California 5 Positive detections for CWD as of 12/15/2025
California 5 Positive detections for CWD as of 12/15/2025
Summary
Positive detections for Chronic Wasting Disease (CWD) in California as of 12/15/2025.
The California Department of Fish and Wildlife (CDFW) has detected Chronic Wasting Disease (CWD) within the state and is working diligently to monitor and manage the presence of the disease within the state’s wildlife populations. Surveillance methods include targeted testing of harvested animals, monitoring of roadkill, and mandatory reporting of sick or unusual-looking animals. Updates will be uploaded as soon as they are available.
This data is associated with the following layers:
Chronic Wasting Disease Sampling Stations - 2025 - CDFW [ds3154] (https://apps.wildlife.ca.gov/bios6/?al=3154),
Participating Meat Processors and Taxidermists - 2025 - CDFW [ds3155] (https://apps.wildlife.ca.gov/bios6/?al=3155),
Chronic Wasting Disease Sampling Stations - 2023-2024 - CDFW [ds3182] (https://apps.wildlife.ca.gov/bios6/?al=3182),
Participating Meat Processors and Taxidermists - 2023-2024 - CDFW [ds3188] (https://apps.wildlife.ca.gov/bios6/?al=3188),
Approved Deer Carcass Disposal Sites - CDFW [ds3156] (https://apps.wildlife.ca.gov/bios6/?al=3156).
These layers include CWD Testing Sites, Participating Meat Processors and Taxidermists (MPT), Carcass Disposal Sites, and comprehensive data on CWD surveillance spanning from 1999 to 2025. This compilation of layers provides a comprehensive view of CWD-related activities, facilitating informed decision-making and strategic planning for wildlife management and disease prevention efforts. For more information please visit: wildlife.ca.gov/CWD.
gis.data.ca.gov/datasets/CDFW::chronic-wasting-disease-positive-detections-2024-2025-cdfw-ds3183/about
Showing rows: 5 of 5
Sample Number ELISA IHC Result County Species Sex Age Hunt Zone DSU Year Sample Type Shape__Area Shape__Length
ODHE2024-026-001 Suspicious Detected Detected Madera Native Deer Male Adult D7 DSU4 2023 Mortality/Non-CWD suspect 51446889.103 25426.378
CWD2024-002-108 Not Tested Suspicious Detected Inyo Native Deer Male Adult X9a DSU5 2024 Roadkill 51684428.124 25485.009
CWD2024-029-011 Suspicious Detected Detected Inyo Native Deer Female Adult X9a DSU5 2024 Clinical 51694526.592 25487.499
CWD2024-030-001 Suspicious Detected Detected Inyo Native Deer Male Adult X9b DSU5 2025 Mortality/Non-CWD suspect 51688387.299 25485.985
CWD2025-031-010 Suspicious Detected Detected Inyo Native Deer Female Adult X9a DSU5 2025 Clinical 51695794.665 25487.811
gis.data.ca.gov/datasets/CDFW::chronic-wasting-disease-positive-detections-2024-2025-cdfw-ds3183/explore?showTable=true
gis.data.ca.gov/datasets/CDFW::chronic-wasting-disease-positive-detections-2024-2025-cdfw-ds3183/about
=====
Sample Number ELISA IHC Result County Species Sex Age Hunt Zone DSU Year Sample Type Shape__Area Shape__Length
CWD2024-002-108 Not Tested Suspicious Detected Inyo Native Deer Male Adult X9a DSU5 2024 Roadkill 51684428.124 25485.009
CWD2024-029-011 Suspicious Detected Detected Inyo Native Deer Female Adult X9a DSU5 2024 Clinical 51694526.592 25487.499
CWD2024-030-001 Suspicious Detected Detected Inyo Native Deer Male Adult X9b DSU5 2025 Mortality/Non-CWD suspect 51688387.299 25485.985
CWD2025-031-010 Suspicious Detected Detected Inyo Native Deer Female Adult X9a DSU5 2025 Clinical 51695794.665 25487.811
ODHE2024-026-001 Suspicious Detected Detected Madera Native Deer Male Adult D7 DSU4 2023 Mortality/Non-CWD suspect 51446889.103 25426.378
gis.data.ca.gov/datasets/CDFW::chronic-wasting-disease-positive-detections-2024-2025-cdfw-ds3183/explore?showTable=true
data-cdfw.opendata.arcgis.com/datasets/CDFW::chronic-wasting-disease-surveillance-cdfw-ds3157-1/explore?layer=1
California Department of Fish and Wildlife Chronic Wasting Disease (CWD) Surveillance Technical Report: 2024
Historic Surveillance
The goal of California’s CWD surveillance program is to detect CWD where it occurs, monitor disease prevalence, and inform management decisions. CDFW has tested over 8,500 California deer and elk for CWD since 2000. The first CWD detections in California were confirmed in May 2024. In response, the Fish and Game Commission adopted temporary amendments to the California Code of Regulations Title 14, Section 708.5 Deer tagging and Reporting Requirements that identified deer hunt zones D7, X9a, X9b, and X9c as CWD Management Zones (CMZs) and required all hunters who harvest a deer within these zones to provide the department with a CWD sample from their harvest (Figure 1). This significantly increased our CWD sampling. Indeed, nearly 20% of all California’s CWD testing since 2000 were from samples collected in 2024. In 2024, the WHL received 1,823 samples for CWD testing, 1,687 of those were from deer or elk that died in 2024, and the remainder were from deer or elk that died in previous years but had not been submitted to the WHL in the year the animal died. Current and historic CWD testing and detection records can be found on the California Department of Fish and Wildlife’s (CDFW) Where is CWD in California? Dashboard at wildlife.ca.gov/CWD. The primary focus of this analysis will be on samples from deer and elk that died in 2024, with supplemental discussions around detections in animals that died in 2023 (n = 1) and 2025 (n = 1).
California’s CWD Detections
The first CWD detections in California were from two adult bucks, one was found dead from unknown causes on September 20, 2023, from Yosemite Lakes Park homeowners association in Madera County and the other from Bishop in Inyo County was found dead on February 6, 2024, after a vehicle collision. Samples from these animals were received at CDFW’s Wildlife Health Lab (WHL) in February and March 2024, respectively, and sent to the Washington Animal Disease Diagnostic Laboratory (WADDL) for testing on April 4, 2024. Preliminary findings were reported by WADDL on April 29, 2024, and confirmatory testing completed at the National Veterinary Services Laboratories (NVSL) in Ames, Iowa on May 6, 2024. Two additional CWD detections were confirmed by WADDL on February 3, 2025, nine months and approximately 1,500 samples after the initial detections. Both were adult deer from the Bishop area, within 5 miles of the first detection in this area. One was a small adult buck found dead of unknown causes but was noted to be skinny and the other an adult female that was euthanized due to clinical signs suggestive of CWD (Figure 2).
2024 Surveillance Synopsis
In 2024, CDFW and partners sampled 1,687 California native deer and elk for CWD testing. Surveillance efforts focused on deer (n = 1,657), only 2% of CWD sampling came from elk. CWD samples were from hunter-harvests (76%), roadkill (12%), clinical suspects (1%), and all other mortality sources (11%). The majority (85%) were from bucks and adult age classes (75%); however, age was not recorded for about 15% of the samples (Table 1). Over half (n = 851) of the 2024 samples came from the four CMZs (Table 2). Of those, 71% were recorded as “Adult” but nearly 20% of age data collected was marked as “Unknown” or was not recorded. Age data is important to better understand disease risk factors and population dynamics. Moving forward, collecting the first incisor for cementum annuli aging will be a priority. Since deer harvest in California is 99% buck and the vast majority of samples from CMZs (>90%) were from hunter-harvested deer, 95% of samples from CMZ’s were from bucks (Table 2).
Preferred CWD samples are retropharyngeal lymph nodes (RPLNs) from deer (preferred) and elk. For elk, the obex (a specific region of the brainstem) may also be included; however, we had sample handling issues with this tissue and many obex submitted were not testable. Once a sample is collected by a hunter, biologist, tribal partner, or participating meat processor and taxidermist, it must be sent to CDFW’s Wildlife Health Lab to be processed. When samples arrive at WHL, data from the data card are recorded in our lab information management system (LIMS), samples are examined,
1 | P a g e California Department of Fish and Wildlife
RPLNs bisected, and half of each RPLN shipped to the diagnostic laboratory for testing via enzyme-linked immunosorbent assay (ELISA) (Figure 3). Samples that were not testable or were non-negative via ELISA were subsequently tested via immunohistochemistry (IHC). During the hunting season, shipments to WHL and from WHL to the diagnostic lab were made weekly. The diagnostic lab, WADDL, had an average turnaround time of three weeks for results once they received samples from WHL (Figure 4).
We confirmed two CWD-positive deer that died and were sampled in 2024, both from the Bishop area. One was reported in May 2024 along with the CWD-positive deer from Yosemite Lakes Park that died in September 2023. A fourth CWD-positive deer died and was sampled in 2025. Enzyme-linked immunosorbent assay (ELISA) conducted on medial retropharyngeal lymph nodes (RPLN) is the preferred rapid test for CDFW’s CWD surveillance. If a sample could not be tested via ELISA due to inappropriate or insufficient samples, these samples went on to immunohistochemistry (IHC) which allows a pathologist to microscopically determine tissue type and presence, or absence of the minimum required of lymphoid follicles to qualify as an official test. Out of 1,687 samples collected in 2024, 75% were “Not Detected” via ELISA, 23% were moved on to IHC testing, and 2% were “Not Tested” because no lymphoid tissue was present in the sample. Of the 390 samples that were not testable via ELISA but forwarded onto IHC testing, 302 were “Not Detected,” 2 tested Positive for CWD, and 86 were unsuitable, unacceptable or had insufficient lymphoid follicle for testing. Thus, a total of two deer sampled in 2024 were CWD-positive and 118 (7%) were recorded as “Not Tested” (Table 3).
Summary and Discussion
Our surveillance targets are to test 300 deer per Deer Sampling Unit (Figure 5) per sampling period (i.e. calendar year). Annual testing targets were exceeded in the two DSUs that contained CMZs with mandatory sampling rules in place. Sampling goals were nearly met in DSU 3 (n = 297); however, half of those samples were collected around Fort Hunter Liggett (FHL) in A South (Table 4). Sampling efforts skewed heavily towards deer populations with tightly controlled hunts like FHL or where regulations required sampling of hunter-harvests. This clumped sampling, both within and between DSUs, may lead to gaps in our ability to detect CWD in new areas and monitor prevalence where CWD has been detected. For example, to date California’s CWD detections have only occurred in roadkill and clinical suspect animals in residential areas (Table 2) yet 76% of our samples statewide and over 92% of our samples from CMZs were from hunter- harvested deer. This discrepancy in detections and sampling effort might make it difficult to detect CWD in residential deer at low prevalence and make it difficult to estimate a robust prevalence where CWD has been detected.
Hunter-harvested samples had the lowest proportion of “Not Tested” results at 4.52% whereas other sampling streams were between 9-15% due to poor sample quality or samples unidentifiable as lymph node (Table 1). This may be due to direction from the WHL that decomposing carcasses can be sampled and tested if an RPLN is identifiable. Where CWD occurs, analyses suggests that deer with clinical signs of CWD and deer killed by vehicle strike are more likely to be CWD positive than the average hunter harvested deer. Thus, these are high value samples for detecting CWD and, despite the increased likelihood of a “Not Tested” result due to sample quality, should still be sampled if a RPLN can be identified.
Current surveillance suggests that detections are likely localized and prevalence in these areas is low. However, when examining the distribution of known harvests tested, the number of samples collected in each hunt zone, and whether any samples were collected in a hunt zone, it becomes clear that many areas remain under sampled. In these areas it is difficult to know the CWD status of deer and elk herds with certainty. This is why it’s important to not only vigilantly sample effected areas to assess prevalence but also sample areas where CWD has not yet been detected, ensuring greater confidence that the disease is absent from those regions as well.
nrm.dfg.ca.gov/FileHandler.ashx?DocumentID=232383
wildlife.ca.gov/Conservation/Laboratories/Wildlife-Investigations/Monitoring/CWD
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California BSE
Tuesday, April 24, 2012
MAD COW DISEASE USA 4TH CASE DOCUMENTED ATYPICAL BSE CALIFORNIA
transmissiblespongiformencephalopathy.blogspot.com/2012/04/mad-cow-disease-usa-4th-case-documented.html
California
Scrapie
www.cdfa.ca.gov/ahfss/Animal_Health/Scrapie_Info.html
California atypical Nor-98 Scrapie Detected
www.researchgate.net/publication/348920361_Atypical_Nor-98_Scrapie_TSE_Prion_USA_State_by_State_Update_January_2021
nor-98.blogspot.com/2011/06/usda-scrapie-report-for-april-2011-new.html
Research Project: Elucidating the Pathobiology and Transmission of Transmissible Spongiform Encephalopathies
Location: Virus and Prion Research
2025 Annual Report
Objectives
Objective 1: Develop highly sensitive detection tools to determine the distribution of CWD and scrapie prions in natural hosts (sheep, goats, cervids) and their environment.
Objective 2: Investigate the pathobiology of CWD, scrapie prion strains, and atypical TSEs in natural hosts including potential cross species transmission events.
Objective 3: Investigate the genetics of CWD susceptibility and resistance in white-tailed deer.
Objective 4: Evaluate the presence of and determine the appropriate methodology for CWD strain determination.
Approach
Eradication or control of a family of diseases is unlikely or impossible when an understanding of the basic mechanisms and influences on transmission are unknown and for which methods to evaluate disease status are lacking. Scrapie and BSE represent the most thoroughly studied TSEs; however, significant knowledge gaps persist with regard to the atypical variants of these diseases. Further, much of the research emphasis to date on genetics of prion disease has focused on the recipient genotype rather than the source. Since both atypical BSE and atypical scrapie have been suggested to occur spontaneously, eradication of these diseases may not be possible unless we expand our understanding of the disease at both the source and recipient level. A better understanding of the tissue distribution and potential transmission of these atypical isolates is critical to understanding what risk these disease variants may pose to ongoing control and eradication efforts. The European epizootic of BSE is waning and efforts to eradicate scrapie in the U.S. and abroad have progressed but are not complete. In the U.S., chronic wasting disease (CWD) presents the most serious challenge to regulatory efforts. CWD appears to be spreading unchecked in both free-ranging and farmed cervids. Methods for antemortem detection of TSEs in general and CWD in particular are needed to fulfill the goal of eradicating scrapie and controlling CWD. Performing these studies will allow us to address critical knowledge gaps that are relevant to developing measures to restrict further disease expansion beyond current, affected populations. Understanding prion disease persistence in animal populations is challenging due to lack of tools for study and a less than complete understanding of transmission among animals within a flock or herd or in naturally occurring reservoirs. In addition to transmission between hosts of like species, free-ranging cervids may come in contact with numerous other species including cattle, sheep, and other susceptible hosts. Transmission of CWD to other species has been studied but limited with regard to the source genotype used. The four primary objectives are inherently linked. Our focus is on developing tools needed for control and research, and using those tools to advance our understanding the complex disease process with the overall goal of eradication and control of disease in livestock, wildlife of economic importance, and potential wildlife reservoirs.
Progress Report
The goals of the project plan for fiscal year (FY) 2025 consisted of 12 milestones, 11 of which were either fully or substantially met. The only milestone in this plan that was not met was due to insufficient animal availability and space constraints. Previous studies utilizing this space are not complete due to longer than anticipated incubation periods and cannot be initiated until those studies are complete. In work toward addressing
Objective 1, “Develop highly sensitive detection tools to determine the distribution of chronic wasting disease (CWD) and scrapie prions in natural hosts (sheep, goats, cervids) and their environment”, we have worked closely with ARS researchers in Pullman, Washington, Animal and Plant Health Inspection Service (APHIS), and university partners. The tools under development are directly utilized by state diagnostic labs and have been shared with the appropriate end users for evaluation. We have also assessed alternative dyes that have do not induce amyloid formation in the amplification based diagnostic assay known as RT-QuIC. While no increase in sensitivity was observed, differences between strains were found offering an additional means to differentiate strains for some TSEs.
Objective 2, “Investigate the pathobiology of CWD, scrapie prion strains, and atypical TSEs in natural hosts including potential cross species transmission events”, the studies in question have been initiated with the goal of furthering the understanding of these TSEs in agriculturally relevant species including the natural host species and other that may be exposed to these TSEs in an agricultural environment. The studies are ongoing and anticipated to last upwards of 5 year and observation of the animals is ongoing. No anticipated signs of disease or relevant reportable information have been seen nor are they expected until near the onset of clinical signs, but if they are observed they will be reported.
Objective 3, “Investigate the genetics of CWD susceptibility and resistance in white-tailed deer”, consists of two subobjectives:
A) Investigate the susceptibility of white-tailed deer to CWD modeling direct contact exposure with infected deer, and
B) Investigate the susceptibility of white-tailed deer to CWD after direct inoculation.
The first of these has been initiated on schedule while the second has been delayed considerably (greater than 3 years at this point) due to insufficient animal space.Upon completion these two studies will aid in understanding the disease and disease progression.
Objective 4, “Evaluate the presence of and determine the appropriate methodology for CWD strain determination”, is dependent upon obtaining a diverse set of CWD isolates. We are continuing the acquisition of these samples. . Strains are one of the least understood aspects of TSEs as a whole and of importance in understanding the risks of CWD. We have initiated studies that will address the biochemical nature of prion strains and how these strains are maintained in a host which will aid in addressing features and differentiation of strains as additional samples become available.
Accomplishments
1. 01 Determined that white-tailed deer (WTD) infected with scrapie from sheep can transmit the disease to other deer under conditions mimicking natural exposure. It has long been suggested that prion disease in deer (chronic wasting disease (CWD)) was caused by the prion agent from sheep. The prion disease that affects sheep, scrapie, has been recognized for hundreds of years. However, chronic wasting disease, a similar disease found in WTD, has only been recognized since the 1960s. ARS researchers in Ames, Iowa, showed that white-tailed deer sick with scrapie from sheep can infect other deer under conditions mimicking natural exposure. Furthermore, this work shows that CWD is difficult to differentiate from WTD infected with scrapie. WTD scrapie prions accumulate in the lymphoreticular system in a manner similar to CWD, meaning that environmental contamination may occur through feces, saliva, and other body fluids of scrapie affected WTD as has been shown for CWD. The presence of WTD infected with scrapie could confound mitigation efforts for chronic wasting disease. This information informs regulatory officials, the farmed cervid industry, and officials tasked with protecting animal health such as state Departments of Agriculture, Natural Resources, or Parks and Wildlife with regard to a disease similar to CWD but arising from sheep scrapie that could be present in WTD that have contact with scrapie affected sheep and/or goats.
2. 02 Showed that gene-targeted mice are capable of reproducing strain specific effects typically limited to natural host species of chronic wasting disease (CWD). CWD is a highly contagious disease of deer, elk, moose, and reindeer found in North America, South Korea, and Scandinavian countries that is caused by misfolded proteins called prions. CWD prions transmit through direct contact between infected animals, or through contaminated soil, grass, or water. All prion diseases exhibit progressive neurodegeneration and ultimately death. Scientists typically study CWD by injecting prions into susceptible animals' brains in lab experiments. Intracranial prion injections are favored because they typically produce shorter incubation periods and higher disease attack rates compared to natural infection. ARS researchers in Ames, Iowa, along with university collaborators showed that this inoculation method can cause the prion strains to change in a way that does not accurately reflect how the disease spreads naturally. They found that using a combination of peripheral inoculation (injection outside the brain) in natural hosts and using novel gene-targeted mice generated in a manner that provides a more natural expression of the inserted prion gene that gives a more accurate picture of how CWD behaves in the real world. The novel mouse model provides an important strategy to precisely assess the zoonotic potential (likelihood of transmission from animals to humans) of CWD and other animal prion diseases using natural routes of transmission. This will impact the tools used and direction of future studies of CWD and other prion diseases allowing more rapid and comprehensive responses to emerging questions aiding both the researchers at the producers they support.
