Friday, February 21, 2025

Distribution of Chronic Wasting Disease in North America February 2025

Distribution of Chronic Wasting Disease in North America 

By National Wildlife Health Center February 10, 2025






Distribution of Chronic Wasting Disease in North America February 2025

I would kindly like to comment please, about my Concerns about Chronic Wasting Disease CWD, Transmissible Spongiform TSE, Prion disease in Cervid. The spread of CWD, and its Environmental and Zoonotic threat to Texas is very real, yet the misinformation about CWD being spread by industry, lobbyists, and hunters, is just as real of a threat. I have followed CWD, TSE, daily, for almost 3 decades, and I have seen this from state to state, as CWD spreads.

Misinformation like;

It’s a government conspiracy to stop hunting.

It’s the insurance companies.

No deer die from CWD.

Yada, yada, yada, I could go on and on, but let’s look at what the science really shows us, shall we.

Please let me explain;

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

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

you cannot cook the TSE prion disease out of meat.

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

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

the TSE prion agent also survives Simulated Wastewater Treatment Processes.

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

you can bury it and it will not go away.

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

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

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


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


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


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

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

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

https://journals.asm.org/doi/10.1128/msphere.00866-24

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

Detection of prions in soils contaminated by multiple routes

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

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

Funded by: Wisconsin Department of Natural Resources

Prion 2023 Abstracts

https://prion2023.org/wp-content/uploads/2023/10/Meeting-book-final-version2.pdf

Chronic wasting disease prions on deer feeders and wildlife visitation to deer feeding areas 

Miranda H. J. Huang, Steve Demarais, Marc D. Schwabenlander, Bronson K. Strickland, Kurt C. VerCauteren, William T. McKinley, Gage Rowden, Corina C. Valencia Tibbitts … See all authors 

First published: 10 February 2025

https://doi.org/10.1002/jwmg.70000

Abstract 

Eliminating supplemental feeding is a common regulatory action within chronic wasting disease (CWD) management zones. These regulations target the potential for increased animal-animal contact and environmental contamination with CWD prions. Prions, the causative agent of CWD, have been detected on feeder surfaces in CWD-positive, captive deer facilities but not among free-ranging populations, and information on the relative risk of transmission at anthropogenic and natural food sources is limited. In this study, we established and maintained 13 gravity feeders from September 2022 to March 2023 in a CWD zone in northern Mississippi, USA (apparent prevalence ~30%). We set up feeders up in 3 ways: no exclusion (deer feeders, n = 7), exclusion of deer using fencing with holes cut at the ground-level to permit smaller wildlife to enter (raccoon feeders, n = 3), and environmental control feeders, which were fully fenced and not filled with feed (control feeders, n = 3). We swabbed feeder spouts at setup and at 4 intervals approximately 6 weeks apart to test for prion contamination via real-time quaking-induced conversion (RT-QuIC). We detected prions 12 weeks after setup on all deer and raccoon feeders. We compared relative transmission risk using camera traps at these feeders, 6 agronomic plantings for wildlife forage (i.e., food plots), and 7 oak mast trees. Weekly visitation rate by white-tailed deer (Odocoileus virginianus; hereafter: deer) differed (P = 0.02) among deer feeders (median = 24.5 deer/week, range = 15.6–65.7), food plots (median = 12.7, range = 3.8–24.7), and mast trees (median = 2.0, range = 0.4–5.1). Contact rates between individual deer also differed between site types (P < 0.01): deer feeders (median = 2.1 deer-to-deer contacts/week, range = 0–10.1), food plots (median = 0.1, range = 0–4.0), and mast trees (median = 0, range = 0–0.3). Raccoons also visited feeders at greater rates than food plots and mast trees (P < 0.04). Finally, we swabbed 19 feeders in 2 areas where CWD was newly detected, finding prion contamination on swabs from 4 feeders. We show that deer feeders in free-ranging populations with high CWD prevalence become contaminated with CWD prions quickly, becoming a potential site of exposure of deer to CWD prions. Our results also demonstrate the ability to find evidence of prion contamination on deer feeders, even in areas where CWD is newly detected.

Snip…

We found that supplemental feeding increased the risk of exposure to CWD prions due to contamination of feeders, increased deer visitation, and increased deer-to-deer contact.

The 12-fold increase in deer visitation to feeders compared to mast trees and 2-fold increase compared to food plots demonstrates increased risk for direct disease spread.

https://wildlife.onlinelibrary.wiley.com/doi/10.1002/jwmg.70000

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

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

https://int-cwd-sympo.org/wp-content/uploads/2023/06/final-agenda-with-abstracts.pdf

Chronic wasting disease detection in environmental and biological samples from a taxidermy site

Results: The PMCA analysis demonstrated CWD seeding activity in some of the components of this facility, including insects involved in head processing, soils, and a trash dumpster.

