Texas Game Wardens Uncover Illegal White-Tailed Deer Smuggling Operation
Texas Game Wardens Uncover Illegal White-Tailed Deer Smuggling Operation
Feb. 6, 2025
Media Contact: TPWD News, Business Hours, 512-389-8030 News
AUSTIN – Texas Game Wardens have concluded an investigation that led to the arrest and conviction of two individuals involved in illegally moving captive white-tailed deer.
A South Texas deer breeder and his business partner were caught attempting to smuggle seven deer from a licensed deer breeding facility in East Texas through Montgomery County to Brazoria and Duval counties, where they intended to illegally release the deer into the wild on private property.
The case unfolded when a Montgomery County Game Warden conducted a traffic stop and discovered the illegally possessed deer being transported without required documentation or identification. Further investigation uncovered significant violations of Texas Parks and Wildlife Department (TPWD) statutes and regulations, as well as criminal and traffic violations. Both individuals were arrested and booked into Montgomery County Jail.
The deer breeder faced 41 total charges: one traffic code violation, 11 penal code violations and 29 deer breeder violations under the Texas Administrative Code and Parks and Wildlife Code. He pleaded guilty to three penal code violations and 29 deer breeder violations. His business partner was charged with two penal code violations and 28 deer breeder violations, of which he was convicted.
Both men were convicted on multiple counts of violations committed with the intent to circumvent disease monitoring and testing requirements. Violations included failure to conduct ante-mortem chronic wasting disease (CWD) testing, failure to obtain valid transfer permits, removal of breeder deer without required identification and illegal possession of live game animals. Combined, they were convicted of a total of 57 deer breeder violations, one alcohol and two dangerous drug violations. They received a total $12,060 in fines.
This case underscores the commitment of TPWD and Texas Game Wardens to protecting the state’s natural resources and upholding wildlife regulations. The possession and movement of deer are regulated, among other reasons, to mitigate the spread of diseases like CWD and to ensure the health of both captive and free-ranging wildlife populations. Anytime a white-tailed deer leaves a breeding facility, it must be uniquely and permanently identified, no matter its age. Breeder deer that have not been properly identified or have had their identification hidden or illegally changed or removed are commonly referred to as “ghost deer.”
“Flagrant violations, such as intentionally transferring deer without identifiers, hinder Texas’ ability to identify the source of a deer in the event of a disease detection,” said Col. Ronald VanderRoest, TPWD Law Enforcement Director. “This creates the potential for negative impacts to the health of both captive and free ranging deer populations, the deer breeder industry, landowners, hunters and Texas’ outdoor and rural based economies, where white-tailed deer hunting has a $9.6 billion annual economic contribution.”
"This case perfectly illustrates the dedication and hard work of Texas Game Wardens by not only uncovering the defendant’s illegal operation but also highlighting the importance of protecting our state’s natural resources," said Ann Kuykendall, Montgomery County assistant district attorney. "This prosecution sends a clear message: those who knowingly violate these laws will be held accountable.”
With no available site for return, their unknown disease status and the unacceptable risks associated with their release into the wild, the “ghost deer” in this case were euthanized in accordance with protocols related to disease testing. The type of activity the suspects were participating in led TPWD to believe a heightened risk of disease exposure existed. Fortunately, the epidemiological investigation revealed no detection of CWD.
About Texas Game Wardens
Texas Game Wardens, within the Law Enforcement Division of the Texas Parks and Wildlife Department, are responsible for enforcing laws related to the conservation and management of natural resources and public safety through community-based law enforcement. Their mission is to provide hunting, fishing and outdoor recreation opportunities for the use and enjoyment of present and future generations. Additionally, they play a crucial role in search and rescue operations during natural disasters, exemplifying their commitment to protecting both the environment and the people of Texas.
Great Job Texas Game Warders, TPWD, et al!
Texas CWD Surveillance Positives Tracking Page is outdated, last figures i have were 1061 Confirmed CWD Cases to date;
Texas CWD total by calendar years
Counties where CWD Exposed Deer were Released
Number of CWD Exposed Deer Released by County
CWD Status Captive Herds
Chronic Wasting Disease CWD TSE Prion can travel upwards to 50MPH or faster, they call it, 'Trucking CWD'.
"In summary, given the volume of tourists, hunters and servicemen moving between GB and North America, the probability of at least one person travelling to/from a CWD affected area and, in doing so, contaminating their clothing, footwear and/or equipment prior to arriving in GB is greater than negligible."
In summary, in endemic areas, there is a medium probability that the soil and surrounding environment is contaminated with CWD prions and in a bioavailable form. In rural areas where CWD has not been reported and deer are present, there is a greater than negligible risk the soil is contaminated with CWD prion.
snip.....
In summary, given the volume of tourists, hunters and servicemen moving between GB and North America, the probability of at least one person travelling to/from a CWD affected area and, in doing so, contaminating their clothing, footwear and/or equipment prior to arriving in GB is greater than negligible... For deer hunters, specifically, the risk is likely to be greater given the increased contact with deer and their environment. However, there is significant uncertainty associated with these estimates.
Friday, December 14, 2012
DEFRA U.K. What is the risk of Chronic Wasting Disease CWD being introduced into Great Britain? A Qualitative Risk Assessment October 2012
snip.....
In the USA, under the Food and Drug Administration's BSE Feed Regulation (21 CFR 589.2000) most material (exceptions include milk, tallow, and gelatin) from deer and elk is prohibited for use in feed for ruminant animals. With regards to feed for non-ruminant animals, under FDA law, CWD positive deer may not be used for any animal feed or feed ingredients. For elk and deer considered at high risk for CWD, the FDA recommends that these animals do not enter the animal feed system. However, this recommendation is guidance and not a requirement by law. Animals considered at high risk for CWD include:
1) animals from areas declared to be endemic for CWD and/or to be CWD eradication zones and
2) deer and elk that at some time during the 60-month period prior to slaughter were in a captive herd that contained a CWD-positive animal.
Therefore, in the USA, materials from cervids other than CWD positive animals may be used in animal feed and feed ingredients for non-ruminants.
The amount of animal PAP that is of deer and/or elk origin imported from the USA to GB can not be determined, however, as it is not specified in TRACES.
It may constitute a small percentage of the 8412 kilos of non-fish origin processed animal proteins that were imported from US into GB in 2011.
Overall, therefore, it is considered there is a __greater than negligible risk___ that (nonruminant) animal feed and pet food containing deer and/or elk protein is imported into GB.
There is uncertainty associated with this estimate given the lack of data on the amount of deer and/or elk protein possibly being imported in these products.
snip.....
36% in 2007 (Almberg et al., 2011). In such areas, population declines of deer of up to 30 to 50% have been observed (Almberg et al., 2011). In areas of Colorado, the prevalence can be as high as 30% (EFSA, 2011). The clinical signs of CWD in affected adults are weight loss and behavioural changes that can span weeks or months (Williams, 2005). In addition, signs might include excessive salivation, behavioural alterations including a fixed stare and changes in interaction with other animals in the herd, and an altered stance (Williams, 2005). These signs are indistinguishable from cervids experimentally infected with bovine spongiform encephalopathy (BSE). Given this, if CWD was to be introduced into countries with BSE such as GB, for example, infected deer populations would need to be tested to differentiate if they were infected with CWD or BSE to minimise the risk of BSE entering the human food-chain via affected venison.
snip..... The rate of transmission of CWD has been reported to be as high as 30% and can approach 100% among captive animals in endemic areas (Safar et al., 2008).
snip.....
In summary, in endemic areas, there is a medium probability that the soil and surrounding environment is contaminated with CWD prions and in a bioavailable form. In rural areas where CWD has not been reported and deer are present, there is a greater than negligible risk the soil is contaminated with CWD prion.
snip.....
In summary, given the volume of tourists, hunters and servicemen moving between GB and North America, the probability of at least one person travelling to/from a CWD affected area and, in doing so, contaminating their clothing, footwear and/or equipment prior to arriving in GB is greater than negligible... For deer hunters, specifically, the risk is likely to be greater given the increased contact with deer and their environment. However, there is significant uncertainty associated with these estimates.
snip.....
Therefore, it is considered that farmed and park deer may have a higher probability of exposure to CWD transferred to the environment than wild deer given the restricted habitat range and higher frequency of contact with tourists and returning GB residents.
snip.....
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.
Abstract
Chronic wasting disease (CWD) is a highly contagious prion disease occurring in free-ranging and farmed cervids. CWD continues to spread uncontrolled across North America, and cases continue to be detected almost every year in the Republic of Korea. CWD-infected animals contaminate the soil by releasing infectious prions through their excreta, and shed prions accumulate and remain infectious in the soil for years. Given that the upper soil levels can become contaminated with prions and serve as infectivity reservoirs facilitating horizontal transmission of CWD, the ability to detect prions in the soil is needed for monitoring and managing CWD spread. Using the protein misfolding cyclic amplification (PMCA) technique, we investigated whether prions could be amplified and detected in farm soil experimentally exposed to CWD-infected brain homogenate as well as in the soil of CWD-affected farms. From each soil sample, we performed 10 serial extractions and used these 10 extracts as PMCA templates. Here, we show that prion seeding activity was detected in extracts from farm soil following 4 years of incubation with CWD-infected brain homogenate. More importantly, 13 of 38 soil samples collected from six CWD-affected farms displayed prion seeding activity, with at least one soil sample in each farm being PMCA positive. Mouse bioassays confirmed the presence of prion infectivity in the soil extracts in which PMCA seeding activity was detected. This is the first report describing the successful detection of prions in soil collected from CWD-affected farms, suggesting that PMCA conducted on serial soil extracts is a sensitive means for prion detection in CWD-contaminated soil. IMPORTANCE
Chronic wasting disease (CWD) is a highly contagious prion disease affecting free-ranging and farmed cervids. CWD continues to spread uncontrollably across North America, and multiple cases are detected annually in the Republic of Korea. Prions shed from CWD-infected animals remain infectious in the soil for years, serving as infectivity reservoirs that facilitate horizontal transmission of the disease. Therefore, the ability to detect CWD prions in soil is crucial for monitoring and managing the spread of the disease. In this study, we have demonstrated for the first time that prions in the soil of CWD-affected farms can be reliably detected using a combination of serial soil extraction and a prion amplification technique. Our data, in which at least one soil sample tested positive for CWD in each of the six CWD-affected farms analyzed, suggest that the approach employed in this study is a sensitive method for prion detection in CWD-contaminated soil.
"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
Aims: Free-ranging animals afflicted with transmissible spongiform encephalopathies frequently shed infectious prions into the broader environment. The quintessential example is chronic wasting disease, the TSE of cervids. Over the course of the disease, an infected animal will shed infectious prions in blood, urine, saliva, and feces. Upon death, the total prion load interred in the animal’s tissues will be deposited wherever the animal falls. This contamination creates substantial risk to naïve animals, and likely contributes to disease spread. Identification and quantification of prions at contamination hotspots is essential for any attempt at mitigation of environmental transmission.
Materials and Methods: Surfactant extraction of soils followed by precipitation yields a sample that is amenable to analysis by real-time quaking induced conversion. However, differences in extraction yield are apparent depending on the properties of the matrix from which the prions are being extracted, principally soil clay content.
