Wednesday, September 13, 2023

Texas Chronic Wasting Disease Detected in Kimble County Deer Breeding Facility

Chronic Wasting Disease Detected in Kimble County Deer Breeding Facility


Sept. 13, 2023


Media Contact: TPWD News,  Business Hours, 512-389-8030


News Image Share on Facebook Share Release URL


AUSTIN — The Texas Parks and Wildlife Department (TPWD) received confirmation of a case of Chronic Wasting Disease (CWD) in a deer-breeding facility in Kimble County, marking the second such detection in a deer-breeding facility located in the county.


A six-year-old doe tested positive through an antemortem (live-animal) test conducted to meet annual CWD surveillance requirements for the facility, and postmortem testing confirmed the initial result.


Texas A&M Veterinary Medical Diagnostic Laboratory in College Station initially analyzed the samples, with the National Veterinary Services Laboratory confirming the CWD detection.


CWD has an incubation period that can span years, meaning the first indication in a herd may likely come through surveillance testing rather than observed clinical signs. Early detection and proactive monitoring improve the state’s response time to the detection of CWD and can greatly reduce the risk of further disease spread. 


Prior to the beginning of all deer hunting seasons, TPWD will establish a surveillance zone encompassing a two-mile radius from this recent detection.  All hunter harvested deer from this new zone must be presented at a check station location, yet to be determined, within 48 hours of harvesting the deer.  All affected landowners within this zone will be contacted by the department after the zone boundaries are established.


CWD is a fatal neurological disease found in certain cervids including deer, elk, moose and other members of the deer family. This slow, progressive disease may not produce visible signs in susceptible species for several years after infection. As the irreversible disease process continues, animals with CWD may show changes in behavior and appearance. Clinical signs may include progressive weight loss, stumbling or tremors with a lack of coordination, loss of appetite, teeth grinding, abnormal head posture and/or drooping ears, and excessive thirst, salivation or urination.


In Texas, the disease was first discovered in 2012 in free-ranging mule deer along a remote area of the Hueco Mountains near the Texas-New Mexico border. CWD has since been detected in Texas captive and free-ranging cervids, including white-tailed deer, mule deer, red deer and elk.


For more information on previous detections in Texas and CWD best management practices for hunters and landowners, visit TPWD’s CWD pageThe recently updated page includes a map of all CWD zones, check stations and positive case tracking. This webpage can be utilized to find answers to frequently asked questions, view videos with information from wildlife veterinarians and review the latest news.


https://tpwd.texas.gov/newsmedia/releases/?req=20230913a


The Cwd tracker page is still outdated, and I spoke with someone at TPWD jus the other day about updating it. They said;


“You are correct, unfortunately we are above that number.  We are in the midst of updating our website and apparently not everything is updating like it should.

I don’t know the exact number off hand, but it’s in the 550 range. I will see about getting that portion of our website updated ASAP.”


https://tpwd.texas.gov/huntwild/wild/diseases/cwd/positive-cases/listing-cwd-cases-texas.phtml#texasCWD


Chronic Wasting Disease in Texas


A Real Disease with Proven Impacts


Produced by a coalition of concerned hunters, landowners, & conservationists (last update 08/2023)


Snip…


Since 2012, CWD has been detected in wild deer in just 7 counties in Texas and is only established in the western panhandle and far west Texas.


In that same period of time, captive deer breeders have exposed almost half of Texas counties to CWD. 


Deer held in captive breeding facilities are confined to much tighter spaces, and have intimate contact with many more animals on a daily basis. By far the greatest factor in amplifying the spread of CWD is the artificial movement of these animals, shipped in livestock trailers hundreds of miles, far outside of their natural home range, and ultimately released to co-mingle with wild deer. 


Each year, Texas captive deer breeders liberate 20,000-30,000 deer from their pens to the wild. 


