TPW Commission Meeting CWD TSE Prion January 21-22, 2026
TPW Commission Meeting CWD TSE Prion January 21-22, 2026
Appointed by the governor and confirmed by the Texas Senate, the Commission adopts policies and rules to carry out all programs of the Texas Parks and Wildlife Department. Every August, the Commission conducts an annual public hearing to receive input from our partners, stakeholders and constituents concerning any issues relating to Department policies, goals, programs, and responsibilities. Anyone who is interested in speaking to the Commission is encouraged to attend. Additional information on this and other public hearings is available at the links below.
TPW Commission Meeting January 21-22, 2026.
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Executive Summary: Staff seeks adoption of proposed amendments to rules governing chronic wasting disease (CWD) detection, response, and management. The proposed amendments would function collectively to acknowledge and accommodate the decision of the Texas Animal Health Commission (TAHC) to cease cooperative efforts with Texas Parks and Wildlife Department (TPWD) with respect to the management of CWD in wildlife resources.
DISEASE DETECTION AND RESPONSE RULES
PROPOSAL PREAMBLE
1. Introduction.
The Texas Parks and Wildlife Department proposes amendments to 31 TAC §§65.81, 65.88, 65.90, 65.91, 65.92, 65.94, 65.95, 65.97, 65.99, and 65.100, concerning Disease Detection and Response, and 65.610, concerning Deer Breeder Permits. The proposed amendments would function collectively to clearly define the areas of respective responsibility between the department and the Texas Animal Health Commission (TAHC) with respect to the management of chronic wasting disease (CWD) in Texas.
CWD is a fatal neurodegenerative disorder that affects some cervid species, including wildlife resources such as white-tailed deer and mule deer, but also exotic species such as elk, red deer, sika, and their hybrids (referred to collectively as “susceptible species”). It is classified as a TSE (transmissible spongiform encephalopathy), a family of diseases that includes scrapie (found in sheep), bovine spongiform encephalopathy (BSE, found in cattle and commonly known as “Mad Cow Disease”), and variant Creutzfeldt-Jakob Disease (vCJD) in humans. CWD is spread by prions (a misfolded protein that is the infectious agent) that other animals can acquire directly or indirectly via bodily fluids or contaminated environments. CWD prions are known to persist in soil, vegetation, water, and carcasses indefinitely and there is no practical method for denaturing them. Thus, if CWD is not contained and controlled, the implications of the disease for Texas and its multi-billion-dollar ranching, hunting, wildlife management, and real estate economies could be significant.
The department has been concerned for over two decades about the emergence of CWD in free-ranging and captive populations of white-tailed and mule deer in Texas. The department is the primary state agency for the management and protection of native wildlife in the state, while TAHC is the state agency responsible for protecting animal agriculture (livestock and poultry) from disease and human health from zoonotic disease. Under Agriculture Code, §161.101(a)(6), CWD is a reportable disease and requires a veterinarian, veterinary diagnostic laboratory, or person having care, custody, or control of an animal to report the existence of CWD to TAHC within 24 hours after diagnosis. Because CWD can be transmitted between wildlife and farmed animals, there is an obvious nexus of interagency responsibilities in certain situations.
A central component of the joint strategy for CWD management was the department’s utilization of TAHC hold orders and quarantines as a regulatory mechanism for isolating and restricting the movement of infected or potentially infected animals. The proposed amendments would remove all references to TAHC (with exceptions as noted), hold orders, quarantines, and herd plans and replace references to hold orders, quarantines, and herd plans, as appropriate, with references to “disease management plan,” which is necessary to create and implement a similar mechanism administered solely by the department and applicable only to white-tailed and mule deer, which are the only two species of native wildlife that are susceptible to CWD.
The proposed amendment to §65.88, concerning Deer Carcass Movement Restrictions, in addition to conforming changes regarding TAHC mentioned earlier in this preamble, would extend the applicability of the section to all dead deer being transported (i.e., not just deer killed by hunting) reword subsection (a) for purposes of clarity, and add new subsection (b) to address the disposal of deer that die within breeding facilities. The disposal methods for deer that die within exposed and positive breeding facilities are currently addressed under TAHC herd plans; therefore, the department must stipulate those standards in department rules in order to prevent the spread of CWD from breeding facilities where it might or has been confirmed to exist. Additionally, the proposed amendment would require persons transporting carcasses of dead breeder deer to a landfill (if the deer are not interred in situ) to possess a completed disposition document on a form approved or supplied by the department, which would be required to accompany deer carcasses during transport and until the carcasses are accepted at the landfill. The proposed amendment is necessary to aid in law enforcement investigations, if necessary, by documenting deer that no longer bear the permanent identification required under Parks and Wildlife Code, Chapter 43, Subchapter L.
The proposed amendment to §65.90, concerning Definitions, consists of a number of related changes intended to address intra-agency roles in CWD management in wildlife contexts and to make clarifications and improvements to definitions used throughout the subchapter. The changes are necessary to prevent misunderstandings and standardize the applicability of various specialized terms.
The proposed amendment would add new paragraph (14) to define “exposed facility” as “a facility that has received exposed deer,” and alter current paragraphs (29) and (45) to make those provisions applicable to all types of facilities and not just to deer breeding facilities. The current rule defines “exposed deer” and “exposure” but does not explicitly address facilities that contain exposed deer. The current definitions in paragraphs (29) and (45) reflect the division of labor with respect to the former role of TAHC in CWD management. Because TAHC hold orders and quarantines will no longer be issued for premises on the basis of CWD in wildlife populations, the affected definitions must be made applicable to all facilities (rather than just to breeding facilities) to accommodate that fact.
The proposed amendment also would make several changes affecting terminology related to administrative mechanisms for authorizing the movement of breeder deer. In order to effectively and efficiently track the movement of breeder deer to and from deer breeders for purposes of law enforcement and disease investigations, the department created a specialized database commonly known as TWIMS, which allowed the automation of many permitting processes. Every location where breeder deer are kept or released is assigned a unique “facility ID” in TWIMS. Although the term “facility” has long been defined by rule to apply to any location required to be registered in TWIMS, the term has, for whatever reason, become synonymous with “deer breeding facility.” Similarly, although the terms “Movement Qualified” (current paragraph (26)) and “Non-Movement Qualified” (current paragraph (28)), under current rule apply only to breeding facilities, they have for whatever reason erroneously become understood to include movement authorizations for other types of facilities, which is technically and legally not the case. The terms were promulgated to reflect the binary opposition states (predicated on compliance with disease-testing requirements) necessary for TWIMS to allow or prevent the activation of a transfer permit that allows deer movement to and from deer breeding facilities or to other types of facilities; however, the terms have become so commonly used to refer to release locations that the department believes it is easier and more effective to simply alter the rules to expand the applicability of the terms to include all types of facilities. Along the same lines, the term “transfer permit” has long been defined in Chapter 65, Subchapter T, to mean the authorization for movement of breeder deer to or from any type of facility, some confusion has arisen as to whether “to or from” means “to and from” even though release locations are terminal destinations (i.e., the transfer permit in such cases is a permanent and final “one-way only” authorization of movement to a location from which the deer cannot ever be removed while still alive). Finally, the proposed amendment would replace the term “release site” (current paragraph (34)), with the term “release facility.” As discussed earlier in this preamble, every location where breeder deer are kept and every location where breeder deer are released are assigned a “facility ID” in TWIMS. To maintain continuity of terminology, the proposed amendments would remove all references to release sites and replace them with references to “release facility.”