Review Publications
www.ars.usda.gov/research/project/?accnNo=440677&fy=202
Cwd, cattle, pigs, sheep, raccoons, oh my!
Price of TSE Prion Poker goes up substantially, all you cattle ranchers and such, better pay close attention here...terry
"Cattle with the E211K polymorphism are susceptible to the CWD agent after oronasal exposure of 0.2 g of infectious material."
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.
prion2023.org/wp-content/uploads/2023/10/Meeting-book-final-version2.pdf
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Prion Conference 2023
Transmission of the chronic wasting disease agent from elk to cattle after oronasal exposure
Conclusions: Cattle with the E211K polymorphism are susceptible to the CWD agent after oronasal exposure of 0.2 g of infectious material.
Strain characterization of chronic wasting disease in bovine-PrP transgenic mice
Conclusions: Altogether, these results exhibit the diversity of CWD strains present in the panel of CWD isolates and the ability of at least some CWD isolates to infect bovine species. Cattle being one of the most important farming species, this ability represents a potential threat to both animal and human health, and consequently deserves further study.
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www.researchgate.net/profile/Syed-Zahid-Shah/publication/378314391_Meeting-book-final-version_prion_2023/links/65d44dad28b7720cecdca95f/Meeting-book-final-version-prion-2023.pdf
Abstract for Prion 2023
Title: Transmission of atypical BSE: a possible origin of Classical BSE in cattle
Authors: Sandor Dudas1, Samuel James Sharpe1, Kristina Santiago-Mateo1, Stefanie Czub1, Waqas Tahir1,2, *
Affiliation: 1National and WOAH reference Laboratory for Bovine Spongiform Encephalopathy, Canadian Food inspection Agency, Lethbridge Laboratory, Lethbridge, Canada. 2Department of Biological Sciences, University of Lethbridge, Lethbridge, Alberta, Canada.
*Corresponding and Presenting Author:
Background: Bovine spongiform encephalopathy (BSE) is a fatal neurodegenerative disease of cattle and is categorized into classical and atypical forms. Classical BSE (CBSE) is linked to the consumption of BSE contaminated feed whereas atypical BSE is considered to be spontaneous in origin. The potential for oral transmission of atypical BSE is yet to be clearly defined.
Aims: To assess the oral transmissibility of atypical BSE (H and L type) in cattle. Should transmission be successful, determine the biochemical characteristics and distribution of PrPSc in the challenge cattle.
Material and Methods: For oral transmission, calves were fed with 100 g of either H (n=3) or L BSE (n=3) positive brain material. Two years post challenge, 1 calf from each of the H and L BSE challenge groups exhibited behavioural signs and were euthanized. Various brain regions of both animals were tested by traditional and novel prion detection methods with inconclusive results. To detect infectivity, brain homogenates from these oral challenge animals (P1) were injected intra-cranially (IC) into steer calves. Upon clinical signs of BSE, 3/4 of IC challenged steer calves were euthanized and tested for PrPSc with ELISA, immunohistochemistry and immunoblot.
Results: After 6 years of incubation, 3/4 animals (2/2 steers IC challenged with brain from P1 L-BSE oral challenge and 1/2 steer IC challenged with brain from P1 H-BSE oral challenge) developed clinical disease. Analysis of these animals revealed high levels of PrPSc in their brains, having biochemical properties similar to that of PrPSc in C-BSE.
Conclusion: These results demonstrate the oral transmission potential of atypical BSE in cattle. Surprisingly, regardless of which atypical type of BSE was used for P1 oral challenge, PrPSc in the P2 animals acquired biochemical characteristics similar to that of PrPSc in C-BSE, suggesting atypical BSE as a possible origin of C-BSE in UK.
Presentation Type: Oral Presentation
Funded by: CFIA, Health Canada, Alberta Livestock and Meat Agency, Alberta Prion
Research Institute
Grant Number: ALMA/APRI: 201400006, HC 414250
Abstract for Prion 2023
Acknowledgement: TSE unit NCAD, Lethbridge (Jianmin Yang, Sarah Bogart, Rachana Muley, Yuanmu Fang, Keri Colwell, Renee Anderson, John Gray, Rakhi Katoch) (CFIA, Canada), Dr. Catherine Graham (NSDA, Canada), Dr. Michel Levy (UCVM, Canada), Dr. Martin Groschup (FLI, Germany), Dr. Christine Fast (FLI, Germany), Dr. Bob Hills (Health Canada, Canada)
Meeting-book-final-version prion 2023 Prion 2023 Congress Organizing Committee and the NeuroPrion Association, we invite you to join us for the International Conference Prion2023 from 16-20 October 2023 in Faro, Portugal.
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Volume 31, Number 1—January 2025
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.
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.
wwwnc.cdc.gov/eid/article/31/1/24-0401_article
Currently, swine rations in the U.S. could contain animal derived components including materials from deer or elk. In addition, feral swine could be exposed to infected carcasses in areas where CWD is present in wildlife populations. The current feed ban in the U.S. is based exclusively on keeping tissues from TSE infected cattle from entering animal feeds. These results indicating the susceptibility of pigs to CWD, coupled with the limitations of the current feed ban, indicates that a revision of the feed ban may be necessary to protect swine production and potentially human health.
The successful transmission of pig-passaged CWD to Tg40 mice reported here suggests that passage of the CWD agent through pigs results in a change of the transmission characteristics which reduces the transmission barrier of Tg40 mice to the CWD agent. If this biological behavior is recapitulated in the original host species, passage of the CWD agent through pigs could potentially lead to increased pathogenicity of the CWD agent in humans. Interestingly, bioassay of material from the longest surviving >6 month orally challenged pig (72 mpc), which was negative for PrPcwd by all other tests, produced a positive bioassay result. Bioassay of material from additional animals is currently underway. This study demonstrates that pigs can serve as potential hosts for CWD, although with low attack rates and scant PrPcwd accumulation. Detection of infectivity in orally challenged pigs using mouse bioassay raises the possibility that naturally exposed pigs act as a reservoir of CWD infectivity, even though affected pigs do not develop overt clinical signs or readily detectable PrPcwd.
www.ars.usda.gov/research/publications/publication/?seqNo115=326166
cwd scrapie pigs oral routes
***> However, at 51 months of incubation or greater, 5 animals were positive by one or more diagnostic methods. Furthermore, positive bioassay results were obtained from all inoculated groups (oral and intracranial; market weight and end of study) suggesting that swine are potential hosts for the agent of scrapie. <***
*** Although the current U.S. feed ban is based on keeping tissues from TSE infected cattle from contaminating animal feed, swine rations in the U.S. could contain animal derived components including materials from scrapie infected sheep and goats. These results indicating the susceptibility of pigs to sheep scrapie, coupled with the limitations of the current feed ban, indicates that a revision of the feed ban may be necessary to protect swine production and potentially human health. <***
***> Results: PrPSc was not detected by EIA and IHC in any RPLNs. All tonsils and MLNs were negative by IHC, though the MLN from one pig in the oral <6 month group was positive by EIA. PrPSc was detected by QuIC in at least one of the lymphoid tissues examined in 5/6 pigs in the intracranial <6 months group, 6/7 intracranial >6 months group, 5/6 pigs in the oral <6 months group, and 4/6 oral >6 months group. Overall, the MLN was positive in 14/19 (74%) of samples examined, the RPLN in 8/18 (44%), and the tonsil in 10/25 (40%).
***> Conclusions: This study demonstrates that PrPSc accumulates in lymphoid tissues from pigs challenged intracranially or orally with the CWD agent, and can be detected as early as 4 months after challenge. CWD-infected pigs rarely develop clinical disease and if they do, they do so after a long incubation period. This raises the possibility that CWD-infected pigs could shed prions into their environment long before they develop clinical disease. Furthermore, lymphoid tissues from CWD-infected pigs could present a potential source of CWD infectivity in the animal and human food chains.
www.ars.usda.gov/research/publications/publication/?seqNo115=353091
www.ars.usda.gov/research/project/?accnNo=432011&fy=2017
www.ars.usda.gov/research/publications/publication/?seqNo115=337105
Conclusions: This study demonstrates that PrPSc accumulates in lymphoid tissues from pigs challenged intracranially or orally with the CWD agent, and can be detected as early as 4 months after challenge. CWD-infected pigs rarely develop clinical disease and if they do, they do so after a long incubation period. This raises the possibility that CWD-infected pigs could shed prions into their environment long before they develop clinical disease. Furthermore, lymphoid tissues from CWD-infected pigs could present a potential source of CWD infectivity in the animal and human food chains.
www.ars.usda.gov/research/publications/publication/?seqNo115=337105
Component 6: Transmissible Spongiform Encephalopathies
Sheep scrapie agent can infect white-tailed deer after oronasal exposure.
The origin of chronic wasting disease (CWD) is not known, but it has many similarities to the sheep prion disease called scrapie. It has long been hypothesized that CWD arose through transmission of sheep scrapie to deer. ARS researchers in Ames, Iowa, conducted research to determine if scrapie derived from sheep could be transmitted to white-tailed deer. The deer inoculated with sheep scrapie developed clinical signs and the abnormal prion protein could be detected in a wide range of tissues. These results indicate that deer may be susceptible to sheep scrapie if exposed to the disease in natural or agricultural settings. In addition, several strong similarities between CWD in white-tailed deer and the experimental cases of scrapie in white-tailed deer suggests that it would be difficult to distinguish scrapie from CWD in deer or identify scrapie if a case occurs. This information should be considered by deer farmers for keeping their herds free from prion diseases.
www.ars.usda.gov/ARSUserFiles/np103/AnnualReports/NP103%20FY2023%20Annual%20Report_Final.pdf
The chronic wasting disease agent from white-tailed deer is highly infectious to humanized mice after passage through raccoons
www.ars.usda.gov/research/publications/publication/?seqNo115=400777
Classical BSE emergence from Nor98/atypical scrapie: Unraveling the shift vs. selection dichotomy in the prion field
Sara Canoyra, Alba Marín-Moreno, Juan Carlos Espinosa , and Juan María Torres
Authors Info & Affiliations Edited by Byron Caughey, National Institute of Allergy and Infectious Diseases (National Institutes of Health), Hamilton, MT; received January 17, 2025; accepted June 7, 2025 by Editorial Board Member Lila M. Gierasch
July 15, 2025
122 (29) e2501104122 doi.org/10.1073/pnas.2501104122
Significance
Classical bovine spongiform encephalopathy (c-BSE) is a fatal cattle prion disease transmissible to humans as variant Creutzfeldt–Jakob Disease (vCJD). Understanding how c-BSE emerges is crucial for preventing future outbreaks and protecting public health. Two main hypotheses explain prion adaptation during cross-species transmission: “conformational shift or deformed templating,” where the species barrier forces a change to a different pathological prion protein, and “conformational selection,” where the species barrier filters preexisting conformers. Our results demonstrate that the conformational shift mechanism explains the emergence of c-BSE when Nor98/atypical scrapie (AS) is transmitted to cattle. This is significant because AS, found in sheep and goats worldwide, can convert to c-BSE. Preventing AS from entering the food chain is crucial to reduce c-BSE/vCJD risks.
Abstract
Prion diseases can manifest with distinct phenotypes in a single species, a phenomenon known as prion strains. Upon cross-species transmission, alterations in the disease phenotype can occur, interpreted as the emergence of a new strain. Two main and non–mutually exclusive evolutionary hypotheses have been proposed to explain this phenomenon: the “conformational shift” or “deformed templating” and the “conformational selection.” The conformational shift hypothesis proposes that the introduction of a new host prion protein (PrPC) forces a change in the conformation of the pathological prion protein (PrPSc), causing the new prion strain emergence. On the contrary, the conformational selection model postulates that prion isolates are a conglomerate of PrPSc conformations with relative distribution frequencies, wherein the species barrier acts as a filter selecting the one fittest for the new species environment. Previous studies reported the emergence of the classical bovine spongiform encephalopathy agent (c-BSE) upon transmission of Nor98/atypical scrapie (AS) onto a bovine PrP. This study investigates the evolutionary dichotomy of this c-BSE emergence by using prion strain thermostability combined with protein misfolding cyclic amplification to distinguish between both strains. Our results suggest that the conformational shift could be the principal mechanism responsible for the c-BSE emergence. Furthermore, the selection model was dismissed as the key mechanism based on the analysis of an artificial c-BSE and AS mixture. The ability of the AS conformers to shift conformation to a c-BSE one supports the hypothesis that the epidemic c-BSE prion may have originated from the transmission of AS in cattle.
www.pnas.org/doi/abs/10.1073/pnas.2501104122?download=true
Published: 04 October 2023
Detection of classical BSE prions in asymptomatic cows after inoculation with atypical/Nor98 scrapie
Marina Betancor, Belén Marín, Alicia Otero, Carlos Hedman, Antonio Romero, Tomás Barrio, Eloisa Sevilla, Jean-Yves Douet, Alvina Huor, Juan José Badiola, Olivier Andréoletti & Rosa Bolea Veterinary Research volume 54, Article number: 89 (2023) Cite this article
Abstract
The emergence of bovine spongiform encephalopathy (BSE) prions from atypical scrapie has been recently observed upon experimental transmission to rodent and swine models. This study aimed to assess whether the inoculation of atypical scrapie could induce BSE-like disease in cattle. Four calves were intracerebrally challenged with atypical scrapie. Animals were euthanized without clinical signs of prion disease and tested negative for PrPSc accumulation by immunohistochemistry and western blotting. However, an emergence of BSE-like prion seeding activity was detected during in vitro propagation of brain samples from the inoculated animals. These findings suggest that atypical scrapie may represent a potential source of BSE infection in cattle.
Snip…
Discussion
Previous studies have demonstrated that C-BSE prions can be present as a minor variant in ovine atypical scrapie isolates and that C-BSE can emerge during the passage of these isolates to pigs and bovine PrP mice [7, 8]. These results pointed to atypical scrapie as a possible origin of C-BSE. Therefore, this study was meant to assess the link between atypical scrapie and C-BSE in the natural host of C-BSE, cattle. Although the intracerebral challenge has some limitations and does not reflect the natural transmission process of prions, bioassays using experimental prion inoculation have allowed to identify and describe the transmission mechanisms of these pathogens. Therefore, we decided to challenge cattle with an atypical scrapie isolate.
It is important to note that none of the animals in this study showed any clinical signs of TSE after inoculation with atypical scrapie, according to the results previously obtained in pigs [8]. In addition, the absence of spongiform changes in brain sections, as well as the absence of PrPSc accumulation by conventional techniques in brain areas from the atypical scrapie-inoculated cows, further highlights the need for highly sensitive techniques such as PMCA to detect low levels of prions. After the in vitro propagation of brain samples from the cows included in this study, seeding activity was detected in reactions seeded with brain material from three out of the four cows, in the areas of frontal cortex, thalamus, and/or cerebellum. Interestingly, none of the samples from the obex, which is one of the most affected areas in prion diseases [14], showed seeding activity. Importantly, the observed glycosylation pattern of the positive PMCA reactions was indistinguishable from that of C-BSE prions and PMCA products from reactions seeded with C-BSE prions. To check whether C-BSE-like prions were present in the original atypical scrapie isolate or if they emerged in the brain of the cows after the inoculation, we performed PMCA of the original inoculum in TgBov substrate, following the same conditions described above. The in vitro amplification of the atypical scrapie inoculum resulted in the propagation of BSE-like seeding activity, biochemically indistinguishable from C-BSE or positive PMCA reactions seeded with brain samples from the inoculated cows, suggesting that, as described before, certain atypical scrapie isolates contain low levels of C-BSE prions [9].
Moreover, in order to rule out a spontaneous in vitro misfolding of bovine PrP during PMCA, we included, as a control for the technique, brain samples from non-inoculated age-matching cows that were also subjected to serial in vitro propagation in TgBov substrate. No positivity was observed in PMCA reactions seeded with samples from these animals, suggesting a true C-BSE-like prion seeding activity and not a spontaneous in vitro misfolding of PrP.
All these results suggest the amplification of C-BSE-like prions during the transmission of ovine atypical scrapie to cows. It is true that, in order to confirm the presence of infectious BSE prions in the challenged cows, strain typing experiments of the PMCA products should be carried out in established mouse lines. Therefore, studies involving a bioassay in bovine and ovine PrP-expressing mice have been started.
Interestingly, the time after inoculation and the BSE-like prion seeding activity were not correlated. As previously stated, the emergence of C-BSE from atypical scrapie has been associated with the presence of low levels of C-BSE prions in the atypical scrapie isolates and our results after the in vitro amplification of the PS152 inoculum support this theory. Therefore, the number of C-BSE conformers contained in the used atypical scrapie isolates may be reduced and not homogeneously distributed, making cows receiving different amounts of C-BSE-like prions. It is true that the emergence of C-BSE-like PMCA seeding activity from the brains of cows could be related to the persistence of prions from the original atypical scrapie inoculum. Previous studies, in which prion seeding activity was detected in the brain of intracerebrally inoculated PrP0/0 mice have highlighted the capacity of prions to persist in non-replicative environments [15]. Nevertheless, cows were intracerebrally challenged in the frontal cortex, and seeding activity was detected in caudal regions of their brains but not in more rostral areas such as the frontal cortex. If these positive PMCA reactions were not a bona fide propagation of C-BSE-like prions but associated to inoculum persistence, it would be expected to detect such amplification in the most rostral areas of the brain. Although all these results support a bona fide propagation of C-BSE-like prions, the possibility of PMCA detecting remaining prions of the inoculum, would be definitely ruled out after in vivo bioassays in mouse lines, which are currently being carried out.
The lack of clinical signs of prion disease in cows after inoculation with atypical scrapie contrasts with results from a previous study in which bovine PrP mice (TgBov) were challenged with atypical scrapie isolates and displayed signs of clinical prion disease, developing neuropathological characteristics of C-BSE [7]. In addition, in the mentioned study, after the first passage, signs of clinical prion disease were only observed in a low proportion of the inoculated mice, and several of the inoculated isolates did not lead to PrPSc accumulation. Three serial passages of atypical scrapie were needed to observe complete attack rates in TgBov mice. Moreover, mice from the first passage that developed clinical signs showed long incubation periods considering the lifespan of a mouse. The cows in this study were also euthanized after a long post-inoculation period (between ~7 and ~11 years). However, the number of C-BSE-like prions present in the original atypical scrapie inoculum was probably too low to produce disease in the cows upon first passage. We also need to consider that TgBov mice overexpress ~8 times bovine PrPC, making them more susceptible to develop disease after the inoculation of C-BSE prions.
Further in vivo experiments challenging different mouse lines have been started in order to confirm the infectivity of the PMCA products obtained in this study. However, in conclusion, our findings show that the propagation of atypical scrapie in cattle leads to the emergence of BSE-like seeding activity. This is a concerning issue with far-reaching implications for public health and food safety. The possibility of interspecies transmission of prion diseases and the emergence of new prion strains highlight the critical need for continued surveillance and monitoring of these diseases in both animal and human populations. Early detection of prion diseases is crucial, and highly sensitive detection techniques such as PMCA can play an important role in this regard.
veterinaryresearch.biomedcentral.com/articles/10.1186/s13567-023-01225-2
Classical BSE prions emerge from asymptomatic pigs challenged with atypical/Nor98 scrapie
Belén Marín, Alicia Otero, Séverine Lugan, Juan Carlos Espinosa, Alba Marín-Moreno, Enric Vidal, Carlos Hedman, Antonio Romero, Martí Pumarola, Juan J. Badiola, Juan María Torres, Olivier Andréoletti & Rosa Bolea
Scientific Reports volume 11, Article number: 17428 (2021) Cite this article
Abstract
Pigs are susceptible to infection with the classical bovine spongiform encephalopathy (C-BSE) agent following experimental inoculation, and PrPSc accumulation was detected in porcine tissues after the inoculation of certain scrapie and chronic wasting disease isolates. However, a robust transmission barrier has been described in this species and, although they were exposed to C-BSE agent in many European countries, no cases of natural transmissible spongiform encephalopathies (TSE) infections have been reported in pigs. Transmission of atypical scrapie to bovinized mice resulted in the emergence of C-BSE prions. Here, we conducted a study to determine if pigs are susceptible to atypical scrapie. To this end, 12, 8–9-month-old minipigs were intracerebrally inoculated with two atypical scrapie sources. Animals were euthanized between 22- and 72-months post inoculation without clinical signs of TSE. All pigs tested negative for PrPSc accumulation by enzyme immunoassay, immunohistochemistry, western blotting and bioassay in porcine PrP mice. Surprisingly, in vitro protein misfolding cyclic amplification demonstrated the presence of C-BSE prions in different brain areas from seven pigs inoculated with both atypical scrapie isolates. Our results suggest that pigs exposed to atypical scrapie prions could become a reservoir for C-BSE and corroborate that C-BSE prions emerge during interspecies passage of atypical scrapie.
snip...
