cervid hunters and people likely to have consumed venison contaminated with chronic wasting disease
=====
https://intcwdsympo.files.wordpress.com/2023/06/final-agenda-with-abstracts.pdf?force_download=true
Fortuitous generation of a zoonotic cervid prion strain
Aims: Whether CWD prions can infect humans remains unclear despite the very substantial scale and long history of human exposure of CWD in many states or provinces of USA and Canada. Multiple in vitro conversion experiments and in vivo animal studies indicate that the CWD-to-human transmission barrier is not unbreakable. A major long-term public health concern on CWD zoonosis is the emergence of highly zoonotic CWD strains. We aim to address the question of whether highly zoonotic CWD strains are possible.
Materials and Methods: We inoculated several sCJD brain samples into cervidized transgenic mice (Tg12), which were intended as negative controls for bioassays of brain tissues from sCJD cases who had potentially been exposed to CWD. Some of the Tg12mice became infected and their brain tissues were further examined by Western blot as well as serial passages in humanized or cervidized mice.
Results: Passage of sCJDMM1 in transgenic mice expressing elk PrP (Tg12) resulted in a “cervidized” CJD strain that we termed CJDElkPrP. We observed 100% transmission of the original CJDElkPrP in transgenic mice expressing human PrP. We passaged CJDElkPrP two more times in the Tg12mice. We found that such second and third passage CJDElkPrP prions retained 100% transmission rate in the humanized mice, despite that the natural elk CWD isolates and CJDElkPrP share the same elk PrP sequence. In contrast, we and others found zero or poor transmission of natural elk CWD isolates in humanized mice.
Conclusions: Our data indicate that highly zoonotic cervid prion strains are not only possible but also can retain zoonotic potential after serial passages in cervids, suggesting a very significant and serious long-term risk of CWD zoonosis given that the broad and continuing spread of CWD prions will provide fertile grounds for the emergence of zoonotic CWD strains over time.
https://prion2023.org/wp-content/uploads/2023/10/Meeting-book-final-version2.pdf
https://web.archive.org/web/20250828201533/https://prion2023.org/wp-content/uploads/2023/10/Meeting-book-final-version2.pdf
https://www.researchgate.net/profile/Syed-Zahid-Shah/publication/378314391_Meeting-book-final-version_prion_2023/links/65d44dad28b7720cecdca95f/Meeting-book-final-version-prion-2023.pdf
Transmission of cervid prions to humanized mice demonstrates the zoonotic potential of CWD
Samia Hannaoui1 · Irina Zemlyankina1 · Sheng Chun Chang1 · Maria Immaculata Arifn1 · Vincent Béringue2 · Debbie McKenzie3 · Hermann M. Schatzl1 · Sabine Gilch1
Received: 24 May 2022 / Revised: 5 August 2022 / Accepted: 7 August 2022
© The Author(s) 2022
Abstract
Prions cause infectious and fatal neurodegenerative diseases in mammals. Chronic wasting disease (CWD), a prion disease of cervids, spreads efficiently among wild and farmed animals. Potential transmission to humans of CWD is a growing concern due to its increasing prevalence. Here, we provide evidence for a zoonotic potential of CWD prions, and its probable signature using mice expressing human prion protein (PrP) as an infection model. Inoculation of these mice with deer CWD isolates resulted in atypical clinical manifestation with prion seeding activity and efficient transmissible infectivity in the brain and, remarkably, in feces, but without classical neuropathological or Western blot appearances of prion diseases. Intriguingly, the protease-resistant PrP in the brain resembled that found in a familial human prion disease and was transmissible upon second passage. Our results suggest that CWD might infect humans, although the transmission barrier is likely higher compared to zoonotic transmission of cattle prions. Notably, our data suggest a different clinical presentation, prion signature, and tissue tropism, which causes challenges for detection by current diagnostic assays. Furthermore, the presence of infectious prions in feces is concerning because if this occurs in humans, it is a source for human-to-human transmission. These findings have strong implications for public health and CWD management.
Keywords Chronic wasting disease · CWD · Zoonotic potential · Prion strains · Zoonotic prions
HIGHLIGHTS OF THIS STUDY
================================
Our results suggest that CWD might infect humans, although the transmission barrier is likely higher compared to zoonotic transmission of cattle prions. Notably, our data suggest a different clinical presentation, prion signature, and tissue tropism, which causes challenges for detection by current diagnostic assays. Furthermore, the presence of infectious prions in feces is concerning because if this occurs in humans, it is a source for human-to-human transmission. These findings have strong implications for public health and CWD management.