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
=====end
Prion 2023 Abstracts
Detection of chronic wasting disease prions in the farm soil of the Republic of Korea
We show that prions can be detected in farm soil up to 4 years after being experimentally contaminated with a range of concentrations of CWD-affected brain homogenate
IMPORTANCE
Chronic wasting disease (CWD) is a highly contagious prion disease affecting free-ranging and farmed cervids. CWD continues to spread uncontrollably across North America, and multiple cases are detected annually in the Republic of Korea. Prions shed from CWD-infected animals remain infectious in the soil for years, serving as infectivity reservoirs that facilitate horizontal transmission of the disease. Therefore, the ability to detect CWD prions in soil is crucial for monitoring and managing the spread of the disease. In this study, we have demonstrated for the first time that prions in the soil of CWD-affected farms can be reliably detected using a combination of serial soil extraction and a prion amplification technique. Our data, in which at least one soil sample tested positive for CWD in each of the six CWD-affected farms analyzed, suggest that the approach employed in this study is a sensitive method for prion detection in CWD-contaminated soil.
Snip…
In this study, we investigated whether CWD prions in the soil of Korean cervid farms can be detected through the combination of repeated extraction and PMCA analysis of these serial extracts. We show that prions can be detected in farm soil up to 4 years after being experimentally contaminated with a range of concentrations of CWD-affected brain homogenate. We also demonstrate that prion seeding activity is present in the soil of the Korean cervid farms in which CWD-positive animals have been identified. Our data suggest that the approach described in this study can be used to detect prions with high sensitivity in CWD-contaminated soil.
Artificial mineral sites that pre-date endemic chronic wasting disease become prion hotspots
The detection of PrPCWD in soils at attractant sites within an endemic CWD zone significantly advances our understanding of environmental PrPCWD accumulation dynamics, providing valuable information for advancing adaptive CWD management approaches.
Chronic wasting disease detection in environmental and biological samples from a taxidermy site
Aims: In this study, we evaluated the presence of infectious prions in a taxidermy facility believed to be exposed to CWD. Detection was performed using the Protein Misfolding Cyclic Amplification (PMCA) technique in biological and inert environmental samples.
Methods: We collected biological and environmental samples (plants, soils, insects, excreta, and others) from a taxidermy facility, and we tested these samples using the PMCA technique. In addition, we swabbed different surfaces possibly exposed to CWD-infected animals. For the PMCA reaction, we directly used a swab piece or 10 µL of 20% w/v homogenized samples.
Results: The PMCA analysis demonstrated CWD seeding activity in some of the components of this facility, including insects involved in head processing, soils, and a trash dumpster.
Conclusions: Different areas of this property were used for various taxidermy procedures. We were able to detect the presence of prions in i) soils that were in contact with the heads of dead animals, ii) insects involved in the cleaning of skulls, and iii) an empty dumpster where animal carcasses were previously placed. This is the first report demonstrating that swabbing is a helpful method to screen for prion infectivity on surfaces potentially contaminated with CWD. These findings are relevant as this swabbing and amplification strategy may be used to evaluate the disease status of other free-ranging and captive settings where there is a concern for CWD transmissions, such as at feeders and water troughs with CWD-exposed properties. This approach could have substantial implications for free-ranging cervid surveillance as well as in epidemiological investigations of CWD.
Prion 2022 Conference abstracts: pushing the boundaries
***> Infectious agent of sheep scrapie may persist in the environment for at least 16 years
***> Nine of these recurrences occurred 14–21 years after culling, apparently as the result of environmental contamination, but outside entry could not always be absolutely excluded.
JOURNAL OF GENERAL VIROLOGY Volume 87, Issue 12
Infectious agent of sheep scrapie may persist in the environment for at least 16 years Free
Rapid recontamination of a farm building occurs after attempted prion removal
First published: 19 January 2019 https://doi.org/10.1136/vr.105054
The data illustrates the difficulty in decontaminating farm buildings from scrapie, and demonstrates the likely contribution of farm dust to the recontamination of these environments to levels that are capable of causing disease. snip...
This study clearly demonstrates the difficulty in removing scrapie infectivity from the farm environment. Practical and effective prion decontamination methods are still urgently required for decontamination of scrapie infectivity from farms that have had cases of scrapie and this is particularly relevant for scrapie positive goatherds, which currently have limited genetic resistance to scrapie within commercial breeds.24 This is very likely to have parallels with control efforts for CWD in cervids.
***>This is very likely to have parallels with control efforts for CWD in cervids.
THE tse prion aka mad cow type disease is not your normal pathogen.
The TSE prion disease survives ashing to 600 degrees celsius, that’s around 1112 degrees farenheit.
you cannot cook the TSE prion disease out of meat.
you can take the ash and mix it with saline and inject that ash into a mouse, and the mouse will go down with TSE.
Prion Infected Meat-and-Bone Meal Is Still Infectious after Biodiesel Production as well.
the TSE prion agent also survives Simulated Wastewater Treatment Processes.
IN fact, you should also know that the TSE Prion agent will survive in the environment for years, if not decades.
you can bury it and it will not go away.
The TSE agent is capable of infected your water table i.e. Detection of protease-resistant cervid prion protein in water from a CWD-endemic area.
it’s not your ordinary pathogen you can just cook it out and be done
New studies on the heat resistance of hamster-adapted scrapie agent: Threshold survival after ashing at 600°C suggests an inorganic template of replication
Prion Infected Meat-and-Bone Meal Is Still Infectious after Biodiesel Production
Detection of protease-resistant cervid prion protein in water from a CWD-endemic area
Prions in Waterways
A Quantitative Assessment of the Amount of Prion Diverted to Category 1 Materials and Wastewater During Processing
Rapid assessment of bovine spongiform encephalopathy prion inactivation by heat treatment in yellow grease produced in the industrial manufacturing process of meat and bone meals
THURSDAY, FEBRUARY 28, 2019
BSE infectivity survives burial for five years with only limited spread
Durkin: Wisconsin DNR says CWD sinking deer herds in disease-endemic areas
PATRICK DURKIN Outdoors Columnist
CWD culprits
According to Wisconsin DNR research, a healthy buck’s annual survival chances are 69% in southwestern Wisconsin, while a CWD-infected buck has only a 17% chance of being alive a year later. The 3-year-old Richland County buck, left, tested positive for CWD in 2020. The yearling buck skeleton couldn’t be tested for CWD, but was found in 2021 on the same infected farm.
If you’re seeing too few deer in southwestern Wisconsin for your hunting or viewing pleasure, it’s time to accept the obvious reason.
The culprit is chronic wasting disease, the always fatal sickness whose infectious prions now kill more female deer in highly contaminated areas than hunters kill with bullets and arrows. Roughly speaking, that’s much of Iowa, Sauk and Richland counties, and western Dane County.
The Department of Natural Resources confirmed that fact for the first time Jan. 22 when releasing the latest findings of its long-running $5 million study into how CWD affects deer populations. The study found that once CWD infects 29% or more of an area’s female deer, the herd starts declining as more deer die each year than reproduction replaces.
As Jasmine Batten, supervisor of the DNR’s wildlife health section, emailed her staff, “CWD mortality has largely replaced antlerless harvest as the primary driver of the deer population’s trajectory in the CWD endemic area (west of Madison).”
Neither Batten nor the agency rushed to that conclusion. The DNR launched its “Southwest Wisconsin CWD, Deer and Predator Study” in autumn 2016, and then caught, tested and fitted GPS collars to 1,249 animals over the next four years across northeastern Grant County, northern Iowa County and northwestern Dane County.
The agency then monitored those 810 adult deer, 323 fawns, 69 coyotes and 47 bobcats to learn where they lived, when and where they moved, and when/how they died. When a collar signaled the animal’s death, researchers hurried in, hoping to learn what killed it.
The DNR says this ongoing study is the “largest and most comprehensive deer research project ever undertaken in Wisconsin.” Although the data will provide more findings, this fact won’t change under current hunting regulations: Other than two-legged hunters targeting bucks, CWD has no deer-killing equal once it’s widespread.
“We can now say it’s not EHD (epizootic hemorrhagic disease), it’s not coyotes, it’s not bobcats, and it’s not earn-a-buck regulations from 15 years ago that are causing the herd declines we’re seeing,” said Dan Storm, the study’s chief researcher. “CWD is the cause, and we have solid evidence to back it up. This is what’s going on, and so let’s proceed with what to do about it.”
The study found that a healthy, uninfected doe age 1 or older is twice as likely to be alive a year later than a CWD-infected doe. Specifically, a healthy doe’s annual survival chances are 83%, while an infected doe’s chances are 41%. CWD-infected bucks age 1 and older fare four times worse than healthy bucks. Specifically, a healthy buck’s annual survival chances are 69%, while an infected buck’s chances are 17%.
CWD-infected deer more often get hit by vehicles, shot by hunters, and killed by starvation and pneumonia. In fact, 51% of dead deer necropsied in the study had pneumonia. Further, preliminary summaries show end-stage wasting — which includes infections and starvation — is the No. 1 cause of death (57%) for CWD-positive adult does. Sick does more often reach that stage than sick bucks, given hunters’ focus on antlers after lawmakers eliminated earn-a-buck regulations in 2011.
So yes, contrary to endemic social-media nonsense, CWD kills deer. In fact, as the cause of death for 57% of infected does, it outpaces the next three causes: hunting, coyotes and unknown causes. For healthy, CWD-free does, hunting and vehicle collisions caused 75% of deaths. Bacterial infections, coyotes and unknown causes killed the other 25%.
Fawn survival in the study was high enough to sustain deer herds. Of the study’s 323 fawns, the annual percentage reaching age 1 ranged from 43% to 51%. Fawn survival rates across North America in recent decades range from 10% to 90%.
The study found that predators (mainly coyotes, but also bobcats) kill about 31% of the unnual fawn “crop,” while diseases like pneumonia, EHD and enterocolitis (inflamed intestines) take 6%; hunters, 4%; human-related causes (vehicles, pet dogs and haying/mowing/brush-hogging), 4%; and starvation, 3%.
Skeptics, of course, ignore CWD while blaming predators and EHD for declining herds. Though they clamor for other hunters to quit shooting antlerless deer, no legitimate deer biologist supports passivity.
“We already did that and look how it went,” Storm said. “Before we lost earn-a-buck (in 2011), hunters dropped Iowa County’s deer herd below 20,000. After earn-a-buck, the herd took 7%, 10% and 12% annual increases until 2020. That herd should have kept growing, but it didn’t. CWD is pulling it down and boxing it in.”
The DNR’s annual post-hunt population estimates show Iowa County’s herd rose 51.3% from 16,900 in 2011 to 25,566, the 2018-2020 three-year average. The herd has since fallen 15.25% to 21,666, the 2021-2023 three-year average.
Bryan Richards, CWD project leader at the USDA’s National Wildlife Health Center in Madison, said backing off would backfire. “You won’t recover a population by letting CWD run its course,” Richards said. “When you try to stockpile deer by not shooting, you protect sick deer, too. Contamination worsens and the healthy proportion of the herd declines. Shooting removes sick deer from the herd sooner than CWD will. They’ll spread fewer prions over time, and you’ll probably shoot them before CWD reaches its worst stages for shedding prions.”