For every deer breeding facility where a CWD positive deer is discovered, an epidemiological investigation is conducted by the Texas Parks & Wildlife Department and the Texas Animal Health Commission to determine how many other deer may have been exposed to the disease and where they have been shipped.  Because of the prolific artificial movement of captive deer, one deer with CWD can impact hundreds of other facilities and ranches across the state.


Unfortunately, released deer in Texas are not required to retain any kind of visible identification (an ear tag), and for this reason, the vast majority of released deer cannot be relocated for testing. 


As of August 2023, 116 Texas counties have received possibly infected breeder deer that cannot be located, putting more than 140,000 landowners at risk of the disease. 


Snip


The state of Texas has been testing for CWD since 2002. Since that time, more than 302,360 captive and free range deer have been tested.  


From 2015-2022, more than 127,000 samples were collected from hunter-harvested and roadkill deer. This sampling rate and risk-based distribution provides scientists confidence that they would have detected the disease if it existed at a very low prevalence (<1%) in any given region at the time sampling began.


Snip…


We have learned from other states where CWD has been present the longest, that a constant increase in the prevalence of the disease may lead to a significant decline in the deer population. When disease prevalence exceeds 20%, deer populations have declined by up to 50%. In some areas of Colorado, where CWD has been present since 1985, mule deer abundance has declined by 45% since that time, despite adequate habitat and no hunting ( Miller et al. 2008 ). Similarly, the South Converse Game Unit in Wyoming has documented CWD prevalence exceeding 50% and has seen an approximate 50% decline in mule deer populations.


Snip…


Rural Economies

Deer hunting is the lifeblood of rural Texas. White-tailed deer hunting is by far the most impactful segment of the hunting economy, representing $4.3 billion, according to a recent Texas A&M Study. And while deer breeders represent a very small segment of that economy (less than 5%), they represent one of the greatest risks. ( Full Texas A&M Report )


Real Estate

Rural land prices are largely driven by recreational buyers with hunting as a top land amenity. Without deer hunting, many of these properties will be worth much less.


Conservation Funding

Deer hunters are the largest funders of wildlife conservation in Texas through excise taxes on firearms, ammunition, and gear along with active membership supporting and funding conservation organizations. If deer hunting suffers due to CWD, all wildlife in Texas lose.


Culture & Health

Texas’ native deer herd has iconic value for all Texans. Deer hunting brings families together, creates camaraderie in communities, and serves to connect Texans to nature.  There is no better protein than wild, locally harvested, non-GMO and totally organic venison.  A healthy deer herd leads to healthy Texans and a healthy and prosperous Texas. 


Snip…


This isn't a disease for our lifetime. It's a disease for our grandchildren's lifetime.    

    - Dr. Bob Dittmar, Former Texas State Wildlife Veterinarian  


Snip…


See the full text with maps, graphs, much more, excellent data…


https://bit.ly/3xL16Gm


Since 2012, CWD has been detected in wild deer in just 7 counties in Texas and is only established in the western panhandle and far west Texas.


In that same period of time, captive deer breeders have exposed almost half of Texas counties to CWD. 


https://bit.ly/3xL16Gm


As of August 2023, 116 Texas counties have received possibly infected breeder deer that cannot be located, putting more than 140,000 landowners at risk of the disease. 


https://bit.ly/3xL16Gm


Texas CWD Surveillance Positives 


https://tpwd.texas.gov/huntwild/wild/diseases/cwd/positive-cases/listing-cwd-cases-texas.phtml#texasCWD 


Counties where CWD Exposed Deer were Released 


https://tpwd.texas.gov/documents/257/CWD-Trace-OutReleaseSites.pdf


Number of CWD Exposed Deer Released by County 


https://tpwd.texas.gov/documents/258/CWD-Trace-OutReleaseSites-NbrDeer.pdf


Chronic Wasting Disease CWD Captive Herds updated April 2023 


https://www.aphis.usda.gov/animal_health/animal_diseases/cwd/downloads/status-of-captive-herds.pdf


