TPWD Executive Order No. 23-003 CWD Emergency Rules Adopted for Movement of Breeder Deer
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.
Emergency Rules Adopted for Movement of Breeder Deer
July 25, 2023
Media Contact: TPWD News, Business Hours, 512-389-8030
AUSTIN — In response to continued positive detections of Chronic Wasting Disease (CWD) in deer breeding facilities, Texas Parks and Wildlife Department (TPWD) has adopted an emergency rule implementing additional movement and testing restrictions for white-tailed deer in deer breeding facilities.
Since June, TPWD has received confirmation of CWD in deer breeding facilities in three counties- Brooks, Frio and Zavala. In 2023 alone, CWD has been detected in nine deer breeding facilities in seven counties. A total of 14 counties have had positive detections since March 2021.
“Since 2021, we have seen an increase in CWD detections from breeder deer at an unprecedented rate,” said John Silovsky, Wildlife Division Director for TPWD. “It’s our hope that these emergency rules will strengthen our surveillance and reduce the number of CWD positive detections across the state.”
This emergency order amends Chapter 31 TAC §65.95, relating to Movement of Breeder Deer. The change requires all breeder deer to be ante-mortem (live-animal) tested for CWD (with a test result of “Not Detected”) before transferring to another deer breeding facility or release site. These changes will be in effect for 120 days but may be extended an additional 60 days.
Additionally, the department has determined that to expedite and facilitate epidemiological investigations, it is necessary to prohibit the removal of identification tags under any circumstance other than allowed by statute. The ability to quickly locate and test breeder deer transferred to a release facility is critical to determining the likelihood of disease transmission.
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.
Visit TPWD’s recently updated CWD page to find a map of all CWD zones, check stations and positive case tracking. The site also provides answers to frequently asked questions, videos with information from wildlife veterinarians, best management practices for hunters and landowners and review the latest news.
Executive Orders
2023
Executive Order No. 23-003
Date: July 24, 2023
Under the provisions of Parks and Wildlife Code, §12.027, if the Texas Parks and Wildlife Commission (the Commission) or the Executive Director of the Texas Parks and Wildlife Department (Executive Director) finds that there is an immediate danger to a species authorized to be regulated by the Department, the Commission or the Executive Director may adopt emergency rules as provided by Government Code, §2001.034.
White-tailed deer and mule deer are game animals subject to regulation by the Commission under the provisions of various chapters of the Parks and Wildlife Code, including Chapters 43 (Subchapters E, L, R, and R-1), 61, 62, and 63. Chronic Wasting Disease (CWD) is a fatal neurodegenerative disorder that affects some cervid species, including white-tailed deer and mule deer.
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.
The emergency rules require all breeder deer to be tested for CWD (with a test result of “Not Detected”) by means of an approved ante-mortem (live-animal) test as a condition of transfer to another deer breeding facility and expressly prohibit the removal of an identification tag prescribed by Parks and Wildlife Code, §43.3561, from a breeder deer except to immediately replace it with an identification tag meeting the requirements of Parks and Wildlife Code, §43.3561(c) or (h).
Therefore, finding that the immediate danger to both captive and free-ranging white-tailed and mule deer populations exists, the Executive Director hereby ORDERS the adoption, on an emergency basis, of an amendment to 31 TAC §65.95, concerning Movement of Breeder Deer, and §65.611 (relating to Prohibited Acts), in response to the ongoing and most recent detections of chronic wasting disease (CWD) in additional deer breeding facilities.
This order is effective immediately upon filing, and authorizes publication of a Notice of Extension of Emergency Adoption in the Texas Register.
This order is issued pursuant to §12.027 of the Texas Parks and Wildlife Code and §2001.034 of the Texas Government Code and is effective immediately.
Signed this 24th day of July, 2023.
Austin Court of Appeals: Breeder Deer Are Not Private Property
Posted on July 15, 2019 by tiffany.dowell
A recent decision from the Austin Court of Appeals in Bailey v. Smith, is important for many Texas landowners involved in the business of raising deer. This case addressed the issue of whether breeder deer–raised by persons with the required TPWD permit–are considered private property of the deer breeder or are owned by the State.
One note here–this case also addressed a number of other technical legal issues such as sovereign immunity, ultra vires action of state officials, and attorney’s fees awards. This blog post will not discuss these issues, but will focus solely on the property rights of breeder deer. To read the entire opinion, click here.
Background
Ken Bailey and Bradley Peterson (“the breeders”) breed whitetail deer. They have the required deer breeder’s permit issued by Texas Parks and Wildlife (TPWD) allowing them to “possess live breeder deer in captivity” and to “engage in the business of breeding breeder deer.”
Bailey and Peterson sued the TPWD and various officials seeking to establish that breeder deer are private property and should not be subject to TPWD requirements for chronic wasting disease testing and limitations on transfer. In particular, they claim a property interest in the breeder deer and claim the Texas Parks and Wildlife Code violate their procedural due process rights.
The trial court found in favor of the TPWD and the officials. Peterson appealed.
Applicable Law
The Texas Legislature has passed regulations requiring “Deer Breeder’s Permits” for persons seeking to possess live breeder deer in captivity. See Tex. Parks & Wildlife Code Section 43.351-43.369. “Breeder deer” are defined as white-tailed or mule deer legally held by a permit. See id. at Section 43.351. “Captivity” is defined as meaning “the keeping of a breeder deer in an enclosure suitable for and capable of retaining the breeder deer it is designed to retain at all times under reasonable and ordinary circumstances and to prevent entry by another deer.” Id.
A person holding a valid deer breeder’s permit may “engage in the business of breeding deer in the immediate locality for which the permit was issued” and may “sell, transfer to another person, or hold in captivity live breeder deer for the purpose of propagation or sale.” Id. at Section 43.357. The permit serves as a complete defense for a deer breeder if accused of unlawful possession or transportation of whitetail or mule deer. Id. at Section 43.353.
These rights are subject to the TPWD’s ability to adopt rules concerning the possession of breeder deer and the procedures and requirements for purchase, transfer, sale, or shipment of breeder deer. See id. The statute further provides that only healthy breeder deer may be transferred, and requires that a transfer permit be obtained if breeder deer are to be moved to or from a facility. See id. Section 43.362. In light of the presence of chronic wasting disease found in captive deer in Texas, TPWD enacted strict rules related to testing and limitations on transport or transfer of captive deer.
Court of Appeals Opinion
The Austin Court of Appeals affirmed the trial court decision. [Read full opinion here.]
The Texas Constitution provides that no person “shall be deprived of life, liberty, property, privileges or immunities” except by the due course of the law of the land. This is analyzed with a two-part test: (1) Did the petitioner possess a liberty or property interest entitled to procedural due process protection; and, if so (2) what process is due?
To have a constitutionally protected property interest, a person must have a “legitimate claim of entitlement” rather than a mere “unilateral expectation.” Historically, with regard to animals, whether property rights existed depended on whether the animal was domestic or ferae naturae (wild) with wild game belonging to the people and held in trust by the State. This was codified by the Legislature in Texas Parks & Wildlife Code Section 1.011, which provides that “all wild animals, fur-bearing animals, wild birds, and wild foul inside the borders of this state are the property of the people of this state.” The Code also provides that restriction of the animals by fences does not affect their status as property of the state. Id. at Section 1.013.
Under this doctrine, a person has no property rights in the wild animal until it is “legally removed from the wild.” See State v. Bartee, 894 S.W.2d 34 (Tex. Ct. App. – San Antonio 1994). Texas law provides that whitetail deer and mule deer are considered game animals, and that no person may capture a game animal from the wild without a permit from the department. Peterson argues that his breeder’s permit allows ownership rights to arise in the breeder deer, but the Court rejected this is argument. The court held that the permit does grant the right to sell, transfer, or hold deer in captivity, but does nothing to make the breeder deer property of the breeder. Further, the fact that deer are held under a permit, which is valid only for a set amount of time, further evidences that nothing in the statute contemplates the breeder retaining any rights over the breeder deer if the permit is expired or revoked. Thus, the court held “we conclude breeder deer are public property held under a permit issued by the Department and, consequently, deer breeders do not acquire common law property rights in them.”
TEXAS COURT OF APPEALS, THIRD DISTRICT, AT AUSTIN
NO. 03-17-00703-CV
Ken Bailey and Bradley Peterson, Appellants v. Carter Smith, Executive Director; Clayton Wolf, Wildlife Division Director; Mitch Lockwood, Big Game Program Director; and Texas Parks & Wildlife Department, Appellees
FROM THE DISTRICT COURT OF TRAVIS COUNTY, 98TH JUDICIAL DISTRICT NO. D-1-GN-15-004391, HONORABLE TIM SULAK, JUDGE PRESIDING O P I N I O N
This is a dispute between commercial deer breeders and the Texas Parks and Wildlife Department (the Department) over the ownership of captive-bred whitetail deer. Ken Bailey and Bradley Peterson each hold a deer breeder’s permit issued by the Department authorizing them “to possess live breeder deer in captivity” and to “engage in the business of breeding breeder deer.” See Tex. Parks & Wild. Code §§ 43.352(a), .357(a)(1). Peterson and Bailey sued the Department and several of its officials to establish that breeder deer are or became private property and to invalidate Department rules requiring breeders to test for chronic wasting disease. The Department responded that breeder deer are wild animals and therefore “property of the people of this state.” See id. § 1.011(a). The district court granted the Department’s partial plea to the jurisdiction and motion for summary judgment, denied Peterson’s cross-motion, and awarded the Department its attorneys’ fees. For the reasons that follow, we will affirm.
Control of Chronic Wasting Disease OMB Control Number: 0579-0189 APHIS-2021-0004 Singeltary Submission
Greetings APHIS et al, i would kindly like to comment on Control of Chronic Wasting Disease OMB Control Number: 0579-0189 APHIS-2021-0004.
Greetings APHIS et al, i would kindly like to comment on Control of Chronic Wasting Disease OMB Control Number: 0579-0189 APHIS-2021-0004.
***> 1st and foremost your biggest problem is 'VOLUNTARY'! AS with the BSE 589.2001 FEED REGULATIONS, especially since it is still voluntary with cervid, knowing full well that cwd and scrapie will transmit to pigs by oral route. VOLUNTARY DOES NOT WORK! all animal products should be banned and be made mandatory, and the herd certification program should be mandatory, or you don't move cervid. IF THE CWD HERD CERTIFICATION IS NOT MANDATORY, it will be another colossal tse prion failure from the start.
***> 2nd USA should declare a Declaration of Extraordinary Emergency due to CWD, and all exports of cervid and cervid products must be stopped internationally, and there should be a ban of interstate movement of cervid, until a live cwd test is available.
***> 3rd Captive Farmed cervid ESCAPEES should be made mandatory to report immediately, and strict regulations for those suspect cwd deer that just happen to disappear. IF a cervid escapes and is not found, that farm should be indefinitely shut down, all movement, until aid MIA cervid is found, and if not ever found, that farm shut down permanently.
***> 4th Captive Farmed Cervid, INDEMNITY, NO MORE Federal indemnity program, or what i call, ENTITLEMENT PROGRAM for game farm industry. NO MORE BAIL OUTS FROM TAX PAYERS. if the captive industry can't buy insurance to protect not only themselves, but also their customers, and especially the STATE, from Chronic Wasting Disease CWD TSE Prion or what some call mad deer disease and harm therefrom, IF they can't afford to buy that insurance that will cover all of it, then they DO NOT GET A PERMIT to have a game farm for anything. This CWD TSE Prion can/could/has caused property values to fall from some reports in some places. roll the dice, how much is a state willing to lose?
***> 5th QUARANTINE OF ALL FARMED CAPTIVE, BREEDERS, URINE, ANTLER, VELVET, SPERM, OR ANY FACILITY, AND THEIR PRODUCTS, that has been confirmed to have Chronic Wasting Disease CWD TSE Prion, the QUARANTINE should be for 21 years due to science showing what scrapie can do. 5 years is NOT near long enough. see; Infectious agent of sheep scrapie may persist in the environment for at least 16 to 21 years.
***> 6th America BSE 589.2001 FEED REGULATIONS CWD TSE Prion
***> 7TH TRUCKING TRANSPORTING CERVID CHRONIC WASTING DISEASE TSE PRION VIOLATING THE LACEY ACT
***> 8TH ALL CAPTIVE FARMING CERVID OPERATIONS MUST BE INSURED TO PAY FOR ANY CLEAN UP OF CWD AND QUARANTINE THERE FROM FOR THE STATE, NO MORE ENTITLEMENT PROGRAM FOR CERVID GAME FARMING PAY TO PLAY FOR CWD TSE PRION OFF THE TAX PAYERS BACK.
***> 9TH ANY STATE WITH DOCUMENTED CWD, INTERSTATE, NATIONAL, AND INTERNATIONAL MOVEMENT OF ALL CERVID, AND ALL CERVID PRODUCTS MUST BE HALTED!
***> 10TH BAN THE SALE OF STRAW BRED BUCKS AND ALL CERVID SEMEN AND URINE PRODUCTS
***> 11th ALL CAPTIVE FARMED CERVID AND THEIR PRODUCTS MUST BE CWD TSE PRION TESTED ANNUALLY AND BEFORE SALE FOR CWD TSE PRION
SEE FULL SCIENCE REFERENCES AND REASONINGS ;
***> 1st and foremost your biggest problem is 'VOLUNTARY'!
''APHIS created a cooperative, voluntary Federal-State-private sector CWD Herd Certification Program designed to identify farmed or captive herds infected with CWD.''
key word failure is 'voluntary'.
WE know for a fact now that voluntary does NOT WORK!
AS with the BSE 589.2001 FEED REGULATIONS (see , another colossal failure, and proven to be a sham, especially since it is still voluntary with cervid, knowing full well that cwd and scrapie will transmit to pigs by oral route. VOLUNTARY DOES NOT WORK! all animal products should be banned and be made mandatory, and the herd certification program should be mandatory, or you don't move cervid. IF THE CWD HERD CERTIFICATION IS NOT MANDATORY, it will be another colossal tse prion failure from the start.
***> 2nd USA should declare a Declaration of Extraordinary Emergency due to CWD, and all exports of cervid and cervid products must be stopped internationally, and there should be a ban of interstate movement of cervid, until a live cwd test is available.
***> 3rd Captive Farmed cervid ESCAPEES should be made mandatory to report immediately, and strict regulations for those suspect cwd deer that just happen to disappear. IF a cervid escapes and is not found, that farm should be indefinitely shut down, all movement, until aid MIA cervid is found, and if not ever found, that farm shut down permanently. ...snip...see full text submission with science references...TSS
Control of Chronic Wasting Disease OMB Control Number: 0579-0189 APHIS-2021-0004 Singeltary Submission
Docket No. APHIS-2018-0011 Chronic Wasting Disease Herd Certification
MONDAY, MAY 15, 2023
TAHC Chapter 40, Chronic Wasting Disease and Scrapie Chapter 60, Singeltary Comment Submission
Greetings TAHC et al,
Thank you kindly for giving me the opportunity to once again comment on CWD and Scrapie.
I want to thank the TAHC and the TPWD for coming together and seems now bring forth sound science, of the real risk factors for both CWD and Scrapie.
With great urgency, i wish to bring your attention on updated Science on Chronic Wasting Disease CWD and Scrapie TSE Prion Environmental Factors and Zoonotic factors, spillover risk factors of CWD and Scrapie to other species i.e. PIGS, our failed feed ban of which now should include all cervid and pigs imo. i saw no mention of atypical Scrapie and the new science from EFSA, i shall include that as well. there is a new TSE Prion disease in a new livestock species the Camel, you should all be aware of. all of this is most important, and should be addressed in any cwd update imo, especially with CWD and Scrapie transmitting to pigs by oral routes.
i will post my concerns below, Thank You Kindly...terry
TAHC Chapter 40, Chronic Wasting Disease and Scrapie Chapter 60, Singeltary Comment Submission
[Federal Register Volume 86, Number 42 (Friday, March 5, 2021)]
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
Greetings again FDA and Mr. Pritchett et al,
UPDATE
***> This report describes the experimental transmission of CWD to red deer following oral inoculation with infectious CWD material of elk origin. At 18 to 20 months post-inoculation, mild to moderate neurological signs and weight loss were observed and animals were euthanized and tested using 3 conventional immunological assays.
Publish Year: 2010
Publication: Can Vet J. 2010 Feb; 51(2): 169-178.
Published: 2010/02
Experimental oral transmission of chronic wasting disease to red deer…
Spongiform encephalopathy was observed in the brain of the 4 infected deer and was characterized by severe and widespread microcavitation primarily of the grey matter, single or multiple intracytoplasmic vacuolation of neurons, neuronal degeneration and loss, mild astrocytic hypertrophy and hyperplasia, and the absence of any significant inflammatory response (Figure 2a).
MONDAY, AUGUST 24, 2020
Very low oral exposure to prions of brain or saliva origin can transmit chronic wasting disease
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 Affiliations expand PMID: 32817706 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.
Conflict of interest statement AstraZeneca Inc.: The funder provided support in the form of salaries for authors [CEH], but did not have any additional role in the study design, data collection and analysis, decision to publish, or preparation of the manuscript. The specific roles of these authors are articulated in the ‘author contributions’ section. This does not alter our adherence to PLOS ONE policies on sharing data and materials.
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.....
THURSDAY, AUGUST 04, 2016
MEETING ON THE FEASIBILITY OF CARRYING OUT EPIDEMIOLOGICAL STUDIES ON CREUTZFELDT JAKOB DISEASE 1978 THE SCRAPIE FILES IN CONFIDENCE CONFIDENTIAL SCJD
TPWD Chronic Wasting Disease Detected in Brooks County Deer Breeding Facility
Chronic Wasting Disease Detected in Brooks County Deer Breeding Facility
July 21, 2023
Media Contact: TPWD News, Business Hours, 512-389-8030
AUSTIN — The Texas Parks and Wildlife Department (TPWD) and Texas Animal Health Commission (TAHC) received notification of a new case of Chronic Wasting Disease (CWD) in a deer-breeding facility in Brooks County. This marks the first detection of the disease in the county and the ninth CWD-positive breeding facility in the state detected in 2023.
A five-year-old doe detected with CWD was transferred in 2022 from a facility in Frio County newly discovered to be positive for CWD. In this case, TPWD regulations required euthanization and testing for CWD as part of the epidemiological investigation.
Texas A&M Veterinary Medical Diagnostic Laboratory in College Station initially analyzed postmortem samples, and the National Veterinary Services Laboratory in Ames, Iowa, confirmed 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.
