Monday, September 08, 2025

Kentucky Confirmed Captive CWD Oct. 14, 2024, this month KDA confirmed eight new CWD positive deer at the same facility

 Kentucky Confirmed Captive CWD Oct. 14, 2024, this month KDA confirmed eight new CWD positive deer at the same facility


In October 2024, the Kentucky Department of Agriculture (KDA) confirmed its first case of CWD in a captive deer at a Breckinridge County farm, marking the state's second overall detection of the disease. This month KDA confirmed eight new CWD positive deer at the same facility.​​​


CHRONIC WASTING DISEASE DETECTED IN CAPTIVE CERVID FROM BRECKINRIDGE COUNTY 

Administration Hunting WildlifeWildlife-Disease-Management

​FRANKFORT, Ky. (Oct. 14, 2024) — Officials from the Kentucky Department of Fish and Wildlife Resources are gathering additional information and carefully evaluating next steps following Monday’s announcement by the Kentucky Department of Agriculture that lab testing confirmed Chronic Wasting Disease (CWD) in a deceased deer from a Breckinridge County deer farm. It marks Kentucky’s first case of CWD in a captive cervid.​​​​

​​​​Chronic Wasting Disease is caused by abnormal proteins called prions and it affects white-tailed deer, elk, and other animals in the deer family. There is no known cure or vaccine, and the disease is always fatal in infected animals. The disease is not known to be transmissible to people, but as a precaution the Centers for Disease Control and Prevention recommends not consuming meat from deer that test positive for the disease. Kentucky Fish and Wildlife always recommends not consuming meat taken from animals that appear to be sick or in poor condition.

The state Department of Agriculture has issued a quarantine restricting movement into or out of the Breckinridge County facility, including live deer or deer products.​​​

​​​​Kentucky Fish and Wildlife officials are in close communication with national, state and local partners and will reference the agency’s CWD Response Plan in response to this new detection.

Since 2002, Kentucky Fish and Wildlife has CWD-tested more than 40,000 deer and elk from across the state.​​​​

​​​​Hunters can aid Kentucky Fish and Wildlife’s statewide monitoring efforts by dropping off the heads of legally harvested and telechecked deer for CWD testing and aging at self-serve CWD Sample Drop-Off sites. This service is provided at no cost to hunters. Detailed location information, instructions and additional resources may be found at the CWD Sample Drop-Off Sites page on the department’s website. Hunters will be promptly notified if a deer they harvested tests positive for CWD.

Deer that appear to be sick but do not have an obvious injury can be reported using the department’s sick deer online reporting form; reports will be reviewed by the agency’s wildlife health program staff, who will contact the person submitting the report if additional information is needed.​​​​

For the latest information on CWD, please visit the department's website (fw.ky.gov) and follow its social media channels. More information about CWD is available at fw.ky.gov/cwd, cwd-info.org and through the CDC website.​​​​​


Deer farm herd killed to stem spread of ‘zombie’ deer disease in Kentucky. Now what?

BY: LIAM NIEMEYER -

SEPTEMBER 8, 2025 5:50 AM

Do deer farms increase the risk that wild deer like this buck will contract a contagious and deadly neurological disease? Opinions differ. (Kentucky Department of Fish and Wildlife Resources) A disease outbreak on a Kentucky deer farm is renewing questions about whether stronger rules are needed for the more than 100 “captive cervid facilities” the state has permitted.

State and federal agencies recently confirmed eight cases of chronic wasting disease (CWD) at a deer farm in Breckinridge County where the illness had first been detected in a single deer in October 2024.

Chronic wasting disease is a fatal prion disorder similar to mad cow disease. Only 10 cases have been confirmed in Kentucky — nine of them on the Breckinridge County farm — out of 40,000 tests since 2002. But the disease’s spread in other states has made preventing it a priority for wildlife managers nationwide because it causes population declines in deer and elk when prevalent.

Much about the neurological condition — dubbed “zombie deer disease” — is unknown. In deer, it causes significant weight loss, listlessness and death. A deer can appear healthy and have CWD for months or years before symptoms appear. Research has produced conflicting conclusions on the risk of it spreading to humans.

In Breckinridge County, more than 100 captive deer were killed in early July at Sinking Creek Whitetails, said co-owner Laura Voyles, whose family started the deer farm in 2020. A Kentucky Department of Agriculture statement said the “depopulation was carried out” at the request of the owner “to protect animal health and prevent further spread. KDA’s role was to collect the necessary samples and submit them to the lab for testing.”

Snip…see full article;


Kentucky CHRONIC WASTING DISEASE DETECTED IN CAPTIVE CERVID FROM BRECKINRIDGE COUNTY

Administration Hunting Wildlife Wildlife-Disease-Management

FRANKFORT, Ky. (Oct. 14, 2024) — Officials from the Kentucky Department of Fish and Wildlife Resources are gathering additional information and carefully evaluating next steps following Monday’s announcement by the Kentucky Department of Agriculture that lab testing confirmed Chronic Wasting Disease (CWD) in a deceased deer from a Breckinridge County deer farm. It marks Kentucky’s first case of CWD in a captive cervid.

Chronic Wasting Disease is caused by abnormal proteins called prions and it affects white-tailed deer, elk, and other animals in the deer family. There is no known cure or vaccine, and the disease is always fatal in infected animals. The disease is not known to be transmissible to people, but as a precaution the Centers for Disease Control and Prevention recommends not consuming meat from deer that test positive for the disease. Kentucky Fish and Wildlife always recommends not consuming meat taken from animals that appear to be sick or in poor condition.

The state Department of Agriculture has issued a quarantine restricting movement into or out of the Breckinridge County facility, including live deer or deer products.

Kentucky Fish and Wildlife officials are in close communication with national, state and local partners and will reference the agency’s CWD Response Plan in response to this new detection.

Since 2002, Kentucky Fish and Wildlife has CWD-tested more than 40,000 deer and elk from across the state.

Hunters can aid Kentucky Fish and Wildlife’s statewide monitoring efforts by dropping off the heads of legally harvested and telechecked deer for CWD testing and aging at self-serve CWD Sample Drop-Off sites. This service is provided at no cost to hunters. Detailed location information, instructions and additional resources may be found at the CWD Sample Drop-Off Sites page on the department’s website. Hunters will be promptly notified if a deer they harvested tests positive for CWD.

Deer that appear to be sick but do not have an obvious injury can be reported using the department’s sick deer online reporting form; reports will be reviewed by the agency’s wildlife health program staff, who will contact the person submitting the report if additional information is needed.

For the latest information on CWD, please visit the department's website (fw.ky.gov) and follow its social media channels. More information about CWD is available at fw.ky.gov/cwd, cwd-info.org and through the CDC website.


Kentucky CWD Response Plan


CWD Updates in Kentucky On 10/14/2024, the Kentucky Department of Agriculture announced that lab testing confirmed CWD in a deceased deer from a Breckinridge County deer farm. It mar ks Kentucky’s first case of CWD in a captive cervid.Officials from the Kentucky Department of Fish and Wildlife Resources are gathering additional information and carefully evaluating next steps. On 12/07/2023, Kentucky Fish and Wildlife announced that a positive case of CWD was detected in Kentucky. The confirmed case was found in a 2.5-year-old male white-tailed deer collected in Ballard County. Multiple tests confirmed the presence of CWD in the deer. The CWD Surveillance Zone has expanded to include Ballard, Carlisle, and McCracken counties, and remains in effect for Hickman, Fulton, Graves, Calloway, and Marshall counties. Kentucky Fish and Wildlife has a CWD Response Plan that calls for the implementation of specific measures following a positive CWD detection in Kentucky. In response to a new detection within KY, this response plan was enacted on 12/06/2023 and aims to contain, reduce, and eliminate the spread of CWD in Kentucky. Previously, Kentucky Fish and Wildlife’s response plan was enacted in September of 2021 in response to a detection within 10 miles from our border.

For the latest information on CWD in Kentucky, please continue to follow our CWD updates and follow the department’s social media channels. Up-to-date news regarding CWD across the US and Canada can be found on the Chronic Wasting Disease Alliance website.


CWD Statues Farmed Cervid


ALERT: CHRONIC WASTING DISEASE (CWD): POSITIVE RESULTS IN WHITETAIL DEER DETECTED IN BALLARD COUNTY, KY.

For more information, please review the press release from the Kentucky Department of Fish and Wildlife.

FARMED CERVIDS

The Office of State Veterinarian (OSV) is currently working with the Kentucky Department of Fish and Wildlife (FW) to maintain a mandatory monitoring surveillance program for Chronic Wasting Disease (CWD) in Kentucky. OSV is responsible for the health requirements of the farmed cervids. Cervids include: deer, elk (including reindeer), moose, etc.

CHRONIC WASTING DISEASE (CWD)

History of CWD

Chronic Wasting Disease (CWD) was first recognized as a clinical disease in 1967 in Colorado. As of December 2023, CWD in free-ranging deer, elk and/or moose has been reported in at least 32 states, including Kentucky, in the continental United States, as well as four provinces in Canada.

What is CWD?

Chronic Wasting Disease (CWD) is a fatal, neurological disease, characterized by spongy degeneration of the brain. It affects white-tailed deer, mule deer, elk, and has recently been confirmed in a moose. CWD belongs to a group of diseases called Transmissible Spongiform Encephalopathies (TSEs), which includes Scrapie in sheep and goats, Bovine Spongiform Encephalopathy (commonly known as "mad cow" disease) in cattle, and Creutzfeldt-Jakob Disease in humans. It is suspected that the agent responsible for causing TSEs is an abnormal protein called a prion. There is currently no treatment or vaccine available. There are currently live testing modalities available, generally reserved for specific indications.

For more information, please see our CWD Frequently Asked Questions under Forms and Documents.

Program Requirements

Program requirements include fencing (monitored by Kentucky Fish & Wildlife), individual animal identification, regular inventories, and testing of all animals over 12 months of age that die for any reason. State agriculture agencies are responsible for safeguarding the health of domestic livestock including alternative livestock species, such as deer and elk. When native wildlife species are farmed, the jurisdictions become more complex. Regulatory authority for farmed cervids in Kentucky lies with the State agriculture agency and the wildlife agency. Kentucky has established CWD surveillance and/or herd certification programs and import requirements for farmed cervids. Please refer to the updated cervid regulations, as well as the one-page HCP Producer document, for more information surrounding specific requirements for the program.

Farmed Deer Herds in Kentucky

Kentucky has approximately 120 farmed deer herds and about 3,350 cervids. All herds are quarterly inspected by a Kentucky Department of Agriculture inspector, as well as a yearly visit by a representative from the Kentucky Department of Fish and Wildlife. An annual census and veterinarian inspection of the herd is also performed. Before applying to the KDA’s CWD Program, you must have an approved facility by the Kentucky Department of Fish and Wildlife. Click here for more information.




Kentucky CWD Detected For First Time

CHRONIC WASTING DISEASE CONFIRMED IN KENTUCKY FOR FIRST TIME

Administration Wildlife Disease Management Wildlife Hunting Commissioner’s Office

FRANKFORT, Ky. (Dec. 7, 2023) — Officials with the Kentucky Department of Fish and Wildlife Resources announced today that Kentucky has joined the list of states across the country with a confirmed detection of Chronic Wasting Disease (CWD), a fatal neurologic disease that affects deer, elk and other species in the deer family.

Two independent types of tests were performed on tissue collected from a 2 ½-year-old male white-tailed deer that was harvested by a hunter in Ballard County in November. Both tests yielded the same test result: the deer was infected with the abnormal proteins that cause CWD.

It is Kentucky’s first documented case of the disease.

While no conclusive evidence exists that CWD can be transmitted to people, the Centers for Disease Control and Prevention (CDC) recommends refraining from eating meat from animals that test positive for CWD. Kentucky Fish and Wildlife always advises against eating the meat from game animals that appear sick or in poor condition.

Deer that appear to be sick but do not have an obvious injury can be reported using the department’s sick deer online reporting form; reports will be reviewed by the agency’s wildlife health program staff, who will contact the person submitting the report if additional information is needed.

As Kentucky Fish and Wildlife staff continue to gather additional details about the infected deer, agency officials are in close communication with national, state and local partners as they carefully consider next steps in response to the detection.