Chronic Wasting Disease CWD Captive Herds updated April 2023 


https://www.aphis.usda.gov/aphis/ourfocus/animalhealth/animal-disease-information/cervid/cervids-cwd/cervids-voluntary-hcp  

TPWD Executive Order No. 23-003 CWD Emergency Rules Adopted for Movement of Breeder Deer 


Executive Orders


2023


Executive Order No. 23-003


Date: July 24, 2023


The Executive Director finds that additional discoveries of CWD in free-ranging white-tailed deer within deer breeding facilities regulated under Parks and Wildlife Code, Chapter 43, Subchapter L and regulations adopted pursuant to that subchapter (31 TAC Chapter 65, Subchapters B and T) constitute an immediate danger to the white-tailed deer and mule deer resources of Texas and that the adoption of rules on an emergency basis with fewer than 30 days’ notice is necessary to address an immediate danger.


https://tpwd.texas.gov/publications/executive_orders/


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.''


see much more about 2 hours long...


https://www.youtube.com/watch?v=O3CAI-EwlgM


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


Commission Agenda Item No. 5 Exhibit B


DISEASE DETECTION AND RESPONSE RULES


PROPOSAL PREAMBLE


1. Introduction. 


snip...


 A third issue is the accuracy of mortality reporting. Department records indicate that for each of the last five years an average of 26 deer breeders have reported a shared total of 159 escapes. Department records for the same time period indicate an average of 31 breeding facilities reported a shared total of 825 missing deer (deer that department records indicate should be present in the facility, but cannot be located or verified). 


https://tpwd.texas.gov/business/feedback/meetings/2022/1104/agenda/item.phtml?item=5


On January 21, 2017 a tornado took down thousands of feet of fence for a 420-acre illegal deer enclosure in Lamar County that had been subject to federal and state investigation for illegally importing white-tailed deer into Mississippi from Texas (a CWD positive state). Native deer were free to move on and off the property before all of the deer were able to be tested for CWD. Testing will be made available for a period of three years for CWD on the property and will be available for deer killed within a 5-mile radius of the property on a voluntary basis. 


https://www.mdwfp.com/media/254796/2016-17-deer-report.pdf


“It is interesting to note that, in 2001, the State of Texas shifted its deer management strategies toward the same leanings that Kroll has suggested for Wisconsin. In Texas, the change was brought about via heavy lobbying from the high-fence deer ranching industry. This pressure helped convince the Texas Parks and Wildlife to change their regulations and allow private landowners to select the own deer biologists.”


http://www.texasmonthly.com/story/which-side-fence-are-you


2012 “For 10 years, Texas has had an aggressive Chronic Wasting Disease prevention and monitoring program. Wildlife agency regulations prohibit importing deer into the state, and the agency has tested more than 26,000 hunter-taken deer and 7,400 animals from the captive-deer industry. None of those deer tested positive.”


http://www.chron.com/news/houston-texas/article/Brain-eating-disease-found-in-Texas-deer-3697731.php


CWD TO HUMANS, What If, has it already happened?


***> Currently, there is scientific evidence to suggest that CWD has zoonotic potential; however, no confirmed cases of CWD have been found in humans.


PART 2. TPWD CHAPTER 65. DIVISION 1. CWD


31 TAC §§65.82, 65.85, 65.88


The Texas Parks and Wildlife Commission in a duly noticed meeting on May 25, 2023 adopted amendments to 31 TAC §§65.82, 65.85, and §65.88, concerning Disease Detection and Response, without changes to the proposed text as published in the April 21, 2023, issue of the Texas Register (48 TexReg 2048). The rules will not be republished.