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 page.
The recently updated TPWD CWD webpage 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. Additional information regarding TAHC requirements, CWD zones, disease information and details pertaining to susceptible exotic species can be found on the TAHC CWD webpage.
TEXAS CWD Detected in Additional Breeding Facilities in Frio and Zavala Counties
Chronic Wasting Disease Detected in Additional Breeding Facilities in Frio and Zavala Counties
July 13, 2023
Media Contact: TPWD News, Business Hours, 512-389-8030 News Image Share on Facebook Share Release URL
AUSTIN — Texas Parks and Wildlife Department (TPWD) received notification of two new cases of Chronic Wasting Disease (CWD) in deer-breeding facilities in Frio and Zavala Counties.
In Frio County, a 2-year-old white-tailed doe died in a deer-breeding facility and was post-mortem tested following CWD surveillance testing requirements. This is the second deer-breeding facility in Frio County to have a positive CWD detection.
In Zavala County, a 3-year-old white-tailed buck died in a deer-breeding facility and was post-mortem tested following CWD surveillance testing requirements. This is the second deer-breeding facility in Zavala County to have a positive CWD detection.
Texas A&M Veterinary Medical Diagnostic Laboratory in College Station initially analyzed postmortem samples; the National Veterinary Services Laboratory in Ames, Iowa, provided a CWD-positive confirmation for both samples.
During the upcoming August meeting of the Texas Parks and Wildlife Commission, TPWD staff will propose the development of CWD surveillance zones within the general vicinity of both CWD-positive facilities. If the proposal passes, the zones will include mandatory sampling of hunter harvested deer, as well as carcass movement and disposal requirements to take effect during the upcoming deer season.
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 a disease outbreak and can greatly reduce the risk of further disease spread.
CWD is a fatal neurological disease found in certain cervids including deer, elk, moose and other members of the deer family. This slow, progressive disease may not produce visible signs in susceptible species for several years after infection. As the disease progresses, 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 page.
Texas Chronic Wasting Disease Discovered in Deer Breeding Facilities in Frio and Hamilton Counties
For Immediate Release
April 11, 2023
Chronic Wasting Disease Discovered in Deer Breeding Facilities in Frio and Hamilton Counties
AUSTIN, TX – Texas Parks and Wildlife Department (TPWD) and Texas Animal Health Commission (TAHC) received confirmation of two new cases of Chronic Wasting Disease (CWD) in separate deer breeding facilities in Hamilton and Frio counties. These cases mark the first detection of the disease in each county.
A single case in a Hamilton County facility was detected using antemortem (live animal) testing conducted to determine if the animal was movement qualified to transfer from the property to a registered release site. A single case in a Frio County facility was detected using postmortem testing following a natural mortality conducted to meet TPWD surveillance requirements.
The samples submitted to the Texas A&M Veterinary Medical Diagnostic Laboratory in College Station were ultimately sent to the National Veterinary Services Laboratory (NVSL) in Ames, Iowa, where the presence of CWD was confirmed in all samples. Officials took immediate action to secure all deer at the facilities. TPWD and TAHC plan to continue working together to conduct additional investigations into the extent of the disease within the facilities.
With an incubation period that can span years, the first indication of CWD in a herd may likely come through testing, rather than observing clinical signs. Early detection and proactive monitoring improve the state’s response time to a disease outbreak and can greatly reduce the risk of further disease spread. Antemortem testing provides a continuous testing baseline that can further clarify the epidemiological uncertainties related to the origin of a disease outbreak. In addition to postmortem testing and other surveillance requirements, this testing helps guide future changes to the disease management strategy.
CWD is a fatal neurological disease found in certain cervids including deer, elk, moose and other members of the deer family. CWD is a slow and progressive disease. Due to a long incubation, cervids infected with CWD may not produce any visible signs for several years after becoming infected. As the disease progresses, animals with CWD show changes in behavior and appearance. Clinical signs may include progressive weight loss, stumbling or tremors with a lack of coordination, excessive thirst, salivation or urination, loss of appetite, teeth grinding, abnormal head posture and/or drooping ears.
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 captive and free-ranging cervids in the state including, white-tailed deer, mule deer, red deer and elk. For more information on previous detections in Texas, visit TPWD’s CWD page.
To date there are no known cases where CWD has infected a human; however, recent research suggests that CWD transmission from infected animals to humans should not be ruled out. As a precaution, it is recommended that hunters test harvested cervid species for CWD, and not consume the meat of infected animals.
For more information about CWD, visit the TPWD website or the TAHC website.
### The Texas Animal Health Commission (TAHC) was established in 1893 as the Livestock Sanitary Commission and charged with protecting the state’s domestic animals “from all contagious or infectious diseases of a malignant character.” TAHC remains true to this charge while evolving with the times to protect the health and marketability of all Texas livestock and poultry. Learn more about the TAHC visit www.tahc.texas.gov.
Texas CWD seven new cases three separate deer-breeding facilities in Zavala, Washington and Gonzales counties 471 confirmed to date
Chronic Wasting Disease Discovered in Deer-Breeding Facilities in Zavala, Washington and Gonzales Counties
March 21, 2023
Media Contact: TPWD News, Business Hours, 512-389-8030 News
Additional Case Detected at High-Fence Release Site in Hunt County
AUSTIN – The Texas Parks and Wildlife Department (TPWD) and Texas Animal Health Commission (TAHC) received confirmation of seven new cases of chronic wasting disease (CWD) in three separate deer-breeding facilities in Zavala, Washington and Gonzales counties. These cases mark the first detection of the disease in each county.
Three cases in a Zavala County facility and one case in a Washington County facility were detected through antemortem (live animal) testing conducted prior to their transfer from the properties to registered release sites. Three cases in a Gonzales County facility were detected by antemortem and postmortem testing, as required by a CWD Herd Plan established after the facility received CWD-exposed deer from an Uvalde County deer breeding facility in which CWD was detected in 2021.
The samples were submitted to the Texas A&M Veterinary Medical Diagnostic Laboratory in College Station and were ultimately sent to the National Veterinary Services Laboratory in Ames, Iowa, where the presence of CWD was confirmed in all seven samples. Officials have taken immediate action to secure all deer at the facilities; TPWD and TAHC plan to continue working together to conduct additional investigations looking into the extent of the disease within the facilities.
“It continues to be imperative for producers to stay diligent with testing susceptible species for CWD,” said Dr. Andy Schwartz, TAHC executive director and state veterinarian. “With an incubation period that can span years, the first indication of this degenerative disease in a herd may likely come through testing, rather than observing clinical signs. Early detection and proactive monitoring improve the state’s response time and can greatly reduce the risk of further disease spread.”
Since November 2021, when the Texas Parks and Wildlife Commission adopted a requirement to antemortem test deer for CWD prior to liberation, this disease surveillance tool has detected CWD in five deer breeding facilities where it was not previously known to exist. Transferring even one CWD-infected deer from a breeding facility could ultimately affect all deer in the vicinity of the transfer, with irreversible impacts.
“With disease surveillance, our goal is to monitor and identify disease expeditiously to minimize the impact of outbreaks,” said Dr. Hunter Reed, TPWD wildlife veterinarian. “This is a continuous process that hopefully results in little to no disease being detected since [ideally] our disease management strategies are effective in limiting transmission. This additional surveillance from antemortem testing not only allows us to respond more quickly to an outbreak, but it also provides us with a robust, continuous testing baseline that can further elucidate the epidemiological uncertainties related to the origin of the disease outbreak, in addition to guiding future changes to our disease management strategy.”
In Hunt County, TPWD and TAHC received confirmation of CWD in a white-tailed doe harvested on a release site located adjacent to a breeding facility already known to have CWD. This is the first positive detection in a free-range deer in the county.
First recognized in the U.S. in 1967, CWD has since been documented in captive and/or free-ranging deer in 30 states and three Canadian provinces.
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 and has since been detected in 471 captive or free-ranging cervids — including white-tailed deer, mule deer, red deer and elk — in 20 Texas counties. For more information on previous detections, visit TPWD’s CWD page.
CWD is a fatal neurological disease found in certain cervids, including deer, elk, moose and other members of the deer family. CWD is a slow and progressive disease. Due to a long incubation, cervids infected with CWD may not produce any visible signs for several years after becoming infected. As the disease progresses, animals with CWD show changes in behavior and appearance. Clinical signs may include progressive weight loss, stumbling or tremors with a lack of coordination, excessive thirst, salivation or urination, loss of appetite, teeth grinding, abnormal head posture and/or drooping ears.
To date there are no known cases where CWD has infected a human; however, recent research suggests that CWD transmission from infected animals to humans should not be ruled out. Consequently, as a precaution, it is recommended that hunters test harvested cervid species for CWD, and that no one consumes the meat of infected animals.
For more information about CWD, visit the TPWD website or the TAHC website.
“A total of 505 cervids (including white-tailed deer, mule deer and elk) have tested positive for CWD in Texas. Free-ranging deer have accounted for 101 of those cases while 404 are associated with a breeding facility or breeder release site.”
Texans spend $4.3 billion annually hunting white-tailed deer, Texas A&M study shows
TEXAS SPORTS NATION
GENERAL
Texans spend $4.3 billion annually hunting white-tailed deer, Texas A&M study shows
Matt Wyatt Staff writer May 26, 2023
Deer hunters and landowners participating in Texas' hugely popular Managed Lands Deer Program, which offers a longer deer season and other liberalized deer hunting rules, will begin paying a modest annual fee for the voluntary program under a law recently adopted by the Texas Legislature. Shannon Tompkins/Houston Chronicle
Few states, if any, can claim a closer connection to white-tailed deer hunting than Texas.
snip...
“One of the things that there was an interest in was better understanding the overall value, or economic importance of whitetail deer within the context of various other ongoing challenges or issues, including chronic wasting disease,” Lopez said.
“There was an interest in trying to better understand the potential economic implications of a challenging issue like chronic wasting disease to this very specific industry.”
A total of 505 cervids (including white-tailed deer, mule deer and elk) have tested positive for CWD in Texas. Free-ranging deer have accounted for 101 of those cases while 404 are associated with a breeding facility or breeder release site.
There is currently no cure for CWD, and it is considered impossible to eradicate once it becomes established.
As this disease continues to creep across the Texas landscape, it could eventually have negative impacts on white-tailed deer populations.
A decline in white-tailed deer numbers could cut into the $4.3 billion spent every year on hunting, spelling disaster for the local economies and communities that depend on that money and the other wildlife species that benefit from it.
ECONOMIC VALUES OF WHITE-TAILED DEER IN TEXAS
2022 SURVEY: PART I
Chronic Wasting Disease (CWD):
2021 Incident
7 Positive Facilities
3 Facilities in Uvalde, 1 in Duval, 1 in Hunt, 1 in Matagorda, & 1 in Mason
1 release site in Hunt co. associated with a positive 2021 facility - NVSL confirmed March 17, 2023.
302 Trace Herds: 177 Breeder Facilities, 116 Release Sites, 4 Nursing Facilities, 5 DMP Sites
Status
Released after meeting requirements: 165 Breeder Facilities, 59 Release Sites/DMPs /Nursing Facilities
Under a Herd Plan: 5 Breeder Facilities (includes positive facilities), 25 Release Sites/DMP
Pending a signed herd plan: 7 Breeder Facilities (includes positive facilities), 41 Release Sites/DMP
Out of State - 8 Facilities
2022 Incident - 84 total involved herds
2 Positive Facilities
Gillespie County – Confirmed August 30, 2022
Limestone County – Confirmed September 13, 2022
82 Trace Facilities
22 Breeder Facilities
59 Release Sites
1 DMP Site
Status
Released after meeting requirements: 10 Breeder Facilities, 5 Release Sites
Signed Herd Plan – 14 Release Sites
Pending Signed Herd Plan: 14 Breeder Facilities (includes positive facilities), 41 Release Sites/DMP
Summary Minutes of the 415th Commission Meeting – 4/04/2023
4
2023 Incident - 44 total affected herds
4 Positive Facilities
Zavala County – confirmed March 10, 2023
Washington County – confirmed March 7, 2023
Gonzales County – confirmed March 17, 2023
Hamilton County – confirmed March 21, 2023
40 Trace Facilities: 10 Breeder Facilities, 28 Release Sites, 1 DMP Site, 1 Nursing Facility
Status
Released after meeting requirements – 1 Breeder Facility
Under a Herd Plan- None at this time: Unconfirmed Frio County Facility- suspect positive notification received March 17, 2023
1 Positive Facility
17 Trace Facilities: 2 Breeder Facilities, 13 Release Sites, 2 DMP Sites
Released after meeting requirements – 2 Breeder Facilities
USDA VS review of the Texas CWD HCP
TAHC is working with TPWD to modify the TWIMS database to better support the HCP
Review of all enrolled herds has begun, and is to be completed by the end of February 2023
Update: USDA extended the deadline. Reviews have been completed in four of the six regions, with good progress being made in the remaining two regions.
“Regarding the current situation involving CWD in permitted deer breeding facilities, TPWD records indicate that within the last five years, the seven CWD-positive facilities transferred a total of 2,530 deer to 270 locations in 102 counties and eight locations in Mexico (the destinations included 139 deer breeding facilities, 118 release sites, five Deer Management Permit sites, and three nursing facilities).'' ...
It is apparent that prior to the recent emergency rules, the CWD detection rules were ineffective at detecting CWD earlier in the deer breeding facilities where it was eventually discovered and had been present for some time; this creates additional concern regarding adequate mitigation of the risk of transferring CWD-positive breeder deer to release sites where released breeder deer come into contact with free-ranging deer...
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).
Commission
September 22, 2020
Chronic Wasting Disease (CWD):
A new CWD positive breeding herd was disclosed in February 2020 in Kimble County. This herd depopulation was completed in July 2020. Including the two index positive deer, an additional eight more positive deer were disclosed (approximate herd prevalence 12%). Since July 2015 and prior to this discovery, five positive captive breeder herds have been disclosed and four of those are in Medina County. One herd in Lavaca and three herds in Medina County were depopulated leaving one large herd in Medina County that is managed on a herd plan. A new zone was established in Val Verde County in December 2019 as a result of a positive free-ranging White-tailed Deer (WTD). A second positive WTD was also disclosed in February 2020 in the same area.
SUMMARY MINUTES OF THE 407th COMMISSION MEETING – 9/22/2020
Scrapie: The flock identified in April 2016 remains under quarantine in Hartley County.
SUMMARY MINUTES OF THE 407th COMMISSION MEETING – 9/22/2020
Texas CWD Herd Kimble County Has approximate prevalence 12% to date
Results: Our results show a 15-fold increase in CWD detection in free-range deer compared with ELISA. Our results unveil the presence of prion infected animals in Texas counties with no previous history of CWD. In the case of captive deer, we detected a 16% more CWD positive animals when compared with IHC. Interestingly, some of these positive samples displayed differences in their electroforetic mobilities, suggesting the presence of different prion strains within the State of Texas. Conclusions: PMCA sensitivity is significantly higher than the current gold standards techniques IHC and ELISA and would be a good tool for rapid CWD screening.
CWD poses a significant threat to the future of hunting in Texas. Deer population declines of 45 and 50 percent have been documented in Colorado and Wyoming. A broad infection of Texas deer populations resulting in similar population impacts would inflict severe economic damage to rural communities and could negatively impact land markets. Specifically, those landowners seeking to establish a thriving herd of deer could avoid buying in areas with confirmed CWD infections. As they do with anthrax-susceptible properties, land brokers may find it advisable to inquire about the status of CWD infections on properties that they present for sale. Prospective buyers should also investigate the status of the wildlife on prospective properties. In addition, existing landowners should monitor developments as TPWD crafts management strategies to identify and contain this deadly disease.
Dr. Gilliland (c-gilliland@tamu.edu) is a research economist with the Texas Real Estate Research Center at Texas A&M University.
Texas CWD Surveillance Positives
Counties where CWD Exposed Deer were Released
Number of CWD Exposed Deer Released by County
Chronic Wasting Disease CWD Captive Herds updated April 2023
Chronic Wasting Disease CWD Captive Herds updated April 2023
Listing of CWD Cases in Texas
TEXAS CWD STRAIN
“Wow,” he said. “Unlike anything we've seen before.”
The prions from the Texas deer were a lot harder to destroy than the ones from the Colorado elk. In fact, the guanidine barely damaged them at all. “We’ve never seen that before in any prion strain, which means that it has a completely different structure than we've ever seen before,” says Zabel. And that suggests that it might be a very different kind of chronic wasting disease. The researchers ran the same test on another Texas deer, with the same results.
TEXAS CWD STRAIN
77. Assessing chronic wasting disease strain differences in free-ranging cervids across the United States
Kaitlyn M. Wagnera, Caitlin Ott-Connb, Kelly Strakab, Bob Dittmarc, Jasmine Battend, Robyn Piercea, Mercedes Hennessya, Elizabeth Gordona, Brett Israela, Jenn Ballarde and Mark D Zabela
aPrion Research Center at Colorado State University; bMichigan Department of Natural Resources; cTexas Parks and Wildlife Department; dMissouri Department of Conservation, 5. Arkansas Game and Fish Commission CONTACT Kaitlyn M. Wagner miedkait@rams.colostate.edu
ABSTRACT
Background/Introduction: Chronic wasting disease (CWD) is an invariably fatal prion disease affecting captive and free-ranging cervids, including white-tailed deer, mule deer, moose, elk, and reindeer. Since the initial description of the disease in the 1960’s, CWD has spread to 23 states, 3 Canadian Provinces, South Korea, Norway and, most recently, Finland. While some outbreaks of CWD were caused by transport of infected animals from endemic regions, the origin of CWD in other epizootics is unclear and has not been characterized. Previous studies have shown that there are two distinct strains of CWD. However, the continuous spread and the unclear origin of several outbreaks warrant continued surveillance and further characterization of strain diversity.
Materials and Methods: To address these knowledge gaps, we used biochemical tests to assess strain differences between CWD outbreaks in Michigan, Texas, Missouri, and Colorado, USA. Brain or lymph node samples were homogenized and digested in 50 µg/mL proteinase K (PK). These samples were then run on a Western blot to assess glycoform ratio and electrophoretic mobility. Texas samples were digested in 100 µg/mL PK. To assess conformational stability, brain or lymph node homogenates were incubated in increasing concentrations of guanidine hydrochloride from 0 M to 4 M in 0.5 M increments. Samples were then precipitated in methanol overnight, washed and PK digested in 50 µg/mL PK before slot blotting.