“We at Kentucky Fish and Wildlife hoped this day would never come but we have been preparing for it,” Kentucky Fish and Wildlife Commissioner Rich Storm said. “Our team of experts first developed our CWD Response Plan more than 20 years ago, and it has been enhanced through the years using the best available science.

“Collaboration with our many partners, including hunters, taxidermists, meat processors, diagnostic testing facilities and other government agencies has enhanced our CWD surveillance efforts.”

The deer was harvested on opening day of modern gun deer season. Biologists collected tissue from the animal as part of ongoing CWD surveillance efforts.

Preliminary tests were conducted at Murray State University’s Breathitt Veterinary Center, where the Enzyme-Linked Immunosorbent Assay (ELISA) CWD test identified the sample as a suspect positive.

Following its CWD Response Plan, Kentucky Fish and Wildlife immediately sent back-up samples to the National Veterinary Services Laboratories (NVSL) in Ames, Iowa for an expedited Immunohistochemistry (IHC), which is a test that is used to detect the deposition of infectious abnormal proteins within specific cervid tissues.

“Results from the IHC confirmed the results of the initial ELISA test and were reported to us on Wednesday as a CWD detection,” said Dr. Christine Casey, wildlife veterinarian with Kentucky Fish and Wildlife. “The combination of the ELISA test and IHC gives us the utmost confidence that the animal was infected with the disease.”

Since its discovery in the late 1960s in Colorado, CWD has spread to more than half the states in the U.S., including six of seven Kentucky-bordering states (Missouri, Illinois, Ohio, West Virginia, Virginia, and Tennessee).

Early detection is critical to slowing the spread of this disease, which can be transmitted through direct contact between animals such as shared body fluids or from plants and soil in a contaminated area. Infected deer can transmit the disease even if they are not currently showing symptoms.

Kentucky Fish and Wildlife established its CWD Response Plan after the disease was detected for the first time east of the Mississippi River, and it has evolved through the past 20-plus years.

The department activated the plan in September 2021 following an announcement by the Tennessee Wildlife Resources Agency that the disease was found just across Kentucky’s s outhern border in northwestern Tennessee.

Kentucky Fish and Wildlife subsequently established a CWD Surveillance Zone in western Kentucky, encompassing Calloway, Marshall, Graves, Fulton and Hickman counties. Special regulations remain in place for those counties.

Kentucky Fish and Wildlife operated mandatory CWD check stations in the surveillance zone in 2021, 2022 and again this year during the first three days of modern gun deer season (Nov. 11-13).

The department collected 1,318 samples last month at its CWD check stations in western Kentucky. Currently, it has received results from 84 percent of those samples, and 35.6 percent of results from samples collected statewide.

Ballard County is adjacent to the surveillance zone. Kentucky Fish and Wildlife staff have been collecting samples from the county for many years as part of the agency’s statewide surveillance efforts, but the disease had never previously been detected.

Since 2002, Kentucky Fish and Wildlife has CWD-tested more than 40,000 deer and elk from across the state, sampling every county.

“Although CWD is always fatal to infected individual animals, by following best practices we can minimize its impact on the long-term health and sustainability of our deer herd so that we can continue to enjoy our deer and elk herds for many generations to come, helping to safeguard the many ways that they benefit the Commonwealth,” Storm said.

With more than a month before deer hunting closes for the season in Kentucky, hunters can aid Kentucky Fish and Wildlife’s statewide monitoring efforts by donating the heads of legally harvested and telechecked deer for CWD testing and aging through the voluntary Deer Sample Collection Station program. There is no cost to hunters. Location information, instructions and more information about the program are available online via fw.ky.gov/cwd. If a hunter-harvested deer tests positive for CWD, the hunter will be contacted upon confirmation of the disease.

For the latest information on CWD, please visit the department's website (fw.ky.gov) and follow its social media channels. More information about CWD is available at fw.ky.gov/cwd, cwd-info.org and through the CDC website .



TUESDAY, OCTOBER 15, 2024

KENTUCKY CHRONIC WASTING DISEASE DETECTED IN CAPTIVE CERVID FROM BRECKINRIDGE COUNTY


FRIDAY, DECEMBER 08, 2023

Kentucky CWD TSE Prion Detected For First Time


TEXAS TRUCKING CWD

“CWD spreads among wild populations at a relatively slow rate, limited by the natural home range and dispersed nature of wild animals.”

NOW HOLD YOUR HORSES, Chronic Wasting Disease CWD of Cervid can spread rather swiftly, traveling around 50 MPH, from the back of truck and trailer, and Here in Texas, we call it ‘Trucking CWD’…

Preventive Veterinary Medicine Volume 234, January 2025, 106385

Use of biosecurity practices to prevent chronic wasting disease in Minnesota cervid herds

Vehicles or trailers that entered the farm were used to transport other live cervids, cervid carcasses, or cervid body parts in past 3 years in 64.3 % (95 % CI 46.3–82.3) of larger elk/reindeer herds compared to 13.6 % (95 % CI 4.7–22.4) of smaller deer herds.

Snip…

Identifying the exact pathway of initial CWD transmission to cervid herds is often not possible, in part due to many potential pathways of transmission for the infection, including both direct and indirect contact with infected farmed or wild cervids (Kincheloe et al., 2021). That study identified that transmissions from infected farmed cervids may occur from direct contact with the movement of cervids from one herd to another and from indirect contact with the sharing of equipment, vehicles, clothing, reproductive equipment, and potentially through semen or embryos.


***> Department records indicate that within the last five years (since January 1, 2020), 30 deer breeding facilities where CWD has been confirmed transferred a total of 8,799 deer to 249 additional deer breeding facilities and 487 release sites located in a total of 144 counties in Texas. <***


Texas Kimble County Farm Chronic Wasting Disease CWD TSE Prion Approximate Herd Prevalence 12%

SUMMARY MINUTES OF THE 407th COMMISSION MEETING Texas Animal Health Commission

September 22, 2020

Chronic Wasting Disease (CWD):

A new CWD positive breeding herd was disclosed in February 2020 in Kimble County. This herd depopulation was completed in July 2020. Including the two index positive deer, an additional eight more positive deer were disclosed (approximate herd prevalence 12%). Since July 2015 and prior to this discovery, five positive captive breeder herds have been disclosed and four of those are in Medina County. One herd in Lavaca and three herds in Medina County were depopulated leaving one large herd in Medina County that is managed on a herd plan. A new zone was established in Val Verde County in December 2019 as a result of a positive free-ranging White-tailed Deer (WTD). A second positive WTD was also disclosed in February 2020 in the same area.

SUMMARY MINUTES OF THE 407th COMMISSION MEETING – 9/22/2020

Scrapie: The flock identified in April 2016 remains under quarantine in Hartley County.

https://www.tahc.texas.gov/agency/meetings/minutes/SummaryMinutes_CommMtg_2020-09-22


State of Knowledge Regarding Transmission, Spread, and Management of Chronic Wasting Disease in U.S. Captive and Free-Ranging Cervid Populations. Washington, DC: The National Academies Press. doi: 10.17226/27449. ×

Appendix F

Data on Cervid Farms and Captive Cervids by State and Costs

This appendix provides an expanded visualization of the cervid data reported in Chiavacci (2022). It also provides descriptions on cervid numbers, number of paid hunting licenses, and years since first detection in wild cervid populations. The committee developed several sets of figures presenting relationships of these data, separated into two frames—states with mule deer and states without mule deer. The appendix concludes with a discussion of public agency costs.

DATA ON CERVID FARMS AND CAPTIVE CERVIDS

Chiavacci (2022) documents the number of cervid farms and captive cervids by state in 2020. Figure F.1 groups those in states with mule deer habitat (Figure F.1a) and those without (Figure F.1b). Most states have less than 150 cervid farms and less than 10,000 captive cervids. The number of cervid farms and captive cervids in Texas exceeds that of others states by over an order of magnitude. Most of the Great Plains and western states with mule deer have less than 50 farms and 3,000 captive cervids. There are, on average, more cervid farms and captive cervids in states with only white-tailed deer habitat (i.e., the central and eastern states).

Some states such as Texas have both breeding and breeding and hunting operations. Little data exist on the scale of those operations apart from the facilities surveyed by Outlaw and others (2017). They determined that the average breeding farm size was found to be 21 acres for breeding and 30 acres for breeding and hunting. The sizes of these facilities are much smaller than those in Alberta documented by Arnot and others (2009), which are in the hundreds of acres.

Figure F.2 plots the years since first detection of chronic wasting disease (CWD) in wild cervids in each state against captive cervids in each state in 2020 in Figure F.2a and Figure F.2b, and against the number of cervid farms in 2020 in Figure F.2c and Figure F.2d.

While CWD was first detected relatively recently in Texas, there is a relatively high number of locales with endemic CWD. The remaining states all have less than 4,000 captive cervids and fewer than 100 farms (Chiavacci, 2022). Both Idaho and Oklahoma have seen a few cases.

For the more eastern states without mule deer, there are regular groupings based on the years since first detection and number of endemic locales, each across the full range of number of cervids and farms. Exceptions to the pattern include Arkansas and Tennessee, which both have only recently detected CWD yet have several endemic locations. New York is also different in that CWD was detected 18 years ago, but few other cases have been found. This is fortuitus for New York as the state has almost 7,500 captive cervids and over 100 farms (Chiavacci, 2022).

Page 181

Suggested Citation:"Appendix F: Data on Cervid Farms and Captive Cervids by State and Costs." National Academies of Sciences, Engineering, and Medicine. 2025. State of Knowledge Regarding Transmission, Spread, and Management of Chronic Wasting Disease in U.S. Captive and Free-Ranging Cervid Populations. Washington, DC: The National Academies Press. doi: 10.17226/27449. ×

FIGURE F.1 Relationships between the number of cervid farms and number of captive cervids by state. *Texas had significantly more cervid farms and captive cervids than any other state with 1,498 cervid farms and 117,120 farmed cervids in 2020. Texas is excluded from panel (a) to keep the two panels comparable.

SOURCE: Data from Chiavacci (2022, Table 1).

Data were obtained by the committee from a variety of digital sources on the state-by-state number of hunting licenses issued annually and populations of wild cervids. (The committee realizes these population estimates are rough and does not employ them in a formal analysis but rather as an indication of the magnitude of those populations at risk.) Considering deer as the most widespread species at risk, for the same states as employed in Chiavacci (2022) and grouped by states with and without mule deer habitat, Figure F.3 plots the number of hunters in 2022 and wild deer populations in 2022. Figure F.3 illustrates that those states with more deer have more hunters, but the general pattern in the states with mule deer habitat is quite different than that of states with just white-tail deer. It is important to note that there may be significant differences in the benefits and costs of hunting across cervid species and states, and the relative proportions of cervids in states vary significantly—for example, many states with mule deer also include significant populations of elk and moose. Also important to note is there is great variation in access to hunting across states and public lands and in resident and non-resident demand for hunting.

Figure F.4 plots the years since first detection and wild deer populations in 2022 in Figure F.4a and Figure F.4b, and the number of hunters in 2022 in Figure F.4c and Figure F.4d.

The plots illustrate again the differences in the pattern of the data between the western/Great Plains states and those further east. For the states with mule deer (Figure F.4a and Figure F.4c), both risk factors (long period of time since first detection and number of endemic locales) increase together apart from Montana (with lower numbers of deer and hunters) and Texas (with higher numbers of deer and hunters), where they have several endemic locales given a relatively recent first detection. The same general risk factor pattern persists for states without mule deer (Figure F.4b and Figure F.4d), although the groupings of each risk factor combination are maintained across broad ranges of deer populations and number of hunters. Again, outliers are Arkansas and Tennessee (having relatively recent detection and high numbers of endemic locales) and New York, which has only had a few cases of CWD since its initial detection many years ago.

National Academies of Sciences, Engineering, and Medicine. 2025. State of Knowledge Regarding Transmission, Spread, and Management of Chronic Wasting Disease in U.S. Captive and Free-Ranging Cervid Populations. Washington, DC: The National Academies Press. https://doi.org/10.17226/27449.