Conclusions: Different areas of this property were used for various taxidermy procedures. We were able to detect the presence of prions in i) soils that were in contact with the heads of dead animals, ii) insects involved in the cleaning of skulls, and iii) an empty dumpster where animal carcasses were previously placed. This is the first report demonstrating that swabbing is a helpful method to screen for prion infectivity on surfaces potentially contaminated with CWD. These findings are relevant as this swabbing and amplification strategy may be used to evaluate the disease status of other free-ranging and captive settings where there is a concern for CWD transmissions, such as at feeders and water troughs with CWD-exposed properties. This approach could have substantial implications for free-ranging cervid surveillance as well as in epidemiological investigations of CWD.

Prion 2022 Conference abstracts: pushing the boundaries

https://www.tandfonline.com/doi/full/10.1080/19336896.2022.2091286

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

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

JOURNAL OF GENERAL VIROLOGY Volume 87, Issue 12

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

https://www.microbiologyresearch.org/content/journal/jgv/10.1099/vir.0.82011-0

Rapid recontamination of a farm building occurs after attempted prion removal

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

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

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

https://bvajournals.onlinelibrary.wiley.com/doi/abs/10.1136/vr.105054

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

https://pubmed.ncbi.nlm.nih.gov/30602491/

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

https://doi.org/10.1002/eap.3089



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

Audrey M. Sandoval, Amy V. Nalls, Erin E. McNulty, Nathaniel D. Denkers, Devon J. Trujillo, Zoe Olmstead, Ethan Barton, Jennifer R. Ballard, Daniel M. Grove, Jeremy S. Dennison, Natalie Stilwell, Christopher A. Cleveland, James M. Crum, Mark G. Ruder, Candace K. Mathiason doi: https://doi.org/10.1101/2025.01.24.634834

ABSTRACT

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

snip…

Overall, this study describes the dissemination of CWD prions throughout tissues and birthing fluids of the pregnancy microenvironment demonstrating that offspring are routinely exposed to the infectious prion in-utero prior to parturition.


Texas CWD Surveillance Positives Tracking Page is still outdated, last figures i have were;

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


Wisconsin Caltive CWD Positives update 1/30/2024

HOLY SMOKES Wisconsin Captive CWD Positives update January 2024

Chronic Wasting Disease Positives in Farm-raised Deer Revised: 1/30/2024



Wisconsin 2024 Cwd


***> Chronic Wasting Disease CWD TSE Prion can travel upwards to 50MPH or faster, they call it, 'Trucking CWD'.

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.....


5 or 6 years quarantine is NOT LONG ENOUGH FOR CWD TSE PRION !!!

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.


Volume 31, Number 1—January 2025

Dispatch

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

Paulina Soto, Francisca Bravo-Risi, Rebeca Benavente, Tucker H. Stimming, Michael J. Bodenchuk, Patrick Whitley, Clint Turnage, Terry R. Spraker, Justin Greenlee, Glenn Telling, Jennifer Malmberg, Thomas Gidlewski, Tracy Nichols, Vienna R. Brown, and Rodrigo Morales Author affiliation: The University of Texas Health Science Center at Houston, Texas, USA (P. Soto, F. Bravo-Risi, R. Benavente, T.H. Stimming, R. Morales); Centro Integrativo de Biologia y Quimica Aplicada, Universidad Bernardo O’Higgins, Santiago, Chile (P. Soto, F. Bravo-Risi, R. Morales); US Department of Agriculture, Fort Collins, Colorado, USA (M.J. Bodenchuk, P. Whitley, C. Turnage, J. Malmberg, T. Gidlewski, T. Nichols, V.R. Brown); Colorado State University, Fort Collins, Colorado, USA (T.R. Spraker, G. Telling); US Department of Agriculture, Ames, Iowa, USA (J. Greenlee) Suggested citation for this article

Abstract

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

Chronic wasting disease (CWD) is a prion disease of particular concern because of its uncontrolled contagious spread among various cervid species in North America (https://www.usgs.gov/media/images/distribution-chronic-wasting-disease-north-america-0ExternalLink), its recent discovery in Nordic countries (1), and its increasingly uncertain zoonotic potential (2). CWD is the only animal prion disease affecting captive as well as wild animals. Persistent shedding of prions by CWD-affected animals and resulting environmental contamination is considered a major route of transmission contributing to spread of the disease. Carcasses of CWD-affected animals represent relevant sources of prion infectivity to multiple animal species that can develop disease or act as vectors to spread infection to new locations.