Results: Our results have found significant differences in glycoform ratio between CWD from Michigan and Colorado, but no differences were observed in conformational stability assays. Interestingly, when testing our CWD isolates from Texas to analyse electrophoretic mobility and glycoform ratio, we found that these samples did not exhibit the characteristic band shift when treated with PK, but PK resistant material remained. Additionally, results from our conformational stability assay demonstrate a unique profile of these Texas isolates. Testing of samples from Missouri is currently underway.
Conclusions: Thus far, our data indicate that there are strain differences between CWD circulating in Michigan and CWD in Colorado and provide important insight into CWD strain differences between two non-contiguous outbreaks. We have also identified a unique strain of CWD in Texas with biochemical strain properties not seen in any of our other CWD isolates. These results highlight the importance of continued surveillance to better understand this devastating disease. These results have important implications for CWD emergence, evolution and our understanding of prion strain heterogeneity on the landscape.
CWD TEXAS SUTTON COUNTY FACILITY
TEXAS REPUBLICAN SB 1372 TAXPAYERS TO PAY FOR GAME FARMS CWD DEPOPULATION?
SB 1372
A BILL TO BE ENTITLED
AN ACT relating to costs associated with the destruction of certain deer.
BE IT ENACTED BY THE LEGISLATURE OF THE STATE OF TEXAS:
SECTION 1. Section 43.955, Parks and Wildlife Code, is amended to read as follows:
Sec. 43.955. COST OF ASSESSMENT AND DESTRUCTION OF DEER [RECOVERY]. (a) The applicable permit holder shall pay all costs associated with:
(1) an epidemiological assessment conducted under this subchapter to the animal health commission; and
(2) except as provided by Subsection (b), the destruction of deer under this subchapter to the department.
(b) Except as provided by Subsection (c), the department shall waive the costs associated with the destruction under this subchapter of breeder deer at a facility covered by a permit issued under Subchapter L where a breeder deer has tested positive for chronic wasting disease in a test performed by a testing laboratory accredited by the Animal and Plant Health Inspection Service of the United States Department of Agriculture.
(c) The department may not waive costs under Subsection (b) if the department determines that the permit holder or an agent of the permit holder, in violation of this chapter or a regulation of the commission, caused:
(1) the introduction of chronic wasting disease into the facility; or
(2) a delay in the detection of chronic wasting disease at the facility.
SECTION 2. Section 43.955, Parks and Wildlife Code, as amended by this Act, applies only to the payment of costs arising from the destruction of deer commenced on or after the effective date of this Act.
SECTION 3. This Act takes effect immediately if it receives a vote of two-thirds of all the members elected to each house, as provided by Section 39, Article III, Texas Constitution. If this Act does not receive the vote necessary for immediate effect, this Act takes effect September 1, 2023.
That can mean the killing of hundreds of expensive animals, and the financial ruin of their rancher.
snip...
“This bill essentially allows Parks and Wildlife to absorb that cost, which we believe helps remove the threat from the landscape quicker, with better landowner relations for the department, and ultimately we think that moves the needle as far as managing the disease,” Dreibelbis said.
snip...
In order to become law, the CWD bill still has to pass the House chamber with a majority vote and then be signed by Gov. Greg Abbott. The chair of the House committee that most recently approved the bill, Rep. Trent Ashby, said in an emailed statement that he was pleased to see the bill making its way through the legislature.
TEXAS REPUBLICAN SB 1372 TAXPAYERS TO PAY FOR CWD TSE PRION DEPOPULATION OF GAME FARMS
The chair of the House committee that most recently approved the bill, Rep. Trent Ashby, said in an emailed statement that he was pleased to see the bill making its way through the legislature.
SO, the taxpayers will have the burden of paying for deer breeders cost of depopulation of their CWD deer herd?...that's crazy if true, and everyone should write Governor Abbott and tell him...taxpayers should not have to pay for game farms cwd depopulation...IMO...terry
what's Governor Abbott history with supporting deer farms?
Governor Abbott on HOW TO LEGISLATE SPREADING CWD TO HELL AND BACK IN TEXAS $$$
i picked up on something that was said, there were several folks complaining that the breeders were getting picked on, and someone said something about trying to 'legislate' there way out of this. folks, this is terrible, i have seen this in other states, and it just spreads cwd even more. hell, it happened right here in Texas in the early days, that's why we are where were at now, you cannot let a bunch of Austin Legislative Socialites regulate CWD, just look what happened in Wisconsin. but i bet this attempted swaying of regulatory power shift from TPWD et al to the Texas Legislature in Austin is happening as we speak. we can't let this happen...
SUNDAY, JANUARY 22, 2017
Texas 85th Legislative Session 2017 Chronic Wasting Disease CWD TSE Prion Cervid Captive Breeder Industry
FRIDAY, JANUARY 27, 2017
TEXAS, Politicians, TAHC, TPWD, and the spread of CWD TSE Prion in Texas
SUNDAY, MAY 14, 2017
85th Legislative Session 2017 AND THE TEXAS TWO STEP Chronic Wasting Disease CWD TSE Prion, and paying to play $$$
Powerful Abbott appointee's lobbying sparks blowback in Legislature
In an ironic twist for Gov. Greg Abbott, who has made ethics reform an urgent political priority, the Texas House is taking aim at what critics call a "pay to play" culture among his appointees.
BY JAY ROOT MAY 12, 2017 12 AM
Houston billionaire Dan Friedkin is chairman of the Texas Parks and Wildlife Commission.
Texas Parks and Wildlife Commission
When Gov. Greg Abbott tapped one of his top campaign donors to become chairman of the Texas Parks and Wildlife Commission, he didn’t get a part-time appointee who would merely draft rules and implement conservation laws passed by the Legislature.
In Dan Friedkin, the governor got a Houston billionaire — with a team of privately funded lobbyists — willing to use his influence to ensure his wildlife interests are taken into account by the Legislature before they pass those laws, interviews and records show.
On the receiving end of that influence, and not in a happy way, is state Rep. Chris Paddie, R-Marshall. Paddie said a lobbyist working for Friedkin’s business empire, which includes a massive South Texas hunting ranch, has been working against his deer breeder management bill, which many large ranchers oppose. The state Parks and Wildlife Department oversees deer breeding regulations in Texas.
“Many times these appointees are well-heeled, very influential people,” Paddie said. “Overall, I feel that it’s inappropriate for an appointee of a board or commission to have personal lobbyists lobbying on issues related to that board or commission.”
Under Texas law, state agencies are barred from lobbying the Legislature. But the powerful people who oversee them aren’t.
If Paddie and dozens of his colleagues get their way, that practice soon will be a Class A misdemeanor.
Last weekend, Paddie attached a ban on appointee lobbying — which would apply to any issues intersecting with their state responsibilities — to an ethics bill that already had powerful friends of the governor in its crosshairs. The provision was adopted unanimously and the bill sailed out of the Texas House on a 91-48 vote Saturday.
The ethics bill, authored by Rep. Lyle Larson, R-San Antonio, would bar big campaign donors from getting appointed by governors in the first place. Anyone who contributed over $2,500 would be barred from serving on state boards and commissions.
Larson pointed to news articles documenting the amount of campaign money appointees have collectively given governors. Last year the San Antonio Express-News calculated that Abbott had received nearly $9 million from people he’s picked for appointed office; before that, a widely cited report from Texans for Public Justice found former Gov. Rick Perry had received $17 million from his own appointees.
Larson said 20 years from now, Texans will be reading the same stories about a future governor unless the Legislature does something about it now.
“We’ve read that article for the last three decades,” Larson said during a brief floor speech. “This is your opportunity to say, 'We need to stop this.' The most egregious ethics violation we’ve got in the state is the pay to play in the governor’s office.”
A prodigious fundraiser, Abbott has put plenty of big donors on prestigious boards and commissions. On the Parks and Wildlife Commission alone, he has installed three mega-donors — pipeline mogul Kelcy Warren, who’s given Abbott more than $800,000 over his statewide political career; Houston businessman S. Reed Morian, who has given $600,000; and Friedkin, who personally donated more than $700,000 — while his Gulf States Toyota PAC gave Abbott another $100,000, according to Ethics Commission records.
Passage of Larson’s HB 3305 represents an ironic twist for Abbott, who for the second session in a row has made ethics reform an urgent political priority — resulting in a bill that's now taking aim at his gubernatorial appointments. Abbott, who has made a habit of ignoring tough questions, hasn't made any public statements about the bill, and his office did not respond to multiple requests for comment.
Friedkin — whose wealth is estimated at $3.4 billion by Forbes — is the owner and CEO of Gulf States Toyota, founded in 1969, which has had the exclusive rights to distribute new Toyotas in Texas and four nearby states. He’d also been a mega-donor to former Gov. Rick Perry, who first appointed Friedkin to the Parks and Wildlife Commission in 2005. Abbott made Friedkin chairman of the commission in 2015.
Requests for comment from Friedkin's office went unanswered.
In addition to his public role as parks and wildlife chairman, a perch that gives him significant influence over deer management issues, Friedkin has private wildlife interests. He owns the sprawling Comanche Ranch in South Texas, according to published news accounts.
The January 2014 edition of Texas Wildlife, published by the Texas Wildlife Association, described Friedkin’s Comanche Ranch as “privately owned and privately hunted” and said it’s “in the business to produce as many trophy bucks as possible, without damaging the native habitat.”
The association, which advocates for private landowners and hunting rights, has locked horns with deer breeding interests at Parks and Wildlife and the Capitol. They compete against each other in the lucrative trophy deer hunting market — and the battle between them perennially spills into the rule-making process at the Parks and Wildlife Commission.
One of their battles centers on how captive deer are tagged so that game wardens and others can distinguish them from native deer. Current law requires a combination of tags and tattoos, and the ranchers and large landowners want to keep it that way. The breeders, meanwhile, favor tagging deer with microchips, which they contend are more accurate and foolproof.
The Wildlife Association said in a Facebook post that removing visible tag or tattoo requirements and allowing microchip tracking “creates real biosecurity risks and blurs ethical lines in the hunting community, as captive deer breeders are allowed to transport and release these animals to be co-mingled with pasture-born deer.” Proponents of the current system say tough rules on breeders are needed to keep out imported deer that may carry Chronic Wasting Disease, which has been found in Texas.
On the other side of the issue is the Texas Deer Association, which represents breeder interests. Executive Director Patrick Tarlton said opposition to his $1.6 billion industry stems less from environmental and health concerns and more from wealthy ranch owners who want to boost profits from trophy-seeking hunters. He notes that Chronic Wasting Disease has been found in both free range and captive deer.
Paddie sided with the breeders by filing House Bill 2855, which would allow breeders to track their deer with microchips instead of relying on physical tags that they say can be torn off.
No one identifying themselves as a Friedkin corporate lobbyist opposed the deer breeding bills during public hearings, according to House and Senate committee records published online.
Behind the scenes, it was a different story.
Paddie said his chief of staff reached out to Laird Doran, one of several lobbyists for Friedkin’s Gulf States Toyota, after hearing that he was trying to convince other legislators to help defeat Paddie's deer microchip bill.
“My chief called him and said, 'Hey, if you’ve got a problem with our bill why aren’t you talking to us?’ ” Paddie said. “He said he represented the Friedkin Group when that happened.”
According to an email from an aide to Sen. Craig Estes, R-Wichita Falls, who is carrying the deer breeding bill in the Senate, Doran also identified himself as a representative of the “Friedkin Group.” That’s the name of the consortium that contains Friedkin's Gulf States Toyota, according to the company’s Linked-In page. He told Estes’ aide that the Friedkin group was opposed to any bill that would “remove requirements for (deer) ear tags,” the senator’s office confirmed.
It’s not clear exactly which Friedkin interests Doran was advancing. Doran is registered at the Texas Ethics Commission with a single entity — Gulf States Toyota — and the agency has no record of a lobbyist working for an entity or individual with the name Friedkin in it, the commission confirmed Wednesday afternoon.
However, Doran checked a variety of non-automotive subject areas in which he is lobbying during this legislative session on behalf of Friedkin’s lucrative distributorship, including “animals,” “parks & wildlife,” “state agencies, boards & commissions,” “environment” and more, his detailed lobby disclosures show.
Doran, director of government relations and senior counsel at the Friedkin Group, did not return phone and email messages left by The Texas Tribune.
Estes said he didn’t have a problem with a governor's appointee engaging in lobbying on issues that affected their private interests, as long as they keep that separate from their state roles.
“I don’t think they should be barred from expressing their views as long as they’re careful to say these are my views, not the views of the agency I’m representing,” Estes said.
But Tarlton, the deer association director, said Friedkin’s use of lobbyists to oppose deer breeders in the Legislature gives the breeders' opponents a huge advantage.
“I think that if the commissioner of Texas Parks and Wildlife is actively lobbying against an industry which his department directly oversees, it absolutely sets up an unfair and closed system of government,” Tarlton said. “The commission is supposed to be the unbiased and equitable oversight for everything wildlife.”
Paddie hopes his amendment to Larsen's ethics bill will even the playing field. He referred to the wealthy Parks and Wildlife chairman (see the 2:29:00 mark in this recorded exchange) when he tacked the appointee-lobbying provision onto Larson’s bill.
Paddie said he’s not singling out anyone. He said it would apply to other powerful gubernatorial appointees in a position to do the same.
“I could have named any number of examples as far as the agencies in particular,” Paddie said. “I want to stop it if anyone serving on any agency is doing this.”
Ryan Murphy contributed to this report.
Disclosure: The Texas Wildlife Association, Texas Parks and Wildlife Department and Gulf States Toyota have been financial supporters of The Texas Tribune. A complete list of Tribune donors and sponsors is available here.
MONDAY, MAY 15, 2023
TAHC Chapter 40, Chronic Wasting Disease and Scrapie Chapter 60, Singeltary Comment Submission
Greetings TAHC et al,
Thank you kindly for giving me the opportunity to once again comment on CWD and Scrapie.
I want to thank the TAHC and the TPWD for coming together and seems now bring forth sound science, of the real risk factors for both CWD and Scrapie.
With great urgency, i wish to bring your attention on updated Science on Chronic Wasting Disease CWD and Scrapie TSE Prion Environmental Factors and Zoonotic factors, spillover risk factors of CWD and Scrapie to other species i.e. PIGS, our failed feed ban of which now should include all cervid and pigs imo. i saw no mention of atypical Scrapie and the new science from EFSA, i shall include that as well. there is a new TSE Prion disease in a new livestock species the Camel, you should all be aware of. all of this is most important, and should be addressed in any cwd update imo, especially with CWD and Scrapie transmitting to pigs by oral routes.
i will post my concerns below, Thank You Kindly...terry
TAHC Chapter 40, Chronic Wasting Disease and Scrapie Chapter 60, Singeltary Comment Submission
***> TEXAS HISTORY OF CWD <***
Singeltary telling TAHC, that CWD was waltzing into Texas from WSMR around Trans Pecos region, starting around 2001, 2002, and every year, there after, until New Mexico finally shamed TAHC et al to test where i had been telling them to test for a decade. 2012 cwd was detected first right there where i had been trying to tell TAHC for 10 years.
***> Singeltary on Texas Chronic Wasting Disease CWD TSE Prion History <***
TUESDAY, JUNE 27, 2023
USAHA Report of the Subcommittee on Farmed Cervidae CWD TSE Prion Herds 2015 to 2023
Chronic Wasting Disease CWD Transmissible Spongiform Encephalopathy TSE Prion PrP ZOONOSIS
“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.
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.
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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.
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Efficient CWD-like transmission of splenic prions in cervidized transgenic mice: a probable diagnostic marker for CWD infection in humans
Xu Qi, Liuting Qing, Manuel Camacho, Ignazio Cali, Qingzhong Kong
Department of Pathology, Case Western Reserve University, Cleveland, USA
***> Such experimentally generated splenic “humanized” CWD prions (termed eHuCWDsp) appear indistinguishable from prions in the brain of sCJDMM1 patients on Western blot.
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
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Transmission
10:00 - 11:40am Thursday, 1st June, 2023
Plaza Ballroom
Moderator Dr. Tracy Nichols
10:00 - 10:20am
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
Abstract
We provide evidence by transmission experiments to different transgenic mouse models and bank voles that Cynomolgus macaques inoculated via different routes with CWD-positive cervid tissues harbor infectious prions. We used tissue materials from macaques inoculated with CWD to inoculate transgenic mice overexpressing cervid PrPC followed by transmission into bank voles. We used RTQuIC, immunoblot and PET blot analysis to assess brains, spinal cords, and tissues of the gastrointestinal tract (GIT) for the presence of prions. Our results show that macaque materials induced clinical disease in transgenic mice with low attack rates. Clinical mice did not display PrPSc in immunoblot, but showed low-levels of prion seeding activity. Further transmission into bank voles led to a 100% attack rate with typical PrPSc signature in immunoblot, and high-level prion seeding activity in brain, spinal cord and GIT tissues. Second passage studies led to 100% attack rate in voles inoculated with brain, spinal cord and small intestine material from first round animals, with shortened survival times indicating adaptation in the new host.
This shows that prions detected in GIT tissues are infectious and transmissible.
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.
***> Our findings demonstrate that macaques, considered the best model for the zoonotic potential of prions, were infected upon CWD challenge, including the oral one.
Transmission of Cervid Prions to Humanized Mice Demonstrates the Zoonotic Potential of CWD
Samia Hannaouia, Irina Zemlyankinaa, Sheng Chun Changa, Maria Immaculata Arifina, Vincent Béringueb, Debbie McKenziec, Hermann M. Schatzla, and Sabine Gilcha
aDepartment of Comparative Biology and Experimental Medicine, Faculty of Veterinary Medicine; Hotchkiss Brain Institute; University of Calgary, Calgary, Canada; bUniversité Paris-Saclay, INRAE, UVSQ, VIM, Jouy-en-Josas, France; cDepartment of Biological Sciences, Center for Prions and Protein Folding Diseases, University of Alberta, Edmonton, Canada
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 tg650 brain 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.
Funded by: We are grateful for financial support from the Natural Sciences and Engineering Research Council of Canada, the National Institutes of Health, Genome Canada, and the Alberta Prion Research Institute. SG is supported by the Canada Research Chairs program.
