Texas Chronic Wasting Disease CWD TSE Prion Dashboard Update August 2025
Texas Chronic Wasting Disease CWD TSE Prion Dashboard Update August 2025
WEDNESDAY, MAY 14, 2025
Texas CWD TSE Prion Cases Rises to 1099 Confirmed Cases To Date
Entries CWD Positives
Positive Number CWD Positive Confirmation Date Free Range Captive County Source Species Sex Age
Positive Number CWD Positive Confirmation Date Free Range Captive County Source Species Sex Age
1099 5/5/25 Breeder Deer Gillespie Facility #14 White-tailed Deer M 4.9
1098 4/24/25 Breeder Deer Zavala Facility #23 White-tailed Deer F 7.8
1097 4/24/25 Breeder Deer Zavala Facility #23 White-tailed Deer F 7.8
1096 4/17/25 Breeder Release Site Zavala N/A White-tailed Deer M 10.5
1095 4/3/25 Breeder Deer Kimble Facility #26 White-tailed Deer F 2.5
1094 4/3/25 Breeder Deer Kimble Facility #26 White-tailed Deer F 6.5
1093 4/3/25 Breeder Deer Kimble Facility #26 White-tailed Deer F 3.5
1092 4/3/25 Breeder Deer Frio Facility #24 White-tailed Deer F 1.7
1091 4/3/25 Breeder Deer Frio Facility #24 White-tailed Deer F 1.7
1090 4/3/25 Breeder Deer Frio Facility #24 White-tailed Deer F 3.7
1089 4/3/25 Breeder Deer Frio Facility #24 White-tailed Deer F 5.7
1088 4/3/25 Breeder Deer Frio Facility #24 White-tailed Deer F 5.7
1087 4/3/25 Breeder Deer Frio Facility #24 White-tailed Deer F 7.7
1086 4/3/25 Breeder Deer Frio Facility #24 White-tailed Deer F 3.7
1085 4/3/25 Breeder Deer Frio Facility #24 White-tailed Deer F 3.7
1084 3/19/25 Free Range El Paso N/A Mule Deer M 6.5
1083 3/14/25 Breeder Deer Frio Facility #24 White-tailed Deer M 1.7
1082 2/27/25 Breeder Deer Kaufman Facility #36 White-tailed Deer F 0.5
1081 2/27/25 Breeder Deer Kaufman Facility #36 White-tailed Deer M 1.5
1080 2/21/25 Breeder Deer Gillespie Facility #15 White-tailed Deer M 2.5
1079 2/19/25 Breeder Deer Frio Facility #24 White-tailed Deer M 1.4
1078 2/13/25 Breeder Release Site Medina Facility #3 Elk F 4
1077 1/14/25 Breeder Deer Frio Facility #24 White-tailed Deer F 2.5
1076 1/14/25 Breeder Deer Frio Facility #24 White-tailed Deer M 1.5
1075 1/14/25 Breeder Deer Frio Facility #24 White-tailed Deer M 1.5
1074 1/24/25 Breeder Deer Zavala Facility #23 White-tailed Deer F 1.5
1073 1/24/25 Breeder Deer Zavala Facility #23 White-tailed Deer F 4.5
1072 1/24/25 Breeder Deer Zavala Facility #23 White-tailed Deer M 2.5
1071 1/24/25 Breeder Deer Zavala Facility #23 White-tailed Deer M 2.5
1070 1/24/25 Breeder Deer Zavala Facility #23 White-tailed Deer M 3.5
1069 2/4/25 Breeder Release Site Brown N/A White-tailed Deer F 2.6
1068 1/23/25 Breeder Release Site Sutton N/A White-tailed Deer M 6.5
1067 1/23/25 Breeder Release Site Medina Facility #3 White-tailed
Snip…see full list of CWD Positives;
WEDNESDAY, MAY 14, 2025
Texas CWD TSE Prion Cases Rises to 1099 Confirmed Cases To Date
December 2024
***> TEXAS CWD TSE PRION POSITIVE SAMPLES BY CALENDAR YEAR JANUARY 1 TO DECEMBER 31 2024 TOTAL TO DATE 1061 CASES CONFIRMED
Texas CWD total by calendar years
May 2024
Texas TAHC TPWD Confirm 132 More Cases of CWD TSE PrP
Jumps from 663 in March, to 795 Positive In May 2024, wow!
TPWD CWD Tracking
Counties where CWD Exposed Deer were Released
Number of CWD Exposed Deer Released by County
TRUCKING CWD
“CWD spreads among wild populations at a relatively slow rate, limited by the natural home range and dispersed nature of wild animals.”
NOW HOLD YOUR HORSES, Chronic Wasting Disease CWD of Cervid can spread rather swiftly, traveling around 50 MPH, from the back of truck and trailer, and Here in Texas, we call it ‘Trucking CWD’…
Preventive Veterinary Medicine Volume 234, January 2025, 106385
Use of biosecurity practices to prevent chronic wasting disease in Minnesota cervid herds
Vehicles or trailers that entered the farm were used to transport other live cervids, cervid carcasses, or cervid body parts in past 3 years in 64.3 % (95 % CI 46.3–82.3) of larger elk/reindeer herds compared to 13.6 % (95 % CI 4.7–22.4) of smaller deer herds.
Snip…
Identifying the exact pathway of initial CWD transmission to cervid herds is often not possible, in part due to many potential pathways of transmission for the infection, including both direct and indirect contact with infected farmed or wild cervids (Kincheloe et al., 2021). That study identified that transmissions from infected farmed cervids may occur from direct contact with the movement of cervids from one herd to another and from indirect contact with the sharing of equipment, vehicles, clothing, reproductive equipment, and potentially through semen or embryos.
***> Department records indicate that within the last five years (since January 1, 2020), 30 deer breeding facilities where CWD has been confirmed transferred a total of 8,799 deer to 249 additional deer breeding facilities and 487 release sites located in a total of 144 counties in Texas. <***
Texas Kimble County Farm Chronic Wasting Disease CWD TSE Prion Approximate Herd Prevalence 12%
SUMMARY MINUTES OF THE 407th COMMISSION MEETING Texas Animal Health Commission
September 22, 2020
Chronic Wasting Disease (CWD):
A new CWD positive breeding herd was disclosed in February 2020 in Kimble County. This herd depopulation was completed in July 2020. Including the two index positive deer, an additional eight more positive deer were disclosed (approximate herd prevalence 12%). Since July 2015 and prior to this discovery, five positive captive breeder herds have been disclosed and four of those are in Medina County. One herd in Lavaca and three herds in Medina County were depopulated leaving one large herd in Medina County that is managed on a herd plan. A new zone was established in Val Verde County in December 2019 as a result of a positive free-ranging White-tailed Deer (WTD). A second positive WTD was also disclosed in February 2020 in the same area.
SUMMARY MINUTES OF THE 407th COMMISSION MEETING – 9/22/2020
Scrapie: The flock identified in April 2016 remains under quarantine in Hartley County.
https://www.tahc.texas.gov/agency/meetings/minutes/SummaryMinutes_CommMtg_2020-09-22
Chronic Wasting Disease in Texas A Real Disease with Proven Impacts
Produced by a coalition of concerned hunters, landowners, & conservationists (last update 1/2025)
Aug 18, 2021
Oh, Deer
Heading Off a Wildlife Epidemic
CWD poses a significant threat to the future of hunting in Texas. Deer population declines of 45 and 50 percent have been documented in Colorado and Wyoming. A broad infection of Texas deer populations resulting in similar population impacts would inflict severe economic damage to rural communities and could negatively impact land markets. Specifically, those landowners seeking to establish a thriving herd of deer could avoid buying in areas with confirmed CWD infections. As they do with anthrax-susceptible properties, land brokers may find it advisable to inquire about the status of CWD infections on properties that they present for sale. Prospective buyers should also investigate the status of the wildlife on prospective properties. In addition, existing landowners should monitor developments as TPWD crafts management strategies to identify and contain this deadly disease.
Dr. Gilliland (c-gilliland@tamu.edu) is a research economist with the Texas Real Estate Research Center at Texas A&M University.
TEXAS BREEDER DEER ESCAPEE WITH CWD IN THE WILD, or so the genetics would show?
OH NO, please tell me i heard this wrong, a potential Texas captive escapee with cwd in the wild, in an area with positive captive cwd herd?
apparently, no ID though. tell me it ain't so please...
23:00 minute mark
''Free Ranging Deer, Dr. Deyoung looked at Genetics of this free ranging deer and what he found was, that the genetics on this deer were more similar to captive deer, than the free ranging population, but he did not see a significant connection to any one captive facility that he analyzed, so we believe, Ahhhhhh, this animal had some captive ahhh, whatnot.''
Commission Agenda Item No. 5 Exhibit B
DISEASE DETECTION AND RESPONSE RULES
PROPOSAL PREAMBLE
1. Introduction.
snip...
A third issue is the accuracy of mortality reporting. Department records indicate that for each of the last five years an average of 26 deer breeders have reported a shared total of 159 escapes. Department records for the same time period indicate an average of 31 breeding facilities reported a shared total of 825 missing deer (deer that department records indicate should be present in the facility, but cannot be located or verified).
On January 21, 2017 a tornado took down thousands of feet of fence for a 420-acre illegal deer enclosure in Lamar County that had been subject to federal and state investigation for illegally importing white-tailed deer into Mississippi from Texas (a CWD positive state). Native deer were free to move on and off the property before all of the deer were able to be tested for CWD. Testing will be made available for a period of three years for CWD on the property and will be available for deer killed within a 5-mile radius of the property on a voluntary basis.
https://www.mdwfp.com/media/254796/2016-17-deer-report.pdf
“It is interesting to note that, in 2001, the State of Texas shifted its deer management strategies toward the same leanings that Kroll has suggested for Wisconsin. In Texas, the change was brought about via heavy lobbying from the high-fence deer ranching industry. This pressure helped convince the Texas Parks and Wildlife to change their regulations and allow private landowners to select the own deer biologists.”
http://www.texasmonthly.com/story/which-side-fence-are-you
Chronic Wasting Disease in Texas
A Real Disease with Proven Impacts
Produced by a coalition of concerned hunters, landowners, & conservationists (last update 08/2023)
Snip…
Since 2012, CWD has been detected in wild deer in just 7 counties in Texas and is only established in the western panhandle and far west Texas.
In that same period of time, captive deer breeders have exposed almost half of Texas counties to CWD.
Deer held in captive breeding facilities are confined to much tighter spaces, and have intimate contact with many more animals on a daily basis. By far the greatest factor in amplifying the spread of CWD is the artificial movement of these animals, shipped in livestock trailers hundreds of miles, far outside of their natural home range, and ultimately released to co-mingle with wild deer.
Each year, Texas captive deer breeders liberate 20,000-30,000 deer from their pens to the wild.
For every deer breeding facility where a CWD positive deer is discovered, an epidemiological investigation is conducted by the Texas Parks & Wildlife Department and the Texas Animal Health Commission to determine how many other deer may have been exposed to the disease and where they have been shipped. Because of the prolific artificial movement of captive deer, one deer with CWD can impact hundreds of other facilities and ranches across the state.
Unfortunately, released deer in Texas are not required to retain any kind of visible identification (an ear tag), and for this reason, the vast majority of released deer cannot be relocated for testing.
As of August 2023, 116 Texas counties have received possibly infected breeder deer that cannot be located, putting more than 140,000 landowners at risk of the disease.
Snip
The state of Texas has been testing for CWD since 2002. Since that time, more than 302,360 captive and free range deer have been tested.
From 2015-2022, more than 127,000 samples were collected from hunter-harvested and roadkill deer. This sampling rate and risk-based distribution provides scientists confidence that they would have detected the disease if it existed at a very low prevalence (<1%) in any given region at the time sampling began.
Snip…
We have learned from other states where CWD has been present the longest, that a constant increase in the prevalence of the disease may lead to a significant decline in the deer population. When disease prevalence exceeds 20%, deer populations have declined by up to 50%. In some areas of Colorado, where CWD has been present since 1985, mule deer abundance has declined by 45% since that time, despite adequate habitat and no hunting ( Miller et al. 2008 ). Similarly, the South Converse Game Unit in Wyoming has documented CWD prevalence exceeding 50% and has seen an approximate 50% decline in mule deer populations.
Snip…
Rural Economies
Deer hunting is the lifeblood of rural Texas. White-tailed deer hunting is by far the most impactful segment of the hunting economy, representing $4.3 billion, according to a recent Texas A&M Study. And while deer breeders represent a very small segment of that economy (less than 5%), they represent one of the greatest risks. ( Full Texas A&M Report )
Real Estate
Rural land prices are largely driven by recreational buyers with hunting as a top land amenity. Without deer hunting, many of these properties will be worth much less.
Conservation Funding
Deer hunters are the largest funders of wildlife conservation in Texas through excise taxes on firearms, ammunition, and gear along with active membership supporting and funding conservation organizations. If deer hunting suffers due to CWD, all wildlife in Texas lose.
Culture & Health
Texas’ native deer herd has iconic value for all Texans. Deer hunting brings families together, creates camaraderie in communities, and serves to connect Texans to nature. There is no better protein than wild, locally harvested, non-GMO and totally organic venison. A healthy deer herd leads to healthy Texans and a healthy and prosperous Texas.
Snip…
This isn't a disease for our lifetime. It's a disease for our grandchildren's lifetime.
- Dr. Bob Dittmar, Former Texas State Wildlife Veterinarian
Snip…
See the full text with maps, graphs, much more, excellent data…
https://bit.ly/3xL16Gm
Since 2012, CWD has been detected in wild deer in just 7 counties in Texas and is only established in the western panhandle and far west Texas.
In that same period of time, captive deer breeders have exposed almost half of Texas counties to CWD.
https://bit.ly/3xL16Gm
As of August 2023, 116 Texas counties have received possibly infected breeder deer that cannot be located, putting more than 140,000 landowners at risk of the disease.
https://bit.ly/3xL16Gm
ECONOMIC VALUES OF WHITE-TAILED DEER IN TEXAS
2022 SURVEY: PART I
http://web.archive.org/web/20230809171452/https://nri.tamu.edu/media/3702/economic-values-of-white-tailed-deer-in-texas-2022-survey-part-i.pdf
Don't mess Texas, or with Mother Nature in Texas, but, seems things went terribly wrong down here in Texas with CWD, be careful what you ask for;
TEXAS CWD STRAIN
“Wow,” he said. “Unlike anything we've seen before.”