Storm put it this way: “The more CWD you have in your area, the more the herd will decline.” Which areas already exceed 29% infection rates for adult does? The latest DNR data from a year ago shows southeastern Richland County on the edge at 27%, northwestern Iowa County at 35%, and the Devil’s Lake area in eastern Sauk County at 34%.
Further, CWD testing of hunter-killed deer in autumn 2024 shows overall (bucks and does) detection rates at or above 29% in six townships (6-mile by 6-mile areas) in Columbia County, three townships in Dane County, eight townships in Iowa County, 11 townships in Richland County, and 15 townships in Sauk County.
How low will deer populations drop where CWD is endemic? Storm said CWD won’t exterminate deer, but no one can predict how it will affect specific valleys, woodlands or watersheds. CWD has spread at varying rates in different Wisconsin habitats, and appears to have leveled off at high infection rates in some areas while still rising and spreading in others.
The disease has so far been verified in wild deer in 48 of Wisconsin’s 72 counties, even though testing has been totally voluntary for years. During the 2024 hunting season, 1,755 more deer tested positive for CWD across the state, a record 10.4% detection rate despite the least amount of samples (16,939) volunteered since 2017. Richland County hunters provided the most samples, 1,335, in 2024, and 444 (33.4%) had CWD.
Southwest Wisconsin CWD, Deer and Predator Study
key takeaways ;
CWD substantially reduces deer survival rates and suppresses population growth.
Where CWD prevalence is high, deer populations are likely declining.
If CWD continues to spread, it will eventually impact deer populations elsewhere.
The effectiveness of harvest for limiting wildlife disease: Insights from 20 years of chronic wasting disease in Wyoming
Wynne E. Moss, Justin Binfet, L. Embere Hall, Samantha E. Allen, William H. Edwards, Jessica E. Jennings-Gaines, Paul C. Cross
First published: 21 January 2025
5 or 6 years quarantine is NOT LONG ENOUGH FOR CWD TSE PRION, imo.
QUARANTINE NEEDS TO BE 21 YEARS FOR CWD TSE PRION !
FRIDAY, APRIL 30, 2021
Should Property Evaluations Contain Scrapie, CWD, TSE PRION Environmental Contamination of the land?
***> 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
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.
Colorado CWD
To: Members of the Colorado Parks and Wildlife Commission
From: Dan Prenzlow, Director
Date: April 22, 2022
Subject: Chronic Wasting Disease Update for Parks and Wildlife Commission
Chronic wasting disease, a fatal neurological disease found in deer, elk, and moose, is well established in herds throughout much of Colorado. We have detected CWD in 40 of our 54 deer herds, 17 of 42 elk herds, and 2 of 9 moose herds. Disease prevalence (percent infected) is highest in deer and lowest in moose. This disease is always fatal and animals die from the disease within about 2-2.5 years of infection. CWD infection shortens the lifespan of infected animals. If infection rates become too high, CWD can affect a herd’s ability to sustain itself.
CWD, Seeing is believing Videos Part 1, Part 2
The below video series is provided by the Mississippi State Deer Lab with many contributing Partners. Click image to
find all videos in the series.
Seeing is Believing is a two part documentary film that hopes to increase awareness about chornic wasting disease (CWD). Although most hunters and landowners may never witness a clinically ill animal in an area with high CWD prevalence, the documentary demonstrates how CWD is certainly present, explains why it is a major concern, and how stakeholders are key to managing the disease. Colorado Parks and Wildlife (CPW) developed these films in partnership with the Wyoming Game and Fish Department, Chronic Wasting Disease Alliance, Colorado Department of Agriculture, Animal and Plant Health Inspection Service, and multiple private conservation organizations.
CWD Seeing is believing part 1 Video
CWD Seeing is believing part 2 Video
The Rocky Mountain Elk Foundation - CWD Informational Video
Cwd videos
How many deer die from cwd? that dog don't hunt no more...
15 minute mark video shows sick deer with cwd, and this deer DIED FROM CWD, IT'S DOCUMENTED, commentator says ''so if anyone every tells you, that a deer has never died from CWD, think of this picture, because the Wisconsin Veterinary Lab told us, what when they looked at her sample under a microscope, she was the hottest animal they had ever seen, and that's in terms of the fluorescents that comes off the slide when the look at it, so, a lot of Prion in her system.''
''SCENTS AND LURES, we know that the Prion is shed in urine, and essentially the production of these products is unregulated, we have no idea, you can't tell where they come from, what species are in them, how many animals, how they are processed, there is really no rules about them, so we are concerned it is a way to bring the disease into new areas, and have us fighting on multiple fronts, AND there are zero risk synthetic options that are readily available in stores, so we have ask hunters to switch to zero risk options.''
see much more about 2 hours long...
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.''
Texas symposium Cwd
Arkansas Cwd
Wyoming Cwd 2022 test results
CDC CWD TSE Prion Update 2025
KEY POINTS
Chronic wasting disease affects deer, elk and similar animals in the United States and a few other countries.
The disease hasn't been shown to infect people.
However, it might be a risk to people if they have contact with or eat meat from animals infected with CWD.
Prions in Muscles of Cervids with Chronic Wasting Disease, Norway
Volume 31, Number 2—February 2025
Research
Prions in Muscles of Cervids with Chronic Wasting Disease, Norway
Snip…
In summary, the results of our study indicate that prions are widely distributed in peripheral and edible tissues of cervids in Norway, including muscles. This finding highlights the risk of human exposure to small amounts of prions through handling and consuming infected cervids.
Appendix
Volume 31, Number 2—February 2025
Dispatch
Detection of Chronic Wasting Disease Prions in Raw, Processed, and Cooked Elk Meat, Texas, USA
Snip…
CWD prions have been detected in the muscle of both farmed and wild deer (10), and at concentrations relevant to sustain disease transmission (11). CWD prions have also been identified across several cervid species and in multiple tissues, including lymph nodes, spleen, tongue, intestines, adrenal gland, eyes, reproductive tissues, ears, lungs, and liver, among others (12–14). Those findings raise concerns about the safety of ingesting processed meats that contain tissues other than skeletal muscle (15) (Appendix). https://wwwnc.cdc.gov/eid/article/31/2/24-0906-app1.pdf .
In addition, those findings highlight the need for continued vigilance and research on the transmission risks of prion diseases and for development of new preventative and detection measures to ensure the safety of the human food supply.
Snip…
Overall, our study results confirm previous reports describing the presence of CWD prions in elk muscles (13). The data also demonstrated CWD prion persistence in food products even after processing through different procedures, including the addition of salts, spices, and other edible elements. Of note, our data show that exposure to high temperatures used to cook the meat increased the availability of prions for in vitro amplification. Considering the potential implications in food safety and public health, we believe that the findings described in this study warrant further research. Our results suggest that although the elk meat used in this study resisted different manipulations involved in subsequent consumption by humans, their zoonotic potential was limited. Nevertheless, even though no cases of CWD transmission to human have been reported, the potential for human infection is still unclear and continued monitoring for zoonotic potential is warranted.
Volume 31, Number 1—January 2025
Dispatch
Detection of Prions in Wild Pigs (Sus scrofa) from Areas with Reported Chronic Wasting Disease Cases, United States
Abstract
Using a prion amplification assay, we identified prions in tissues from wild pigs (Sus scrofa) living in areas of the United States with variable chronic wasting disease (CWD) epidemiology. Our findings indicate that scavenging swine could play a role in disseminating CWD and could therefore influence its epidemiology, geographic distribution, and interspecies spread.
Detection of chronic wasting disease prions in processed meats
Results: Our results show positive prion detection in all the samples analyzed using deer and elk substrates. Surprisingly, cooked meats displayed increased seeding activities. This data suggests that CWD-prions are available to people even after meats are processed and cooked.
Conclusions: These results suggest CWD prions are accessible to humans through meats, even after processing and cooking. Considering the fact that these samples were collected from already processed specimens, the availability of CWD prions to humans is probably underestimated.
"Our results show positive prion detection in all the samples analyzed using deer and elk substrates. Surprisingly, cooked meats displayed increased seeding activities."
The detection and decontamination of chronic wasting disease prions during venison processing
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
DETECTION OF CHRONIC WASTING DISEASE PRIONS IN PROCESSED MEATS.
In this study, we analyzed different processed meats derived from a pre-clinical, CWD-positive free-ranging elk. Products tested included filets, sausages, boneless steaks, burgers, ham steaks, seasoned chili meats, and spiced meats. CWD-prion presence in these products were assessed by PMCA using deer and elk substrates. Our results show positive prion detection in all products. To confirm the resilience of CWD-prions to traditional cooking methods, we grilled and boiled the meat products and evaluated them for any remnant PMCA seeding activity. Results confirmed the presence of CWD-prions in these meat products suggesting that infectious particles may still be available to people even after cooking. Our results strongly suggest ongoing human exposure to CWD-prions and raise significant concerns of zoonotic transmission through ingestion of CWD contaminated meat products.
***> Products tested included filets, sausages, boneless steaks, burgers, ham steaks, seasoned chili meats, and spiced meats.
***> CWD-prion presence in these products were assessed by PMCA using deer and elk substrates.
***> Our results show positive prion detection in all products.
***> Results confirmed the presence of CWD-prions in these meat products suggesting that infectious particles may still be available to people even after cooking.
***> Our results strongly suggest ongoing human exposure to CWD-prions and raise significant concerns of zoonotic transmission through ingestion of CWD contaminated meat products.
Transmission of prion infectivity from CWD-infected macaque tissues to rodent models demonstrates the zoonotic potential of chronic wasting disease.
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
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Transmission of Cervid Prions to Humanized Mice Demonstrates the Zoonotic Potential of CWD
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.
The finding that infectious PrPSc was shed in fecal material of CWD-infected humanized mice and induced clinical disease, different tropism, and typical three banding pattern-PrPres in bank voles that is transmissible upon second passage is highly concerning for public health. The fact that this biochemical signature in bank voles resembles that of the Wisc-1 original deer isolate and is different from that of bvWisc-1, in the migration profile and the glyco-form-ratio, is valid evidence that these results are not a product of contamination in our study. If CWD in humans is found to be contagious and transmissible among humans, as it is in cervids [57], the spread of the disease within humans might become endemic.
Transmission of cervid prions to humanized mice demonstrates the zoonotic potential of CWD
Acta Neuropathol 144, 767–784 (2022). https://doi.org/10.1007/s00401-022-02482-9
Published
22 August 2022
Fortuitous generation of a zoonotic cervid prion strain
Results: Passage of sCJDMM1 in transgenic mice expressing elk PrP (Tg12) resulted in a “cervidized” CJD strain that we termed CJDElkPrP. We observed 100% transmission of the original CJDElkPrP in transgenic mice expressing human PrP. We passaged CJDElkPrP two more times in the Tg12 mice. We found that such second and third passage CJDElkPrP prions retained 100% transmission rate in the humanized mice, despite that the natural elk CWD isolates and CJDElkPrP share the same elk PrP sequence. In contrast, we and others found zero or poor transmission of natural elk CWD isolates in humanized mice.
Conclusions: Our data indicate that highly zoonotic cervid prion strains are not only possible but also can retain zoonotic potential after serial passages in cervids, suggesting a very significant and serious long-term risk of CWD zoonosis given that the broad and continuing spread of CWD prions will provide fertile grounds for the emergence of zoonotic CWD strains over time.