Acknowledgement: We thank Dr. Trent Bollinger, WCVM, University of Saskatchewan, Saskatoon, Canada, for providing brain tissue from the WTD-116AG isolate, Dr. Stéphane Haïk, ICM, Paris, France, for providing brain tissue from vCJD and sCJD cases, and Dr. Umberto Agrimi, Istituto Superiore di Sanità, Italy, for the bank vole model. We thank animal facility staff for animal care, Dr. Stephanie Anderson for veterinary oversight, and Yo-Ching Cheng for preparing recombinant PrP substrates. Thank you to Dr. Stephanie Booth and Jennifer Myskiw, Public Health Agency of Canada, Canada.
The chronic wasting disease agent from white-tailed deer is infectious to humanized mice after passage through raccoons
Eric Cassmanna, Xu Qib, Qingzhong Kongb, and Justin Greenleea
aNational Animal Disease Center, Agricultural Research Service, US Department of Agriculture, Ames, IA, USA
bDepartments of Pathology, Neurology, National Center for Regenerative Medicine, and National Prion Disease Pathology Surveillance Center, Case Western Reserve University, Cleveland, Ohio, USA
Aims: Evaluate the zoonotic potential of the raccoon passaged chronic wasting disease (CWD) agent in humanized transgenic mice in comparison with the North American CWD agent from the original white-tailed deer host.
Material and Methods: Pooled brain material (GG96) from a CWD positive herd was used to oronasally inoculate two white-tailed deer with wild-type prion protein genotype and intracranially inoculate a raccoon. Brain homogenates (10% w/v) from the raccoon and the two white-tailed deer were used to intracranially inoculate separate groups of transgenic mice that express human prion protein with methionine (M) at codon 129 (Tg40h). Brains and spleens were collected from mice at experimental endpoints of clinical disease or approximately 700 days post-inoculation. Tissues were divided and homogenized or fixed in 10% buffered neutral formalin. Immunohistochemistry, enzyme immunoassay, and western blot were used to detect misfolded prion protein (PrPSc) in tissue.
Results: Humanized transgenic mice inoculated with the raccoon passaged CWD agent from white-tailed deer exhibited a 100% (12/12) attack rate with an average incubation period of 605 days. PrPScwas detected in brain tissue by enzyme immunoassay with an average optical density of 3.6/4.0 for positive brains. PrPScalso was detected in brain tissue by western blot and immunohistochemistry. No PrPScwas detected in the spleens of mice inoculated with the raccoon passaged CWD agent. Humanized mice inoculated with the CWD agent from white-tailed deer did not have detectable PrPScusing conventional immunoassay techniques.
Conclusions: The host range of the CWD agent from white-tailed deer was expanded in our experimental model after one passage through raccoons.
Funded by: This research was funded in its entirety by congressionally appropriated funds to the United States Department of Agriculture, Agricultural Research Service. The funders of the work did not influence study design, data collection and analysis, decision to publish, or preparation of the manuscript.
Acknowledgement: We thank Quazetta Brown, Lexi Frese, Rylie Frese, Kevin Hassall, Leisa Mandell, and Trudy Tatum for providing excellent technical support to this project.
Stable and highly zoonotic cervid prion strain is possible
Manuel Camacho, Xu Qi, Liuting Qing, Sydney Smith, Jieji Hu, Wanyun Tao, Ignazio Cali, and Qingzhong Kong
Department of Pathology, Case Western Reserve University, Cleveland, USA
Aims: Whether CWD prions can infect humans remains unclear despite the very substantial scale and long history of human exposure of CWD in some areas. Multiple in vitro conversion experiments and in vivo animal studies suggest that the CWD-to-human transmission barrier is not unbreakable. A major public health concern on CWD zoonosis is the emergence of highly zoonotic CWD strains. We aim to address the question of whether highly zoonotic CWD strains are possible.
Material and Methods: We inoculated a few sCJD brain samples into cervidized transgenic mice, which were intended as negative controls for bioassays of brain tissues from sCJD cases who had hunted or consumed vension from CWD-endemic states. Some of these mice became infected and their brain tissues were further examined by serial passages in humanized or cervidized mice.
Results: Passage of sCJDMM1 in transgenic mice expressing elk PrP (Tg12) resulted in a ‘cervidized’ CJD strain that we termed CJDElkPrP. We observed 100% transmission of CJDElkPrPin transgenic mice expressing human PrP (Tg40h). We passaged CJDElkPrPtwo more times in the Tg12 mice. We found that such second and third passage CJDElkPrPprions also led to 100% infection in the Tg40h mice. In contrast, we and others found zero or poor transmission of natural elk CWD isolates in humanized mice, despite that natural elk CWD isolates and CJDElkPrPshare the same elk PrP sequence.
Conclusions: Our data demonstrate that highly zoonotic cervid prion strains are not only possible but also can be stably maintained in cervids and that CWD zoonosis is prion strain-dependent.
Funded by: NIH
Grant number: R01NS052319, R01NS088604, R01NS109532
Acknowledgement: We want to thank the National Prion Disease Pathology Surveillance Center and Drs. Allen Jenny and Katherine O’Rourke for providing the sCJD samples and the CWD samples, respectively.
Adaptation of chronic wasting disease (CWD) prion strains in hosts with different PRNP genotypes
Camilo Duque Velasqueza,c, Elizabeth Triscotta,c, Chiye Kima,c, Diana Morenoa,c, Judd Aikenb,c, and Debbie McKenziea,c
aDepartment of Biological Science, University of Alberta, Edmonton, AB T6G 2G8, Canada; bDepartment of Agriculture, Food & Nutritional Science, University of Alberta, Edmonton, AB T6G 2G8, Canada; cCentre for Prions and Protein Folding Diseases, University of Alberta, Edmonton, AB T6G 2M8, Canada
Aims: The contagious nature of CWD epizootics and the PrPCamino acid variation of cervids (and susceptible sympatric species) guarantee the expansion of prion conformational diversity and selective landscapes where new strains can arise. CWD strains can have novel transmission properties including altered host range that may increase zoonotic risk as circulating strains diversify and evolve. We are characterizing the host adaptability of characterized CWD strains as well as CWD isolates from different cervid species in various enzootic regions.
Material and Methods: Characterized CWD strains as well as a number of isolates from hunter-harvested deer were bioassayed in our rodent panel (transgenic mice expressing cervid alleles G96, S96 and H95-PrPC, elk PrPC, bovine PrPC, and both hamsters and non-transgenic laboratory mice). Strain characteristics were compared using computer based scoring of brain pathology (e.g. PrPCWDbrain distribution), western blot and protein misfolding cyclic amplification (PMCA).
Results: Transmission of various isolates resulted in the selection of strain mixtures in hosts expressing similar PrPC, particularly for polymorphic white-tailed deer and for Norwegian reindeer. As of the second passage, transmission of P153 moose prions from Norway has not resulted in emergence of strains with properties similar to any North American CWD strains in our taxonomic collection (Wisc-1, CWD2, H95+and 116AG).
Conclusions: Our data indicates polymorphic white-tailed deer can favor infection with more than one strain. Similar to transmission studies of Colorado CWD isolates from cervids expressing a single PrPCprimary structure, the isolate from Norway reindeer (V214) represents a strain mixture, suggesting intrinsic strain diversity in the Nordfjella epizootic. The diversity of CWD strains with distinct transmission characteristics represents a threat to wildlife, sympatric domestic animals and public health.
Funded by: Genome Canada and Genome Alberta (Alberta Prion Research Institute and Alberta Agriculture & Forestry); NSERC
Grant number: #LSARP 10205; NSERC RGPIN-2017-05539
Acknowledgement: We would like to thank Margo Pybus (Alberta Environment and Parks) Trent Bollinger (University of Saskatchewan) for providing us with tissue samples from hunter-harvested deer and Sylvie Benestad for providing moose and reindeer samples.
Application of PMCA to understand CWD prion strains, species barrier and zoonotic potential
Sandra Pritzkowa, Damian Gorskia, Frank Ramireza, Fei Wanga, Glenn C. Tellingb, Justin J. Greenleec, Sylvie L. Benestadd, and Claudio Sotoa
aDepartment of Neurology, University of Texas Medical School at Houston, Houston, Texas, USA; bDepartment of Microbiology, Immunology and Pathology, Colorado State University, Fort Collins, Colorado, USA; cVirus and Prion Research Unit, United States Department of Agriculture, Ames, Iowa, USA; dNorwegian Veterinary Institute, OIE Reference Laboratory for CWD, Ås, Norway
Aims: Chronic wasting disease (CWD) is a prion disease affecting various species of cervids that continues to spread uncontrollably across North America and has recently been detected in Scandinavia (Norway, Sweden and Finland). The mechanisms responsible for the natural transmission of CWD are largely unknown. Furthermore, the risk of CWD transmission to other species, including humans, is also unknown and remains a dangerous enigma. In this study, we investigated the potential of CWD prions to infect several other animal species (sheep, cattle, pig, hamster, and mouse) including humans, by examining their capacity to convert the normal prion protein of distinct species in a PMCA reaction. Moreover, we also investigated whether the in vivo passage of CWD through intermediate species alters their capacity for zoonotic transmission, which may represent a major hazard to human health.
Material and Methods: For these studies, we used brain material from CWD-infected white-tailed deer (Odocoileus virginianus), elk (Cervus canadensis), and mule deer (Odocoileus hemionus) as species native to North America. We also used CWD-infected Moose (Alces alces), reindeer (Rangifer tarandus) and red deer (Cervus elaphus) as Norwegian cervids. We also used brains from cattle, sheep and pigs experimentally infected by CWD. To study interspecies-transmission and zoonotic potential, samples were tested via PMCA for the conversion of PrPCinto PrPScusing different combinations of inoculum and host species. Based on these analyses we estimated the spillover and zoonotic potential for different CWD isolates. We define and quantify spillover and zoonotic potential indices as the efficiency by which CWD prions sustain prion generation in vitro at the expense of normal prion proteins from various mammals and human, respectively.
Results: Our results show that prions from some cervid species, especially those found in Northern Europe, have a higher potential to transmit disease characteristics to other animals. Conversely, CWD-infected cervids originated in North America appear to have a greater potential to generate human PrPSc. We also found that in vivo transmission of CWD to cattle, but not to sheep or pigs substantially increases the ability of these prions to convert human PrPCby PMCA.
Conclusions: Our findings support the existence of different CWD prion strains with distinct spillover and zoonotic potentials. We also conclude that transmission of CWD to other animal species may increase the risk for CWD transmission to humans. Our studies may provide a tool to predict the array of animal species that a given CWD prion could affect and may contribute to understanding the risk of CWD for human health.
Funded by: National Institute of Health
Grant number: P01 AI077774
Generation of human chronic wasting disease in transgenic mice
Zerui Wanga, Kefeng Qinb, Manuel V. Camachoa, Ignazio Cali a,c, Jue Yuana, Pingping Shena, Tricia Gillilanda, Syed Zahid Ali Shaha, Maria Gerasimenkoa, Michelle Tanga, Sarada Rajamanickama, Anika Yadatia, Lawrence B. Schonbergerd, Justin Greenleee, Qingzhong Konga,c, James A. Mastriannib, and Wen-Quan Zoua,c
aDepartment of Pathology, Case Western Reserve University School of Medicine, Cleveland, OH, USA; bDepartment of Neurology and Center for Comprehensive Care and Research on Memory Disorders, the University of Chicago Pritzker School of Medicine, Chicago, USA; cNational Prion Disease Pathology Surveillance Center, Case Western Reserve University School of Medicine, Cleveland, OH 44106, USA; dDivision of High-Consequence Pathogens and Pathology, Centers for Disease Control and Prevention, 1600 Clifton Rd, Atlanta, GA, USA; eVirus and Prion Research Unit, National Animal Disease Center, USDA, Agricultural Research Service, 1920 Dayton Avenue, Ames, IA, USA
Aims: Chronic wasting disease (CWD) results from the accumulation of an infectious misfolded conformer (PrPSc) of cellular prion protein (PrPC) in the brains of deer and elk. It has been spreading rapidly throughout many regions of North America, exported inadvertently to South Korea, and more recently identified in Europe. Mad cow disease has caused variant Creutzfeldt-Jakob disease (vCJD) in humans and is currently the only known zoonotic prion disease. Whether CWD is transmissible to humans remains uncertain. The aims of our study were not only to confirm whether CWD prion isolates can convert human brain PrPCinto PrPScin vitro by serial protein misfolding cyclic amplification (sPMCA) but also to determine whether the sPMCA-induced CWD-derived human PrPScis infectious.
Material and Methods: Eight CWD prion isolates from 7 elks and 1 deer were used as the seeds while normal human brain homogenates containing either PrP-129 MM (n = 2) or PrP-129 VV (n = 1) were used as the substrates for sPMCA assay. A normal elk brain tissue sample was used as a negative control seed. Two lines of humanized transgenic (Tg) mice expressing either human PrP-129VV or −129 MM polymorphism were included for transmission studies to determine the infectivity of PMCA-amplified PrPSc. Wester blotting and immunohistochemistry and hematoxylin & eosin staining were used for determining PrPScand neuropathological changes of inoculated animals.
Results: We report here the generation of the first CWD-derived infectious human PrPScusing elk CWD PrPScto initiate conversion of human PrPCfrom normal human brain homogenates with PMCA in vitro. Western blotting with a human PrP selective antibody confirmed that the PMCA-generated protease-resistant PrPScwas derived from the human brain PrPCsubstrate. Two lines of humanized transgenic mice expressing human PrPCwith 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 PrPScpatterns and neuropathological changes in the brain.
Conclusions: Our study, using PMCA and animal bioassays, provides the first evidence that CWD PrPSchas the potential to overcome the species barrier and directly convert human PrPCinto infectious PrPScthat can produce bona fide prion disease when inoculated into humanized transgenic mice.
Funded by: CJD Foundation and NIH
PRION 2018 CONFERENCE
Oral transmission of CWD into Cynomolgus macaques: signs of atypical disease, prion conversion and infectivity in macaques and bio-assayed transgenic mice
Hermann M. Schatzl, Samia Hannaoui, Yo-Ching Cheng, Sabine Gilch (Calgary Prion Research Unit, University of Calgary, Calgary, Canada) Michael Beekes (RKI Berlin), Walter Schulz-Schaeffer (University of Homburg/Saar, Germany), Christiane Stahl-Hennig (German Primate Center) & Stefanie Czub (CFIA Lethbridge).
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 detected in spinal cord and brain of some 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 pre-clinical mice are currently tested using various read-outs and by second passage in mice. Transgenic mice expressing human PrP were so far negative for clear clinical prion disease (some mice >300 days p.i.). In parallel, the same macaque materials are inoculated into bank voles.
Taken together, there is strong evidence of transmissibility of CWD orally into macaques and from macaque tissues into transgenic mouse models, although with an incomplete attack rate.
The clinical and pathological presentation in macaques was mostly atypical, with a strong emphasis on spinal cord pathology. Our ongoing studies will show whether the transmission of CWD into macaques and passage in transgenic mice represents a form of non-adaptive prion amplification, and whether macaque-adapted prions have the potential to infect mice expressing human PrP.
The notion that CWD can be transmitted orally into both new-world and old-world non-human primates asks for a careful reevaluation of the zoonotic risk of CWD..
***> The notion that CWD can be transmitted orally into both new-world and old-world non-human primates asks for a careful reevaluation of the zoonotic risk of CWD. <***
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https://prion2018.org/
171. Schatzl HM, Hannaoui S, Cheng Y‐C, Gilch S, Beekes M, Schulz‐Schaeffer W, Stahl‐Hennig C and Czub S, 2018. Oral transmission of CWD into cynomolgus macaques: signs of atypical disease, prion conversion and infectivity in macaques and bio‐assayed transgenic mice. Prion, 2018, 35–36.
P219 First evidence of intracranial and peroral transmission of Chronic Wasting Disease (CWD) into Cynomolgus macaques: a work in progress
Stefanie Czub1, Walter Schulz-Schaeffer2, Christiane Stahl-Hennig3, Michael Beekes4, Hermann Schaetzl5 and Dirk Motzkus6 1 University of Calgary Faculty of Veterinary Medicine/Canadian Food Inspection Agency; 2Universitätsklinikum des Saarlandes und Medizinische Fakultät der Universität des Saarlandes; 3 Deutsches Primaten Zentrum/Goettingen; 4 Robert-Koch-Institut Berlin; 5 University of Calgary Faculty of Veterinary Medicine; 6 presently: Boehringer Ingelheim Veterinary Research Center; previously: Deutsches Primaten Zentrum/Goettingen
This is a progress report of a project which started in 2009. 21 cynomolgus macaques were challenged with characterized CWD material from white-tailed deer (WTD) or elk by intracerebral (ic), oral, and skin exposure routes. Additional blood transfusion experiments are supposed to assess the CWD contamination risk of human blood product. Challenge materials originated from symptomatic cervids for ic, skin scarification and partially per oral routes (WTD brain). Challenge material for feeding of muscle derived from preclinical WTD and from preclinical macaques for blood transfusion experiments. We have confirmed that the CWD challenge material contained at least two different CWD agents (brain material) as well as CWD prions in muscle-associated nerves.
Here we present first data on a group of animals either challenged ic with steel wires or per orally and sacrificed with incubation times ranging from 4.5 to 6.9 years at postmortem. Three animals displayed signs of mild clinical disease, including anxiety, apathy, ataxia and/or tremor. In four animals wasting was observed, two of those had confirmed diabetes. All animals have variable signs of prion neuropathology in spinal cords and brains and by supersensitive IHC, reaction was detected in spinal cord segments of all animals. Protein misfolding cyclic amplification (PMCA), real-time quaking-induced conversion (RT-QuiC) and PET-blot assays to further substantiate these findings are on the way, as well as bioassays in bank voles and transgenic mice.
At present, a total of 10 animals are sacrificed and read-outs are ongoing. Preclinical incubation of the remaining macaques covers a range from 6.4 to 7.10 years. Based on the species barrier and an incubation time of > 5 years for BSE in macaques and about 10 years for scrapie in macaques, we expected an onset of clinical disease beyond 6 years post inoculation.
https://cjdfoundation.org/files/pdf/CWD%20study%20oral%20transmission%20of%20CWD%20to%20primates.pdf
Subject: PRION 2017 CONFERENCE DECIPHERING NEURODEGENERATIVE DISORDERS VIDEO
PRION 2017 CONFERENCE DECIPHERING NEURODEGENERATIVE DISORDERS
PRION 2017 CONFERENCE VIDEO
Cervid to human prion transmission
Kong, Qingzhong Case Western Reserve University, Cleveland, OH, United States
We hypothesize that:
(1) The classic CWD prion strain can infect humans at low levels in the brain and peripheral lymphoid tissues;
(2) The cervid-to-human transmission barrier is dependent on the cervid prion strain and influenced by the host (human) prion protein (PrP) primary sequence;
(3) Reliable essays can be established to detect CWD infection in humans; and
(4) CWD transmission to humans has already occurred. We will test these hypotheses in 4 Aims using transgenic (Tg) mouse models and complementary in vitro approaches.