The disease devastating deer herds may also threaten human health
Scientists are exploring the origins of chronic wasting disease before it becomes truly catastrophic.
Rae Ellen Bichell
Image credit: David Parsons/Istock
April 8, 2019
This story was published in collaboration with the Mountain West News Bureau, a collaboration between Wyoming Public Media, Boise State Public Radio in Idaho, KUER in Salt Lake City and KRCC and KUNC in Colorado.
SNIP...
One day in late February, in their laboratory in Fort Collins, Colorado, Wagner and Zabel compared the prions from the brains of CWD-infected deer in Texas with those of elk in Colorado. They want to know if the proteins were all mangled in the same way, or not. “If they are different, this would suggest that we have different strain properties, which is evidence as we're building our case that we might have multiple strains of CWD circulating in the U.S.,” says Wagner.
Step one is to see if they’re equally easy to destroy using a chemical called guanidine. The shape of a prion dictates everything, including the way it interacts with an animal’s cells and the ease with which chemicals can unfold it.
“Moment of truth,” said Wagner, as she and Zabel huddled around a computer, waiting for results to come through. When they did, Zabel was surprised.
“Wow,” he said. “Unlike anything we've seen before.”
The prions from the Texas deer were a lot harder to destroy than the ones from the Colorado elk. In fact, the guanidine barely damaged them at all. “We’ve never seen that before in any prion strain, which means that it has a completely different structure than we've ever seen before,” says Zabel. And that suggests that it might be a very different kind of chronic wasting disease. The researchers ran the same test on another Texas deer, with the same results.
Now, these are only the preliminary results from a few animals. Wagner and Zabel have a lot more experiments to do. But if future tests come to the same conclusion, it would support their hypothesis that there are multiple strains of chronic wasting disease out there, all with different origins. That, in turn, could mean that this disease will become even trickier to manage than it already is.
And, Zabel adds, there’s something else. “If it's still evolving, it may still evolve into a form that could potentially, eventually affect humans,” he says.
Zabel is not the only one worried about that possibility.
OSTERHOLM, THE EPIDEMIOLOGIST from Minnesota, is also concerned. He directs the Center for Infectious Disease Research and Policy at the University of Minnesota, and is serving a one-year stint as a “Science Envoy for Health Security” with the U.S. State Department. In February, he told Minnesota lawmakers that when it comes to chronic wasting disease, we are playing with fire. “You are going to hear from people that this is not going to be a problem other than a game farm issue. You're going to hear from people that it's not going to transmit to people, and I hope they're right, but I wouldn't bet on it,” he said. “And if we lose this one and haven’t done all we can do, we will pay a price.”
If that wasn’t warning enough, he added: “Just remember what happened in England.”
He was talking about mad cow disease. Decades ago, Osterholm got involved in studying the potential for the newly emerging condition — bovine spongiform encephalopathy, or BSE for short — to be transmitted to humans.
At that point, researchers had yet to document a prion disease in animals that could infect people. They did, however, have a few pieces of the puzzle. For one, work in Papua New Guinea had shown that people could transmit prion diseases to each other if they practiced cannibalism, especially of the brain-eating variety. They also knew that BSE was spreading quickly between cattle. Osterholm says he and others worried that the more widespread it became, the more chances it might have to change into something that could sicken people.
“A lot of people thought that it was an overreaction,” says Osterholm. “Then, of course, in 1996, 10 years later, we recognized that in fact transmission had occurred.” Variant Creutzfeldt-Jakob disease, as the illness is called when it appears in human beings, has infected about 230 people worldwide. Osterholm says he feels like he’s having déjà vu, except that instead of mad cow, now it’s chronic wasting disease that’s spreading in animals, with the potential to cross the species barrier to infect humans.
SNIP...SEE FULL TEXT;
https://www.hcn.org/articles/wildlife-the-disease-devastating-deer-herds-may-also-threaten-human-health-science
TEXAS CWD STRAIN
77. Assessing chronic wasting disease strain differences in free-ranging cervids across the United States
Kaitlyn M. Wagnera, Caitlin Ott-Connb, Kelly Strakab, Bob Dittmarc, Jasmine Battend, Robyn Piercea, Mercedes Hennessya, Elizabeth Gordona, Brett Israela, Jenn Ballarde and Mark D Zabela
aPrion Research Center at Colorado State University; bMichigan Department of Natural Resources; cTexas Parks and Wildlife Department; dMissouri Department of Conservation, 5. Arkansas Game and Fish Commission CONTACT Kaitlyn M. Wagner miedkait@rams.colostate.edu
ABSTRACT
Background/Introduction: Chronic wasting disease (CWD) is an invariably fatal prion disease affecting captive and free-ranging cervids, including white-tailed deer, mule deer, moose, elk, and reindeer. Since the initial description of the disease in the 1960’s, CWD has spread to 23 states, 3 Canadian Provinces, South Korea, Norway and, most recently, Finland. While some outbreaks of CWD were caused by transport of infected animals from endemic regions, the origin of CWD in other epizootics is unclear and has not been characterized. Previous studies have shown that there are two distinct strains of CWD. However, the continuous spread and the unclear origin of several outbreaks warrant continued surveillance and further characterization of strain diversity.
Materials and Methods: To address these knowledge gaps, we used biochemical tests to assess strain differences between CWD outbreaks in Michigan, Texas, Missouri, and Colorado, USA. Brain or lymph node samples were homogenized and digested in 50 µg/mL proteinase K (PK). These samples were then run on a Western blot to assess glycoform ratio and electrophoretic mobility. Texas samples were digested in 100 µg/mL PK. To assess conformational stability, brain or lymph node homogenates were incubated in increasing concentrations of guanidine hydrochloride from 0 M to 4 M in 0.5 M increments. Samples were then precipitated in methanol overnight, washed and PK digested in 50 µg/mL PK before slot blotting.
Results: Our results have found significant differences in glycoform ratio between CWD from Michigan and Colorado, but no differences were observed in conformational stability assays. Interestingly, when testing our CWD isolates from Texas to analyse electrophoretic mobility and glycoform ratio, we found that these samples did not exhibit the characteristic band shift when treated with PK, but PK resistant material remained. Additionally, results from our conformational stability assay demonstrate a unique profile of these Texas isolates. Testing of samples from Missouri is currently underway.
Conclusions: Thus far, our data indicate that there are strain differences between CWD circulating in Michigan and CWD in Colorado and provide important insight into CWD strain differences between two non-contiguous outbreaks. We have also identified a unique strain of CWD in Texas with biochemical strain properties not seen in any of our other CWD isolates. These results highlight the importance of continued surveillance to better understand this devastating disease. These results have important implications for CWD emergence, evolution and our understanding of prion strain heterogeneity on the landscape.
http://www.tandfonline.com/doi/full/10.1080/19336896.2019.1615197
Texas Game Wardens Bust Illegal Deer Operations Across the State Feb. 27, 2025
Media Contact: TPWD News, Business Hours, 512-389-8030
AUSTIN – A recent investigation by Texas Game Wardens resulted in approximately 1,200 pending charges and 22 suspects from across the state involved in the deer breeding industry and black-market wildlife trade.
The suspects and charges are associated with three deer breeding facilities, ten release sites, one deer management pen and three illegal facilities not registered in the Texas Wildlife Information Management Services (TWIMS) database, meaning they were operating or receiving deer in violation of registration requirements and disease monitoring protocols.
https://tpwd.texas.gov/newsmedia/releases/?req=20250227b
Texas Game Wardens Bust Illegal Deer Operations Across the State Feb. 27, 2025
https://chronic-wasting-disease.blogspot.com/2025/02/texas-game-wardens-bust-illegal-deer.html
TUESDAY, FEBRUARY 25, 2025
TEXAS ANIMAL HEALTH COMMISSION 423rd Commission Meeting CWD Update February 25, 2025
https://chronic-wasting-disease.blogspot.com/2025/02/texas-animal-health-commission-423rd.html
SUNDAY, MAY 04, 2025
Texas Senate Bill 2649 creation of a statewide Chronic Wasting Disease plan
https://chronic-wasting-disease.blogspot.com/2025/05/texas-senate-bill-2649-creation-of.html
SUNDAY, MAY 04, 2025
Texas Senate Bill 2651 establishment of a pilot program to breed deer resistant to CWD TSE Prion, what could go wrong?
https://chronic-wasting-disease.blogspot.com/2025/05/texas-senate-bill-2651-establishment-of_4.html
Texas S.B. 2843 Directs TPWD to conduct a comprehensive study of current measures to control chronic wasting disease (CWD) in deer
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
https://chronic-wasting-disease.blogspot.com/2025/04/texas-sb-2843-directs-tpwd-to-conduct.html
FRIDAY, APRIL 04, 2025
Trucking CWD TSE Prion
“CWD spreads among wild populations at a relatively slow rate, limited by the natural home range and dispersed nature of wild animals.”
NOW HOLD YOUR HORSES, Chronic Wasting Disease CWD of Cervid can spread rather swiftly, traveling around 50 MPH, from the back of truck and trailer, and Here in Texas, we call it ‘Trucking CWD’…
Preventive Veterinary Medicine Volume 234, January 2025, 106385
Use of biosecurity practices to prevent chronic wasting disease in Minnesota cervid herds
Vehicles or trailers that entered the farm were used to transport other live cervids, cervid carcasses, or cervid body parts in past 3 years in 64.3 % (95 % CI 46.3–82.3) of larger elk/reindeer herds compared to 13.6 % (95 % CI 4.7–22.4) of smaller deer herds.
Snip…
Identifying the exact pathway of initial CWD transmission to cervid herds is often not possible, in part due to many potential pathways of transmission for the infection, including both direct and indirect contact with infected farmed or wild cervids (Kincheloe et al., 2021). That study identified that transmissions from infected farmed cervids may occur from direct contact with the movement of cervids from one herd to another and from indirect contact with the sharing of equipment, vehicles, clothing, reproductive equipment, and potentially through semen or embryos.
https://www.sciencedirect.com/science/article/abs/pii/S016758772400271X
Snip…see;
Trucking CWD TSE Prion
https://chronic-wasting-disease.blogspot.com/2025/04/trucking-cwd-tse-prion.html
CWD Status Captive Herds
https://www.aphis.usda.gov/sites/default/files/status-of-captive-herds.pdf
THURSDAY, APRIL 24, 2025
***> US Captive CWD Positive Herds Update April 2025
https://chronic-wasting-disease.blogspot.com/2025/04/us-captive-cwd-positive-herds-update.html
P.S., a bit of recent science on CWD tse prion, that you might should be aware of, if you are not already. You’re not dealing with an ordinary pathogen. Cwd tse PrP is nasty stuff, think Chernobyl. Think Cwd is not capable of transmitting to humans, think again. We now know Cwd will transmit by oral routes, to cattle, sheep, pigs, Cervid, primates, and an even more worrisome findings recently;
Published: 05 August 2025
Vertical transmission of chronic wasting disease in free-ranging white-tailed deer populations
Abstract Chronic wasting disease (CWD) is a fatal neurodegenerative disease affecting cervids across North America, Northern Europe, and Asia. Disease transmission among cervids has historically been attributed to direct animal-to-animal contact with ‘secreta’ (saliva, blood, urine, and feces) containing the infectious agent, and indirect contact with the agent shed to the environment in these bodily components. Mounting evidence provides another mechanism of CWD transmission, that from mother-to-offspring, including during pregnancy (vertical transmission). Here we describe the detection of the infectious CWD agent and prion seeding in fetal and reproductive tissues collected from healthy-appearing free-ranging white-tailed deer (Odocoileus virginianus) from multiple U.S. states by mouse bioassay and in vitro prion amplification assays. This is the first report of the infectious agent in multiple in utero derived fetal and maternal-fetal reproductive tissues, providing evidence that CWD infections are propagated within gestational fetal tissues of white-tailed deer populations. This work confirms previous experimental and field findings in several cervid species supporting vertical transmission as an additional mechanism of CWD transmission and may help to further explain the facile dissemination of this disease among captive and free-ranging cervid populations.
Snip…
We report infectious prions in the reproductive and fetal tissue of naturally exposed free-ranging white-tailed deer suggesting that in utero maternal transmission is likely an underappreciated mode of CWD transmission. Our study shows that vertical transmission is indeed a viable route of infection within the southeastern U.S. and is another potential factor contributing to the relentless spread of chronic wasting disease.
https://www.nature.com/articles/s41598-025-12727-8
SUNDAY, AUGUST 02, 2015
TEXAS CWD, Have you been ThunderStruck, deer semen, straw bred bucks, super ovulation, and the potential TSE Prion connection, what if?
http://chronic-wasting-disease.blogspot.com/2015/08/texas-cwd-have-you-been-thunderstruck.html
Problem Statement 6B: Reveal genetics of prion disease susceptibility.
Greater frequency of chronic wasting disease in free-ranging elk genetically tolerant to disease progression raises concerns related to prion transmission and strain evolution.
Animal Disease Research Unit, Pullman, Washington
Genetic variations in the prion protein gene of Rocky Mountain elk do not confer complete resistance to fatal infection by chronic wasting disease. However, elk carrying one or two copies of the amino acid leucine (L) variant at position 132 of the prion protein (132L*, where * is either M for methionine or L) survive much longer than 132MM elk. An ARS researcher in Pullman, Washington, in collaboration with researchers at the University of Wyoming, the University of California at Davis, the National Park Service, and the Animal and Plant Health Inspection Service, found a higher frequency of 132L* elk in areas of Wyoming with high infection rates, consistent with the expected positive effect of prolonged survival on reproduction. However, the frequency of chronic wasting disease infection in 132L* elk was also higher than previous estimates. To improve the long-term management of native elk populations, these findings underscore the importance of determining the effects of prolonged infection on disease transmission from 132L* elk and the potential for driving prion strain diversification.
https://www.ars.usda.gov/ARSUserFiles/np103/AnnualReports/Final%20NP103%20FY2024%20Annual%20Report.updated%205.30.25.pdf
Research Project: Elucidating the Pathobiology and Transmission of Transmissible Spongiform Encephalopathies
Location: Virus and Prion Research
Title: Update: CWD genetic resistance project at NADC
Author item Cassmann, Eric item Greenlee, Justin Submitted to: North American Deer Farmer Publication Type: Trade Journal Publication Acceptance Date: 11/5/2023 Publication Date: 11/15/2023 Citation: Cassmann, E.D., Greenlee, J.J. 2023. Update: CWD genetic resistance project at NADC. North American Deer Farmer. P. 83.