The finding that infectious PrPSc was shed in fecal material of CWD-infected humanized mice and induced clinical disease, different tropism, and typical three banding pattern-PrPres in bank voles that is transmissible upon second passage is highly concerning for public health. The fact that this biochemical signature in bank voles resembles that of the Wisc-1 original deer isolate and is different from that of bvWisc-1, in the migration profile and the glyco-form-ratio, is valid evidence that these results are not a product of contamination in our study. If CWD in humans is found to be contagious and transmissible among humans, as it is in cervids [57], the spread of the disease within humans might become endemic.
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.
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.
“suggesting a potential for human-to-human transmission and a real iatrogenic risk that might be unrecognizable.”
=================================
Supplementary Information The online version contains supplementary material available at
snip...see full text;
Pigs, CWD, TSE, Prion, and feed, what if?
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
WE NOW KNOW, that CWD will transmit, BY ORAL ROUTES, to cattle, sheep, pigs, Cervid, monkeys, and probably any species, if fed large enough doses of Cwd, and held long enough…so, it is of utmost urgency to update and enhance the old 1997 mad cow feed ban…it’s just science…terry
Drug Administration's BSE Feed Regulation (21 CFR 589.2000) Singeltary Another Request for Update 2023
The infamous 1997 mad cow feed ban i.e. Food and Drug Administration's BSE Feed Regulation (21 CFR 589.2000) most material (exceptions include milk, tallow, and gelatin) from deer and elk is prohibited for use in feed for ruminant animals. With regards to feed for non-ruminant animals, under FDA law, CWD positive deer may not be used for any animal feed or feed ingredients. For elk and deer considered at high risk for CWD, the FDA recommends that these animals do not enter the animal feed system. However, this recommendation is guidance and not a requirement by law.
***>However, this recommendation is guidance and not a requirement by law.
WITH GREAT URGENCY, THE Food and Drug Administration's BSE Feed Regulation (21 CFR 589.2000) MUST BE ENHANCED AND UPDATED TO INCLUDE CERVID, PIGS, AND SHEEP, SINCE RECENT SCIENCE AND TRANSMISSION STUDIES ALL, INCLUDING CATTLE, HAVE SHOWN ORAL TSE PrP TRANSMISSIONS BETWEEN THE SPECIES, AND THIS SHOULD BE DONE WITH THE UTMOST URGENCY…terry
2016
Docket No. FDA-2003-D-0432 (formerly 03D-0186) Use of Material from Deer and Elk in Animal Feed
PUBLIC SUBMISSION
Comment from Terry Singeltary Sr.
Posted by the Food and Drug Administration on May 17, 2016 Comment
Docket No. FDA-2003-D-0432 (formerly 03D-0186) Use of Material from Deer and Elk in Animal Feed Singeltary Submission
WA2 Oral transmission of CWD into Cynomolgus macaques: signs of atypical disease, prion conversion and infectivity in macaques and bio-assayed transgenic mice
Schatzl HM (1, 2), Hannaoui S (1, 2), Cheng Y-C (1, 2), Gilch S (1, 2), Beekes M (3), SchulzSchaeffer W (4), Stahl-Hennig C (5) and Czub S (2, 6)
(1) University of Calgary, Calgary Prion Research Unit, Calgary, Canada (2) University of Calgary, Faculty of Veterinary Medicine, Calgary, Canada, (3) Robert Koch Institute, Berlin, Germany, (4) University of Homburg/Saar, Homburg, Germany, (5) German Primate Center, Goettingen, Germany, (6) Canadian Food Inspection Agency (CFIA), Lethbridge, Canada.
To date, BSE is the only example of interspecies transmission of an animal prion disease into humans. The potential zoonotic transmission of CWD is an alarming issue and was addressed by many groups using a variety of in vitro and in vivo experimental systems. Evidence from these studies indicated a substantial, if not absolute, species barrier, aligning with the absence of epidemiological evidence suggesting transmission into humans. Studies in non-human primates were not conclusive so far, with oral transmission into new-world monkeys and no transmission into old-world monkeys. Our consortium has challenged 18 Cynomolgus macaques with characterized CWD material, focusing on oral transmission with muscle tissue. Some macaques have orally received a total of 5 kg of muscle material over a period of 2 years. After 5-7 years of incubation time some animals showed clinical symptoms indicative of prion disease, and prion neuropathology and PrPSc deposition were found in spinal cord and brain of euthanized animals. PrPSc in immunoblot was weakly detected in some spinal cord materials and various tissues tested positive in RT-QuIC, including lymph node and spleen homogenates. To prove prion infectivity in the macaque tissues, we have intracerebrally inoculated 2 lines of transgenic mice, expressing either elk or human PrP. At least 3 TgElk mice, receiving tissues from 2 different macaques, showed clinical signs of a progressive prion disease and brains were positive in immunoblot and RT-QuIC. Tissues (brain, spinal cord and spleen) from these and preclinical mice are currently tested using various read-outs and by second passage in mice. Transgenic mice expressing human PrP were so far negative for clear clinical prion disease (some mice >300 days p.i.). In parallel, the same macaque materials are inoculated into bank voles. Taken together, there is strong evidence of transmissibility of CWD orally into macaques and from macaque tissues into transgenic mouse models, although with an incomplete attack rate. The clinical and pathological presentation in macaques was mostly atypical, with a strong emphasis on spinal cord pathology. Our ongoing studies will show whether the transmission of CWD into macaques and passage in transgenic mice represents a form of non-adaptive prion amplification, and whether macaque-adapted prions have the potential to infect mice expressing human PrP. The notion that CWD can be transmitted orally into both new-world and old-world non-human primates asks for a careful reevaluation of the zoonotic risk of CWD.
***> The notion that CWD can be transmitted orally into both new-world and old-world non-human primates asks for a careful reevaluation of the zoonotic risk of CWD.
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WA16 Monitoring Potential CWD Transmission to Humans
Belay ED
Centers for Disease Control and Prevention (CDC), National Center for Emerging and Zoonotic Infectious Diseases, Atlanta, GA, USA.
The spread of chronic wasting disease (CWD) in animals has raised concerns about increasing human exposure to the CWD agent via hunting and venison consumption, potentially facilitating CWD transmission to humans. Several studies have explored this possibility, including limited epidemiologic studies, in vitro experiments, and laboratory studies using various types of animal models. Most human exposures to the CWD agent in the United States would be expected to occur in association with deer and elk hunting in CWD-endemic areas. The Centers for Disease Control and Prevention (CDC) collaborated with state health departments in Colorado, Wisconsin, and Wyoming to identify persons at risk of CWD exposure and to monitor their vital status over time. Databases were established of persons who hunted in Colorado and Wyoming and those who reported consumption of venison from deer that later tested positive in Wisconsin. Information from the databases is periodically cross-checked with mortality data to determine the vital status and causes of death for deceased persons. Long-term follow-up of these hunters is needed to assess their risk of development of a prion disease linked to CWD exposure.
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P166 Characterization of CJD strain profiles in venison consumers and non-consumers from Alberta and Saskatchewan
Stephanie Booth (1,2), Lise Lamoureux (1), Debra Sorensen (1), Jennifer L. Myskiw (1,2), Megan Klassen (1,2), Michael Coulthart (3), Valerie Sim (4)
(1) Zoonotic Diseases and Special Pathogens, National Microbiology Laboratory, Public Health Agency of Canada, Winnipeg (2) Department of Medical Microbiology and Infectious Diseases, University of Manitoba, Winnipeg (3) Canadian CJD Surveillance System, Public Health Agency of Canada, Ottawa (4) Division of Neurology, Department of Medicine Centre for Prions and Protein Folding Diseases, University of Alberta, Edmonton.
Chronic wasting disease (CWD) is spreading rapidly through wild cervid populations in the Canadian provinces of Alberta and Saskatchewan. While this has implications for tourism and hunting, there is also concern over possible zoonotic transmission to humans who eat venison from infected deer. Whilst there is no evidence of any human cases of CWD to date, the Canadian CJD Surveillance System (CJDSS) in Canada is staying vigilant. When variant CJD occurred following exposure to BSE, the unique biochemical fingerprint of the pathologic PrP enabled a causal link to be confirmed. However, we cannot be sure what phenotype human CWD prions would present with, or indeed, whether this would be distinct from that see in sporadic CJD. Therefore we are undertaking a systematic analysis of the molecular diversity of CJD cases of individuals who resided in Alberta and Saskatchewan at their time of death comparing venison consumers and non-consumers, using a variety of clinical, imaging, pathological and biochemical markers. Our initial objective is to develop novel biochemical methodologies that will extend the baseline glycoform and genetic polymorphism typing that is already completed by the CJDSS. Firstly, we are reviewing MRI, EEG and pathology information from over 40 cases of CJD to select clinically affected areas for further investigation. Biochemical analysis will include assessment of the levels of protease sensitive and resistant prion protein, glycoform typing using 2D gel electrophoresis, testing seeding capabilities and kinetics of aggregation by quaking-induced conversion, and determining prion oligomer size distributions with asymmetric flow field fractionation with in-line light scattering. Progress and preliminary data will be presented. Ultimately, we intend to further define the relationship between PrP structure and disease phenotype and establish a baseline for the identification of future atypical CJD cases that may arise as a result of exposure to CWD.
=====
Source Prion Conference 2018 Abstracts
http://prionconference.blogspot.com/2018/
Volume 24, Number 8—August 2018
Research Susceptibility of Human Prion Protein to Conversion by Chronic Wasting Disease Prions
Marcelo A. BarriaComments to Author , Adriana Libori, Gordon Mitchell, and Mark W. Head Author affiliations: National CJD Research and Surveillance Unit, University of Edinburgh, Edinburgh, Scotland, UK (M.A. Barria, A. Libori, M.W. Head); National and OIE Reference Laboratory for Scrapie and CWD, Canadian Food Inspection Agency, Ottawa, Ontario, Canada (G. Mitchell)
Abstract Chronic wasting disease (CWD) is a contagious and fatal neurodegenerative disease and a serious animal health issue for deer and elk in North America. The identification of the first cases of CWD among free-ranging reindeer and moose in Europe brings back into focus the unresolved issue of whether CWD can be zoonotic like bovine spongiform encephalopathy. We used a cell-free seeded protein misfolding assay to determine whether CWD prions from elk, white-tailed deer, and reindeer in North America can convert the human prion protein to the disease-associated form. We found that prions can convert, but the efficiency of conversion is affected by polymorphic variation in the cervid and human prion protein genes. In view of the similarity of reindeer, elk, and white-tailed deer in North America to reindeer, red deer, and roe deer, respectively, in Europe, a more comprehensive and thorough assessment of the zoonotic potential of CWD might be warranted.
snip...
The prion hypothesis proposes that direct molecular interaction between PrPSc and PrPC is necessary for conversion and prion replication. Accordingly, polymorphic variants of the PrP of host and agent might play a role in determining compatibility and potential zoonotic risk. In this study, we have examined the capacity of the human PrPC to support in vitro conversion by elk, white-tailed deer, and reindeer CWD PrPSc. Our data confirm that elk CWD prions can convert the human PrPC, at least in vitro, and show that the homologous PRNP polymorphisms at codon 129 and 132 in humans and cervids affect conversion efficiency. Other species affected by CWD, particularly caribou or reindeer, also seem able to convert the human PrP. It will be important to determine whether other polymorphic variants found in other CWD-affected Cervidae or perhaps other factors (17) exert similar effects on the ability to convert human PrP and thus affect their zoonotic potential.