*** 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).***
8. Even though human TSE‐exposure risk through consumption of game from European cervids can be assumed to be minor, if at all existing, no final conclusion can be drawn due to the overall lack of scientific data. In particular the US data do not clearly exclude the possibility of human (sporadic or familial) TSE development due to consumption of venison. The Working Group thus recognizes a potential risk to consumers if a TSE would be present in European cervids. It might be prudent considering appropriate measures to reduce such a risk, e.g. excluding tissues such as CNS and lymphoid tissues from the human food chain, which would greatly reduce any potential risk for consumers. However, it is stressed that currently, no data regarding a risk of TSE infections from cervid products are available.
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The tissue distribution of infectivity in CWD‐infected cervids is now known to extend beyond CNS and lymphoid tissues. While the removal of these specific tissues from the food chain would reduce human dietary exposure to infectivity, exclusion from the food chain of the whole carcass of any infected animal would be required to eliminate human dietary exposure.
***> 1993 cjd report finds relationship with eat venison and cjd increases 9 fold
FINDINGS
*** 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). ***
*** 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). ***
*** 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 ;
GAME FARM INDUSTRY WANTS TO COVER UP FINDINGS OF INCREASE RISK TO CJD FROM CERVID
BSE INQUIRY
CJD9/10022
October 1994
Mr R.N. Elmhirst Chairman British Deer Farmers Association Holly Lodge Spencers Lane
BerksWell Coventry CV7 7BZ
Dear Mr Elmhirst,
CREUTZFELDT-JAKOB DISEASE (CJD) SURVEILLANCE UNIT REPORT
Thank you for your recent letter concerning the publication of the third annual report from the CJD Surveillance Unit. I am sorry that you are dissatisfied with the way in which this report was published.
The Surveillance Unit is a completely independant outside body and the Department of Health is committed to publishing their reports as soon as they become available. In the circumstances it is not the practice to circulate the report for comment since the findings of the report would not be amended.. In future we can ensure that the British Deer Farmers Association receives a copy of the report in advance of publication.
The Chief Medical Officer has undertaken to keep the public fully informed of the results of any research in respect of CJD. This report was entirely the work of the unit and was produced completely independantly of the the Department.
The statistical results reqarding the consumption of venison was put into perspective in the body of the report and was not mentioned at all in the press release. Media attention regarding this report was low key but gave a realistic presentation of the statistical findings of the Unit. This approach to publication was successful in that consumption of venison was highlighted only once by the media ie. in the News at one television proqramme.
I believe that a further statement about the report, or indeed statistical links between CJD and consumption of venison, would increase, and quite possibly give damaging credence, to the whole issue. From the low key media reports of which I am aware it seems unlikely that venison consumption will suffer adversely, if at all.
http://web.archive.org/web/20030511010117/http://www.bseinquiry.gov.uk/files/yb/1994/10/00003001.pdf
2004
Jeff Swann and his Mom, cwd link... sporadic CJD?, CBC NEWS Jeff Schwan sCJD, CWD, and Professor Aguzzi on BSE and sporadic CJD
????: CBCnews
Transmission Studies
Mule deer transmissions of CWD were by intracerebral inoculation and compared with natural cases {the following was written but with a single line marked through it ''first passage (by this route)}....TSS
resulted in a more rapidly progressive clinical disease with repeated episodes of synocopy ending in coma. One control animal became affected, it is believed through contamination of inoculum (?saline). Further CWD transmissions were carried out by Dick Marsh into ferret, mink and squirrel monkey. Transmission occurred in ALL of these species with the shortest incubation period in the ferret.
snip....
TUESDAY, MAY 11, 2021
> A Unique Presentation of Creutzfeldt-Jakob Disease in a Patient Consuming Deer Antler Velvet <
Conclusion
We believe that our patient’s case of CJD is highly suspicious for cervid etiology given the circumstances of the case as well as the strong evidence of plausibility reported in published literature. This is the first known case of CJD in a patient who had consumed deer antler velvet. Despite the confirmed diagnosis of CJD, a causal relationship between the patient’s disease and his consumption of deer antler velvet cannot be definitively concluded.
Supplemental data including molecular tissue sample analysis and autopsy findings could yield further supporting evidence. Given this patient’s clinical resemblance to CBD and the known histological similarities of CBD with CJD, clinicians should consider both diseases in the differential diagnosis of patients with a similarly esoteric presentation. Regardless of the origin of this patient’s disease, it is clear that the potential for prion transmission from cervids to humans should be further investigated by the academic community with considerable urgency.
''We believe that our patient’s case of CJD is highly suspicious for cervid etiology given the circumstances of the case as well as the strong evidence of plausibility reported in published literature. This is the first known case of CJD in a patient who had consumed deer antler velvet. Despite the confirmed diagnosis of CJD, a causal relationship between the patient’s disease and his consumption of deer antler velvet cannot be definitively concluded.''
CREUTZFELDT JAKOB DISEASE: A Unique Presentation of Creutzfeldt-Jakob Disease in a Patient Consuming Deer Antler Velvet
i was warning England and the BSE Inquiry about just this, way back in 1998, and was ask to supply information to the BSE Inquiry. for anyone that might be interested, see;
Singeltary submission to the BSE Inquiry on CJD and Nutritional Supplements 1998
ABOUT that deer antler spray and CWD TSE PRION... I have been screaming this since my neighbors mom died from cjd, and she had been taking a supplement that contained bovine brain, bovine eyeball, and other SRMs specified risk materials, the most high risk for mad cow disease. just saying...
I made a submission to the BSE Inquiry long ago during the BSE Inquiry days, and they seemed pretty interested.
Sender: "Patricia Cantos"
To: "Terry S Singeltary Sr. (E-mail)"
Subject: Your submission to the Inquiry
Date: Fri, 3 Jul 1998 10:10:05 +0100 3 July 1998
Mr Terry S Singeltary Sr. E-Mail: Flounder at wt.net Ref: E2979
Dear Mr Singeltary, Thank you for your E-mail message of the 30th of June 1998 providing the Inquiry with your further comments. Thank you for offering to provide the Inquiry with any test results on the nutritional supplements your mother was taking before she died. As requested I am sending you our general Information Pack and a copy of the Chairman's letter. Please contact me if your system cannot read the attachments. Regarding your question, the Inquiry is looking into many aspects of the scientific evidence on BSE and nvCJD.
I would refer you to the transcripts of evidence we have already heard which are found on our internet site at ;
http://www.bse.org.uk.
Could you please provide the Inquiry with a copy of the press article you refer to in your e-mail? If not an approximate date for the article so that we can locate it? In the meantime, thank you for you comments. Please do not hesitate to contact me on... snip...end...tss
everyone I tell this too gets it screwed up...MY MOTHER WAS NOT TAKING THOSE SUPPLEMENTS IPLEX (that I ever knew of). this was my neighbors mother that died exactly one year previously and to the day of sporadic CJD that was diagnosed as Alzheimer’s at first. my mother died exactly a year later from the Heidenhain Variant of Creutzfeldt Jakob Disease hvCJD, and exceedingly rare strains of the ever growing sporadic CJD’s. both cases confirmed. ...
kind regards, terry
TSEs i.e. mad cow disease's BSE/BASE and NUTRITIONAL SUPPLEMENTS IPLEX, mad by standard process; vacuum dried bovine BRAIN, bone meal, bovine EYE, veal Bone, bovine liver powder, bovine adrenal, vacuum dried bovine kidney, and vacuum dried porcine stomach. also; what about potential mad cow candy bars ? see their potential mad cow candy bar list too... THESE are just a few of MANY of just this ONE COMPANY...TSS
''So, in sum, dietary supplements sold in the United States often contain ruminant tissues from undisclosed sources. Personally, I am rather squeamish and I don't think I would be eating prostate or testicle or pituitary, but I am also a little bit wary of consuming products with those glands, not just out of personal repugnance but simply out of a health concern.''
DEPARTMENT OF HEALTH AND HUMAN SERVICES FOOD AND DRUG ADMINISTRATION CENTER FOR BIOLOGICS EVALUATION AND RESEARCH TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES ADVISORY COMMITTEE Friday, January 19, 2001
snip...
15 Open Public Hearing
16 DR. FREAS: We are opening the open public hearing
17 now. We have received one response to speak in this
18 afternoon's open public hearing. That is from Dr. Scott
19 Norton. If Dr. Norton is here, would you please come
20 forward. You can either use the podium or the microphone,
21 whichever is your choice.
22 DR. NORTON: I am Scott Norton and I am a
23 physician in the Washington D.C. area. I am here speaking
24 as a private citizen today.
25 I first became concerned about the presence of 231
1 tissues from ruminant animals in dietary supplements about
2 six months ago and expressed my concern in a letter that was 3 published in New England Journal of Medicine in July of Year 4 2000. 5 A couple of the products that I had looked at, and 6 examined their labels, that raised these concerns I brought 7 in right here. I will just read some of the organs that are 8 found in one that is called Male Power. Deer antler, 9 pancreas, orchic--despite what we just heard that the FDA
10 prefers the term "testicular tissue" to be written on the
11 labels, I have never seen a dietary supplement say
12 "testicle." They always say "orchis" or "orchic" which may
13 sound rather flowery to the etymologically impaired--thymus,
14 adrenal, heart, lymph node, prostate, spleen and pituitary.
15 There are actually seventeen organs in that particular
16 product.
17 There is another product that is called Brain
18 Nutrition that tells us that it is vitamins and minerals
19 essential for important brain function. It does not mention
20 that there is any glandulars on at least the bold print. 21 But if you look at the small print on the back, we learn
22 that it has brain extract and pituitary extract, raw, in
23 there.
24 We know that many of the organs that can be found
25 in the dietary supplements do fall in that list of organs
232
1 that are suspect for contamination with TSEs, the labels, in 2 nearly all cases, identify neither the animal source nor the 3 geographic location from which the organs were derived. I 4 have seen one line that did specify from New Zealand cattle 5 but no other manufacturer will list either the species or 6 the geographic location. 7 The FDA's and the USDA's import alerts that we 8 just learned about prohibit the use of these organs in 9 foods, medicines and medical devices. But my reading of the
10 alert, 17-04, suggests that DSHEA does allow some loopholes
11 for these tissues to possible slip in.
12 I will just read from 17-04 that we heard. On the
13 first page, it says that, "This alert does not establish any
14 obligations on regulated entities." I love seeing
15 legislation that starts out with that caveat.
16 Then it says, further, "The USDA regulations do
17 not apply to bovine-derived materials intended for human
18 consumption as finished dietary supplements." We also learn
19 that the prohibition, or the import alert, is limited to
20 bulk lots of these tissues, completed tissues, from BSE-
21 derived countries. It does not mention if it is not a bulk
22 import or if it is raw materials rather than finished
23 materials.
24 Further, we know that it is strongly recommended
25 but not actually prohibited in the language here. So I have
233
1 not taken the assurances from that import alert that Dr. 2 Moore was trying to convey to us. 3 So, in sum, dietary supplements sold in the United 4 States often contain ruminant tissues from undisclosed 5 sources. Personally, I am rather squeamish and I don't 6 think I would be eating prostate or testicle or pituitary, 7 but I am also a little bit wary of consuming products with 8 those glands, not just out of personal repugnance but simply 9 out of a health concern.
10 So my question to the advisory committee is this;
11 is my caution reasonable and, if it is, should we take
12 further efforts to inform, or even protect, the American
13 public from such exposure.
14 I was curious about Dr. Moore's remarks. I sensed
15 two messages. One was the initial reassurance that FDA has
16 the regulatory authority but then I also learned that it is
17 the manufacturer's responsibility to provide those 18 assurances, that the FDA doesn't actually inspect.
19 I think that the FDA commissioners from Harvey
20 Wylie to David Kessler would say that that track record has
21 proven itself.
22 Thank you very much.
23 [Applause.]
24 DR. BROWN: Thanks, Dr. Norton. 25 Committee Discussion snip...
17 But I think that we could exhibit some quite 18 reasonable concern about blood donors who are taking dietary 19 supplements that contain a certain amount of unspecified- 20 origin brain, brain-related, brain and pituitary material. 21 If they have done this for more than a sniff or something 22 like that, then, perhaps, they should be deferred as blood 23 donors. 24 That is probably worse than spending six months in 25 the U.K. 1/19/01 3681t2.rtf(845) page 501 http://www.fda.gov/ohrms/dockets/ac/cber01.htm
Advisory Committees: CBER 2001 Meeting Documents
see actual paper;
-------- Original Message --------
Subject: METABOLIFE AND TSEs GAO-03-494 ''URGENT DATA''
Date: Thu, 01 May 2003 11:23:01 -0500
From: "Terry S. Singeltary Sr."
To: NelliganJ at gao.gov
The General Accounting Office (GAO) today released the following reports and testimonies:
REPORTS
1. Dietary Supplements: Review of Health-Related Call Records for Users of Metabolife 356. GAO-03-494, March 31.
see updated url link;
GREETINGS GAO:
i was surprised that i did not see any listing of bovine tissue in metabolife on it's label. have they ceased using these desiccated tissues???
i see that the lable on this product METABOLIFE 356, does not state that it has any tissues of desiccated bovine organs? i no the product use to, so i am curious if they have ceased the use of the tissues of cattle they use to use (see below)???
METABOLIFE 356 BOVINE COMPLEX/GLANDULAR SYSTEM OVARIES, PROSTATE, SCROTUM AND ADRENAL USDA SOURCE CATTLE
i tried warning them years ago of this potential threat of CJD/TSEs;
From: Randy Smith To: "'flounder at wt.net'" Subject: Metabolife Date: Mon, 7 Dec 1998 14:21:35 -0800
Dear Sir,
We are looking at reformulation. I agree that slow virus diseases present a problem in some areas of the world.
Our product uses healthy USDA inspected cattle for the glandular extract.
If you have any links to more information on this subject I would like to examine them.
Thank you for your interest and concern,
Dr. Smith ============
snip...
see full text links of this archived information ;
zoonosis zoonotic cervid tse prion cwd to humans, preparing for the storm
***An alternative to modeling the species barrier is the cell-free conversion assay which points to CWD as the animal prion disease with the greatest zoonotic potential, after (and very much less than) BSE.116***
2023 CWD ZOONOSIS
***> 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.
U of M expert warns of increasing likelihood of CWD transmission to humans
Cathy Wurzer and Gretchen Brown June 5, 2023 1:30 PM
Minnesota scientists have watched chronic wasting disease (CWD) — a fatal, neurological illness — kill deer and elk.
Now, they’re studying its potential to jump to humans.
The University of Minnesota’s Center for Infectious Disease Research and Policy has received more than $1.5 million in state money to start prepping for the possibility of CWD spreading to cows, pigs and possibly humans.
Michael Osterholm, Ph.D. is a world-renowned epidemiologist who heads the center.
He said transmission to humans has not yet been confirmed, but research suggests it is increasingly likely — especially as the disease continues to spread among deer and elk.
“None of us want to believe this could happen,” he told MPR News host Cathy Wurzer. “But you know, as much as you hope it isn't going to happen, hope is not a strategy.”
Current testing can be done only if animals die or are killed, and lymph nodes or brain matter is removed for testing to verify the disease.
That means captive deer often aren’t tested until they die or show symptoms of the disease, and that’s often too late to stop the spread of the disease.
And there aren’t yet adequate tests for humans, Osterholm said — let alone protocols in place if a human were to test positive for the disease.
snip...see;
U of M expert warns of increasing likelihood of CWD transmission to humans
Published: 22 August 2022
WEDNESDAY, JUNE 14, 2023
Texas TPWD CWD 508 Cases Confirmed To Date
TUESDAY, MAY 30, 2023
Texas Chronic Wasting Disease Detected in a Free-Range Deer in Bexar County 506 Cases and Mounting
SATURDAY, MAY 27, 2023
TEXAS CWD NOW CONFIRMED 505 Cervid, 101 Wild and 404 associated with breeding facility or breeder release site
MONDAY, MAY 08, 2023
TEXAS Chronic Wasting Disease Discovered in Deer Breeding Facility in Sutton County
TUESDAY, APRIL 11, 2023
Texas TAHC Chronic Wasting Disease Discovered in Deer Breeding Facilities in Frio and Hamilton Counties
TUESDAY, MARCH 21, 2023
Texas CWD seven new cases three separate deer-breeding facilities in Zavala, Washington and Gonzales counties 471 confirmed to date
FRIDAY, FEBRUARY 17, 2023
TEXAS OVERVIEW OF STATE RESPONSE TO CHRONIC WASTING DISEASE CWD TSE PRION April 2019 a Review
Why doesn't the DNR want to routinely test fawns?
The DNR highly discourages the testing of any fawns regardless of where they were harvested. Of the more than 15,000 fawns from the CWD-MZ that have been tested, only 23 were test positive, and most of those were nearly one year old. It is exceedingly unlikely that a deer less than one year old would test positive for CWD, even in the higher CWD prevalence areas of southern Wisconsin. Few fawns will have been exposed to CWD, and because this disease spreads through the deer's body very slowly, it is very rare in a fawn that the disease has progressed to a level that is detectable. This means that testing a fawn provides almost no information valuable to understanding CWD in Wisconsin's deer herd and does not provide information of great value to the hunter in making a decision about venison consumption.
Six fawns tested positive for CWD, five fawns from the core study area, including the youngest (5 months) free-ranging cervid to test positive.
Saturday, February 04, 2012
Wisconsin 16 MONTH age limit on testing dead deer Game Farm CWD Testing Protocol Needs To Be Revised
***> 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
PMCID: PMC5845664
PMID: 29058651
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.
snip...