Interpretive Summary: Technical Abstract: In March of 2020, we began a study to examine the susceptibility of whitetail deer with rare prion protein genotypes to chronic wasting disease (CWD). In the sequence of amino acids that make up the deer prion protein, there are several locations that are variable. These variations are sometimes called polymorphisms. In the data collected from depopulations, whitetail deer with certain prion gene polymorphisms were not positive for CWD. In 2019, Dr. Nick Haley published a paper that showed H95/S96, HH95, and S96/K226 deer from depopulated herds in the US were not CWD positive. Based on the overall low number of deer with these genotypes () we’re unable to determine if they were resistant to CWD or if there were too few deer with these genotypes to be statistically represented in the positive cases. It’s also possible that they could be partially susceptible with longer incubation times than deer with generic (wild type) prion genotypes. Samples gathered at depopulation represent a snapshot of the herd. It is possible these rare genotypes were exposed, but had not yet accumulated abnormal prion protein to a level detectable by the detection methods used. The NADC susceptibility study was initiated to help answer these questions. We studied deer with polymorphisms at 3 amino acid locations (codons): 95, 96, and 226. Wild type deer are QQ95GG96QQ226. Whitetail deer with wild type prion genotypes were inoculated with CWD and co-housed with other whitetail deer (contact deer) that had rare prion protein genotypes. The genotypes of contact deer included QH95GS96QQ226, QH95GG96QK226, QQ95GS96QQ226, QQ95SS96QQ226, Q95GS96QK226, and QQ95GG96KK226 (bolded text indicates a prion gene polymorphism). During the first year, we collected feces, saliva, nasal swabs, skin, blood, and rectal biopsies from the inoculated and contact deer to determine if deer are CWD positive and the period of CWD shedding. After the first year, we started collecting rectal biopsies annually on the contact deer, but all other samples are still collected every three months. Eight out of ten (8/10) inoculated deer developed clinical signs for CWD and tested positive after necropsy (Figure 1). The average time from inoculation to euthanasia of these eight inoculated deer was 23 months. Two inoculated deer are still on-study; one of these deer has tested positive for CWD on rectal biopsy IHC. To date, two deer from the contact group have developed CWD clinical signs and tested positive (Figure 2). The positive deer from the contact group had the GS96QK226 and KK226 genotypes. We have detected CWD prions in rectal biopsies with IHC in three other contact deer as of October 2023. Their prion genotypes are GS96, QH95GS96, and GS96QK226. As the experiment continues, we hope to answer 2 main questions. (1) Are there any prion protein polymorphisms that make deer resistant to CWD, and (2) what are the CWD shedding dynamics in deer with detectable CWD. One potential outcome of the study would be identifying genotypes with very long incubation periods that, while susceptible to CWD, still could be used to manage CWD.
https://www.ars.usda.gov/research/publications/publication/?seqNo115=410188
Update: CWD genetic resistance project at NADC 1) Are there any prion protein polymorphisms that make deer resistant to CWD, and (2) what are the CWD shedding dynamics in deer with detectable CWD. One potential outcome of the study would be identifying genotypes with very long incubation periods that, while susceptible to CWD, still could be used to manage CWD.
https://www.ars.usda.gov/research/publications/publication/?seqNo115=410188
Another potential and likely outcome of this study, imo, is that genotypes developed with very long incubation, could therefore, if released into the wild, could help spread cwd even further, exposing even more wild species, and surrounding environments, for even longer periods of time, due to the longer incubation, a terrible potential outcome, one that must be avoided at all cost, imo…terry
Detection of Prions in Wild Pigs (Sus scrofa) from Areas with Reported Chronic Wasting Disease Cases, United States
Volume 31, Number 1—January 2025
Abstract
Using a prion amplification assay, we identified prions in tissues from wild pigs (Sus scrofa) living in areas of the United States with variable chronic wasting disease (CWD) epidemiology. Our findings indicate that scavenging swine could play a role in disseminating CWD and could therefore influence its epidemiology, geographic distribution, and interspecies spread.
Snip…
Conclusions
In summary, results from this study showed that wild pigs are exposed to cervid prions, although the pigs seem to display some resistance to infection via natural exposure. Future studies should address the susceptibility of this invasive animal species to the multiple prion strains circulating in the environment. Nonetheless, identification of CWD prions in wild pig tissues indicated the potential for pigs to move prions across the landscape, which may, in turn, influence the epidemiology and geographic spread of CWD.
https://wwwnc.cdc.gov/eid/article/31/1/24-0401_article
Although the current U.S. feed ban is based on keeping tissues from TSE infected cattle from contaminating animal feed, swine rations in the U.S. could contain animal derived components including materials from scrapie infected sheep and goats. These results indicating the susceptibility of pigs to sheep scrapie, coupled with the limitations of the current feed ban, indicates that a revision of the feed ban may be necessary to protect swine production and potentially human health.
2. Determined that pigs naturally exposed to chronic wasting disease (CWD) may act as a reservoir of CWD infectivity. Chronic wasting disease is a naturally occurring, fatal, neurodegenerative disease of cervids. The potential for swine to serve as a host for the agent of CWD disease is unknown. The purpose of this study was to investigate the susceptibility of swine to the CWD agent following experimental oral or intracranial inoculation. Pigs were assigned to 1 of 3 groups: intracranially inoculated; orally inoculated; or non-inoculated. At market weight age, half of the pigs in each group were tested ('market weight' groups). The remaining pigs ('aged' groups) were allowed to incubate for up to 73 months post inoculation (MPI). Tissues collected at necropsy were examined for disease-associated prion protein (PrPSc) by multiple diagnostic methods. Brain samples from selected pigs were bioassayed in mice expressing porcine prion protein. Some pigs from each inoculated group were positive by one or more tests. Bioassay was positive in 4 out of 5 pigs assayed. Although only small amounts of PrPSc were detected using sensitive methods, this study demonstrates that pigs can serve as hosts for CWD. Detection of infectivity in orally inoculated pigs using mouse bioassay raises the possibility that naturally exposed pigs could act as a reservoir of CWD infectivity. Currently, swine rations in the U.S. could contain animal derived components including materials from deer or elk. In addition, feral swine could be exposed to infected carcasses in areas where CWD is present in wildlife populations. The current feed ban in the U.S. is based exclusively on keeping tissues from TSE infected cattle from entering animal feeds. These results indicating the susceptibility of pigs to CWD, coupled with the limitations of the current feed ban, indicates that a revision of the feed ban may be necessary to protect swine production and potentially human health.
https://www.ars.usda.gov/research/publications/publication/?seqNo115=353091
https://www.ars.usda.gov/research/project/?accnNo=432011&fy=2017
https://www.ars.usda.gov/research/publications/publication/?seqNo115=337105
https://www.ars.usda.gov/research/publications/publication/?seqNo115=326166
Addressing chronic wasting disease in Korean farms: topsoil removal and 2N NaOH treatment before cervid restocking
Kyung-Je Park , Hoo-Chang Park , Yu-Ran Lee , In-Soon Roh , Gordon Mitchell , Young Pyo Choi …
Published online: 08 Jul 2025
Abstract
Chronic wasting disease (CWD) is a highly contagious prion disease occurring in free-ranging and farmed cervids. In the Republic of Korea, cases of CWD continue to be detected almost annually, on both new and occasionally previously infected farms. CWD-infected animals contaminate soil and other environmental components by shedding prions through their excreta. Since shed prions remain infectious for years in the environment, they can act as infectivity reservoirs facilitating horizontal transmission of CWD. To prevent the further spread of CWD and allow farms to resume operations, control measures on infected farms, including topsoil removal and thorough environmental treatment with 2N NaOH, have been implemented in the Republic of Korea. Restocking remediated farms with cervids was permitted after confirming the absence of prion seeding activity in soil samples using protein misfolding cyclic amplification (PMCA). A total of 215 samples from 18 remediated farms were collected and analysed using PMCA, with only 3 samples from 3 farms displaying prion seeding activity. While the disease control measures effectively eliminated prion seeding activity in CWD-affected farms, CWD recurred at two of the 18 remediated farms 4 to 5 years after restocking animals. It remains unclear whether the recurrence of CWD at the two farms was due to residual prions in the environment after the control measures, or the introduction of the infected animals from other farms. This uncertainty is heightened by the annual occurrence of CWD at multiple farms and the absence of a traceability system for farmed cervids.
Keywords: Chronic wasting disease (CWD); NaOH; Protein-misfolding cyclic amplification (PMCA); Republic of Korea; farm; prions; remediation; topsoil.
https://www.tandfonline.com/doi/full/10.1080/19336896.2025.2527588
“While the disease control measures effectively eliminated prion seeding activity in CWD-affected farms, CWD recurred at two of the 18 remediated farms 4 to 5 years after restocking animals.”
I remember what “deep throat” told me about Scrapie back around 2001, during early days of my BSE investigation, after my Mom died from hvCJD, I never forgot, and it seems it’s come to pass;
***> Confidential!!!!
***> As early as 1992-3 there had been long studies conducted on small pastures containing scrapie infected sheep at the sheep research station associated with the Neuropathogenesis Unit in Edinburgh, Scotland. Whether these are documented...I don't know. But personal recounts both heard and recorded in a daily journal indicate that leaving the pastures free and replacing the topsoil completely at least 2 feet of thickness each year for SEVEN years....and then when very clean (proven scrapie free) sheep were placed on these small pastures.... the new sheep also broke out with scrapie and passed it to offspring. I am not sure that TSE contaminated ground could ever be free of the agent!! A very frightening revelation!!!
---end personal email---end...tss
and so it seems…
so, this is what we leave our children and grandchildren?
Rapid recontamination of a farm building occurs after attempted prion removal
First published: 19 January 2019 https://doi.org/10.1136/vr.105054
The data illustrates the difficulty in decontaminating farm buildings from scrapie, and demonstrates the likely contribution of farm dust to the recontamination of these environments to levels that are capable of causing disease.
snip...
This study clearly demonstrates the difficulty in removing scrapie infectivity from the farm environment. Practical and effective prion decontamination methods are still urgently required for decontamination of scrapie infectivity from farms that have had cases of scrapie and this is particularly relevant for scrapie positive goatherds, which currently have limited genetic resistance to scrapie within commercial breeds.24 This is very likely to have parallels with control efforts for CWD in cervids.
https://bvajournals.onlinelibrary.wiley.com/doi/abs/10.1136/vr.105054
***>This is very likely to have parallels with control efforts for CWD in cervids.
https://pubmed.ncbi.nlm.nih.gov/30602491/
Front. Vet. Sci., 14 September 2015 | https://doi.org/10.3389/fvets.2015.00032
Objects in contact with classical scrapie sheep act as a reservoir for scrapie transmission
In conclusion, the results in the current study indicate that removal of furniture that had been in contact with scrapie-infected animals should be recommended, particularly since cleaning and decontamination may not effectively remove scrapie infectivity (31), even though infectivity declines considerably if the pasture and the field furniture have not been in contact with scrapie-infected sheep for several months. As sPMCA failed to detect PrPSc in furniture that was subjected to weathering, even though exposure led to infection in sheep, this method may not always be reliable in predicting the risk of scrapie infection through environmental contamination.
http://journal.frontiersin.org/article/10.3389/fvets.2015.00032/full
"Additionally, we have determined that prion seeding activity is retained for at least fifteen years at a contaminated site following attempted remediation."
15 YEARS!
Detection of prions in soils contaminated by multiple routes
Results: We are able to detect prion seeding activity at multiple types of environmental hotspots, including carcass sites, contaminated captive facilities, and scrapes (i.e. urine and saliva). Differences in relative prion concentration vary depending on the nature and source of the contamination. Additionally, we have determined that prion seeding activity is retained for at least fifteen years at a contaminated site following attempted remediation.
Conclusions: Detection of prions in the environment is of the utmost importance for controlling chronic wasting disease spread. Here, we have demonstrated a viable method for detection of prions in complex environmental matrices. However, it is quite likely that this method underestimates the total infectious prion load in a contaminated sample, due to incomplete recovery of infectious prions. Further refinements are necessary for accurate quantification of prions in such samples, and to account for the intrinsic heterogeneities found in the broader environment.
Funded by: Wisconsin Department of Natural Resources
Prion 2023 Abstracts
https://prion2023.org/wp-content/uploads/2023/10/Meeting-book-final-version2.pdf
SUNDAY, APRIL 06, 2025
Failure to prevent classical scrapie after repeated decontamination of a barn
https://scrapie-usa.blogspot.com/2025/04/failure-to-prevent-classical-scrapie.html
https://prpsc.proboards.com/thread/165/failure-prevent-scrapie-repeated-decontamination
CWD, So, this is what we leave our children and grandchildren?
Detection of chronic wasting disease prions in the farm soil of the Republic of Korea
Here, we show that prion seeding activity was detected in extracts from farm soil following 4 years of incubation with CWD-infected brain homogenate.
https://journals.asm.org/doi/10.1128/msphere.00866-24
=====***>
"Additionally, we have determined that prion seeding activity is retained for at least fifteen years at a contaminated site following attempted remediation."
=====***>
Detection of prions in soils contaminated by multiple routes
Results: We are able to detect prion seeding activity at multiple types of environmental hotspots, including carcass sites, contaminated captive facilities, and scrapes (i.e. urine and saliva). Differences in relative prion concentration vary depending on the nature and source of the contamination. Additionally, we have determined that prion seeding activity is retained for at least fifteen years at a contaminated site following attempted remediation.
Conclusions: Detection of prions in the environment is of the utmost importance for controlling chronic wasting disease spread. Here, we have demonstrated a viable method for detection of prions in complex environmental matrices. However, it is quite likely that this method underestimates the total infectious prion load in a contaminated sample, due to incomplete recovery of infectious prions. Further refinements are necessary for accurate quantification of prions in such samples, and to account for the intrinsic heterogeneities found in the broader environment.