Dr. Barria is a research scientist working at the National CJD Research and Surveillance Unit, University of Edinburgh. His research has focused on understanding the molecular basis of a group of fatal neurologic disorders called prion diseases.
Volume 30, Number 12—December 2024
Research Letter
Zoonotic Potential of Chronic Wasting Disease After Adaptation in Intermediate Species
Tomás BarrioComments to Author , Sylvie L. Benestad, Jean-Yves Douet, Alvina Huor, Séverine Lugan, Naïma Aron, Hervé Cassard, Juan Carlos Espinosa, Alicia Otero, Rosa Bolea, Juan María Torres, and Olivier Andréolett
Author affiliation: Unité 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, Toulouse, France (T. Barrio, J.-Y. Douet, A. Huor, S. Lugan, N. Aron, H. Cassard, O. Andréoletti); Norwegian Veterinary Institute, Ås, Norway (S.L. Benestad); Consejo Superior de Investigaciones Científicas, Madrid, Spain (J.C. Espinosa, J.M. Torres); Universidad de Zaragoza, Zaragoza, Spain (A. Otero, R. Bolea)
Abstract
Chronic wasting disease (CWD) is an emerging disease in Europe. We report an increase in interspecies transmission capacity and zoonotic potential of a moose CWD isolate from Europe after passage in an ovine prion protein–expressing host. Those results indicated some CWD prions could acquire enhanced zoonotic properties following adaptation in an intermediate species.
Chronic wasting disease (CWD) is a highly contagious prion disease affecting members of the Cervidae family. CWD is widely spread across North America, where it endangers the survival of free-ranging cervid populations. In Europe, CWD was reported in a reindeer (Rangifer tarandus tarandus) from Norway in 2016 (1). Since 2016, several cases have been reported in Norway, Sweden, and Finland in multiple species, including reindeer, red deer (Cervus elaphus), and moose (Alces alces) (2).
Whereas CWD strains circulating in North America exhibit some uniformity (3), the cases found in Europe are more variable. Transmission into rodent models has revealed multiple CWD strains that are apparently different than strains in North America, and moose cases in Norway have demonstrated biochemical patterns distinct from previous cases in Europe (4). We characterized the interspecies transmission potential of 1 moose CWD isolate from Norway (Norwegian Veterinary Institute identification no. 16–60-P153) (4) by intracerebral injection of mouse models expressing the normal prion protein (PrPC) sequences from several species (Figure, panel A).
We anesthetized and inoculated 6–10-week-old mice with 2 mg of equivalent tissue (20 µL of 10% brain homogenate) in the right parietal lobe. We monitored the inoculated animals daily and humanely euthanized animals at the onset of clinical signs or after the preestablished endpoint of 700 days postinfection (dpi). We conducted a systematic proteinase K–resistant prion protein (PrPres) detection by using Western blot.
Inoculation of the original CWD isolate did not cause the propagation of detectable prions in Tg340 mice expressing methionine (TgMet) or Tg361 mice expressing valine (TgVal) at position 129 of human PrPC. We did not observe PrPres in brain tissue or disease occurrence in bovine PrPC-expressing mice (BoTg110) after intracerebral inoculation of the CWD isolate (Table; Figure, panel B).
We inoculated the CWD isolate in Tg338 mice, which overexpress ovine PrP ≈8 times. At 612 and 717 dpi (Table), 2 of 12 animals showed clinical signs of prion disease and we detected PrPres accumulation in their brain tissue (Figure, panel B). Of note, the 2 animals showed different PrPres banding patterns, with the nonglycosylated band migrating to 19 kDa in the first mouse and to 21 kDa in the second. Both PrPres-containing brains transmitted disease with 100% efficacy to second-passage Tg338mice, which contained 21-kDa PrPres in their brains (Figure, panel B). A third passage resulted in the incubation period shortening (95 ± 5 dpi). Our observations are consistent with a progressive adaptation of the moose CWD prion to the ovine-PrPC expressing model and suggest moose CWD prions in Europe may have an intrinsic capability to propagate in ovine species with the VRQ genotype.
We next determined whether adaptation of this moose CWD agent to Tg338 altered its capacity to cross species barriers. For that purpose, we inoculated Tg338-adapted moose CWD prions (passaged twice in Tg338) to the same panel of PrPC-expressing mice models. Inoculation of the Tg338-adapted isolate to BoTg110 resulted in 100% disease transmission that showed a banding pattern and intermediate molecular weight from 19–21 kDa (Figure, panel C; Appendix Figure) and an incubation period of 431 ± 32 dpi (Table), which suggested the lack of a major transmission barrier. In addition, 1 of 8 inoculated TgMet mice showed clinical signs at 561 dpi (Table). PrPres in the brain of that mouse was revealed by a mixed 19 + 21 kDa banding pattern (Figure, panel C). A second passage in TgMet is underway.
Inoculation of TgVal resulted in efficient transmission (5/6 animals); the mean incubation period was 483 ± 35 dpi (Table) and accumulation was 21 kDa PrPres (Figure, panel C). On second passage, transmission was 100% and we observed a shorter incubation period (311 ± 12 dpi).
The incubation periods and PrPres biochemical profiles of the CWD prions that propagated in the TgMet and TgVal mice greatly differed from those observed in mice inoculated with the most prevalent human prion strains or with classic bovine spongiform encephalopathy (BSE), sheep-adapted BSE, or Tg338-adapted c-BSE (Table; Figure, panel D). Those results might suggest this CWD-derived prion strain differs from other strains documented in those models. Further investigation is necessary.
The evolution of moose CWD zoonotic potential after its passage in an ovine PrPC-expressing host is reminiscent of the well-documented altered capacities of the c-BSE agent to cross the human species barrier after adaptation in sheep and goats (9). The codon 129-dependent response to infection of humanized mice with Tg338-adapted CWD is also compatible with studies demonstrating the role of this polymorphism in susceptibility to prions (10).
In summary, our results demonstrate the potential capacity of some CWD agents to transmit to sheep or other farmed animals. Our results highlight the need to experimentally assess and monitor this transmission risk under natural exposure conditions. In addition, the dramatic changes of the zoonotic capacity of the CWD isolate we documented from Europe clearly demonstrate the risk adaptation and propagation of cervid prions into farmed animals represents. Although additional studies are needed to characterize these emerging agents, our findings have major potential implications for animal and public health.
Dr. Barrio is a research scientist with Institut National de Recherche pour l’Agriculture, l’Alimentation et l’Environnement. His research interests include animal and human prion diseases and other neurodegenerative disorders linked to misfolded proteins.
Prion 2017 Conference Abstracts
First evidence of intracranial and peroral transmission of Chronic Wasting Disease (CWD) into Cynomolgus macaques: a work in progress
Stefanie Czub1, Walter Schulz-Schaeffer2, Christiane Stahl-Hennig3, Michael Beekes4, Hermann Schaetzl5 and Dirk Motzkus6 1 University of Calgary Faculty of Veterinary Medicine/Canadian Food Inspection Agency; 2Universitatsklinikum des Saarlandes und Medizinische Fakultat der Universitat des Saarlandes; 3 Deutsches Primaten Zentrum/Goettingen; 4 Robert-Koch-Institut Berlin; 5 University of Calgary Faculty of Veterinary Medicine; 6 presently: Boehringer Ingelheim Veterinary Research Center; previously: Deutsches Primaten Zentrum/Goettingen
This is a progress report of a project which started in 2009.
21 cynomolgus macaques were challenged with characterized CWD material from white-tailed deer (WTD) or elk by intracerebral (ic), oral, and skin exposure routes. Additional blood transfusion experiments are supposed to assess the CWD contamination risk of human blood product. Challenge materials originated from symptomatic cervids for ic, skin scarification and partially per oral routes (WTD brain). Challenge material for feeding of muscle derived from preclinical WTD and from preclinical macaques for blood transfusion experiments. We have confirmed that the CWD challenge material contained at least two different CWD agents (brain material) as well as CWD prions in muscle-associated nerves. Here we present first data on a group of animals either challenged ic with steel wires or per orally and sacrificed with incubation times ranging from 4.5 to 6.9 years at postmortem. Three animals displayed signs of mild clinical disease, including anxiety, apathy, ataxia and/or tremor. In four animals wasting was observed, two of those had confirmed diabetes. All animals have variable signs of prion neuropathology in spinal cords and brains and by supersensitive IHC, reaction was detected in spinal cord segments of all animals. Protein misfolding cyclic amplification (PMCA), real-time quaking-induced conversion (RT-QuiC) and PET-blot assays to further substantiate these findings are on the way, as well as bioassays in bank voles and transgenic mice. At present, a total of 10 animals are sacrificed and read-outs are ongoing. Preclinical incubation of the remaining macaques covers a range from 6.4 to 7.10 years. Based on the species barrier and an incubation time of > 5 years for BSE in macaques and about 10 years for scrapie in macaques, we expected an onset of clinical disease beyond 6 years post inoculation.
PRION 2017 DECIPHERING NEURODEGENERATIVE DISORDERS ABSTRACTS REFERENCE
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.
SATURDAY, FEBRUARY 23, 2019
Chronic Wasting Disease CWD TSE Prion and THE FEAST 2003 CDC an updated review of the science 2019
TUESDAY, NOVEMBER 04, 2014
Six-year follow-up of a point-source exposure to CWD contaminated venison in an Upstate New York community: risk behaviours and health outcomes 2005–2011 Authors, though, acknowledged the study was limited in geography and sample size and so it couldn't draw a conclusion about the risk to humans. They recommended more study. Dr. Ermias Belay was the report's principal author but he said New York and Oneida County officials are following the proper course by not launching a study. "There's really nothing to monitor presently. No one's sick," Belay said, noting the disease's incubation period in deer and elk is measured in years. "
Transmission Studies Mule deer transmissions of CWD were by intracerebral inoculation and compared with natural cases {the following was written but with a single line marked through it ''first passage (by this route)}....TSS resulted in a more rapidly progressive clinical disease with repeated episodes of synocopy ending in coma. One control animal became affected, it is believed through contamination of inoculum (?saline). Further CWD transmissions were carried out by Dick Marsh into ferret, mink and squirrel monkey. Transmission occurred in ALL of these species with the shortest incubation period in the ferret.
snip....
Prion Infectivity in Fat of Deer with Chronic Wasting Disease▿
Brent Race#, Kimberly Meade-White#, Richard Race and Bruce Chesebro* + Author Affiliations In mice, prion infectivity was recently detected in fat. Since ruminant fat is consumed by humans and fed to animals, we determined infectivity titers in fat from two CWD-infected deer. Deer fat devoid of muscle contained low levels of CWD infectivity and might be a risk factor for prion infection of other species.
http://jvi.asm.org/content/83/18/9608.full Prions in Skeletal Muscles of Deer with Chronic Wasting Disease Here bioassays in transgenic mice expressing cervid prion protein revealed the presence of infectious prions in skeletal muscles of CWD-infected deer, demonstrating that humans consuming or handling meat from CWD-infected deer are at risk to prion exposure.