Free-ranging deer are sympatric with multiple animal species, including some that act as predators, scavengers, or both. Experimental transmissions to study the potential for interspecies CWD transmissions have been attempted in raccoons, ferrets, cattle, sheep, and North American rodents (3–7). Potential interspecies CWD transmission has also been addressed using transgenic (Tg) mice expressing prion proteins (PrP) from relevant animal species (8). Although no reports of natural interspecies CWD transmissions have been documented, experimental studies strongly suggest the possibility for interspecies transmission in nature exists (3–7). Inoculation and serial passage studies reveal the potential of CWD prions to adapt to noncervid species, resulting in emergence of novel prion strains with unpredicted features (9–11).

Wild pigs (Sus scrofa), also called feral swine, are an invasive population comprising domestic swine, Eurasian wild boar, and hybrids of the 2 species (12). Wild pig populations have become established in the United States (Appendix Figure 1, panel A), enabled by their high rates of fecundity; omnivorous and opportunistic diet; and widespread, often human-mediated movement (13). Wild pigs scavenge carcasses on the landscape and have an intimate relationship with the soil because of their routine rooting and wallowing behaviors (14). CWD prions have been experimentally transmitted to domestic pigs by intracerebral and oral exposure routes (15), which is relevant because wild pigs coexist with cervids in CWD endemic areas and reportedly prey on fawns and scavenge deer carcasses. Considering the species overlap in many parts of the United States (Appendix Figure 1, panel B), we studied potential interactions between wild pigs and CWD prions.

Snip…

Conclusions

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


2019

-----Original Message----- 
From: Terry S. Singeltary Sr. <flounder9@verizon.net
To: Terry Singeltary <flounder9@verizon.net
Sent: Fri, Dec 6, 2019 2:36 pm 

Subject: Feral hogs and cwd tse prion

Feral hogs and cwd tse prion

woman was just killed in Texas by feral hogs. also, cwd and pigs, well, it could happen, plus, can one imagine if cwd ever did transmit to feral hogs in the wild, or even if it didn't, those hogs digging up everything, if in a cwd zone, could help spread cwd to hell and back. just thinking out of the box a bit, bbbut...... cwd scrapie pigs oral routes

***> cattle, pigs, sheep, cwd, tse, prion, oh my!…terrible

and 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, REASONS AS FOLLOW.

First off I will start with a single BSE feed breach 10 years after 1997 partial ban. If you got to the archived link, all the way down to bottom…THE NEXT YEAR I RECALL ONE WITH 10,000,000+ banned products recall…see this records at the bottom…terry

REASON The feed was manufactured from materials that may have been contaminated with mammalian protein.

VOLUME OF PRODUCT IN COMMERCE 27,694,240 lbs DISTRIBUTION MI

snip..... end

***>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;


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

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

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

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

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

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

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

"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


How in the hell do you make a complete recall of 27,694,240 lbs of feed that was manufactured from materials that may have been contaminated with mammalian protein, in one state, Michigan, 2006? Wonder how much was fed out?

RECALLS AND FIELD CORRECTIONS: VETERINARY MEDICINE -- CLASS II

______________________________

PRODUCT

a) CO-OP 32% Sinking Catfish, Recall # V-100-6;

b) Performance Sheep Pell W/Decox/A/N, medicated, net wt. 50 lbs, Recall # V-101-6;

c) Pro 40% Swine Conc Meal -- 50 lb, Recall # V-102-6;

d) CO-OP 32% Sinking Catfish Food Medicated, Recall # V-103-6;

e) "Big Jim’s" BBB Deer Ration, Big Buck Blend, Recall # V-104-6;

f) CO-OP 40% Hog Supplement Medicated Pelleted, Tylosin 100 grams/ton, 50 lb. bag, Recall # V-105-6;

g) Pig Starter Pell II, 18% W/MCDX Medicated 282020, Carbadox -- 0.0055%, Recall # V-106-6;

h) CO-OP STARTER-GROWER CRUMBLES, Complete Feed for Chickens from Hatch to 20 Weeks, Medicated, Bacitracin Methylene Disalicylate, 25 and 50 Lbs, Recall # V-107-6;

i) CO-OP LAYING PELLETS, Complete Feed for Laying Chickens, Recall # 108-6;

j) CO-OP LAYING CRUMBLES, Recall # V-109-6;

k) CO-OP QUAIL FLIGHT CONDITIONER MEDICATED, net wt 50 Lbs, Recall # V-110-6;

l) CO-OP QUAIL STARTER MEDICATED, Net Wt. 50 Lbs, Recall # V-111-6;

m) CO-OP QUAIL GROWER MEDICATED, 50 Lbs, Recall # V-112-6

CODE Product manufactured from 02/01/2005 until 06/06/2006

RECALLING FIRM/MANUFACTURER

 Alabama Farmers Cooperative, Inc., Decatur, AL, by telephone, fax, email and visit on June 9, 2006.