The proposed amendment to §65.91, concerning General Provisions, would eliminate references to TAHC and replace the term “herd plan” with the term “disease management plan” for reasons previously discussed in this preamble. The proposed amendment to subsection (d) would address situations in which a premise is subject to TAHC movement restrictions because of CWD exposure in a susceptible species other than white-tailed deer or mule deer. The department has determined that because native cervids are susceptible species, allowing breeder deer to be moved from an exposed location represents an unacceptable risk of spreading CWD to native free-ranging and captive deer populations unless a determination based on the particulars of a given circumstance indicate that risk is either non-existent or acceptable. The proposed amendment also would alter subsection (e) to create an exception that would allow the transfer of deer to or from a facility designated NMQ if authorized under a disease management plan. The department has determined that there may be unforeseen situations in which compliance with a disease management plan provides epidemiological confidence that the transfer of deer by a facility otherwise not allowed to move deer can be allowed. Finally, the proposed amendment would alter subsection (f) to clarify that the provisions of the subsection apply to facilities where CWD has been confirmed as well as facilities where CWD is suspected to be present, which is necessary to address situations in which a facility nominally linked to a positive facility can be cleared following epidemiological investigation.
The proposed amendment to §65.92, concerning CWD Testing, would make conforming changes discussed previously in this preamble.
The proposed amendment to §65.94, concerning Breeding Facility Minimum Movement Qualification, would make conforming changes discussed previously in this preamble.
The proposed amendment to §65.95, concerning Movement of Breeder Deer, makes conforming changes as discussed previously in this preamble and would stipulate that changes in land ownership do not affect the status of a property as a trace-out release site. The department has determined that because CWD is an existential threat to native wildlife, it is necessary to eliminate the potential for unscrupulous persons to evade disease-management obligations by way of real estate transactions.
The proposed amendment to §65.97, concerning Testing and Movement of Deer Pursuant to a Triple T or TTP Permit, would make conforming changes discussed previously in this preamble.
The proposed amendment to §65.99, concerning Breeding Facilities Epidemiologically Connected to Deer Infected with CWD; Positive Deer Breeding Facilities, would make conforming changes discussed previously in this preamble.
The proposed amendment to §65.100, concerning Violations and Penalties, would make conforming changes discussed previously in this preamble.
The proposed amendment to §65.610, concerning Transfer of Deer, would make conforming changes discussed previously in this preamble.
Robert Macdonald, Regulations Coordinator, has determined that for each of the first five years that the rules as proposed are in effect, there will be no fiscal implications to state and local governments as a result of enforcing or administering the rules as proposed, as department personnel currently allocated to the administration and enforcement of disease management activities will administer and enforce the rules as part of their current job duties.
Mr. Macdonald also has determined that for each of the first five years the amendments as proposed are in effect:
(A) The public benefit anticipated as a result of enforcing or administering the rules as proposed will be the continued efficacy of department efforts to prevent the spread of CWD from locations where it does or has a reasonable probability to exist, thus ensuring the public of continued enjoyment of the resource and also ensuring the continued beneficial economic impacts of hunting in Texas.
(B) There will be no adverse economic impact on persons required to comply with the rules as proposed.
(C) Under provisions of Government Code, Chapter 2006, a state agency must prepare an economic impact statement and a regulatory flexibility analysis for a rule that may have an adverse economic effect on small businesses, micro-businesses, and rural communities. As required by Government Code, §2006.002(g), in April 2008, the Office of the Attorney General issued guidelines to assist state agencies in determining a proposed rule’s potential adverse economic impact on small businesses, micro-businesses, and rural communities. Those guidelines state that an agency need only consider a proposed rule’s "direct adverse economic impacts" to small businesses and micro-businesses to determine if any further analysis is required. For that purpose, the department considers "direct economic impact" to mean a requirement that would directly impose recordkeeping or reporting requirements; impose taxes or fees; result in lost sales or profits; adversely affect market competition; or require the purchase or modification of equipment or services.
Government Code, §2006.001(1), defines a small or micro-business as a legal entity "formed for the purpose of making a profit" and "independently owned and operated." A micro-business is a business with 20 or fewer employees. A small business is defined as a business with fewer than 100 employees, or less than $6 million in annual gross receipts. The department has determined that the proposed rules will not result in direct economic costs to small businesses and microbusinesses.
The department has determined that the proposed rules will not affect rural communities because the rules do not directly regulate any rural community.
(D) The department has not drafted a local employment impact statement under the Administrative Procedures Act, §2001.022, as the agency has determined that the rules as proposed will not result in direct impacts to local economies.
(E) The department has determined that Government Code, §2001.0225 (Regulatory Analysis of Major Environmental Rules), does not apply to the proposed rules.
(F) The department has determined that there will not be a taking of private real property, as defined by Government Code, Chapter 2007, as a result of the proposed rules. Any impacts resulting from the discovery of CWD in or near private real property would be the result of the discovery of CWD and not the proposed rule.
(G) In compliance with the requirements of Government Code, §2001.0221, the department has prepared the following Government Growth Impact Statement (GGIS). The rules as proposed, if adopted, will:
(1) neither create nor eliminate a government program;
(2) not result in an increase or decrease in the number of full-time equivalent employee needs;
(3) not result in a need for additional General Revenue funding;
(4) not affect the amount of any fee;
(5) not create a new regulation or repeal an existing regulation, but will modify existing rules to accommodate the cessation of TAHC involvement in the management of CWD efforts with respect to native wildlife;
(6) not increase the number of individuals subject to regulation; and
(7) not positively or adversely affect the state’s economy.
4. Request for Public Comment.
Comments on the proposed rules may be submitted to Kory Gann, Big Game Program Director, Texas Parks and Wildlife Department, 4200 Smith School Road, Austin, Texas, 78744; (512) 389-4363, (e-mail: kory.gann@tpwd.texas.gov); or via the department’s website at www.tpwd.texas.gov.
5. Statutory Authority.
The amendments are proposed under the authority of Parks and Wildlife Code, Chapter 43, Subchapter C, which requires the commission to adopt rules to govern the collecting, holding, possession, propagation, release, display, or transport of protected wildlife for scientific research, educational display, zoological collection, or rehabilitation; Subchapter E, which requires the commission to adopt rules for the trapping, transporting, and transplanting of game animals and game birds, urban white-tailed deer removal, and trapping and transporting surplus white-tailed deer; Subchapter L, which authorizes the commission to make regulations governing the possession, transfer, purchase, sale, of breeder deer held under the authority of the subchapter; Subchapters R and R-1, which authorize the commission to establish the conditions of a deer management permit for white-tailed and mule deer, respectively; and §61.021, which provides that no person may possess a game animal at any time or in any place except as permitted under a proclamation of the commission.
The proposed amendments affect Parks and Wildlife Code, Chapter 43, Subchapters C, E, L, R, R-1, and Chapter 61.
6. Rule Text.
§65.81. Risk Mitigation Provisions.
(a) (No change.)
(b) Breeder Deer.
(1) – (7) (No change.)
(8) Deer that escape from a breeding facility any part of which is within five linear miles of a location where CWD has been detected in a free-range white-tailed deer or susceptible species, or within 25 linear miles of a location where CWD has been detected in a free-range mule deer, may not be recaptured and/or returned to a breeding facility except as expressly authorized in writing by the department or in a disease management[herd] plan.
(9) (No change.)
(c) (No change.)
§65.88. Deer Carcass Movement Restrictions.
(a) In addition to the provisions of §65.10 of this title (Possession of Wildlife Resources) and except as may be otherwise prohibited by this subchapter or a disease management plan, a dead white-tailed deer, mule deer, or susceptible species (or parts thereof) may be transported into or within this state from the location where the animal was killed or found, provided the[, a department herd plan, or a quarantine or hold order issued by TAHC, a white-tailed deer or mule deer or part of a white-tailed or mule deer killed in this state or a susceptible species or part of a susceptible species harvested outside of Texas may be transported from the location where the animal was killed as provided in this section. The] parts of the animal not retained for cooking, storage or taxidermy purposes are[shall be] disposed of as quickly as practicable by one of the following methods:
(1) – (3) (No change.)
(b) A white-tailed deer or mule deer that dies in an exposed breeding facility or positive breeding facility must be disposed of only as provided in subsection (a)(1) or (2) of this section. If a breeder deer is disposed of as provided in subsection (a)(1) of this section, a completed disposition document on a form provided or approved by the department must accompany the carcass(es) to the landfill and remain with the possessor until the carcass(es) has/have been accepted by the landfill.