In this study, we evaluated the zoonotic potential of CWD using a transgenic mouse model overexpressing human M129-PrPC (tg650 [12]). We inoculated tg650mice intracerebrally with two deer CWD isolates, Wisc-1 and 116AG [22, 23, 27, 29]. We demonstrate that this transgenic line was susceptible to infection with CWD prions and displayed a distinct leading clinical sign, an atypical PrPSc signature and unusual fecal shedding of infectious prions. Importantly, these prions generated by the human PrP transgenic mice were transmissible upon passage. Our results are the first evidence of a zoonotic risk of CWD when using one of the most common CWD strains, Wisc-1/CWD1 for infection. We demonstrated in a human transgenic mouse model that the species barrier for transmission of CWD to humans is not absolute. The fact that its signature was not typical raises the questions whether CWD would manifest in humans as a subclinical infection, whether it would arise through direct or indirect transmission including an intermediate host, or a silent to uncovered human-to-human transmission, and whether current detection techniques will be suffcient to unveil its presence.
Our findings strongly suggest that CWD should be regarded as an actual public health risk. Here, we use humanized mice to show that CWD prions can cross the species barrier to humans, and remarkably, infectious prions can be excreted in feces.
Our results indicate that if CWD crosses the species-barrier to humans, it is unlikely to resemble the most common forms of human prion diseases with respect to clinical signs, tissue tropism and PrPSc signature. For instance, PrPSc in variable protease-sensitive prionopathy (VPSPr), a sporadic form of human prion disease, and in the genetic form Gerstmann-Sträussler-Scheinker syndrome (GSS) is defined by an atypical PK-resistant PrPSc fragment that is non-glycosylated and truncated at both C- and N-termini, with a molecular weight between 6 and 8 kDa [24, 44–46]. These biochemical features are unique and distinctive from PrPSc (PrP27-30) found in most other human or animal prion disease. The atypical PrPSc signature detected in brain homogenate of tg650 mice #321 (1st passage) and #3063 (2nd passage), and the 7–8 kDa fragment (Figs. 2, 4) are very similar to that of GSS, both in terms of migration profile and the N-terminal cleavage site.
CWD in humans might remain subclinical but with PrPSc deposits in the brain with an unusual morphology that does not resemble the patterns usually seen in different prion diseases (e.g., mouse #328; Fig. 3), clinical with untraceable abnormal PrP (e.g., mouse #327) but still transmissible and uncovered upon subsequent passage (e.g., mouse #3063; Fig. 4), or prions have other reservoirs than the usual ones, hence the presence of infectivity in feces (e.g., mouse #327) suggesting a potential for human-to-human transmission and a real iatrogenic risk that might be unrecognizable.
“suggesting a potential for human-to-human transmission and a real iatrogenic risk that might be unrecognizable.”
=================================
Supplementary Information The online version contains supplementary material available at
https://doi.org/10.1007/s00401-022-02482-9
snip...see full text;
https://link.springer.com/article/10.1007/s00401-022-02482-9
https://link.springer.com/content/pdf/10.1007/s00401-022-02482-9.pdf
Transmission of Cervid Prions to Humanized Mice Demonstrates the Zoonotic Potential of CWD
Samia Hannaouia, Irina Zemlyankinaa, Sheng Chun Changa, Maria Immaculata Arifina, Vincent Béringueb, Debbie McKenziec, Hermann M. Schatzla, and Sabine Gilcha
Results: Here, we provide the strongest evidence supporting the zoonotic potential of CWD prions, and their possible phenotype in humans. Inoculation of mice expressing human PrPCwith deer CWD isolates (strains Wisc-1 and 116AG) resulted in atypical clinical manifestations in > 75% of the mice, with myoclonus as leading clinical sign. Most of tg650brain homogenates were positive for seeding activity in RT-QuIC. Clinical disease and presentation was transmissible to tg650mice and bank voles. Intriguingly, protease-resistant PrP in the brain of tg650 mice resembled that found in a familial human prion disease and was transmissible upon passage. Abnormal PrP aggregates upon infection with Wisc-1 were detectable in thalamus, hypothalamus, and midbrain/pons regions.
Unprecedented in human prion disease, feces of CWD-inoculated tg650 mice harbored prion seeding activity and infectious prions, as shown by inoculation of bank voles and tg650 with fecal homogenates.
Conclusions: This is the first evidence that CWD can infect humans and cause disease with a distinctive clinical presentation, signature, and tropism, which might be transmissible between humans while current diagnostic assays might fail to detect it. These findings have major implications for public health and CWD-management.
https://www.tandfonline.com/doi/full/10.1080/19336896.2022.2091286
Macaque tissues to rodent models demonstrates the zoonotic potential of chronic wasting disease.