Discussion The outbreak of C-BSE was followed by the appearance of TSE in species that had never been diagnosed with prion diseases and the emergence in humans of vCJD16,17,18. However, no natural prion disease has been described in pigs, even though they were exposed to C-BSE contaminated feed12. Posterior experimental challenges in pigs and mice expressing porcine PrP have demonstrated that, although they are not completely resistant, pigs present a robust transmission barrier for C-BSE prions4,14,19.
However, the possible transmission of a TSE to swine is a public health concern due to the wide use of pork as a source of human food, and the increasing use of pigs as tissue donors, being reported a case of vCJD in a human patient receiving a swine dura mater graft20. Although pigs are apparently non-susceptible to C-BSE after oral challenge4,5,21, infectivity has been detected in tissues from pigs orally inoculated with classical scrapie or CWD10,11. In addition, these positive orally inoculated pigs are often subclinical, what could represent a public health concern, considering that these animals could reach the slaughterhouse without showing signs suggestive of prion disease.
In the present study, we evaluated the transmissibility of atypical scrapie to pigs. Pigs were euthanized between 22- and 72-months post inoculation (mpi), and their tissues tested for PrPSc accumulation and infectivity. We did not find evidence of transmission of atypical scrapie to any of the animals by EIA (Table 2), western blotting, or mouse bioassay (Table 3). PrPSc accumulation can be detected in BSE-challenged pigs at 34 mpi4, and at 22 mpi when inoculated with SBSE7. Although scrapie or CWD-inoculated pigs do not show clinical signs, PrPSc presence can be found in scrapie-challenged animals at 51 mpi11 and as early as 6 mpi in the case of CWD10.
Our main goal was to test the ability of atypical scrapie/Nor98 strain to propagate in swine, given that mice expressing porcine PrP (PoPrP-Tg001/tgPo mice) showed to be susceptible to atypical scrapie inoculation. One atypical scrapie isolate adapted to this transgenic line, reaching a 100% attack rate and rapid incubation periods in serial passages13, a similar adaptation to that observed with the C-BSE agent19. However, when this atypical scrapie isolate was tested for propagation in tgPo mice again, together with other atypical scrapie isolates, no positive results were obtained, in vitro nor in vivo14. These results, together with the negative transmissions showed in the present study, reinforce the conclusion that porcine species is highly resistant to atypical scrapie. However, we only performed one passage in tgPo mice, and further passages in this line and/or PMCA analysis of tgPo brains to detect any possible prion replication would be of interest.
However, it was demonstrated that C-BSE prions can be present as a minor variant in ovine atypical scrapie isolates and that C-BSE can emerge during the passage of these isolates to bovine PrP mice15. Considering that the aforementioned atypical scrapie isolate also acquired BSE-like properties when transmitted to tgPo mice13, and that C-BSE is the only prion that efficiently propagates in swine PrP4,7,14, we decided to investigate whether C-BSE prions could emerge from atypical scrapie during the ovine-porcine interspecies transmission.
Interestingly, PMCA reactions seeded with brain material from 7 pigs propagated in tgBov substrate showing PrPres with identical biochemical characteristics to those of C-BSE (Fig. 1). Positive C-BSE amplification was detected in the brain of pigs inoculated with either the PS152 or TOA3 atypical scrapie isolates, at minimum incubation periods of 28- and 35-months post inoculation, respectively. From each animal, positive reactions were not obtained from all brain areas tested (Supplementary table 1). Although PrPres amplified from the pigs showed C-BSE biochemical characteristics, further bioassays in tgBov mice are required to know whether these prions replicate the neuropathological features of C-BSE.
Altogether, our results and data obtained from transmission studies of prions to pigs, tgPo mice and in vitro studies using porcine substrate have shown that pig PrP has a very limited ability to sustain prion replication. No significant polymorphisms have been described for pig PRNP22, and it has been suggested that the conformational flexibility of pig PrP sequence is very low, limiting the number of PrPSc conformations able to produce misfolding14. No differences have been found between pig and minipig PrP sequences either23, suggesting that the conclusions obtained here could be extrapolated to domestic, non-experimental pigs. However, using tgBov substrate, we have demonstrated in vitro the presence of C-BSE seeding activity in some pig brain areas, suggesting that C-BSE prions emerged during the transmission of ovine atypical scrapie prions to pigs. Interestingly, C-BSE prions did not emerge from brain material of all the pigs, and, of those from which it did emerge, it was not detected in all brarsain areas tested. No correlation between time after inoculation and BSE emergence was found either. When the emergence of C-BSE from atypical scrapie in PMCA was described, it was associated to low levels of C-BSE prions that were present in the original atypical scrapie isolates15. It is possible that this result is related to the great resistance that pigs present to prion diseases, making the penetrance of the BSE prions that could be present in the original inoculum incomplete. In addition, considering that the amount of C-BSE conformers in the atypical scrapie inocula is probably very reduced and perhaps not homogeneously distributed throughout the isolate, it is also possible that not all the pigs received a sufficient amount of C-BSE conformers capable of being detected by PMCA. Finally, we should consider that PMCA amplification of prions is sometimes a stochastic phenomenon, which could explain why no C-BSE propagation was obtained from some of the pigs. It could be also discussed that C-BSE emergence from the pig brains could be related to persistence of the original atypical scrapie inoculum. However, C-BSE amplification was not obtained from all of the pigs and, in some of them (i.e. P-1217 and P-1231) C-BSE propagation was detected in caudal regions of the brain (cerebellum or occipital cortex) but not in more rostral areas (such as parietal cortex). If C-BSE amplification from pig brain samples were associated to inoculum persistence and not bona fide propagation of C-BSE prions it would be expected that such amplification would be detected mainly in the most rostral areas of the brain. Finally, even though the titer generated was not enough to produce disease in the pigs, these results evidence again the issue that pigs could act as subclinical reservoirs for prion diseases as observed with scrapie and CWD, and that the presence of prions can be detected in pigs short after exposure to prions7,10,11.
In conclusion, our findings suggest that, although pigs present a strong transmission barrier against the propagation of atypical scrapie, they can propagate low levels of C-BSE prions. The prevalence of atypical scrapie and the presence of infectivity in tissues from atypical scrapie infected sheep are underestimated24,25. Given that pigs have demonstrated being susceptible to other prion diseases, and to propagate prions without showing signs of disease, the measures implemented to ban the inclusion of ruminant proteins in livestock feed must not be interrupted.
www.nature.com/articles/s41598-021-96818-2
The prevalence of atypical scrapie and the presence of infectivity in tissues from atypical scrapie infected sheep are underestimated24,25.
Given that pigs have demonstrated being susceptible to other prion diseases, and to propagate prions without showing signs of disease, the measures implemented to ban the inclusion of ruminant proteins in livestock feed must not be interrupted.
nor-98.blogspot.com/2021/10/classical-bse-prions-emerge-from.html
nor-98.blogspot.com/
EFSA atypical Scrapie
***> AS is considered more likely (subjective probability range 50–66%) that AS is a non-contagious, rather than a contagious, disease.
SNIP...SEE;
THURSDAY, JULY 8, 2021
EFSA Scientific report on the analysis of the 2‐year compulsory intensified monitoring of atypical scrapie
***> AS is considered more likely (subjective probability range 50–66%) that AS is a non-contagious, rather than a contagious, disease.
efsa.onlinelibrary.wiley.com/doi/10.2903/j.efsa.2021.6686
efsa.onlinelibrary.wiley.com/doi/full/10.2903/j.efsa.2021.6686
efsa.onlinelibrary.wiley.com/doi/epdf/10.2903/j.efsa.2021.6686
efsaopinionbseanimalprotein.blogspot.com/2021/07/efsa-scientific-report-on-analysis-of.html
***> Incomplete inactivation of atypical scrapie following recommended autoclave decontamination procedures <***
John Spiropoulos Richard Lockey Katy E. Beck Chris Vickery Thomas M. Holder Leigh Thorne Mark Arnold Olivier Andreoletti Marion M Simmons Linda A. Terry First published: 21 May 2019 doi.org/10.1111/tbed.13247 This article has been accepted for publication and undergone full peer review but has not been through the copyediting, typesetting, pagination and proofreading process, which may lead to differences between this version and the Version of Record. Please cite this article as doi: 10.1111/tbed.13247
Summary Prions are highly resistant to the decontamination procedures normally used to inactivate conventional pathogens. This is a challenging problem not only in the medical and veterinary fields for minimising the risk of transmission from potentially infective sources, but also for ensuring the safe disposal or subsequent use of animal by‐products. Specific pressure autoclaving protocols were developed for this purpose, but different strains of prions have been reported to have differing resistance patterns to established prion decontamination procedures, and as additional TSE strains are identified it is necessary to determine the effectiveness of such procedures. In this study we assessed the efficacy of sterilisation using the EU recommended autoclave procedure for prions (133o C, 3 Bar for 20 min) on the atypical or Nor98 (AS/Nor98) scrapie strain of sheep and goats. Using a highly sensitive murine mouse model (tg338) that overexpresses ovine PrPC, we determined that this method of decontamination reduced the infectivity titre by 1010. Infectivity was nonetheless still detected after applying the recommended autoclaving protocol. This shows that AS/Nor98 can survive the designated legislative decontamination conditions, albeit with a significant decrease in titre. The infectivity of a classical scrapie isolate subjected to the same decontamination conditions was reduced by 106 suggesting that the AS/Nor98 isolate is less sensitive to decontamination than the classical scrapie source. This article is protected by copyright. All rights reserved.
onlinelibrary.wiley.com/doi/abs/10.1111/tbed.13247
nor-98.blogspot.com/
***> SCRAPIE TSE Prion USA RAPID RESPONSE URGENT UPDATES DECEMBER 25, 2025 <***
scrapie-usa.blogspot.com/2025/12/scrapie-tse-prion-usa-rapid-response.html
prpsc.proboards.com/thread/186/scrapie-prion-response-urgent-updates
2026 USDA EXPLANATORY NOTES, APHIS, CWD, BSE, Scrapie, TSE, Prion
transmissiblespongiformencephalopathy.blogspot.com/2025/12/2026-usda-explanatory-notes-aphis-cwd.html
transmissiblespongiformencephalopathy.blogspot.com/2025/08/transmissible-spongiform-encephalopathy.html
Final rule on the Importation of Sheep, Goats, and Certain Other Ruminants (APHIS-2009-0095) Scrapie, BSE, CWD, TSE Prion Singeltary Submission
scrapie-usa.blogspot.com/2021/12/final-rule-on-importation-of-sheep.html
APHIS USDA Captive CWD Herds Update by State December 2025 Update
chronic-wasting-disease.blogspot.com/2025/12/aphis-usda-captive-cwd-herds-update-by.html
prpsc.proboards.com/thread/187/aphis-captive-herds-update-december
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?
chronic-wasting-disease.blogspot.com/2025/05/texas-senate-bill-2651-establishment-of_4.html
FRIDAY, NOVEMBER 21, 2025
Chronic Wasting Disease CWD TSE Prion Herd Declines
chronic-wasting-disease.blogspot.com/2025/11/chronic-wasting-disease-cwd-tse-prion.html
FRIDAY, OCTOBER 31, 2025
Captive Cervid and the Economic Burden of Chronic Wasting Disease CWD TSE Prion?
The economic burden of ignoring CWD would be far greater, imo, with time, if no cervid were left, or just a select few, if the environment/property was so exposed and saturated with CWD, that you couldn’t sell it, you couldn’t grow crops because of the soil saturation of the CWD, water tables saturated with CWD, saturation of hay, grains, from crops uptake on said property, cervid meat saturated from Cervid CWD, remember, You cannot cook the TSE prion disease out of meat, In fact new data now shows that exposure to high temperatures used to cook the meat increased the availability of prions for in vitro amplification. So, what Do we do, how many humans and animals do we continue to expose, continue to saturate with the CWD TSE Prion, …
chronic-wasting-disease.blogspot.com/2025/10/captive-cervid-and-economic-burden-of.html
prpsc.proboards.com/thread/183/captive-cervid-economic-burden-prion
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
www.regulations.gov/comment/FDA-2003-D-0432-0011
www.regulations.gov/docket/FDA-2003-D-0432
USA BSE Testing and Surveillance?
Bottom line, USA is testing so few cows for BSE (<25k tested annually)
www.aphis.usda.gov/livestock-poultry-disease/cattle/bse/bse-surveillance-program
BUT, even at those low testing figures, the USA did just confirm another case of BSE just here recently. Feed ban has failed terribly, and CWD is spreading in the USA, at an alarming rate. Recent transmission studies show oral transmission of CWD of Cervid to cattle. Studies also show links of sporadic CJD to BSE, Scrapie, and CWD. It’s a Whole new game of Prion poker now$$$
Wednesday, May 24, 2023
***> WAHIS, WOAH, OIE, United States of America Bovine spongiform encephalopathy Immediate notification
wahis.woah.org/#/in-review/5067
woahoie.blogspot.com/2023/05/wahis-woah-oie-united-states-of-america.html
prpsc.proboards.com/thread/125/wahis-woah-oie-immediate-notification
SATURDAY, MAY 20, 2023
***> Tennessee State Veterinarian Alerts Cattle Owners to Disease Detection Mad Cow atypical L-Type BSE
bse-atypical.blogspot.com/2023/05/tennessee-state-veterinarian-alerts.html
prpsc.proboards.com/thread/123/tennessee-veterinarian-alerts-cattle-confirmed
MAY 19, 2023
www.aphis.usda.gov/aphis/newsroom/stakeholder-info/sa_by_date/sa-2023/bse
2 weeks before the announcement of this recent mad cow case in the USA, i submitted this to the APHIS et al;
***> APPRX. 2 weeks before the recent mad cow case was confirmed in the USA, in Tennessee, atypical L-Type BSE, I submitted this to the APHIS et al;
Document APHIS-2023-0027-0001 BSE Singeltary Comment Submission May 2, 2023
''said 'burden' cost, will be a heavy burden to bear, if we fail with Bovine Spongiform Encephalopathy BSE TSE Prion disease, that is why this information collection is so critical''...
www.regulations.gov/comment/APHIS-2023-0027-0002
downloads.regulations.gov/APHIS-2023-0027-0002/attachment_1.pdf
Bovine Spongiform Encephalopathy BSE TSE Prion Origin USA?, what if?
Research Project: Pathobiology, Genetics, and Detection of Transmissible Spongiform Encephalopathies Location: Virus and Prion Research
Title: Sheep are susceptible to the agent of TME by intracranial inoculation and have evidence of infectivity in lymphoid tissues
Author item CASSMANN, ERIC - Oak Ridge Institute For Science And Education (ORISE) item MOORE, SARA - Oak Ridge Institute For Science And Education (ORISE) item SMITH, JODI - Iowa State University item Greenlee, Justin
Submitted to: Frontiers in Veterinary Science Publication Type: Peer Reviewed Journal Publication Acceptance Date: 11/14/2019 Publication Date: 11/29/2019 Citation: Cassmann, E.D., Moore, S.J., Smith, J.D., Greenlee, J.J. 2019.
Sheep are susceptible to the agent of TME by intracranial inoculation and have evidence of infectivity in lymphoid tissues.
Frontiers in Veterinary Science. 6:430. doi.org/10.3389/fvets.2019.00430. DOI: doi.org/10.3389/fvets.2019.00430
Interpretive Summary: Prion diseases are protein misfolding diseases that are transmissible between animals. The outcome of prion infection is irreversible brain damage and death. Transmission can occur between animals of the same or different species, however, transmission between different species is usually less efficient due to the species barrier, which results from differences in the amino acid sequence of the prion protein between the donor and recipient species. The present work evaluated whether transmissible mink encephalopathy (TME) can infect sheep. Our results demonstrate that sheep are susceptible to the TME agent and that the TME agent has similar properties to the agent of L-type atypical bovine spongiform encephalopathy (L-BSE). This work supports the ideas that L-BSE is a possible source for TME in mink and that the practice of feeding cattle with neurologic disease to mink should be avoided. This information is important to farmers who raise cattle, sheep, or mink.
Technical Abstract: Transmissible mink encephalopathy (TME) is a food borne prion disease. Epidemiological and experimental evidence suggests similarities between the agent of TME and L-BSE. This experiment demonstrates the susceptibility of four different genotypes of sheep to the agent of TME by intracranial inoculation. The four genotypes of sheep used in this experiment had polymorphisms corresponding to codons 136 and 171 of the prion gene: VV136QQ171, AV136QQ171, AA136QQ171, and AA136QR171. All intracranially inoculated sheep without comorbidities (15/15) developed clinical scrapie and had detectable PrPSc by immunohistochemistry, western blot, and enzyme immunoassay (EIA). The mean incubation periods in TME infected sheep correlated with their relative genotypic susceptibility. There was peripheral distribution of PrPSc in the trigeminal ganglion and neuromuscular spindles; however, unlike classical scrapie and C-BSE in sheep, ovine TME did not accumulate in the lymphoid tissue. To rule out the presence of infectious, but proteinase K susceptible PrPSc, the lymph nodes of two sheep genotypes, VV136QQ171 and AA136QQ171, were bioassayed in transgenic ovinized mice. None of the mice (0/32) inoculated by the intraperitoneal route had detectable PrPSc by EIA. Interestingly, mice intracranially inoculated with RPLN tissue from a VV136QQ171 sheep were EIA positive (3/17) indicating that sheep inoculated with TME harbor infectivity in their lymph nodes. Western blot analysis demonstrated similarities in the migration patterns between ovine TME and the bovine TME inoculum. Overall, these results demonstrate that sheep are susceptible to the agent of TME, and that the tissue distribution of PrPSc in TME infected sheep is distinct from classical scrapie.
www.ars.usda.gov/research/publications/publication/?seqNo115=363305
www.ars.usda.gov/research/publications/publication/?seqNo115=360665
www.ars.usda.gov/research/publications/publication/?seqNo115=373668
Previous work has shown that the Stetsonville, WI outbreak of TME could have been precipitated by feeding mink a downer cow with atypical BSE; therefore, it very well may have originated from a cow with L-BSE. The agent of TME appears to remain stable, and it has a high transmission efficiency after a sequence of interspecies transmission events. Although C-BSE is the archetypal foodborne TSE, our findings indicate that L-BSE and bTME have greater transmission efficiencies in bovinized mice. Previous work has demonstrated that L-BSE also is more virulent than C-BSE in mice expressing the human prion protein [46, 55]. Although the documented incidence of L-BSE is low, the propensity of L-BSE and the TME agent to cross species barriers support the continued monitoring for atypical BSE.
bmcvetres.biomedcentral.com/articles/10.1186/s12917-020-02611-0
***>This work supports the ideas that L-BSE is a possible source for TME in mink and that the practice of feeding cattle with neurologic disease to mink should be avoided. This information is important to farmers who raise cattle, sheep, or mink.<***
1985
Evidence That Transmissible Mink Encephalopathy Results from Feeding Infected Cattle Over the next 8-10 weeks, approximately 40% of all the adult mink on the farm died from TME.
snip...