FDA initiated recall is complete.

REASON

Animal and fish feeds which were possibly contaminated with ruminant based protein not labeled as "Do not feed to ruminants".

VOLUME OF PRODUCT IN COMMERCE

125 tons

DISTRIBUTION

AL and FL

______________________________

PRODUCT

Bulk custom dairy feds manufactured from concentrates, Recall # V-113-6 CODE All dairy feeds produced between 2/1/05 and 6/16/06 and containing H. J. Baker recalled feed products.

RECALLING FIRM/MANUFACTURER Vita Plus Corp., Gagetown, MI, by visit beginning on June 21, 2006.

Firm initiated recall is complete.

REASON

The feed was manufactured from materials that may have been contaminated with mammalian protein.

VOLUME OF PRODUCT IN COMMERCE

27,694,240 lbs

DISTRIBUTION

MI
______________________________

PRODUCT

Bulk custom made dairy feed, Recall # V-114-6

CODE None

RECALLING FIRM/MANUFACTURER Burkmann Feeds LLC, Glasgow, KY, by letter on July 14, 2006. Firm initiated recall is ongoing.

REASON

Custom made feeds contain ingredient called Pro-Lak, which may contain ruminant derived meat and bone meal.

VOLUME OF PRODUCT IN COMMERCE

???

DISTRIBUTION

KY

END OF ENFORCEMENT REPORT FOR AUGUST 2, 2006

###


***> Deer don’t die from CWD TSE Prion?

CWD is 100% fatal to a Cervid, if something else don’t kill it first…

“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.”

https://www.antigojournal.com/sports/outdoors/durkin-wisconsin-dnr-says-cwd-sinking-deer-herds-in-disease-endemic-areas/article_cb73b5ca-dd9e-11ef-853c-d3fb206ddf8c.ht

***> Deer don’t die from CWD, it’s the insurance companies?

For all you …folks, that keep saying deer don’t die form CWD, here’s your sign…

“The deer was found dead by a landowner and was severely emaciated.”

CWD-POSITIVE DETECTED IN CARBON COUNTY

February 12, 2025

HARRISBURG -- The Pennsylvania Game Commission today announced an additional CWD-positive deer has been detected in the northeastern part of the state.

The deer, an adult male, was detected in Packer Township, Carbon County. This detection is the first in Carbon County and is more than 10 miles from any other confirmed CWD-positive deer. The deer was found dead by a landowner and was severely emaciated.

https://www.pa.gov/agencies/pgc/newsroom/pheasants-to-be-released-next-week/cwd-positive-detected-in-carbon-county.html

Ever seen a dead deer from Cwd?

That dog don’t hunt!

First chronic wasting disease case confirmed in Spokane County

SPOKANE- Washington’s first case of chronic wasting disease (CWD) has been confirmed in an adult female white-tailed deer that was found dead in the Fairwood area of north Spokane.

https://wdfw.wa.gov/newsroom/news-release/first-chronic-wasting-disease-case-confirmed-spokane-county

Case of Chronic Wasting Disease found in dead deer at Breckinridge County farm Oct 14, 2024 Updated Oct 14, 2024 The Kentucky Department of Fish and Wildlife said Monday that a case of the disease was found in a dead deer from a Breckinridge County deer farm. This is Kentucky's first case of CWD in a captive group of deer, the department said in a news release.

https://www.wdrb.com/news/case-of-chronic-wasting-disease-found-in-dead-deer-at-breckinridge-county-farm/article_e874f26c-8a95-11ef-b4fb-2f583a5d3105.html

Oklahoma CIMARRON COUNTY SSA ENLARGED AFTER CHRONIC WASTING DISEASE CONFIRMED IN DEAD DEER

https://www.wildlifedepartment.com/outdoor-news/cimarron-county-ssa-enlarged-after-chronic-wasting-disease-confirmed-dead-deer

MADISON, Wis. – The Wisconsin Department of Natural Resources (DNR) confirms the first positive test result for chronic wasting disease (CWD) in a wild deer in Waushara County. The deer was found dead in early February in the town of Wautoma and is within 10 miles of the Marquette and Portage county borders.

https://dnr.wisconsin.gov/newsroom/release/91086

Ever see a dead deer from Cwd?