Samia Hannaoui1,2, Ginny Cheng1,2, Wiebke Wemheuer3, Walter Schulz-Schaeffer3, Sabine Gilch1,2, Hermann Schatzl1,2 1University of Calgary, Calgary, Canada. 2Calgary Prion Research Unit, Calgary, Canada. 3Institute of Neuropathology, Medical Faculty, Saarland University, Homburg/Saar, Germany
Snip…
***> Further passage to cervidized mice revealed transmission with a 100% attack rate.
***> Our findings demonstrate that macaques, considered the best model for the zoonotic potential of prions, were infected upon CWD challenge, including the oral one.
****> The disease manifested as atypical in macaques and initial transgenic mouse transmissions, but with infectivity present at all times, as unveiled in the bank vole model with an unusual tissue tropism.
***> Epidemiologic surveillance of prion disease among cervid hunters and people likely to have consumed venison contaminated with chronic wasting disease
=====
https://intcwdsympo.files.wordpress.com/2023/06/final-agenda-with-abstracts.pdf?force_download=true
18. Zoonotic potential of moose-derived chronic wasting disease prions after adaptation in intermediate species
Tomás Barrioa, Jean-Yves Doueta, Alvina Huora, Séverine Lugana, Naïma Arona, Hervé Cassarda, Sylvie L. Benestadb, Juan Carlos Espinosac, Juan María Torresc, Olivier Andréolettia
aUnité Mixte de Recherche de l’Institut National de Recherche pour l’Agriculture, l’Alimentation et l’Environnement 1225 Interactions Hôtes-Agents Pathogènes, École Nationale Vétérinaire de Toulouse, 31076 Toulouse, France; bNorwegian Veterinary Institute, P.O. Box 64, NO-1431 Ås, Norway; cCentro de Investigación en Sanidad Animal (CISA-INIA), 28130, Valdeolmos, Madrid, Spain
Aims: Chronic wasting disease (CWD) is an emerging prion disease in Europe. To date, cases have been reported in three Nordic countries and in several species, including reindeer (Rangifer tarandus), moose (Alces alces) and red deer (Cervus elaphus). Cumulating data suggest that the prion strains responsible for the European cases are distinct from those circulating in North America. The biological properties of CWD prions are still poorly documented, in particular their spillover and zoonotic capacities. In this study, we aimed at characterizing the interspecies transmission potential of Norwegian moose CWD isolates.
Materials and Methods: For that purpose, we performed experimental transmissions in a panel of transgenic models expressing the PrPC sequence of various species.
Results: On first passage, one moose isolate propagated in the ovine PrPC-expressing model (Tg338). After adaptation in this host, moose CWD prions were able to transmit in mice expressing either bovine or human PrPC with high efficacy.
Conclusions: These results suggest that CWD prions can acquire enhanced zoonotic properties following adaptation in an intermediate species.
Funding
Grant number: AAPG2020 EU-CWD, ICRAD2020 TCWDE, NRC2022 NorCWD
Acknowledgement
https://www.tandfonline.com/doi/full/10.1080/19336896.2024.2424058
“ After adaptation in this host, moose CWD prions were able to transmit in mice expressing either bovine or human PrPC with high efficacy.”
“Also, we do not claim that "no-one has ever been infected with prion disease from eating venison." Our conclusion stating that we found no strong evidence of CWD transmission to humans in the article you quoted or in any other forum is limited to the patients we investigated.”
*** now, let’s see what the authors said about this casual link, personal communications years ago, and then the latest on the zoonotic potential from CWD to humans from the TOKYO PRION 2016 CONFERENCE.
see where it is stated NO STRONG evidence. so, does this mean there IS casual evidence ????
“Our conclusion stating that we found no strong evidence of CWD transmission to humans”
Subject: CWD aka MAD DEER/ELK TO HUMANS ???
Date: September 30, 2002 at 7:06 am PST
From: "Belay, Ermias"
To: Cc: "Race, Richard (NIH)" ; ; "Belay, Ermias"
Sent: Monday, September 30, 2002 9:22 AM
Subject: RE: TO CDC AND NIH - PUB MED- 3 MORE DEATHS - CWD - YOUNG HUNTERS
Dear Sir/Madam, In the Archives of Neurology you quoted (the abstract of which was attached to your email), we did not say CWD in humans will present like variant CJD.. That assumption would be wrong. I encourage you to read the whole article and call me if you have questions or need more clarification (phone: 404-639-3091).
Also, we do not claim that "no-one has ever been infected with prion disease from eating venison." Our conclusion stating that we found no strong evidence of CWD transmission to humans in the article you quoted or in any other forum is limited to the patients we investigated.