The rancher was a ''dead stock'' feeder using mostly (>95%) downer or dead dairy cattle...
web.archive.org/web/20090506002258/http://www.bseinquiry.gov.uk/files/mb/m09/tab05.pdf
web.archive.org/web/20090506001031/http://www.bseinquiry.gov.uk/files/mb/m09a/tab01.pdf
web.archive.org/web/20090506024922/http://www.bseinquiry.gov.uk/files/yb/1987/06/10004001.pdf
FRIDAY, NOVEMBER 21, 2025
While no one was watching: Tenuous status of CDC prion unit, risk of CWD to people worry scientists
chronic-wasting-disease.blogspot.com/2025/11/while-no-one-was-watching-tenuous.html
WEDNESDAY, OCTOBER 15, 2025
US NATIONAL PRION DISEASE PATHOLOGY SURVEILLANCE CENTER CJD TSE REPORT 2025
prionunitusaupdate.blogspot.com/2025/10/us-national-prion-disease-pathology.html
MONDAY, DECEMBER 29, 2025
ARS Research Elucidating the Pathobiology and Transmission of Transmissible Spongiform Encephalopathies 2025 Annual Report
transmissiblespongiformencephalopathy.blogspot.com/2025/12/ars-research-elucidating-pathobiology.html
Trucking CWD TSE Prion
Chronic Wasting Disease CWD TSE Prion of Cervid
“CWD spreads among wild populations at a relatively slow rate, limited by the natural home range and dispersed nature of wild animals.”
NOW HOLD YOUR HORSES, Chronic Wasting Disease CWD of Cervid can spread rather swiftly, traveling around 50 MPH, from the back of truck and trailer, and Here in Texas, we call it ‘Trucking CWD’…
Preventive Veterinary Medicine Volume 234, January 2025, 106385
Use of biosecurity practices to prevent chronic wasting disease in Minnesota cervid herds
Vehicles or trailers that entered the farm were used to transport other live cervids, cervid carcasses, or cervid body parts in past 3 years in 64.3 % (95 % CI 46.3–82.3) of larger elk/reindeer herds compared to 13.6 % (95 % CI 4.7–22.4) of smaller deer herds.
Snip…
Identifying the exact pathway of initial CWD transmission to cervid herds is often not possible, in part due to many potential pathways of transmission for the infection, including both direct and indirect contact with infected farmed or wild cervids (Kincheloe et al., 2021). That study identified that transmissions from infected farmed cervids may occur from direct contact with the movement of cervids from one herd to another and from indirect contact with the sharing of equipment, vehicles, clothing, reproductive equipment, and potentially through semen or embryos.
www.sciencedirect.com/science/article/abs/pii/S016758772400271X
“Chronic Wasting Disease (CWD) is a fatal neurological disease and can devastate deer populations by silently spreading through direct animal contact and contaminated environments. Without close monitoring, illegal movement of captive deer increases the risk of introducing CWD to areas it is not known to exist, potentially leading to widespread outbreaks which will impact more than just the health of Texas deer.”
tpwd.texas.gov/newsmedia/releases/?req=20250227b
Texas Chronic Wasting Disease CWD TSE Prion Dashboard Update August 2025
SEE NEW DASHBOARD FOR CWD POSITIVES!
experience.arcgis.com/experience/8f6c27330c444a19b4b57beb7ffabb8b/page/Dashboard#data_s=id%3AdataSource_3-1966d773e34-layer-10%3A29
Texas CWD total by calendar years
chronic-wasting-disease.blogspot.com/2024/12/texas-cwd-tse-prion-positive-samples-by.html
tpwd.texas.gov/huntwild/wild/diseases/cwd/positive-cases/listing-cwd-cases-texas.phtml#texasCWD
Counties where CWD Exposed Deer were Released
tpwd.texas.gov/documents/257/CWD-Trace-OutReleaseSites.pdf
Number of CWD Exposed Deer Released by County
tpwd.texas.gov/documents/258/CWD-Trace-OutReleaseSites-NbrDeer.pdf
CWD Status Captive Herds
www.aphis.usda.gov/sites/default/files/status-of-captive-herds.pdf
THURSDAY, AUGUST 14, 2025
Texas Game Wardens Near Conclusion of ‘Ghost Deer’ Case with 24 Suspects, 1,400 Charges Filed Statewide
chronic-wasting-disease.blogspot.com/2025/08/texas-game-wardens-near-conclusion-of.html
prpsc.proboards.com/thread/178/texas-game-wardens-conclusion-ghost
WEDNESDAY, MAY 14, 2025
Texas CWD TSE Prion Cases Rises to 1099 Confirmed Cases To Date
chronic-wasting-disease.blogspot.com/2025/05/texas-cwd-tse-prion-cases-rises-to-1099.html
TAHC 425th Commission Meeting CWD 1:45:00
* See CWD speakers expressing their concerns with changed regulations…
2:00 hr mark
m.youtube.com/watch?v=bWawHpdn_7I
TEXAS ANIMAL HEALTH COMMISSION 423rd Commission Meeting CWD Update February 25, 2025
chronic-wasting-disease.blogspot.com/2025/02/texas-animal-health-commission-423rd.html
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
web.archive.org/web/20201017124040/https://www.tahc.texas.gov/agency/meetings/minutes/SummaryMinutes_CommMtg_2020-09-22.pdf
WEDNESDAY, DECEMBER 17, 2025
Texas TPWD Confirms 116 More Cases CWD, Total To Date 1,215 Positives
chronic-wasting-disease.blogspot.com/2025/12/texas-tpwd-confirms-116-more-cases-cwd.html
THURSDAY, APRIL 10, 2025
***> CWD TSE Prion, Politics, Friendly Fire, Unforeseen Consequences, What If?
chronic-wasting-disease.blogspot.com/2025/04/cwd-tse-prion-politics-friendly-fire.html
Texas S.B. 2843 Directs TPWD to conduct a comprehensive study of current measures to control chronic wasting disease (CWD) in deer
Trying to legislate CWD is what got Texas in this CWD mess to begin with, how did that work out$$$ Legislators and Politicians need to stay away and let TPWD and TAHC et try and contain this mess that Legislators and Politicians got us in, called CWD TSE Prion…terry
chronic-wasting-disease.blogspot.com/2025/04/texas-sb-2843-directs-tpwd-to-conduct.html
SUNDAY, MAY 04, 2025
Texas Senate Bill 2651 establishment of a pilot program to breed deer resistant to CWD TSE Prion
chronic-wasting-disease.blogspot.com/2025/05/texas-senate-bill-2651-establishment-of_4.html
TPW Commission Meeting CWD TSE Prion January 21-22, 2026 FINAL
Texas Parks and Wildlife Commission Appointed by the governor and confirmed by the Texas Senate, the Commission adopts policies and rules to carry out all programs of the Texas Parks and Wildlife Department. Every August, the Commission conducts an annual public hearing to receive input from our partners, stakeholders and constituents concerning any issues relating to Department policies, goals, programs, and responsibilities. Anyone who is interested in speaking to the Commission is encouraged to attend. Additional information on this and other public hearings is available at the links below.
TPW Commission Meeting January 21-22, 2026.
Summary English Summary Resumen en español
Executive Summary: Staff seeks adoption of proposed amendments to rules governing chronic wasting disease (CWD) detection, response, and management. The proposed amendments would function collectively to acknowledge and accommodate the decision of the Texas Animal Health Commission (TAHC) to cease cooperative efforts with Texas Parks and Wildlife Department (TPWD) with respect to the management of CWD in wildlife resources.
DISEASE DETECTION AND RESPONSE RULES
PROPOSAL PREAMBLE
1. Introduction.
snip…see;
tpwd.texas.gov/business/feedback/public_comment/proposals/202601_disease_detection_and_response_rules.phtml
TPW Commission Meeting CWD TSE Prion January 21-22, 2026
prpsc.proboards.com/thread/185/tpw-commission-prion-january-2026
chronic-wasting-disease.blogspot.com/2025/12/tpw-commission-meeting-cwd-tse-prion.html
Texas Confirms 116 More Cases CWD, Total To Date 1,215 Positives
TPWD CWD Dashboard 1,215 Total Positive Samples
experience.arcgis.com/experience/8f6c27330c444a19b4b57beb7ffabb8b/page/Dashboard#data_s=id%3AdataSource_3-1966d773e34-layer-10%3A2
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%). Scrapie: The flock identified in April 2016 remains under quarantine in Hartley County.
web.archive.org/web/20201017124040/https://www.tahc.texas.gov/agency/meetings/minutes/SummaryMinutes_CommMtg_2020-09-22.pdf
TEXAS PARKS & WILDLIFE: 50 CWD CASES AT SITE OF INITIAL POSITIVE IN WASHINGTON CO., BUT NO NEW CASES IN WILD
Josh Blaschke
October 29, 2025
Fifty cases of Chronic Wasting Disease (CWD) were reported after a deer herd depopulation operation this summer at the location of Washington County’s first recorded case, but state officials say those cases were all contained to the original site.
Texas Parks and Wildlife District 9 Leader Bobby Eichler (right), with Texas Game Warden Vinicius Mathias, provides an update to Washington County Commissioners on Tuesday about the current state of Chronic Wasting Disease in the county. Texas Parks and Wildlife Department (TPWD) District 9 Leader Bobby Eichler informed Washington County Commissioners on Tuesday that 158 adult deer and 63 fawns were euthanized as part of the operation. The depopulation occurred in the overnight hours between August 5th and 6th at the deer-breeding facility north of Brenham, where the county’s first case of CWD was reported in early 2023 in a doe that was born in the facility.
Eichler said the 50 positive cases represented roughly a third of the facility’s adult herd – the fawns, none older than 5 months of age, were not tested – and were spread across all age groups and both sexes. He said at the time of the depopulation, 72 deer were missing from the reported herd inventory and were presumed dead.
According to Eichler, since the initial positive was detected in 2023, none of the deer that have since tested positive were found in the wild; all were at the site of the first case.
CWD is a degenerative prion disease that erodes the neurological functions of deer. Victims experience symptoms like weight loss, stumbling, salivating and an overall appearance of “wasting” away. It is ultimately fatal, and there is no treatment or vaccine.
The test samples were submitted to the National Veterinary Services Laboratories in Ames, Iowa, and the results were returned on September 30th. Eichler said after the first positive case from 2023, the herd was quarantined, and additional live testing resulted in no new detections, though he noted that post-mortem testing is typically more effective. Captive deer-breeding facilities undergo annual CWD testing requirements to ensure deer are safe to be released to other breeders or ranchers.
Eichler said as part of an agreement reached this summer between the facility owner, the TPWD and the Texas Animal Health Commission, the owner voluntarily accepted USDA indemnity funds of an undisclosed amount. The herd was depopulated as a condition of that agreement, and the carcasses were buried deep underground on-site.
When asked if the affected deer-breeding facility would be able to re-open, TPWD Regional Wildlife Health Specialist Megan Hahn answered that most USDA herd plans require a quarantine period of at least 60 months before discussion can begin on re-introducing CWD-susceptible species. She said those plans also involve high-intensity cleaning and disinfecting of related equipment, troughs and fencing, while non-metallic items can be burned.
Across the state, Hahn said there have been roughly 1,100 positive CWD detections, with a little over 140 of those being considered free-ranging. Most of the cases are out of the Panhandle and West Texas. Hahn said testing efforts will remain constant as the state works to understand where the disease is located, as well as its prevalence and spread.
Eichler encouraged the continued use of the check station located in the parking lot east of the constables’ offices for dropping off samples to be tested.
Snip…
He said at the time of the depopulation, 72 deer were missing from the reported herd inventory and were presumed dead.
kwhi.com/2025/10/29/texas-parks-wildlife-50-cwd-cases-at-site-of-initial-positive-in-washington-co-but-no-new-cases-in-wild/
Eichler updates county on Chronic Wasting Disease
By Jason May
Snip…
“After receiving confirmation that the sample was CWD positive, the herd was quarantined. The facility conducted additional antemortem or live testing with no additional detections,” he said. “Ultimately, the facility owner voluntarily accepted USDA indemnity funds, and the herd was depopulated as a condition of that agreement.”
He detailed how the operation was carried out.
“Texas Parks and Wildlife staff determined that using chemical immobilization drugs and a captive penetrating bolt gun were the two most humane methods to collect the deer and the safest means for personnel involved,” Eichler said. “A bolt gun is a simple device that uses a .22 blank cartridge to drive a bolt into the skull. It is not an actual firearm and does not fire a projectile.”
The carcasses were buried on site as agreed upon with the facility, the Texas Animal Health Commission and the USDA.
Eichler noted that approximately 30 percent of the herd tested positive for CWD.
“All 158 adult deer were sampled. The only deer not tested were fawns under five months of age,” he said. “Samples were sent directly to the National Veterinary Services Laboratory, a USDA facility in Ames, Iowa. Results were returned to Texas Parks and Wildlife on Sept. 30. Of the 158 samples, 50 were positive for CWD, representing 31 percent of the herd. Positive deer were found across all age groups and both sexes.”
Eichler said testing for CWD continues statewide.
kdhnews.com/news/texas/eichler-updates-county-on-chronic-wasting-disease/article_ac83accb-3002-561c-adc2-bb34e2e04b87.html
Iowa 79.8 percent of the deer tested positive CWD and Wisconsin Buckhorn Flats Nearly 80% CWD positive
For Immediate Release
Thursday, October 2, 2014 Dustin Vande Hoef
TEST RESULTS FROM CAPTIVE DEER HERD WITH CHRONIC WASTING DISEASE RELEASED 79.8 percent of the deer tested positive for the disease
DES MOINES – The Iowa Department of Agriculture and Land Stewardship today announced that the test results from the depopulation of a quarantined captive deer herd in north-central Iowa showed that 284 of the 356 deer, or 79.8% of the herd, tested positive for Chronic Wasting Disease (CWD). The owners of the quarantined herd have entered into a fence maintenance agreement with the Iowa Department of Agriculture and Land Stewardship, which requires the owners to maintain the 8’ foot perimeter fence around the herd premises for five years after the depopulation was complete and the premises had been cleaned and disinfected
CWD is a progressive, fatal, degenerative neurological disease of farmed and free-ranging deer, elk, and moose. There is no known treatment or vaccine for CWD. CWD is not a disease that affects humans.
On July 18, 2012, USDA Animal and Plant Health Inspection Service’s (APHIS) National Veterinary Services Lab in Ames, IA confirmed that a male white tail deer harvested from a hunting preserve in southeast IA was positive for CWD. An investigation revealed that this animal had just been introduced into the hunting preserve from the above-referenced captive deer herd in north-central Iowa.
The captive deer herd was immediately quarantined to prevent the spread of CWD. The herd has remained in quarantine until its depopulation on August 25 to 27, 2014.
The Iowa Department of Agriculture and Land Stewardship participated in a joint operation to depopulate the infected herd with USDA Veterinary Services, which was the lead agency, and USDA Wildlife Services.
Federal indemnity funding became available in 2014. USDA APHIS appraised the captive deer herd of 376 animals at that time, which was before depopulation and testing, at $1,354,250. At that time a herd plan was developed with the owners and officials from USDA and the Iowa Department of Agriculture and Land Stewardship.
Once the depopulation was complete and the premises had been cleaned and disinfected, indemnity of $917,100.00 from the USDA has been or will be paid to the owners as compensation for the 356 captive deer depopulated.
The Iowa Department of Agriculture and Land Stewardship operates a voluntary CWD program for farms that sell live animals. Currently 145 Iowa farms participate in the voluntary program. The above-referenced captive deer facility left the voluntary CWD program prior to the discovery of the disease as they had stopped selling live animals. All deer harvested in a hunting preserve must be tested for CWD.
-30-
www.iowaagriculture.gov/press/2014press/press10022014.asp
web.archive.org/web/20141006172620/https://www.iowaagriculture.gov/press/2014press/press10022014.asp
DES MOINES – The Iowa Department of Agriculture and Land Stewardship today announced that the test results from the depopulation of a quarantined captive deer herd in north-central Iowa showed that 284 of the 356 deer, or 79.8% of the herd, tested positive for Chronic Wasting Disease (CWD).
web.archive.org/web/20141006172620/https://www.iowaagriculture.gov/press/2014press/press10022014.asp
Wisconsin Buckhorn Flats CWD
SUBJECT: Almond Deer Farm Update
The first case of Chronic Wasting Disease (CWD) among Wisconsin's farm-raised deer occurred in a white-tailed deer buck shot by a hunter at the property (formerly known as Buckhorn Flats) in September 2002. This situation prompted the eventual depopulation of the entire farm.
The deer, a mix of does and yearlings, were destroyed on January 17, 2006- 4 years later- by U.S. Department of Agriculture shooters under a USDA agreement with the farm owner.
Sixty of the 76 animals tested positive for CWD. The 76 deer constituted the breeding herd in the breeding facility on the farm. The property also had a hunting preserve until 2005. Four deer, two does and two fawns, the only deer remaining in the former preserve, were killed and tested as well. CWD was not detected in those animals.
The total number of deer to test positive from this farm from the initial discovery to final depopulation is 82. The nearly 80% prevalence rate discovered on Buckhorn Flats is the highest prevalence recorded in any captive cervid operation in North America.
web.archive.org/web/20140831060348/http://dnr.wi.gov/about/nrb/2011/december/12-11-2b2.pdf
Colorado CWD TSE Prion
“The overall incidence of clinical CWD in white-tailed deer was 82%“
Epidemiology of Chronic Wasting Disease in Captive White-Tailed and Mule Deer
The overall incidence of clinical CWD in white-tailed deer was 82% Species (cohort) CWD (cases/total) Incidence (%) Age at CWD death (mo)
cpw.state.co.us/Documents/Hunting/BigGame/CWD/PDF/ResearchArticles/JWDEpiCWD.pdf
web.archive.org/web/20150908134715/https://cpw.state.co.us/Documents/Hunting/BigGame/CWD/PDF/ResearchArticles/JWDEpiCWD.pdf
THURSDAY, APRIL 10, 2025
***> CWD TSE Prion, Politics, Friendly Fire, Unforeseen Consequences, What If?
chronic-wasting-disease.blogspot.com/2025/04/cwd-tse-prion-politics-friendly-fire.html
Texas S.B. 2843 Directs TPWD to conduct a comprehensive study of current measures to control chronic wasting disease (CWD) in deer
Trying to legislate CWD is what got Texas in this CWD mess to begin with, how did that work out$$$ Legislators and Politicians need to stay away and let TPWD and TAHC et try and contain this mess that Legislators and Politicians got us in, called CWD TSE Prion…terry
chronic-wasting-disease.blogspot.com/2025/04/texas-sb-2843-directs-tpwd-to-conduct.html
SUNDAY, MAY 04, 2025
Texas Senate Bill 2651 establishment of a pilot program to breed deer resistant to CWD TSE Prion
chronic-wasting-disease.blogspot.com/2025/05/texas-senate-bill-2651-establishment-of_4.html
Arkansas CWD Deer Study Final 2025
4. Objective 4 and 6 - Infection rates and population modeling
a. In 2024, CWD sample prevalence was 40% across the study area, with higher rates seen in males (65%) than in females (34%).
b. Approximately 50% of males tested positive for CWD by the age of 2.5.
c. White-tailed deer abundance in the study area declined, driven by reduced lifespans and lower lifetime reproduction.
d. If survival does not increase, this population is expected to continue to decline.
drive.google.com/file/d/1jN5mtvXvz7IYFDQjv4Rasrw60dGe4KMJ/view
Louisiana House of Representative Aug 27, 9:30 AM, HCR-6 CWD
Louisiana House of Representative
Chronic Wasting Disease CWD
(A letter written from a Mississippi farmer who’s farm has been in his family for more than 100 years, and submitted it in this video presentation, 28 minute mark, another wake up call for sure, of what some have been warning for years, about CWD, but sadly will go by the wayside by the conspiracy theorists spreading fake news…terry)
Alston Ross
Marshall County, Mississippi
My family owns a 2,000 acre farm in Marshall County, which is in North Mississippi. CWD has plagued my farm since 2018 and has become progressively worse over time. We no longer have mature deer over the age of 3 years old on our property. Every buck harvested on our land has tested positive this year. The owners of our neighboring properties have continued to feed deer and ignore MDWFP regulations, which has exacerbated the spread of the disease throughout our area. This farm has been in my family for over 100 years, and due to the rapid spread of CWD, we are concerned about the future of our deer herd and the value of our hunting land…end
Snip…
Arkansas
Snip…
40:35 “…and conversely, I was co-Principle Investigator in NW Arkansas, where prevalence is approaching 50 percent.”