(c)[(b)] The rendering of carcass parts is not a lawful method of disposal.
(d)[(c)] The carcass of a white-tailed or mule deer may be deboned at any location prior to transportation to a final destination, provided:
(1) – (6) (No change.)
(e)[(d)] It is an offense for any person to dispose of those parts of an animal that the possessor does not retain for cooking, storage, or taxidermy purposes except as follows:
(1) – (3) (No change.)
Issued in Austin, Texas, on
The amendments are proposed under the authority of Parks and Wildlife Code, Chapter 43, Subchapter C, which requires the commission to adopt rules to govern the collecting, holding, possession, propagation, release, display, or transport of protected wildlife for scientific research, educational display, zoological collection, or rehabilitation; Subchapter E, which requires the commission to adopt rules for the trapping, transporting, and transplanting of game animals and game birds, urban white-tailed deer removal, and trapping and transporting surplus white-tailed deer; Subchapter L, which authorizes the commission to make regulations governing the possession, transfer, purchase, sale, of breeder deer held under the authority of the subchapter; Subchapters R and R-1, which authorize the commission to establish the conditions of a deer management permit for white-tailed and mule deer, respectively; and §61.021, which provides that no person may possess a game animal at any time or in any place except as permitted under a proclamation of the commission.
The proposed amendments affect Parks and Wildlife Code, Chapter 43, Subchapters C, E, L, R, R-1, and Chapter 61.
§65.90. Definitions. The following words and terms shall have the following meanings, except in cases where the context clearly indicates otherwise.
(1) – (11) (No change.)
(12) Disease management plan--A set of requirements for disease testing and management developed by the department.
(13)[(12)] Exposed deer — A deer that meets any of the following criteria:
(A) – (C) (No change.)
(14) Exposed facility—A facility that has received an exposed deer.
(15)[(13)] Exposure — The period of time that has elapsed following the introduction of an exposed deer to a breeding facility.
(16)[(14)] Facility — Any location required to be registered in TWIMS under a deer breeder’s permit, Triple T permit, TTP permit, or DMP, including release sites and/or trap sites.
(17)[(15)] Free-range deer — A deer that is not a breeder deer.
[(16) Herd Plan--A set of requirements for disease testing and management developed by the department and TAHC.]
(18)[(17)] Hunter-harvested deer — A deer required to be tagged under the provisions of Subchapter A of this chapter (relating to Statewide Hunting Proclamation).
(19)[(18)] Hunting year — That period of time between September 1 and August 31 of any year when it is lawful to hunt deer under the provisions of Subchapter A of this chapter (relating to Statewide Hunting Proclamation).
(20)[(19)] Inconclusive — A test result that is neither "positive" nor "not detected" on the basis of clinical deficiency.
(21)[(20)] "Insufficient follicles" — A test result indicating that a tonsil or rectal biopsy sample contained an insufficient number of lymphoid follicles to produce a valid test result.
(22)[(21)] Landowner (owner) — Any person who has an ownership interest in a tract of land and includes landowner’s authorized agent.
(23)[(22)] Landowner’s authorized agent (agent) — A person designated by a landowner to act on the landowner’s behalf.
(24)[(23)] Last known exposure — The last date a deer in a trace-out or trace-in breeding facility was exposed to a trace deer prior to the death or transfer of that trace deer.
(25)[(24)] Liberated deer — A free-ranging deer that bears evidence of having been a breeder deer, including, but not limited to, a tattoo (including partial or illegible tattooing), or evidence of having been eartagged at any time (holes, rips, notches, etc. in the ear tissue), electronic identification devices, or any other signs that the deer was at any time a breeder deer.
(26)[(25)] Location of detection — The exact geographic location, to the extent that it can be determined, at which a deer or susceptible species confirmed to be positive for CWD died.
(27)[(26)] Movement Qualified (MQ) — A designation made by the department pursuant to this division that allows:
(A) a deer breeder to [lawfully] transfer breeder deer to another facility; or
(B) a facility to receive breeder deer.
(28)[(27)] Not available/unavailable for testing — For a Category B trace-out deer breeding facility, a deer that is no longer present in a facility and cannot be found or the whereabouts of which are otherwise unknown.
(29)[(28)] Not Movement Qualified (NMQ) — A designation made by the department pursuant to this division that prohibits:
(A) the transfer of deer by a deer breeder; or
(B) a facility from receiving breeder deer.
(30)[(29)] Positive [breeding] facility — A [deer breeding] facility where CWD has been confirmed to exist.
(31)[(30)] Post-mortem test — A CWD test performed on a dead deer.
(32)[(31)] Properly executed — A form or report required by this division on which all required information has been entered.
(33)[(32)] Reconciled herd — The breeder deer held in a breeding facility for which every birth, mortality, and transfer of breeder deer has been accurately reported as required by this division.
(34)[(33)] Release — The act of liberating a deer from captivity. For the purposes of this division the terms "release" and "liberate" are synonymous.
(35)[(34)] Release facility[site] — A specific tract of land to which deer are released, including the release of deer under the provisions of this chapter or Parks and Wildlife Code, Chapter 43, Subchapters E, L, R, or R-1.
(36)[(35)] Reporting year — For a deer breeder’s permit, the period of time from April 1 of one calendar year through March 31 of the next calendar year.
(37)[(36)] RFID tag — A button-type ear tag conforming to the 840 standards of the United States Department of Agriculture’s Animal Identification Number system.
(38)[(37)] Submit — When used in the context of test results, provided to the department, either directly from a deer breeder or via an accredited testing laboratory.
(39)[(38)] Susceptible species — Any cervid species or part of a cervid species that is susceptible to CWD.
(40)[(39)] Suspect — An initial CWD test result of "detected" that has not been confirmed.
(41)[(40)] TAHC — Texas Animal Health Commission.
(42)[(41)] Test-eligible —
(A) – (B) (No change.)
(43)[(42)] Test, Test Result(s), or Test Requirement — A CWD test, CWD test result, or CWD test requirement as provided in this division.
(44)[(43)] Trace deer — A deer that the department has determined had been in a CWD-positive deer breeding facility on or after the date the facility was first exposed to CWD, if known; otherwise, within the previous five years from the reported mortality date of the CWD-positive deer, or the date of the ante-mortem test result.
(45)[(44)] Trace-in breeding facility — A breeding facility that meets either of the following criteria:
(A) – (B) (No change.)
(46)[(45)] Trace-out [breeding] facility — A breeding or release facility that has received an exposed deer that was in a CWD-positive deer breeding facility.
(47) Transfer—The movement of breeder deer under a transfer permit executed as provided in Subchapter T of this chapter:
(A) from or to another breeding facility; or
(B) from a breeding facility to another type of facility.
(48)[(46)] Trap Site — A specific tract of land approved by the department for the trapping of deer under this chapter and Parks and Wildlife Code, Chapter 43, Subchapters E, L, R, and R-1.
(49)[(47)] Triple T permit — A permit to trap, transport, and transplant white-tailed or mule deer (Triple T permit) issued under the provisions of Parks and Wildlife Code, Chapter 43, Subchapter E, and Subchapter C of this chapter (relating to Permits for Trapping, Transporting, and Transplanting Game Animals and Game Birds).
(50)[(48)] Trap, Transport and Process (TTP) permit — A permit issued under the provisions of Parks and Wildlife Code, Chapter 43, Subchapter E, and Subchapter C of this chapter (relating to Permits for Trapping, Transporting, and Transplanting Game Animals and Game Birds), to trap, transport, and process surplus white-tailed deer (TTP permit).
(51)[(49)] TWIMS — The department’s Texas Wildlife Information Management Services (TWIMS) online application.
(52)[(50)] Whole-herd test — The administration of an ante-mortem test to the entirety of test-eligible deer in the inventory of a breeding facility.