***> Currently, there is scientific evidence to suggest that CWD has zoonotic potential; however, no confirmed cases of CWD have been found in humans.


https://www.sos.texas.gov/texreg/archive/June302023/Adopted%20Rules/31.NATURAL%20RESOURCES%20AND%20CONSERVATION.html#57


17 DETECTION OF CHRONIC WASTING DISEASE PRIONS IN PROCESSED MEATS.


Rebeca Benavente1, Francisca Bravo1,2, Paulina Soto1,2, J. Hunter Reed3, Mitch Lockwood3, Rodrigo Morales1,2


1Department of Neurology, McGovern Medical School, University of Texas Health Science Center at Houston, Houston, USA. 2Universidad Bernardo O’Higgins, Santiago, Chile. 3Texas Parks and Wildlife, Austin, USA


Abstract


The zoonotic potential of chronic wasting disease (CWD) remains unknown. Currently, there are no known natural cases of CWD transmission to humans but increasing evidence suggests that the host range of CWD is not confined only to cervid species. Alarmingly, recent experimental evidence suggests that certain CWD isolates can induce disease in non-human primates. While the CDC strongly recommends determining CWD status in animals prior to consumption, this practice is voluntary. Consequently, it is plausible that a proportion of the cervid meat entering the human food chain may be contaminated with CWD. Of additional concern is that traditional diagnostic techniques used to detect CWD have relatively low sensitivity and are only approved for use in tissues other than those typically ingested by humans. In this study, we analyzed different processed meats derived from a pre-clinical, CWD-positive free-ranging elk. Products tested included filets, sausages, boneless steaks, burgers, ham steaks, seasoned chili meats, and spiced meats. CWD-prion presence in these products were assessed by PMCA using deer and elk substrates. 


***> Our results show positive prion detection in all products. 


***>To confirm the resilience of CWD-prions to traditional cooking methods, we grilled and boiled the meat products and evaluated them for any remnant PMCA seeding activity. Results confirmed the presence of CWD-prions in these meat products suggesting that infectious particles may still be available to people even after cooking. 


***> Our results strongly suggest ongoing human exposure to CWD-prions and raise significant concerns of zoonotic transmission through ingestion of CWD contaminated meat products. 


***> Products tested included filets, sausages, boneless steaks, burgers, ham steaks, seasoned chili meats, and spiced meats. 


***> CWD-prion presence in these products were assessed by PMCA using deer and elk substrates. 


***> Our results show positive prion detection in all products. 


***> Results confirmed the presence of CWD-prions in these meat products suggesting that infectious particles may still be available to people even after cooking.


***> Our results strongly suggest ongoing human exposure to CWD-prions and raise significant concerns of zoonotic transmission through ingestion of CWD contaminated meat products. 


=====


Transmission of prion infectivity from CWD-infected macaque tissues to rodent models demonstrates the zoonotic potential of chronic wasting disease.


Samia Hannaoui1,2, Ginny Cheng1,2, Wiebke Wemheuer3, Walter Schulz-Schaeffer3, Sabine Gilch1,2, Hermann Schatzl1,2 1University of Calgary, Calgary, Canada. 2Calgary Prion Research Unit, Calgary, Canada. 3Institute of Neuropathology, Medical Faculty, Saarland University, Homburg/Saar, Germany


***> Further passage to cervidized mice revealed transmission with a 100% attack rate. 


***> Our findings demonstrate that macaques, considered the best model for the zoonotic potential of prions, were infected upon CWD challenge, including the oral one. 


****> The disease manifested as atypical in macaques and initial transgenic mouse transmissions, but with infectivity present at all times, as unveiled in the bank vole model with an unusual tissue tropism. 


***> Epidemiologic surveillance of prion disease among cervid hunters and people likely to have consumed venison contaminated with chronic wasting disease


=====


https://intcwdsympo.files.wordpress.com/2023/06/final-agenda-with-abstracts.pdf?force_download=true


9 Carrot plants as potential vectors for CWD transmission.


Paulina Soto1,2, Francisca Bravo-Risi1,2, Claudio Soto1, Rodrigo Morales1,2


1Department of Neurology, McGovern Medical School, University of Texas Health Science Center at Houston, Houston, USA. 2Universidad Bernardo O’Higgins, Santiago, Chile


***> We show that edible plant components can absorb prions from CWD-contaminated soils and transport them to their aerial parts.


