Friday, February 21, 2025

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


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.


TEXAS BREEDER DEER ESCAPEE WITH CWD IN THE WILD, or so the genetics would show?

OH NO, please tell me i heard this wrong, a potential Texas captive escapee with cwd in the wild, in an area with positive captive cwd herd?

apparently, no ID though. tell me it ain't so please...

23:00 minute mark

''Free Ranging Deer, Dr. Deyoung looked at Genetics of this free ranging deer and what he found was, that the genetics on this deer were more similar to captive deer, than the free ranging population, but he did not see a significant connection to any one captive facility that he analyzed, so we believe, Ahhhhhh, this animal had some captive ahhh, whatnot.''


Texas symposium Cwd


Arkansas Cwd


Wyoming Cwd 2022 test results


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 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.



Friday, February 21, 2025

Distribution of Chronic Wasting Disease in North America February 2025


Terry S. Singeltary Sr.





posted by Terry S. Singeltary Sr. at 3:10 PM

0 Comments:

Post a Comment

Subscribe to Post Comments [Atom]

<< Home