Funded by: Wisconsin Department of Natural Resources
Prion 2023 Abstracts
https://prion2023.org/wp-content/uploads/2023/10/Meeting-book-final-version2.pdf
Artificial mineral sites that pre-date endemic chronic wasting disease become prion hotspots
The detection of PrPCWD in soils at attractant sites within an endemic CWD zone significantly advances our understanding of environmental PrPCWD accumulation dynamics, providing valuable information for advancing adaptive CWD management approaches.
https://int-cwd-sympo.org/wp-content/uploads/2023/06/final-agenda-with-abstracts.pdf
Chronic wasting disease detection in environmental and biological samples from a taxidermy site
Results: The PMCA analysis demonstrated CWD seeding activity in some of the components of this facility, including insects involved in head processing, soils, and a trash dumpster.
Conclusions: Different areas of this property were used for various taxidermy procedures. We were able to detect the presence of prions in i) soils that were in contact with the heads of dead animals, ii) insects involved in the cleaning of skulls, and iii) an empty dumpster where animal carcasses were previously placed. This is the first report demonstrating that swabbing is a helpful method to screen for prion infectivity on surfaces potentially contaminated with CWD. These findings are relevant as this swabbing and amplification strategy may be used to evaluate the disease status of other free-ranging and captive settings where there is a concern for CWD transmissions, such as at feeders and water troughs with CWD-exposed properties. This approach could have substantial implications for free-ranging cervid surveillance as well as in epidemiological investigations of CWD.
Prion 2022 Conference abstracts: pushing the boundaries
https://www.tandfonline.com/doi/full/10.1080/19336896.2022.2091286
https://intcwdsympo.files.wordpress.com/2023/06/final-agenda-with-abstracts.pdf?force_download=true
***> Infectious agent of sheep scrapie may persist in the environment for at least 16 years
***> Nine of these recurrences occurred 14–21 years after culling, apparently as the result of environmental contamination, but outside entry could not always be absolutely excluded.
JOURNAL OF GENERAL VIROLOGY Volume 87, Issue 12
Infectious agent of sheep scrapie may persist in the environment for at least 16 years Free
https://www.microbiologyresearch.org/content/journal/jgv/10.1099/vir.0.82011-0
Rapid recontamination of a farm building occurs after attempted prion removal
First published: 19 January 2019 https://doi.org/10.1136/vr.105054
The data illustrates the difficulty in decontaminating farm buildings from scrapie, and demonstrates the likely contribution of farm dust to the recontamination of these environments to levels that are capable of causing disease. snip...
This study clearly demonstrates the difficulty in removing scrapie infectivity from the farm environment. Practical and effective prion decontamination methods are still urgently required for decontamination of scrapie infectivity from farms that have had cases of scrapie and this is particularly relevant for scrapie positive goatherds, which currently have limited genetic resistance to scrapie within commercial breeds.24 This is very likely to have parallels with control efforts for CWD in cervids.
https://bvajournals.onlinelibrary.wiley.com/doi/abs/10.1136/vr.105054
***>This is very likely to have parallels with control efforts for CWD in cervids.
https://pubmed.ncbi.nlm.nih.gov/30602491/
Chronic Wasting Disease CWD TSE Prion
THE CWD TSE Prion aka mad cow type disease is not your normal pathogen.
The TSE prion disease survives ashing to 600 degrees celsius, that’s around 1112 degrees farenheit.
you cannot cook the TSE prion disease out of meat.
you can take the ash and mix it with saline and inject that ash into a mouse, and the mouse will go down with TSE.
Prion Infected Meat-and-Bone Meal Is Still Infectious after Biodiesel Production as well.
the TSE prion agent also survives Simulated Wastewater Treatment Processes.
IN fact, you should also know that the TSE Prion agent will survive in the environment for years, if not decades.
you can bury it and it will not go away.
The TSE agent is capable of infected your water table i.e. Detection of protease-resistant cervid prion protein in water from a CWD-endemic area.
it’s not your ordinary pathogen you can just cook it out and be done
New studies on the heat resistance of hamster-adapted scrapie agent: Threshold survival after ashing at 600°C suggests an inorganic template of replication
http://www.pnas.org/content/97/7/3418.full
Prion Infected Meat-and-Bone Meal Is Still Infectious after Biodiesel Production
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2493038/
March 13, 2025
Prion Partitioning and Persistence in Environmental Waters
https://pubs.acs.org/doi/epdf/10.1021/acs.est.4c11497?ref=article_openPDF
Prions in Waterways
https://vimeo.com/898941380?fbclid=IwAR3Di7tLuU-iagCetdt4-CVPrOPQQrv037QS1Uxz0tX3z7BuvPeYlwIp7IY
Detection of protease-resistant cervid prion protein in water from a CWD-endemic area
https://www.ncbi...nlm.nih.gov/pmc/articles/PMC2802782/pdf/prion0303_0171.pdf
A Quantitative Assessment of the Amount of Prion Diverted to Category 1 Materials and Wastewater During Processing
http://onlinelibrary.wiley.com/doi/10.1111/j.1539-6924.2012.01922.x/abstract
Rapid assessment of bovine spongiform encephalopathy prion inactivation by heat treatment in yellow grease produced in the industrial manufacturing process of meat and bone meals
https://bmcvetres.biomedcentral.com/track/pdf/10.1186/1746-6148-9-134.pdf
THURSDAY, FEBRUARY 28, 2019
BSE infectivity survives burial for five years with only limited spread
https://link.springer.com/content/pdf/10.1007%2Fs00705-019-04154-8.pdf
So, this is what we leave our children and grandchildren?
Aug 18, 2021
Oh, Deer
Heading Off a Wildlife Epidemic
CWD poses a significant threat to the future of hunting in Texas. Deer population declines of 45 and 50 percent have been documented in Colorado and Wyoming. A broad infection of Texas deer populations resulting in similar population impacts would inflict severe economic damage to rural communities and could negatively impact land markets. Specifically, those landowners seeking to establish a thriving herd of deer could avoid buying in areas with confirmed CWD infections. As they do with anthrax-susceptible properties, land brokers may find it advisable to inquire about the status of CWD infections on properties that they present for sale. Prospective buyers should also investigate the status of the wildlife on prospective properties. In addition, existing landowners should monitor developments as TPWD crafts management strategies to identify and contain this deadly disease.
Dr. Gilliland (c-gilliland@tamu.edu) is a research economist with the Texas Real Estate Research Center at Texas A&M University.
https://www.recenter.tamu.edu/articles/tierra-grande/oh-d
So, this is what we leave our children and grandchildren?
CDC CWD TSE Prion Update 2025
KEY POINTS
Chronic wasting disease affects deer, elk and similar animals in the United States and a few other countries.
The disease hasn't been shown to infect people.
However, it might be a risk to people if they have contact with or eat meat from animals infected with CWD.
https://www.cdc.gov/chronic-wasting/about/index.html
Prions in Muscles of Cervids with Chronic Wasting Disease, Norway
Volume 31, Number 2—February 2025
Research
Prions in Muscles of Cervids with Chronic Wasting Disease, Norway
Snip…
In summary, the results of our study indicate that prions are widely distributed in peripheral and edible tissues of cervids in Norway, including muscles. This finding highlights the risk of human exposure to small amounts of prions through handling and consuming infected cervids. Nevertheless, we note that this study did not investigate the zoonotic potential of the Norway CWD prions. In North America, humans have historically consumed meat from CWD-infected animals, which has been documented to harbor prions (35,44–47). Despite the potential exposure to prions, no epidemiologic evidence indicates a correlation between the occurrence of CWD cases in animals and the prevalence of human prion diseases (48). A recent bioassay study reported no transmissions from 3 Nordic isolates into transgenic mice expressing human PrP (49). Therefore, our findings should be interpreted with caution in terms of human health implications, and further research is required to determine the zoonotic potential of these CWD strains.
The presence of prions in peripheral tissues indicates that CWD may have a systemic nature in all Norwegian cervid species, challenging the view that prions are exclusively localized in the CNS in sporadic CWD of moose and red deer. Our findings expand the notion of just how widely distributed prions can be in cervids affected with CWD and call into question the capability of emerging CWD strains in terms of infectivity to other species, including humans.
Appendix
https://wwwnc.cdc.gov/eid/article/31/2/24-0903-app1.pdf
https://wwwnc.cdc.gov/eid/article/31/2/24-0903_article
Volume 31, Number 2—February 2025
Dispatch
Detection of Chronic Wasting Disease Prions in Raw, Processed, and Cooked Elk Meat, Texas, USA
Rebeca Benavente, Fraser Brydon, Francisca Bravo-Risi, Paulina Soto, J. Hunter Reed, Mitch Lockwood, Glenn Telling, Marcelo A. Barria, and Rodrigo MoralesComments to Author
Snip…
CWD prions have been detected in the muscle of both farmed and wild deer (10), and at concentrations relevant to sustain disease transmission (11). CWD prions have also been identified across several cervid species and in multiple tissues, including lymph nodes, spleen, tongue, intestines, adrenal gland, eyes, reproductive tissues, ears, lungs, and liver, among others (12–14). Those findings raise concerns about the safety of ingesting processed meats that contain tissues other than skeletal muscle (15) (Appendix). https://wwwnc.cdc.gov/eid/article/31/2/24-0906-app1.pdf .
In addition, those findings highlight the need for continued vigilance and research on the transmission risks of prion diseases and for development of new preventative and detection measures to ensure the safety of the human food supply.
Snip…
Overall, our study results confirm previous reports describing the presence of CWD prions in elk muscles (13). The data also demonstrated CWD prion persistence in food products even after processing through different procedures, including the addition of salts, spices, and other edible elements. Of note, our data show that exposure to high temperatures used to cook the meat increased the availability of prions for in vitro amplification. Considering the potential implications in food safety and public health, we believe that the findings described in this study warrant further research. Our results suggest that although the elk meat used in this study resisted different manipulations involved in subsequent consumption by humans, their zoonotic potential was limited. Nevertheless, even though no cases of CWD transmission to human have been reported, the potential for human infection is still unclear and continued monitoring for zoonotic potential is warranted.
https://wwwnc.cdc.gov/eid/article/31/2/24-0906_article
Volume 31, Number 1—January 2025
Dispatch
Detection of Prions in Wild Pigs (Sus scrofa) from Areas with Reported Chronic Wasting Disease Cases, United States
Abstract
Using a prion amplification assay, we identified prions in tissues from wild pigs (Sus scrofa) living in areas of the United States with variable chronic wasting disease (CWD) epidemiology. Our findings indicate that scavenging swine could play a role in disseminating CWD and could therefore influence its epidemiology, geographic distribution, and interspecies spread.
Snip…
Conclusions In summary, results from this study showed that wild pigs are exposed to cervid prions, although the pigs seem to display some resistance to infection via natural exposure. Future studies should address the susceptibility of this invasive animal species to the multiple prion strains circulating in the environment. Nonetheless, identification of CWD prions in wild pig tissues indicated the potential for pigs to move prions across the landscape, which may, in turn, influence the epidemiology and geographic spread of CWD.
https://wwwnc.cdc.gov/eid/article/%2031/1/24-0401_article
***> Price of TSE Prion Poker goes up substantially, all you cattle ranchers and such, better pay close attention here...terry <***
Transmission of the chronic wasting disease agent from elk to cattle after oronasal exposure
Justin Greenlee, Jifeng Bian, Zoe Lambert, Alexis Frese, and Eric Cassmann Virus and Prion Research Unit, National Animal Disease Center, USDA-ARS, Ames, IA, USA
Aims: The purpose of this study was to determine the susceptibility of cattle to chronic wasting disease agent from elk.
Materials and Methods: Initial studies were conducted in bovinized mice using inoculum derived from elk with various genotypes at codon 132 (MM, LM, LL). Based upon attack rates, inoculum (10% w/v brain homogenate) from an LM132 elk was selected for transmission studies in cattle. At approximately 2 weeks of age, one wild type steer (EE211) and one steer with the E211K polymorphism (EK211) were fed 1 mL of brain homogenate in a quart of milk replacer while another 1 mL was instilled intranasally. The cattle were examined daily for clinical signs for the duration of the experiment. One steer is still under observation at 71 months post-inoculation (mpi).
Results: Inoculum derived from MM132 elk resulted in similar attack rates and incubation periods in mice expressing wild type or K211 bovine PRNP, 35% at 531 days post inoculation (dpi) and 27% at 448 dpi, respectively. Inoculum from LM132 elk had a slightly higher attack rates in mice: 45% (693 dpi) in wild type cattle PRNP and 33% (468) in K211 mice. Inoculum from LL132 elk resulted in the highest attack rate in wild type bovinized mice (53% at 625 dpi), but no K211 mice were affected at >700 days. At approximately 70 mpi, the EK211 genotype steer developed clinical signs suggestive of prion disease, depression, low head carriage, hypersalivation, and ataxia, and was necropsied. Enzyme immunoassay (IDEXX) was positive in brainstem (OD=4.00, but non-detect in retropharyngeal lymph nodes and palatine tonsil. Immunoreactivity was largely limited to the brainstem, midbrain, and cervical spinal cord with a pattern that was primarily glia-associated.
Conclusions: Cattle with the E211K polymorphism are susceptible to the CWD agent after oronasal exposure of 0.2 g of infectious material.
Funded by: This research was funded in its entirety by congressionally appropriated funds to the United States Department of Agriculture, Agricultural Research Service. The funders of the work did not influence study design, data collection and analysis, decision to publish, or preparation of the manuscript.
*****>>> "Cattle with the E211K polymorphism are susceptible to the CWD agent after oronasal exposure of 0.2 g of infectious material." <<<*****
=====end
Strain characterization of chronic wasting disease in bovine-PrP transgenic mice
Nuria Jerez-Garrido1, Sara Canoyra1, Natalia Fernández-Borges1, Alba Marín Moreno1, Sylvie L. Benestad2, Olivier Andreoletti3, Gordon Mitchell4, Aru Balachandran4, Juan María Torres1 and Juan Carlos Espinosa1. 1 Centro de Investigación en Sanidad Animal, CISA-INIA-CSIC, Madrid, Spain. 2 Norwegian Veterinary Institute, Ås, Norway. 3 UMR Institut National de la Recherche Agronomique (INRA)/École Nationale Vétérinaire de Toulouse (ENVT), Interactions Hôtes Agents Pathogènes, Toulouse, France. 4 Canadian Food Inspection Agency, Ottawa, Canada.
Aims: Chronic wasting disease (CWD) is an infectious prion disease that affects cervids. Various CWD prion strains have been identified in different cervid species from North America and Europe. The properties of the infectious prion strains are influenced by amino acid changes and polymorphisms in the PrP sequences of different cervid species. This study, aimed to assess the ability of a panel of CWD prion isolates from diverse cervid species from North America and Europe to infect bovine species, as well as to investigate the properties of the prion strains following the adaptation to the bovine-PrP context.