Texas Game Wardens Near Conclusion of ‘Ghost Deer’ Case with 24 Suspects, 1,400 Charges Filed Statewide

Aug. 14, 2025

Media Contact: TPWD News, Business Hours, 512-389-8030

AUSTIN – The Texas Game Warden investigation known as "Ghost Deer" has reached a possible conclusion after two additional suspects turned themselves in on felony charges. This brings the total number of individuals implicated in the case to 24, with approximately 1,400 charges filed across 11 Texas counties.

Ken Schlaudt, 64, of San Antonio, the owner of four deer breeding facilities and one release site, along with facility manager Bill Bowers, 55, of San Angelo, surrendered to the Travis County District Attorney’s Office on charges of felony tampering with a governmental record. Both men allegedly entered false information into the Texas Wildlife Information Management System (TWIMS) to facilitate illegal smuggling of white-tailed breeder deer. They also face more than 100 misdemeanor charges related to unlawful breeder deer activities in Tom Green County.

The "Ghost Deer" investigation has uncovered widespread, coordinated deer breeding violations including, but not limited to: smuggling captive breeder deer and free-range whitetail deer between breeder facilities and ranches, Chronic Wasting Disease (CWD) testing violations, license violations and misdemeanor and felony drug charges relating to the possession and mishandling of prescribed sedation drugs classified as controlled substances.

The suspects charged in the case include:

Evan Bircher, 59, San Antonio Vernon Carr, 55, Corpus Christi Jarrod Croaker, 47, Corpus Christi Terry Edwards, 54, Angleton Joshua Jurecek, 41, Alice Justin Leinneweber, 36, Orange Grove James Mann, 53, Odem Gage McKinzie, 28, Normanna Herbert “Tim” McKinzie, 47, Normanna Eric Olivares, 47, Corpus Christi Bruce Pipkin, 57, Beaumont Dustin Reynolds, 38, Robstown Kevin Soto, 55, Hockley Jared Utter, 52, Pipe Creek Reed Vollmering, 32, Orange Grove Clint West, 56, Beaumont James Whaley, 49, Sevierville, Tenn. Ryder Whitstine, 19, Rockport Ryker Whitstine, 21, Rockport Claude Wilhelm, 52, Orange Cases are pending adjudication in Bandera, Bee, Brazoria, Duval, Edwards, Jim Wells, Live Oak, Montgomery, Tom Green, Travis and Webb counties.

The investigation began in March 2024 when game wardens discovered the first violations during a traffic stop.


That incident led wardens to the much larger network of violations,


resulting in one of the largest deer smuggling operations in Texas history.

About Texas Game Wardens

Texas Game Wardens, within the Law Enforcement Division of Texas Parks and Wildlife Department, are responsible for enforcing laws related to the conservation and management of natural resources and public safety through community-based law enforcement. Their mission is to provide hunting, fishing and outdoor recreation opportunities for the use and enjoyment of present and future generations. Additionally, they play a crucial role in search and rescue operations during natural disasters, exemplifying their commitment to protecting both the environment and the people of Texas.

If you witness a fishing, wildlife or boating violation in progress, please call 1-800-792-GAME(4263) immediately and report it to Operation Game Thief (OGT), Texas’ Wildlife Crime-Stoppers Program. You can also text your tip by sending the keyword TXOGT plus your tip to 847411 or through the Texas OGT App, available for iOS and Android devices. Dispatchers are available 24/7.


Texas Chronic Wasting Disease CWD TSE Prion Dashboard Update August 2025


WEDNESDAY, MAY 14, 2025

Texas CWD TSE Prion Cases Rises to 1099 Confirmed Cases To Date

Entries CWD Positives

Positive Number CWD Positive Confirmation Date Free Range Captive County Source Species Sex Age

1099 5/5/25 Breeder Deer Gillespie Facility #14 White-tailed Deer M 4.9
1098 4/24/25 Breeder Deer Zavala Facility #23 White-tailed Deer F 7.8
1097 4/24/25 Breeder Deer Zavala Facility #23 White-tailed Deer F 7.8
1096 4/17/25 Breeder Release Site Zavala N/A White-tailed Deer M 10.5
1095 4/3/25 Breeder Deer Kimble Facility #26 White-tailed Deer F 2.5
1094 4/3/25 Breeder Deer Kimble Facility #26 White-tailed Deer F 6.5
1093 4/3/25 Breeder Deer Kimble Facility #26 White-tailed Deer F 3.5
1092 4/3/25 Breeder Deer Frio Facility #24 White-tailed Deer F 1.7
1091 4/3/25 Breeder Deer Frio Facility #24 White-tailed Deer F 1.7
1090 4/3/25 Breeder Deer Frio Facility #24 White-tailed Deer F 3.7
1089 4/3/25 Breeder Deer Frio Facility #24 White-tailed Deer F 5.7
1088 4/3/25 Breeder Deer Frio Facility #24 White-tailed Deer F 5.7
1087 4/3/25 Breeder Deer Frio Facility #24 White-tailed Deer F 7.7
1086 4/3/25 Breeder Deer Frio Facility #24 White-tailed Deer F 3.7
1085 4/3/25 Breeder Deer Frio Facility #24 White-tailed Deer F 3.7
1084 3/19/25 Free Range El Paso N/A Mule Deer M 6.5
1083 3/14/25 Breeder Deer Frio Facility #24 White-tailed Deer M 1.7
1082 2/27/25 Breeder Deer Kaufman Facility #36 White-tailed Deer F 0.5
1081 2/27/25 Breeder Deer Kaufman Facility #36 White-tailed Deer M 1.5
1080 2/21/25 Breeder Deer Gillespie Facility #15 White-tailed Deer M 2.5
1079 2/19/25 Breeder Deer Frio Facility #24 White-tailed Deer M 1.4
1078 2/13/25 Breeder Release Site Medina Facility #3 Elk F 4
1077 1/14/25 Breeder Deer Frio Facility #24 White-tailed Deer F 2.5
1076 1/14/25 Breeder Deer Frio Facility #24 White-tailed Deer M 1.5
1075 1/14/25 Breeder Deer Frio Facility #24 White-tailed Deer M 1.5
1074 1/24/25 Breeder Deer Zavala Facility #23 White-tailed Deer F 1.5
1073 1/24/25 Breeder Deer Zavala Facility #23 White-tailed Deer F 4.5
1072 1/24/25 Breeder Deer Zavala Facility #23 White-tailed Deer M 2.5
1071 1/24/25 Breeder Deer Zavala Facility #23 White-tailed Deer M 2.5
1070 1/24/25 Breeder Deer Zavala Facility #23 White-tailed Deer M 3.5
1069 2/4/25 Breeder Release Site Brown N/A White-tailed Deer F 2.6
1068 1/23/25 Breeder Release Site Sutton N/A White-tailed Deer M 6.5
1067 1/23/25 Breeder Release Site Medina Facility #3 White-tailed Deer M 5.5
1066 1/24/25 Breeder Release Site Hunt N/A White-tailed Deer M 2.5
1065 1/14/25 Breeder Release Site Zavala N/A White-tailed Deer M 5.5
1064 1/14/25 Breeder Release Site Zavala N/A White-tailed Deer M 5.5
1063 1/16/25 Free Range Hudspeth N/A Mule Deer M 8.5
1062 1/7/25 Breeder Deer Real Facility #29 White-tailed Deer F 3.4
1061 12/26/24 Breeder Release Site Brown N/A White-tailed Deer F 3.5

Snip…see full list of CWD Positives;

Snip…see full list of CWD Positives;


WEDNESDAY, MAY 14, 2025

Texas CWD TSE Prion Cases Rises to 1099 Confirmed Cases To Date


December 2024

***> TEXAS CWD TSE PRION POSITIVE SAMPLES BY CALENDAR YEAR JANUARY 1 TO DECEMBER 31 2024 TOTAL TO DATE 1061 CASES CONFIRMED

Texas CWD total by calendar years


May 2024

Texas TAHC TPWD Confirm 132 More Cases of CWD TSE PrP

Jumps from 663 in March, to 795 Positive In May 2024, wow!




Counties where CWD Exposed Deer were Released


Number of CWD Exposed Deer Released by County


Published: 05 August 2025

Vertical transmission of chronic wasting disease in free-ranging white-tailed deer populations

Abstract Chronic wasting disease (CWD) is a fatal neurodegenerative disease affecting cervids across North America, Northern Europe, and Asia. Disease transmission among cervids has historically been attributed to direct animal-to-animal contact with ‘secreta’ (saliva, blood, urine, and feces) containing the infectious agent, and indirect contact with the agent shed to the environment in these bodily components. Mounting evidence provides another mechanism of CWD transmission, that from mother-to-offspring, including during pregnancy (vertical transmission). Here we describe the detection of the infectious CWD agent and prion seeding in fetal and reproductive tissues collected from healthy-appearing free-ranging white-tailed deer (Odocoileus virginianus) from multiple U.S. states by mouse bioassay and in vitro prion amplification assays. This is the first report of the infectious agent in multiple in utero derived fetal and maternal-fetal reproductive tissues, providing evidence that CWD infections are propagated within gestational fetal tissues of white-tailed deer populations. This work confirms previous experimental and field findings in several cervid species supporting vertical transmission as an additional mechanism of CWD transmission and may help to further explain the facile dissemination of this disease among captive and free-ranging cervid populations.

Snip…

We report infectious prions in the reproductive and fetal tissue of naturally exposed free-ranging white-tailed deer suggesting that in utero maternal transmission is likely an underappreciated mode of CWD transmission. Our study shows that vertical transmission is indeed a viable route of infection within the southeastern U.S. and is another potential factor contributing to the relentless spread of chronic wasting disease.


***> Politicians, sperm mills, Semen, And CWD, what if?

Jerking for Dollars, and CWD TSE Prion, what if?

Talk about big bucks: Deer semen donations are fueling South Texas campaign Each deer semen straw — from bucks with names like Gladiator Sunset, Sweet Dreams and Bandit — was assigned a $1,000 value, according to her campaign finance report.

THURSDAY, APRIL 10, 2025

CWD TSE Prion, Politics, Friendly Fire, Unforeseen Consequences, What If?


SUNDAY, AUGUST 02, 2015

TEXAS CWD, Have you been ThunderStruck, deer semen, straw bred bucks, super ovulation, and the potential TSE Prion connection, what if?


Detection of chronic wasting disease prions in soil at an illegal white-tailed deer carcass disposal site

Published online: 06 Jun 2025

Abstract

Chronic wasting disease (CWD) is a contagious prion disorder affecting cervids such as deer, elk, caribou, and moose, causing progressive and severe neurological degeneration followed by eventual death. As CWD prions (PrPSc) accumulate in the body, they are shed through excreta and secreta, as well as through decomposing carcasses. Prions can persist in the environment for years, posing significant concerns for ongoing transmission to susceptible cervids and pose an unknown risk to sympatric species. We used a validated protocol for real-time quaking-induced conversion (RT-QuIC) in vitro prion amplification assay to detect prions in soil collected within and around an illegal white-tailed deer (Odocoileus virginianus, WTD) carcass disposal site and associated captive WTD farm in Beltrami County, Minnesota. We detected PrPSc in 26 of 201 soil samples across 15 locations within the illegal disposal site and one on the farm that housed the cervids. Importantly, a subset of RT-QuIC positive soil samples was collected from soils where carcasses were recovered, providing direct evidence that environmental contamination resulted from this illegal activity. These findings reveal that improper cervid carcass disposal practices may have important implications for ongoing CWD transmission through the environment.

Snip…

Conclusions

Using RT-QuIC, we detected PrPSc in 26 of 201 soil samples collected across 16 locations on public land where WTD carcasses had been disposed and the captive facility from where they originated. Within the disposal site, 25 out of 124 soil samples (20%) tested positive for PrPSc. Among those positive detections, 17, or 68%, were collected from locations where CWD-positive WTD remains had been previously recovered. This environmental investigation demonstrates how improper cervid carcass disposal practices can result in persistent environmental contamination, posing a potential risk to wildlife health. Given that disposal of livestock on the landscape is a common practice among producers [Citation54–56], these findings underscore the need for improved disposal practices and further investigation of environmental impacts. Expanding on this area of environmental research is crucial as the geographic range of CWD continues to expand [Citation57]. The use of RT-QuIC for prion detection in environmental samples offers an exciting advancement to environmental surveillance for prions, though as we demonstrate here and in Grunklee et al. [Citation41], assay optimization and validation for use with different environmental samples, including new soil types, is still necessary. Further enhancements to RT-QuIC and other methodologies for prion detection will facilitate more opportunities to explore the persistence, degradation, transport, and remediation of environmental prions.