*** 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
spontaneous = 325,650 hits
key word here is 'reported'. science has shown that CWD in humans will look like sporadic CJD.
SO, how can one assume that CWD has not already transmitted to humans? they can't, and it's as simple as that. from all recorded science to date, CWD has already transmitted to humans, and it's being misdiagnosed as sporadic CJD. ...terry
*** LOOKING FOR CWD IN HUMANS AS nvCJD or as an ATYPICAL CJD, LOOKING IN ALL THE WRONG PLACES $$$ ***
> However, to date, no CWD infections have been reported in people. key word here is ‘reported’. science has shown that CWD in humans will look like sporadic CJD. SO, how can one assume that CWD has not already transmitted to humans? they can’t, and it’s as simple as that. from all recorded science to date, CWD has already transmitted to humans, and it’s being misdiagnosed as sporadic CJD. …terry
*** LOOKING FOR CWD IN HUMANS AS nvCJD or as an ATYPICAL CJD, LOOKING IN ALL THE WRONG PLACES $$$ ***
*** These results would seem to suggest that CWD does indeed have zoonotic potential, at least as judged by the compatibility of CWD prions and their human PrPC target. Furthermore, extrapolation from this simple in vitro assay suggests that if zoonotic CWD occurred, it would most likely effect those of the PRNP codon 129-MM genotype and that the PrPres type would be similar to that found in the most common subtype of sCJD (MM1).***
CWD TSE PRION AND ZOONOTIC, ZOONOSIS, FACTORS
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@ References:
Dear Terry,
An excellent piece of review as this literature is desperately 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
====
''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...see full text;
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
1997-11-10: Panorama - The British disease
***Moreover, sporadic disease has never been observed in breeding colonies or primate research laboratories, most notably among hundreds of animals over several decades of study at the National Institutes of Health25, and in nearly twenty older animals continuously housed in our own facility.***
Even if the prevailing view is that sporadic CJD is due to the spontaneous formation of CJD prions, it remains possible that its apparent sporadic nature may, at least in part, result from our limited capacity to identify an environmental origin.
Prion Conference 2023
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.
"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
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.
"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
Cattle with the EK211 PRNP polymorphism are susceptible to the H-type bovine spongiform encephalopathy agent from either E211K or wild type donors after oronasal inoculation
Justin J. Greenleea, Eric D. Cassmanna, S. Jo Moorea,b, and M. Heather West Greenleec
aVirus and Prion Research Unit, National Animal Disease Center, ARS, United States Department of Agriculture, Ames, IA, USA; bOak Ridge Institute for Science and Education (ORISE), U.S. Department of Energy, Oak Ridge, TN, US; cDepartment of Biomedical Sciences, Iowa State University College of Veterinary Medicine, Ames, IA, US
Aims: In 2006, a case of H-type bovine spongiform encephalopathy (H-BSE) was reported in a cow with a previously unreported prion protein polymorphism (E211K). The E211K polymorphism is heritable and homologous to the E200K mutation in humans that is the most frequent PRNP mutation associated with familial Creutzfeldt-Jakob disease. Although the prevalence of the E211K polymorphism is low, cattle carrying the K211 allele develop H-type BSE with a rapid onset after experimental inoculation by the intracranial route. The purpose of this study was to investigate whether the agents of H-type BSE or H-type BSE associated with the E211K polymorphism transmit to wild type cattle or cattle with the K211 allele after oronasal exposure.
Material and Methods: Wild type (EE211) or heterozygous (EK211) cattle were oronasally inoculated with the H-BSE agent from either the US 2004 case (wild type donor; n = 3) or from the US 2006 case with the E211K polymorphism (n = 4). Cattle were observed daily throughout the course of the experiment for the development of clinical signs. When signs were noted, animals were euthanized and necropsied. Cattle were confirmed positive for abnormal BSE prions by enzyme immunoassay (EIA; Idexx HerdChek BSE Ag Test), anti-PrP immunohistochemistry (IHC) on brainstem, and microscopic examination for vacuolation.
Results: Three-out-of-four (75%) calves with the EK211 genotype developed clinical signs of H-BSE including inattentiveness, loss of body condition, weakness, ataxia, and muscle fasciculations and were euthanized. Two of the positive EK211 steers received H-BSE US 2004 inoculum (Incubation Period (IP): 59.3 and 72.3 months) while the other positive steer received the E211K H-BSE inoculum (IP: 49.7 months). EIA confirmed that abundant misfolded protein (O.D. 2.57–4.0) in the brainstem, and IHC demonstrated PrPScthroughout the brain. All wild type recipient cattle and a single EK211 steer remained asymptomatic for the duration of the experiment (approximately 7 years post-inoculation) and no abnormal prion protein was detected in these cattle by EIA.
Conclusions: This study demonstrates that the H-type BSE agent is transmissible by the oronasal route. Cattle with the EK211 genotype are oronasally susceptible to small doses of the H-BSE agent from either EK211 or EE211 (wild type) donors. Wild-type EE211 cattle remained asymptomatic for the duration of the experiment with this small dose (0.1 g) of inoculum. These results reinforce the need for ongoing surveillance for classical and atypical BSE to minimize the risk of potentially infectious tissues entering the animal or human food chains.
Funded by: US Department of Agriculture
***>However, this recommendation is guidance and not a requirement by law.
THIS MUST CHANGE ASAP!
“For elk and deer considered at high risk for CWD, the FDA recommends that these animals do not enter the animal feed system. However, this recommendation is guidance and not a requirement by law.”
Friday, December 14, 2012
DEFRA U.K. What is the risk of Chronic Wasting Disease CWD being introduced into Great Britain? A Qualitative Risk Assessment October 2012
snip.....
In the USA, under the Food and Drug Administration's BSE Feed Regulation (21 CFR 589.2000) most material (exceptions include milk, tallow, and gelatin) from deer and elk is prohibited for use in feed for ruminant animals. With regards to feed for non-ruminant animals, under FDA law, CWD positive deer may not be used for any animal feed or feed ingredients. For elk and deer considered at high risk for CWD, the FDA recommends that these animals do not enter the animal feed system. However, this recommendation is guidance and not a requirement by law. Animals considered at high risk for CWD include:
1) animals from areas declared to be endemic for CWD and/or to be CWD eradication zones and
2) deer and elk that at some time during the 60-month period prior to slaughter were in a captive herd that contained a CWD-positive animal.
Therefore, in the USA, materials from cervids other than CWD positive animals may be used in animal feed and feed ingredients for non-ruminants.
The amount of animal PAP that is of deer and/or elk origin imported from the USA to GB can not be determined, however, as it is not specified in TRACES.
It may constitute a small percentage of the 8412 kilos of non-fish origin processed animal proteins that were imported from US into GB in 2011.
Overall, therefore, it is considered there is a __greater than negligible risk___ that (nonruminant) animal feed and pet food containing deer and/or elk protein is imported into GB.
There is uncertainty associated with this estimate given the lack of data on the amount of deer and/or elk protein possibly being imported in these products.
snip.....
PLoS One. 2020 Aug 20;15(8):e0237410. doi: 10.1371/journal.pone.0237410. eCollection 2020.
Very low oral exposure to prions of brain or saliva origin can transmit chronic wasting disease
Nathaniel D Denkers 1 , Clare E Hoover 2 , Kristen A Davenport 3 , Davin M Henderson 1 , Erin E McNulty 1 , Amy V Nalls 1 , Candace K Mathiason 1 , Edward A Hoover 1
PMID: 32817706 PMCID: PMC7446902 DOI: 10.1371/journal.pone.0237410
Abstract
The minimum infectious dose required to induce CWD infection in cervids remains unknown, as does whether peripherally shed prions and/or multiple low dose exposures are important factors in CWD transmission. With the goal of better understand CWD infection in nature, we studied oral exposures of deer to very low doses of CWD prions and also examined whether the frequency of exposure or prion source may influence infection and pathogenesis. We orally inoculated white-tailed deer with either single or multiple divided doses of prions of brain or saliva origin and monitored infection by serial longitudinal tissue biopsies spanning over two years. We report that oral exposure to as little as 300 nanograms (ng) of CWD-positive brain or to saliva containing seeding activity equivalent to 300 ng of CWD-positive brain, were sufficient to transmit CWD disease. This was true whether the inoculum was administered as a single bolus or divided as three weekly 100 ng exposures. However, when the 300 ng total dose was apportioned as 10, 30 ng doses delivered over 12 weeks, no infection occurred. While low-dose exposures to prions of brain or saliva origin prolonged the time from inoculation to first detection of infection, once infection was established, we observed no differences in disease pathogenesis. These studies suggest that the CWD minimum infectious dose approximates 100 to 300 ng CWD-positive brain (or saliva equivalent), and that CWD infection appears to conform more with a threshold than a cumulative dose dynamic.
Snip…
Discussion
As CWD expands across North America and Scandinavia, how this disease is transmitted so efficiently remains unclear, given the low concentrations of prions shed in secretions and excretions [13, 14]. The present studies demonstrated that a single oral exposure to as little as 300nmg of CWD-positive brain or equivalent saliva can initiate infection in 100% of exposed white-tailed deer. However, distributing this dose as 10, 30 ng exposures failed to induce infection. Overall, these results suggest that the minimum oral infectious exposure approaches 100 to 300 ng of CWD-positive brain equivalent. These dynamics also invite speculation as to whether potential infection co-factors, such as particle binding [46, 47] or compromises in mucosal integrity may influence infection susceptibility, as suggested from two studies in rodent models [48, 49].
PRION 2023 CONTINUED;
Prion 2023 Experimental Oronasal Inoculation of the Chronic Wasting Disease Agent into White Tailed Deer
Author list: Sarah Zurbuchena,b , S. Jo Moorea,b , Jifeng Biana , Eric D. Cassmanna , and Justin J. Greenleea . a. Virus and Prion Research Unit, National Animal Disease Center, ARS, United States Department of Agriculture, Ames, IA, US b. Oak Ridge Institute for Science and Education (ORISE), U.S. Department of Energy, Oak Ridge, TN, United States
Aims: The purpose of this experiment was to determine whether white-tailed deer (WTD) are susceptible to inoculation of chronic wasting disease (CWD) via oronasal exposure.
Materials and methods: Six male, neutered WTD were oronasally inoculated with brainstem material (10% w/v) from a CWD-positive wild-type WTD. The genotypes of five inoculated deer were Q95/G96 (wild-type). One inoculated deer was homozygous S at codon 96 (96SS). Cervidized (Tg12; M132 elk PrP) mice were inoculated with 1% w/v brainstem homogenate from either a 96GG WTD (n=10) or the 96SS WTD (n=10).
Results: All deer developed characteristic clinical signs of CWD including weight loss, regurgitation, and ataxia. The 96SS individual had a prolonged disease course and incubation period compared to the other deer. Western blots of the brainstem on all deer yielded similar molecular profiles. All deer had widespread lymphoid distribution of PrPCWD and neuropathologic lesions associated with transmissible spongiform encephalopathies. Both groups of mice had a 100% attack rate and developed clinical signs, including loss of body condition, ataxia, and loss of righting reflex. Mice inoculated with material from the 96SS deer had a significantly shorter incubation period than mice inoculated with material from 96GG deer (Welch two sample T-test, P<0.05). Serial dilutions of each inocula suggests that differences in incubation period were not due to a greater concentration of PrPCWD in the 96SS inoculum. Molecular profiles from western blot of brain homogenates from mice appeared similar regardless of inoculum and appear similar to those of deer used for inoculum.