§65.91. General Provisions.
(a) – (b) (No change.)
(c) Except as provided in this division or as expressly authorized and in accordance with the provisions of a disease management[herd] plan, [no person shall transfer deer to or from] any facility for which a CWD test result of "suspect" or "positive" has been obtained from an accredited testing laboratory, irrespective of how the sample was obtained or who collected the sample, is automatically NMQ and the[The] provisions of this subsection take effect immediately [upon the notification of a CWD "suspect" test result, and continue in effect until the department expressly authorizes the resumption of permitted activities at that facility].
(d) Notwithstanding any provision of this division, no person may cause or allow breeder deer to be transferred from a facility subject to[moved from a facility for any purpose if such movement is prohibited by a herd plan associated with] a TAHC hold order or TAHC quarantine applicable to a trace susceptible species unless specifically authorized to do so under a disease management plan or the department has authorized movement following an epidemiological assessment.
(e) No person may transfer deer to or from a facility that has been designated NMQ by the department unless:
(A) specifically authorized by the department for the holder of a scientific research permit when the proposed research is determined to be of use in advancing the etiology of CWD in susceptible species; or
(B) authorized by a disease management plan.
(f) Immediately upon the notification that a facility has received a CWD "suspect" test result (a CWD-suspect facility) or a CWD “positive” test result (a CWD-positive facility), all facilities that have received[that have been in possession of] a deer [that was] held in or transferred to the [CWD suspect] facility within the previous five years shall be designated NMQ by the department until it is determined that the facility is not epidemiologically linked to the CWD-suspect or CWD-positive[CWD suspect] deer, or it is determined upon further testing that the "suspect" deer is not a confirmed positive.
(g) – (i) (No change.)
§65.92. CWD Testing.
(a) (No change.)
(b) Except as provided in §65.95(c)(7) of this title (relating to Movement of Breeder Deer) or subsection (d) of this section, an ante-mortem CWD test is not valid unless it is performed by an accredited laboratory on retropharyngeal lymph node, rectal mucosa, or tonsillar tissue with at least six lymphoid follicles collected within eight months of submission by a licensed veterinarian authorized pursuant to statutes and regulations governing the practice of veterinary medicine in Texas [and regulations of the TAHC] from a live deer that:
(1) — (2) (No change.)
(c) – (j) (No change.)
(k) Upon notification by the department that CWD is suspected or confirmed in a deer as a result of ante-mortem testing in a facility, the facility is automatically NMQ and the permittee shall:
(1) — (2) (No change.)
(l) (No change.)
§65.94. Breeding Facility Minimum Movement Qualification.
(a) Notwithstanding any other provision of this division, a breeding facility is designated NMQ and is prohibited from transferring breeder deer anywhere for any purpose if the breeding facility:
(1) (No change.)
(2) is not authorized pursuant to a disease management plan[herd plan associated with a TAHC hold order or TAHC quarantine];
(3) — (4) (No change.)
(b) – (d) (No change.)
(e) The department may decline to designate a facility as MQ under subsection (d) of this section:
(1) (No change.)
(2) upon the recommendation of a licensed veterinarian or epidemiologist employed by the department [or TAHC]. The recommendation must:
(A) — (B) (No change.)
(f) – (i) (No change.)
§65.95. Movement of Breeder Deer.
(a) – (b) (No change.)
(c) Release Facilities [Sites]; Release of Breeder Deer.
(1) An approved release facility[site] consists solely of the specific tract of land to which deer are released and the acreage is designated as a release facility[site] in TWIMS. A release facility[site] owner may modify the acreage registered as the release facility[site] to recognize changes in acreage (such as the removal of cross-fencing or the purchase of adjoining land), so long as the release facility[site] owner notifies the department of such modifications prior to the acreage modification. The release facility[site] requirements set forth in this division apply to the entire acreage modified under the provisions of this paragraph.
(2) Liberated breeder deer must have complete, unrestricted access to the entirety of the release facility[site]; provided, however, deer may be excluded from areas for safety reasons (such as airstrips) or for the purpose of protecting areas such as crops, orchards, ornamental plants, and lawns from depredation.
(3) All release facility[sites] onto which breeder deer are liberated must be surrounded by a fence of at least seven feet in height that is capable of retaining deer at all times under reasonable and ordinary circumstances. The owner of the release facility[site] is responsible for ensuring that the fence and associated infrastructure retain deer under reasonable and ordinary circumstances.
(4) The department will not authorize the liberation of breeder deer at a release facility[site] registered in TWIMS following the effective date of this subsection unless the owner of the release facility[site] submits to the department a letter of endorsement by a person authorized by the department to conduct fence inspections under the provisions of §65.603 of this title (relating to Application and Permit Issuance) stating that the person has personally conducted an on-site inspection at the releasefacility identified in the application and affirming that the release facility[site] is surrounded by a perimeter fence meeting the requirements of paragraph (3) of this subsection. This paragraph does not apply to release facility[sites] that have received deer prior to the effective date of this paragraph. It is an offense for any person the department has authorized as a facility inspector to submit the letter of endorsement required by this paragraph if the person has not personally conducted an onsite inspection at the facility.
(5) No person may intentionally cause or allow any live deer to leave or escape from a release facility[site] onto which breeder deer have been liberated.
(6) The owner of a release facility[site] where deer from a facility subject to the provisions of §65.99 of this title (relating to Breeding Facilities Epidemiologically Connected to Deer Infected with CWD; Positive Deer Breeding Facilities) or deer from a CWD-positive facility have been released shall maintain a harvest log at the release facility[site] that complies with §65.93 of this title (relating to Harvest Log).
(7) No person may transfer a breeder deer to a release facility or cause or allow a breeder deer to be transferred to a release facility unless:
(A) — (B) (No change.)
(C) the deer bears the identification prescribed by Parks and Wildlife Code, §43.3561, and any applicable disease management[herd]plan.
(D) – (F) (No change.)
(d) Trace-out Release Facility[Site].
(1) A release facility[site] is a trace-out release facility [site] if it has[:]
[(A)] received trace deer directly or indirectly from a positive breeding facility, unless the department has determined that the landowner of the release facility has satisfied the requirements of a disease management plan for the property[; and]
[(B) it has not been released from a hold order or quarantine related to activity described in subparagraph (A) of this paragraph].
(2) The landowner of a trace-out release facility[site] must:
(A) within 60 days of notification by the department that trace-out release status has been confirmed, remove every trace deer at the release facility[site], either by lawful hunting or as specifically authorized in writing by the department (or both), and submit post-mortem CWD samples for each deer within seven days of mortality; and
(B) submit post-mortem CWD test results for 100 percent of all hunter-harvested deer until the department is confident that CWD is not present at the release facility[site] or as prescribed in a disease management[herd] plan.
(3) No breeder deer may be transferred to a trace-out release facility[site] unless the deer has been tagged in one ear with a button-type RFID tag approved by the department.
(4) A change in ownership of a tract of land does not affect the status of the property as a trace-out release site for the purposes of this subchapter.
(e) The owner of a trace-out release facility[site] that is not in compliance with applicable provisions of this division is ineligible for enrollment or continued participation in the Managed Lands Deer Program under Subchapter A of this chapter.
§65.97. Testing and Movement of Deer Pursuant to a Triple T or TTP Permit.
(a) General.
(1) – (2) (No change.)
(3) In addition to the reasons for denying a Triple T permit as provided in §65.107 of this title (relating to Permit Application and Processing) and §65.109 of this title (relating to Issuance of Permit), the department will not issue a Triple T permit if the department determines, based on epidemiological assessment, [and consultation with TAHC]that to do so would create an unacceptable risk for the spread of CWD.
(4) – (7) (No change.)
(b) – (c) (No change.)
§65.99. Breeding Facilities Epidemiologically Connected to Deer Infected with CWD; Positive Deer Breeding Facilities.
(a) (No change.)