While the disease control measures effectively eliminated prion seeding activity in CWD-affected farms, CWD recurred at two of the 18 remediated farms 4 to 5 years after restocking animals. It remains unclear whether the recurrence of CWD at the two farms was due to residual prions in the environment after the control measures, or the introduction of the infected animals from other farms. This uncertainty is heightened by the annual occurrence of CWD at multiple farms and the absence of a traceability system for farmed cervids.

Keywords: Chronic wasting disease (CWD); NaOH; Protein-misfolding cyclic amplification (PMCA); Republic of Korea; farm; prions; remediation; topsoil.


“While the disease control measures effectively eliminated prion seeding activity in CWD-affected farms, CWD recurred at two of the 18 remediated farms 4 to 5 years after restocking animals.”

I remember what “deep throat” told me about Scrapie back around 2001, during early days of my BSE investigation, after my Mom died from hvCJD, I never forgot, and it seems it’s come to pass;

***> Confidential!!!!

***> As early as 1992-3 there had been long studies conducted on small pastures containing scrapie infected sheep at the sheep research station associated with the Neuropathogenesis Unit in Edinburgh, Scotland. Whether these are documented...I don't know. But personal recounts both heard and recorded in a daily journal indicate that leaving the pastures free and replacing the topsoil completely at least 2 feet of thickness each year for SEVEN years....and then when very clean (proven scrapie free) sheep were placed on these small pastures.... the new sheep also broke out with scrapie and passed it to offspring. I am not sure that TSE contaminated ground could ever be free of the agent!! A very frightening revelation!!!

---end personal email---end...tss

and so it seems…

so, this is what we leave our children and grandchildren?

Rapid recontamination of a farm building occurs after attempted prion removal

First published: 19 January 2019 https://doi.org/10.1136/vr.105054

The data illustrates the difficulty in decontaminating farm buildings from scrapie, and demonstrates the likely contribution of farm dust to the recontamination of these environments to levels that are capable of causing disease.

snip...

This study clearly demonstrates the difficulty in removing scrapie infectivity from the farm environment. Practical and effective prion decontamination methods are still urgently required for decontamination of scrapie infectivity from farms that have had cases of scrapie and this is particularly relevant for scrapie positive goatherds, which currently have limited genetic resistance to scrapie within commercial breeds.24 This is very likely to have parallels with control efforts for CWD in cervids.


***>This is very likely to have parallels with control efforts for CWD in cervids.


Front. Vet. Sci., 14 September 2015 | https://doi.org/10.3389/fvets.2015.00032

Objects in contact with classical scrapie sheep act as a reservoir for scrapie transmission

In conclusion, the results in the current study indicate that removal of furniture that had been in contact with scrapie-infected animals should be recommended, particularly since cleaning and decontamination may not effectively remove scrapie infectivity (31), even though infectivity declines considerably if the pasture and the field furniture have not been in contact with scrapie-infected sheep for several months. As sPMCA failed to detect PrPSc in furniture that was subjected to weathering, even though exposure led to infection in sheep, this method may not always be reliable in predicting the risk of scrapie infection through environmental contamination.


"Additionally, we have determined that prion seeding activity is retained for at least fifteen years at a contaminated site following attempted remediation."

15 YEARS!

Detection of prions in soils contaminated by multiple routes

Results: We are able to detect prion seeding activity at multiple types of environmental hotspots, including carcass sites, contaminated captive facilities, and scrapes (i.e. urine and saliva). Differences in relative prion concentration vary depending on the nature and source of the contamination. Additionally, we have determined that prion seeding activity is retained for at least fifteen years at a contaminated site following attempted remediation.

Conclusions: Detection of prions in the environment is of the utmost importance for controlling chronic wasting disease spread. Here, we have demonstrated a viable method for detection of prions in complex environmental matrices. However, it is quite likely that this method underestimates the total infectious prion load in a contaminated sample, due to incomplete recovery of infectious prions. Further refinements are necessary for accurate quantification of prions in such samples, and to account for the intrinsic heterogeneities found in the broader environment.

Funded by: Wisconsin Department of Natural Resources

Prion 2023 Abstracts


SUNDAY, APRIL 06, 2025

Failure to prevent classical scrapie after repeated decontamination of a barn



CWD, So, this is what we leave our children and grandchildren?

Detection of chronic wasting disease prions in the farm soil of the Republic of Korea

Here, we show that prion seeding activity was detected in extracts from farm soil following 4 years of incubation with CWD-infected brain homogenate.


=====***>

"Additionally, we have determined that prion seeding activity is retained for at least fifteen years at a contaminated site following attempted remediation."

=====***>

Detection of prions in soils contaminated by multiple routes

Results: We are able to detect prion seeding activity at multiple types of environmental hotspots, including carcass sites, contaminated captive facilities, and scrapes (i.e. urine and saliva). Differences in relative prion concentration vary depending on the nature and source of the contamination. Additionally, we have determined that prion seeding activity is retained for at least fifteen years at a contaminated site following attempted remediation.

Conclusions: Detection of prions in the environment is of the utmost importance for controlling chronic wasting disease spread. Here, we have demonstrated a viable method for detection of prions in complex environmental matrices. However, it is quite likely that this method underestimates the total infectious prion load in a contaminated sample, due to incomplete recovery of infectious prions. Further refinements are necessary for accurate quantification of prions in such samples, and to account for the intrinsic heterogeneities found in the broader environment.

Funded by: Wisconsin Department of Natural Resources

Prion 2023 Abstracts


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

The detection of PrPCWD in soils at attractant sites within an endemic CWD zone significantly advances our understanding of environmental PrPCWD accumulation dynamics, providing valuable information for advancing adaptive CWD management approaches.


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



***> Infectious agent of sheep scrapie may persist in the environment for at least 16 years

***> Nine of these recurrences occurred 14–21 years after culling, apparently as the result of environmental contamination, but outside entry could not always be absolutely excluded.

JOURNAL OF GENERAL VIROLOGY Volume 87, Issue 12

Infectious agent of sheep scrapie may persist in the environment for at least 16 years Free


Rapid recontamination of a farm building occurs after attempted prion removal

First published: 19 January 2019 https://doi.org/10.1136/vr.105054

The data illustrates the difficulty in decontaminating farm buildings from scrapie, and demonstrates the likely contribution of farm dust to the recontamination of these environments to levels that are capable of causing disease. snip...

This study clearly demonstrates the difficulty in removing scrapie infectivity from the farm environment. Practical and effective prion decontamination methods are still urgently required for decontamination of scrapie infectivity from farms that have had cases of scrapie and this is particularly relevant for scrapie positive goatherds, which currently have limited genetic resistance to scrapie within commercial breeds.24 This is very likely to have parallels with control efforts for CWD in cervids.


***>This is very likely to have parallels with control efforts for CWD in cervids.


Chronic Wasting Disease CWD TSE Prion

THE CWD TSE Prion aka mad cow type disease is not your normal pathogen.

The TSE prion disease survives ashing to 600 degrees celsius, that’s around 1112 degrees farenheit.

you cannot cook the TSE prion disease out of meat.

you can take the ash and mix it with saline and inject that ash into a mouse, and the mouse will go down with TSE.

Prion Infected Meat-and-Bone Meal Is Still Infectious after Biodiesel Production as well.

the TSE prion agent also survives Simulated Wastewater Treatment Processes.

IN fact, you should also know that the TSE Prion agent will survive in the environment for years, if not decades.

you can bury it and it will not go away.

The TSE agent is capable of infected your water table i.e. Detection of protease-resistant cervid prion protein in water from a CWD-endemic area.

it’s not your ordinary pathogen you can just cook it out and be done

New studies on the heat resistance of hamster-adapted scrapie agent: Threshold survival after ashing at 600°C suggests an inorganic template of replication


Prion Infected Meat-and-Bone Meal Is Still Infectious after Biodiesel Production


March 13, 2025

Prion Partitioning and Persistence in Environmental Waters


Prions in Waterways


Detection of protease-resistant cervid prion protein in water from a CWD-endemic area


A Quantitative Assessment of the Amount of Prion Diverted to Category 1 Materials and Wastewater During Processing


Rapid assessment of bovine spongiform encephalopathy prion inactivation by heat treatment in yellow grease produced in the industrial manufacturing process of meat and bone meals


THURSDAY, FEBRUARY 28, 2019

BSE infectivity survives burial for five years with only limited spread


So, this is what we leave our children and grandchildren?

CDC CWD TSE Prion Update 2025

KEY POINTS

Chronic wasting disease affects deer, elk and similar animals in the United States and a few other countries.

The disease hasn't been shown to infect people.

However, it might be a risk to people if they have contact with or eat meat from animals infected with CWD.


Prions in Muscles of Cervids with Chronic Wasting Disease, Norway

Volume 31, Number 2—February 2025

Research

Prions in Muscles of Cervids with Chronic Wasting Disease, Norway

Snip…

In summary, the results of our study indicate that prions are widely distributed in peripheral and edible tissues of cervids in Norway, including muscles. This finding highlights the risk of human exposure to small amounts of prions through handling and consuming infected cervids. Nevertheless, we note that this study did not investigate the zoonotic potential of the Norway CWD prions. In North America, humans have historically consumed meat from CWD-infected animals, which has been documented to harbor prions (35,44–47). Despite the potential exposure to prions, no epidemiologic evidence indicates a correlation between the occurrence of CWD cases in animals and the prevalence of human prion diseases (48). A recent bioassay study reported no transmissions from 3 Nordic isolates into transgenic mice expressing human PrP (49). Therefore, our findings should be interpreted with caution in terms of human health implications, and further research is required to determine the zoonotic potential of these CWD strains.

The presence of prions in peripheral tissues indicates that CWD may have a systemic nature in all Norwegian cervid species, challenging the view that prions are exclusively localized in the CNS in sporadic CWD of moose and red deer. Our findings expand the notion of just how widely distributed prions can be in cervids affected with CWD and call into question the capability of emerging CWD strains in terms of infectivity to other species, including humans.

Appendix



Volume 31, Number 2—February 2025

Dispatch

Detection of Chronic Wasting Disease Prions in Raw, Processed, and Cooked Elk Meat, Texas, USA

Rebeca Benavente, Fraser Brydon, Francisca Bravo-Risi, Paulina Soto, J. Hunter Reed, Mitch Lockwood, Glenn Telling, Marcelo A. Barria, and Rodrigo MoralesComments to Author

Snip…

CWD prions have been detected in the muscle of both farmed and wild deer (10), and at concentrations relevant to sustain disease transmission (11). CWD prions have also been identified across several cervid species and in multiple tissues, including lymph nodes, spleen, tongue, intestines, adrenal gland, eyes, reproductive tissues, ears, lungs, and liver, among others (12–14). Those findings raise concerns about the safety of ingesting processed meats that contain tissues other than skeletal muscle (15) (Appendix). https://wwwnc.cdc.gov/eid/article/31/2/24-0906-app1.pdf .

In addition, those findings highlight the need for continued vigilance and research on the transmission risks of prion diseases and for development of new preventative and detection measures to ensure the safety of the human food supply.

Snip…

Overall, our study results confirm previous reports describing the presence of CWD prions in elk muscles (13). The data also demonstrated CWD prion persistence in food products even after processing through different procedures, including the addition of salts, spices, and other edible elements. Of note, our data show that exposure to high temperatures used to cook the meat increased the availability of prions for in vitro amplification. Considering the potential implications in food safety and public health, we believe that the findings described in this study warrant further research. Our results suggest that although the elk meat used in this study resisted different manipulations involved in subsequent consumption by humans, their zoonotic potential was limited. Nevertheless, even though no cases of CWD transmission to human have been reported, the potential for human infection is still unclear and continued monitoring for zoonotic potential is warranted.