Materials and Methods: BoPrP-Tg110 mice overexpressing the bovine-PrP sequence were inoculated by intracranial route with a panel of CWD prion isolates from both North America (two white-tailed deer and two elk) and Europe (one reindeer, one moose and one red deer).
Results: Our results show distinct behaviours in the transmission of the CWD isolates to the BoPrP-Tg110 mouse model. Some of these isolates did not transmit even after the second passage. Those able to transmit displayed differences in terms of attack rate, survival times, biochemical properties of brain PrPres, and histopathology.
Conclusions: Altogether, these results exhibit the diversity of CWD strains present in the panel of CWD isolates and the ability of at least some CWD isolates to infect bovine species. Cattle being one of the most important farming species, this ability represents a potential threat to both animal and human health, and consequently deserves further study.
Funded by: MCIN/AEI /10.13039/501100011033 and by European Union NextGeneration EU/PRTR
Grant number: PCI2020-120680-2 ICRAD
"Altogether, these results exhibit the diversity of CWD strains present in the panel of CWD isolates and the ability of at least some CWD isolates to infect bovine species. Cattle being one of the most important farming species, this ability represents a potential threat to both animal and human health, and consequently deserves further study."
=====end
https://prion2023.org/wp-content/uploads/2023/10/Meeting-book-final-version2.pdf
so, this is what we leave our children and grandchildren?
Redefining the zoonotic potential of chronic wasting disease
Project Number 5R01NS121016-04
Contact PI/Project Leader SCHATZL, HERMANN M
Other PIs
Awardee Organization
UNIVERSITY OF CALGARY
Description
Abstract Text
The rapid expansion of chronic wasting disease (CWD), a prion disease of free-ranging and farmed deer, elk and moose, is a major and ongoing threat in North America. Approximately 1 in 36 Americans hunt deer and elk and eat venison, and it is estimated that 7,000 – 15,000 CWD-infected cervids are consumed annually. This fuels growing concerns about the human health risks imposed by CWD. There are no documented cases of CWD transmission to humans, even though with the long incubation periods of all prion diseases and the unknown presentation of CWD in humans definite conclusions are not possible. The zoonotic potential of prion diseases has been exemplified by bovine spongiform encephalopathy (BSE, mad cow disease) which resulted in a new form of human prion disease (vCJD). BSE was transmissible to Cynomolgus macaques and transgenic mice expressing the human prion protein. Initial results of CWD transmission studies to the same non-human primate and mouse models of human prion disease were not successful, corroborating the conclusion that the zoonotic potential of CWD is low, if not absent. Our groups were part of a consortium that inoculated Cynomolgus macaques via different routes with CWD. Some animals exhibited subtle clinical signs reminiscent of prion disease, and upon euthanasia, weak signs of vacuolation, PrPSc deposition and astrocytosis in the brain were found, while no proteinase K (PK) resistant prion protein (PrP) was detectable. We have now demonstrated for the first time that CWD from macaques can transmit clinical prion disease to transgenic mouse models of CWD and human prion disease, albeit in the absence of detectable PK-resistant PrP. Bona fide PrPSc was only detected upon 3rd passage from mouse to bank vole models. Altogether, this is the first evidence that CWD very likely has zoonotic potential. The goal of the current proposal is to redefine the zoonotic potential of CWD by characterizing the biological properties of CWD prions emerging upon experimental transmission into macaques, for obtaining important information on how CWD could manifest in humans.
In Aim 1, we will study whether CWD from macaque (CWDmac) in bank voles represents a new prion strain, by comparing biochemical and biological properties to an array of known prion strains from different species.
Aim 2 addresses the question whether CWDmac represents an intermediate prion strain, adaptable to cervids or humans upon passage, and possessing an expanded host range. We will address this by in vivo passage in cervidized or humanized mouse models. In vitro, we will utilize serial PMCA and a newly generated PrP0/0 cell culture model for infection, upon reconstitution with PrP from different species.
In Aim 3, we will shed light on the observed dissociation between infectivity and the presence of bona fide PrPSc. We propose to identify atypical PrP fragments associated with CWDmac, and we will elucidate brain cell responses to CWDmac exposure by innovative single cell RNA sequencing. In summary, our studies will uncover the possible manifestation of CWD in humans, which is of critical importance for drawing definite conclusions about the zoonotic potential of CWD.
Public Health Relevance Statement
The zoonotic potential of chronic wasting disease (CWD) is unclear to date. We provide the first evidence by transmission experiments to different transgenic mouse models and bank voles that Cynomolgus macaques inoculated via different routes with CWD-positive cervid tissues harbor infectious prions that elicit clinical disease in rodents. Our proposed studies will unravel the properties of these prions, how they will adapt to humans and which pathways are activated in brain cells and associated with clinical disease. Results from these studies uncover the potential manifestation of CWD in humans, which is highly relevant for human health.
https://eventos.galoa.com.br/prion-2025/page/5178-home
Project 3A: CWD Prion Shedding and Environmental Contamination: Role in Transmission and Zoonotic
Parent Project Number 5P01AI077774-14
Sub-Project ID 5512
Contact PI/Project Leader HOOVER, EDWARD ARTHUR
Awardee Organization UNIVERSITY OF TEXAS HLTH SCI CTR HOUSTON
Description
Abstract Text
Chronic wasting disease (CWD) is an emergent, highly transmissible, geographically expanding, prion disease of both wild and captive cervids. CWD is unique among prion diseases in its facile contagion and environmental persistence. Its expanding geographical range, combined with the increasing transport of animals and animal products, portend its continued expansion and diversification. The zoonotic potential of CWD remains poorly understood. CWD endemic areas interface cervids with livestock species and humans, posing obvious zoonotic risks that over time will increase. While it is known that strains of CWD exist, nothing is known about the zoonotic potential of these strains. Work from our applicant group has shown that CWD infected cervids continually shed prions into the environment and that previously unrecognized environmental factors can influence the emergence of a dominant strain from a mixture. The ability to recognize the zoonotic potential of CWD strains is central to mitigating CWD transmission risk. The central hypothesis for work described here is that CWD strains evolve continuously due to a combination of both host and environmental factors. We will test this hypothesis by:
i) determining the evolution and zoonotic impact of CWD strains in the native cervid species;
ii) leveraging our unique animal resources, expertise, and in vivo & in vitro methodologies to assess environmental factors that alter CWD strain selection and evolution and
iii) evaluate zoonotic potential of CWD strains by a complementary combination of in vitro amplification assays and animal transmission studies.
The results will provide new information about this emergent transmissible prion disease and the risk it poses to humans and other species.
https://reporter.nih.gov/project-details/11056111#description
Project 3B: Pathogenesis Transmission and Detection of Zoonotic Prion Diseases
Parent Project Number 5P01AI077774-14
Sub-Project ID 5513
Contact PI/Project Leader BARTZ, JASON C
Awardee Organization UNIVERSITY OF TEXAS HLTH SCI CTR HOUSTON
Description Abstract Text
Project Summary: Chronic wasting disease (CWD) is an emergent, highly transmissible, geographically expanding, prion disease of both wild and captive cervids. CWD is unique among prion diseases in its facile contagion and environmental persistence. Its expanding geographical range, combined with the increasing transport of animals and animal products, portend its continued expansion and diversification. The zoonotic potential of CWD remains poorly understood. CWD endemic areas interface cervids with livestock species and humans, posing obvious zoonotic risks that over time will increase. While it is known that strains of CWD exist, nothing is known about the zoonotic potential of these strains. Work from our applicant group has shown that CWD- infected cervids continually shed prions into the environment and that previously unrecognized environmental factors can influence the emergence of a dominant strain from a mixture. The ability to recognize the zoonotic potential of CWD strains is central to mitigating CWD transmission risk. The central hypothesis for work described here is that CWD strains evolve continuously due to a combination of both host and environmental factors. We will test this hypothesis by:
i) determining the evolution and zoonotic impact of CWD strains in the native cervid species;
ii) leveraging our unique animal resources, expertise, and in vivo & in vitro methodologies to assess environmental factors that alter CWD strain selection and evolution and
iii) evaluate zoonotic potential of CWD strains by a complementary combination of in vitro amplification assays and animal transmission studies.
The results will provide new information about this emergent transmissible prion disease and the risk it poses to humans and other species.
https://reporter.nih.gov/project-details/11056115#description
Project 1: Modeling the Mechanisms of Prion Transmission, Strain Selection, Mutation and Species Barrier in Transgenic Mice
Parent Project Number 5P01AI077774-14
Sub-Project ID 5510
Contact PI/Project Leader TELLING, GLENN C
Awardee Organization UNIVERSITY OF TEXAS HLTH SCI CTR HOUSTON
Description Abstract Text
Our broad, long-term objectives are to are to decipher the mechanisms by which infectious prions replicate, encode strain information, and evolve to acquire new properties. We propose four Specific Aims to address our central hypothesis that incompletely adapted prion strains are comprised of poorly optimized ensembles of PrPSc quasi species conformers that evolve under selective pressure towards states of enhanced stability and pathogenicity. Our particular focus is chronic wasting disease (CWD), an uncontrollable contagious epidemic of cervids of uncertain zoonotic potential. Using genetically engineered CWD-susceptible mice, cultured cells, cell free amplification, and antibodies recognizing defined conformation-dependent PrP epitopes,
Aim I will address the mechanism of adaptation of unstable emergent CWD prions in response to physical and chemical constraints.
In Aim II we will address the hypothesis that that residue 226 and other cervid PrP polymorphisms influence selection of distinct portfolios of CWD strain conformers with different adaptive potentials. Using gene targeted mice expressing physiologically controlled levels of PrP variants and in vitro systems for prion replication, we will characterize the properties of strains propagated in these backgrounds and explore whether interference between them affects selection and adaptation of CWD.
In Aim III, we will assess the properties of emergent Norwegian moose and reindeer CWD strains experimentally propagated in deer and compare with established North American CWD.
Aim IV will address an unmet need in the field of significant importance, namely the paucity of model systems and tools for studying human prions. Using newly generated gene targeted mice expressing physiological levels of human PrP and novel approaches to derive susceptible human neuroblastoma cells, we will assess the zoonotic potential of emergent CWD strains and their adapted derivatives propagated in different cervid PrP backgrounds. Our ultimate goal is to assess and manage the risk posed to humans from continually evolving prions, specifically those causing CWD, by understanding the means by which they propagate and exist as heritable strains with protean host range properties that adapt and evolve under selective pressure.
https://reporter.nih.gov/project-details/11056096#description
Project 2
Parent Project Number 5P01AI077774-14
Sub-Project ID 5511
Contact PI/Project Leader SOTO, CLAUDIO
Awardee Organization UNIVERSITY OF TEXAS HLTH SCI CTR HOUSTON
Description Abstract Text
ABSTRACT Chronic wasting disease (CWD) affecting various species of cervids in North American and Northern Europe represents a serious problem, because it continues to propagate uncontrollably among wild and captive cervids. CWD appears to be very heterogeneous with multiple different strains and can be transmitted to other animal species. The risk of CWD transmission to humans is unknown which is a major concern because the number of sick animals and their geographical distribution is rapidly increasing. The mechanism by which CWD propagates so efficiently among cervids is also unknown. The main goal of this project is to utilize a set of highly innovative techniques to study the cellular, molecular and structural features of naturally occurring CWD strains and their potential for inter- species transmission, particularly focusing on the possibility that certain CWD strains may infect humans. We will also attempt to elucidate the atomic resolution structure of CWD prions using cryo-electron microscopy. The overarching hypothesis is that CWD exists as multiple strains in distinct individuals and even within the same individual in different brain cells and that inter- species transmission and zoonotic potential depend on the specific strain characteristics. The project is divided in the following specific aims:
(1) Study the structural and molecular diversity of natural CWD strains and the high resolution three-dimensional structure of CWD prions.
(2) Understand CWD prion strain diversity in single brain cells isolated by laser capture microdissection and subsequently amplified by PMCA.
(3) Evaluate CWD inter-species transmission spillover potential and its effect on zoonotic potential.
(4) Analyze the deer-human prion species barrier in vivo using chimeric mice harboring human and cervid neuronal cells.
The studies included in this projects will address some of the most pressing questions regarding CWD, including
(i) the CWD prion strain variability,
(ii) the zoonotic potential of different CWD prion strains,
(iii) the atomic resolution structure of infectious prions and the structural basis of prion strains,
(iv) the cellular distribution of CWD prion strains in the brain and its gene expression consequences,
(v) the spillover potential of CWD to other animal species,
(vi) the potential role of intermediate species in the transmission of CWD prions to humans.
The findings generated in this project will be essential to design measures to prevent further propagation of CWD, and to avoid the emergence of new diseases with potentially disastrous consequences.
https://reporter.nih.gov/search/fXQ8kEmVa0mNDk1JNnx3Cw/project-details/11056103#description
18. Zoonotic potential of moose-derived chronic wasting disease prions after adaptation in intermediate species
Tomás Barrioa, Jean-Yves Doueta, Alvina Huora, Séverine Lugana, Naïma Arona, Hervé Cassarda, Sylvie L. Benestadb, Juan Carlos Espinosac, Juan María Torresc, Olivier Andréolettia
aUnité Mixte de Recherche de l’Institut National de Recherche pour l’Agriculture, l’Alimentation et l’Environnement 1225 Interactions Hôtes-Agents Pathogènes, École Nationale Vétérinaire de Toulouse, 31076 Toulouse, France; bNorwegian Veterinary Institute, P.O. Box 64, NO-1431 Ås, Norway; cCentro de Investigación en Sanidad Animal (CISA-INIA), 28130, Valdeolmos, Madrid, Spain
Aims: Chronic wasting disease (CWD) is an emerging prion disease in Europe. To date, cases have been reported in three Nordic countries and in several species, including reindeer (Rangifer tarandus), moose (Alces alces) and red deer (Cervus elaphus). Cumulating data suggest that the prion strains responsible for the European cases are distinct from those circulating in North America. The biological properties of CWD prions are still poorly documented, in particular their spillover and zoonotic capacities. In this study, we aimed at characterizing the interspecies transmission potential of Norwegian moose CWD isolates.
Materials and Methods: For that purpose, we performed experimental transmissions in a panel of transgenic models expressing the PrPC sequence of various species.