Ermias Belay, M.D. Centers for Disease Control and Prevention
Subject: TO CDC AND NIH - PUB MED- 3 MORE DEATHS - CWD - YOUNG HUNTERS
Sunday, November 10, 2002 6:26 PM .......snip........end..............TSS
-----Original Message-----
From:
Sent: Sunday, September 29, 2002 10:15 AM
To: rr26k@nih.gov; rrace@niaid.nih.gov; ebb8@CDC.GOV
Subject: TO CDC AND NIH - PUB MED- 3 MORE DEATHS - CWD - YOUNG HUNTERS
Sunday, November 10, 2002 6:26 PM .......snip........end..............TSS
Thursday, April 03, 2008
A prion disease of cervids: Chronic wasting disease 2008 1: Vet Res. 2008 Apr 3;39(4):41 A prion disease of cervids: Chronic wasting disease Sigurdson CJ.
snip...
*** twenty-seven CJD patients who regularly consumed venison were reported to the Surveillance Center, however there have been no unusual or novel prion subtypes that might indicate the appearance of a new prion strain [7, 41].
snip... full text ;
https://www.vetres.org/articles/vetres/abs/2008/04/v08092/v08092.html
https://chronic-wasting-disease.blogspot.com/2008/04/prion-disease-of-cervids-chronic.html
“regular venison eating associated with a 9 FOLD INCREASE IN RISK OF CJD”
Subject: Re: DEER SPONGIFORM ENCEPHALOPATHY SURVEY & HOUND STUDY
Date: Fri, 18 Oct 2002 23:12:22 +0100
From: Steve Dealler Reply-To: Bovine Spongiform Encephalopathy Organization: Netscape Online member
To: BSE-L@ …
######## Bovine Spongiform Encephalopathy <BSE-L@UNI-KARLSRUHE.DE> #########
Dear Terry,
An excellent piece of review as this literature is desparately difficult to get back from Government sites. What happened with the deer was that an association between deer meat eating and sporadic CJD was found in about 1993. The evidence was not great but did not disappear after several years of asking CJD cases what they had eaten. I think that the work into deer disease largely stopped because it was not helpful to the UK industry...and no specific cases were reported.
Well, if you dont look adequately like they are in USA currenly then you wont find any!
Steve Dealler
########### http://mailhost.rz.uni-karlsruhe.de/warc/bse-l.html ############
Subject: DEER SPONGIFORM ENCEPHALOPATHY SURVEY & HOUND STUDY
From: "Terry S. Singeltary Sr." <flounder@WT.NET>
Reply To: Bovine Spongiform Encephalopathy <BSE-L@UNI-KARLSRUHE.DE>
Date: Thu, 17 Oct 2002 17:04:51 -0700
snip...
''The association between venison eating and risk of CJD shows similar pattern, with regular venison eating associated with a 9 FOLD INCREASE IN RISK OF CJD (p = 0.04).''
CREUTZFELDT JAKOB DISEASE SURVEILLANCE IN THE UNITED KINGDOM THIRD ANNUAL REPORT AUGUST 1994
snip...see full report ;
http://web.archive.org/web/20090506050043/http://www.bseinquiry.gov.uk/files/yb/1994/08/00004001.pdf
http://web.archive.org/web/20090506050007/http://www.bseinquiry.gov.uk/files/yb/1994/10/00003001.pdf
http://web.archive.org/web/20090506050244/http://www.bseinquiry.gov.uk/files/yb/1994/07/00001001.pdf
Stephen Dealler is a consultant medical microbiologist deal@airtime.co.uk BSE Inquiry Steve Dealler Management In Confidence BSE: Private Submission of Bovine Brain Dealler
snip...end
########### http://mailhost.rz.uni-karlsruhe.de/warc/bse-l.html ############
*** These results would seem to suggest that CWD does indeed have zoonotic potential, at least as judged by the compatibility of CWD prions and their human PrPC target. Furthermore, extrapolation from this simple in vitro assay suggests that if zoonotic CWD occurred, it would most likely effect those of the PRNP codon 129-MM genotype and that the PrPres type would be similar to that found in the most common subtype of sCJD (MM1).***
http://www.tandfonline.com/doi/full/10.4161/pri.28124?src=recsys
http://www.tandfonline.com/doi/pdf/10.4161/pri.28124?needAccess=true
https://wwwnc.cdc.gov/eid/article/20/1/13-0858_article
Two Hunters from the Same Lodge Afflicted with Sporadic CJD: Is Chronic Wasting Disease to Blame?