Snip…
41:00 “Specific to the work in Arkansas, in 2020, the state agency was showing the Prevalence at 30 percent in the Northwest part of the State, so flip a coin, so, 1 out of every 3 deer had the disease. We started that research in 2020, and now, the prevalence rate is now exceeding 40% in both sexes, and 50% in males.”
43:00 “what we’re seeing Arkansas now is, that population is declining about 11% a year.”
Snip…see full video presentation;
house.louisiana.gov/H_Video/VideoArchivePlayer?v=house/2025/Aug/0827_25_NR_Joint
CWD IS RAVAGING MY FAMILY’S LAND, BUT IT’S NOT TOO LATE FOR YOU
September 9, 2025 By: Paul Annear
My first season deer hunting in Wisconsin was 2001, the same season that produced Wisconsin’s first deer to test positive for chronic wasting disease. CWD has always been at the forefront of deer hunting discussions in my time as a hunter, and I’ve watched the disease slowly spread and worsen. Since 2019, eight of 11 deer I’ve taken on my family’s property in Richland County in Southwest Wisconsin have tested positive for CWD – including the buck in the photo above.
Aside from harvesting otherwise perfectly healthy-looking deer that test positive for CWD, we are now seeing live deer walking around in the awful final stages of this disease. Research has now confirmed what I’ve seen occurring on our hunting land in the last five to six years: CWD is beginning to reduce deer populations in high-prevalence areas like mine.
It didn’t have to reach this point. Hunters in areas with low CWD prevalence can keep infection rates low and deer populations healthy overall by accepting and implementing certain strategies. Some of the strategies I will lay out will challenge you as a hunter to play the “long game,” but there are ways to slow the spread of CWD in areas where it is newly discovered and infection rates are still low.
If you’re rolling your eyes at another guy talking about CWD, I get it, but I urge you to keep reading. Hear my personal story, how it has affected my hunting experiences, and what can happen if hunters ignore CWD.
“Where Are the Deer?”
…snip…see full text;
deerassociation.com/cwd-is-ravaging-my-familys-land-but-its-not-too-late-for-you/
This CWD Study Could Change Deer Hunting FOREVER | The Check Station October 8, 2025 NW Arkansas
NW Arkansas CWD 11:25 minutes;
50% of all deer positive for CWD.
35% of Does are Positive for CWD.
68% Bucks are Positive for CWD.
Most Bucks NW Arkansas that where Tested, are Positive for CWD.
m.youtube.com/watch?v=kTicUE-xsQU&t=695s&pp=2AG3BZACAQ%3D%3D
MEMORANDUM
To: Members of the Colorado Parks and Wildlife Commission
From: Dan Prenzlow, Director
Date: April 22, 2022
Subject: Chronic Wasting Disease Update for Parks and Wildlife Commission Chronic wasting disease, a fatal neurological disease found in deer, elk, and moose, is well established in herds throughout much of Colorado. We have detected CWD in 40 of our 54 deer herds, 17 of 42 elk herds, and 2 of 9 moose herds. Disease prevalence (percent infected) is highest in deer and lowest in moose. This disease is always fatal and animals die from the disease within about 2-2.5 years of infection. CWD infection shortens the lifespan of infected animals. If infection rates become too high, CWD can affect a herd’s ability to sustain itself.
Snip…
web.archive.org/web/20220609004350/https://cpw.state.co.us/Documents/Commission/2022/May/Item.11-PWC_Memo_CWD_Update_EckertMillerWood_April2022-Matthew_Eckert-DNR.pdf
18% of mule deer in northeastern Montana have deadly chronic wasting disease “In the 2024-25 hunting FWP submitted 9,066 samples for chronic wasting disease testing – the largest number of CWD samples ever collected in a single year. More than 1,100 of these samples were collected by hunters. Of those samples, 335 tested positive for the disease, including 202 white-tailed deer, 127 mule deer and six elk.”
billingsgazette.com/outdoors/article_de5278b8-f2e1-11ef-b479-cf42652717a4.html
The effectiveness of harvest for limiting wildlife disease: Insights from 20 years of chronic wasting disease in Wyoming
First published: 21 January 2025
doi.org/10.1002/eap.3089
esajournals.onlinelibrary.wiley.com/doi/10.1002/eap.3089
www.usgs.gov/news/national-news-release/new-study-finds-deer-hunting-can-help-keep-chronic-wasting-disease-check
Since identifying its first cases of CWD in captive deer in the 70s and finding the first wild infected deer in 1985, Wyoming has seen the disease slowly spread throughout the state. CWD has now been documented in members of the deer family in most of Wyoming’s deer hunting areas, with 20% to 40% percent of mule deer affected in some herds. A 2017 study estimated a 21% annual population decline as a result of the fatal disease.
freerangeamerican.us/chronic-wasting-disease-wyoming/#:~:text=CWD%20has%20now%20been%20documented,result%20of%20the%20fatal%20disease.
How does CWD impact deer, elk, and moose populations?
Recent research in Wyoming has demonstrated declines in both mule and white-tailed deer populations in deer hunt area 65 due to CWD (see below for citations). These declines are in the core endemic area where prevalence is highest. In areas with lower prevalence, effects of CWD are poorly understood but are considered additive along with other factors that can negatively affect deer populations in Wyoming (i.e. habitat loss, predation, other diseases). The distribution and prevalence of CWD in Wyoming elk is less than that of deer. Currently there are no documented direct population impacts in Wyoming elk from CWD; however, research from Rocky Mountain National Park suggests that CWD could impact elk populations at higher prevalence (13%). While CWD has been found in free ranging moose, there have been few detections, and there is no evidence that CWD is currently having an impact on moose populations.
wgfd.wyo.gov/Wildlife-in-Wyoming/More-Wildlife/Wildlife-Disease/Chronic-Wasting-Disease
PLoS One. 2016 Aug 30;11(8):e0161127. doi: 10.1371/journal.pone.0161127. eCollection 2016.
Chronic Wasting Disease Drives Population Decline of White-Tailed Deer
We show that a chronic disease that becomes endemic in wildlife populations has the potential to be population-limiting and the strong population-level effects of CWD suggest affected populations are not sustainable at high disease prevalence under current harvest levels.
journals.plos.org/plosone/article?id=10.1371/journal.pone.0161127
Friday, December 14, 2012
DEFRA U.K. What is the risk of Chronic Wasting Disease CWD being introduced into Great Britain? A Qualitative Risk Assessment October 2012
snip.....
36% in 2007 (Almberg et al., 2011). In such areas, population declines of deer of up to 30 to 50% have been observed (Almberg et al., 2011). In areas of Colorado, the prevalence can be as high as 30% (EFSA, 2011).
snip.....
The rate of transmission of CWD has been reported to be as high as 30% and can approach 100% among captive animals in endemic areas (Safar et al., 2008). snip.....
web.archive.org/web/20170404125557/http://webarchive.nationalarchives.gov.uk/20130822084033/http://www.defra.gov.uk/animal-diseases/files/qra_chronic-wasting-disease-121029.pdf
Chronic Wasting Disease in Texas A Real Disease with Proven Impacts
Produced by a coalition of concerned hunters, landowners, & conservationists (last update 1/2025)
storymaps.arcgis.com/stories/b93f528938ac48e9b56dcc79953cbec0
Aug 18, 2021
Oh, Deer
Heading Off a Wildlife Epidemic
CWD poses a significant threat to the future of hunting in Texas. Deer population declines of 45 and 50 percent have been documented in Colorado and Wyoming. A broad infection of Texas deer populations resulting in similar population impacts would inflict severe economic damage to rural communities and could negatively impact land markets. Specifically, those landowners seeking to establish a thriving herd of deer could avoid buying in areas with confirmed CWD infections. As they do with anthrax-susceptible properties, land brokers may find it advisable to inquire about the status of CWD infections on properties that they present for sale. Prospective buyers should also investigate the status of the wildlife on prospective properties. In addition, existing landowners should monitor developments as TPWD crafts management strategies to identify and contain this deadly disease.
Dr. Gilliland (
www.recenter.tamu.edu/articles/tierra-grande/oh-d
Thursday, October 2, 2014
TEST RESULTS FROM CAPTIVE DEER HERD WITH CHRONIC WASTING DISEASE RELEASED 79.8 percent of the deer tested positive for the disease
DES MOINES – The Iowa Department of Agriculture and Land Stewardship today announced that the test results from the depopulation of a quarantined captive deer herd in north-central Iowa showed that 284 of the 356 deer, or 79.8% of the herd, tested positive for Chronic Wasting Disease (CWD).
web.archive.org/web/20141006172620/https://www.iowaagriculture.gov/press/2014press/press10022014.asp
Wisconsin Buckhorn Flats CWD
SUBJECT: Almond Deer Farm Update
Sixty of the 76 animals tested positive for CWD. The 76 deer constituted the breeding herd in the breeding facility on the farm. The property also had a hunting preserve until 2005. Four deer, two does and two fawns, the only deer remaining in the former preserve, were killed and tested as well. CWD was not detected in those animals.
The total number of deer to test positive from this farm from the initial discovery to final depopulation is 82. The nearly 80% prevalence rate discovered on Buckhorn Flats is the highest prevalence recorded in any captive cervid operation in North America.
web.archive.org/web/20140831060348/http://dnr.wi.gov/about/nrb/2011/december/12-11-2b2.pdf
Colorado CWD TSE Prion
“The overall incidence of clinical CWD in white-tailed deer was 82% “
Epidemiology of Chronic Wasting Disease in Captive White-Tailed and Mule Deer
web.archive.org/web/20150908134715/https://cpw.state.co.us/Documents/Hunting/BigGame/CWD/PDF/ResearchArticles/JWDEpiCWD.pdf
Chronic Wasting Disease CWD TSE Prion Environmental & Zoonosis Factors Update September 2025
Chronic wasting disease (CWD) prion detection in environmental and biological samples from a taxidermy site and nursing facility, and instruments used in surveillance activities
Available online 9 April 2025
Highlights
• CWD prions were identified in a taxidermy and deer nursing facility.
• Contaminated samples included waters, soils, dermestid beetles, domestic flies and a dumpster.
• Surgical instruments used to collect deer samples can get contaminated with CWD prions.
• Some of the infectious particles are readily released from surgical instruments when washed.
• Our results suggest that taxidermy practices actively contribute in the spreading of CWD.
Snip…
In summary, the information provided in this report demonstrate how anthropogenic activities, specifically taxidermy practices, animal processing, and rehabilitation of CWD susceptible species, may facilitate CWD transmission through the environmental dissemination of CWD prions. This study, along with future research efforts characterizing the overall level of infectivity, provides relevant information on managing CWD and to control its rapid geographic expansion. …
www.sciencedirect.com/science/article/abs/pii/S0048969725009544
Chronic wasting disease detection in environmental and biological samples from a taxidermy site
Results: The PMCA analysis demonstrated CWD seeding activity in some of the components of this facility, including insects involved in head processing, soils, and a trash dumpster.
Conclusions: Different areas of this property were used for various taxidermy procedures. We were able to detect the presence of prions in
i) soils that were in contact with the heads of dead animals, ii) insects involved in the cleaning of skulls, and iii) an empty dumpster where animal carcasses were previously placed.
This is the first report demonstrating that swabbing is a helpful method to screen for prion infectivity on surfaces potentially contaminated with CWD. These findings are relevant as this swabbing and amplification strategy may be used to evaluate the disease status of other free-ranging and captive settings where there is a concern for CWD transmissions, such as at feeders and water troughs with CWD-exposed properties. This approach could have substantial implications for free-ranging cervid surveillance as well as in epidemiological investigations of CWD.
Prion 2022 Conference abstracts: pushing the boundaries
www.tandfonline.com/doi/full/10.1080/19336896.2022.2091286
Artificial mineral sites that pre-date endemic chronic wasting disease become prion hotspots
The Ames Research and Educational Center property, centrally located within the CWD zone of southwest Tennessee, contains 49 historical mineral supplementation sites that were decommissioned in 2012. Here, we demonstrate that 32 of the 49 (65%) mineral sites within Ames established prior to the regional CWD outbreak, serve as foci of environmental PrPCWD contamination. Detection of PrPCWD in soils from these artificial mineral sites was dependent on site-specific management efforts. Soil physical properties were very similar across sites and no correlation between PrPCWD detection and soil physical properties was found. The detection of PrPCWD in soils at attractant sites within an endemic CWD zone significantly advances our understanding of environmental PrPCWD accumulation dynamics, providing valuable information for advancing adaptive CWD management approaches.
intcwdsympo.files.wordpress.com/2023/06/final-agenda-with-abstracts.pdf
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.
www.tandfonline.com/doi/full/10.1080/19336896.2025.2527588
Rapid recontamination of a farm building occurs after attempted prion removal
First published: 19 January 2019 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.
bvajournals.onlinelibrary.wiley.com/doi/abs/10.1136/vr.105054
***>This is very likely to have parallels with control efforts for CWD in cervids.
pubmed.ncbi.nlm.nih.gov/30602491/
Front. Vet. Sci., 14 September 2015 | 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.
journal.frontiersin.org/article/10.3389/fvets.2015.00032/full
SUNDAY, APRIL 06, 2025
Failure to prevent classical scrapie after repeated decontamination of a barn
scrapie-usa.blogspot.com/2025/04/failure-to-prevent-classical-scrapie.html
prpsc.proboards.com/thread/165/failure-prevent-scrapie-repeated-decontamination
"Additionally, we have determined that prion seeding activity is retained for at least fifteen years at a contaminated site following attempted remediation."
15 YEARS!
Detection of prions in soils contaminated by multiple routes
Results: We are able to detect prion seeding activity at multiple types of environmental hotspots, including carcass sites, contaminated captive facilities, and scrapes (i.e. urine and saliva). Differences in relative prion concentration vary depending on the nature and source of the contamination. Additionally, we have determined that prion seeding activity is retained for at least fifteen years at a contaminated site following attempted remediation.
Conclusions: Detection of prions in the environment is of the utmost importance for controlling chronic wasting disease spread. Here, we have demonstrated a viable method for detection of prions in complex environmental matrices. However, it is quite likely that this method underestimates the total infectious prion load in a contaminated sample, due to incomplete recovery of infectious prions. Further refinements are necessary for accurate quantification of prions in such samples, and to account for the intrinsic heterogeneities found in the broader environment.
Funded by: Wisconsin Department of Natural Resources
Meeting-book-final-version prion 2023 Prion 2023 Congress Organizing Committee and the NeuroPrion Association, we invite you to join us for the International Conference Prion2023 from 16-20 October 2023 in Faro, Portugal.
web.archive.org/web/20250828201533/https://prion2023.org/wp-content/uploads/2023/10/Meeting-book-final-version2.pdf
www.researchgate.net/profile/Syed-Zahid-Shah/publication/378314391_Meeting-book-final-version_prion_2023/links/65d44dad28b7720cecdca95f/Meeting-book-final-version-prion-2023.pdf
***> Infectious agent of sheep scrapie may persist in the environment for at least 16 years
***> Nine of these recurrences occurred 14–21 years after culling, apparently as the result of environmental contamination, but outside entry could not always be absolutely excluded.
JOURNAL OF GENERAL VIROLOGY Volume 87, Issue 12
Infectious agent of sheep scrapie may persist in the environment for at least 16 years Free
www.microbiologyresearch.org/content/journal/jgv/10.1099/vir.0.82011-0
Shedding of Chronic Wasting Disease Prions in Multiple Excreta Throughout Disease Course in White-tailed Deer
Conclusions: These studies demonstrate: (a) CWD prion excretion occurs throughout infection; (2) PRNP genotype (GG≫GS/NT) influences the excreta shedding; and (3) detection sensitivity in excreta can vary with different RT-QuIC protocols. These results provide a more complete perspective of prion shedding in deer during the course of CWD infection.
Prion 2022 Conference abstracts: pushing the boundaries
www.tandfonline.com/doi/full/10.1080/
***>This is very likely to have parallels with control efforts for CWD in cervids.
pubmed.ncbi.nlm.nih.gov/30602491/
I remember what “deep throat” told me about Scrapie back around 2001, during early days of my BSE investigation, after my Mom died from hvCJD, I never forgot, and it seems it’s come to pass;
***> Confidential!!!!
***> As early as 1992-3 there had been long studies conducted on small pastures containing scrapie infected sheep at the sheep research station associated with the Neuropathogenesis Unit in Edinburgh, Scotland. Whether these are documented...I don't know. But personal recounts both heard and recorded in a daily journal indicate that leaving the pastures free and replacing the topsoil completely at least 2 feet of thickness each year for SEVEN years....and then when very clean (proven scrapie free) sheep were placed on these small pastures.... the new sheep also broke out with scrapie and passed it to offspring. I am not sure that TSE contaminated ground could ever be free of the agent!! A very frightening revelation!!!
---end personal email---end...tss
and so it seems…
Chronic Wasting Disease CWD TSE Prion
THE CWD TSE Prion aka mad cow type disease is not your normal pathogen.
The TSE prion disease survives ashing to 600 degrees celsius, that’s around 1112 degrees farenheit.
You cannot cook the TSE prion disease out of meat. In fact new data now shows that exposure to high temperatures used to cook the meat increased the availability of prions for in vitro amplification.
you can take the ash and mix it with saline and inject that ash into a mouse, and the mouse will go down with TSE.
Prion Infected Meat-and-Bone Meal Is Still Infectious after Biodiesel Production as well.
the TSE prion agent also survives Simulated Wastewater Treatment Processes.
IN fact, you should also know that the TSE Prion agent will survive in the environment for years, if not decades.
you can bury it and it will not go away.
The TSE agent is capable of infected your water table i.e. Detection of protease-resistant cervid prion protein in water from a CWD-endemic area.
it’s not your ordinary pathogen you can just cook it out and be done
New studies on the heat resistance of hamster-adapted scrapie agent: Threshold survival after ashing at 600°C suggests an inorganic template of replication
www.pnas.org/content/97/7/3418.full
Prion Infected Meat-and-Bone Meal Is Still Infectious after Biodiesel Production
www.ncbi.nlm.nih.gov/pmc/articles/PMC2493038/
Rapid assessment of bovine spongiform encephalopathy prion inactivation by heat treatment in yellow grease produced in the industrial manufacturing process of meat and bone meals
bmcvetres.biomedcentral.com/track/pdf/10.1186/1746-6148-9-134.pdf
THURSDAY, FEBRUARY 28, 2019
BSE infectivity survives burial for five years with only limited spread
link.springer.com/content/pdf/10.1007%2Fs00705-019-04154-8.pdf
Chronic wasting disease prions on deer feeders and wildlife visitation to deer feeding areas
First published: 10 February 2025
Snip…
Finally, we swabbed 19 feeders in 2 areas where CWD was newly detected, finding prion contamination on swabs from 4 feeders. We show that deer feeders in free-ranging populations with high CWD prevalence become contaminated with CWD prions quickly, becoming a potential site of exposure of deer to CWD prions. Our results also demonstrate the ability to find evidence of prion contamination on deer feeders, even in areas where CWD is newly detected.
Snip…
We found that supplemental feeding increased the risk of exposure to CWD prions due to contamination of feeders, increased deer visitation, and increased deer-to-deer contact.
The 12-fold increase in deer visitation to feeders compared to mast trees and 2-fold increase compared to food plots demonstrates increased risk for direct disease spread.
wildlife.onlinelibrary.wiley.com/doi/10.1002/jwmg.70000
2025
Cwd, cattle, pigs, sheep, raccoons, oh my!
Price of TSE Prion Poker goes up substantially, all you cattle ranchers and such, better pay close attention here...terry
"Cattle with the E211K polymorphism are susceptible to the CWD agent after oronasal exposure of 0.2 g of infectious material."