Results: On first passage, one moose isolate propagated in the ovine PrPC-expressing model (Tg338). After adaptation in this host, moose CWD prions were able to transmit in mice expressing either bovine or human PrPC with high efficacy.
Conclusions: These results suggest that CWD prions can acquire enhanced zoonotic properties following adaptation in an intermediate species.
Funding
Grant number: AAPG2020 EU-CWD, ICRAD2020 TCWDE, NRC2022 NorCWD
Acknowledgement
https://www.tandfonline.com/doi/full/10.1080/19336896.2024.2424058
“ After adaptation in this host, moose CWD prions were able to transmit in mice expressing either bovine or human PrPC with high efficacy.”
regular venison eating associated with a 9 FOLD INCREASE IN RISK OF CJD
Subject: Re: DEER SPONGIFORM ENCEPHALOPATHY SURVEY & HOUND STUDY
Date: Fri, 18 Oct 2002 23:12:22 +0100
From: Steve Dealler
Reply-To: Bovine Spongiform Encephalopathy Organization: Netscape Online member
To: BSE-L@ …
######## Bovine Spongiform Encephalopathy <BSE-L@UNI-KARLSRUHE.DE> #########
Dear Terry,
An excellent piece of review as this literature is desparately difficult to get back from Government sites.
What happened with the deer was that an association between deer meat eating and sporadic CJD was found in about 1993. The evidence was not great but did not disappear after several years of asking CJD cases what they had eaten. I think that the work into deer disease largely stopped because it was not helpful to the UK industry...and no specific cases were reported.
Well, if you dont look adequately like they are in USA currenly then you wont find any!
Steve Dealler
########### http://mailhost.rz.uni-karlsruhe.de/warc/bse-l.html ############
Subject: DEER SPONGIFORM ENCEPHALOPATHY SURVEY & HOUND STUDY
From: "Terry S. Singeltary Sr." <flounder@WT.NET>
Reply To: Bovine Spongiform Encephalopathy <BSE-L@UNI-KARLSRUHE.DE>
Date: Thu, 17 Oct 2002 17:04:51 -0700
snip...
''The association between venison eating and risk of CJD shows similar pattern, with regular venison eating associated with a 9 FOLD INCREASE IN RISK OF CJD (p = 0.04).''
CREUTZFELDT JAKOB DISEASE SURVEILLANCE IN THE UNITED KINGDOM THIRD ANNUAL REPORT AUGUST 1994
Consumption of venison and veal was much less widespread among both cases and controls. For both of these meats there was evidence of a trend with increasing frequency of consumption being associated with increasing risk of CJD. (not nvCJD, but sporadic CJD...tss) These associations were largely unchanged when attention was restricted to pairs with data obtained from relatives. ...
Table 9 presents the results of an analysis of these data.
There is STRONG evidence of an association between ‘’regular’’ veal eating and risk of CJD (p = .0.01).
Individuals reported to eat veal on average at least once a year appear to be at 13 TIMES THE RISK of individuals who have never eaten veal.
There is, however, a very wide confidence interval around this estimate. There is no strong evidence that eating veal less than once per year is associated with increased risk of CJD (p = 0.51).
The association between venison eating and risk of CJD shows similar pattern, with regular venison eating associated with a 9 FOLD INCREASE IN RISK OF CJD (p = 0.04).
There is some evidence that risk of CJD INCREASES WITH INCREASING FREQUENCY OF LAMB EATING (p = 0.02).
The evidence for such an association between beef eating and CJD is weaker (p = 0.14). When only controls for whom a relative was interviewed are included, this evidence becomes a little STRONGER (p = 0.08).
snip...
It was found that when veal was included in the model with another exposure, the association between veal and CJD remained statistically significant (p = < 0.05 for all exposures), while the other exposures ceased to be statistically significant (p = > 0.05).
snip...
In conclusion, an analysis of dietary histories revealed statistical associations between various meats/animal products and INCREASED RISK OF CJD. When some account was taken of possible confounding, the association between VEAL EATING AND RISK OF CJD EMERGED AS THE STRONGEST OF THESE ASSOCIATIONS STATISTICALLY. ...
snip...
In the study in the USA, a range of foodstuffs were associated with an increased risk of CJD, including liver consumption which was associated with an apparent SIX-FOLD INCREASE IN THE RISK OF CJD. By comparing the data from 3 studies in relation to this particular dietary factor, the risk of liver consumption became non-significant with an odds ratio of 1.2 (PERSONAL COMMUNICATION, PROFESSOR A. HOFMAN. ERASMUS UNIVERSITY, ROTTERDAM). (???...TSS)
snip...see full report ;
http://web.archive.org/web/20090506050043/http://www.bseinquiry.gov.uk/files/yb/1994/08/00004001.pdf
http://web.archive.org/web/20090506050007/http://www.bseinquiry.gov.uk/files/yb/1994/10/00003001.pdf
http://web.archive.org/web/20090506050244/http://www.bseinquiry.gov.uk/files/yb/1994/07/00001001.pdf
Stephen Dealler is a consultant medical microbiologist deal@airtime.co.uk
BSE Inquiry Steve Dealler
Management In Confidence
BSE: Private Submission of Bovine Brain Dealler
snip...end
########### http://mailhost.rz.uni-karlsruhe.de/warc/bse-l.html ############
BSE INQUIRY
CJD9/10022
October 1994
Mr R.N. Elmhirst Chairman British Deer Farmers Association Holly Lodge Spencers Lane
BerksWell Coventry CV7 7BZ
Dear Mr Elmhirst,
CREUTZFELDT-JAKOB DISEASE (CJD) SURVEILLANCE UNIT REPORT
Thank you for your recent letter concerning the publication of the third annual report from the CJD Surveillance Unit. I am sorry that you are dissatisfied with the way in which this report was published.
The Surveillance Unit is a completely independant outside body and the Department of Health is committed to publishing their reports as soon as they become available. In the circumstances it is not the practice to circulate the report for comment since the findings of the report would not be amended.. In future we can ensure that the British Deer Farmers Association receives a copy of the report in advance of publication.
The Chief Medical Officer has undertaken to keep the public fully informed of the results of any research in respect of CJD. This report was entirely the work of the unit and was produced completely independantly of the the Department.
The statistical results reqarding the consumption of venison was put into perspective in the body of the report and was not mentioned at all in the press release. Media attention regarding this report was low key but gave a realistic presentation of the statistical findings of the Unit. This approach to publication was successful in that consumption of venison was highlighted only once by the media ie. in the News at one television proqramme.
I believe that a further statement about the report, or indeed statistical links between CJD and consumption of venison, would increase, and quite possibly give damaging credence, to the whole issue. From the low key media reports of which I am aware it seems unlikely that venison consumption will suffer adversely, if at all.
http://web.archive.org/web/20030511010117/http://www.bseinquiry.gov.uk/files/yb/1994/10/00003001.pdf
TSE in wild UK deer? The first case of BSE (as we now realise) was in a nyala in London zoo and the further zoo cases in ungulates were simply thought of as being interesting transmissions of scrapie initially. The big problem started to appear with animals in 1993-5 when it became clear that there was an increase in the CJD cases in people that had eaten deer although the statistics involved must have been questionable. The reason for this was that the CJD Surveillance was well funded to look into the diet of people dying of CJD. This effect is not clear with vCJD...if only because the numbers involved are much smaller and hence it is difficult to gain enough statistics. They found that many other foods did not appear to have much association at all but that deer certainly did and as years went by the association actually became clearer. The appearance of vCJD in 1996 made all this much more difficult in that it was suddenly clearer that the cases of sporadic CJD that they had been checking up until then probably had nothing to do with beef...and the study decreased. During the period there was an increasing worry that deer were involved with CJD..
see references:
DEER BRAIN SURVEY
https://web.archive.org/web/20090506025229/http://www.bseinquiry.gov.uk/files/yb/1991/11/20004001.pdf
CONFIDENTIAL AND IN CONFIDENCE TRANSMISSION TO CHIMPANZEES AND PIGS
IN CONFIDENCE
TRANSMISSION TO CHIMPANZEES
Kuru and CJD have been successfully transmitted to chimpanzees but scrapie and TME have not.
We cannot say that scrapie will not transmit to chimpanzees. There are several scrapie strains and I am not aware that all have been tried (that would have to be from mouse passaged material). Nor has a wide enough range of field isolates subsequently strain typed in mice been inoculated by the appropriate routes (i/c, i/p and i/v).
I believe the proposed experiment to determine transmissibility, if conducted, would only show the susceptibility or resistance of the chimpanzee to infection/disease by the routes used and the result could not be interpreted for the predictability of the susceptibility for man. proposals for prolonged oral exposure of chimpanzees to milk from cattle were suggested a long while ago and rejected.
In view of Dr Gibbs' probable use of chimpazees Mr Wells' comments (enclosed) are pertinent. I have yet to receive a direct communication from Dr Schellekers but before any collaboration or provision of material we should identify the Gibbs' proposals and objectives.
A positive result from a chimpanzee challenged severely would likely create alarm in some circles even if the result could not be interpreted for man. I have a view that all these agents could be transmitted provided a large enough dose by appropriate routes was given and the animals kept long enough. Until the mechanisms of the species barrier are more clearly understood it might be best to retain that hypothesis.
A negative result would take a lifetime to determine but that would be a shorter period than might be available for human exposure and it would still not answer the question regarding mans ‘susceptibility. In the meantime no doubt the negativity would be used defensively. It would however be counterproductive if the experiment finally became positive. We may learn more about public reactions following next Monday's meeting.
R Bradley
CVO (+ Mr Wells’ commenters 23 September 1990 Dr T W A Little Dr B J Shreeve
90/9.23/1.1
https://web.archive.org/web/20090506041740/http://www.bseinquiry.gov.uk/files/yb/1990/09/23001001.pdf
*** now, let’s see what the authors said about this casual link, personal communications years ago, and then the latest on the zoonotic potential from CWD to humans from the TOKYO PRION 2016 CONFERENCE.
see where it is stated NO STRONG evidence. so, does this mean there IS casual evidence ????
“Our conclusion stating that we found no strong evidence of CWD transmission to humans”
From: TSS Subject: CWD aka MAD DEER/ELK TO HUMANS ???
Date: September 30, 2002 at 7:06 am PST
From: "Belay, Ermias"
To: Cc: "Race, Richard (NIH)" ; ; "Belay, Ermias"
Sent: Monday, September 30, 2002 9:22 AM
Subject: RE: TO CDC AND NIH - PUB MED- 3 MORE DEATHS - CWD - YOUNG HUNTERS
Dear Sir/Madam, In the Archives of Neurology you quoted (the abstract of which was attached to your email), we did not say CWD in humans will present like variant CJD.. That assumption would be wrong. I encourage you to read the whole article and call me if you have questions or need more clarification (phone: 404-639-3091).
Also, we do not claim that "no-one has ever been infected with prion disease from eating venison." Our conclusion stating that we found no strong evidence of CWD transmission to humans in the article you quoted or in any other forum is limited to the patients we investigated.
Ermias Belay, M.D. Centers for Disease Control and Prevention
-----Original Message----- From:
Sent: Sunday, September 29, 2002 10:15 AM
To: rr26k@nih.gov; rrace@niaid.nih.gov; ebb8@CDC.GOV
Subject: TO CDC AND NIH - PUB MED- 3 MORE DEATHS - CWD - YOUNG HUNTERS
Sunday, November 10, 2002 6:26 PM .......snip........end..............TSS
Thursday, April 03, 2008
A prion disease of cervids: Chronic wasting disease 2008 1: Vet Res. 2008 Apr 3;39(4):41 A prion disease of cervids: Chronic wasting disease Sigurdson CJ.
snip... *** twenty-seven CJD patients who regularly consumed venison were reported to the Surveillance Center***,
snip... full text ;
http://chronic-wasting-disease.blogspot.com/2008/04/prion-disease-of-cervids-chronic.html
However, to date, no CWD infections have been reported in people.
sporadic, spontaneous CJD, 85%+ of all human TSE, did not just happen. never in scientific literature has this been proven. if one looks up the word sporadic or spontaneous at pubmed, you will get a laundry list of disease that are classified in such a way;
sporadic = 54,983 hits
https://www.ncbi.nlm.nih.gov/pubmed/?term=sporadic
spontaneous = 325,650 hits
https://www.ncbi.nlm.nih.gov/pubmed/?term=spontaneous
key word here is 'reported'. science has shown that CWD in humans will look like sporadic CJD.
SO, how can one assume that CWD has not already transmitted to humans? they can't, and it's as simple as that. from all recorded science to date, CWD has already transmitted to humans, and it's being misdiagnosed as sporadic CJD. ...terry
*** LOOKING FOR CWD IN HUMANS AS nvCJD or as an ATYPICAL CJD, LOOKING IN ALL THE WRONG PLACES $$$ ***
However, to date, no CWD infections have been reported in people. key word here is ‘reported’. science has shown that CWD in humans will look like sporadic CJD. SO, how can one assume that CWD has not already transmitted to humans? they can’t, and it’s as simple as that. from all recorded science to date, CWD has already transmitted to humans, and it’s being misdiagnosed as sporadic CJD. …terry
*** LOOKING FOR CWD IN HUMANS AS nvCJD or as an ATYPICAL CJD, LOOKING IN ALL THE WRONG PLACES $$$ ***
*** These results would seem to suggest that CWD does indeed have zoonotic potential, at least as judged by the compatibility of CWD prions and their human PrPC target. Furthermore, extrapolation from this simple in vitro assay suggests that if zoonotic CWD occurred, it would most likely effect those of the PRNP codon 129-MM genotype and that the PrPres type would be similar to that found in the most common subtype of sCJD (MM1).***
http://www.tandfonline.com/doi/full/10.4161/pri.28124?src=recsys
http://www.tandfonline.com/doi/pdf/10.4161/pri.28124?needAccess=true
https://wwwnc.cdc.gov/eid/article/20/1/13-0858_article
So, this is what we leave our children and grandchildren?
CDC CWD TSE Prion Update 2025
KEY POINTS
Chronic wasting disease affects deer, elk and similar animals in the United States and a few other countries.
The disease hasn't been shown to infect people.