(P7-13.002) Jonathan Trout, Matthew Roberts, Michel Tabet, Eithan Kotkowski, and Sarah HornAUTHORS INFO & AFFILIATIONS April 9, 2024 issue 102 (17_supplement_1) https://doi.org/10.1212/WNL.0000000000204407
Abstract Publication History Information & Authors Metrics & Citations Share Abstract
Objective:
This study presents a cluster of Creutzfeldt-Jakob disease (CJD) cases after exposure to chronic wasting disease (CWD)-infected deer, suggestive of potential prion transmission from CWD-infected deer to humans.
Background:
CJD is a rapidly progressive central nervous system disorder caused by misfolded prion proteins. CWD, a prion disease prevalent in North American deer, has raised concerns due to its possible link to CJD. Although no conclusive evidence of cross-species prion transmission exists, vigilance for such cases is crucial for public health.
Design/Methods:
Not applicable.
Results:
In 2022, a 72-year-old man with a history of consuming meat from a CWD-infected deer population presented with rapid-onset confusion and aggression. His friend, who had also eaten venison from the same deer population, recently died of CJD, raising concerns about a potential link between CWD and human prion disease. Despite aggressive symptomatic treatment of seizures and agitation, the patient’s condition deteriorated and he died within a month of initial presentation. The diagnosis was confirmed postmortem as sporadic CJD with homozygous methionine at codon 129 (sCJDMM1). The patient’s history, including a similar case in his social group, suggests a possible novel animal-to-human transmission of CWD. Based on non-human primate and mouse models, cross-species transmission of CJD is plausible. Due to the challenge of distinguishing sCJDMM1 from CWD without detailed prion protein characterization, it is not possible to definitively rule out CWD in these cases. Although causation remains unproven, this cluster emphasizes the need for further investigation into the potential risks of consuming CWD-infected deer and its implications for public health.
Conclusions:
Clusters of sporadic CJD cases may occur in regions with CWD-confirmed deer populations, hinting at potential cross-species prion transmission. Surveillance and further research are essential to better understand this possible association.
Disclosure: Mr. Trout has nothing to disclose. Dr. Roberts has nothing to disclose. Dr. Tabet has nothing to disclose. Dr. Kotkowski has nothing to disclose. Dr. Horn has received personal compensation in the range of $500-$4,999 for serving as a Consultant for Cala Trio. The institution of Dr. Horn has received research support from Alzheimer's Association.
https://www.neurology.org/doi/abs/10.1212/WNL.0000000000204407
TUESDAY, MAY 11, 2021
A Unique Presentation of Creutzfeldt-Jakob Disease in a Patient Consuming Deer Antler Velvet
Conclusion
We believe that our patient’s case of CJD is highly suspicious for cervid etiology given the circumstances of the case as well as the strong evidence of plausibility reported in published literature. This is the first known case of CJD in a patient who had consumed deer antler velvet. Despite the confirmed diagnosis of CJD, a causal relationship between the patient’s disease and his consumption of deer antler velvet cannot be definitively concluded.
Supplemental data including molecular tissue sample analysis and autopsy findings could yield further supporting evidence. Given this patient’s clinical resemblance to CBD and the known histological similarities of CBD with CJD, clinicians should consider both diseases in the differential diagnosis of patients with a similarly esoteric presentation. Regardless of the origin of this patient’s disease, it is clear that the potential for prion transmission from cervids to humans should be further investigated by the academic community with considerable urgency.
https://thescipub.com/pdf/ajidsp.2021.43.48.pdf
''We believe that our patient’s case of CJD is highly suspicious for cervid etiology given the circumstances of the case as well as the strong evidence of plausibility reported in published literature. This is the first known case of CJD in a patient who had consumed deer antler velvet. Despite the confirmed diagnosis of CJD, a causal relationship between the patient’s disease and his consumption of deer antler velvet cannot be definitively concluded.''
https://thescipub.com/pdf/ajidsp.2021.43.48.pdf
CREUTZFELDT JAKOB DISEASE: A Unique Presentation of Creutzfeldt-Jakob Disease in a Patient Consuming Deer Antler Velvet
i was warning England and the BSE Inquiry about just this, way back in 1998, and was ask to supply information to the BSE Inquiry. for anyone that might be interested, see;
Singeltary submission to the BSE Inquiry on CJD and Nutritional Supplements 1998
ABOUT that deer antler spray and CWD TSE PRION... I have been screaming this since my neighbors mom died from cjd, and she had been taking a supplement that contained bovine brain, bovine eyeball, and other SRMs specified risk materials, the most high risk for mad cow disease. just saying...