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

https://www.youtube.com/watch?v=fvDTHEwnmO8

CWD Seeing is believing part 2 Video

https://www.youtube.com/watch?v=BbaYYLWewNg

Cwd videos

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...

https://www.youtube.com/watch?v=O3CAI-EwlgM&t=922s

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.''

https://youtu.be/aoPDeGL6mpQ?t=1384

Wyoming Cwd 2022 test results

https://m.youtube.com/watch?v=cy_CDnNKQSE

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.

https://dnr.wisconsin.gov/topic/research/projects/dpp/StudyResults

***> LEGISLATING CWD TSE Prion, Bills to release Genetically Modified Cervid into the wild, what could go wrong?

“If slower disease progression results in longer-lived, infected deer with longer periods of infectiousness, resistance may lead to increased disease transmission rates, higher prion concentrations in the environment, and increased prevalence, as has been observed in some captive deer herds (Miller et al., 2006; Keane et al., 2008a).”

Genetic susceptibility to chronic wasting disease in free-ranging white-tailed deer: Complement component C1q and Prnp polymorphisms§

Julie A. Blanchong a, *, Dennis M. Heisey b , Kim T. Scribner c , Scot V. Libants d , Chad Johnson e , Judd M. Aiken e , Julia A. Langenberg f , Michael D. Samuel g

snip...

Identifying the genetic basis for heterogeneity in disease susceptibility or progression can improve our understanding of individual variation in disease susceptibility in both free-ranging and captive populations. What this individual variation in disease susceptibility means for the trajectory of disease in a population, however, is not straightforward. For example, the greater, but not complete, resistance to CWD in deer with at least one Serine (S) at amino acid 96 of the Prnp gene appears to be associated with slower progression of disease (e.g., Johnson et al., 2006; Keane et al., 2008a). If slower disease progression results in longer-lived, infected deer with longer periods of infectiousness, resistance may lead to increased disease transmission rates, higher prion concentrations in the environment, and increased prevalence, as has been observed in some captive deer herds (Miller et al., 2006; Keane et al., 2008a). Alternatively, if the slower progression of disease in resistant deer is not associated with longer periods of infectiousness, but might instead indicate a higher dose of PrPCWD is required for infection, transmission rates in the population could decline especially if, as in Wisconsin, deer suffer high rates of mortality from other sources (e.g., hunting). Clearly, determining the relationship between genetic susceptibility to infection, dose requirements, disease progression, and the period of PrPCWD infectiousness are key components for understanding the consequences of CWD to free-ranging populations.



Volume 30, Number 10—October 2024

Research

Temporal Characterization of Prion Shedding in Secreta of White-Tailed Deer in Longitudinal Study of Chronic Wasting Disease, United States

Our findings suggest that deer expressing alternative PRNP polymorphisms might live longer and, although they shed fewer prions throughout CWD course, might over their extended lifespan increase CWD prions in the environment


Prion protein gene sequence and chronic wasting disease susceptibility in white-tailed deer (Odocoileus virginianus)

Adam L Brandt, Amy C Kelly, Michelle L Green, Paul Shelton, Jan Novakofski & Nohra E Mateus-Pinilla

Pages 449-462 | Received 21 Sep 2015, Accepted 23 Oct 2015, Published online: 21 Dec 2015 https://doi.org/10.1080/19336896.2015.1115179

The presence of aa96S has been associated with slowed disease progression, longer life span among captive deer,Citation26,27 and does not appear to affect the rate at which prions are shed from infected individuals.Citation38 Additionally, CWD infected mule deer have been found to excrete pathogenic prions while asymptomatic.Citation39 This contributes to concerns that wild deer with aa96S may be shedding infectious prions into the environment for longer periods of time than deer lacking the mutation, but are not symptomatic or detectable by immunohistochemical procedures.



''There are no known familial or genetic TSEs of animals, although polymorphisms in the PRNP gene of some species (sheep for example) may influence the length of the incubation period and occurrence of disease.''

c) The commonest form of CJD occurs as a sporadic disease, the cause of which is unknown, although genetic factors (particularly the codon 129 polymorphism in the prion protein gene (PRNP)) influence disease susceptibility. The familial forms of human TSEs (see Box 1) appear to have a solely genetic origin and are closely associated with mutations or insertions in the PRNP gene. Most, but not all, of the familial forms of human TSEs have been transmitted experimentally to animals. There are no known familial or genetic TSEs of animals, although polymorphisms in the PRNP gene of some species (sheep for example) may influence the length of the incubation period and occurrence of disease.


P-145 Estimating chronic wasting disease resistance in cervids using real time quaking- induced conversion

Nicholas J Haley1, Rachel Rielinqer2, Kristen A Davenport3, W. David Walter4, Katherine I O'Rourke5, Gordon Mitchell6, Juergen A Richt2 1

Our studies demonstrate that in vitro amplification metrics predict in vivo susceptibility, and that alleles with multiple codons, each influencing resistance independently, do not necessarily contribute additively to resistance. Importantly, we found that the white-tailed deer 226K substrate exhibited the slowest amplification rate among those evaluated, suggesting that further investigation of this allele and its resistance in vivo are warranted to determine if absolute resistance to CWD is possible. ***at present, no cervid PrP allele conferring absolute resistance to prion infection has been identified.