***> Our results indicate that edible plants could participate as vectors of CWD transmission.


=====


https://intcwdsympo.files.wordpress.com/2023/06/final-agenda-with-abstracts.pdf?force_download=true


Transmission of Cervid Prions to Humanized Mice Demonstrates the Zoonotic Potential of CWD


Aims: Chronic wasting disease (CWD), a prion disease of cervids, spreads efficiently among wild and farmed animals. Potential transmission to humans of CWD is a growing concern due to its increasing prevalence. Here, we aimed to determine the zoonotic potential of CWD using a mouse model for human prion diseases.


Material and Methods: Transgenic mice overexpressing human PrPChomozygous for methionine at codon 129 (tg650) were inoculated intracerebrally with brain homogenates of white-tailed deer infected with Wisc-1/CWD1 or 116AG CWD strains. Mice were monitored for clinical signs and were euthanized at terminal disease. Brains were tested by RT-QuIC, western blot upon PK digestion, and immunohistochemistry; fecal homogenates were analyzed by RT-QuIC. Brain/spinal cord and fecal homogenates of CWD-inoculated tg650 mice were inoculated into tg650 mice or bank voles. Brain homogenates of bank voles inoculated with fecal homogenates of CWD-infected tg650 mice were used for second passage in bank voles.


Results: Here, we provide the strongest evidence supporting the zoonotic potential of CWD prions, and their possible phenotype in humans. Inoculation of mice expressing human PrPCwith deer CWD isolates (strains Wisc-1 and 116AG) resulted in atypical clinical manifestations in > 75% of the mice, with myoclonus as leading clinical sign. Most of tg650brain homogenates were positive for seeding activity in RT-QuIC. Clinical disease and presentation was transmissible to tg650 mice and bank voles. Intriguingly, protease-resistant PrP in the brain of tg650 mice resembled that found in a familial human prion disease and was transmissible upon passage. Abnormal PrP aggregates upon infection with Wisc-1 were detectable in thalamus, hypothalamus, and midbrain/pons regions.


Unprecedented in human prion disease, feces of CWD-inoculated tg650 mice harbored prion seeding activity and infectious prions, as shown by inoculation of bank voles and tg650 with fecal homogenates.


Conclusions: This is the first evidence that CWD can infect humans and cause disease with a distinctive clinical presentation, signature, and tropism, which might be transmissible between humans while current diagnostic assays might fail to detect it. These findings have major implications for public health and CWD-management.


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


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

Abstract

Prions cause infectious and fatal neurodegenerative diseases in mammals. Chronic wasting disease (CWD), a prion disease of cervids, spreads efficiently among wild and farmed animals. Potential transmission to humans of CWD is a growing concern due to its increasing prevalence. Here, we provide evidence for a zoonotic potential of CWD prions, and its probable signature using mice expressing human prion protein (PrP) as an infection model. Inoculation of these mice with deer CWD isolates resulted in atypical clinical manifestation with prion seeding activity and efficient transmissible infectivity in the brain and, remarkably, in feces, but without classical neuropathological or Western blot appearances of prion diseases. Intriguingly, the protease-resistant PrP in the brain resembled that found in a familial human prion disease and was transmissible upon second passage. Our results suggest that CWD might infect humans, although the transmission barrier is likely higher compared to zoonotic transmission of cattle prions. Notably, our data suggest a different clinical presentation, prion signature, and tissue tropism, which causes challenges for detection by current diagnostic assays. Furthermore, the presence of infectious prions in feces is concerning because if this occurs in humans, it is a source for human-to-human transmission. These findings have strong implications for public health and CWD management.

snip…

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


PLoS One. 2020; 15(8): e0237410. Published online 2020 Aug 20. doi: 10.1371/journal.pone.0237410 PMCID: PMC7446902 PMID: 32817706 

Very low oral exposure to prions of brain or saliva origin can transmit chronic wasting disease 

Abstract 

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...