(b) No deer from a facility subject to the provisions of this section may be transferred or liberated except as provided in this section or expressly authorized in a disease management[herd] plan and then only in accordance with the provisions of this division and the disease management[herd] plan.
(c) (No change.)
(d) Category A trace-out breeding facility.
(1) – (3) (No change.)
(4) The department [in consultation with TAHC] may decline to authorize a custom testing plan under subsection (h) of this section if an epidemiological assessment determines that a custom testing plan is inappropriate.
(5) (No change.)
(e) Category B trace-out breeding facility.
(1) – (4) (No change.)
(5) The department [in consultation with TAHC] may decline to authorize a custom testing plan under subsection (h) of this section if an epidemiological assessment determines that a custom testing plan is inappropriate.
(6) (No change.)
(f) The department shall, provided the provisions of this subchapter do not otherwise prevent restoration of MQ status, restore MQ status to a breeding facility that has been designated NMQ under the provisions of subsection (e) of this section as provided in this paragraph.
(1) MQ status may be restored for a facility in which all trace deer available for testing are tested in accordance with subsection (e) of this section and trace deer unavailable for testing were received by the trace facility less than 36 months prior to the date of detection in the positive breeding facility, provided:
(A) – (D) (No change.)
(E) Compliance with the requirements of this subsection does not relieve any person of any obligation or requirement of a disease management[herd] plan.
(2) MQ status may be restored for a facility in which:
(A) – (D) (No change.)
(E) Compliance with the requirements of this subsection does not relieve any person of any obligation or requirement of a disease management[herd] plan.
(g) Trace-in breeding facility. Immediately upon notification by the department of trace-in facility status, a facility is automatically NMQ.
(1) – (3) (No change.)
(4) The department [in consultation with TAHC] may decline to authorize a custom testing plan under subsection (g) of this section if an epidemiological assessment determines that a custom testing plan is inappropriate.
(5) (No change.)
(h) Custom Testing Plan. Within seven days of being notified by the department that a breeding facility has been designated a Category A, Category B, or trace-in facility, a permittee may, in lieu of meeting the applicable testing requirements of subsections (d) — (g) of this section, request the development of a custom testing plan by the department [in consultation with TAHC] based upon an epidemiological assessment conducted by the department [and TAHC. A custom testing plan under this subsection is not valid unless it has been approved by the department and TAHC].
(1) – (5) (No change.)
(i) Positive Facility.
(1) Upon notification by the department that CWD is suspected in a deer in a facility, the facility is automatically NMQ and the permittee shall:
(A) – (C) (No change.)
(D) euthanize all trace deer within seven days of confirmation of the positive test result, unless authorized by the department or in a disease management [herd] plan;
(E) – (F) (No change.)
(2) Unless otherwise provided in writing by the department, a permittee must enter into a disease management[herd] plan within six months of being designated a positive facility or agree to conduct a depopulation of the breeder deer within the facility.
(3) Fencing meeting the specifications in §65.605 of this title shall be installed around a positive facility no later than the completion of the disease management[herd] plan and removal of a quarantine unless the owner of the facility conducts a complete depopulation of the breeder deer.
§65.100. Violations and Penalties.
(a) A person who violates a provision of this division or a condition of a deer breeder’s permit, DMP, Triple T permit, TTP permit, disease management[herd] plan, or custom testing plan commits an offense and is subject to the penalties prescribed by the applicable provisions of the Parks and Wildlife Code.
(b) [A person who possesses or receives white-tailed deer or mule deer under the provisions of this division and/or Subchapters C, D, or T of this chapter is subject to the provisions of TAHC regulations at 4 TAC Chapter 40 (relating to Chronic Wasting Disease) that are applicable to white-tailed or mule deer].
[(c)] A person who fails to comply with a provision of this division or a condition of a deer’s breeder permit, DMP, Triple T permit, TTP permit, disease management[herd] plan, or custom testing plan may be prohibited by the department from future permit eligibility or issuance.
This agency hereby certifies that the proposal has been reviewed by legal counsel and found to be within the agency’s authority to adopt.
Issued in Austin, Texas, on
The amendment is are proposed under the authority of Parks and Wildlife Code, Chapter 43, Subchapter L, which authorizes the commission to make regulations governing the possession, transfer, purchase, sale, of breeder deer held under the authority of the subchapter
The proposed amendments affect Parks and Wildlife Code, Chapter 43, Subchapter L.
§65.610. Transfer Permits.
(a) – (d) (No change.)
(e) Release.
(1) – (4) (No change,)
(5) It is an offense for any person to:
(A) release, cause, allow, or participate in the release of a breeder deer that does not bear the identification prescribed by Parks and Wildlife Code, §43.3561, and any applicable disease management[herd] plan; or
(B) (No change.)
This agency hereby certifies that the proposal has been reviewed by legal counsel and found to be within the agency’s authority to adopt.
Issued in Austin, Texas, on
SUMMARY MINUTES OF THE 407th COMMISSION MEETING Texas Animal Health Commission
September 22, 2020
http://web.archive.org/web/20201017124040/https://www.tahc.texas.gov/agency/meetings/minutes/SummaryMinutes_CommMtg_2020-09-22.pdf
https://transmissiblespongiformencephalopathy.blogspot.com/2025/12/2026-usda-explanatory-notes-aphis-cwd.html
***> CWD TSE Prion, Politics, Friendly Fire, Unforeseen Consequences, What If?
https://chronic-wasting-disease.blogspot.com/2025/04/cwd-tse-prion-politics-friendly-fire.html
Texas S.B. 2843 Directs TPWD to conduct a comprehensive study of current measures to control chronic wasting disease (CWD) in deer
Trying to legislate CWD is what got Texas in this CWD mess to begin with, how did that work out$$$ Legislators and Politicians need to stay away and let TPWD and TAHC et try and contain this mess that Legislators and Politicians got us in, called CWD TSE Prion…terry
https://chronic-wasting-disease.blogspot.com/2025/04/texas-sb-2843-directs-tpwd-to-conduct.html
SUNDAY, MAY 04, 2025
Texas Senate Bill 2651 establishment of a pilot program to breed deer resistant to CWD TSE Prion
https://chronic-wasting-disease.blogspot.com/2025/05/texas-senate-bill-2651-establishment-of_4.html
4. Objective 4 and 6 - Infection rates and population modeling
a. In 2024, CWD sample prevalence was 40% across the study area, with higher rates seen in males (65%) than in females (34%).
b. Approximately 50% of males tested positive for CWD by the age of 2.5.
c. White-tailed deer abundance in the study area declined, driven by reduced lifespans and lower lifetime reproduction.
d. If survival does not increase, this population is expected to continue to decline.
https://drive.google.com/file/d/1jN5mtvXvz7IYFDQjv4Rasrw60dGe4KMJ/view
Louisiana House of Representative Aug 27, 9:30 AM, HCR-6 CWD
Louisiana House of Representative
Chronic Wasting Disease CWD
(A letter written from a Mississippi farmer who’s farm has been in his family for more than 100 years, and submitted it in this video presentation, 28 minute mark, another wake up call for sure, of what some have been warning for years, about CWD, but sadly will go by the wayside by the conspiracy theorists spreading fake news…terry)
Alston Ross
Marshall County, Mississippi
My family owns a 2,000 acre farm in Marshall County, which is in North Mississippi. CWD has plagued my farm since 2018 and has become progressively worse over time. We no longer have mature deer over the age of 3 years old on our property. Every buck harvested on our land has tested positive this year. The owners of our neighboring properties have continued to feed deer and ignore MDWFP regulations, which has exacerbated the spread of the disease throughout our area. This farm has been in my family for over 100 years, and due to the rapid spread of CWD, we are concerned about the future of our deer herd and the value of our hunting land…end
Snip…
Arkansas
Snip…
40:35 “…and conversely, I was co-Principle Investigator in NW Arkansas, where prevalence is approaching 50 percent.”