PRION 2016 CONFERENCE TOKYO



***> at present, no PrPC allele conferring absolute resistance in cervids has been identified.

J Gen Virol. 2017 Nov; 98(11): 2882–2892.

Published online 2017 Oct 23. doi: 10.1099/jgv.0.000952

Estimating chronic wasting disease susceptibility in cervids using real-time quaking-induced conversion

Chronic wasting disease (CWD) resistance in cervids is often characterized as decreased prevalence and/or protracted disease progression in individuals with specific alleles; at present, no PrPC allele conferring absolute resistance in cervids has been identified.


***> CWD TSE Prion Zoonotic Zoonosis, what if?

CDC CWD TSE Prion Update 2025

KEY POINTS

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

The disease hasn't been shown to infect people.

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


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

=====


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 tg650with 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;


ARS RESEARCH Generation of human chronic wasting disease in transgenic mice

Publication Acceptance Date: 9/8/2021

Research Project: Pathobiology, Genetics, and Detection of Transmissible Spongiform Encephalopathies Location: Virus and Prion Research

Title: Generation of human chronic wasting disease in transgenic mice

Author item WANG, ZERUI - Case Western Reserve University (CWRU) item QIN, KEFENG - University Of Chicago item CAMACHO, MANUEL - Case Western Reserve University (CWRU) item SHEN, PINGPING - Case Western Reserve University (CWRU) item YUAN, JUE - Case Western Reserve University (CWRU) item Greenlee, Justin item CUI, LI - Jilin University item KONG, QINGZHONG - Case Western Reserve University (CWRU) item MASTRIANNI, JAMES - University Of Chicago item ZOU, WEN-QUAN - Case Western Reserve University (CWRU)

Submitted to: Acta Neuropathologica Publication Type: Peer Reviewed Journal Publication Acceptance Date: 9/8/2021 Publication Date: N/A Citation: N/A

Interpretive Summary: Prion diseases are invariably fatal neurologic diseases for which there is no known prevention or cure. Chronic wasting disease (CWD) is the prion disease of deer and elk and is present in farmed and free ranging herds throughout North America. To date there is no clear evidence that the CWD agent could be transmitted to humans. This manuscript describes the use of an in vitro technique, cell-free serial protein misfolding cyclic amplification (sPMCA), to generate a CWD prion that is infectious to transgenic mice expressing the human prion protein. This study provides the first evidence that CWD prions may be able to cause misfolding in the human prion protein. This information will impact medical experts and those involved in making policy for farmed cervids and wildlife.

Technical Abstract: Chronic wasting disease (CWD) is a cervid spongiform encephalopathy or prion disease caused by the infectious prion or PrPSc, a misfolded conformer of cellular prion protein (PrPC). It has rapidly spread in North America and also has been found in Asia and Europe. In contrast to the zoonotic mad cow disease that is the first animal prion disease found transmissible to humans, the transmissibility of CWD to humans remains uncertain although most previous studies have suggested that humans may not be susceptible to CWD. Here we report the generation of an infectious human PrPSc by seeding CWD PrPSc in normal human brain PrPC through the in vitro cell-free serial protein misfolding cyclic amplification (sPMCA). Western blotting confirms that the sPMCA-induced proteinase K-resistant PrPSc is a human form, evidenced by a PrP-specific antibody that recognizes human but not cervid PrP. Remarkably, two lines of humanized transgenic (Tg) mice expressing human PrP-129Val/Val (VV) or -129Met/Met (MM) polymorphism develop prion disease at 233 ± 6 (mean ± SE) days post-inoculation (dpi) and 552 ± 27 dpi, respectively, upon intracerebral inoculation with the sPMCA-generated PrPSc. The brain of diseased Tg mice reveals the electrophoretic profile of PrPSc similar to sporadic Creutzfeldt-Jakob disease (sCJD) MM1 or VV2 subtype but different neuropathological patterns. We believe that our study provides the first evidence that CWD PrPSc is able to convert human PrPC into PrPSc in vitro and the CWD-derived human PrPSc mimics atypical sCJD subtypes in humanized Tg mice.


''The brain of diseased Tg mice reveals the electrophoretic profile of PrPSc similar to sporadic Creutzfeldt-Jakob disease (sCJD) MM1 or VV2 subtype but different neuropathological patterns.''

''We believe that our study provides the first evidence that CWD PrPSc is able to convert human PrPC into PrPSc in vitro and the CWD-derived human PrPSc mimics atypical sCJD subtypes in humanized Tg mice.''