Volume 31, Number 1—January 2025

Dispatch

Detection of Prions in Wild Pigs (Sus scrofa) from Areas with Reported Chronic Wasting Disease Cases, United States

Abstract

Using a prion amplification assay, we identified prions in tissues from wild pigs (Sus scrofa) living in areas of the United States with variable chronic wasting disease (CWD) epidemiology. Our findings indicate that scavenging swine could play a role in disseminating CWD and could therefore influence its epidemiology, geographic distribution, and interspecies spread.

Snip…

Conclusions In summary, results from this study showed that wild pigs are exposed to cervid prions, although the pigs seem to display some resistance to infection via natural exposure. Future studies should address the susceptibility of this invasive animal species to the multiple prion strains circulating in the environment. Nonetheless, identification of CWD prions in wild pig tissues indicated the potential for pigs to move prions across the landscape, which may, in turn, influence the epidemiology and geographic spread of CWD.


Although the current U.S. feed ban is based on keeping tissues from TSE infected cattle from contaminating animal feed, swine rations in the U.S. could contain animal derived components including materials from scrapie infected sheep and goats. These results indicating the susceptibility of pigs to sheep scrapie, coupled with the limitations of the current feed ban, indicates that a revision of the feed ban may be necessary to protect swine production and potentially human health.

2. Determined that pigs naturally exposed to chronic wasting disease (CWD) may act as a reservoir of CWD infectivity. Chronic wasting disease is a naturally occurring, fatal, neurodegenerative disease of cervids. The potential for swine to serve as a host for the agent of CWD disease is unknown. The purpose of this study was to investigate the susceptibility of swine to the CWD agent following experimental oral or intracranial inoculation. Pigs were assigned to 1 of 3 groups: intracranially inoculated; orally inoculated; or non-inoculated. At market weight age, half of the pigs in each group were tested ('market weight' groups). The remaining pigs ('aged' groups) were allowed to incubate for up to 73 months post inoculation (MPI). Tissues collected at necropsy were examined for disease-associated prion protein (PrPSc) by multiple diagnostic methods. Brain samples from selected pigs were bioassayed in mice expressing porcine prion protein. Some pigs from each inoculated group were positive by one or more tests. Bioassay was positive in 4 out of 5 pigs assayed. Although only small amounts of PrPSc were detected using sensitive methods, this study demonstrates that pigs can serve as hosts for CWD. Detection of infectivity in orally inoculated pigs using mouse bioassay raises the possibility that naturally exposed pigs could act as a reservoir of CWD infectivity. Currently, swine rations in the U.S. could contain animal derived components including materials from deer or elk. In addition, feral swine could be exposed to infected carcasses in areas where CWD is present in wildlife populations. The current feed ban in the U.S. is based exclusively on keeping tissues from TSE infected cattle from entering animal feeds. These results indicating the susceptibility of pigs to CWD, coupled with the limitations of the current feed ban, indicates that a revision of the feed ban may be necessary to protect swine production and potentially human health.





***> Price of TSE Prion Poker goes up substantially, all you cattle ranchers and such, better pay close attention here...terry <***

Transmission of the chronic wasting disease agent from elk to cattle after oronasal exposure

Justin Greenlee, Jifeng Bian, Zoe Lambert, Alexis Frese, and Eric Cassmann Virus and Prion Research Unit, National Animal Disease Center, USDA-ARS, Ames, IA, USA

Aims: The purpose of this study was to determine the susceptibility of cattle to chronic wasting disease agent from elk.

Materials and Methods: Initial studies were conducted in bovinized mice using inoculum derived from elk with various genotypes at codon 132 (MM, LM, LL). Based upon attack rates, inoculum (10% w/v brain homogenate) from an LM132 elk was selected for transmission studies in cattle. At approximately 2 weeks of age, one wild type steer (EE211) and one steer with the E211K polymorphism (EK211) were fed 1 mL of brain homogenate in a quart of milk replacer while another 1 mL was instilled intranasally. The cattle were examined daily for clinical signs for the duration of the experiment. One steer is still under observation at 71 months post-inoculation (mpi).

Results: Inoculum derived from MM132 elk resulted in similar attack rates and incubation periods in mice expressing wild type or K211 bovine PRNP, 35% at 531 days post inoculation (dpi) and 27% at 448 dpi, respectively. Inoculum from LM132 elk had a slightly higher attack rates in mice: 45% (693 dpi) in wild type cattle PRNP and 33% (468) in K211 mice. Inoculum from LL132 elk resulted in the highest attack rate in wild type bovinized mice (53% at 625 dpi), but no K211 mice were affected at >700 days. At approximately 70 mpi, the EK211 genotype steer developed clinical signs suggestive of prion disease, depression, low head carriage, hypersalivation, and ataxia, and was necropsied. Enzyme immunoassay (IDEXX) was positive in brainstem (OD=4.00, but non-detect in retropharyngeal lymph nodes and palatine tonsil. Immunoreactivity was largely limited to the brainstem, midbrain, and cervical spinal cord with a pattern that was primarily glia-associated.

Conclusions: Cattle with the E211K polymorphism are susceptible to the CWD agent after oronasal exposure of 0.2 g of infectious material.

Funded by: This research was funded in its entirety by congressionally appropriated funds to the United States Department of Agriculture, Agricultural Research Service. The funders of the work did not influence study design, data collection and analysis, decision to publish, or preparation of the manuscript.

*****>>> "Cattle with the E211K polymorphism are susceptible to the CWD agent after oronasal exposure of 0.2 g of infectious material." <<<*****

=====end

Strain characterization of chronic wasting disease in bovine-PrP transgenic mice

Nuria Jerez-Garrido1, Sara Canoyra1, Natalia Fernández-Borges1, Alba Marín Moreno1, Sylvie L. Benestad2, Olivier Andreoletti3, Gordon Mitchell4, Aru Balachandran4, Juan María Torres1 and Juan Carlos Espinosa1. 1 Centro de Investigación en Sanidad Animal, CISA-INIA-CSIC, Madrid, Spain. 2 Norwegian Veterinary Institute, Ås, Norway. 3 UMR Institut National de la Recherche Agronomique (INRA)/École Nationale Vétérinaire de Toulouse (ENVT), Interactions Hôtes Agents Pathogènes, Toulouse, France. 4 Canadian Food Inspection Agency, Ottawa, Canada.

Aims: Chronic wasting disease (CWD) is an infectious prion disease that affects cervids. Various CWD prion strains have been identified in different cervid species from North America and Europe. The properties of the infectious prion strains are influenced by amino acid changes and polymorphisms in the PrP sequences of different cervid species. This study, aimed to assess the ability of a panel of CWD prion isolates from diverse cervid species from North America and Europe to infect bovine species, as well as to investigate the properties of the prion strains following the adaptation to the bovine-PrP context.

Materials and Methods: BoPrP-Tg110 mice overexpressing the bovine-PrP sequence were inoculated by intracranial route with a panel of CWD prion isolates from both North America (two white-tailed deer and two elk) and Europe (one reindeer, one moose and one red deer).

Results: Our results show distinct behaviours in the transmission of the CWD isolates to the BoPrP-Tg110 mouse model. Some of these isolates did not transmit even after the second passage. Those able to transmit displayed differences in terms of attack rate, survival times, biochemical properties of brain PrPres, and histopathology.

Conclusions: Altogether, these results exhibit the diversity of CWD strains present in the panel of CWD isolates and the ability of at least some CWD isolates to infect bovine species. Cattle being one of the most important farming species, this ability represents a potential threat to both animal and human health, and consequently deserves further study.

Funded by: MCIN/AEI /10.13039/501100011033 and by European Union NextGeneration EU/PRTR

Grant number: PCI2020-120680-2 ICRAD

"Altogether, these results exhibit the diversity of CWD strains present in the panel of CWD isolates and the ability of at least some CWD isolates to infect bovine species. Cattle being one of the most important farming species, this ability represents a potential threat to both animal and human health, and consequently deserves further study."

=====end


so, this is what we leave our children and grandchildren?

Redefining the zoonotic potential of chronic wasting disease

Project Number 5R01NS121016-04

Contact PI/Project Leader SCHATZL, HERMANN M

Other PIs

Awardee Organization

UNIVERSITY OF CALGARY

Description

Abstract Text

The rapid expansion of chronic wasting disease (CWD), a prion disease of free-ranging and farmed deer, elk and moose, is a major and ongoing threat in North America. Approximately 1 in 36 Americans hunt deer and elk and eat venison, and it is estimated that 7,000 – 15,000 CWD-infected cervids are consumed annually. This fuels growing concerns about the human health risks imposed by CWD. There are no documented cases of CWD transmission to humans, even though with the long incubation periods of all prion diseases and the unknown presentation of CWD in humans definite conclusions are not possible. The zoonotic potential of prion diseases has been exemplified by bovine spongiform encephalopathy (BSE, mad cow disease) which resulted in a new form of human prion disease (vCJD). BSE was transmissible to Cynomolgus macaques and transgenic mice expressing the human prion protein. Initial results of CWD transmission studies to the same non-human primate and mouse models of human prion disease were not successful, corroborating the conclusion that the zoonotic potential of CWD is low, if not absent. Our groups were part of a consortium that inoculated Cynomolgus macaques via different routes with CWD. Some animals exhibited subtle clinical signs reminiscent of prion disease, and upon euthanasia, weak signs of vacuolation, PrPSc deposition and astrocytosis in the brain were found, while no proteinase K (PK) resistant prion protein (PrP) was detectable. We have now demonstrated for the first time that CWD from macaques can transmit clinical prion disease to transgenic mouse models of CWD and human prion disease, albeit in the absence of detectable PK-resistant PrP. Bona fide PrPSc was only detected upon 3rd passage from mouse to bank vole models. Altogether, this is the first evidence that CWD very likely has zoonotic potential. The goal of the current proposal is to redefine the zoonotic potential of CWD by characterizing the biological properties of CWD prions emerging upon experimental transmission into macaques, for obtaining important information on how CWD could manifest in humans.

In Aim 1, we will study whether CWD from macaque (CWDmac) in bank voles represents a new prion strain, by comparing biochemical and biological properties to an array of known prion strains from different species.

Aim 2 addresses the question whether CWDmac represents an intermediate prion strain, adaptable to cervids or humans upon passage, and possessing an expanded host range. We will address this by in vivo passage in cervidized or humanized mouse models. In vitro, we will utilize serial PMCA and a newly generated PrP0/0 cell culture model for infection, upon reconstitution with PrP from different species.

In Aim 3, we will shed light on the observed dissociation between infectivity and the presence of bona fide PrPSc. We propose to identify atypical PrP fragments associated with CWDmac, and we will elucidate brain cell responses to CWDmac exposure by innovative single cell RNA sequencing. In summary, our studies will uncover the possible manifestation of CWD in humans, which is of critical importance for drawing definite conclusions about the zoonotic potential of CWD.

Public Health Relevance Statement

The zoonotic potential of chronic wasting disease (CWD) is unclear to date. We provide the first evidence by transmission experiments to different transgenic mouse models and bank voles that Cynomolgus macaques inoculated via different routes with CWD-positive cervid tissues harbor infectious prions that elicit clinical disease in rodents. Our proposed studies will unravel the properties of these prions, how they will adapt to humans and which pathways are activated in brain cells and associated with clinical disease. Results from these studies uncover the potential manifestation of CWD in humans, which is highly relevant for human health.