Snip…
41:00 “Specific to the work in Arkansas, in 2020, the state agency was showing the Prevalence at 30 percent in the Northwest part of the State, so flip a coin, so, 1 out of every 3 deer had the disease. We started that research in 2020, and now, the prevalence rate is now exceeding 40% in both sexes, and 50% in males.”
43:00 “what we’re seeing Arkansas now is, that population is declining about 11% a year.”
Snip…see full video presentation;
https://house.louisiana.gov/H_Video/VideoArchivePlayer?v=house/2025/Aug/0827_25_NR_Joint
CWD IS RAVAGING MY FAMILY’S LAND, BUT IT’S NOT TOO LATE FOR YOU
September 9, 2025 By: Paul Annear
My first season deer hunting in Wisconsin was 2001, the same season that produced Wisconsin’s first deer to test positive for chronic wasting disease. CWD has always been at the forefront of deer hunting discussions in my time as a hunter, and I’ve watched the disease slowly spread and worsen. Since 2019, eight of 11 deer I’ve taken on my family’s property in Richland County in Southwest Wisconsin have tested positive for CWD – including the buck in the photo above.
Aside from harvesting otherwise perfectly healthy-looking deer that test positive for CWD, we are now seeing live deer walking around in the awful final stages of this disease. Research has now confirmed what I’ve seen occurring on our hunting land in the last five to six years: CWD is beginning to reduce deer populations in high-prevalence areas like mine.
It didn’t have to reach this point. Hunters in areas with low CWD prevalence can keep infection rates low and deer populations healthy overall by accepting and implementing certain strategies. Some of the strategies I will lay out will challenge you as a hunter to play the “long game,” but there are ways to slow the spread of CWD in areas where it is newly discovered and infection rates are still low.
If you’re rolling your eyes at another guy talking about CWD, I get it, but I urge you to keep reading. Hear my personal story, how it has affected my hunting experiences, and what can happen if hunters ignore CWD.
“Where Are the Deer?”
…snip…see full text;
https://deerassociation.com/cwd-is-ravaging-my-familys-land-but-its-not-too-late-for-you/
This CWD Study Could Change Deer Hunting FOREVER | The Check Station October 8, 2025 NW Arkansas
NW Arkansas CWD 11:25 minutes;
50% of all deer positive for CWD.
35% of Does are Positive for CWD.
68% Bucks are Positive for CWD.
Most Bucks NW Arkansas that where Tested, are Positive for CWD.
https://m.youtube.com/watch?v=kTicUE-xsQU&t=695s&pp=2AG3BZACAQ%3D%3D
MEMORANDUM
To: Members of the Colorado Parks and Wildlife Commission
From: Dan Prenzlow, Director
Date: April 22, 2022
Subject: Chronic Wasting Disease Update for Parks and Wildlife Commission Chronic wasting disease, a fatal neurological disease found in deer, elk, and moose, is well established in herds throughout much of Colorado. We have detected CWD in 40 of our 54 deer herds, 17 of 42 elk herds, and 2 of 9 moose herds. Disease prevalence (percent infected) is highest in deer and lowest in moose. This disease is always fatal and animals die from the disease within about 2-2.5 years of infection. CWD infection shortens the lifespan of infected animals. If infection rates become too high, CWD can affect a herd’s ability to sustain itself.
Snip…
http://web.archive.org/web/20220609004350/https://cpw.state.co.us/Documents/Commission/2022/May/Item.11-PWC_Memo_CWD_Update_EckertMillerWood_April2022-Matthew_Eckert-DNR.pdf
18% of mule deer in northeastern Montana have deadly chronic wasting disease “In the 2024-25 hunting FWP submitted 9,066 samples for chronic wasting disease testing – the largest number of CWD samples ever collected in a single year. More than 1,100 of these samples were collected by hunters. Of those samples, 335 tested positive for the disease, including 202 white-tailed deer, 127 mule deer and six elk.”
https://billingsgazette.com/outdoors/article_de5278b8-f2e1-11ef-b479-cf42652717a4.html
The effectiveness of harvest for limiting wildlife disease: Insights from 20 years of chronic wasting disease in Wyoming
First published: 21 January 2025
https://doi.org/10.1002/eap.3089
https://esajournals.onlinelibrary.wiley.com/doi/10.1002/eap.3089
https://www.usgs.gov/news/national-news-release/new-study-finds-deer-hunting-can-help-keep-chronic-wasting-disease-check
Since identifying its first cases of CWD in captive deer in the 70s and finding the first wild infected deer in 1985, Wyoming has seen the disease slowly spread throughout the state. CWD has now been documented in members of the deer family in most of Wyoming’s deer hunting areas, with 20% to 40% percent of mule deer affected in some herds. A 2017 study estimated a 21% annual population decline as a result of the fatal disease.
https://freerangeamerican.us/chronic-wasting-disease-wyoming/#:~:text=CWD%20has%20now%20been%20documented,result%20of%20the%20fatal%20disease.
How does CWD impact deer, elk, and moose populations?
Recent research in Wyoming has demonstrated declines in both mule and white-tailed deer populations in deer hunt area 65 due to CWD (see below for citations). These declines are in the core endemic area where prevalence is highest. In areas with lower prevalence, effects of CWD are poorly understood but are considered additive along with other factors that can negatively affect deer populations in Wyoming (i.e. habitat loss, predation, other diseases). The distribution and prevalence of CWD in Wyoming elk is less than that of deer. Currently there are no documented direct population impacts in Wyoming elk from CWD; however, research from Rocky Mountain National Park suggests that CWD could impact elk populations at higher prevalence (13%). While CWD has been found in free ranging moose, there have been few detections, and there is no evidence that CWD is currently having an impact on moose populations.
https://wgfd.wyo.gov/Wildlife-in-Wyoming/More-Wildlife/Wildlife-Disease/Chronic-Wasting-Disease
PLoS One. 2016 Aug 30;11(8):e0161127. doi: 10.1371/journal.pone.0161127. eCollection 2016.
Chronic Wasting Disease Drives Population Decline of White-Tailed Deer
We show that a chronic disease that becomes endemic in wildlife populations has the potential to be population-limiting and the strong population-level effects of CWD suggest affected populations are not sustainable at high disease prevalence under current harvest levels.
https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0161127
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.....
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).
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.....
https://web.archive.org/web/20170404125557/http://webarchive.nationalarchives.gov.uk/20130822084033/http://www.defra.gov.uk/animal-diseases/files/qra_chronic-wasting-disease-121029.pdf
Chronic Wasting Disease in Texas A Real Disease with Proven Impacts
Produced by a coalition of concerned hunters, landowners, & conservationists (last update 1/2025)
https://storymaps.arcgis.com/stories/b93f528938ac48e9b56dcc79953cbec0
Aug 18, 2021
Oh, Deer
Heading Off a Wildlife Epidemic
CWD poses a significant threat to the future of hunting in Texas. Deer population declines of 45 and 50 percent have been documented in Colorado and Wyoming. A broad infection of Texas deer populations resulting in similar population impacts would inflict severe economic damage to rural communities and could negatively impact land markets. Specifically, those landowners seeking to establish a thriving herd of deer could avoid buying in areas with confirmed CWD infections. As they do with anthrax-susceptible properties, land brokers may find it advisable to inquire about the status of CWD infections on properties that they present for sale. Prospective buyers should also investigate the status of the wildlife on prospective properties. In addition, existing landowners should monitor developments as TPWD crafts management strategies to identify and contain this deadly disease.