However, it might be a risk to people if they have contact with or eat meat from animals infected with CWD.
https://www.cdc.gov/chronic-wasting/about/index.html
Volume 31, Number 4—April 2025
Research
Detection and Decontamination of Chronic Wasting Disease Prions during Venison Processing
https://wwwnc.cdc.gov/eid/article/31/4/24-1176_article
Prions in Muscles of Cervids with Chronic Wasting Disease, Norway
Volume 31, Number 2—February 2025
Research
Prions in Muscles of Cervids with Chronic Wasting Disease, Norway
Snip…
In summary, the results of our study indicate that prions are widely distributed in peripheral and edible tissues of cervids in Norway, including muscles. This finding highlights the risk of human exposure to small amounts of prions through handling and consuming infected cervids. Nevertheless, we note that this study did not investigate the zoonotic potential of the Norway CWD prions. In North America, humans have historically consumed meat from CWD-infected animals, which has been documented to harbor prions (35,44–47). Despite the potential exposure to prions, no epidemiologic evidence indicates a correlation between the occurrence of CWD cases in animals and the prevalence of human prion diseases (48). A recent bioassay study reported no transmissions from 3 Nordic isolates into transgenic mice expressing human PrP (49). Therefore, our findings should be interpreted with caution in terms of human health implications, and further research is required to determine the zoonotic potential of these CWD strains.
The presence of prions in peripheral tissues indicates that CWD may have a systemic nature in all Norwegian cervid species, challenging the view that prions are exclusively localized in the CNS in sporadic CWD of moose and red deer. Our findings expand the notion of just how widely distributed prions can be in cervids affected with CWD and call into question the capability of emerging CWD strains in terms of infectivity to other species, including humans.
Appendix
https://wwwnc.cdc.gov/eid/article/31/2/24-0903-app1.pdf
https://wwwnc.cdc.gov/eid/article/31/2/24-0903_article
Volume 31, Number 2—February 2025
Dispatch
Detection of Chronic Wasting Disease Prions in Raw, Processed, and Cooked Elk Meat, Texas, USA
Rebeca Benavente, Fraser Brydon, Francisca Bravo-Risi, Paulina Soto, J. Hunter Reed, Mitch Lockwood, Glenn Telling, Marcelo A. Barria, and Rodrigo MoralesComments to Author
Snip…
CWD prions have been detected in the muscle of both farmed and wild deer (10), and at concentrations relevant to sustain disease transmission (11). CWD prions have also been identified across several cervid species and in multiple tissues, including lymph nodes, spleen, tongue, intestines, adrenal gland, eyes, reproductive tissues, ears, lungs, and liver, among others (12–14). Those findings raise concerns about the safety of ingesting processed meats that contain tissues other than skeletal muscle (15) (Appendix). https://wwwnc.cdc.gov/eid/article/31/2/24-0906-app1.pdf .
In addition, those findings highlight the need for continued vigilance and research on the transmission risks of prion diseases and for development of new preventative and detection measures to ensure the safety of the human food supply.
Snip…
Overall, our study results confirm previous reports describing the presence of CWD prions in elk muscles (13). The data also demonstrated CWD prion persistence in food products even after processing through different procedures, including the addition of salts, spices, and other edible elements. Of note, our data show that exposure to high temperatures used to cook the meat increased the availability of prions for in vitro amplification. Considering the potential implications in food safety and public health, we believe that the findings described in this study warrant further research. Our results suggest that although the elk meat used in this study resisted different manipulations involved in subsequent consumption by humans, their zoonotic potential was limited. Nevertheless, even though no cases of CWD transmission to human have been reported, the potential for human infection is still unclear and continued monitoring for zoonotic potential is warranted.
https://wwwnc.cdc.gov/eid/article/31/2/24-0906_article
Volume 31, Number 1—January 2025
Dispatch
Detection of Prions in Wild Pigs (Sus scrofa) from Areas with Reported Chronic Wasting Disease Cases, United States
Abstract
Using a prion amplification assay, we identified prions in tissues from wild pigs (Sus scrofa) living in areas of the United States with variable chronic wasting disease (CWD) epidemiology. Our findings indicate that scavenging swine could play a role in disseminating CWD and could therefore influence its epidemiology, geographic distribution, and interspecies spread.
Snip…
Conclusions In summary, results from this study showed that wild pigs are exposed to cervid prions, although the pigs seem to display some resistance to infection via natural exposure. Future studies should address the susceptibility of this invasive animal species to the multiple prion strains circulating in the environment. Nonetheless, identification of CWD prions in wild pig tissues indicated the potential for pigs to move prions across the landscape, which may, in turn, influence the epidemiology and geographic spread of CWD.
https://wwwnc.cdc.gov/eid/article/%2031/1/24-0401_article
Detection of chronic wasting disease prions in processed meats
Rebeca Benavente1 , Francisca Bravo1,2, J. Hunter Reed3 , Mitch Lockwood3 , Glenn Telling4 , Rodrigo Morales1,2 1 Department of Neurology, McGovern Medical School, University of Texas Health Science Center at Houston, Texas, USA; 2 Universidad Bernardo O’Higgins. Santiago, Chile; 3 Texas Parks and Wildlife Department, Texas, USA. 4 Prion Research Center, Department of Microbiology, Immunology, and Pathology, Colorado State University, Fort Collins, CO, USA
Aims: identify the presence of CWD prions in processed meats derived from elk.
Materials and Methods: In this study, we analyzed different processed meats derived from a CWD-positive (pre-clinical) free-ranging elk. Products tested included filets, sausages, boneless steaks, burgers, seasoned chili meats, and spiced meats. The presence of CWD-prions in these samples were assessed by PMCA using deer and elk substrates. The same analyses were performed in grilled and boiled meats to evaluate the resistance of the infectious agent to these procedures.
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.
Funded by: NIH and USDA
Grant number: 1R01AI132695 and APP-20115 to RM
Acknowledgement: We would like to thank TPWD personnel for providing us with valuable samples
"Our results show positive prion detection in all the samples analyzed using deer and elk substrates. Surprisingly, cooked meats displayed increased seeding activities."
end...
PRION 2023 CONTINUED;
https://prion2023.org/wp-content/uploads/2023/10/Meeting-book-final-version2.pdf
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
https://prion2023.org/wp-content/uploads/2023/10/Meeting-book-final-version2.pdf
DETECTION OF CHRONIC WASTING DISEASE PRIONS IN PROCESSED MEATS.
Abstract
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.
https://intcwdsympo.files.wordpress.com/2023/06/final-agenda-with-abstracts.pdf?force_download=true
Transmission of prion infectivity from CWD-infected macaque tissues to rodent models demonstrates the zoonotic potential of chronic wasting disease.
Samia Hannaoui1,2, Ginny Cheng1,2, Wiebke Wemheuer3, Walter Schulz-Schaeffer3, Sabine Gilch1,2, Hermann Schatzl1,2 1University of Calgary, Calgary, Canada. 2Calgary Prion Research Unit, Calgary, Canada. 3Institute of Neuropathology, Medical Faculty, Saarland University, Homburg/Saar, Germany
Snip…
***> Further passage to cervidized mice revealed transmission with a 100% attack rate.
***> Our findings demonstrate that macaques, considered the best model for the zoonotic potential of prions, were infected upon CWD challenge, including the oral one.
****> The disease manifested as atypical in macaques and initial transgenic mouse transmissions, but with infectivity present at all times, as unveiled in the bank vole model with an unusual tissue tropism.
***> Epidemiologic surveillance of prion disease among cervid hunters and people likely to have consumed venison contaminated with chronic wasting disease
=====
https://intcwdsympo.files.wordpress.com/2023/06/final-agenda-with-abstracts.pdf?force_download=true
Transmission of Cervid Prions to Humanized Mice Demonstrates the Zoonotic Potential of CWD
Samia Hannaouia, Irina Zemlyankinaa, Sheng Chun Changa, Maria Immaculata Arifina, Vincent Béringueb, Debbie McKenziec, Hermann M. Schatzla, and Sabine Gilcha
Results: Here, we provide the strongest evidence supporting the zoonotic potential of CWD prions, and their possible phenotype in humans. Inoculation of mice expressing human PrPCwith deer CWD isolates (strains Wisc-1 and 116AG) resulted in atypical clinical manifestations in > 75% of the mice, with myoclonus as leading clinical sign. Most of tg650brain homogenates were positive for seeding activity in RT-QuIC. Clinical disease and presentation was transmissible to tg650 mice and bank voles. Intriguingly, protease-resistant PrP in the brain of tg650 mice resembled that found in a familial human prion disease and was transmissible upon passage. Abnormal PrP aggregates upon infection with Wisc-1 were detectable in thalamus, hypothalamus, and midbrain/pons regions.
Unprecedented in human prion disease, feces of CWD-inoculated tg650 mice harbored prion seeding activity and infectious prions, as shown by inoculation of bank voles and tg650 with fecal homogenates.
Conclusions: This is the first evidence that CWD can infect humans and cause disease with a distinctive clinical presentation, signature, and tropism, which might be transmissible between humans while current diagnostic assays might fail to detect it. These findings have major implications for public health and CWD-management.
https://www.tandfonline.com/doi/full/10.1080/19336896.2022.2091286
The finding that infectious PrPSc was shed in fecal material of CWD-infected humanized mice and induced clinical disease, different tropism, and typical three banding pattern-PrPres in bank voles that is transmissible upon second passage is highly concerning for public health. The fact that this biochemical signature in bank voles resembles that of the Wisc-1 original deer isolate and is different from that of bvWisc-1, in the migration profile and the glyco-form-ratio, is valid evidence that these results are not a product of contamination in our study. If CWD in humans is found to be contagious and transmissible among humans, as it is in cervids [57], the spread of the disease within humans might become endemic.
Transmission of cervid prions to humanized mice demonstrates the zoonotic potential of CWD
Acta Neuropathol 144, 767–784 (2022). https://doi.org/10.1007/s00401-022-02482-9
Published
22 August 2022
https://link.springer.com/article/10.1007/s00401-022-02482-9
Fortuitous generation of a zoonotic cervid prion strain
Aims: Whether CWD prions can infect humans remains unclear despite the very substantial scale and long history of human exposure of CWD in many states or provinces of USA and Canada. Multiple in vitro conversion experiments and in vivo animal studies indicate that the CWD-to-human transmission barrier is not unbreakable. A major long-term public health concern on CWD zoonosis is the emergence of highly zoonotic CWD strains. We aim to address the question of whether highly zoonotic CWD strains are possible.
Materials and Methods: We inoculated several sCJD brain samples into cervidized transgenic mice (Tg12), which were intended as negative controls for bioassays of brain tissues from sCJD cases who had potentially been exposed to CWD. Some of the Tg12 mice became infected and their brain tissues were further examined by Western blot as well as serial passages in humanized or cervidized mice.
Results: Passage of sCJDMM1 in transgenic mice expressing elk PrP (Tg12) resulted in a “cervidized” CJD strain that we termed CJDElkPrP. We observed 100% transmission of the original CJDElkPrP in transgenic mice expressing human PrP. We passaged CJDElkPrP two more times in the Tg12 mice. We found that such second and third passage CJDElkPrP prions retained 100% transmission rate in the humanized mice, despite that the natural elk CWD isolates and CJDElkPrP share the same elk PrP sequence. In contrast, we and others found zero or poor transmission of natural elk CWD isolates in humanized mice.
Conclusions: Our data indicate that highly zoonotic cervid prion strains are not only possible but also can retain zoonotic potential after serial passages in cervids, suggesting a very significant and serious long-term risk of CWD zoonosis given that the broad and continuing spread of CWD prions will provide fertile grounds for the emergence of zoonotic CWD strains over time.
https://prion2023.org/wp-content/uploads/2023/10/Meeting-book-final-version2.pdf
The finding that infectious PrPSc was shed in fecal material of CWD-infected humanized mice and induced clinical disease, different tropism, and typical three banding pattern-PrPres in bank voles that is transmissible upon second passage is highly concerning for public health. The fact that this biochemical signature in bank voles resembles that of the Wisc-1 original deer isolate and is different from that of bvWisc-1, in the migration profile and the glyco-form-ratio, is valid evidence that these results are not a product of contamination in our study. If CWD in humans is found to be contagious and transmissible among humans, as it is in cervids [57], the spread of the disease within humans might become endemic.
Transmission of cervid prions to humanized mice demonstrates the zoonotic potential of CWD
Acta Neuropathol 144, 767–784 (2022). https://doi.org/10.1007/s00401-022-02482-9
Published
22 August 2022
https://link.springer.com/article/10.1007/s00401-022-02482-9
Transmission of cervid prions to humanized mice demonstrates the zoonotic potential of CWD
Samia Hannaoui1 · Irina Zemlyankina1 · Sheng Chun Chang1 · Maria Immaculata Arifn1 · Vincent Béringue2 · Debbie McKenzie3 · Hermann M. Schatzl1 · Sabine Gilch1
Received: 24 May 2022 / Revised: 5 August 2022 / Accepted: 7 August 2022
© The Author(s) 2022
Abstract
Prions cause infectious and fatal neurodegenerative diseases in mammals. Chronic wasting disease (CWD), a prion disease of cervids, spreads efficiently among wild and farmed animals. Potential transmission to humans of CWD is a growing concern due to its increasing prevalence. Here, we provide evidence for a zoonotic potential of CWD prions, and its probable signature using mice expressing human prion protein (PrP) as an infection model. Inoculation of these mice with deer CWD isolates resulted in atypical clinical manifestation with prion seeding activity and efficient transmissible infectivity in the brain and, remarkably, in feces, but without classical neuropathological or Western blot appearances of prion diseases. Intriguingly, the protease-resistant PrP in the brain resembled that found in a familial human prion disease and was transmissible upon second passage. Our results suggest that CWD might infect humans, although the transmission barrier is likely higher compared to zoonotic transmission of cattle prions. Notably, our data suggest a different clinical presentation, prion signature, and tissue tropism, which causes challenges for detection by current diagnostic assays. Furthermore, the presence of infectious prions in feces is concerning because if this occurs in humans, it is a source for human-to-human transmission. These findings have strong implications for public health and CWD management.
Keywords Chronic wasting disease · CWD · Zoonotic potential · Prion strains · Zoonotic prions
HIGHLIGHTS OF THIS STUDY
================================
Our results suggest that CWD might infect humans, although the transmission barrier is likely higher compared to zoonotic transmission of cattle prions. Notably, our data suggest a different clinical presentation, prion signature, and tissue tropism, which causes challenges for detection by current diagnostic assays. Furthermore, the presence of infectious prions in feces is concerning because if this occurs in humans, it is a source for human-to-human transmission. These findings have strong implications for public health and CWD management.