Project 3A: CWD Prion Shedding and Environmental Contamination: Role in Transmission and Zoonotic

Parent Project Number 5P01AI077774-14

Sub-Project ID 5512

Contact PI/Project Leader HOOVER, EDWARD ARTHUR

Awardee Organization UNIVERSITY OF TEXAS HLTH SCI CTR HOUSTON

Description

Abstract Text

Chronic wasting disease (CWD) is an emergent, highly transmissible, geographically expanding, prion disease of both wild and captive cervids. CWD is unique among prion diseases in its facile contagion and environmental persistence. Its expanding geographical range, combined with the increasing transport of animals and animal products, portend its continued expansion and diversification. The zoonotic potential of CWD remains poorly understood. CWD endemic areas interface cervids with livestock species and humans, posing obvious zoonotic risks that over time will increase. While it is known that strains of CWD exist, nothing is known about the zoonotic potential of these strains. Work from our applicant group has shown that CWD infected cervids continually shed prions into the environment and that previously unrecognized environmental factors can influence the emergence of a dominant strain from a mixture. The ability to recognize the zoonotic potential of CWD strains is central to mitigating CWD transmission risk. The central hypothesis for work described here is that CWD strains evolve continuously due to a combination of both host and environmental factors. We will test this hypothesis by:

i) determining the evolution and zoonotic impact of CWD strains in the native cervid species;

ii) leveraging our unique animal resources, expertise, and in vivo & in vitro methodologies to assess environmental factors that alter CWD strain selection and evolution and

iii) evaluate zoonotic potential of CWD strains by a complementary combination of in vitro amplification assays and animal transmission studies.

The results will provide new information about this emergent transmissible prion disease and the risk it poses to humans and other species.


Project 3B: Pathogenesis Transmission and Detection of Zoonotic Prion Diseases

Parent Project Number 5P01AI077774-14

Sub-Project ID 5513

Contact PI/Project Leader BARTZ, JASON C

Awardee Organization UNIVERSITY OF TEXAS HLTH SCI CTR HOUSTON

Description Abstract Text

Project Summary: Chronic wasting disease (CWD) is an emergent, highly transmissible, geographically expanding, prion disease of both wild and captive cervids. CWD is unique among prion diseases in its facile contagion and environmental persistence. Its expanding geographical range, combined with the increasing transport of animals and animal products, portend its continued expansion and diversification. The zoonotic potential of CWD remains poorly understood. CWD endemic areas interface cervids with livestock species and humans, posing obvious zoonotic risks that over time will increase. While it is known that strains of CWD exist, nothing is known about the zoonotic potential of these strains. Work from our applicant group has shown that CWD- infected cervids continually shed prions into the environment and that previously unrecognized environmental factors can influence the emergence of a dominant strain from a mixture. The ability to recognize the zoonotic potential of CWD strains is central to mitigating CWD transmission risk. The central hypothesis for work described here is that CWD strains evolve continuously due to a combination of both host and environmental factors. We will test this hypothesis by:

i) determining the evolution and zoonotic impact of CWD strains in the native cervid species;

ii) leveraging our unique animal resources, expertise, and in vivo & in vitro methodologies to assess environmental factors that alter CWD strain selection and evolution and

iii) evaluate zoonotic potential of CWD strains by a complementary combination of in vitro amplification assays and animal transmission studies.

The results will provide new information about this emergent transmissible prion disease and the risk it poses to humans and other species.


Project 1: Modeling the Mechanisms of Prion Transmission, Strain Selection, Mutation and Species Barrier in Transgenic Mice

Parent Project Number 5P01AI077774-14

Sub-Project ID 5510

Contact PI/Project Leader TELLING, GLENN C

Awardee Organization UNIVERSITY OF TEXAS HLTH SCI CTR HOUSTON

Description Abstract Text

Our broad, long-term objectives are to are to decipher the mechanisms by which infectious prions replicate, encode strain information, and evolve to acquire new properties. We propose four Specific Aims to address our central hypothesis that incompletely adapted prion strains are comprised of poorly optimized ensembles of PrPSc quasi species conformers that evolve under selective pressure towards states of enhanced stability and pathogenicity. Our particular focus is chronic wasting disease (CWD), an uncontrollable contagious epidemic of cervids of uncertain zoonotic potential. Using genetically engineered CWD-susceptible mice, cultured cells, cell free amplification, and antibodies recognizing defined conformation-dependent PrP epitopes,

Aim I will address the mechanism of adaptation of unstable emergent CWD prions in response to physical and chemical constraints.

In Aim II we will address the hypothesis that that residue 226 and other cervid PrP polymorphisms influence selection of distinct portfolios of CWD strain conformers with different adaptive potentials. Using gene targeted mice expressing physiologically controlled levels of PrP variants and in vitro systems for prion replication, we will characterize the properties of strains propagated in these backgrounds and explore whether interference between them affects selection and adaptation of CWD.

In Aim III, we will assess the properties of emergent Norwegian moose and reindeer CWD strains experimentally propagated in deer and compare with established North American CWD.

Aim IV will address an unmet need in the field of significant importance, namely the paucity of model systems and tools for studying human prions. Using newly generated gene targeted mice expressing physiological levels of human PrP and novel approaches to derive susceptible human neuroblastoma cells, we will assess the zoonotic potential of emergent CWD strains and their adapted derivatives propagated in different cervid PrP backgrounds. Our ultimate goal is to assess and manage the risk posed to humans from continually evolving prions, specifically those causing CWD, by understanding the means by which they propagate and exist as heritable strains with protean host range properties that adapt and evolve under selective pressure.


Project 2

Parent Project Number 5P01AI077774-14

Sub-Project ID 5511

Contact PI/Project Leader SOTO, CLAUDIO

Awardee Organization UNIVERSITY OF TEXAS HLTH SCI CTR HOUSTON

Description Abstract Text

ABSTRACT Chronic wasting disease (CWD) affecting various species of cervids in North American and Northern Europe represents a serious problem, because it continues to propagate uncontrollably among wild and captive cervids. CWD appears to be very heterogeneous with multiple different strains and can be transmitted to other animal species. The risk of CWD transmission to humans is unknown which is a major concern because the number of sick animals and their geographical distribution is rapidly increasing. The mechanism by which CWD propagates so efficiently among cervids is also unknown. The main goal of this project is to utilize a set of highly innovative techniques to study the cellular, molecular and structural features of naturally occurring CWD strains and their potential for inter- species transmission, particularly focusing on the possibility that certain CWD strains may infect humans. We will also attempt to elucidate the atomic resolution structure of CWD prions using cryo-electron microscopy. The overarching hypothesis is that CWD exists as multiple strains in distinct individuals and even within the same individual in different brain cells and that inter- species transmission and zoonotic potential depend on the specific strain characteristics. The project is divided in the following specific aims:

(1) Study the structural and molecular diversity of natural CWD strains and the high resolution three-dimensional structure of CWD prions.

(2) Understand CWD prion strain diversity in single brain cells isolated by laser capture microdissection and subsequently amplified by PMCA.

(3) Evaluate CWD inter-species transmission spillover potential and its effect on zoonotic potential.

(4) Analyze the deer-human prion species barrier in vivo using chimeric mice harboring human and cervid neuronal cells.

The studies included in this projects will address some of the most pressing questions regarding CWD, including

(i) the CWD prion strain variability,

(ii) the zoonotic potential of different CWD prion strains,

(iii) the atomic resolution structure of infectious prions and the structural basis of prion strains,

(iv) the cellular distribution of CWD prion strains in the brain and its gene expression consequences,

(v) the spillover potential of CWD to other animal species,

(vi) the potential role of intermediate species in the transmission of CWD prions to humans.

The findings generated in this project will be essential to design measures to prevent further propagation of CWD, and to avoid the emergence of new diseases with potentially disastrous consequences.


18. Zoonotic potential of moose-derived chronic wasting disease prions after adaptation in intermediate species

Tomás Barrioa, Jean-Yves Doueta, Alvina Huora, Séverine Lugana, Naïma Arona, Hervé Cassarda, Sylvie L. Benestadb, Juan Carlos Espinosac, Juan María Torresc, Olivier Andréolettia

aUnité Mixte de Recherche de l’Institut National de Recherche pour l’Agriculture, l’Alimentation et l’Environnement 1225 Interactions Hôtes-Agents Pathogènes, École Nationale Vétérinaire de Toulouse, 31076 Toulouse, France; bNorwegian Veterinary Institute, P.O. Box 64, NO-1431 Ås, Norway; cCentro de Investigación en Sanidad Animal (CISA-INIA), 28130, Valdeolmos, Madrid, Spain

Aims: Chronic wasting disease (CWD) is an emerging prion disease in Europe. To date, cases have been reported in three Nordic countries and in several species, including reindeer (Rangifer tarandus), moose (Alces alces) and red deer (Cervus elaphus). Cumulating data suggest that the prion strains responsible for the European cases are distinct from those circulating in North America. The biological properties of CWD prions are still poorly documented, in particular their spillover and zoonotic capacities. In this study, we aimed at characterizing the interspecies transmission potential of Norwegian moose CWD isolates.

Materials and Methods: For that purpose, we performed experimental transmissions in a panel of transgenic models expressing the PrPC sequence of various species.

Results: On first passage, one moose isolate propagated in the ovine PrPC-expressing model (Tg338). After adaptation in this host, moose CWD prions were able to transmit in mice expressing either bovine or human PrPC with high efficacy.

Conclusions: These results suggest that CWD prions can acquire enhanced zoonotic properties following adaptation in an intermediate species.

Funding

Grant number: AAPG2020 EU-CWD, ICRAD2020 TCWDE, NRC2022 NorCWD

Acknowledgement


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

regular venison eating associated with a 9 FOLD INCREASE IN RISK OF CJD

Subject: Re: DEER SPONGIFORM ENCEPHALOPATHY SURVEY & HOUND STUDY

Date: Fri, 18 Oct 2002 23:12:22 +0100

From: Steve Dealler

Reply-To: Bovine Spongiform Encephalopathy Organization: Netscape Online member

To: BSE-L@ …

######## Bovine Spongiform Encephalopathy <BSE-L@UNI-KARLSRUHE.DE> #########

Dear Terry,

An excellent piece of review as this literature is desparately difficult to get back from Government sites.

What happened with the deer was that an association between deer meat eating and sporadic CJD was found in about 1993. The evidence was not great but did not disappear after several years of asking CJD cases what they had eaten. I think that the work into deer disease largely stopped because it was not helpful to the UK industry...and no specific cases were reported.

Well, if you dont look adequately like they are in USA currenly then you wont find any!

Steve Dealler

########### http://mailhost.rz.uni-karlsruhe.de/warc/bse-l.html ############

Subject: DEER SPONGIFORM ENCEPHALOPATHY SURVEY & HOUND STUDY

From: "Terry S. Singeltary Sr." <flounder@WT.NET>

Reply To: Bovine Spongiform Encephalopathy <BSE-L@UNI-KARLSRUHE.DE>

Date: Thu, 17 Oct 2002 17:04:51 -0700

snip...

''The association between venison eating and risk of CJD shows similar pattern, with regular venison eating associated with a 9 FOLD INCREASE IN RISK OF CJD (p = 0.04).''

CREUTZFELDT JAKOB DISEASE SURVEILLANCE IN THE UNITED KINGDOM THIRD ANNUAL REPORT AUGUST 1994

Consumption of venison and veal was much less widespread among both cases and controls. For both of these meats there was evidence of a trend with increasing frequency of consumption being associated with increasing risk of CJD. (not nvCJD, but sporadic CJD...tss) These associations were largely unchanged when attention was restricted to pairs with data obtained from relatives. ...

Table 9 presents the results of an analysis of these data.

There is STRONG evidence of an association between ‘’regular’’ veal eating and risk of CJD (p = .0.01).

Individuals reported to eat veal on average at least once a year appear to be at 13 TIMES THE RISK of individuals who have never eaten veal.

There is, however, a very wide confidence interval around this estimate. There is no strong evidence that eating veal less than once per year is associated with increased risk of CJD (p = 0.51).

The association between venison eating and risk of CJD shows similar pattern, with regular venison eating associated with a 9 FOLD INCREASE IN RISK OF CJD (p = 0.04).

There is some evidence that risk of CJD INCREASES WITH INCREASING FREQUENCY OF LAMB EATING (p = 0.02).

The evidence for such an association between beef eating and CJD is weaker (p = 0.14). When only controls for whom a relative was interviewed are included, this evidence becomes a little STRONGER (p = 0.08).

snip...

It was found that when veal was included in the model with another exposure, the association between veal and CJD remained statistically significant (p = < 0.05 for all exposures), while the other exposures ceased to be statistically significant (p = > 0.05).

snip...

In conclusion, an analysis of dietary histories revealed statistical associations between various meats/animal products and INCREASED RISK OF CJD. When some account was taken of possible confounding, the association between VEAL EATING AND RISK OF CJD EMERGED AS THE STRONGEST OF THESE ASSOCIATIONS STATISTICALLY. ...

snip...