I made a submission to the BSE Inquiry long ago during the BSE Inquiry days, and they seemed pretty interested.
Sender: "Patricia Cantos"
To: "Terry S Singeltary Sr. (E-mail)"
Subject: Your submission to the Inquiry
Date: Fri, 3 Jul 1998 10:10:05 +0100 3 July 1998
Mr Terry S Singeltary Sr. E-Mail: Flounder at wt.netRef: E2979
Dear Mr Singeltary, Thank you for your E-mail message of the 30th of June 1998 providing the Inquiry with your further comments. Thank you for offering to provide the Inquiry with any test results on the nutritional supplements your mother was taking before she died. As requested I am sending you our general Information Pack and a copy of the Chairman's letter. Please contact me if your system cannot read the attachments. Regarding your question, the Inquiry is looking into many aspects of the scientific evidence on BSE and nvCJD.
I would refer you to the transcripts of evidence we have already heard which are found on our internet site at ;
http://www.bse.org.uk.
Could you please provide the Inquiry with a copy of the press article you refer to in your e-mail? If not an approximate date for the article so that we can locate it? In the meantime, thank you for you comments. Please do not hesitate to contact me on... snip...end...tss
everyone I tell this too gets it screwed up...MY MOTHER WAS NOT TAKING THOSE SUPPLEMENTS IPLEX (that I ever knew of). this was my neighbors mother that died exactly one year previously and to the day of sporadic CJD that was diagnosed as Alzheimer’s at first. my mother died exactly a year later from the Heidenhain Variant of Creutzfeldt Jakob Disease hvCJD, and exceedingly rare strains of the ever growing sporadic CJD’s. both cases confirmed. ...kind regards, terry
*** now, let’s see what the authors said about this casual link, personal communications years ago, and then the latest on the zoonotic potential from CWD to humans from the TOKYO PRION 2016 CONFERENCE.
see where it is stated NO STRONG evidence. so, does this mean there IS casual evidence ????
“Our conclusion stating that we found no strong evidence of CWD transmission to humans”
Subject: CWD aka MAD DEER/ELK TO HUMANS ???
Date: September 30, 2002 at 7:06 am PST
From: "Belay, Ermias"
To: Cc: "Race, Richard (NIH)" ; ; "Belay, Ermias"
Sent: Monday, September 30, 2002 9:22 AM
Subject: RE: TO CDC AND NIH - PUB MED- 3 MORE DEATHS - CWD - YOUNG HUNTERS
Dear Sir/Madam, In the Archives of Neurology you quoted (the abstract of which was attached to your email), we did not say CWD in humans will present like variant CJD.. That assumption would be wrong. I encourage you to read the whole article and call me if you have questions or need more clarification (phone: 404-639-3091).
Also, we do not claim that "no-one has ever been infected with prion disease from eating venison." Our conclusion stating that we found no strong evidence of CWD transmission to humans in the article you quoted or in any other forum is limited to the patients we investigated.
Ermias Belay, M.D. Centers for Disease Control and Prevention
Subject: TO CDC AND NIH - PUB MED- 3 MORE DEATHS - CWD - YOUNG HUNTERS
Sunday, November 10, 2002 6:26 PM .......snip........end..............TSS
-----Original Message-----
From:
Sent: Sunday, September 29, 2002 10:15 AM
To: rr26k@nih.gov; rrace@niaid.nih.gov; ebb8@CDC.GOV
Subject: TO CDC AND NIH - PUB MED- 3 MORE DEATHS - CWD - YOUNG HUNTERS
Sunday, November 10, 2002 6:26 PM .......snip........end..............TSS
Thursday, April 03, 2008
A prion disease of cervids: Chronic wasting disease 2008 1: Vet Res. 2008 Apr 3;39(4):41 A prion disease of cervids: Chronic wasting disease Sigurdson CJ.
snip...
*** twenty-seven CJD patients who regularly consumed venison were reported to the Surveillance Center, however there have been no unusual or novel prion subtypes that might indicate the appearance of a new prion strain [7, 41].
snip... full text ;
https://www.vetres.org/articles/vetres/abs/2008/04/v08092/v08092.html
https://chronic-wasting-disease.blogspot.com/2008/04/prion-disease-of-cervids-chronic.html
“regular venison eating associated with a 9 FOLD INCREASE IN RISK OF CJD”
Subject: Re: DEER SPONGIFORM ENCEPHALOPATHY SURVEY & HOUND STUDY
Date: Fri, 18 Oct 2002 23:12:22 +0100
From: Steve Dealler Reply-To: Bovine Spongiform Encephalopathy Organization: Netscape Online member
To: BSE-L@ …
######## Bovine Spongiform Encephalopathy <BSE-L@UNI-KARLSRUHE.DE> #########
Dear Terry,
An excellent piece of review as this literature is desparately difficult to get back from Government sites. What happened with the deer was that an association between deer meat eating and sporadic CJD was found in about 1993. The evidence was not great but did not disappear after several years of asking CJD cases what they had eaten. I think that the work into deer disease largely stopped because it was not helpful to the UK industry...and no specific cases were reported.