Dr. Gilliland (c-gilliland@tamu.edu) is a research economist with the Texas Real Estate Research Center at Texas A&M University.
https://www.recenter.tamu.edu/articles/tierra-grande/oh-d
TEST RESULTS FROM CAPTIVE DEER HERD WITH CHRONIC WASTING DISEASE RELEASED 79.8 percent of the deer tested positive for the disease
DES MOINES – The Iowa Department of Agriculture and Land Stewardship today announced that the test results from the depopulation of a quarantined captive deer herd in north-central Iowa showed that 284 of the 356 deer, or 79.8% of the herd, tested positive for Chronic Wasting Disease (CWD).
http://web.archive.org/web/20141006172620/https://www.iowaagriculture.gov/press/2014press/press10022014.asp
Wisconsin Buckhorn Flats CWD
SUBJECT: Almond Deer Farm Update
Sixty of the 76 animals tested positive for CWD. The 76 deer constituted the breeding herd in the breeding facility on the farm. The property also had a hunting preserve until 2005. Four deer, two does and two fawns, the only deer remaining in the former preserve, were killed and tested as well. CWD was not detected in those animals.
The total number of deer to test positive from this farm from the initial discovery to final depopulation is 82. The nearly 80% prevalence rate discovered on Buckhorn Flats is the highest prevalence recorded in any captive cervid operation in North America.
http://web.archive.org/web/20140831060348/http://dnr.wi.gov/about/nrb/2011/december/12-11-2b2.pdf
Colorado CWD TSE Prion
“The overall incidence of clinical CWD in white-tailed deer was 82% “
Epidemiology of Chronic Wasting Disease in Captive White-Tailed and Mule Deer
http://web.archive.org/web/20150908134715/https://cpw.state.co.us/Documents/Hunting/BigGame/CWD/PDF/ResearchArticles/JWDEpiCWD.pdf
Available online 9 April 2025
Highlights
• CWD prions were identified in a taxidermy and deer nursing facility.
• Contaminated samples included waters, soils, dermestid beetles, domestic flies and a dumpster.
• Surgical instruments used to collect deer samples can get contaminated with CWD prions.
• Some of the infectious particles are readily released from surgical instruments when washed.
• Our results suggest that taxidermy practices actively contribute in the spreading of CWD.
Snip…
In summary, the information provided in this report demonstrate how anthropogenic activities, specifically taxidermy practices, animal processing, and rehabilitation of CWD susceptible species, may facilitate CWD transmission through the environmental dissemination of CWD prions. This study, along with future research efforts characterizing the overall level of infectivity, provides relevant information on managing CWD and to control its rapid geographic expansion. …
https://www.sciencedirect.com/science/article/abs/pii/S0048969725009544
Chronic wasting disease detection in environmental and biological samples from a taxidermy site
Results: The PMCA analysis demonstrated CWD seeding activity in some of the components of this facility, including insects involved in head processing, soils, and a trash dumpster.
Conclusions: Different areas of this property were used for various taxidermy procedures. We were able to detect the presence of prions in
i) soils that were in contact with the heads of dead animals, ii) insects involved in the cleaning of skulls, and iii) an empty dumpster where animal carcasses were previously placed.
This is the first report demonstrating that swabbing is a helpful method to screen for prion infectivity on surfaces potentially contaminated with CWD. These findings are relevant as this swabbing and amplification strategy may be used to evaluate the disease status of other free-ranging and captive settings where there is a concern for CWD transmissions, such as at feeders and water troughs with CWD-exposed properties. This approach could have substantial implications for free-ranging cervid surveillance as well as in epidemiological investigations of CWD.
Prion 2022 Conference abstracts: pushing the boundaries
https://www.tandfonline.com/doi/full/10.1080/19336896.2022.2091286
Artificial mineral sites that pre-date endemic chronic wasting disease become prion hotspots
The Ames Research and Educational Center property, centrally located within the CWD zone of southwest Tennessee, contains 49 historical mineral supplementation sites that were decommissioned in 2012. Here, we demonstrate that 32 of the 49 (65%) mineral sites within Ames established prior to the regional CWD outbreak, serve as foci of environmental PrPCWD contamination. Detection of PrPCWD in soils from these artificial mineral sites was dependent on site-specific management efforts. Soil physical properties were very similar across sites and no correlation between PrPCWD detection and soil physical properties was found. The detection of PrPCWD in soils at attractant sites within an endemic CWD zone significantly advances our understanding of environmental PrPCWD accumulation dynamics, providing valuable information for advancing adaptive CWD management approaches.
https://intcwdsympo.files.wordpress.com/2023/06/final-agenda-with-abstracts.pdf
Keywords: Chronic wasting disease (CWD); NaOH; Protein-misfolding cyclic amplification (PMCA); Republic of Korea; farm; prions; remediation; topsoil.
https://www.tandfonline.com/doi/full/10.1080/19336896.2025.2527588
First published: 19 January 2019 https://doi.org/10.1136/vr.105054
The data illustrates the difficulty in decontaminating farm buildings from scrapie, and demonstrates the likely contribution of farm dust to the recontamination of these environments to levels that are capable of causing disease.
snip...
This study clearly demonstrates the difficulty in removing scrapie infectivity from the farm environment. Practical and effective prion decontamination methods are still urgently required for decontamination of scrapie infectivity from farms that have had cases of scrapie and this is particularly relevant for scrapie positive goatherds, which currently have limited genetic resistance to scrapie within commercial breeds.24 This is very likely to have parallels with control efforts for CWD in cervids.
https://bvajournals.onlinelibrary.wiley.com/doi/abs/10.1136/vr.105054
***>This is very likely to have parallels with control efforts for CWD in cervids.
https://pubmed.ncbi.nlm.nih.gov/30602491/
Front. Vet. Sci., 14 September 2015 | https://doi.org/10.3389/fvets.2015.00032
Objects in contact with classical scrapie sheep act as a reservoir for scrapie transmission
In conclusion, the results in the current study indicate that removal of furniture that had been in contact with scrapie-infected animals should be recommended, particularly since cleaning and decontamination may not effectively remove scrapie infectivity (31), even though infectivity declines considerably if the pasture and the field furniture have not been in contact with scrapie-infected sheep for several months. As sPMCA failed to detect PrPSc in furniture that was subjected to weathering, even though exposure led to infection in sheep, this method may not always be reliable in predicting the risk of scrapie infection through environmental contamination.
http://journal.frontiersin.org/article/10.3389/fvets.2015.00032/full
Failure to prevent classical scrapie after repeated decontamination of a barn
https://scrapie-usa.blogspot.com/2025/04/failure-to-prevent-classical-scrapie.html
https://prpsc.proboards.com/thread/165/failure-prevent-scrapie-repeated-decontamination
"Additionally, we have determined that prion seeding activity is retained for at least fifteen years at a contaminated site following attempted remediation."
15 YEARS!
Detection of prions in soils contaminated by multiple routes
Results: We are able to detect prion seeding activity at multiple types of environmental hotspots, including carcass sites, contaminated captive facilities, and scrapes (i.e. urine and saliva). Differences in relative prion concentration vary depending on the nature and source of the contamination. Additionally, we have determined that prion seeding activity is retained for at least fifteen years at a contaminated site following attempted remediation.
Conclusions: Detection of prions in the environment is of the utmost importance for controlling chronic wasting disease spread. Here, we have demonstrated a viable method for detection of prions in complex environmental matrices. However, it is quite likely that this method underestimates the total infectious prion load in a contaminated sample, due to incomplete recovery of infectious prions. Further refinements are necessary for accurate quantification of prions in such samples, and to account for the intrinsic heterogeneities found in the broader environment.
Funded by: Wisconsin Department of Natural Resources
Prion 2023 Congress Organizing Committee and the NeuroPrion Association, we invite you to join us for the International Conference Prion2023 from 16-20 October 2023 in Faro, Portugal.
***> Nine of these recurrences occurred 14–21 years after culling, apparently as the result of environmental contamination, but outside entry could not always be absolutely excluded.
JOURNAL OF GENERAL VIROLOGY Volume 87, Issue 12
Infectious agent of sheep scrapie may persist in the environment for at least 16 years Free
https://www.microbiologyresearch.org/content/journal/jgv/10.1099/vir.0.82011-0
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.