In summary, evaluating the amplification rates and efficiencies of recombinant PrPC substrates by RT-QuIC could be a useful tool for estimating the susceptibility of rare or newly discovered PRNP alleles, allowing researchers to target specific alleles for downstream evaluation in challenge studies. In the face of an ever-expanding CWD-endemic area, it is increasingly important to characterize the natural susceptibility of these alleles, as well as their geographical distribution and the evolutionary basis for their rarity. Do the QGAK, 225F and 225Y alleles represent recent, random anomalies, or are they more primitive mutations that adversely affect reproductive fitness? Perhaps they are an indication that cervids with these rare alleles were themselves once the target of a primordial prion strain. While some evidence has been presented for distinct strains of CWD, little is known about their geographical distribution or virulence in cervid hosts of diverse PRNP backgrounds. It is possible that, with the appropriate framework, RT-QuIC could allow for the discrimination of known and novel prion strains. Without further research into disease management and prevention, including resistance, the only certainty seems to be that CWD will continue its insidious spread, with further discoveries in new hosts and geographical locations.
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
Department of Microbiology and Immunology, Midwestern University, United States; 2Department of Diagnostic Medicine and Pathobiology, Kansas State University; 3Prion Research Center; Colorado State University; 4U.S. Geological Survey, Pennsylvania Cooperative Fish and Wildlife Research Unit; 5Agricultural Research Service, United States Department of Agriculture; 6Canadian Food Inspection Agency, National and OlE Reference Laboratory for Scrapie and CWO
In mammalian species, the susceptibility to prion diseases is affected, in part, by the sequence of the host's prion protein (PrP). In sheep, a gradation from scrapie susceptible to resistant has been established both in vivo and in vitro based on the amino acids present at PrP positions 136, 154, and 171, which has led to global breeding programs to reduce the prevalence of scrapie in domestic sheep. In cervids, resistance is commonly characterized as a delayed progression of chronic wasting disease (CWD); at present, no cervid PrP allele conferring absolute resistance to prion infection has been identified. To model the susceptibility of various naturally-occurring and hypothetical cervid PrP alleles in vitro, we compared the amplification rates and efficiency of various CWD isolates in recombinant PrPC using real time quaking-induced conversion. We hypothesized that amplification metrics of these isolates in cervid PrP substrates would correlate to in vivo susceptibility - allowing susceptibility prediction for alleles found at 10 frequency in nature, and that there would be an additive effect of multiple resistant codons in hypothetical alleles. 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 cervid PrP allele conferring absolute resistance to prion infection has been identified.
''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.
''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.''
ADOPTED: 26 September 2019 doi: 10.2903/j.efsa.2019.5863 Update on chronic wasting disease (CWD) III
snip...
3.2.1.2. Non-cervid domestic species
The remarkably high rate of natural CWD transmission in the ongoing NA epidemics raises the question of the risk to livestock grazing on CWD-contaminated shared rangeland and subsequently developing a novel CWD-related prion disease. This issue has been investigated by transmitting CWD via experimental challenge to cattle, sheep and pigs and to tg mouse lines expressing the relevant species PrP.
For cattle challenged with CWD, PrPSc was detected in approximately 40% of intracerebrally inoculated animals (Hamir et al., 2005, 2006a, 2007). Tg mice expressing bovine PrP have also been challenged with CWD and while published studies have negative outcomes (Tamguney et al., 2009b), unpublished data provided for the purposes of this Opinion indicate that some transmission of individual isolates to bovinised mice is possible (Table 1).
In small ruminant recipients, a low rate of transmission was reported between 35 and 72 months post-infection (mpi) in ARQ/ARQ and ARQ/VRQ sheep intracerebrally challenged with mule deer CWD (Hamir et al., 2006b), while two out of two ARQ/ARQ sheep intracerebrally inoculated with elk CWD developed clinical disease after 28 mpi (Madsen-Bouterse et al., 2016). However, tg mice expressing ARQ sheep PrP were resistant (Tamguney et al., 2006) and tg mice expressing the VRQ PrP allele were poorly susceptible to clinical disease (Beringue et al., 2012; Madsen-Bouterse et al., 2016). In contrast, tg mice expressing VRQ sheep PrP challenged with CWD have resulted in highly efficient, life-long asymptomatic replication of these prions in the spleen tissue (Beringue et al., 2012).
A recent study investigated the potential for swine to serve as hosts of the CWD agent(s) by intracerebral or oral challenge of crossbred piglets (Moore et al., 2016b, 2017). Pigs sacrificed at 6 mpi, approximately the age at which pigs reach market weight, were clinically healthy and negative by diagnostic tests, although low-level CWD agent replication could be detected in the CNS by bioassay in tg cervinised mice. Among pigs that were incubated for up to 73 mpi, some gave diagnostic evidence of CWD replication in the brain between 42 and 72 mpi. Importantly, this was observed also in one orally challenged pig at 64 mpi and the presence of low-level CWD replication was confirmed by mouse bioassay. The authors of this study argued that pigs can support low-level amplification of CWD prions, although the species barrier to CWD infection is relatively high and that the detection of infectivity in orally inoculated pigs with a mouse bioassay raises the possibility that naturally exposed pigs could act as a reservoir of CWD infectivity.
3.2.1.3. Other species
Studies have demonstrated that the CWD agent(s) can be transmitted by the IC route in several species of rodents, such as voles (Subfamily Arvicolinae), deer mice (Peromyscus maniculatus), mice and hamsters (Subfamily Cricetinae). The susceptibility was, however, variable, being high in voles and deer mice but lower in mice and hamsters (Raymond et al., 2007; Heisey et al., 2010; Kurt et al., 2011; Di et al., 2013; Lee et al., 2013). Mink (subfamily Mustelinae) (Harrington et al., 2008), ferrets (Mustela putorius) (Bartz et al., 1998; Sigurdson et al., 2008) and cats (Mathiason et al., 2013) were susceptible to IC challenge with NA CWD sources, while CWD transmitted poorly to raccoons (Procyon lotor) by the IC route (Moore et al., 2019).
3.2.2. European isolates
The host range of CWD in Europe has been much less investigated so far, due to its recent identification. Among the cervid species involved in the CWD epidemics in North America, only some species (such as moose and reindeer) inhabit Europe; mule deer, white-tailed deer and elk/wapiti are American cervid species, although a few populations of white-tailed deer have been introduced into Europe. Others cervids that mainly inhabit Europe are red deer and roe deer. After the first detection in a reindeer in Norway in 2016 (Benestad et al., 2016), CWD has been detected in wild reindeer, moose and one red deer in Norway (Mysterud and Edmunds, 2019), in a moose in Finland in March 2018 and in three moose in Sweden in March, May and September 2019. CWD has not been detected
Chronic Wasting Disease (CWD) III www.efsa.europa.eu/efsajournal 14 EFSA Journal 2019;17(11):5863
so far in wild roe deer, fallow deer or white-tailed deer nor in any farmed cervid species. However, for fallow deer and white-tailed deer, the number of animals tested by the surveillance systems is still very low.
The potential host range of European CWD strains is under investigation by bioassay experiments in a range of model species; most of these studies are ongoing and there are no published data available so far. Data from the experiments that are known to be ongoing in different laboratories have been gathered for the purposes of this Opinion. Overall, reindeer CWD, moose CWD and red deer CWD brain isolates (and LRS isolates from some selected cases) are being tested for transmissibility in mice, hamsters, bank voles and in a range of tg mouse lines expressing PrP sequences from: cervids (Q226 or E226 deer PrP variants), small ruminants (ARQ, VRQ, AHQ and ARR PrP polymorphic variants), cattle, pig, vulture and human (M129 and V129 PrP polymorphic variants) (see Section 3.3.1). Importantly, in most of these animal models, the transmissibility of European CWD isolates will be directly comparable with the outcome of similar (published or ongoing) experiments with CWD isolates from North America.
While most of these studies are still ongoing, some experiments with CWD isolates from Europe have already produced evidence of transmission in some recipient species (Table 1). These include bank voles, conventional laboratory mice and tg mice expressing cervid PrP, sheep PrP and mouse PrP. The same rodent models are also susceptible to NA CWD isolates and will therefore allow comparative strain typing of NA and European CWD strains in due course. There is no strong evidence so far for rodent models being widely susceptible to NA isolates but not to European isolates or vice versa.
Table 1 summarises more than 500 ongoing, published or unpublished primary transmission experiments of NA or European CWD isolates from different cervids into various rodent models, which have been gathered following the requests described in Section 2.2. The CWD isolates are grouped according to geographical origin and cervid species, with each column summarising the results obtained with one or more CWD isolates from a given species and country. Rodent models are grouped according to the PrP species expressed. Some species have polymorphic PrP sequences, so more than one PrP sequence per species has been modelled. In these cases, each row summarises the data obtained with more than one PrP variant of a given species. Therefore, conventional mice include wt mice expressing PRNPa or PRNPb mouse PrP variants; bank voles include two genetic lines with different amino acids at codon 109 (Bv109M and Bv109I); tg-cervidPrP mice include mouse lines expressing several cervid PrP variants (the deer wt Q226, the elk wt E226, the WTD variant S96, the elk variant M132); tg-sheepPrP mice include mouse lines expressing the ARQ, VRQ, AHQ or ARR small ruminant PrP variants; finally, tg-humanPrP mice include mouse lines expressing M or V at the human PrP polymorphic codon 129. Therefore, each box in the Table 1 summarises the outcome of bioassay experiments with one or more CWD isolates (from the same species and origin) in one or more recipient rodent models (expressing PrP from a single given species).
Chronic Wasting Disease (CWD) III www.efsa.europa.eu/efsajournal 15 EFSA Journal 2019;17(11):5863
Most of the studies conducted by molecular/biochemical methods are still ongoing. The preliminary data obtained by molecular/biochemical methods were difficult to summarise and will not be reported in the present Opinion. This was mainly due to lack of detail in the results obtained by direct PrPSc analyses (PrPres typing, conformational stability, proteinase K resistance, which are intended to investigate CWD strains) and to the different methodological approaches employed in amplification assays (PMCA and RT-QuIC). The information gathered by this activity shows that experiments aimed at modelling the species barrier for NA or European CWD isolates into different animal species, including humans, are underway in different laboratories and will be of help for understanding the potential host range of CWD strains.
3.2.3 Impact of the PRNP gene on transmissibility
Polymorphisms in the PRNP gene are known to influence susceptibility/resistance to prion disease in both small ruminants and humans (for recent review, see EFSA BIOHAZ Panel 2014, EFSA BIOHAZ Panel, 2017; Diack et al., 2014). Effects of host PRNP polymorphisms on CWD susceptibility/resistance have also been described in a number of cervid species (reviewed in EFSA BIOHAZ Panel, 2017, 2018).
However, deer and elk wild-type PrP primary structures are equivalent, except at residue 226, which is glutamate in elk and glutamine in deer. The effect of this difference on CWD pathogenesis has been recently investigated using a gene-targeting approach in which the mouse PrP coding sequence was replaced with elk or deer PrP. The results obtained following experimental challenge with deer and elk CWD inocula from NA showed that the resulting GtE226 and GtQ226 mice had distinct kinetics of disease onset, with incubation times shorter in GtE226 than in GtQ226 mice, indicating that amino acid differences at PrP residue 226 dictate the selection and propagation of divergent strains in deer and elk with CWD. As prion strain properties largely dictate host range potential, these findings suggest that prion strains from elk and deer might pose distinct risks to sympatric species or humans exposed to CWD (Bian et al., 2019).
The most common cervid species in Europe (moose, red deer, reindeer and roe deer) share the same PrP primary structure, i.e. Q226. However, red deer PrP is polymorphic at residue 226 and can therefore code for either Q226 or E226. Interestingly, CWD cases detected so far in four Norwegian moose, the first Swedish moose and one Norwegian reindeer are all homozygous for Q226 (Benestad, 2019b,c,d), but the CWD case in red deer is instead homozygous for E226 (Vikøren et al., 2019). The impact of these differences in PrP genotype on the transmissibility and strain properties of European CWD isolates is currently under investigation using GtE226 and GtQ226 mice (Bian et al., 2019). PRNP genotypes of the other reindeer from Norway and of the other moose cases in Sweden and Finland are not in the public domain.
Data on the transmissibility of CWD in species with different PrP sequences obtained by in vivo or in vitro modelling allow the investigation of the structural basis of the transmission barriers for CWD. This in turn could provide hints for predicting, to some extent, the susceptibility of non-cervid species to CWD. Taken together, studies with CWD isolates from NA suggest that the 165–175 sequence similarity between cervid and host PrP is one important factor governing the susceptibility of different species to CWD (reviewed by Kurt et al., 2016). In particular, polymorphisms at N/S170 in the recipient species might be important for susceptibility, with species that have N170 being more susceptible than those with S170 (Kurt et al., 2016). However, this must not be seen as an absolute rule, as species having S170 in their PrP, such as squirrel monkeys, have also been reported to be susceptible to CWD. It is however pertinent to note that all livestock species and humans have PrP sequences with S170, so they should not be considered among the species with supposedly high susceptibility to NA CWD isolates. Ongoing experiments in rodent models seem to indicate a similar trend for European CWD isolates, as rodent models, apparently more susceptible to European CWD isolates such as bank voles and tg mice expressing deer PrP, are N170.
Little information is currently known about the genetics of either wild or farmed cervid populations in Europe. A recent published study of several deer species (mostly in Great Britain) reported that red deer showed the most PRNP gene variation, with polymorphisms at codons 98, 168, 226 and 247 and marked variability in genotype frequencies in different regions. Other deer species showed less variation, with roe and fallow deer having identical PRNP gene sequences in all the animals sampled. Based on comparison with PRNP sequences of NA cervids affected by CWD and limited experimental challenge data, the authors conclude that a high proportion of wild deer in Great Britain may be susceptible to CWD (Robinson et al., 2019). A similar conclusion was reached by a previous study of 715 genotyped cervids (red deer, roe deer and chamois) from the UK and Italy (Peletto et al., 2009).
3.2.4. Concluding remarks
• The transmission of prions between species is limited by the ‘transmission barrier’ and the amino acid sequence of the host PrP plays a very key role in the overall susceptibility to TSE. Even for prions deriving from the same species, the host range may vary according to the prion strain, implying that different CWD strains might have different host ranges and different potential for transmitting to livestock species and to humans.
• Whether the natural host range of CWD in NA extends beyond the family Cervidae is currently unclear and no natural infections have been reported so far in other wildlife species (e.g. predators and scavengers) with overlapping geographical ranges.
• NA CWD has been transmitted experimentally to cattle and sheep, but with incomplete attack rates. The species barrier appears higher for pigs, although challenged animals can support low-level prion amplification.
• Experimental transmission to tg mice and other rodent models shows some difference in the host ranges of different isolates but, particularly for the European isolates, many bioassays are still ongoing and data are not yet available.
• The number of strains, the strain diversity, the prevalence and the potential host range of disease in both NA and Europe CWD may be underestimated.
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The disease devastating deer herds may also threaten human health
Scientists are exploring the origins of chronic wasting disease before it becomes truly catastrophic.
Rae Ellen Bichell
Image credit: David Parsons/Istock
April 8, 2019
This story was published in collaboration with the Mountain West News Bureau, a collaboration between Wyoming Public Media, Boise State Public Radio in Idaho, KUER in Salt Lake City and KRCC and KUNC in Colorado.
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One day in late February, in their laboratory in Fort Collins, Colorado, Wagner and Zabel compared the prions from the brains of CWD-infected deer in Texas with those of elk in Colorado. They want to know if the proteins were all mangled in the same way, or not. “If they are different, this would suggest that we have different strain properties, which is evidence as we're building our case that we might have multiple strains of CWD circulating in the U.S.,” says Wagner.
Step one is to see if they’re equally easy to destroy using a chemical called guanidine. The shape of a prion dictates everything, including the way it interacts with an animal’s cells and the ease with which chemicals can unfold it.
“Moment of truth,” said Wagner, as she and Zabel huddled around a computer, waiting for results to come through. When they did, Zabel was surprised.
“Wow,” he said. “Unlike anything we've seen before.”
The prions from the Texas deer were a lot harder to destroy than the ones from the Colorado elk. In fact, the guanidine barely damaged them at all. “We’ve never seen that before in any prion strain, which means that it has a completely different structure than we've ever seen before,” says Zabel. And that suggests that it might be a very different kind of chronic wasting disease. The researchers ran the same test on another Texas deer, with the same results.
Now, these are only the preliminary results from a few animals. Wagner and Zabel have a lot more experiments to do. But if future tests come to the same conclusion, it would support their hypothesis that there are multiple strains of chronic wasting disease out there, all with different origins. That, in turn, could mean that this disease will become even trickier to manage than it already is.
And, Zabel adds, there’s something else. “If it's still evolving, it may still evolve into a form that could potentially, eventually affect humans,” he says.
Zabel is not the only one worried about that possibility.
OSTERHOLM, THE EPIDEMIOLOGIST from Minnesota, is also concerned. He directs the Center for Infectious Disease Research and Policy at the University of Minnesota, and is serving a one-year stint as a “Science Envoy for Health Security” with the U.S. State Department. In February, he told Minnesota lawmakers that when it comes to chronic wasting disease, we are playing with fire. “You are going to hear from people that this is not going to be a problem other than a game farm issue. You're going to hear from people that it's not going to transmit to people, and I hope they're right, but I wouldn't bet on it,” he said. “And if we lose this one and haven’t done all we can do, we will pay a price.”
If that wasn’t warning enough, he added: “Just remember what happened in England.”
He was talking about mad cow disease. Decades ago, Osterholm got involved in studying the potential for the newly emerging condition — bovine spongiform encephalopathy, or BSE for short — to be transmitted to humans.
At that point, researchers had yet to document a prion disease in animals that could infect people. They did, however, have a few pieces of the puzzle. For one, work in Papua New Guinea had shown that people could transmit prion diseases to each other if they practiced cannibalism, especially of the brain-eating variety. They also knew that BSE was spreading quickly between cattle. Osterholm says he and others worried that the more widespread it became, the more chances it might have to change into something that could sicken people.
“A lot of people thought that it was an overreaction,” says Osterholm. “Then, of course, in 1996, 10 years later, we recognized that in fact transmission had occurred.” Variant Creutzfeldt-Jakob disease, as the illness is called when it appears in human beings, has infected about 230 people worldwide. Osterholm says he feels like he’s having déjà vu, except that instead of mad cow, now it’s chronic wasting disease that’s spreading in animals, with the potential to cross the species barrier to infect humans.
SNIP...SEE FULL TEXT;
***> 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.''
Biologists Stress Testing Harvests for Chronic Wasting Disease During Deer Season
Dec. 2, 2022
Media Contact: TPWD News, Business Hours, 512-389-8030
April 22, 2016
Scrapie Confirmed in a Hartley County Sheep
AUSTIN - Texas Animal Health Commission (TAHC) officials have confirmed scrapie in a Hartley County ewe. The ewe was tested by TAHC after the owner reported signs of weight loss and lack of coordination to their local veterinarian. The premises was quarantined and a flock plan for monitoring is being developed by the TAHC and USDA.