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
Prion Conference 2023
Transmission of the chronic wasting disease agent from elk to cattle after oronasal exposure
Conclusions: Cattle with the E211K polymorphism are susceptible to the CWD agent after oronasal exposure of 0.2 g of infectious material.
Strain characterization of chronic wasting disease in bovine-PrP transgenic mice
Conclusions: Altogether, these results exhibit the diversity of CWD strains present in the panel of CWD isolates and the ability of at least some CWD isolates to infect bovine species. Cattle being one of the most important farming species, this ability represents a potential threat to both animal and human health, and consequently deserves further study.
web.archive.org/web/20231116212109/https://prion2023.org/wp-content/uploads/2023/10/Meeting-book-final-version2.pdf
www.researchgate.net/profile/Syed-Zahid-Shah/publication/378314391_Meeting-book-final-version_prion_2023/links/65d44dad28b7720cecdca95f/Meeting-book-final-version-prion-2023.pdf
Volume 31, Number 1—January 2025
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.
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.
wwwnc.cdc.gov/eid/article/31/1/24-0401_article
Currently, swine rations in the U.S. could contain animal derived components including materials from deer or elk. In addition, feral swine could be exposed to infected carcasses in areas where CWD is present in wildlife populations. The current feed ban in the U.S. is based exclusively on keeping tissues from TSE infected cattle from entering animal feeds. These results indicating the susceptibility of pigs to CWD, coupled with the limitations of the current feed ban, indicates that a revision of the feed ban may be necessary to protect swine production and potentially human health.
The successful transmission of pig-passaged CWD to Tg40 mice reported here suggests that passage of the CWD agent through pigs results in a change of the transmission characteristics which reduces the transmission barrier of Tg40 mice to the CWD agent. If this biological behavior is recapitulated in the original host species, passage of the CWD agent through pigs could potentially lead to increased pathogenicity of the CWD agent in humans. Interestingly, bioassay of material from the longest surviving >6 month orally challenged pig (72 mpc), which was negative for PrPcwd by all other tests, produced a positive bioassay result. Bioassay of material from additional animals is currently underway. This study demonstrates that pigs can serve as potential hosts for CWD, although with low attack rates and scant PrPcwd accumulation. Detection of infectivity in orally challenged pigs using mouse bioassay raises the possibility that naturally exposed pigs act as a reservoir of CWD infectivity, even though affected pigs do not develop overt clinical signs or readily detectable PrPcwd.
www.ars.usda.gov/research/publications/publication/?seqNo115=326166
cwd scrapie pigs oral routes
***> However, at 51 months of incubation or greater, 5 animals were positive by one or more diagnostic methods. Furthermore, positive bioassay results were obtained from all inoculated groups (oral and intracranial; market weight and end of study) suggesting that swine are potential hosts for the agent of scrapie. <***
*** Although the current U.S. feed ban is based on keeping tissues from TSE infected cattle from contaminating animal feed, swine rations in the U.S. could contain animal derived components including materials from scrapie infected sheep and goats. These results indicating the susceptibility of pigs to sheep scrapie, coupled with the limitations of the current feed ban, indicates that a revision of the feed ban may be necessary to protect swine production and potentially human health. <***
***> Results: PrPSc was not detected by EIA and IHC in any RPLNs. All tonsils and MLNs were negative by IHC, though the MLN from one pig in the oral <6 month group was positive by EIA. PrPSc was detected by QuIC in at least one of the lymphoid tissues examined in 5/6 pigs in the intracranial <6 months group, 6/7 intracranial >6 months group, 5/6 pigs in the oral <6 months group, and 4/6 oral >6 months group. Overall, the MLN was positive in 14/19 (74%) of samples examined, the RPLN in 8/18 (44%), and the tonsil in 10/25 (40%).
***> Conclusions: This study demonstrates that PrPSc accumulates in lymphoid tissues from pigs challenged intracranially or orally with the CWD agent, and can be detected as early as 4 months after challenge. CWD-infected pigs rarely develop clinical disease and if they do, they do so after a long incubation period. This raises the possibility that CWD-infected pigs could shed prions into their environment long before they develop clinical disease. Furthermore, lymphoid tissues from CWD-infected pigs could present a potential source of CWD infectivity in the animal and human food chains.
www.ars.usda.gov/research/publications/publication/?seqNo115=353091
www.ars.usda.gov/research/project/?accnNo=432011&fy=2017
www.ars.usda.gov/research/publications/publication/?seqNo115=337105
Conclusions: This study demonstrates that PrPSc accumulates in lymphoid tissues from pigs challenged intracranially or orally with the CWD agent, and can be detected as early as 4 months after challenge. CWD-infected pigs rarely develop clinical disease and if they do, they do so after a long incubation period. This raises the possibility that CWD-infected pigs could shed prions into their environment long before they develop clinical disease. Furthermore, lymphoid tissues from CWD-infected pigs could present a potential source of CWD infectivity in the animal and human food chains.
www.ars.usda.gov/research/publications/publication/?seqNo115=337105
Component 6: Transmissible Spongiform Encephalopathies
Sheep scrapie agent can infect white-tailed deer after oronasal exposure.
The origin of chronic wasting disease (CWD) is not known, but it has many similarities to the sheep prion disease called scrapie. It has long been hypothesized that CWD arose through transmission of sheep scrapie to deer. ARS researchers in Ames, Iowa, conducted research to determine if scrapie derived from sheep could be transmitted to white-tailed deer. The deer inoculated with sheep scrapie developed clinical signs and the abnormal prion protein could be detected in a wide range of tissues. These results indicate that deer may be susceptible to sheep scrapie if exposed to the disease in natural or agricultural settings. In addition, several strong similarities between CWD in white-tailed deer and the experimental cases of scrapie in white-tailed deer suggests that it would be difficult to distinguish scrapie from CWD in deer or identify scrapie if a case occurs. This information should be considered by deer farmers for keeping their herds free from prion diseases.
www.ars.usda.gov/ARSUserFiles/np103/AnnualReports/NP103%20FY2023%20Annual%20Report_Final.pdf
SCRAPIE TSE Prion USA RAPID RESPONSE URGENT UPDATES DECEMBER 25, 2025
scrapie-usa.blogspot.com/2025/12/scrapie-tse-prion-usa-rapid-response.html
prpsc.proboards.com/thread/186/scrapie-prion-response-urgent-updates
The chronic wasting disease agent from white-tailed deer is highly infectious to humanized mice after passage through raccoons
www.ars.usda.gov/research/publications/publication/?seqNo115=400777
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
www.regulations.gov/comment/FDA-2003-D-0432-0011
www.regulations.gov/docket/FDA-2003-D-0432
WHO IS GETTING PAID OFF CWD, IS IT DNR, INSURANCE COMPANIES, GOVERNMENT, CONSPIRACY, OR COULD IT BE…indemnity for captive Cervid industry?
USDA EXPLANATORY NOTES ANIMAL AND PLANT HEALTH INSPECTION SERVICE 2025-2014 CHRONIC WASTING DISEASE CWD TSE CERVID
chronic-wasting-disease.blogspot.com/2025/09/usda-explanatory-notes-animal-and-plant.html
TUESDAY, NOVEMBER 11, 2025
USAHA 128th Annual Meeting October 2024 CWD, TSE, Prion Update
chronic-wasting-disease.blogspot.com/2025/11/usaha-128th-annual-meeting-october-2024.html
FRIDAY, OCTOBER 31, 2025
Captive Cervid and the Economic Burden of Chronic Wasting Disease CWD TSE Prion?
The economic burden of ignoring CWD would be far greater, imo, with time, if no cervid were left, or just a select few, if the environment/property was so exposed and saturated with CWD, that you couldn’t sell it, you couldn’t grow crops because of the soil saturation of the CWD, water tables saturated with CWD, saturation of hay, grains, from crops uptake on said property, cervid meat saturated from Cervid CWD, remember, You cannot cook the TSE prion disease out of meat, In fact new data now shows that exposure to high temperatures used to cook the meat increased the availability of prions for in vitro amplification. So, what Do we do, how many humans and animals do we continue to expose, continue to saturate with the CWD TSE Prion, …
chronic-wasting-disease.blogspot.com/2025/10/captive-cervid-and-economic-burden-of.html
prpsc.proboards.com/thread/183/captive-cervid-economic-burden-prion
CWD Status Captive Herds
www.aphis.usda.gov/sites/default/files/status-of-captive-herds.pdf
www.thewildlifenews.com/2025/12/03/elk-feedlots-and-chronic-wasting-disease/
Human CWD TSE PrP, what if?
the problem is, to date, there is NO diagnostic criteria set in stone that would confirm a case of human Cwd, like there was with nvCJD (my Mom died from confirmed hvCJD a rare strain of the infamous sporadic CJDs with new strains mounting, sporadic CJD simply means ‘unknown’, IT DOES NOT MEAN 85%+ SPORADIC CJD IS ALL SPONTANEOUS, that’s all iatrogenic CJD is sporadic CJD, until the iatrogenic event is detected, confirmed, traced back, confirmed, put into the academic domain, and finally, if your lucky, finally published to the media, and finally the public domain.) sorry, I got off course…but let me perfectly clear here, all science to date shows, Human CWD will not look like New Variant Creutzfeldt Jakob disease nvCJD. CWD to humans will look like some variant of sporadic Creutzfeldt Jakob Disease. And here me out very clearly, and this is from the to TSE Prion Gods themselves, old correspondence from way back during my investigations early BSE nvCJD days…2002
“Also, we do not claim that "no-one has ever been infected with prion disease from eating venison." Our conclusion stating that we found no strong evidence of CWD transmission to humans in the article you quoted or in any other forum is limited to the patients we investigated.”
*** now, let’s see what the authors said about this casual link, personal communications years ago, and then the latest on the zoonotic potential from CWD to humans from the TOKYO PRION 2016 CONFERENCE.
see where it is stated NO STRONG evidence. so, does this mean there IS casual evidence
?“Our conclusion stating that we found no strong evidence of CWD transmission to humans”
Subject: CWD aka MAD DEER/ELK TO HUMANS
Date: September 30, 2002 at 7:06 am PST From: "Belay, Ermias" To: Cc: "Race, Richard (NIH)" ; ; "Belay, Ermias" Sent: Monday, September 30, 2002 9:22 AMSubject: 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:
Also, we do not claim that "no-one has ever been infected with prion disease from eating venison." Our conclusion stating that we found no strong evidence of CWD transmission to humans in the article you quoted or in any other forum is limited to the patients we investigated.
Ermias Belay, M.D. Centers for Disease Control and Prevention
Subject: TO CDC AND NIH - PUB MED- 3 MORE DEATHS - CWD - YOUNG HUNTERS
Sunday, November 10, 2002 6:26 PM .......snip........end..............TSS
-----Original Message-----
From: Sent: Sunday, September 29, 2002 10:15 AM
To:
Subject: TO CDC AND NIH - PUB MED- 3 MORE DEATHS - CWD - YOUNG HUNTERS
Sunday, November 10, 2002 6:26 PM .......snip........end..............TSS
Thursday, April 03, 2008
A prion disease of cervids: Chronic wasting disease 2008 1: Vet Res. 2008 Apr 3;39(4):41 A prion disease of cervids: Chronic wasting disease Sigurdson CJ.
snip...
*** twenty-seven CJD patients who regularly consumed venison were reported to the Surveillance Center, however there have been no unusual or novel prion subtypes that might indicate the appearance of a new prion strain [7, 41].
snip... full text ;
www.vetres.org/articles/vetres/abs/2008/04/v08092/v08092.html
chronic-wasting-disease.blogspot.com/2008/04/prion-disease-of-cervids-chronic.html
“regular venison eating associated with a 9 FOLD INCREASE IN RISK OF CJD”
Subject: Re: DEER SPONGIFORM ENCEPHALOPATHY SURVEY & HOUND STUDY Date: Fri, 18 Oct 2002 23:12:22 +0100 From: Steve Dealler Reply-To: Bovine Spongiform Encephalopathy Organization: Netscape Online member
To: BSE-L@ …
######## Bovine Spongiform Encephalopathy <
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
########### mailhost.rz.uni-karlsruhe.de/warc/bse-l.html ############
Subject: DEER SPONGIFORM ENCEPHALOPATHY SURVEY & HOUND STUDY From: "Terry S. Singeltary Sr." <
snip...
''The association between venison eating and risk of CJD shows similar pattern, with regular venison eating associated with a 9 FOLD INCREASE IN RISK OF CJD (p = 0.04).''
CREUTZFELDT JAKOB DISEASE SURVEILLANCE IN THE UNITED KINGDOM THIRD ANNUAL REPORT AUGUST 1994
snip...see full report ;
web.archive.org/web/20090506050043/http://www.bseinquiry.gov.uk/files/yb/1994/08/00004001.pdf
web.archive.org/web/20090506050007/http://www.bseinquiry.gov.uk/files/yb/1994/10/00003001.pdf
web.archive.org/web/20090506050244/http://www.bseinquiry.gov.uk/files/yb/1994/07/00001001.pdf
Stephen Dealler is a consultant medical microbiologist
snip...end
########### mailhost.rz.uni-karlsruhe.de/warc/bse-l.html ############
*** These results would seem to suggest that CWD does indeed have zoonotic potential, at least as judged by the compatibility of CWD prions and their human PrPC target. Furthermore, extrapolation from this simple in vitro assay suggests that if zoonotic CWD occurred, it would most likely effect those of the PRNP codon 129-MM genotype and that the PrPres type would be similar to that found in the most common subtype of sCJD (MM1).***
www.tandfonline.com/doi/full/10.4161/pri.28124?src=recsys
www.tandfonline.com/doi/pdf/10.4161/pri.28124?needAccess=true
wwwnc.cdc.gov/eid/article/20/1/13-0858_article
So, this is what we leave our children and grandchildren?
What does CDC say?
CDC CWD TSE Prion Update 2025
KEY POINTS
Chronic wasting disease affects deer, elk and similar animals in the United States and a few other countries.
The disease hasn't been shown to infect people.
However, it might be a risk to people if they have contact with or eat meat from animals infected with CWD.
www.cdc.gov/chronic-wasting/about/index.html
Prions in Muscles of Cervids with Chronic Wasting Disease, Norway
Volume 31, Number 2—February 2025
Research
Prions in Muscles of Cervids with Chronic Wasting Disease, Norway
Snip…
In summary, the results of our study indicate that prions are widely distributed in peripheral and edible tissues of cervids in Norway, including muscles. This finding highlights the risk of human exposure to small amounts of prions through handling and consuming infected cervids. Nevertheless, we note that this study did not investigate the zoonotic potential of the Norway CWD prions. In North America, humans have historically consumed meat from CWD-infected animals, which has been documented to harbor prions (35,44–47). Despite the potential exposure to prions, no epidemiologic evidence indicates a correlation between the occurrence of CWD cases in animals and the prevalence of human prion diseases (48). A recent bioassay study reported no transmissions from 3 Nordic isolates into transgenic mice expressing human PrP (49). Therefore, our findings should be interpreted with caution in terms of human health implications, and further research is required to determine the zoonotic potential of these CWD strains.
The presence of prions in peripheral tissues indicates that CWD may have a systemic nature in all Norwegian cervid species, challenging the view that prions are exclusively localized in the CNS in sporadic CWD of moose and red deer. Our findings expand the notion of just how widely distributed prions can be in cervids affected with CWD and call into question the capability of emerging CWD strains in terms of infectivity to other species, including humans.
Appendix
wwwnc.cdc.gov/eid/article/31/2/24-0903-app1.pdf
wwwnc.cdc.gov/eid/article/31/2/24-0903_article
Volume 31, Number 2—February 2025
Dispatch
Detection of Chronic Wasting Disease Prions in Raw, Processed, and Cooked Elk Meat, Texas, USA
Rebeca Benavente, Fraser Brydon, Francisca Bravo-Risi, Paulina Soto, J. Hunter Reed, Mitch Lockwood, Glenn Telling, Marcelo A. Barria, and Rodrigo MoralesComments to Author
Snip…
CWD prions have been detected in the muscle of both farmed and wild deer (10), and at concentrations relevant to sustain disease transmission (11). CWD prions have also been identified across several cervid species and in multiple tissues, including lymph nodes, spleen, tongue, intestines, adrenal gland, eyes, reproductive tissues, ears, lungs, and liver, among others (12–14). Those findings raise concerns about the safety of ingesting processed meats that contain tissues other than skeletal muscle (15) (Appendix). 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.
wwwnc.cdc.gov/eid/article/31/2/24-0906_article
The detection and decontamination of chronic wasting disease prions during venison processing
Aims: There is a growing concern that chronic wasting disease (CWD) prions in venison pose a risk to human health. CWD prions accumulate in infected deer tissues that commonly enter the human food chain through meat processing and consumption. The United States (US) Food and Drug Administration and US Department of Agriculture now formally consider CWD-positive venison unfit for human and animal consumption. Yet, the degree to which prion contamination occurs during routine venison processing is unknown. Here, we use environmental surface swab methods to:
a) experimentally test meat processing equipment (i.e., stainless steel knives and polyethylene cutting boards) before and after processing CWD-positive venison and
b) test the efficacy of five different disinfectant types (i.e., Dawn dish soap, Virkon-S, Briotech, 10% bleach, and 40% bleach) to determine prion decontamination efficacy.
Materials and Methods: We used a real-time quaking-induced conversion (RT-QuIC) assay to determine CWD infection status of venison and to detect CWD prions in the swabs. We collected three swabs per surface and ran eight technical replicates on RT-QuIC.
Results: CWD prions were detected on all cutting boards (n= 3; replicates= 8/8, 8/8, 8/8 and knives (n= 3; replicates= 8/8, 8/8, 8/8) used in processing CWD-positive venison, but not on those used for CWD-negative venison. After processing CWD-positive venison, allowing the surfaces to dry, and washing the cutting board with Dawn dish soap, we detected CWD prions on the cutting board surface (n= 3; replicates= 8/8, 8/8, 8/8) but not on the knife (n= 3, replicates = 0/8, 0/8, 0/8). Similar patterns were observed with Briotech (cutting board: n= 3; replicates= 7/8, 1/8, 0/8; knife: n= 3; replicates = 0/8, 0/8, 0/8). We did not detect CWD prions on the knives or cutting boards after disinfecting with Virkon-S, 10% bleach, and 40% bleach.
Conclusions: These preliminary results suggest that Dawn dish soap and Briotech do not reliably decontaminate CWD prions from these surfaces. Our data suggest that Virkon-S and various bleach concentrations are more effective in reducing prion contamination of meat processing surfaces; however, surface type may also influence the ability of prions to adsorb to surfaces, preventing complete decontamination. Our results will directly inform best practices to prevent the introduction of CWD prions into the human food chain during venison processing.
Prion 2023 Abstracts
web.archive.org/web/20231116212109/https://prion2023.org/wp-content/uploads/2023/10/Meeting-book-final-version2.pdf
www.researchgate.net/profile/Syed-Zahid-Shah/publication/378314391_Meeting-book-final-version_prion_2023/links/65d44dad28b7720cecdca95f/Meeting-book-final-version-prion-2023.pdf
DETECTION OF CHRONIC WASTING DISEASE PRIONS IN PROCESSED MEATS.
The zoonotic potential of chronic wasting disease (CWD) remains unknown. Currently, there are no known natural cases of CWD transmission to humans but increasing evidence suggests that the host range of CWD is not confined only to cervid species. Alarmingly, recent experimental evidence suggests that certain CWD isolates can induce disease in non-human primates. While the CDC strongly recommends determining CWD status in animals prior to consumption, this practice is voluntary. Consequently, it is plausible that a proportion of the cervid meat entering the human food chain may be contaminated with CWD. Of additional concern is that traditional diagnostic techniques used to detect CWD have relatively low sensitivity and are only approved for use in tissues other than those typically ingested by humans. In this study, we analyzed different processed meats derived from a pre-clinical, CWD-positive free-ranging elk. Products tested included filets, sausages, boneless steaks, burgers, ham steaks, seasoned chili meats, and spiced meats. CWD-prion presence in these products were assessed by PMCA using deer and elk substrates. Our results show positive prion detection in all products. To confirm the resilience of CWD-prions to traditional cooking methods, we grilled and boiled the meat products and evaluated them for any remnant PMCA seeding activity. Results confirmed the presence of CWD-prions in these meat products suggesting that infectious particles may still be available to people even after cooking. Our results strongly suggest ongoing human exposure to CWD-prions and raise significant concerns of zoonotic transmission through ingestion of CWD contaminated meat products.