The results demonstrate: (a) that the minimum CWD oral infectious dose is vastly lower than historical studies used to establish infection; (b) that a direct relationship exists between dose and incubation time to first prion replication detection in tonsils, irrespective of genotype; (c) that a difference was not discernible between brain vs. saliva source prions in ability to establish infection or in resultant disease course; and (d) that the CWD infection process appears to conform more to a threshold dose than an accumulative dose dynamic. 


*** now, let’s see what the authors said way back about this casual link, personal communications years ago, and then the latest on the zoonotic potential from CWD to humans from the TOKYO PRION 2016 CONFERENCE. see where it is stated NO STRONG evidence. so, does this mean there IS casual evidence ???? “Our conclusion stating that we found no strong evidence of CWD transmission to humans” 

From: TSS Subject: CWD aka MAD DEER/ELK TO HUMANS ??? 

Date: September 30, 2002 at 7:06 am PST 

From: "Belay, Ermias" 

To: Cc: "Race, Richard (NIH)" ; ; "Belay, Ermias" 

Sent: Monday, September 30, 2002 9:22 AM Subject: RE: TO CDC AND NIH - PUB MED- 3 MORE DEATHS - CWD - YOUNG HUNTERS 

Dear Sir/Madam, In the Archives of Neurology you quoted (the abstract of which was attached to your email), we did not say CWD in humans will present like variant CJD.. That assumption would be wrong. I encourage you to read the whole article and call me if you have questions or need more clarification (phone: 404-639-3091). 

Also, we do not claim that "no-one has ever been infected with prion disease from eating venison." Our conclusion stating that we found no strong evidence of CWD transmission to humans in the article you quoted or in any other forum is limited to the patients we investigated. 

Ermias Belay, M.D. Centers for Disease Control and Prevention 

-----Original Message----- From: 

Sent: Sunday, September 29, 2002 10:15 AM 
To: rr26k@nih.gov; rrace@niaid.nih.gov; ebb8@CDC.GOV 

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

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


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

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

sporadic = 54,983 hits 

 
spontaneous = 325,650 hits 

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

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

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

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

key word here is ‘reported’. science has shown that CWD in humans will look like sporadic CJD. SO, how can one assume that CWD has not already transmitted to humans? they can’t, and it’s as simple as that. from all recorded science to date, CWD has already transmitted to humans, and it’s being misdiagnosed as sporadic CJD. …terry

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

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




CWD TSE PRION AND ZOONOTIC, ZOONOSIS, POTENTIAL

Subject: Re: DEER SPONGIFORM ENCEPHALOPATHY SURVEY & HOUND STUDY 

Date: Fri, 18 Oct 2002 23:12:22 +0100 

From: Steve Dealler 

Reply-To: Bovine Spongiform Encephalopathy Organization: Netscape Online member 

To: BSE-L@ References: 

Dear Terry,

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

What happened with the deer was that an association between deer meat eating and sporadic CJD was found in about 1993. The evidence was not great but did not disappear after several years of asking CJD cases what they had eaten. I think that the work into deer disease largely stopped because it was not helpful to the UK industry...and no specific cases were reported. Well, if you dont look adequately like they are in USA currenly then you wont find any!

Steve Dealler 

=====

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

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

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

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

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

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

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

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

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

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

snip...

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

snip...

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

snip...

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

snip...see full report ;



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 scrapiepositive goatherds, which currently have limited genetic resistance to scrapie within commercial breeds.24 This is very likely to have parallels with control efforts for CWD in cervids.