"The TAHC is working closely with the flock owner, sharing all of the options for disease eradication," said Dr. David Finch, TAHC Region 1 Director. "We are thankful the producer was proactive in identifying a problem and seeking veterinary help immediately."
Texas leads the nation in sheep and goat production. Since 2008, there have been no confirmed cases of scrapie in Texas. The last big spike in Texas scrapie cases was in 2006 when nine infected herds were identified and the last herd was released from restrictions in 2013.
According to USDA regulations, Texas must conduct adequate scrapie surveillance by collecting a minimum of 598 sheep samples annually. Since USDA slaughter surveillance started in FY 2003, the percent of cull sheep found positive for scrapieat slaughter (once adjusted for face color) has decreased 90 percent.
Scrapie is the oldest known transmissible spongiform encephalopathies, and under natural conditions only sheep and goats are known to be affected by scrapie. It is a fatal disease that affects the central nervous system of sheep and goats. It is not completely understood how scrapie is passed from one animal to the next and apparently healthy sheep infected with scrapie can spread the disease. Sheep and goats are typically infected as young lambs or kids, though adult sheep and goats can become infected.
The most effective method of scrapie prevention is to maintain a closed flock. Raising replacement ewes, purchasing genetically resistant rams and ewes,or buying from a certified-free scrapie flock are other options to reduce the risk of scrapie. At this time the resistant genetic markers in goats have not been identified, therefore it is important to maintain your sheep and goat herds separately.
The incubation period for Scrapie is typically two to five years. Producers should record individual identification numbers and the seller's premise identification number on purchase and sales records. These records must be maintained for a minimum of five years.
Producers should notify the Texas Animal Health Commission (800-550-8242) or the USDA-Austin Office (512-383-2400) if they have an adult sheep or goat with neurologic signs such as incoordination, behavioral changes, or intense itching with wool loss. Producers may order scrapie identification tags by calling 866-873-2824. For more information, please visit our website at:
web.archive.org/web/20160607024701/http://www.tahc.texas.gov/news/pr/2016/2016-04-22_TAHCScrapie.pdf
Scrapie: The flock identified in April 2016 remains under quarantine in Hartley County.
Scrapie Field Trial Experiments Mission, Texas, The Moore Air Force Base Scrapie TSE Prion Experiment 1964 How Did CWD Get Way Down In Medina County, Texas?
DISCUSSION
Observations of natural outbreaks of scrapie indicated that the disease spread from flock to flock by the movement of infected, but apparently normal, sheep which were incubating the disease.
There was no evidence that the disease spread to adjacent flocks in the absent of such movements or that vectors or other host species were involved in the spread of scrapie to sheep or goats; however, these possibilities should be kept open...
snip...PLEASE READ THE FULL REPORT ON THE SCRAPIE FIELD TRIAL EXPERIMENTS IN MISSION, TEXAS!!!
4 MOST ENDANGERED WHITETAIL DESTINATIONS IN AMERICA
Mark Kenyon
MARK KENYON Jun 3, 2022
4 Most Endangered Whitetail Destinations in America
It would not be hyperbole to say that we’re quite possibly living in the “golden age” of whitetail deer hunting.
Deer populations might be higher now than ever before and, at least since records have been kept, bigger, older bucks have never been more numerous. Hunters smash world and state records every year. The good times sure seem to be rolling.
But this isn’t true across all aspects or locales within the whitetail range, nor is it guaranteed to remain true into the future. All good things can and do come to an end.
The future of deer and deer hunting, as is the case with almost every aspect of the natural world today, exists on a precipice. Serious threats like disease, habitat loss, resource management, and public opinion all loom on the horizon. Four specific threatened locations, in particular, stand out as representative of larger issues threatening our nation’s deer hunting future. These are, in our estimation, the four most endangered whitetail destinations in America.
Read on for an introduction to these special yet threatened whitetail locales. And find out what we can do as deer hunters and stewards of the land to address the challenges in these specific locations and across the nation.
SOUTHWESTERN WISCONSIN
Greatest Threat: Chronic Wasting Disease
Southwest Wisconsin, a world-renowned big buck destination, is also ground zero for chronic wasting disease. The 100% fatal neurological disease impacting whitetails and other deer species has now spread to 29 states across the country. CWD is widely recognized as possibly the greatest existential threat to the future of whitetail hunting, and no place is it more ubiquitous than Wisconsin’s driftless area.
In some regions here, hunters are observing population-level impacts and CWD prevalence rates have hit as high as 30%. In more practical terms, this means that some areas of the whitetail-crazy state of Wisconsin might be experiencing the beginnings of downward trends in populations due to CWD. Almost one in three deer tested in these areas are testing positive. While CWD’s large-scale impact on deer populations is no joke, an equally concerning risk is the impact that positive tests have on the desire to hunt and eat deer at all. While transmission from deer to humans hasn’t been documented, it’s theoretically possible—akin to what happened with Mad Cow Disease in the 1990s. For this reason, the CDC currently advises hunters not to consume venison from a CWD-positive deer. The result of all this is that a lot of hard-earned venison is getting thrown in the dump already, and things, hypothetically, stand to worsen.
This worst-in-class state of affairs is partly due to a passive approach to CWD management that Wisconsin adopted in 2012, moving away from their “earn a buck” rule, stopping targeted population controls, and making testing in known CWD areas only voluntary.
“Because of the passive management approach taken by Wisconsin, CWD is endemic to five southwest counties, has spread to surrounding counties, and has been found in 38 of the state’s 72 counties,” said southwestern Wisconsin resident, hunter, and land consultant Doug Duren. “In some areas in those counties where prevalence is being studied, over 50% of adult bucks and over 35% of adult does are CWD positive.”
In conversations with other area residents, Duren heard anecdotal reports of seeing fewer older deer and mature bucks, increasing numbers of late-stage infected animals in need of putting down, and already dead deer. “One member of a group of hunters with a lease in Iowa County, Wisconsin told me they decided to give up their lease and find opportunity elsewhere as every buck they killed in the past three years tested positive for CWD,” he said. “This is a cautionary tale.”
While there is no single simple fix to this problem, the recently introduced Chronic Wasting Disease Research and Management Act would designate $35 million in badly needed funding for CWD research and another $35 million for management and surveillance that would certainly help the situation in Wisconsin and beyond. Click here to let your senators know this is an issue of supreme importance to deer hunters in your state.
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TEXAS
Greatest Threat: Captive Deer Industry
The great state of Texas sports one of the most robust and proud deer hunting cultures in the nation, but it’s also home to what some consider the greatest threat to deer hunting in all of America: the captive deer industry.
The debate around the captive deer industry is complicated, long-standing, and fraught, but the issues can be distilled into two main categories. First is the well-documented risk of spreading CWD by way of the transfer and sale of captive deer. Second is the negative impact that captive deer shooting facilities, and the media created around them, can have on the public perception of hunting in America and the North American Model of Conservation.
Texas is home to more captive deer facilities than any other state by a long shot, with 858 locations. The conditions present at such facilities, with high numbers of animals in close quarters, are well known to be a perfect storm for the spread of CWD. Not to mention the fact that given the transactional nature of captive deer breeding, many animals are sold and shipped across wide swaths of the country, potentially cross-contaminating new herds of deer all along the way.
While there have been increasing amounts of testing and monitoring of these herds for CWD, the effectiveness of these efforts are feared to be sub-par at best. “The profit motive is so great, it is common for deer breeders to hide infections, or simply not test, and thus spread the disease,” writes Whit Fosborg, CEO of the Theodore Roosevelt Conservation Partnership.
All of this makes Texas a likely ground zero for future CWD issues, a perfect example being a 2021 investigation that identified the release of more than 1,700 deer from seven Texas captive deer facilities that could have been exposed to chronic wasting disease. “Overwhelmingly, the CWD hot zone maps radiate from captive facilities across the state,” said Texas resident and bowhunter K.C. Smith.
Furthermore, the proliferation of captive deer facilities and “canned shooting preserves” threaten to shine a poor light on the larger hunting public, potentially hemorrhaging support for the free-range pursuit of whitetails in Texas and elsewhere. While the vast majority of non-hunters support hunting for food, those figures reverse when considering “trophy hunting.” Animals that are custom-bred to grow the largest antlers possible and then housed in high-fenced small enclosures and sold off to be shot by the highest bidder represents the most egregious example of what trophy hunting could be percieved as. Regardless of whether or not most high-fence facilities fit this description, the worst offenders are unfortunately what most people notice. We as whitetail hunters risk being defined by our most fringe element, especially in the Lone Star state.
It’s important to note that many of the high fence deer facilities in Texas very well might be well-managed and owned by good honest deer-loving people, Smith was quick to remind me. This is not as cut and dry of an issue as some non-Texans want to believe it is.
“I have an easy set of values to live by: don’t hurt people and don’t take their stuff,” he said. “However, when the deer ‘owned’ by another person are threatening to take away the future of my kids’ and everyone’s deer hunting, something must be done.”
Support for the Chronic Wasting Disease Research and Management Act will help just as much here as in Wisconsin, as would advocating for greater oversightof the captive deer industry in Texas and beyond.
Detection of infectious prions in tissues of feral hogs
PAULINA SOTO1,2, Francisca Bravo-Risi3,4, Rebeca Benavente3, Michael J. Bodenchuk5, Patrick Whitley Whitley6, Clint Turnage6, Tracy A Nichols7, Terry Spraker, Vienna R Brown6, 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. 3Department of Neurology, McGovern Medical School, University of Texas Health Science Center at Houston, Houston, Chile. 4Universidad Bernardo O’Higgins, Santigo, Chile. 5United States Department of Agriculture, Animal and Plant Health Inspection Service, Wildlife Services, San Antonio, USA. 6USDA APHIS Wildlife Services, Fort Collins, USA. 7Veterinary Services Cervid Health Program, United States Department of Agriculture, Animal and Plant Health Inspection Service, Fort Collins, USA
Abstract
Chronic wasting disease (CWD) is the prion disease with the greatest potential for spreading, affecting at least seven cervid species. An essential feature of prions lies in their ability to infect some species and not others. This phenomenon, known as a species barrier, seems to be largely dictated by the similarities between the donor (infectious) and recipient prion protein (PrP) sequences. Considering this, some potentially susceptible carnivores are proposed to act as vectors of CWD transmission as they may get infected. Alternatively, predators or scavengers may not get infected but spread infectious particles after they cross their digestive tracts. This project aims to identify the presence of infectious prions in feral hogs living in CWD-endemic areas. To do this, PMCA seeding activity was analyzed on feral hogs tissues such as the brain and retropharyngeal and submandibular lymph nodes using homologous pig PrP substrate or heterologous deer PrP substrate. We furthe! r injected selected feral hogs tissues into mice expressing the cervid and porcine versions of the prion protein to assess their potential to transmit disease. Our results show positive in vitro PrPSc detection using porcine and cervid substrates. The considerably higher detection using cervid substrate suggests that although feral hogs are exposed to CWD prions, disease transmission is inefficient. Bioassays confirmed these results and demonstrated that the infectivity carried by feral hogs is not enough to induce disease. In summary, these results suggest that feral hogs may play a role in disseminating CWD prions across the landscape.
***> In summary, these results suggest that feral hogs may play a role in disseminating CWD prions across the landscape.
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THURSDAY, MARCH 08, 2018
WILD HOGS AND CHRONIC WASTING DISEASE CWD TSE PRION
i have been worried about this for some time, but i don't see why others are not worried as well. these feral hogs that run rampant across states, can dig up a great deal of territory. what else can they dig up? i.e. CWD TSE PRION, and can they spread cwd tse prion to hell and back?
CWD TO PIGS
Research Project: TRANSMISSION, DIFFERENTIATION, AND PATHOBIOLOGY OF TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES
Location: Virus and Prion Research
Title: Disease-associated prion protein detected in lymphoid tissues from pigs challenged with the agent of chronic wasting disease
Author item Moore, Sarah item Kunkle, Robert item Kondru, Naveen item Manne, Sireesha item Smith, Jodi item Kanthasamy, Anumantha item West Greenlee, M item Greenlee, Justin
Submitted to: Prion Publication Type: Abstract Only Publication Acceptance Date: 3/15/2017 Publication Date: N/A Citation: N/A Interpretive Summary:
Technical Abstract: Aims: Chronic wasting disease (CWD) is a naturally-occurring, fatal neurodegenerative disease of cervids. We previously demonstrated that disease-associated prion protein (PrPSc) can be detected in the brain and retina from pigs challenged intracranially or orally with the CWD agent. In that study, neurological signs consistent with prion disease were observed only in one pig: an intracranially challenged pig that was euthanized at 64 months post-challenge. The purpose of this study was to use an antigen-capture immunoassay (EIA) and real-time quaking-induced conversion (QuIC) to determine whether PrPSc is present in lymphoid tissues from pigs challenged with the CWD agent.
Methods: At two months of age, crossbred pigs were challenged by the intracranial route (n=20), oral route (n=19), or were left unchallenged (n=9). At approximately 6 months of age, the time at which commercial pigs reach market weight, half of the pigs in each group were culled (<6 challenge="" groups="" month="" pigs="" remaining="" the="">6 month challenge groups) were allowed to incubate for up to 73 months post challenge (mpc). The retropharyngeal lymph node (RPLN) was screened for the presence of PrPSc by EIA and immunohistochemistry (IHC). The RPLN, palatine tonsil, and mesenteric lymph node (MLN) from 6-7 pigs per challenge group were also tested using EIA and QuIC.
Results: PrPSc was not detected by EIA and IHC in any RPLNs. All tonsils and MLNs were negative by IHC, though the MLN from one pig in the oral <6 5="" 6="" at="" by="" detected="" eia.="" examined="" group="" in="" intracranial="" least="" lymphoid="" month="" months="" of="" one="" pigs="" positive="" prpsc="" quic="" the="" tissues="" was="">6 months group, 5/6 pigs in the oral <6 4="" and="" group="" months="" oral="">6 months group. Overall, the MLN was positive in 14/19 (74%) of samples examined, the RPLN in 8/18 (44%), and the tonsil in 10/25 (40%). Conclusions:
This study demonstrates that PrPSc accumulates in lymphoid tissues from pigs challenged intracranially or orally with the CWD agent, and can be detected as early as 4 months after challenge.
CWD-infected pigs rarely develop clinical disease and if they do, they do so after a long incubation period. This raises the possibility that CWD-infected pigs could shed prions into their environment long before they develop clinical disease.
Furthermore, lymphoid tissues from CWD-infected pigs could present a potential source of CWD infectivity in the animal and human food chains.
CONFIDENTIAL
EXPERIMENTAL PORCINE SPONGIFORM ENCEPHALOPATHY
While this clearly is a cause for concern we should not jump to the conclusion that this means that pigs will necessarily be infected by bone and meat meal fed by the oral route as is the case with cattle. ...
we cannot rule out the possibility that unrecognised subclinical spongiform encephalopathy could be present in British pigs though there is no evidence for this: only with parenteral/implantable pharmaceuticals/devices is the theoretical risk to humans of sufficient concern to consider any action.
Our records show that while some use is made of porcine materials in medicinal products, the only products which would appear to be in a hypothetically ''higher risk'' area are the adrenocorticotrophic hormone for which the source material comes from outside the United Kingdom, namely America China Sweden France and Germany. The products are manufactured by Ferring and Armour. A further product, ''Zenoderm Corium implant'' manufactured by Ethicon, makes use of porcine skin - which is not considered to be a ''high risk'' tissue, but one of its uses is described in the data sheet as ''in dural replacement''. This product is sourced from the United Kingdom.....
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WEDNESDAY, APRIL 05, 2017
Disease-associated prion protein detected in lymphoid tissues from pigs challenged with the agent of chronic wasting disease
Snip…see;
THURSDAY, MARCH 08, 2018
Cervid, Wild Hogs, Coyotes, Wolves, Cats, Rodents, Gut Piles and Scavengers, A Potential Risk as Regards Disease Transmission CWD TSE Prion
TUESDAY, JUNE 27, 2023
USAHA Report of the Subcommittee on Farmed Cervidae CWD TSE Prion Herds 2015 to 2023
Chronic wasting disease detection in environmental and biological samples from a taxidermy site
Paulina Sotoa,b, J. Hunter Reedc, Mitch Lockwoodc, and Rodrigo Moralesa,b aDepartment of Neurology, McGovern Medical School, University of Texas Health Science Center at Houston, Texas, USA; bUniversidad Bernardo O’Higgins, Santiago, Chile; cTexas Parks and Wildlife Department, Texas, USA
Chronic wasting disease (CWD) is a transmissible spongiform encephalopathy affecting captive and free-ranging cervids (e.g., mule deer, white-tailed deer, elk, reindeer, and moose). Nowadays, CWD is widely distributed in North America. It is suggested that CWD spreads due to direct animal contact or through exposure to contaminated environments previously inhabited by infected animals. CWD may also be spread through the movement of infected animals and carcasses. Taxidermy practices involve processing deer tissues (or whole animal carcasses). In many cases, the CWD status of processed animals is unknown. This can generate risks of disease spread and transmission. Taxidermy practices include different steps involving physical, chemical, and biological procedures. Without proper tissue handling or disposal practices, taxidermist facilities may become a focus of prion infectivity.
Aims: In this study, we evaluated the presence of infectious prions in a taxidermy facility believed to be exposed to CWD. Detection was performed using the Protein Misfolding Cyclic Amplification (PMCA) technique in biological and inert environmental samples.
Methods: We collected biological and environmental samples (plants, soils, insects, excreta, and others) from a taxidermy facility, and we tested these samples using the PMCA technique. In addition, we swabbed different surfaces possibly exposed to CWD-infected animals. For the PMCA reaction, we directly used a swab piece or 10 µL of 20% w/v homogenized samples. Results: The PMCA analysis demonstrated CWD seeding activity in some of the components of this facility, including insects involved in head processing, soils, and a trash dumpster.
Conclusions: Different areas of this property were used for various taxidermy procedures. We were able to detect the presence of prions in
i) soils that were in contact with the heads of dead animals,
ii) insects involved in the cleaning of skulls, and
iii) an empty dumpster where animal carcasses were previously placed.