***> Products tested included filets, sausages, boneless steaks, burgers, ham steaks, seasoned chili meats, and spiced meats.
***> CWD-prion presence in these products were assessed by PMCA using deer and elk substrates.
***> Our results show positive prion detection in all products.
***> Results confirmed the presence of CWD-prions in these meat products suggesting that infectious particles may still be available to people even after cooking.
***> Our results strongly suggest ongoing human exposure to CWD-prions and raise significant concerns of zoonotic transmission through ingestion of CWD contaminated meat products.
intcwdsympo.files.wordpress.com/2023/06/final-agenda-with-abstracts.pdf?force_download=true
Detection of chronic wasting disease prions in processed meats
Results: Our results show positive prion detection in all the samples analyzed using deer and elk substrates. Surprisingly, cooked meats displayed increased seeding activities. This data suggests that CWD-prions are available to people even after meats are processed and cooked.
Conclusions: These results suggest CWD prions are accessible to humans through meats, even after processing and cooking. Considering the fact that these samples were collected from already processed specimens, the availability of CWD prions to humans is probably underestimated.
"Our results show positive prion detection in all the samples analyzed using deer and elk substrates. Surprisingly, cooked meats displayed increased seeding activities."
web.archive.org/web/20231116212109/https://prion2023.org/wp-content/uploads/2023/10/Meeting-book-final-version2.pdf
www.researchgate.net/profile/Syed-Zahid-Shah/publication/378314391_Meeting-book-final-version_prion_2023/links/65d44dad28b7720cecdca95f/Meeting-book-final-version-prion-2023.pdf
Fortuitous generation of a zoonotic cervid prion strain
Aims: Whether CWD prions can infect humans remains unclear despite the very substantial scale and long history of human exposure of CWD in many states or provinces of USA and Canada. Multiple in vitro conversion experiments and in vivo animal studies indicate that the CWD-to-human transmission barrier is not unbreakable. A major long-term public health concern on CWD zoonosis is the emergence of highly zoonotic CWD strains. We aim to address the question of whether highly zoonotic CWD strains are possible.
Materials and Methods: We inoculated several sCJD brain samples into cervidized transgenic mice (Tg12), which were intended as negative controls for bioassays of brain tissues from sCJD cases who had potentially been exposed to CWD. Some of the Tg12mice became infected and their brain tissues were further examined by Western blot as well as serial passages in humanized or cervidized mice.
Results: Passage of sCJDMM1 in transgenic mice expressing elk PrP (Tg12) resulted in a “cervidized” CJD strain that we termed CJDElkPrP. We observed 100% transmission of the original CJDElkPrP in transgenic mice expressing human PrP. We passaged CJDElkPrP two more times in the Tg12mice. We found that such second and third passage CJDElkPrP prions retained 100% transmission rate in the humanized mice, despite that the natural elk CWD isolates and CJDElkPrP share the same elk PrP sequence. In contrast, we and others found zero or poor transmission of natural elk CWD isolates in humanized mice.
Conclusions: Our data indicate that highly zoonotic cervid prion strains are not only possible but also can retain zoonotic potential after serial passages in cervids, suggesting a very significant and serious long-term risk of CWD zoonosis given that the broad and continuing spread of CWD prions will provide fertile grounds for the emergence of zoonotic CWD strains over time.
prion2023.org/wp-content/uploads/2023/10/Meeting-book-final-version2.pdf
web.archive.org/web/20250828201533/https://prion2023.org/wp-content/uploads/2023/10/Meeting-book-final-version2.pdf
www.researchgate.net/profile/Syed-Zahid-Shah/publication/378314391_Meeting-book-final-version_prion_2023/links/65d44dad28b7720cecdca95f/Meeting-book-final-version-prion-2023.pdf
Transmission of cervid prions to humanized mice demonstrates the zoonotic potential of CWD
Samia Hannaoui1 · Irina Zemlyankina1 · Sheng Chun Chang1 · Maria Immaculata Arifn1 · Vincent Béringue2 · Debbie McKenzie3 · Hermann M. Schatzl1 · Sabine Gilch1
Received: 24 May 2022 / Revised: 5 August 2022 / Accepted: 7 August 2022
© The Author(s) 2022
Abstract
Prions cause infectious and fatal neurodegenerative diseases in mammals. Chronic wasting disease (CWD), a prion disease of cervids, spreads efficiently among wild and farmed animals. Potential transmission to humans of CWD is a growing concern due to its increasing prevalence. Here, we provide evidence for a zoonotic potential of CWD prions, and its probable signature using mice expressing human prion protein (PrP) as an infection model. Inoculation of these mice with deer CWD isolates resulted in atypical clinical manifestation with prion seeding activity and efficient transmissible infectivity in the brain and, remarkably, in feces, but without classical neuropathological or Western blot appearances of prion diseases. Intriguingly, the protease-resistant PrP in the brain resembled that found in a familial human prion disease and was transmissible upon second passage. Our results suggest that CWD might infect humans, although the transmission barrier is likely higher compared to zoonotic transmission of cattle prions. Notably, our data suggest a different clinical presentation, prion signature, and tissue tropism, which causes challenges for detection by current diagnostic assays. Furthermore, the presence of infectious prions in feces is concerning because if this occurs in humans, it is a source for human-to-human transmission. These findings have strong implications for public health and CWD management.
Keywords Chronic wasting disease · CWD · Zoonotic potential · Prion strains · Zoonotic prions
HIGHLIGHTS OF THIS STUDY
================================
Our results suggest that CWD might infect humans, although the transmission barrier is likely higher compared to zoonotic transmission of cattle prions. Notably, our data suggest a different clinical presentation, prion signature, and tissue tropism, which causes challenges for detection by current diagnostic assays. Furthermore, the presence of infectious prions in feces is concerning because if this occurs in humans, it is a source for human-to-human transmission. These findings have strong implications for public health and CWD management.
In this study, we evaluated the zoonotic potential of CWD using a transgenic mouse model overexpressing human M129-PrPC (tg650 [12]). We inoculated tg650mice intracerebrally with two deer CWD isolates, Wisc-1 and 116AG [22, 23, 27, 29]. We demonstrate that this transgenic line was susceptible to infection with CWD prions and displayed a distinct leading clinical sign, an atypical PrPSc signature and unusual fecal shedding of infectious prions. Importantly, these prions generated by the human PrP transgenic mice were transmissible upon passage. Our results are the first evidence of a zoonotic risk of CWD when using one of the most common CWD strains, Wisc-1/CWD1 for infection. We demonstrated in a human transgenic mouse model that the species barrier for transmission of CWD to humans is not absolute. The fact that its signature was not typical raises the questions whether CWD would manifest in humans as a subclinical infection, whether it would arise through direct or indirect transmission including an intermediate host, or a silent to uncovered human-to-human transmission, and whether current detection techniques will be suffcient to unveil its presence.
Our findings strongly suggest that CWD should be regarded as an actual public health risk. Here, we use humanized mice to show that CWD prions can cross the species barrier to humans, and remarkably, infectious prions can be excreted in feces.
Our results indicate that if CWD crosses the species-barrier to humans, it is unlikely to resemble the most common forms of human prion diseases with respect to clinical signs, tissue tropism and PrPSc signature. For instance, PrPSc in variable protease-sensitive prionopathy (VPSPr), a sporadic form of human prion disease, and in the genetic form Gerstmann-Sträussler-Scheinker syndrome (GSS) is defined by an atypical PK-resistant PrPSc fragment that is non-glycosylated and truncated at both C- and N-termini, with a molecular weight between 6 and 8 kDa [24, 44–46]. These biochemical features are unique and distinctive from PrPSc (PrP27-30) found in most other human or animal prion disease. The atypical PrPSc signature detected in brain homogenate of tg650 mice #321 (1st passage) and #3063 (2nd passage), and the 7–8 kDa fragment (Figs. 2, 4) are very similar to that of GSS, both in terms of migration profile and the N-terminal cleavage site.
CWD in humans might remain subclinical but with PrPSc deposits in the brain with an unusual morphology that does not resemble the patterns usually seen in different prion diseases (e.g., mouse #328; Fig. 3), clinical with untraceable abnormal PrP (e.g., mouse #327) but still transmissible and uncovered upon subsequent passage (e.g., mouse #3063; Fig. 4), or prions have other reservoirs than the usual ones, hence the presence of infectivity in feces (e.g., mouse #327) suggesting a potential for human-to-human transmission and a real iatrogenic risk that might be unrecognizable.
“suggesting a potential for human-to-human transmission and a real iatrogenic risk that might be unrecognizable.”
=================================
Supplementary Information The online version contains supplementary material available at
doi.org/10.1007/s00401-022-02482-9
snip...see full text;
link.springer.com/article/10.1007/s00401-022-02482-9
link.springer.com/content/pdf/10.1007/s00401-022-02482-9.pdf
Macaque tissues to rodent models demonstrates the zoonotic potential of chronic wasting disease.
Samia Hannaoui1,2, Ginny Cheng1,2, Wiebke Wemheuer3, Walter Schulz-Schaeffer3, Sabine Gilch1,2, Hermann Schatzl1,2 1University of Calgary, Calgary, Canada. 2Calgary Prion Research Unit, Calgary, Canada. 3Institute of Neuropathology, Medical Faculty, Saarland University, Homburg/Saar, Germany
Snip…
***> Further passage to cervidized mice revealed transmission with a 100% attack rate.
***> Our findings demonstrate that macaques, considered the best model for the zoonotic potential of prions, were infected upon CWD challenge, including the oral one.
****> The disease manifested as atypical in macaques and initial transgenic mouse transmissions, but with infectivity present at all times, as unveiled in the bank vole model with an unusual tissue tropism.
***> Epidemiologic surveillance of prion disease among cervid hunters and people likely to have consumed venison contaminated with chronic wasting disease
=====
intcwdsympo.files.wordpress.com/2023/06/final-agenda-with-abstracts.pdf?force_download=true
Transmission of Cervid Prions to Humanized Mice Demonstrates the Zoonotic Potential of CWD
Samia Hannaouia, Irina Zemlyankinaa, Sheng Chun Changa, Maria Immaculata Arifina, Vincent Béringueb, Debbie McKenziec, Hermann M. Schatzla, and Sabine Gilcha
Results: Here, we provide the strongest evidence supporting the zoonotic potential of CWD prions, and their possible phenotype in humans. Inoculation of mice expressing human PrPCwith deer CWD isolates (strains Wisc-1 and 116AG) resulted in atypical clinical manifestations in > 75% of the mice, with myoclonus as leading clinical sign. Most of tg650brain homogenates were positive for seeding activity in RT-QuIC. Clinical disease and presentation was transmissible to tg650mice and bank voles. Intriguingly, protease-resistant PrP in the brain of tg650 mice resembled that found in a familial human prion disease and was transmissible upon passage. Abnormal PrP aggregates upon infection with Wisc-1 were detectable in thalamus, hypothalamus, and midbrain/pons regions.
Unprecedented in human prion disease, feces of CWD-inoculated tg650 mice harbored prion seeding activity and infectious prions, as shown by inoculation of bank voles and tg650 with fecal homogenates.
Conclusions: This is the first evidence that CWD can infect humans and cause disease with a distinctive clinical presentation, signature, and tropism, which might be transmissible between humans while current diagnostic assays might fail to detect it. These findings have major implications for public health and CWD-management.
www.tandfonline.com/doi/full/10.1080/19336896.2022.2091286
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
www.tandfonline.com/doi/full/10.1080/19336896.2024.2424058
“ After adaptation in this host, moose CWD prions were able to transmit in mice expressing either bovine or human PrPC with high efficacy.”
While no one was watching: Tenuous status of CDC prion unit, risk of CWD to people worry scientists
Mary Van Beusekom, MS Today at 9:15 a.m.
Chronic Wasting Disease BSE CWD zone deer disposal site Lorie Shaull / Flickr cc
Nine months ago, Janie Johnston, 73, left her home in the Chicago suburbs to drive to her doctor's office for routine care. She made it as far as the side of the street opposite the clinic but couldn't figure out how to get there, so she returned home, where she struggled to remember the abbreviation "GPS."
That was the first sign that something was seriously wrong. Soon, the semi-retired geologist couldn't speak in full sentences or feed herself. Within 2 months, the woman who had been reviewing proposals for the National Science Foundation in the weeks leading up to symptom onset was dead of a terrifying neurological disease her family had never heard of: Creutzfeldt-Jakob disease (CJD).
CWD may cause CJD-like disease if it infects people Rather than being genetic or acquired, Johnston's CJD developed when normal prions in her brain spontaneously began misfolding. The abnormal prions accumulated rather than being shed, triggering confusion and fatigue that doctors initially mistook for stroke, meningitis, or alcohol withdrawal. The disease usually occurs in older adults.
Seeing what my mom went through, I do not want anyone else to have to experience that, nor their family members. Kristal Enter
While no one is certain, experts think that another always-fatal prion disease—this one currently known to occur only in cervids such as deer, moose, and elk—may behave the same way if it should jump the species barrier and infect people.
Chronic wasting disease (CWD) has been decimating cervid populations throughout North America since it was first diagnosed in a captive Colorado mule deer in 1967. While mitigation measures such as hunting may help slow its spread, it can't be stopped.
This is because cervids are ubiquitous and free ranging, the interval from infection to symptom onset can take years, and prions spread easily from animal to animal and through environmental contamination, which can persist for years.
Johnston's daughter, Kristal Enter, 39, a fundraiser in Boston, is familiar with CWD and its potential implications for human health. "Seeing what my mom went through, I do not want anyone else to have to experience that, nor their family members," she told CIDRAP News. "The more we're on top of chronic wasting disease and thinking about it, the better."
But the frightening thing is that, for well over a month during the recent US government shutdown, no one was watching the human disease landscape for CWD, a highly infectious disease with no treatment or cure.
If cases slip by, it will be too late Nine days after the government shutdown began, all four staff members of the Centers for Disease Control and Prevention's (CDC's) National Center for Emerging and Zoonotic Infectious Diseases Prion and Public Health Office were sent home after receiving reduction-in-force (RIF) notices. While the end of the shutdown led all four to be reinstated through at least January, layoffs after that time are possible.
Within the past few months, two other researchers who had been part of the team also had to be let go after their fellowship contracts weren't renewed, per the administration's policy of blocking contract renewals.
The prion unit, which monitors the nation for human prion diseases, is part of the Division of High-Consequence Pathogens and Pathology. It launched in the mid-1990s in response to the outbreak of bovine spongiform encephalopathy (BSE, or "mad cow disease") in UK cattle. BSE prions were inadvertently consumed by people who ate contaminated beef, causing the human form of BSE, variant CJD (vCJD). All infected people—more than 230—died.
The initial goal of the Prion and Public Health Office was to watch for any cases of vCJD in the US population. Since then, its focus has expanded to include advising hospitals on how to prevent and respond to prion contamination of instruments used in neurosurgery (prions are resistant to many usual sterilization methods), as well as working with state health departments on disease surveillance. Unit members also answer questions from the public.
Today, as CWD continues its inexorable march across the landscape, exposing more and more people, the prion unit's priority is conducting surveillance for signs of a CWD species jump into high-risk people such as hunters. Without this expertise, no one will be able to evaluate whether a suspected case of CWD prion transmission to humans is likely from an animal.
The prion unit has launched several epidemiologic studies in collaboration with multiple states to look at whether more hunters are dying of prion diseases than would be expected.
Janie Johnston Janie Johnston / Courtesy of Kristal Enter As an example of the unit's work, last spring, a cluster of CJD cases in Oregon was widely conjectured to be linked to CWD. Such cases require autopsy and an epidemiologic investigation to determine whether CWD was involved and, if so, what kind of public health measures are needed. The prion unit shared ideas and strategy with the Oregon state health department in this investigation, which, thankfully, found no link.
But experts say that without anyone looking for these deviations from normal—particularly given that signs of illness may take years to appear—cases could easily go unnoticed, and it will be too late to implement public health measures that could mitigate some of these consequences.
Lawrence Schonberger, MD, MPH, retired chief of the Prion and Public Health Office, said that, as was the situation with BSE, CWD containment efforts must continue. "Unlike with mad cow disease, however, these efforts to date have not been successful," he said. Surveillance and research "should continue to help people recognize any emerging risk to humans from this agent now and in the future, when this agent's pathogenicity [ability to cause disease] may change."
'Worst time to get rid of such a division' Brian Appleby, MD, is director of the National Prion Disease Pathology Surveillance Center at Case Western University, which conducts diagnostic testing for human prion diseases and conducted Johnston's autopsy. The CDC funds the center, which collaborates with the Prion and Public Health Office on public health efforts and research projects.
When you don't have a neutral party investigating these things or doing neuropathology to confirm or refute those things, you really have no idea what's going on in the public health space. Brian Appleby, MD
If the CDC prion unit were eliminated, "no one would be looking at prion disease," Appleby said. "We wouldn't be able to tell if we have an increase in cases or where they're going or coming from. And when you don't have a neutral party investigating these things or doing neuropathology to confirm or refute those things, you really have no idea what's going on in the public health space."
And with the threat of CWD, "this is probably the worst time to get rid of such a division," he added.
While there have been no stated plans to eliminate the unit, history hints that its continued existence may be in jeopardy. In fact, it was removed from President Donald Trump's budget during both of his administrations, before the House of Representatives and Senate reinstated it, Appleby said.
In the first Trump administration, report language stated that human prion surveillance is redundant because cattle are now screened for BSE, and the National Institutes of Health cover research, said Appleby, who refuted the assertions.
"Part of the reason why we are a safe export country for beef is not just the cattle surveillance for BSE, but the human surveillance for variant CJD," he said, adding that monitoring is a separate function from research. "When we were removed from the president's budget this time around, there was no report language, so we have no signal to know why."
Always 'one step behind' Debbie Yobs, president and executive director of the CJD Foundation, a patient-advocacy organization that works with Appleby's center to provide medical lectures, support groups, and other programs, emphasized the importance of sustained surveillance. "You can't have gaps in monitoring a deadly disease like prion disease," she said.
It's like combining symptoms of Alzheimer's, Parkinson's, and ALS [amyotrophic lateral sclerosis, or Lou Gehrig's disease] and then speeding it all up. Debbie Yobs
CJD is devastating for patients and families, said Yobs, whose husband, Patrick, died at age 45 of the less common, genetic form of the disease. "It's like combining symptoms of Alzheimer's, Parkinson's, and ALS [amyotrophic lateral sclerosis, or Lou Gehrig's disease] and then speeding it all up," she added. "There's no definitive diagnosis except through autopsy."
Indeed, Enter called her family's ordeal "unreal," because although Johnston's case was typical of a sporadic case, CJD affects only about 500 to 600 people in the United States each year, per the CDC. At the same time as the family was grieving, they were trying to learn how hospice staff could best manage Johnston's symptoms, which none of them had dealt with before.