In the study in the USA, a range of foodstuffs were associated with an increased risk of CJD, including liver consumption which was associated with an apparent SIX-FOLD INCREASE IN THE RISK OF CJD. By comparing the data from 3 studies in relation to this particular dietary factor, the risk of liver consumption became non-significant with an odds ratio of 1.2 (PERSONAL COMMUNICATION, PROFESSOR A. HOFMAN. ERASMUS UNIVERSITY, ROTTERDAM). (???...TSS)

snip...see full report ;




Stephen Dealler is a consultant medical microbiologist deal@airtime.co.uk

BSE Inquiry Steve Dealler

Management In Confidence

BSE: Private Submission of Bovine Brain Dealler

snip...end

########### http://mailhost.rz.uni-karlsruhe.de/warc/bse-l.html ############

BSE INQUIRY

CJD9/10022

October 1994

Mr R.N. Elmhirst Chairman British Deer Farmers Association Holly Lodge Spencers Lane

BerksWell Coventry CV7 7BZ

Dear Mr Elmhirst,

CREUTZFELDT-JAKOB DISEASE (CJD) SURVEILLANCE UNIT REPORT

Thank you for your recent letter concerning the publication of the third annual report from the CJD Surveillance Unit. I am sorry that you are dissatisfied with the way in which this report was published.

The Surveillance Unit is a completely independant outside body and the Department of Health is committed to publishing their reports as soon as they become available. In the circumstances it is not the practice to circulate the report for comment since the findings of the report would not be amended.. In future we can ensure that the British Deer Farmers Association receives a copy of the report in advance of publication.

The Chief Medical Officer has undertaken to keep the public fully informed of the results of any research in respect of CJD. This report was entirely the work of the unit and was produced completely independantly of the the Department.

The statistical results reqarding the consumption of venison was put into perspective in the body of the report and was not mentioned at all in the press release. Media attention regarding this report was low key but gave a realistic presentation of the statistical findings of the Unit. This approach to publication was successful in that consumption of venison was highlighted only once by the media ie. in the News at one television proqramme.

I believe that a further statement about the report, or indeed statistical links between CJD and consumption of venison, would increase, and quite possibly give damaging credence, to the whole issue. From the low key media reports of which I am aware it seems unlikely that venison consumption will suffer adversely, if at all.


TSE in wild UK deer? The first case of BSE (as we now realise) was in a nyala in London zoo and the further zoo cases in ungulates were simply thought of as being interesting transmissions of scrapie initially. The big problem started to appear with animals in 1993-5 when it became clear that there was an increase in the CJD cases in people that had eaten deer although the statistics involved must have been questionable. The reason for this was that the CJD Surveillance was well funded to look into the diet of people dying of CJD. This effect is not clear with vCJD...if only because the numbers involved are much smaller and hence it is difficult to gain enough statistics. They found that many other foods did not appear to have much association at all but that deer certainly did and as years went by the association actually became clearer. The appearance of vCJD in 1996 made all this much more difficult in that it was suddenly clearer that the cases of sporadic CJD that they had been checking up until then probably had nothing to do with beef...and the study decreased. During the period there was an increasing worry that deer were involved with CJD..

see references:

DEER BRAIN SURVEY


CONFIDENTIAL AND IN CONFIDENCE TRANSMISSION TO CHIMPANZEES AND PIGS

IN CONFIDENCE

TRANSMISSION TO CHIMPANZEES

Kuru and CJD have been successfully transmitted to chimpanzees but scrapie and TME have not.

We cannot say that scrapie will not transmit to chimpanzees. There are several scrapie strains and I am not aware that all have been tried (that would have to be from mouse passaged material). Nor has a wide enough range of field isolates subsequently strain typed in mice been inoculated by the appropriate routes (i/c, i/p and i/v).

I believe the proposed experiment to determine transmissibility, if conducted, would only show the susceptibility or resistance of the chimpanzee to infection/disease by the routes used and the result could not be interpreted for the predictability of the susceptibility for man. proposals for prolonged oral exposure of chimpanzees to milk from cattle were suggested a long while ago and rejected.

In view of Dr Gibbs' probable use of chimpazees Mr Wells' comments (enclosed) are pertinent. I have yet to receive a direct communication from Dr Schellekers but before any collaboration or provision of material we should identify the Gibbs' proposals and objectives.

A positive result from a chimpanzee challenged severely would likely create alarm in some circles even if the result could not be interpreted for man. I have a view that all these agents could be transmitted provided a large enough dose by appropriate routes was given and the animals kept long enough. Until the mechanisms of the species barrier are more clearly understood it might be best to retain that hypothesis.

A negative result would take a lifetime to determine but that would be a shorter period than might be available for human exposure and it would still not answer the question regarding mans ‘susceptibility. In the meantime no doubt the negativity would be used defensively. It would however be counterproductive if the experiment finally became positive. We may learn more about public reactions following next Monday's meeting.

R Bradley

CVO (+ Mr Wells’ commenters 23 September 1990 Dr T W A Little Dr B J Shreeve

90/9.23/1.1


*** now, let’s see what the authors said about this casual link, personal communications years ago, and then the latest on the zoonotic potential from CWD to humans from the TOKYO PRION 2016 CONFERENCE.

see where it is stated NO STRONG evidence. so, does this mean there IS casual evidence ????

“Our conclusion stating that we found no strong evidence of CWD transmission to humans”

From: TSS Subject: CWD aka MAD DEER/ELK TO HUMANS ???

Date: September 30, 2002 at 7:06 am PST

From: "Belay, Ermias"

To: Cc: "Race, Richard (NIH)" ; ; "Belay, Ermias"

Sent: Monday, September 30, 2002 9:22 AM

Subject: RE: TO CDC AND NIH - PUB MED- 3 MORE DEATHS - CWD - YOUNG HUNTERS

Dear Sir/Madam, In the Archives of Neurology you quoted (the abstract of which was attached to your email), we did not say CWD in humans will present like variant CJD.. That assumption would be wrong. I encourage you to read the whole article and call me if you have questions or need more clarification (phone: 404-639-3091).

Also, we do not claim that "no-one has ever been infected with prion disease from eating venison." Our conclusion stating that we found no strong evidence of CWD transmission to humans in the article you quoted or in any other forum is limited to the patients we investigated.

Ermias Belay, M.D. Centers for Disease Control and Prevention

-----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***,

snip... full text ;


However, to date, no CWD infections have been reported in people.

sporadic, spontaneous CJD, 85%+ of all human TSE, did not just happen. never in scientific literature has this been proven. if one looks up the word sporadic or spontaneous at pubmed, you will get a laundry list of disease that are classified in such a way;

sporadic = 54,983 hits


spontaneous = 325,650 hits


key word here is 'reported'. science has shown that CWD in humans will look like sporadic CJD.

SO, how can one assume that CWD has not already transmitted to humans? they can't, and it's as simple as that. from all recorded science to date, CWD has already transmitted to humans, and it's being misdiagnosed as sporadic CJD. ...terry

*** LOOKING FOR CWD IN HUMANS AS nvCJD or as an ATYPICAL CJD, LOOKING IN ALL THE WRONG PLACES $$$ ***

However, to date, no CWD infections have been reported in people. key word here is ‘reported’. science has shown that CWD in humans will look like sporadic CJD. SO, how can one assume that CWD has not already transmitted to humans? they can’t, and it’s as simple as that. from all recorded science to date, CWD has already transmitted to humans, and it’s being misdiagnosed as sporadic CJD. …terry

*** LOOKING FOR CWD IN HUMANS AS nvCJD or as an ATYPICAL CJD, LOOKING IN ALL THE WRONG PLACES $$$ ***

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




So, this is what we leave our children and grandchildren?

CDC CWD TSE Prion Update 2025

KEY POINTS

Chronic wasting disease affects deer, elk and similar animals in the United States and a few other countries.

The disease hasn't been shown to infect people.

However, it might be a risk to people if they have contact with or eat meat from animals infected with CWD.


Volume 31, Number 4—April 2025

Research

Detection and Decontamination of Chronic Wasting Disease Prions during Venison Processing


Transmission of Cervid Prions to Humanized Mice Demonstrates the Zoonotic Potential of CWD

Samia Hannaouia, Irina Zemlyankinaa, Sheng Chun Changa, Maria Immaculata Arifina, Vincent Béringueb, Debbie McKenziec, Hermann M. Schatzla, and Sabine Gilcha

Results: Here, we provide the strongest evidence supporting the zoonotic potential of CWD prions, and their possible phenotype in humans. Inoculation of mice expressing human PrPCwith deer CWD isolates (strains Wisc-1 and 116AG) resulted in atypical clinical manifestations in > 75% of the mice, with myoclonus as leading clinical sign. Most of tg650brain homogenates were positive for seeding activity in RT-QuIC. Clinical disease and presentation was transmissible to tg650 mice and bank voles. Intriguingly, protease-resistant PrP in the brain of tg650 mice resembled that found in a familial human prion disease and was transmissible upon passage. Abnormal PrP aggregates upon infection with Wisc-1 were detectable in thalamus, hypothalamus, and midbrain/pons regions.

Unprecedented in human prion disease, feces of CWD-inoculated tg650 mice harbored prion seeding activity and infectious prions, as shown by inoculation of bank voles and tg650 with fecal homogenates.

Conclusions: This is the first evidence that CWD can infect humans and cause disease with a distinctive clinical presentation, signature, and tropism, which might be transmissible between humans while current diagnostic assays might fail to detect it. These findings have major implications for public health and CWD-management.


Transmission of prion infectivity from CWD-infected macaque tissues to rodent models demonstrates the zoonotic potential of chronic wasting disease.

Samia Hannaoui1,2, Ginny Cheng1,2, Wiebke Wemheuer3, Walter Schulz-Schaeffer3, Sabine Gilch1,2, Hermann Schatzl1,2 1University of Calgary, Calgary, Canada. 2Calgary Prion Research Unit, Calgary, Canada. 3Institute of Neuropathology, Medical Faculty, Saarland University, Homburg/Saar, Germany

***> Further passage to cervidized mice revealed transmission with a 100% attack rate.

***> Our findings demonstrate that macaques, considered the best model for the zoonotic potential of prions, were infected upon CWD challenge, including the oral one.

****> The disease manifested as atypical in macaques and initial transgenic mouse transmissions, but with infectivity present at all times, as unveiled in the bank vole model with an unusual tissue tropism.

***> Epidemiologic surveillance of prion disease among cervid hunters and people likely to have consumed venison contaminated with chronic wasting disease

=====


The finding that infectious PrPSc was shed in fecal material of CWD-infected humanized mice and induced clinical disease, different tropism, and typical three banding pattern-PrPres in bank voles that is transmissible upon second passage is highly concerning for public health. The fact that this biochemical signature in bank voles resembles that of the Wisc-1 original deer isolate and is different from that of bvWisc-1, in the migration profile and the glyco-form-ratio, is valid evidence that these results are not a product of contamination in our study. If CWD in humans is found to be contagious and transmissible among humans, as it is in cervids [57], the spread of the disease within humans might become endemic.

Transmission of cervid prions to humanized mice demonstrates the zoonotic potential of CWD

Acta Neuropathol 144, 767–784 (2022). https://doi.org/10.1007/s00401-022-02482-9

Published

22 August 2022


Fortuitous generation of a zoonotic cervid prion strain

Aims: Whether CWD prions can infect humans remains unclear despite the very substantial scale and long history of human exposure of CWD in many states or provinces of USA and Canada. Multiple in vitro conversion experiments and in vivo animal studies indicate that the CWD-to-human transmission barrier is not unbreakable. A major long-term public health concern on CWD zoonosis is the emergence of highly zoonotic CWD strains. We aim to address the question of whether highly zoonotic CWD strains are possible.

Materials and Methods: We inoculated several sCJD brain samples into cervidized transgenic mice (Tg12), which were intended as negative controls for bioassays of brain tissues from sCJD cases who had potentially been exposed to CWD. Some of the Tg12 mice became infected and their brain tissues were further examined by Western blot as well as serial passages in humanized or cervidized mice.