Conclusions: This study characterizes the lesions and clinical course of CWD in WTD inoculated in a similar manner to natural conditions. It supports previous findings that 96SS deer have a prolonged disease course. Further, it describes a first pass of inoculum from a 96SS deer in cervidized mice which shortened the incubation period.
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, analysis, decision to publish, or preparation of the manuscript.
Acknowledgement: We thank Ami Frank and Kevin Hassall for their technical contributions to this project.
=====end
PRION 2023 CONTINUED;
Texas Chronic Wasting Disease CWD TSE Prion
TEXAS CHRONIC WASTING DISEASE CWD TSE PRION UPDATE DECEMBER 2024
i have lost count, and the TPWD et al CWD Tracker page has NOT been updated since May 30, 2024.
THE October increase of 132 more cases to 1008 total CWD Cases to date, was an updated cwd report i got from TPWD et al via request, although that increase has yet to be added to the total cwd tally, so i am confused...terry
THURSDAY, MAY 30, 2024
Texas TAHC TPWD Confirm 132 More Cases of CWD TSE PrP 795 Positive To Date
TUESDAY, OCTOBER 01, 2024
Texas TAHC TPWD Confirm 213 More Cases of CWD TSE PrP 1008 Positive To Date
SUMMARY MINUTES OF THE 422 nd COMMISSION MEETING Texas Animal Health Commission
November 12, 2024
• Chronic Wasting Disease (CWD): There have been seven positive breeding facilities since January 1, 2024. Dr. Jessica Monday, TAHC State Epidemiologist, will give an update under Agenda Item #9.
Chronic Wasting Disease:
o 103 Positive Deer
o Six Breeder Deer facilities with fifteen positive deer
o 2024 Medina County Facility – HCP Breeder Facility
▪ Suspect sample collected July 22, 2024 and confirmed July 29th via post-mortem sampling
▪ Trace-out to 2023 positive herd
▪ Herd visit completed, seeking depopulation
o There were 245 traces closed from 2021, 23 for 2022, 209 for 2023, and 54 for 2024
SUMMARY MINUTES OF THE 421 st COMMISSION MEETING Texas Animal Health Commission
July 16, 2024
▪ Chronic Wasting Disease (CWD): Positive breeding facilities since January 1, 2024: Five CWD Positive / Trace Herd Update: Dr. Trey James, (TAHC Field Epidemiologist) will give an update under Agenda Item #9
snip...
• Chronic Wasting Disease:
o 5 Positive Breeder Facilities with 11 Positive Deer
o 2024 Zavala County Facility – 5 th Year HCP Breeder Facility
▪ Suspect sample collected April 11th, 2024 and confirmed April 24th via post-mortem sampling
▪ Trace-out to Frio County #2 positive breeder facility
▪ Thirty-five traces: 29 trace outs and 6 trace ins
▪ Pending a herd visit
o 2024 Trinity County Facility – HCP Certified Breeder Facility
▪ Suspect sample collected on May 31st and confirmed June 6th via postmortem sampling
▪ Tier and trace connections to 2021 and 2023 positive facilities
▪ 14 traces; 6 trace outs and 8 trace-in
▪ Pending herd visit
o 2024 Sutton County Facility – HCP Certified Breeder Facility
▪ Suspect sample collected June 11th, and confirmed June 26th via postmortem sampling
▪ No prior trace history
▪ Adjacent breeder herd on shared premises and under same ownership has tier and trace connections to 2021 and 2023 positive herds
▪ 51 traces: 21 trace outs and 30 trace ins
o There were 239 traces closed from 2021, 23 for 2022, 204 for 2023, and 41 for 2024
OFFICIAL MINUTES OF THE 420th COMMISSION MEETING Texas Animal Health Commission
April 30, 2024
• Chronic Wasting Disease (CWD):
Summary Minutes of the 420th Commission Meeting – 4/30/2024
3 Positive breeding facilities in 2024
CWD Positive / Trace Herd Update: Dr. Trey James, (Acting State Epidemiologist) will give update under Agenda Item # 10
snip...
• Chronic Wasting Disease:
o 5th year Real County Breeder Facility suspended due to non-compliance
Suspect sample collected March 11th, 2024 and confirmed March 25th via post-mortem sampling. The positive sample was banked and animal was not reported deceased for two months before being submitted to the lab for regulatory testing
Two additional positives since initial detection
Fifty-seven traces; 44 trace outs and 13 trace-in
o 5th Year Zavala County Breeder Facility had suspect sample collected on April 11th and confirmed April 24th.
It was a trace out to Frio County positive breeder facility
35 traces; 29 trace outs and 6 trace-in
Summary Minutes of the 420th Commission Meeting – 4/30/2024
o There were 239 traces closed in 2021, 22 in 2022, and 193 in 2023
OFFICIAL MINUTES OF THE 419th COMMISSION MEETING Texas Animal Health Commission
January 23, 2024
• Chronic Wasting Disease (CWD):
5th Virtual Chronic Wasting Disease Stakeholder and Tribal Nations Update, January 8- 11, 2024
Texas – 5- Cooperative Agreement Reports
o 2 – TAHC – Helped secure funding
- Dr. Chris Seabury TAMU – Accurate Genomic Predictions for CWD in U.S. Elk
- Bud Dinges DVM TAHC – Evaluating Long Range Low Energy Ear Tags for Tracking Whitetailed Deer “Released” from CWD Positive Deer Breeding Facility into a Hunting Enclosure
o 3 – TPWD – Helped secure funding – presented by J Hunter Reed DVM TWPD
CWD Positive / Trace Herd Update: Dr. Jessie Monday, State Epidemiologist will give update under Agenda Item # 10
snip...
Cervidae: Chronic Wasting Disease
• 40 positive deer in 2023
Chronic Wasting Disease Detected in Kerr County Deer Breeding Facility Oct. 31, 2024
TPWD CWD Tracker page still not updated;
TUESDAY, OCTOBER 01, 2024
Texas TAHC TPWD Confirm 213 More Cases of CWD TSE PrP 1008 Positive To Date
Texas TAHC TPWD Confirm 132 More Cases of CWD TSE PrP 795 Positive To Date
Friday, August 16, 2024
TPWD Chronic Wasting Disease (CWD) Detection and Response Rules – Recommended Adoption of New Surveillance Zones August 22, 2024
Friday, August 02, 2024
TPWD Chronic Wasting Disease Detected in Medina County Deer Breeding Fifth Facility
Chronic Wasting Disease Detected in Sutton County Deer Breeding Facility, marking the second facility where CWD has been detected in the county
June 27, 2024
Media Contact: TPWD News, Business Hours, 512-389-8030
AUSTIN — Texas Parks and Wildlife Department (TPWD) received confirmation of one case of Chronic Wasting Disease (CWD) in a Sutton County deer breeding facility, marking the second facility where CWD has been detected in the county, located in the Edward Plateau region of Texas.
A two-year-old female white-tailed deer tested positive using postmortem testing conducted to meet CWD surveillance requirements for the facility. Texas A&M Veterinary Medical Diagnostic Laboratory (TVMDL) initially analyzed the samples, and the National Veterinary Services Laboratory in Iowa confirmed the CWD detection.
CWD has an incubation period that can span years, so the first indication of the disease in a herd is often found through routine surveillance testing rather than observed clinical signs. Early detection and proactive monitoring improve the state’s response time to the detection of CWD and can greatly reduce the risk of further disease spread. TPWD reminds all deer breeders of requirements to report mortalities within seven days of detection and submit CWD test samples within seven days of collection.
CWD is a fatal neurological disease found in certain cervids including deer, elk, moose and other members of the deer family. This slow, progressive disease may not produce visible signs in susceptible species for several years after infection. As the disease process continues, animals with CWD may show changes in behavior and appearance. Clinical signs may include progressive weight loss, stumbling or tremors with a lack of coordination, loss of appetite, teeth grinding, abnormal head posture and/or drooping ears, and excessive thirst, salivation or urination.
In Texas, the disease was first discovered in 2012 in free-ranging mule deer along a remote area of the Hueco Mountains near the Texas-New Mexico border. CWD has since been detected in Texas captive and free-ranging cervids, including white-tailed deer, mule deer, red deer and elk.
For more information on previous detections in Texas, surveillance and containment zones, movement restrictions, and CWD best management practices for hunters and landowners, visit TPWD’s CWD page.
TAHC Chronic Wasting Disease Detected in Trinity County Deer Breeding Facility
For Immediate Release
June 14, 2024
Chronic Wasting Disease Detected in Trinity County Deer Breeding Facility
AUSTIN, TX – Texas Parks and Wildlife Department (TPWD) and Texas Animal Health Commission (TAHC) received confirmation of one case of Chronic Wasting Disease (CWD) in a Trinity County deer breeding facility, marking the first detection in the county.
A two-year-old female white-tailed deer tested positive using postmortem testing conducted to meet CWD surveillance requirements for the facility. Texas A&M Veterinary Medical Diagnostic Laboratory (TVMDL) initially analyzed the samples, and the National Veterinary Services Laboratory in Iowa confirmed the CWD detections.
CWD has an incubation period that can span years, so the first indication of the disease in a herd is often found through routine surveillance testing rather than observed clinical signs. Early detection and proactive monitoring improve the state’s response time to the detection of CWD and can greatly reduce the risk of further disease spread. TAHC and TPWD remind all deer breeders of requirements to report mortalities within seven days of detection and submit CWD test samples within seven days of collection.
CWD is a fatal neurological disease found in certain cervids including deer, elk, moose and other members of the deer family. This slow, progressive disease may not produce visible signs in susceptible species for several years after infection. As the disease process continues, animals with CWD may show changes in behavior and appearance. Clinical signs may include progressive weight loss, stumbling or tremors with a lack of coordination, loss of appetite, teeth grinding, abnormal head posture and/or drooping ears, and excessive thirst, salivation or urination.
In Texas, the disease was first discovered in 2012 in free-ranging mule deer along a remote area of the Hueco Mountains near the Texas-New Mexico border. CWD has since been detected in Texas captive and free-ranging cervids, including white-tailed deer, mule deer, red deer and elk.
For more information on previous detections in Texas, surveillance and containment zones, movement restrictions, and CWD best management practices for hunters and landowners, visit TPWD’s CWD page or the TAHC’s CWD page.
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Texas TAHC TPWD Confirm 132 More Cases of CWD TSE PrP
Jumps from 663 in March, to 795 Positive In May 2024, wow!
THURSDAY, MARCH 07, 2024
Texas TPWD CWD Cases Jump to 663 Confirmed To Date
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.
In the case of the Brooks County breeding facility, department records indicate that the facility has within the last five years transferred 1,057 deer to 51 deer breeding facilities, five Deer Management Permit (DMP) sites, and 77 release sites located in a total of 67 counties, as well as to three destinations in Mexico.