"It becomes incumbent upon the family members to become the experts to guide the care," she said. "What they say about CJD is that every day is another new symptom or new complication to have to try to address. And you always feel like you're one step behind."
www.cidrap.umn.edu/chronic-wasting-disease/while-no-one-was-watching-tenuous-status-cdc-prion-unit-risk-cwd-people
“While no one was watching: Tenuous status of CDC prion unit, risk of CWD to people worry scientists”
FRIDAY, NOVEMBER 21, 2025
While no one was watching: Tenuous status of CDC prion unit, risk of CWD to people worry scientists
chronic-wasting-disease.blogspot.com/2025/11/while-no-one-was-watching-tenuous.html
2004
Jeff Swann and his Mom, cwd link... sporadic CJD?, CBC NEWS Jeff Schwan sCJD, CWD, and Professor Aguzzi on BSE and sporadic CJD
?: CBCnewshistodb15.usz.ch/pages/Images/videos/video-004/video-004.html
2004
April 22, 2004, 10:30 AM CDT Guests: Patrick Singh, Terry Schwan, Janet Skarbek, Bill Fielding (BEGIN VIDEOTAPE) ANNOUNCER: DEBORAH NORVILLE TONIGHT.
www.nbcnews.com/id/wbna4806886
1997-11-10: Panorama - The British disease
histodb15.usz.ch/pages/Images/videos/video-009/video-009.html
Two Hunters from the Same Lodge Afflicted with Sporadic CJD: Is Chronic Wasting Disease to Blame?
(P7-13.002) Jonathan Trout, Matthew Roberts, Michel Tabet, Eithan Kotkowski, and Sarah HornAUTHORS INFO & AFFILIATIONS April 9, 2024 issue 102 (17_supplement_1) 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.
www.neurology.org/doi/abs/10.1212/WNL.0000000000204407
TUESDAY, MAY 11, 2021
A Unique Presentation of Creutzfeldt-Jakob Disease in a Patient Consuming Deer Antler Velvet <
Conclusion
We believe that our patient’s case of CJD is highly suspicious for cervid etiology given the circumstances of the case as well as the strong evidence of plausibility reported in published literature. This is the first known case of CJD in a patient who had consumed deer antler velvet. Despite the confirmed diagnosis of CJD, a causal relationship between the patient’s disease and his consumption of deer antler velvet cannot be definitively concluded.
Supplemental data including molecular tissue sample analysis and autopsy findings could yield further supporting evidence. Given this patient’s clinical resemblance to CBD and the known histological similarities of CBD with CJD, clinicians should consider both diseases in the differential diagnosis of patients with a similarly esoteric presentation. Regardless of the origin of this patient’s disease, it is clear that the potential for prion transmission from cervids to humans should be further investigated by the academic community with considerable urgency.
thescipub.com/pdf/ajidsp.2021.43.48.pdf
''We believe that our patient’s case of CJD is highly suspicious for cervid etiology given the circumstances of the case as well as the strong evidence of plausibility reported in published literature. This is the first known case of CJD in a patient who had consumed deer antler velvet. Despite the confirmed diagnosis of CJD, a causal relationship between the patient’s disease and his consumption of deer antler velvet cannot be definitively concluded.''
thescipub.com/pdf/ajidsp.2021.43.48.pdf
CREUTZFELDT JAKOB DISEASE: A Unique Presentation of Creutzfeldt-Jakob Disease in a Patient Consuming Deer Antler Velvet
i was warning England and the BSE Inquiry about just this, way back in 1998, and was ask to supply information to the BSE Inquiry. for anyone that might be interested, see;
Singeltary submission to the BSE Inquiry on CJD and Nutritional Supplements 1998
ABOUT that deer antler spray and CWD TSE PRION... I have been screaming this since my neighbors mom died from cjd, and she had been taking a supplement that contained bovine brain, bovine eyeball, and other SRMs specified risk materials, the most high risk for mad cow disease. just saying...
I made a submission to the BSE Inquiry long ago during the BSE Inquiry days, and they seemed pretty interested.
Sender: "Patricia Cantos"
To: "Terry S Singeltary Sr. (E-mail)"
Subject: Your submission to the Inquiry
Date: Fri, 3 Jul 1998 10:10:05 +0100 3 July 1998
Mr Terry S Singeltary Sr. E-Mail: Flounder at wt.netRef: E2979
Dear Mr Singeltary, Thank you for your E-mail message of the 30th of June 1998 providing the Inquiry with your further comments. Thank you for offering to provide the Inquiry with any test results on the nutritional supplements your mother was taking before she died. As requested I am sending you our general Information Pack and a copy of the Chairman's letter. Please contact me if your system cannot read the attachments. Regarding your question, the Inquiry is looking into many aspects of the scientific evidence on BSE and nvCJD.
I would refer you to the transcripts of evidence we have already heard which are found on our internet site at ;
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
creutzfeldt-jakob-disease.blogspot.com/2021/05/a-unique-presentation-of-creutzfeldt.html
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.
efsa.onlinelibrary.wiley.com/doi/full/10.2903/j.efsa.2018.5132
SATURDAY, FEBRUARY 23, 2019
Chronic Wasting Disease CWD TSE Prion and THE FEAST 2003 CDC an updated review of the science 2019
chronic-wasting-disease.blogspot.com/2019/02/chronic-wasting-disease-cwd-tse-prion.html
TUESDAY, NOVEMBER 04, 2014
Six-year follow-up of a point-source exposure to CWD contaminated venison in an Upstate New York community: risk behaviours and health outcomes 2005–2011 Authors, though, acknowledged the study was limited in geography and sample size and so it couldn't draw a conclusion about the risk to humans. They recommended more study. Dr. Ermias Belay was the report's principal author but he said New York and Oneida County officials are following the proper course by not launching a study. "There's really nothing to monitor presently. No one's sick," Belay said, noting the disease's incubation period in deer and elk is measured in years. "
chronic-wasting-disease.blogspot.com/2014/11/six-year-follow-up-of-point-source.html
Transmission Studies Mule deer transmissions of CWD were by intracerebral inoculation and compared with natural cases {the following was written but with a single line marked through it ''first passage (by this route)}....TSS resulted in a more rapidly progressive clinical disease with repeated episodes of synocopy ending in coma. One control animal became affected, it is believed through contamination of inoculum (?saline). Further CWD transmissions were carried out by Dick Marsh into ferret, mink and squirrel monkey. Transmission occurred in ALL of these species with the shortest incubation period in the ferret.
snip....
web.archive.org/web/20090506002237/http://www..bseinquiry.gov.uk/files/mb/m11b/tab01.pdf
Docket No. FDA-2003-D-0432 (formerly 03D-0186) Use of Material from Deer and Elk in Animal Feed
PUBLIC SUBMISSION Comment from Terry Singeltary Sr.
Posted by the Food and Drug Administration on May 17, 2016
Comment Docket No. FDA-2003-D-0432 (formerly 03D-0186) Use of Material from Deer and Elk in Animal Feed Singeltary Submission
www.regulations.gov/comment/FDA-2003-D-0432-0011
www.regulations.gov/docket/FDA-2003-D-0432
Control of Chronic Wasting Disease OMB Control Number: 0579-0189APHIS-2021-0004 Singeltary Submission
www.regulations.gov/comment/APHIS-2021-0004-0002
downloads.regulations.gov/APHIS-2021-0004-0002/attachment_1.pdf
Docket No. APHIS-2018-0011 Chronic Wasting Disease Herd Certification
www.regulations.gov/document/APHIS-2018-0011-0003
downloads.regulations.gov/APHIS-2018-0011-0003/attachment_1.pdf
APHIS Indemnity Regulations [Docket No. APHIS-2021-0010] RIN 0579-AE65 Singeltary Comment Submission
Comment from Singeltary Sr., Terry
Posted by the Animal and Plant Health Inspection Service on Sep 8, 2022
www.regulations.gov/comment/APHIS-2021-0010-0003
downloads.regulations.gov/APHIS-2021-0010-0003/attachment_1.pdf
MONDAY, SEPTEMBER 15, 2025
Chronic Wasting Disease CWD TSE Prion Environmental Factors Update
chronic-wasting-disease.blogspot.com/2025/09/chronic-wasting-disease-cwd-tse-prion.html
https://prpsc.proboards.com/thread/180/chronic-wasting-disease-environmental-factors
SUNDAY, MARCH 20, 2022
CHRONIC WASTING DISEASE CASES CWD STATUS OF CAPTIVE HERDS AS OF February 2022
chronic-wasting-disease.blogspot.com/2022/03/chronic-wasting-disease-cases-cwd.html
THURSDAY, APRIL 24, 2025
US Captive CWD Positive Herds Update April 2025
chronic-wasting-disease.blogspot.com/2025/04/us-captive-cwd-positive-herds-update.html
chronic wasting disease cwd TSE Prion, deer don’t die from cwd, show me a picture of a prion, it’s a conspiracy, the insurance companies, money grab you say, blah, blah, blah,…science, research, especially long term research on TSE Prion disease, and housing large animals, for long periods of time, all cost money,…cwd, money grab you say, folks be like the DNR et al are all about money for nothing and the chicks are for free, where does the money go? besides research, Indemnity, year after year after year, paying out deer farmers for cwd herds…
2026 USDA EXPLANATORY NOTES, APHIS, CWD, BSE, Scrapie, TSE, Prion
transmissiblespongiformencephalopathy.blogspot.com/2025/12/2026-usda-explanatory-notes-aphis-cwd.html
Captive Cervid and the Economic Burden of Chronic Wasting Disease CWD TSE Prion?
chronic-wasting-disease.blogspot.com/2025/10/captive-cervid-and-economic-burden-of.html
prpsc.proboards.com/thread/183/captive-cervid-economic-burden-prion
The economic costs of chronic wasting disease in the United States
The study found that the federal government spent over $280 million on chronic wasting disease over the 21-year period from 2000-2021. Most of that spending was under the U.S. Department of Agriculture’s Animal and Plant Health Inspection Service, which included over $16 million in indemnity payments to cervid farmers.
New USGS Study Offers Roadmap to the Economics of Chronic Wasting Disease | U.S. Geological Survey usgs.gov favicon.ico
The economic costs of chronic wasting disease in the United States December 8, 2022
www.usgs.gov/publications/economic-costs-chronic-wasting-disease-united-states
chronic-wasting-disease.blogspot.com/2023/01/the-economic-costs-of-chronic-wasting.html
i have followed the science of all the Transmissible Spongiform Encephalopathy TSE Prion disease, in all species, even the camel, every day, for 28 years, trying to help warn others, and stop the spread. I’ve seen it, it’s a nasty way to die. my Mom died from confirmed Heidenhain Variant Creutzfeldt Jakob Disease hvCJD. So Cry me a river, about breeders captive cervid industry, raising Cervid to be released, to be killed and slaughtered, in a pen, that have CWD or exposed to CWD (some of which have ignored CWD regulations), Come back and talk to me after you have signed on the dotted line for them to cut your Mothers…daughters, wife, brain cut out her head, to ship to Washington, so Scientists can study this Transmissible Spongiform Encephalopathy TSE Prion disease, which is all Chronic Wasting Disease CWD is, to try and save lives, lives like like yourself, folks that don’t believe, your children, your family, some of which still refuse to see the forest, because of the trees, or because of the bottom dollar. If you don’t think CWD is capable of jumping to other species, including humans, if it has not already, then you got another thing coming, and it’s coming, and friendly fire or pass it forward, iatrogenic, that’s just part of it, In fact science shows it’s already happened in some cases (I’ll spare you that drama). But Back in 97, when Mom was dying from this transmissible spongiform encephalopathy, which is all CWD is, she did everything Linda Blair did in the movie, The Exorcist, except spin her head 360 degrees. She did levitate in bed jerking so bad, it took three grown adults to hold her down, all the while she was screaming WHY CANT I STOP THIS? you never forget. just made a promise to Mom, don’t let them forget, you got to stop it…terry
Washington Times - Washington,DC, USA NIH may destroy human brain collection By Steve Mitchell Medical Correspondent Washington, DC, Mar. 24 (UPI)
www.upi.com/Science_News/2005/03/24/NIH-may-destroy-human-brain-collection/84811111671758/
NIH sends mixed signals on CJD brains By Steve Mitchell Medical Correspondent
www.upi.com/Science_News/2005/04/07/NIH-sends-mixed-signals-on-CJD-brains/25701112902231/
JOHN CORNYN TEXAS UNITED STATES SENATE WASHINGTON, DC 20510-4305 May 18,2005 Mr. Terry Singeltary,… Bacliff, Texas 77518
Dear Mr. Singeltary:
Enclosed is the reply I received from the Department of Health and Human Services in response to my earlier inquiry on your behalf. I hope this will be useful to you. I appreciate having the opportunity to represent you in the United States Senate.
Thank you for taking time to contact me.
Sincerely,
JOHN CORNYN United States Senate JC:djl Enclosure
DEPARTMENT OF HEALTH & HUMAN SERVICES National Institutes of HealthNational Institute of Neurological Disorders and Stroke NINDS Building 31, Room 8A52
May 10, 2005
The Honorable John Cornyn United States Senator Occidental Tower
Dear Senator Cornyn:
Your letter to the National Institutes of Health (NIH) forwarding correspondence from Mr. Terry S. Singeltary, Sr., has been forwarded to me for reply. Mr. Singeltary is concerned about the preservation of Creutzfeldt-Jakob disease (CJD) brain samples that have been maintained by the National Institute of Neurological Disorders and Stroke (NINDS) Intramural Research program for many years.
I am sorry to learn that Mr. Singeltary's mother died of CJD and can certainly understand his desire that any tissues that could help investigators unravel the puzzle of this deadly disease are preserved. I hope he will be pleased to learn that all the brains and other tissues with potential to help scientists learn about CJD are, and will continue to be, conserved. (The tissues that are discarded are those that have either decayed to an extent that renders them no longer appropriate for research or those for which we do not have sufficient identification.)
The purpose of gathering these brains and tissues is to help scientists learn about CJD. To that end, some of the NINDS-held samples are distributed to investigators who can demonstrate that they have a compelling research or public health need for such materials. For example, samples have been transferred to NIH grantee Dr. Pierluigi Gambetti, who heads the National Prion Diseases Pathology Surveillance Center at Case Western Reserve University in Ohio and works with the Centers for Disease Control and Prevention to monitor all cases of CJD in the United States. Dr. Gambetti studies the tissues to learn about the formation, physical and chemical properties, and pathogenic mechanisms of prion proteins, which are believed to be involved in the cause of CJD. Samples have also been transferred to Dr. David Asher, at the U.S. Food and Drug Administration, for use in assessing a potential diagnostic test for CJD.
Page 2 - The Honorable John Cornyn
in closing, we know that donating organs and tissue from loved ones is a very difficult and personal choice that must often be made at the most stressful of times. We at the NINDS are grateful to those stalwart family members who make this choice in the selfless hope that it will help others afflicted with CJD. We also know the invaluable contribution such donations make to the advancement of medical science, and we are dedicated to the preservation of all of the tissue samples that can help in our efforts to overcome CJD.
I hope this information is helpful to you in responding to Mr. Singeltary.
Sincerely,
Story C. Landis, Ph.D. Director, National Institute of Neurological Disorder and Stroke
NIH says it will preserve CJD brains
By STEVE MITCHELL MAY 31, 2005 / 5:26 PM
www.upi.com/Science_News/2005/05/31/NIH-says-it-will-preserve-CJD-brains/67711117574761/
2001 Singeltary on CJD, Journal of American Medical Association
February 14, 2001
Diagnosis and Reporting of Creutzfeldt-Jakob Disease
Terry S. Singeltary, Sr
Author Affiliations
JAMA. 2001;285(6):733-734. doi:10-1001/pubs.JAMA-ISSN-0098-7484-285-6-jlt0214
To the Editor: In their Research Letter, Dr Gibbons and colleagues1 reported that the annual US death rate due to Creutzfeldt-Jakob disease (CJD) has been stable since 1985. These estimates, however, are based only on reported cases, and do not include misdiagnosed or preclinical cases. It seems to me that misdiagnosis alone would drastically change these figures. An unknown number of persons with a diagnosis of Alzheimer disease in fact may have CJD, although only a small number of these patients receive the postmortem examination necessary to make this diagnosis. Furthermore, only a few states have made CJD reportable. Human and animal transmissible spongiform encephalopathies should be reportable nationwide and internationally.
February 14, 2001
Diagnosis and Reporting of Creutzfeldt-Jakob Disease
Terry S. Singeltary, Sr
Author Affiliations
JAMA. 2001;285(6):733-734. doi:10-1001/pubs.JAMA-ISSN-0098-7484-285-6-jlt0214
jamanetwork.com/journals/jama/article-abstract/1031186
2023
creutzfeldt-jakob-disease.blogspot.com/2023/09/professor-john-collinge-on-tackling.html
FRIDAY, NOVEMBER 21, 2025
While no one was watching: Tenuous status of CDC prion unit, risk of CWD to people worry scientists
chronic-wasting-disease.blogspot.com/2025/11/while-no-one-was-watching-tenuous.html
kindest regards, terry
APHIS USDA Captive CWD Herds Update by State December 2025 Update
CHRONIC WASTING DISEASE CASES
Date of Index Case Confirmation Index Case State County Species Herd Type HCP Enrolled HCP Certified Number of Animals Herd Status
11/1/2025 ukn TX Limestone WTD Hunt No No 132 Quarantine
10/27/2025 3 YR Make WI Richland WTD Breeder Yes Yes ukn Quarantine
10/9/2025 2 YR Female TX Duvall WTD Breeder No No 94+ Quarantine
10/9/2025 2 YR Male PA Franklin WTD Breeder No No 23 Quarantine
10/8/2025 3.5 YR Male PA Huntingdon WTD Hobby No No 2 Quarantine
10/8/2025 3 YR Male WI Portage WTD Fallow Hunt No No 132 Quarantine
9/26/2025 8.5 YR Female TX Navaro WTD Breeder No No 650 Quarantine
9/16/2025 3 YR Female PA Dauphin WTD Breeder Yes Yes 85 Quarantine
9/5/2025 3 YR Male TX Duvall WTD Breeder No No 107+ Quarantine
8/6/2025 Adult Female PA Fulton WTD Breeder No No 14 Quarantine
7/21/2025 4 YR Female PA Bedford WTD Breeder No No 34 Quarantine
Updated December 2025 CHRONIC WASTING DISEASE CASES
6/3/2025 11 YR Female PA Blair WTD Breeder No No 45 Quarantine
6/3/2025 8 YR Female PA Bedford WTD Breeder No No 6 Quarantine
5/16/2025 5.5 YR Female WI Rock WTD Breeder No No ~46 Quarantine
5/14/2025 3 YR Female UT Weber Elk Hunt No No ukn Quarantine
4/30/2025 4.5 YR Male PA Jefferson WTD Hunt No No 36 Depopulated
4/18/2025 10+ YR Ukn TX Zavala WTD Hunt No No 190 Quarantine
4/9/2025 6 YR Male MI Montcalm WTD Breeder No No 86 Quarantine
3/28/2025 3.5 YR Male PA Huntingdon WTD Hobby No No 2 Quarantine
3/28/2025 3.5 YR Female PA Wayne Red Deer Hunt No no 31 Depopulated
2/26/2025 1.5 YR Male TX Kauffman WTD Breeder Yes Yes 400 Quarantine
2/26/2025 3.5 Yr Male PA Lancaster WTD Breeder Yes Yes 105 Quarantine
2/21/2025 4 YR Male CO Montrose Elk Hunt No No 97 Quarantine
Updated December 2025 CHRONIC WASTING DISEASE CASES
2/21/2025 7 YR Female MI Osceola WTD Hunt No No 201 Quarantine
2/10/2025 3.5 YR Male PA Perry WTD Hunt No No 15 Quarantine
1/7/2025 4 YR Female CO Mesa Elk Hunt No No 217 Quarantine
1/7/2025 2 YR Male UT Duchesne Elk Hunt No No 0 No animals
snip…see more;
www.aphis.usda.gov/sites/default/files/status-of-captive-herds.pdf
Remember, a quarantined captive CWD Herd, is a ticking environmental time bomb just waiting to go off, think Chernobyl, the longer held in quarantine, the greater chance of environmental spread of CWD. litigation of CWD can take what seems to be an eternity, and CWD TSE Prion saturation into the environment grows each day left in quarantine. …terry
APHIS USDA Captive CWD Herds Update by State December 2025 Update
chronic-wasting-disease.blogspot.com/2025/12/aphis-usda-captive-cwd-herds-update-by.html
prpsc.proboards.com/thread/187/aphis-captive-herds-update-december
Terry S. Singeltary Sr.
posted by Terry S. Singeltary Sr. at
4:07 PM
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