Results: Passage of sCJDMM1 in transgenic mice expressing elk PrP (Tg12) resulted in a “cervidized” CJD strain that we termed CJDElkPrP. We observed 100% transmission of the original CJDElkPrP in transgenic mice expressing human PrP. We passaged CJDElkPrP two more times in the Tg12 mice. We found that such second and third passage CJDElkPrP prions retained 100% transmission rate in the humanized mice, despite that the natural elk CWD isolates and CJDElkPrP share the same elk PrP sequence. In contrast, we and others found zero or poor transmission of natural elk CWD isolates in humanized mice.

Conclusions: Our data indicate that highly zoonotic cervid prion strains are not only possible but also can retain zoonotic potential after serial passages in cervids, suggesting a very significant and serious long-term risk of CWD zoonosis given that the broad and continuing spread of CWD prions will provide fertile grounds for the emergence of zoonotic CWD strains over time.


The finding that infectious PrPSc was shed in fecal material of CWD-infected humanized mice and induced clinical disease, different tropism, and typical three banding pattern-PrPres in bank voles that is transmissible upon second passage is highly concerning for public health. The fact that this biochemical signature in bank voles resembles that of the Wisc-1 original deer isolate and is different from that of bvWisc-1, in the migration profile and the glyco-form-ratio, is valid evidence that these results are not a product of contamination in our study. If CWD in humans is found to be contagious and transmissible among humans, as it is in cervids [57], the spread of the disease within humans might become endemic.

Transmission of cervid prions to humanized mice demonstrates the zoonotic potential of CWD

Acta Neuropathol 144, 767–784 (2022). https://doi.org/10.1007/s00401-022-02482-9

Published

22 August 2022


Transmission of cervid prions to humanized mice demonstrates the zoonotic potential of CWD

Samia Hannaoui1 · Irina Zemlyankina1 · Sheng Chun Chang1 · Maria Immaculata Arifn1 · Vincent Béringue2 · Debbie McKenzie3 · Hermann M. Schatzl1 · Sabine Gilch1

Received: 24 May 2022 / Revised: 5 August 2022 / Accepted: 7 August 2022

© The Author(s) 2022

Abstract

Prions cause infectious and fatal neurodegenerative diseases in mammals. Chronic wasting disease (CWD), a prion disease of cervids, spreads efficiently among wild and farmed animals. Potential transmission to humans of CWD is a growing concern due to its increasing prevalence. Here, we provide evidence for a zoonotic potential of CWD prions, and its probable signature using mice expressing human prion protein (PrP) as an infection model. Inoculation of these mice with deer CWD isolates resulted in atypical clinical manifestation with prion seeding activity and efficient transmissible infectivity in the brain and, remarkably, in feces, but without classical neuropathological or Western blot appearances of prion diseases. Intriguingly, the protease-resistant PrP in the brain resembled that found in a familial human prion disease and was transmissible upon second passage. Our results suggest that CWD might infect humans, although the transmission barrier is likely higher compared to zoonotic transmission of cattle prions. Notably, our data suggest a different clinical presentation, prion signature, and tissue tropism, which causes challenges for detection by current diagnostic assays. Furthermore, the presence of infectious prions in feces is concerning because if this occurs in humans, it is a source for human-to-human transmission. These findings have strong implications for public health and CWD management.

Keywords Chronic wasting disease · CWD · Zoonotic potential · Prion strains · Zoonotic prions

HIGHLIGHTS OF THIS STUDY

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

Our results suggest that CWD might infect humans, although the transmission barrier is likely higher compared to zoonotic transmission of cattle prions. Notably, our data suggest a different clinical presentation, prion signature, and tissue tropism, which causes challenges for detection by current diagnostic assays. Furthermore, the presence of infectious prions in feces is concerning because if this occurs in humans, it is a source for human-to-human transmission. These findings have strong implications for public health and CWD management.

In this study, we evaluated the zoonotic potential of CWD using a transgenic mouse model overexpressing human M129-PrPC (tg650 [12]). We inoculated tg650 mice intracerebrally with two deer CWD isolates, Wisc-1 and 116AG [22, 23, 27, 29]. We demonstrate that this transgenic line was susceptible to infection with CWD prions and displayed a distinct leading clinical sign, an atypical PrPSc signature and unusual fecal shedding of infectious prions. Importantly, these prions generated by the human PrP transgenic mice were transmissible upon passage. Our results are the first evidence of a zoonotic risk of CWD when using one of the most common CWD strains, Wisc-1/CWD1 for infection. We demonstrated in a human transgenic mouse model that the species barrier for transmission of CWD to humans is not absolute. The fact that its signature was not typical raises the questions whether CWD would manifest in humans as a subclinical infection, whether it would arise through direct or indirect transmission including an intermediate host, or a silent to uncovered human-to-human transmission, and whether current detection techniques will be suffcient to unveil its presence.

Our findings strongly suggest that CWD should be regarded as an actual public health risk. Here, we use humanized mice to show that CWD prions can cross the species barrier to humans, and remarkably, infectious prions can be excreted in feces.

Our results indicate that if CWD crosses the species-barrier to humans, it is unlikely to resemble the most common forms of human prion diseases with respect to clinical signs, tissue tropism and PrPSc signature. For instance, PrPSc in variable protease-sensitive prionopathy (VPSPr), a sporadic form of human prion disease, and in the genetic form Gerstmann-Sträussler-Scheinker syndrome (GSS) is defined by an atypical PK-resistant PrPSc fragment that is non-glycosylated and truncated at both C- and N-termini, with a molecular weight between 6 and 8 kDa [24, 44–46]. These biochemical features are unique and distinctive from PrPSc (PrP27-30) found in most other human or animal prion disease. The atypical PrPSc signature detected in brain homogenate of tg650 mice #321 (1st passage) and #3063 (2nd passage), and the 7–8 kDa fragment (Figs. 2, 4) are very similar to that of GSS, both in terms of migration profile and the N-terminal cleavage site.

CWD in humans might remain subclinical but with PrPSc deposits in the brain with an unusual morphology that does not resemble the patterns usually seen in different prion diseases (e.g., mouse #328; Fig. 3), clinical with untraceable abnormal PrP (e.g., mouse #327) but still transmissible and uncovered upon subsequent passage (e.g., mouse #3063; Fig. 4), or prions have other reservoirs than the usual ones, hence the presence of infectivity in feces (e.g., mouse #327) suggesting a potential for human-to-human transmission and a real iatrogenic risk that might be unrecognizable.

“suggesting a potential for human-to-human transmission and a real iatrogenic risk that might be unrecognizable.”

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

Supplementary Information The online version contains supplementary material available at


snip...see full text;



EFSA Panel on Biological Hazards (BIOHAZ) Antonia Ricci Ana Allende Declan Bolton Marianne Chemaly Robert Davies Pablo Salvador Fernández Escámez ...

First published: 17 January 2018 https://doi.org/10.2903/j.efsa.2018.5132

also, see;

8. Even though human TSE‐exposure risk through consumption of game from European cervids can be assumed to be minor, if at all existing, no final conclusion can be drawn due to the overall lack of scientific data.

***> In particular the US data do not clearly exclude the possibility of human (sporadic or familial) TSE development due to consumption of venison.

The Working Group thus recognizes a potential risk to consumers if a TSE would be present in European cervids. It might be prudent considering appropriate measures to reduce such a risk, e.g. excluding tissues such as CNS and lymphoid tissues from the human food chain, which would greatly reduce any potential risk for consumers.. However, it is stressed that currently, no data regarding a risk of TSE infections from cervid products are available.


2004

Jeff Swann and his Mom, cwd link... sporadic CJD?, CBC NEWS Jeff Schwan sCJD, CWD, and Professor Aguzzi on BSE and sporadic CJD

????: CBCnews


2004

April 22, 2004, 10:30 AM CDT Guests: Patrick Singh, Terry Schwan, Janet Skarbek, Bill Fielding (BEGIN VIDEOTAPE) ANNOUNCER: DEBORAH NORVILLE TONIGHT.


1997-11-10: Panorama - The British disease


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.


''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.''


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.net Ref: E2979

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

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

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

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

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

kind regards, terry

TSEs i.e. mad cow disease's BSE/BASE and NUTRITIONAL SUPPLEMENTS IPLEX, mad by standard process; vacuum dried bovine BRAIN, bone meal, bovine EYE, veal Bone, bovine liver powder, bovine adrenal, vacuum dried bovine kidney, and vacuum dried porcine stomach. also; what about potential mad cow candy bars ? see their potential mad cow candy bar list too... THESE are just a few of MANY of just this ONE COMPANY...TSS






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.


***> Creutzfeldt Jakob Disease CJD TSE Prion Cases Increasing March 2025


***> Creutzfeldt Jakob Disease CJD, BSE, CWD, TSE, Prion, December 14, 2024 Annual Update



Iatrogenic Transmissible Spongiform Encephalopathy TSE Prion, CWD, our worst nightmare, what if?


So, this is what we leave our children and grandchildren?

THURSDAY, JUNE 12, 2025

***> Redefining the zoonotic potential of chronic wasting disease Singeltary Review


TUESDAY, JULY 08, 2025

Addressing chronic wasting disease in Korean farms: topsoil removal and 2N NaOH treatment before cervid restocking


THURSDAY, JULY 10, 2025

Distribution of chronic wasting disease (CWD) prions in tissues from experimentally exposed coyotes (Canis latrans) Published: July 9, 2025


THURSDAY, JULY 10, 2025

Modelling the effect of genotype (PRNP) linked to susceptibility, infection duration and prion shedding on chronic wasting disease dynamics of cervids


WEDNESDAY, MAY 14, 2025

Texas CWD TSE Prion Cases Rises to 1099 Confirmed Cases To Date



FRIDAY, APRIL 04, 2025

Trucking CWD TSE Prion

“CWD spreads among wild populations at a relatively slow rate, limited by the natural home range and dispersed nature of wild animals.”

NOW HOLD YOUR HORSES, Chronic Wasting Disease CWD of Cervid can spread rather swiftly, traveling around 50 MPH, from the back of truck and trailer, and Here in Texas, we call it ‘Trucking CWD’…


SUNDAY, MAY 04, 2025

Texas Senate Bill 2649 creation of a statewide Chronic Wasting Disease plan


SUNDAY, MAY 04, 2025

Texas Senate Bill 2651 establishment of a pilot program to breed deer resistant to CWD TSE Prion, what could go wrong?


Texas S.B. 2843 Directs TPWD to conduct a comprehensive study of current measures to control chronic wasting disease (CWD) in deer


Friday, February 21, 2025

Deer don’t die from CWD, it’s the insurance companies, or it's a Government conspiracy?


Friday, February 21, 2025

CWD, BAITING, AND MINERAL LICKS, WHAT IF?


SUNDAY, MAY 05, 2024

Chronic Wasting Disease, Cervid Captive Herd CWD Infection rates, Zoonosis, and Environmental Risk Factors


Texas Game Wardens Bust Illegal Deer Operations Across the State Feb. 27, 2025


TUESDAY, FEBRUARY 25, 2025

TEXAS ANIMAL HEALTH COMMISSION 423rd Commission Meeting CWD Update February 25, 2025


CWD Status Captive Herds


THURSDAY, APRIL 24, 2025

***> US Captive CWD Positive Herds Update April 2025


Control of Chronic Wasting Disease OMB Control Number: 0579-0189APHIS-2021-0004 Singeltary Submission



Docket No. APHIS-2018-0011 Chronic Wasting Disease Herd Certification



Docket No. FDA-2003-D-0432 (formerly 03D-0186) Use of Material from Deer and Elk in Animal Feed

PUBLIC SUBMISSION

Comment from Terry Singeltary Sr.

Posted by the Food and Drug Administration on May 17, 2016 Comment

Docket No. FDA-2003-D-0432 (formerly 03D-0186) Use of Material from Deer and Elk in Animal Feed Singeltary Submission



APHIS Indemnity Regulations [Docket No. APHIS-2021-0010] RIN 0579-AE65 Singeltary Comment Submission

Comment from Singeltary Sr., Terry

Posted by the Animal and Plant Health Inspection Service on Sep 8, 2022



Terry S. Singeltary Sr.

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