Well, if you dont look adequately like they are in USA currenly then you wont find any!
Steve Dealler
########### http://mailhost.rz.uni-karlsruhe.de/warc/bse-l.html ############
Subject: DEER SPONGIFORM ENCEPHALOPATHY SURVEY & HOUND STUDY
From: "Terry S. Singeltary Sr." <flounder@WT.NET>
Reply To: Bovine Spongiform Encephalopathy <BSE-L@UNI-KARLSRUHE.DE>
Date: Thu, 17 Oct 2002 17:04:51 -0700
snip...
''The association between venison eating and risk of CJD shows similar pattern, with regular venison eating associated with a 9 FOLD INCREASE IN RISK OF CJD (p = 0.04).''
CREUTZFELDT JAKOB DISEASE SURVEILLANCE IN THE UNITED KINGDOM THIRD ANNUAL REPORT AUGUST 1994
snip...see full report ;
http://web.archive.org/web/20090506050043/http://www.bseinquiry.gov.uk/files/yb/1994/08/00004001.pdf
http://web.archive.org/web/20090506050007/http://www.bseinquiry.gov.uk/files/yb/1994/10/00003001.pdf
http://web.archive.org/web/20090506050244/http://www.bseinquiry.gov.uk/files/yb/1994/07/00001001.pdf
Stephen Dealler is a consultant medical microbiologist deal@airtime.co.uk BSE Inquiry Steve Dealler Management In Confidence BSE: Private Submission of Bovine Brain Dealler
snip...end
########### http://mailhost.rz.uni-karlsruhe.de/warc/bse-l.html ############
*** These results would seem to suggest that CWD does indeed have zoonotic potential, at least as judged by the compatibility of CWD prions and their human PrPC target. Furthermore, extrapolation from this simple in vitro assay suggests that if zoonotic CWD occurred, it would most likely effect those of the PRNP codon 129-MM genotype and that the PrPres type would be similar to that found in the most common subtype of sCJD (MM1).***
http://www.tandfonline.com/doi/full/10.4161/pri.28124?src=recsys
http://www.tandfonline.com/doi/pdf/10.4161/pri.28124?needAccess=true
https://wwwnc.cdc.gov/eid/article/20/1/13-0858_article
Two Hunters from the Same Lodge Afflicted with Sporadic CJD: Is Chronic Wasting Disease to Blame?
(P7-13.002) Jonathan Trout, Matthew Roberts, Michel Tabet, Eithan Kotkowski, and Sarah HornAUTHORS INFO & AFFILIATIONS April 9, 2024 issue 102 (17_supplement_1) https://doi.org/10.1212/WNL.0000000000204407
Abstract Publication History Information & Authors Metrics & Citations Share Abstract
Objective:
This study presents a cluster of Creutzfeldt-Jakob disease (CJD) cases after exposure to chronic wasting disease (CWD)-infected deer, suggestive of potential prion transmission from CWD-infected deer to humans.
Background:
CJD is a rapidly progressive central nervous system disorder caused by misfolded prion proteins. CWD, a prion disease prevalent in North American deer, has raised concerns due to its possible link to CJD. Although no conclusive evidence of cross-species prion transmission exists, vigilance for such cases is crucial for public health.
Design/Methods:
Not applicable.
Results:
In 2022, a 72-year-old man with a history of consuming meat from a CWD-infected deer population presented with rapid-onset confusion and aggression. His friend, who had also eaten venison from the same deer population, recently died of CJD, raising concerns about a potential link between CWD and human prion disease. Despite aggressive symptomatic treatment of seizures and agitation, the patient’s condition deteriorated and he died within a month of initial presentation. The diagnosis was confirmed postmortem as sporadic CJD with homozygous methionine at codon 129 (sCJDMM1). The patient’s history, including a similar case in his social group, suggests a possible novel animal-to-human transmission of CWD. Based on non-human primate and mouse models, cross-species transmission of CJD is plausible. Due to the challenge of distinguishing sCJDMM1 from CWD without detailed prion protein characterization, it is not possible to definitively rule out CWD in these cases. Although causation remains unproven, this cluster emphasizes the need for further investigation into the potential risks of consuming CWD-infected deer and its implications for public health.