In this study, we evaluated the zoonotic potential of CWD using a transgenic mouse model overexpressing human M129-PrPC (tg650 [12]). We inoculated tg650 mice intracerebrally with two deer CWD isolates, Wisc-1 and 116AG [22, 23, 27, 29]. We demonstrate that this transgenic line was susceptible to infection with CWD prions and displayed a distinct leading clinical sign, an atypical PrPSc signature and unusual fecal shedding of infectious prions. Importantly, these prions generated by the human PrP transgenic mice were transmissible upon passage. Our results are the first evidence of a zoonotic risk of CWD when using one of the most common CWD strains, Wisc-1/CWD1 for infection. We demonstrated in a human transgenic mouse model that the species barrier for transmission of CWD to humans is not absolute. The fact that its signature was not typical raises the questions whether CWD would manifest in humans as a subclinical infection, whether it would arise through direct or indirect transmission including an intermediate host, or a silent to uncovered human-to-human transmission, and whether current detection techniques will be suffcient to unveil its presence.
Our findings strongly suggest that CWD should be regarded as an actual public health risk. Here, we use humanized mice to show that CWD prions can cross the species barrier to humans, and remarkably, infectious prions can be excreted in feces.
Our results indicate that if CWD crosses the species-barrier to humans, it is unlikely to resemble the most common forms of human prion diseases with respect to clinical signs, tissue tropism and PrPSc signature. For instance, PrPSc in variable protease-sensitive prionopathy (VPSPr), a sporadic form of human prion disease, and in the genetic form Gerstmann-Sträussler-Scheinker syndrome (GSS) is defined by an atypical PK-resistant PrPSc fragment that is non-glycosylated and truncated at both C- and N-termini, with a molecular weight between 6 and 8 kDa [24, 44–46]. These biochemical features are unique and distinctive from PrPSc (PrP27-30) found in most other human or animal prion disease. The atypical PrPSc signature detected in brain homogenate of tg650 mice #321 (1st passage) and #3063 (2nd passage), and the 7–8 kDa fragment (Figs. 2, 4) are very similar to that of GSS, both in terms of migration profile and the N-terminal cleavage site.
CWD in humans might remain subclinical but with PrPSc deposits in the brain with an unusual morphology that does not resemble the patterns usually seen in different prion diseases (e.g., mouse #328; Fig. 3), clinical with untraceable abnormal PrP (e.g., mouse #327) but still transmissible and uncovered upon subsequent passage (e.g., mouse #3063; Fig. 4), or prions have other reservoirs than the usual ones, hence the presence of infectivity in feces (e.g., mouse #327) suggesting a potential for human-to-human transmission and a real iatrogenic risk that might be unrecognizable.
“suggesting a potential for human-to-human transmission and a real iatrogenic risk that might be unrecognizable.”
=================================
Supplementary Information The online version contains supplementary material available at
https://doi.org/10.1007/s00401-022-02482-9
snip...see full text;
https://link.springer.com/article/10.1007/s00401-022-02482-9
https://link.springer.com/content/pdf/10.1007/s00401-022-02482-9.pdf
EFSA Panel on Biological Hazards (BIOHAZ) Antonia Ricci Ana Allende Declan Bolton Marianne Chemaly Robert Davies Pablo Salvador Fernández Escámez ...
First published: 17 January 2018 https://doi.org/10.2903/j.efsa.2018.5132
also, see;
8. Even though human TSE‐exposure risk through consumption of game from European cervids can be assumed to be minor, if at all existing, no final conclusion can be drawn due to the overall lack of scientific data.
***> In particular the US data do not clearly exclude the possibility of human (sporadic or familial) TSE development due to consumption of venison.
The Working Group thus recognizes a potential risk to consumers if a TSE would be present in European cervids. It might be prudent considering appropriate measures to reduce such a risk, e.g. excluding tissues such as CNS and lymphoid tissues from the human food chain, which would greatly reduce any potential risk for consumers.. However, it is stressed that currently, no data regarding a risk of TSE infections from cervid products are available.
https://efsa.onlinelibrary.wiley.com/doi/full/10.2903/j.efsa.2018.5132
2004
Jeff Swann and his Mom, cwd link... sporadic CJD?, CBC NEWS Jeff Schwan sCJD, CWD, and Professor Aguzzi on BSE and sporadic CJD
????: CBCnews
https://histodb15.usz.ch/pages/Images/videos/video-004/video-004.html
2004
April 22, 2004, 10:30 AM CDT Guests: Patrick Singh, Terry Schwan, Janet Skarbek, Bill Fielding (BEGIN VIDEOTAPE) ANNOUNCER: DEBORAH NORVILLE TONIGHT.
https://www.nbcnews.com/id/wbna4806886
1997-11-10: Panorama - The British disease
https://histodb15.usz.ch/pages/Images/videos/video-009/video-009.html
TUESDAY, MAY 11, 2021
A Unique Presentation of Creutzfeldt-Jakob Disease in a Patient Consuming Deer Antler Velvet <
Conclusion
We believe that our patient’s case of CJD is highly suspicious for cervid etiology given the circumstances of the case as well as the strong evidence of plausibility reported in published literature. This is the first known case of CJD in a patient who had consumed deer antler velvet. Despite the confirmed diagnosis of CJD, a causal relationship between the patient’s disease and his consumption of deer antler velvet cannot be definitively concluded.
Supplemental data including molecular tissue sample analysis and autopsy findings could yield further supporting evidence. Given this patient’s clinical resemblance to CBD and the known histological similarities of CBD with CJD, clinicians should consider both diseases in the differential diagnosis of patients with a similarly esoteric presentation. Regardless of the origin of this patient’s disease, it is clear that the potential for prion transmission from cervids to humans should be further investigated by the academic community with considerable urgency.
https://thescipub.com/pdf/ajidsp.2021.43.48.pdf
''We believe that our patient’s case of CJD is highly suspicious for cervid etiology given the circumstances of the case as well as the strong evidence of plausibility reported in published literature. This is the first known case of CJD in a patient who had consumed deer antler velvet. Despite the confirmed diagnosis of CJD, a causal relationship between the patient’s disease and his consumption of deer antler velvet cannot be definitively concluded.''
https://thescipub.com/pdf/ajidsp.2021.43.48.pdf
CREUTZFELDT JAKOB DISEASE: A Unique Presentation of Creutzfeldt-Jakob Disease in a Patient Consuming Deer Antler Velvet
i was warning England and the BSE Inquiry about just this, way back in 1998, and was ask to supply information to the BSE Inquiry. for anyone that might be interested, see;
Singeltary submission to the BSE Inquiry on CJD and Nutritional Supplements 1998
ABOUT that deer antler spray and CWD TSE PRION... I have been screaming this since my neighbors mom died from cjd, and she had been taking a supplement that contained bovine brain, bovine eyeball, and other SRMs specified risk materials, the most high risk for mad cow disease. just saying...
I made a submission to the BSE Inquiry long ago during the BSE Inquiry days, and they seemed pretty interested.
Sender: "Patricia Cantos"
To: "Terry S Singeltary Sr. (E-mail)"
Subject: Your submission to the Inquiry
Date: Fri, 3 Jul 1998 10:10:05 +0100 3 July 1998
Mr Terry S Singeltary Sr. E-Mail: Flounder at wt.net Ref: E2979
Dear Mr Singeltary, Thank you for your E-mail message of the 30th of June 1998 providing the Inquiry with your further comments. Thank you for offering to provide the Inquiry with any test results on the nutritional supplements your mother was taking before she died. As requested I am sending you our general Information Pack and a copy of the Chairman's letter. Please contact me if your system cannot read the attachments. Regarding your question, the Inquiry is looking into many aspects of the scientific evidence on BSE and nvCJD.
I would refer you to the transcripts of evidence we have already heard which are found on our internet site at ;
http://www.bse.org.uk.
Could you please provide the Inquiry with a copy of the press article you refer to in your e-mail? If not an approximate date for the article so that we can locate it? In the meantime, thank you for you comments. Please do not hesitate to contact me on... snip...end...tss
everyone I tell this too gets it screwed up...MY MOTHER WAS NOT TAKING THOSE SUPPLEMENTS IPLEX (that I ever knew of). this was my neighbors mother that died exactly one year previously and to the day of sporadic CJD that was diagnosed as Alzheimer’s at first. my mother died exactly a year later from the Heidenhain Variant of Creutzfeldt Jakob Disease hvCJD, and exceedingly rare strains of the ever growing sporadic CJD’s. both cases confirmed. ...
kind regards, terry
TSEs i.e. mad cow disease's BSE/BASE and NUTRITIONAL SUPPLEMENTS IPLEX, mad by standard process; vacuum dried bovine BRAIN, bone meal, bovine EYE, veal Bone, bovine liver powder, bovine adrenal, vacuum dried bovine kidney, and vacuum dried porcine stomach. also; what about potential mad cow candy bars ? see their potential mad cow candy bar list too... THESE are just a few of MANY of just this ONE COMPANY...TSS
https://wwwnc.cdc.gov/eid/article/15/5/08-1458_article
http://www.spiegel.de/spiegel/print/d-18578755.html
http://chronic-wasting-disease.blogspot.com/2009/03/chronic-wasting-disease-prions-in-elk.html
http://creutzfeldt-jakob-disease.blogspot.com/2013/11/large-cjd-tse-prion-potential-case.html
http://tseac.blogspot.com/2011/02/usa-50-state-bse-mad-cow-conference.html
Two Hunters from the Same Lodge Afflicted with Sporadic CJD: Is Chronic Wasting Disease to Blame?
(P7-13.002) Jonathan Trout, Matthew Roberts, Michel Tabet, Eithan Kotkowski, and Sarah HornAUTHORS INFO & AFFILIATIONS April 9, 2024 issue 102 (17_supplement_1) https://doi.org/10.1212/WNL.0000000000204407
Abstract Publication History Information & Authors Metrics & Citations Share Abstract
Objective:
This study presents a cluster of Creutzfeldt-Jakob disease (CJD) cases after exposure to chronic wasting disease (CWD)-infected deer, suggestive of potential prion transmission from CWD-infected deer to humans.
Background:
CJD is a rapidly progressive central nervous system disorder caused by misfolded prion proteins. CWD, a prion disease prevalent in North American deer, has raised concerns due to its possible link to CJD. Although no conclusive evidence of cross-species prion transmission exists, vigilance for such cases is crucial for public health.
Design/Methods:
Not applicable.
Results:
In 2022, a 72-year-old man with a history of consuming meat from a CWD-infected deer population presented with rapid-onset confusion and aggression. His friend, who had also eaten venison from the same deer population, recently died of CJD, raising concerns about a potential link between CWD and human prion disease. Despite aggressive symptomatic treatment of seizures and agitation, the patient’s condition deteriorated and he died within a month of initial presentation. The diagnosis was confirmed postmortem as sporadic CJD with homozygous methionine at codon 129 (sCJDMM1). The patient’s history, including a similar case in his social group, suggests a possible novel animal-to-human transmission of CWD. Based on non-human primate and mouse models, cross-species transmission of CJD is plausible. Due to the challenge of distinguishing sCJDMM1 from CWD without detailed prion protein characterization, it is not possible to definitively rule out CWD in these cases. Although causation remains unproven, this cluster emphasizes the need for further investigation into the potential risks of consuming CWD-infected deer and its implications for public health.
Conclusions:
Clusters of sporadic CJD cases may occur in regions with CWD-confirmed deer populations, hinting at potential cross-species prion transmission. Surveillance and further research are essential to better understand this possible association.
Disclosure: Mr. Trout has nothing to disclose. Dr. Roberts has nothing to disclose. Dr. Tabet has nothing to disclose. Dr. Kotkowski has nothing to disclose. Dr. Horn has received personal compensation in the range of $500-$4,999 for serving as a Consultant for Cala Trio. The institution of Dr. Horn has received research support from Alzheimer's Association.
https://www.neurology.org/doi/abs/10.1212/WNL.0000000000204407
THURSDAY, JUNE 12, 2025
***> Redefining the zoonotic potential of chronic wasting disease Singeltary Review
https://chronic-wasting-disease.blogspot.com/2025/06/redefining-zoonotic-potential-of.html
TUESDAY, JULY 08, 2025
Addressing chronic wasting disease in Korean farms: topsoil removal and 2N NaOH treatment before cervid restocking
https://chronic-wasting-disease.blogspot.com/2025/07/addressing-chronic-wasting-disease-in.html
THURSDAY, JULY 10, 2025
Distribution of chronic wasting disease (CWD) prions in tissues from experimentally exposed coyotes (Canis latrans) Published: July 9, 2025
https://chronic-wasting-disease.blogspot.com/2025/07/distribution-of-chronic-wasting-disease.html
THURSDAY, JULY 10, 2025
Modelling the effect of genotype (PRNP) linked to susceptibility, infection duration and prion shedding on chronic wasting disease dynamics of cervids
https://chronic-wasting-disease.blogspot.com/2025/07/modelling-effect-of-genotype-prnp.html
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.
https://prion2023.org/wp-content/uploads/2023/10/Meeting-book-final-version2.pdf
https://chronic-wasting-disease.blogspot.com/2023/10/transmission-of-chronic-wasting-disease.html
MONDAY, AUGUST 4, 2025
Canadian 2021 H-type Bovine Spongiform Encephalopathy case associated with a novel E211K polymorphism in prion protein gene novel E211K polymorphism in prion protein gene, Singeltary Review
https://bovineprp.blogspot.com/2025/08/canadian-2021-h-type-bovine-spongiform.html
***> Creutzfeldt Jakob Disease CJD TSE Prion Cases Increasing March 2025
https://creutzfeldt-jakob-disease.blogspot.com/2025/03/creutzfeldt-jakob-disease-tse-prion.html
***> Creutzfeldt Jakob Disease CJD, BSE, CWD, TSE, Prion, December 14, 2024 Annual Update
https://creutzfeldt-jakob-disease.blogspot.com/2024/12/creutzfeldt-jacob-disease-cjd-bse-cwd.html
https://creutzfeldt-jakob-disease.blogspot.com/
Iatrogenic Transmissible Spongiform Encephalopathy TSE Prion, CWD, our worst nightmare, what if?
https://itseprion.blogspot.com/
So, this is what we leave our children and grandchildren?
terry
posted by Terry S. Singeltary Sr. at
4:11 PM
0 Comments