In the case of the Frio County breeding facility, department records indicate that the facility has "certified herd" status under the TAHC herd certification program and within the last five years has transferred 627 deer to 46 deer breeding facilities, two nursing facilities, two DMP sites, and 29 release sites located in a total of 41 counties.
In the case of the Zavala County breeding facility, department records indicate that within the last five years the facility has transferred 276 deer to three deer breeding facilities, one DMP facility, and 21 release sites located in a total of 14 counties.
In the case of the Kimble County breeding facility, the facility was the source or destination for 282 deer, including deer sent to seven release sites.
In the case of the Cherokee County breeding facility, the facility received 17 deer from four breeding facilities but did not transfer deer to another breeding facility or release site.
The breeding facilities, nursing facilities, DMP facilities, and release sites that have received deer from the positive facilities are directly connected to those facilities and are of epidemiological concern. These facilities are by current rule also prohibited from receiving or transferring deer unless and until epidemiological investigation determines that Movement Qualified (MQ) status can be restored. Deer breeding facilities that received deer from one or more of the directly connected breeding facilities (referred to as "Tier 1" facilities) are indirectly connected to the positive facilities and are of epidemiological concern because they have received exposed deer that were in a trace-out breeding facility.
The recent detections of CWD in breeding facilities located in Brooks, Frio, Zavala, Kimble, and Cherokee counties are part of an ongoing outbreak of CWD in deer breeding facilities.
Since March 29, 2021, CWD has been detected in 15 counties.
In 2023 alone, CWD has been detected in 12 deer breeding facilities located in nine counties.
Prior to 2021, CWD was detected in six deer breeding facilities located in four counties.
In response to the magnitude and the potential severity of this situation, the emergency rules require the ante-mortem testing of test eligible deer prior to transfer from a breeding facility to another breeding facility.
The emergency action is necessary to protect the state's white-tailed deer populations, as well as associated industries.
TAHC 2 does tested positive and additional testing resulted in 3 subsequent CWD detections Edwards County Deer Breeding Facility
April 25, 2024
Chronic Wasting Disease Detected in Edwards County Deer Breeding Facility
AUSTIN, TX – Texas Parks and Wildlife Department (TPWD) and Texas Animal Health Commission (TAHC) received confirmation of two cases of chronic wasting disease (CWD) in an Edwards County deer breeding facility, marking the first detections in the county.
A pair of two-year-old does tested positive using antemortem testing conducted to meet CWD surveillance requirements for deer. Texas A&M Veterinary Medical Diagnostic Laboratory (TVMDL) initially analyzed the samples, and the National Veterinary Services Laboratory in Iowa confirmed the CWD detection. Proactive removal of deer penned with the positive deer and additional testing resulted in three subsequent CWD detections.
CWD has an incubation period that can span years, so the first indication of the disease in a herd is often found through surveillance testing rather than observed clinical signs. Early detection and proactive monitoring improve the state’s response time to the detection of CWD and can greatly reduce the risk of further disease spread. TAHC and TPWD remind all deer breeders of requirements to report mortalities within seven days of detection and submit CWD test samples within seven days of collection.
CWD is a fatal neurological disease found in certain cervids including deer, elk, moose and other members of the deer family. This slow, progressive disease may not produce visible signs in susceptible species for several years after infection. As the disease process continues, animals with CWD may show changes in behavior and appearance. Clinical signs may include progressive weight loss, stumbling or tremors with a lack of coordination, loss of appetite, teeth grinding, abnormal head posture and/or drooping ears, and excessive thirst, salivation or urination.
In Texas, the disease was first discovered in 2012 in free-ranging mule deer along a remote area of the Hueco Mountains near the Texas-New Mexico border. CWD has since been detected in Texas captive and free-ranging cervids, including white-tailed deer, mule deer, red deer and elk.
TAHC Detected in Edwards County Deer Breeding Facility
A pair of two-year-old does tested positive
additional testing resulted in three subsequent CWD detections.
Texas Chronic Wasting Disease Detected in Real County Deer Breeding Facility
Chronic Wasting Disease Detected in Real County Deer Breeding Facility
April 8, 2024 Media Contact: TPWD News, Business Hours, 512-389-8030 News
AUSTIN — Texas Parks and Wildlife Department (TPWD) and Texas Animal Health Commission (TAHC) received confirmation of two cases of Chronic Wasting Disease (CWD) in a Real County deer breeding facility, marking the first detections in the county.
A 10-year-old and a 6.5-year-old female white-tailed deer tested positive through postmortem testing conducted to meet CWD surveillance requirements for the facility. Texas A&M Veterinary Medical Diagnostic Laboratory (TVMDL) initially analyzed the samples, and the National Veterinary Services Laboratory in Iowa confirmed the CWD detections.
CWD has an incubation period that can span years, so the first indication of the disease in a herd is often found through surveillance (routine) testing rather than observed clinical signs. Early detection and proactive monitoring improve the state’s response time to the detection of CWD and can greatly reduce the risk of further disease spread. All deer breeders are required to report mortalities within seven days of detection and submit CWD test samples within seven days of collection. TAHC and TPWD continue to stress the importance of following all rules pertaining to appropriate sample submission for deer breeding facilities.
CWD is a fatal neurological disease found in certain cervids including deer, elk, moose and other members of the deer family. This slow, progressive disease may not produce visible signs in susceptible species for several years after infection. As the disease process continues, animals with CWD may show changes in behavior and appearance. Clinical signs may include progressive weight loss, stumbling or tremors with a lack of coordination, loss of appetite, teeth grinding, abnormal head posture and/or drooping ears, and excessive thirst, salivation or urination.
In Texas, the disease was first discovered in 2012 in free-ranging mule deer along a remote area of the Hueco Mountains near the Texas-New Mexico border. CWD has since been detected in Texas captive and free-ranging cervids, including white-tailed deer, mule deer, red deer and elk.
For more information on previous detections in Texas, surveillance and containment zones, movement restrictions, and CWD best management practices for hunters and landowners, visit TPWD’s CWD page or the TAHC’s CWD page.
Friday, February 16, 2024 Texas TPWD CWD TSE Prion Positives Jump To 637 Confirmed Cases To Date Texas TPWD CWD TSE Prion Positives Jump To 637 Confirmed Cases To Date
Listing of CWD Cases in Texas
Show 25
Positive Number CWD Positive Confirmation Date Free Range Captive County Source Species Sex Age
637 2024-02-09 White-tailed Deer Hunt Facility #9 White-tailed Deer - Breeder Deer M 2.6
636 2024-02-09 White-tailed Deer Hunt Facility #9 White-tailed Deer - Breeder Deer M 1.5
635 2024-02-09 White-tailed Deer Hunt Facility #9 White-tailed Deer - Breeder Deer F 4.6
634 2024-02-12 White-tailed Deer Hunt Facility #9 White-tailed Deer - Breeder Deer M 3.5
633 2024-01-31 White-tailed Deer Hunt Facility #9 White-tailed Deer - Breeder Deer M 3.5
632 2024-01-31 White-tailed Deer Hunt Facility #9 White-tailed Deer - Breeder Deer M 2.5
631 2024-01-31 White-tailed Deer Hunt Facility #9 White-tailed Deer - Breeder Deer F 4.5
630 2024-01-31 White-tailed Deer Gillespie Facility #14 White-tailed Deer - Breeder Deer M 2.5
629 2024-02-09 White-tailed Deer Hunt N/A White-tailed Deer - Breeder Release Site F 3.5
628 2024-01-31 White-tailed Deer Hunt N/A White-tailed Deer - Breeder Release Site F 3.5
627 2024-01-31 White-tailed Deer Kaufman N/A White-tailed Deer - Breeder Release Site M 5.5
626 2024-01-31 White-tailed Deer Hunt N/A White-tailed Deer - Breeder Release Site F 1.5
625 2024-01-18 White-tailed Deer Medina Facility #4 White-tailed Deer - Breeder Release Site M 8.5
624 2024-01-18 White-tailed Deer Medina N/A White-tailed Deer - Free Range F 3.5
623 2024-01-04 White-tailed Deer Zavala Facility #23 White-tailed Deer - Breeder Deer M 1.5
622 2024-01-04 White-tailed Deer Hunt Facility #9 White-tailed Deer - Breeder Deer F 2.5
621 2024-01-04 White-tailed Deer Hunt Facility #9 White-tailed Deer - Breeder Deer M 5.5
620 2024-01-04 White-tailed Deer Hunt Facility #9 White-tailed Deer - Breeder Deer F 3.5
619 2024-01-04 White-tailed Deer Hunt Facility #9 White-tailed Deer - Breeder Deer M 2.5
618 2024-01-02 White-tailed Deer Frio Facility #21 White-tailed Deer - Breeder Deer M 2.5
617 2024-01-03 White-tailed Deer Frio Facility #24 White-tailed Deer - Breeder Deer F 2.5
616 2024-01-03 White-tailed Deer Hunt Facility #9 White-tailed Deer - Breeder Deer M 2.5
615 2024-01-03 White-tailed Deer Kimble Facility #26 White-tailed Deer - Breeder Deer F 5.5
614 2024-01-03 White-tailed Deer Hunt Facility #9 White-tailed Deer - Breeder Deer F 4.5
Showing 1 to 24 of 637
*CWD Positive Confirmation Dates marked with * are dates confirmed by Texas A&M Veterinary Diagnostic Laboratory rather than the National Veterinary Diagnostic Laboratory.
*CWD Positive Confirmation Dates marked with * are dates confirmed by Texas A&M Veterinary Diagnostic Laboratory rather than the National Veterinary Diagnostic Laboratory.
TPWD Chronic Wasting Disease Surveillance Weekly Update February 05, 2024 CWD Confirmed to Date 628 Positive
Chronic Wasting Disease Surveillance Weekly Update
February 05, 2024
CWD surveillance efforts have been under way since March 1, 2023. Statewide CWD sampling goals for the 2023-2024 collection year are to collect approximately 7,982 samples, and all samples within the CWD designated zones. Wildlife Division staff are collecting CWD samples from a variety of locations which include, road kill deer, locker plants and deer processors, private ranches, WMA and State Parks, and check stations. The first sample reported for this season was collected on March 1, 2023 and was a road kill deer. Exotic species which have been sampled include axis deer, red deer, sika, sambar and elk. A total of 14,753 CWD samples have been collected to date which is approximately 184.83% of the statewide goal of 7,982 samples. Summary of current results are listed below along with maps illustrating distribution of CWD samples.
SUMMARY
snip...see full text;
Friday, January 05, 2024
Texas CWD Cases Mount, 624 documented cases statewide, with 181 cases reported in 2023 alone
CWD in Mississippi with Kamen Campell and William McKinley MS Outdoors Podcast December 4, 2024, reported some very grim CWD news.
CWD in Mississippi is now compared to a “wildfire”.
CWD in Benton County is now reporting 1 in 5 deer now have CWD.
Ultimate Danger question about 15 minute mark?
New Information coming in.
Arkansas GPS Deer collar showing CWD is killing as many deer as hunters are.
West Virginia is showing CWD is killing 1 1/2 times as many deer as hunters are.
“The disease is having a Population Level Impact on herds in the South East”
U.S. Geological Survey science strategy to address chronic wasting disease and cervid health in 2024–2028
December 11, 2024
Terry S. Singeltary Sr.
posted by Terry S. Singeltary Sr. at
2:05 PM
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