Conclusions:
Clusters of sporadic CJD cases may occur in regions with CWD-confirmed deer populations, hinting at potential cross-species prion transmission. Surveillance and further research are essential to better understand this possible association.
Disclosure: Mr. Trout has nothing to disclose. Dr. Roberts has nothing to disclose. Dr. Tabet has nothing to disclose. Dr. Kotkowski has nothing to disclose. Dr. Horn has received personal compensation in the range of $500-$4,999 for serving as a Consultant for Cala Trio. The institution of Dr. Horn has received research support from Alzheimer's Association.
https://www.neurology.org/doi/abs/10.1212/WNL.0000000000204407
TUESDAY, MAY 11, 2021
A Unique Presentation of Creutzfeldt-Jakob Disease in a Patient Consuming Deer Antler Velvet
Conclusion
We believe that our patient’s case of CJD is highly suspicious for cervid etiology given the circumstances of the case as well as the strong evidence of plausibility reported in published literature. This is the first known case of CJD in a patient who had consumed deer antler velvet. Despite the confirmed diagnosis of CJD, a causal relationship between the patient’s disease and his consumption of deer antler velvet cannot be definitively concluded.
Supplemental data including molecular tissue sample analysis and autopsy findings could yield further supporting evidence. Given this patient’s clinical resemblance to CBD and the known histological similarities of CBD with CJD, clinicians should consider both diseases in the differential diagnosis of patients with a similarly esoteric presentation. Regardless of the origin of this patient’s disease, it is clear that the potential for prion transmission from cervids to humans should be further investigated by the academic community with considerable urgency.
https://thescipub.com/pdf/ajidsp.2021.43.48.pdf
''We believe that our patient’s case of CJD is highly suspicious for cervid etiology given the circumstances of the case as well as the strong evidence of plausibility reported in published literature. This is the first known case of CJD in a patient who had consumed deer antler velvet. Despite the confirmed diagnosis of CJD, a causal relationship between the patient’s disease and his consumption of deer antler velvet cannot be definitively concluded.''
https://thescipub.com/pdf/ajidsp.2021.43.48.pdf
CREUTZFELDT JAKOB DISEASE: A Unique Presentation of Creutzfeldt-Jakob Disease in a Patient Consuming Deer Antler Velvet
i was warning England and the BSE Inquiry about just this, way back in 1998, and was ask to supply information to the BSE Inquiry. for anyone that might be interested, see;
Singeltary submission to the BSE Inquiry on CJD and Nutritional Supplements 1998
ABOUT that deer antler spray and CWD TSE PRION... I have been screaming this since my neighbors mom died from cjd, and she had been taking a supplement that contained bovine brain, bovine eyeball, and other SRMs specified risk materials, the most high risk for mad cow disease. just saying...
I made a submission to the BSE Inquiry long ago during the BSE Inquiry days, and they seemed pretty interested.
Sender: "Patricia Cantos"
To: "Terry S Singeltary Sr. (E-mail)"
Subject: Your submission to the Inquiry
Date: Fri, 3 Jul 1998 10:10:05 +0100 3 July 1998
Mr Terry S Singeltary Sr. E-Mail: Flounder at wt.netRef: E2979
Dear Mr Singeltary, Thank you for your E-mail message of the 30th of June 1998 providing the Inquiry with your further comments. Thank you for offering to provide the Inquiry with any test results on the nutritional supplements your mother was taking before she died. As requested I am sending you our general Information Pack and a copy of the Chairman's letter. Please contact me if your system cannot read the attachments. Regarding your question, the Inquiry is looking into many aspects of the scientific evidence on BSE and nvCJD.
I would refer you to the transcripts of evidence we have already heard which are found on our internet site at ;
http://www.bse.org.uk.
Could you please provide the Inquiry with a copy of the press article you refer to in your e-mail? If not an approximate date for the article so that we can locate it? In the meantime, thank you for you comments. Please do not hesitate to contact me on... snip...end...tss
everyone I tell this too gets it screwed up...MY MOTHER WAS NOT TAKING THOSE SUPPLEMENTS IPLEX (that I ever knew of). this was my neighbors mother that died exactly one year previously and to the day of sporadic CJD that was diagnosed as Alzheimer’s at first. my mother died exactly a year later from the Heidenhain Variant of Creutzfeldt Jakob Disease hvCJD, and exceedingly rare strains of the ever growing sporadic CJD’s. both cases confirmed. ...kind regards, terry
Good Luck!
Terry S. Singeltary Sr.
posted by Terry S. Singeltary Sr. at
6:06 PM
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