This is the first report demonstrating that swabbing is a helpful method to screen for prion infectivity on surfaces potentially contaminated with CWD. These findings are relevant as this swabbing and amplification strategy may be used to evaluate the disease status of other free-ranging and captive settings where there is a concern for CWD transmissions, such as at feeders and water troughs with CWD-exposed properties. This approach could have substantial implications for free-ranging cervid surveillance as well as in epidemiological investigations of CWD.
Funded by: USDA Grant number: AP20VSSPRS00C143
PRION 2022 ABSTRACTS, AND A BIG THANK YOU TO On behalf of the Prion2020/2022 Congress Organizing Committee and the NeuroPrion Association, we heartily invite you to join us for the International Conference Prion2020/2022 from 13.-16. September 2022 in Göttingen.
Prion 2022 Conference abstracts: pushing the boundaries
Large-scale PMCA screening of retropharyngeal lymph nodes and in white-tailed deer and comparisons with ELISA and IHC: the Texas CWD study
Rebeca Benaventea, Paulina Sotoa, Mitch Lockwoodb, and Rodrigo Moralesa aDepartment of Neurology, McGovern Medical School, University of Texas Health Science Center at Houston, Texas, USA; bTexas Park and Wildlife Department, Texas, USA
Chronic wasting disease (CWD) is a transmissible spongiform encephalopathy that affects various species of cervids, and both free-ranging and captive animals. Until now, CWD has been detected in 3 continents: North America, Europe, and Asia. CWD prevalence in some states may reach 30% of total animals. In Texas, the first case of CWD was reported in a free-range mule deer in Hudspeth and now it has been detected in additional 14 counties. Currently, the gold standard techniques used for CWD screening and detection are ELISA and immunohistochemistry (IHC) of obex and retropharyngeal lymph nodes (RPLN). Unfortunately, these methods are known for having a low diagnostic sensitivity. Hence, many CWD-infected animals at pre-symptomatic stages may be misdiagnosed. Two promising in vitro prion amplification techniques, including the real-time quaking-induced conversion (RT-QuIC) and the protein misfolding cyclic amplification (PMCA) have been used to diagnose CWD and other prion diseases in several tissues and bodily fluids. Considering the low cost and speed of RT-QuIC, two recent studies have communicated the potential of this technique to diagnose CWD prions in RPLN samples. Unfortunately, the data presented in these articles suggest that identification of CWD positive samples is comparable to the currently used ELISA and IHC protocols. Similar studies using the PMCA technique have not been reported.
Aims: Compare the CWD diagnostic potential of PMCA with ELISA and IHC in RPLN samples from captive and free-range white-tailed deer. Material and Methods: In this study we analyzed 1,003 RPLN from both free-ranging and captive white-tailed deer collected in Texas. Samples were interrogated with the PMCA technique for their content of CWD prions. PMCA data was compared with the results obtained through currently approved techniques.
Results: Our results show a 15-fold increase in CWD detection in free-range deer compared with ELISA. Our results unveil the presence of prion infected animals in Texas counties with no previous history of CWD. In the case of captive deer, we detected a 16% more CWD positive animals when compared with IHC. Interestingly, some of these positive samples displayed differences in their electroforetic mobilities, suggesting the presence of different prion strains within the State of Texas.
Conclusions: PMCA sensitivity is significantly higher than the current gold standards techniques IHC and ELISA and would be a good tool for rapid CWD screening.
Funded by: USDA
Grant number: AP20VSSPRS00C143
PRION 2022 ABSTRACTS, AND A BIG THANK YOU TO On behalf of the Prion2020/2022 Congress Organizing Committee and the NeuroPrion Association, we heartily invite you to join us for the International Conference Prion2020/2022 from 13.-16. September 2022 in Göttingen.
Prion 2022 Conference abstracts: pushing the boundaries
Shedding of Chronic Wasting Disease Prions in Multiple Excreta Throughout Disease Course in White-tailed Deer
Nathaniel D. Denkersa, Erin E. McNultya, Caitlyn N. Krafta, Amy V. Nallsa, Joseph A. Westricha, Wilfred Goldmannb, Candace K. Mathiasona, and Edward A. Hoovera
aPrion Research Center, College of Veterinary Medicine and Biological Sciences, Department of Microbiology, Immunology, and Pathology; Colorado State University, Fort Collins, CO, USA; bDivision of Infection and Immunity, The Roslin Institute and the Royal Dick School of Veterinary Studies, University of Edinburgh, Midlothian, UK
Aims: Chronic wasting disease (CWD) now infects cervids in South Korea, North America, and Scandinavia. CWD is unique in its efficient transmission and shedding of prions in body fluids throughout long course infections. Questions remain as to the magnitude of shedding and the route of prion acquisition. As CWD continues to expand, the need to better understand these facets of disease becomes more pertinent. The purpose of the studies described was to define the longitudinal shedding profile of CWD prions in urine, saliva, and feces throughout the course of infection in white-tailed deer.
Material and Methods: Twelve (12) white-tailed deer were inoculated with either 1 mg or 300ng of CWD. Urine, saliva, and feces were collected every 3-month post-inoculation (MPI) throughout the study duration. Cohorts were established based on PNRP genotype: codon 96 GG (n = 6) and alternate codons 96 GS (n = 5) & 103NT (n = 1). Urine and saliva were analyzed using iron-oxide magnetic extraction (IOME) and real-time quaking induced conversion (RT-QuIC)(IQ). Feces were subjected to IOME, followed by 4 rounds protein misfolding cyclic amplification (PMCA) with products analyzed by RT-QuIC (IPQ). To determine whether IPQ may be superior to IQ, a subset of urine and saliva were also tested by IPQ. Results were compared with clinical disease status.
Results: Within the 96 GG cohort, positive seeding activity was detected in feces from all deer (100%), in saliva from 5 of 6 (83%), and in urine from 4 of 6 (66%). Shedding in all excreta occurred at, or just after, the first positive tonsil biopsy result. In the 96 GS/103NT cohort, positive seeding activity could be detected in feces from 3 of 6 (50%) deer, saliva in 2 of 6 (33%), and urine in 1 of 6 (16%). Shedding in excreta was detected >5 months after the first tonsil positive result. Four of six 96 GG deer developed clinical signs of CWD, whereas only 2 of the 96 GS/103NT did. Shedding was more frequently detected in deer with clinical disease. The IPQ protocol did not significantly improve detection in saliva or urine samples, however, it significantly augmented detection in feces by eliminating non-specific background commonly experienced with IQ. Negative control samples remained negative in samples tested.
Conclusions: These studies demonstrate: (a) CWD prion excretion occurs throughout infection; (2) PRNP genotype (GG≫GS/NT) influences the excreta shedding; and (3) detection sensitivity in excreta can vary with different RT-QuIC protocols. These results provide a more complete perspective of prion shedding in deer during the course of CWD infection.
Funded by: National Institutes of Health (NIH)
Grant number: RO1-NS061902-09 R to EAH, PO1-AI077774 to EAH, and R01-AI112956-06 to CKM
Acknowledgement: We abundantly thank Sallie Dahmes at WASCO and David Osborn and Gino D’Angelo at the University of Georgia Warnell School of Forestry and Natural Resources for their long-standing support of this work through provision of the hand-raised, CWD-free, white-tailed deer used in these studies
Carrot plants as potential vectors for CWD transmission
Paulina Sotoa,b, Francisca Bravo-Risia,b, Claudio Sotoa, and Rodrigo Moralesa,b
aDepartment of Neurology, McGovern Medical School, University of Texas Health Science Center at Houston, Texas, USA; bUniversidad Bernardo O’Higgins, Santiago, Chile
Prion diseases are infectious neurodegenerative disorders afflicting humans and other mammals. These diseases are generated by the misfolding of the cellular prion protein into a disease-causing isoform. Chronic wasting disease (CWD) is a prevalent prion disease affecting cervids (captive and free-range). CWD is thought to be transmitted through direct animal contact or by indirect exposure to contaminated environments. Many studies have shown that infectious prions can enter the environment through saliva, feces, or urine from infected animals and decaying carcasses. However, we do not fully understand the specific contribution of each component to disease transmission events. Plants are logical environmental components to be evaluated since they grow in environments contaminated with CWD prions and are relevant for animal and human nutrition.
Aims: The main objective of this study is to study whether prions are transported to the roots and leaves of carrots, an edible plant commonly used in the human diet and as deer bait.
Methods: We have grown carrot plants in CWD-infected soils. After 90 days, we harvested the carrots and separated them from the leaves. The experiment was controlled by growing plants in soil samples treated with brain extracts from healthy animals. These materials were interrogated for their prion seeding activity using the Protein Misfolding Cyclic Amplification (PMCA) technique. Infectivity was evaluated in mouse bioassays (intracerebral injections in Tg1536 mice). The animals were sacrificed when they showed established signs of prion disease. Animals not displaying clinical signs were sacrificed at 600 days post-inoculation.
Results: The PMCA analysis demonstrated CWD seeding activity in soils contaminated with CWD prions, as well as in carrot plants (leaves and roots) grown on them. Bioassays demonstrated that both leaves and roots contained CWD prions in sufficient quantities to induce disease (92% attack rate). As expected, animals treated with prion-infected soils developed prion disease at shorter incubation periods (and complete attack rates) compared to plant components. Animals treated with soil and plant components exposed with CWD-free brain extracts did not display prion-associated clinical signs or evidence of sub-clinical prion infection.
Conclusions: We show that edible plant components can absorb prions from CWD contaminated soils and transport them to their aerial parts. Our results indicate that plants could participate as vectors of CWD transmission. Importantly, plants designated for human consumption represent a risk of introducing CWD prions into the human food chain.
Funded by: NIH
Grant number: R01AI132695
October 6th-12th, 126th Meeting 2022 Resolutions
RESOLUTION NUMBER: 30 Approved
SOURCE: COMMITTEE ON WILDLIFE
SUBJECT MATTER: Chronic Wasting Disease Carcass Disposal Dumpster Management and Biosecurity
BACKGROUND INFORMATION:
State and tribal wildlife agencies may identify collection points (dumpsters) within an identified chronic wasting disease (CWD) management zone for the disposal of hunter-harvested cervid carcasses to remove potentially infected carcasses off the landscape for disposal by an approved method (Gillin & Mawdsley, 2018, chap.14). However, depending on their placement and maintenance these dumpsters could potentially increase the risk of CWD transmission.
In several different states, photographic evidence has shown dumpsters in state identified CWD management zones overflowing with deer carcasses and limbs scattered on the land nearby. This could provide an opportunity for scavengers to potentially move infected carcass material to non-infected zones or increase contamination of the ground material around the dumpster’s location.
Federal guidance does not explicitly address uniform standards for collection locations for carcasses of free-ranging cervids; however, the United States Department of Agriculture, Animal and Plant Health Inspection Service, Veterinary Services Program Standards on CWD outlines procedures for carcass disposal, equipment sanitation, and decontamination of premises for captive cervid facilities.
RESOLUTION:
The United States Animal Health Association urges the Association of Fish and Wildlife Agencies (AFWA), Wildlife Health Committee to further refine the AFWA Technical Report on Best Management Practices for Prevention, Surveillance, and Management of Chronic Wasting Disease; Chapter 14, Carcass Disposal to address the placement and management of chronic wasting disease carcass disposal dumpsters or other carcass collection containers.
Reference:
1. Gillin, Colin M., and Mawdsley, Jonathan R. (eds.). 2018. AFWA Technical Report on Best Management Practices for Surveillance, Management and Control of Chronic Wasting Disease. Association of Fish and Wildlife Agencies, Washington, D. C. 111 pp.
ENVIRONMENT FACTORS FOR THE TRANSMISSION OF CWD TSE PRP
Sensitive detection of chronic wasting disease prions recovered from environmentally relevant surfaces
Environment International
Available online 13 June 2022, 107347
Environment International
Sensitive detection of chronic wasting disease prions recovered from environmentally relevant surfaces
Qi Yuana Gag e Rowdenb Tiffany M.Wolfc Marc D.Schwabenlanderb Peter A.LarsenbShannon L.Bartelt-Huntd Jason C.Bartza
a Department of Medical Microbiology and Immunology, Creighton University, Omaha, Nebraska, 68178, United States of America
b Department of Veterinary and Biomedical Sciences, University of Minnesota, Saint Paul, MN, 55108, United States of America
c Department of Veterinary Population Medicine, University of Minnesota, Saint Paul, MN, 55108, United States of America
d Department of Civil and Environmental Engineering, Peter Kiewit Institute, University of Nebraska-Lincoln, Omaha, Nebraska, 68182, United States of America
Received 26 April 2022, Revised 8 June 2022, Accepted 9 June 2022, Available online 13 June 2022.
Get rights and content
Under a Creative Commons license Open access
Highlights • An innovative method for prion recovery from swabs was developed.
• Recovery of prions decreased as swab-drying time was increased.
• Recovery of CWD prions from stainless steel and glass was approximately 30%.
• RT-QuIC enhanced CWD prion detection by 4 orders of magnitude.
• Surface-recovered CWD prion was sufficient for efficient RT-QuIC detection.
Abstract
Chronic wasting disease (CWD) has been identified in 30 states in the United States, four provinces in Canada, and recently emerged in Scandinavia. The association of CWD prions with environmental materials such as soil, plants, and surfaces may enhance the persistence of CWD prion infectivity in the environment exacerbating disease transmission. Identifying and quantifying CWD prions in the environment is significant for prion monitoring and disease transmission control. A systematic method for CWD prion quantification from associated environmental materials, however, does not exist. In this study, we developed an innovative method for extracting prions from swabs and recovering CWD prions swabbed from different types of surfaces including glass, stainless steel, and wood. We found that samples dried on swabs were unfavorable for prion extraction, with the greatest prion recovery from wet swabs. Using this swabbing technique, the recovery of CWD prions dried to glass or stainless steel was approximately 30% in most cases, whereas that from wood was undetectable by conventional prion immunodetection techniques. Real-time quake-induced conversion (RT-QuIC) analysis of these same samples resulted in an increase of the detection limit of CWD prions from stainless steel by 4 orders of magnitude. More importantly, the RT-QuIC detection of CWD prions recovered from stainless steel surfaces using this method was similar to the original CWD prion load applied to the surface. This combined surface swabbing and RT-QuIC detection method provides an ultrasensitive means for prion detection across many settings and applications.
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5. Conclusions
Chronic wasting disease is spreading in North America and it is hypothesized that in CWD-endemic areas environmental persistence of CWD prions can exacerbate disease transmission. The development of a sensitive CWD prion detection method from environmentally relevant surfaces is significant for monitoring, risk assessment, and control of CWD. In this study, we developed a novel swab-extraction procedure for field deployable sampling of CWD prions from stainless steel, glass, and wood. We found that extended swab-drying was unfavorable for extraction, indicating that hydrated storage of swabs after sampling aided in prion recovery. Recoverable CWD prions from stainless steel and glass was approximately 30%, which was greater than from wood. RT-QuIC analysis of the swab extracts resulted in an increase of the detection limit of CWD prions from stainless steel by 4 orders of magnitude compared to conventional immunodetection techniques. More importantly, the RT-QuIC detection of CWD prions recovered from stainless steel surfaces using this developed method was similar to the original CWD prion load without surface contact. This method of prion sampling and recovery, in combination with ultrasensitive detection methods, allows for prion detection from contaminated environmental surfaces.
Research Paper
Cellular prion protein distribution in the vomeronasal organ, parotid, and scent glands of white-tailed deer and mule deer
Anthony Ness, Aradhana Jacob, Kelsey Saboraki, Alicia Otero, Danielle Gushue, Diana Martinez Moreno, Melanie de Peña, Xinli Tang, Judd Aiken, Susan Lingle & Debbie McKenzie ORCID Icon show less
Pages 40-57 | Received 03 Feb 2022, Accepted 13 May 2022, Published online: 29 May 2022
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ABSTRACT
Chronic wasting disease (CWD) is a contagious and fatal transmissible spongiform encephalopathy affecting species of the cervidae family. CWD has an expanding geographic range and complex, poorly understood transmission mechanics. CWD is disproportionately prevalent in wild male mule deer and male white-tailed deer. Sex and species influences on CWD prevalence have been hypothesized to be related to animal behaviours that involve deer facial and body exocrine glands. Understanding CWD transmission potential requires a foundational knowledge of the cellular prion protein (PrPC) in glands associated with cervid behaviours. In this study, we characterized the presence and distribution of PrPC in six integumentary and two non-integumentary tissues of hunter-harvested mule deer (Odocoileus hemionus) and white-tailed deer (O. virginianus). We report that white-tailed deer expressed significantly more PrPC than their mule deer in the parotid, metatarsal, and interdigital glands. Females expressed more PrPC than males in the forehead and preorbital glands. The distribution of PrPC within the integumentary exocrine glands of the face and legs were localized to glandular cells, hair follicles, epidermis, and immune cell infiltrates. All tissues examined expressed sufficient quantities of PrPC to serve as possible sites of prion initial infection, propagation, and shedding.
KEYWORDS: Prion chronic wasting diseasesex differences species differences disease prevalence cervid protein expression glands
Paper
Rapid recontamination of a farm building occurs after attempted prion removal
Kevin Christopher Gough BSc (Hons), PhD Claire Alison Baker BSc (Hons) Steve Hawkins MIBiol Hugh Simmons BVSc, MRCVS, MBA, MA Timm Konold DrMedVet, PhD, MRCVS … See all authors
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.
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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
Gudmundur Georgsson1, Sigurdur Sigurdarson2, Paul Brown3
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
imageTimm Konold1*, imageStephen A. C. Hawkins2, imageLisa C. Thurston3, imageBen C. Maddison4, imageKevin C. Gough5, imageAnthony Duarte1 and imageHugh A. Simmons1
The findings of this study highlight the role of field furniture used by scrapie-infected sheep to act as a reservoir for disease re-introduction although infectivity declines considerably if the field furniture has not been in contact with scrapie-infected sheep for several months. PMCA may not be as sensitive as VRQ/VRQ sheep to test for environmental contamination.
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Discussion
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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
Kyung Je Park, Hoo Chang Park, In Soon Roh, Hyo Jin Kim, Hae-Eun Kang and Hyun Joo Sohn
Foreign Animal Disease Division, Animal and Plant Quarantine Agency, Gimcheon, Gyeongsangbuk-do, Korea
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
MONDAY, APRIL 19, 2021
Evaluation of the application for new alternative biodiesel production process for rendered fat including Category 1 animal by-products (BDI-RepCat® process, AT) ???
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---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
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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.
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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)
Terry S. Singeltary Sr.
posted by Terry S. Singeltary Sr. at
10:12 AM
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