Published: 26 September 2021

Generation of human chronic wasting disease in transgenic mice

Zerui Wang, Kefeng Qin, Manuel V. Camacho, Ignazio Cali, Jue Yuan, Pingping Shen, Justin Greenlee, Qingzhong Kong, James A. Mastrianni & Wen-Quan Zou

Acta Neuropathologica Communications volume 9, Article number: 158 (2021)

Abstract

Chronic wasting disease (CWD) is a cervid prion disease caused by the accumulation of an infectious misfolded conformer (PrPSc) of cellular prion protein (PrPC). It has been spreading rapidly in North America and also found in Asia and Europe. Although bovine spongiform encephalopathy (i.e. mad cow disease) is the only animal prion disease known to be zoonotic, the transmissibility of CWD to humans remains uncertain. Here we report the generation of the first CWD-derived infectious human PrPSc by elk CWD PrPSc-seeded conversion of PrPC in normal human brain homogenates using in vitro protein misfolding cyclic amplification (PMCA). Western blotting with human PrP selective antibody confirmed that the PMCA-generated protease-resistant PrPSc was derived from the human PrPC substrate. Two lines of humanized transgenic mice expressing human PrP with either Val or Met at the polymorphic codon 129 developed clinical prion disease following intracerebral inoculation with the PMCA-generated CWD-derived human PrPSc. Diseased mice exhibited distinct PrPSc patterns and neuropathological changes in the brain. Our study, using PMCA and animal bioassays, provides the first evidence that CWD PrPSc can cross the species barrier to convert human PrPC into infectious PrPSc that can produce bona fide prion disease when inoculated into humanized transgenic mice.

Snip...

It is worth noting that the annual number of sporadic CJD (sCJD) cases in the USA has increased, with the total number of suspected and confirmed sCJD cases rising from 284 in 2003 to 511 in 2017 (https://www.cdc.gov/prions/cjd/occurrence-transmission.html). The greatly enhanced CJD surveillance and an aging population in the USA certainly contributed to the observed increase in annual sCJD case numbers in recent years, but the possibility cannot be excluded that some of the increased sCJD prevalence is linked to CWD exposure.

In the present study, using serial protein misfolding cyclic amplification (sPMCA) assay we generate PrPSc by seeding CWD prions in normal human brain homogenates. Importantly, we reveal that two lines of humanized Tg mice expressing human PrP-129VV and 129MM develop prion diseases upon intracerebral inoculation of the abnormal PrP generated by sPMCA. We believe that our study provides the first opportunity to dissect the clinical, pathological and biochemical features of the CWD-derived human prion disease in two lines of humanized Tg mice expressing two major human PrP genotypes, respectively.


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.

See also poster P103

***> 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.

Source Prion Conference 2018 Abstracts


*** 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.govrrace@niaid.nih.govebb8@CDC.GOV


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


Sunday, November 10, 2002 6:26 PM .......snip........end..............TSS


Thursday, April 03, 2008


A prion disease of cervids: Chronic wasting disease 2008 1: Vet Res. 2008 Apr 3;39(4):41 A prion disease of cervids: Chronic wasting disease Sigurdson CJ.


snip... *** twenty-seven CJD patients who regularly consumed venison were reported to the Surveillance Center***,


snip... full text ;



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


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


sporadic = 54,983 hits



spontaneous = 325,650 hits



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


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


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


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


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


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





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: <3daf5023 .4080804="" wt.net="">


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

Dear Terry,

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

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

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

Steve Dealler

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

Subject: DEER SPONGIFORM ENCEPHALOPATHY SURVEY & HOUND STUDY 

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

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

Date: Thu, 17 Oct 2002 17:04:51 -0700 Content-Type: text/plain Parts/Attachments: text/plain (102 lines) 

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

Greetings BSE-L,

is there any other CWD surveys/testing in the UK on their deer? what sort of testing has been done to date on UK/EU deer? any input would be helpful... thank you

DEER SPONGIFORM ENCEPHALOPATHY SURVEY

http://www.bse.org.uk/files/yb/1991/11/20004001.pdf

http://www.bse.org.uk/files/yb/1992/11/04002001.pdf

hope they did not go by the wayside as the hound study;

http://www.bse.org.uk/files/yb/1991/10/18001001.pdf

http://www.bse.org.uk/files/yb/1993/12/06001001.pdf

37.Putative TSE in hounds - work started 1990 -(see para 41)

Robert Higgins, a Veterinary Investigation Officer at Thirsk, had been working on a hound survey in 1990. Gerald Wells and I myself received histological sections from this survey along with the accompanying letter (YB90/11.28/1.1) dated November 1990. This letter details spongiform changes found in brains from hunt hounds failing to keep up with the rest of the pack, along with the results of SAF extractions from fresh brain material from these same animals. SAFs were not found in brains unless spongiform changes were also present. The spongiform changes were not pathognomonic (ie. conclusive proof) for prion disease, as they were atypical, being largely present in white matter rather than grey matter in the brain and spinal cord. However, Tony Scott, then head of electron microscopy work on TSEs, had no doubt that these SAFs were genuine and that these hounds therefore must have had a scrapie-like disease. I reviewed all the sections myself (original notes appended) and although the pathology was not typical, I could not exclude the possibility that this was a scrapie-like disorder, as white matter vacuolation is seen in TSEs and Wallerian degeneration was also present in the white matter of the hounds, another feature of scrapie.