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


***> 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


Front. Vet. Sci., 14 September 2015 | https://doi.org/10.3389/fvets.2015.00032

Objects in contact with classical scrapie sheep act as a reservoir for scrapie transmission

In conclusion, the results in the current study indicate that removal of furniture that had been in contact with scrapie-infected animals should be recommended, particularly since cleaning and decontamination may not effectively remove scrapie infectivity (31), even though infectivity declines considerably if the pasture and the field furniture have not been in contact with scrapie-infected sheep for several months. As sPMCA failed to detect PrPSc in furniture that was subjected to weathering, even though exposure led to infection in sheep, this method may not always be reliable in predicting the risk of scrapie infection through environmental contamination. 


172. Establishment of PrPCWD extraction and detection methods in the farm soil

Conclusions: Our studies showed that PrPCWD persist in 0.001% CWD contaminated soil for at least 4 year and natural CWD-affected farm soil. When cervid reintroduced into CWD outbreak farm, the strict decontamination procedures of the infectious agent should be performed in the environment of CWD-affected cervid habitat.


THE tse prion aka mad cow type disease is not your normal pathogen. 

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

you cannot cook the TSE prion disease out of meat. 

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

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

the TSE prion agent also survives Simulated Wastewater Treatment Processes. 

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

you can bury it and it will not go away. 

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

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

***> that’s what’s so worrisome about Iatrogenic mode of transmission, a simple autoclave will not kill this TSE prion agent.

1: J Neurol Neurosurg Psychiatry 1994 Jun;57(6):757-8 

***> Transmission of Creutzfeldt-Jakob disease to a chimpanzee by electrodes contaminated during neurosurgery. 

Gibbs CJ Jr, Asher DM, Kobrine A, Amyx HL, Sulima MP, Gajdusek DC. 

Laboratory of Central Nervous System Studies, National Institute of 

Neurological Disorders and Stroke, National Institutes of Health, 

Bethesda, MD 20892. 

Stereotactic multicontact electrodes used to probe the cerebral cortex of a middle aged woman with progressive dementia were previously implicated in the accidental transmission of Creutzfeldt-Jakob disease (CJD) to two younger patients. The diagnoses of CJD have been confirmed for all three cases. More than two years after their last use in humans, after three cleanings and repeated sterilisation in ethanol and formaldehyde vapour, the electrodes were implanted in the cortex of a chimpanzee. Eighteen months later the animal became ill with CJD. This finding serves to re-emphasise the potential danger posed by reuse of instruments contaminated with the agents of spongiform encephalopathies, even after scrupulous attempts to clean them. 

PMID: 8006664 [PubMed - indexed for MEDLINE] 


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 


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


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 early BSE days---end...tss

and so it seems...

Scrapie Agent (Strain 263K) Can Transmit Disease via the Oral Route after Persistence in Soil over Years

Published: May 9, 2007

snip...

Our results showed that 263K scrapie agent can persist in soil at least over 29 months. Strikingly, not only the contaminated soil itself retained high levels of infectivity, as evidenced by oral administration to Syrian hamsters, but also feeding of aqueous soil extracts was able to induce disease in the reporter animals. We could also demonstrate that PrPSc in soil, extracted after 21 months, provides a catalytically active seed in the protein misfolding cyclic amplification (PMCA) reaction. PMCA opens therefore a perspective for considerably improving the detectability of prions in soil samples from the field.

snip...


Dr. Paul Brown Scrapie Soil Test BSE Inquiry Document


 Published: 06 September 2021

***> Chronic wasting disease: a cervid prion infection looming to spillover

Alicia Otero, Camilo Duque Velásquez, Judd Aiken & Debbie McKenzie 

Veterinary Research volume 52, Article number: 115 (2021) 


MONDAY, SEPTEMBER 11, 2023 

Professor John Collinge on tackling prion diseases sCJD around 1 in 5000 deaths worldwide

“The best-known human prion disease is sporadic Creutzfeldt-Jakob disease (sCJD), a rapidly progressive dementia which accounts for around 1 in 5000 deaths worldwide.”




Terry S. Singeltary Sr.

0 Comments:

Post a Comment

Subscribe to Post Comments [Atom]

<< Home