38.I reviewed the literature on hound neuropathology, and discovered that micrographs and descriptive neuropathology from papers on 'hound ataxia' mirrored those in material from Robert Higgins' hound survey. Dr Tony Palmer (Cambridge) had done much of this work, and I obtained original sections from hound ataxia cases from him. This enabled me provisionally to conclude that Robert Higgins had in all probability detected hound ataxia, but also that hound ataxia itself was possibly a TSE. Gerald Wells confirmed in 'blind' examination of single restricted microscopic fields that there was no distinction between the white matter vacuolation present in BSE and scrapie cases, and that occurring in hound ataxia and the hound survey cases.

39.Hound ataxia had reportedly been occurring since the 1930's, and a known risk factor for its development was the feeding to hounds of downer cows, and particularly bovine offal. Circumstantial evidence suggests that bovine offal may also be causal in FSE, and TME in mink. Despite the inconclusive nature of the neuropathology, it was clearly evident that this putative canine spongiform encephalopathy merited further investigation.

40.The inconclusive results in hounds were never confirmed, nor was the link with hound ataxia pursued. I telephoned Robert Higgins six years after he first sent the slides to CVL. I was informed that despite his submitting a yearly report to the CVO including the suggestion that the hound work be continued, no further work had been done since 1991. This was surprising, to say the very least.

41.The hound work could have provided valuable evidence that a scrapie-like agent may have been present in cattle offal long before the BSE epidemic was recognised. The MAFF hound survey remains unpublished.

Histopathological support to various other published MAFF experiments

42.These included neuropathological examination of material from experiments studying the attempted transmission of BSE to chickens and pigs (CVL 1991) and to mice (RVC 1994).

http://www.bse.org.uk/witness/htm/stat067.htm

nothing to offer scientifically;

http://www.bse.org.uk/files/yb/1991/10/17001001.pdf

maddogs and Englishman

http://www.bse.org.uk/files/yb/1990/11/28001001.pdf

kind regards, terry

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

snip...

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


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


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


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


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


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


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


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


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


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


snip...


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


snip...


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


snip...


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


snip...see full report ;





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


BSE Inquiry Steve Dealler


Management In Confidence


BSE: Private Submission of Bovine Brain Dealler


snip...end

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

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


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




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




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


PUBLIC SUBMISSION


Comment from Terry Singeltary Sr.


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


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




Wednesday, May 24, 2023


***> WAHIS, WOAH, OIE, United States of America Bovine spongiform encephalopathy Immediate notification


https://wahis.woah.org/#/in-review/5067


https://woahoie.blogspot.com/2023/05/wahis-woah-oie-united-states-of-america.html


https://prpsc.proboards.com/thread/125/wahis-woah-oie-immediate-notification


SATURDAY, MAY 20, 2023


***> Tennessee State Veterinarian Alerts Cattle Owners to Disease Detection Mad Cow atypical L-Type BSE


https://bse-atypical.blogspot.com/2023/05/tennessee-state-veterinarian-alerts.html


https://prpsc.proboards.com/thread/123/tennessee-veterinarian-alerts-cattle-confirmed


MAY 19, 2023


https://www.aphis.usda.gov/aphis/newsroom/stakeholder-info/sa_by_date/sa-2023/bse


2 weeks before the announcement of this recent mad cow case in the USA, i submitted this to the APHIS et al;


***> APPRX. 2 weeks before the recent mad cow case was confirmed in the USA, in Tennessee, atypical L-Type BSE, I submitted this to the APHIS et al;


Document APHIS-2023-0027-0001 BSE Singeltary Comment Submission May 2, 2023


''said 'burden' cost, will be a heavy burden to bear, if we fail with Bovine Spongiform Encephalopathy BSE TSE Prion disease, that is why this information collection is so critical''...


https://www.regulations.gov/comment/APHIS-2023-0027-0002



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


Expanding Distribution of Chronic Wasting Disease

Active

By National Wildlife Health Center February 10, 2025


Wasted Days and Wasted Nights…Freddy Fender

Terry S. Singeltary Sr. Flounder9@verizon.net Bacliff, Texas 77518

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