Prion 2022 Conference abstracts: pushing the boundaries
https://www.tandfonline.com/doi/full/10.1080/
https://pubmed.ncbi.nlm.nih.gov/30602491/
I remember what “deep throat” told me about Scrapie back around 2001, during early days of my BSE investigation, after my Mom died from hvCJD, I never forgot, and it seems it’s come to pass;
***> 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…
Chronic Wasting Disease CWD TSE Prion
THE CWD TSE Prion aka mad cow type disease is not your normal pathogen.
The TSE prion disease survives ashing to 600 degrees celsius, that’s around 1112 degrees farenheit.
You cannot cook the TSE prion disease out of meat. In fact new data now shows that exposure to high temperatures used to cook the meat increased the availability of prions for in vitro amplification.
you can take the ash and mix it with saline and inject that ash into a mouse, and the mouse will go down with TSE.
Prion Infected Meat-and-Bone Meal Is Still Infectious after Biodiesel Production as well.
the TSE prion agent also survives Simulated Wastewater Treatment Processes.
IN fact, you should also know that the TSE Prion agent will survive in the environment for years, if not decades.
you can bury it and it will not go away.
The TSE agent is capable of infected your water table i.e. Detection of protease-resistant cervid prion protein in water from a CWD-endemic area.
it’s not your ordinary pathogen you can just cook it out and be done
New studies on the heat resistance of hamster-adapted scrapie agent: Threshold survival after ashing at 600°C suggests an inorganic template of replication
http://www.pnas.org/content/97/7/3418.full
Prion Infected Meat-and-Bone Meal Is Still Infectious after Biodiesel Production
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2493038/
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
https://bmcvetres.biomedcentral.com/track/pdf/10.1186/1746-6148-9-134.pdf
THURSDAY, FEBRUARY 28, 2019
BSE infectivity survives burial for five years with only limited spread
https://link.springer.com/content/pdf/10.1007%2Fs00705-019-04154-8.pdf
Chronic wasting disease prions on deer feeders and wildlife visitation to deer feeding areas
First published: 10 February 2025
Snip…
Finally, we swabbed 19 feeders in 2 areas where CWD was newly detected, finding prion contamination on swabs from 4 feeders. We show that deer feeders in free-ranging populations with high CWD prevalence become contaminated with CWD prions quickly, becoming a potential site of exposure of deer to CWD prions. Our results also demonstrate the ability to find evidence of prion contamination on deer feeders, even in areas where CWD is newly detected.
Snip…
We found that supplemental feeding increased the risk of exposure to CWD prions due to contamination of feeders, increased deer visitation, and increased deer-to-deer contact.
The 12-fold increase in deer visitation to feeders compared to mast trees and 2-fold increase compared to food plots demonstrates increased risk for direct disease spread.
https://wildlife.onlinelibrary.wiley.com/doi/10.1002/jwmg.70000
2025
Cwd, cattle, pigs, sheep, raccoons, oh my!
Price of TSE Prion Poker goes up substantially, all you cattle ranchers and such, better pay close attention here...terry
"Cattle with the E211K polymorphism are susceptible to the CWD agent after oronasal exposure of 0.2 g of infectious material."
Transmission of the chronic wasting disease agent from elk to cattle after oronasal exposure
Justin Greenlee, Jifeng Bian, Zoe Lambert, Alexis Frese, and Eric Cassmann Virus and Prion Research Unit, National Animal Disease Center, USDA-ARS, Ames, IA, USA
Aims: The purpose of this study was to determine the susceptibility of cattle to chronic wasting disease agent from elk.
Materials and Methods: Initial studies were conducted in bovinized mice using inoculum derived from elk with various genotypes at codon 132 (MM, LM, LL). Based upon attack rates, inoculum (10% w/v brain homogenate) from an LM132 elk was selected for transmission studies in cattle. At approximately 2 weeks of age, one wild type steer (EE211) and one steer with the E211K polymorphism (EK211) were fed 1 mL of brain homogenate in a quart of milk replacer while another 1 mL was instilled intranasally. The cattle were examined daily for clinical signs for the duration of the experiment. One steer is still under observation at 71 months post-inoculation (mpi).
Results: Inoculum derived from MM132 elk resulted in similar attack rates and incubation periods in mice expressing wild type or K211 bovine PRNP, 35% at 531 days post inoculation (dpi) and 27% at 448 dpi, respectively. Inoculum from LM132 elk had a slightly higher attack rates in mice: 45% (693 dpi) in wild type cattle PRNP and 33% (468) in K211 mice. Inoculum from LL132 elk resulted in the highest attack rate in wild type bovinized mice (53% at 625 dpi), but no K211 mice were affected at >700 days. At approximately 70 mpi, the EK211 genotype steer developed clinical signs suggestive of prion disease, depression, low head carriage, hypersalivation, and ataxia, and was necropsied. Enzyme immunoassay (IDEXX) was positive in brainstem (OD=4.00, but non-detect in retropharyngeal lymph nodes and palatine tonsil. Immunoreactivity was largely limited to the brainstem, midbrain, and cervical spinal cord with a pattern that was primarily glia-associated.
Conclusions: Cattle with the E211K polymorphism are susceptible to the CWD agent after oronasal exposure of 0.2 g of infectious material.
https://prion2023.org/wp-content/uploads/2023/10/Meeting-book-final-version2.pdf
Prion 2023 Congress Organizing Committee and the NeuroPrion Association, we invite you to join us for the International Conference Prion2023 from 16-20 October 2023 in Faro, Portugal.
Transmission of the chronic wasting disease agent from elk to cattle after oronasal exposure
Conclusions: Cattle with the E211K polymorphism are susceptible to the CWD agent after oronasal exposure of 0.2 g of infectious material.
Strain characterization of chronic wasting disease in bovine-PrP transgenic mice
Conclusions: Altogether, these results exhibit the diversity of CWD strains present in the panel of CWD isolates and the ability of at least some CWD isolates to infect bovine species. Cattle being one of the most important farming species, this ability represents a potential threat to both animal and human health, and consequently deserves further study.
https://prion2023.org/wp-content/uploads/2023/10/Meeting-book-final-version2.pdf
Detection of Prions in Wild Pigs (Sus scrofa) from Areas with Reported Chronic Wasting Disease Cases, United States
Abstract
Using a prion amplification assay, we identified prions in tissues from wild pigs (Sus scrofa) living in areas of the United States with variable chronic wasting disease (CWD) epidemiology. Our findings indicate that scavenging swine could play a role in disseminating CWD and could therefore influence its epidemiology, geographic distribution, and interspecies spread.
Conclusions
In summary, results from this study showed that wild pigs are exposed to cervid prions, although the pigs seem to display some resistance to infection via natural exposure. Future studies should address the susceptibility of this invasive animal species to the multiple prion strains circulating in the environment. Nonetheless, identification of CWD prions in wild pig tissues indicated the potential for pigs to move prions across the landscape, which may, in turn, influence the epidemiology and geographic spread of CWD.
https://wwwnc.cdc.gov/eid/article/31/1/24-0401_article
Currently, swine rations in the U.S. could contain animal derived components including materials from deer or elk. In addition, feral swine could be exposed to infected carcasses in areas where CWD is present in wildlife populations. The current feed ban in the U.S. is based exclusively on keeping tissues from TSE infected cattle from entering animal feeds. These results indicating the susceptibility of pigs to CWD, coupled with the limitations of the current feed ban, indicates that a revision of the feed ban may be necessary to protect swine production and potentially human health.
The successful transmission of pig-passaged CWD to Tg40 mice reported here suggests that passage of the CWD agent through pigs results in a change of the transmission characteristics which reduces the transmission barrier of Tg40 mice to the CWD agent. If this biological behavior is recapitulated in the original host species, passage of the CWD agent through pigs could potentially lead to increased pathogenicity of the CWD agent in humans. Interestingly, bioassay of material from the longest surviving >6 month orally challenged pig (72 mpc), which was negative for PrPcwd by all other tests, produced a positive bioassay result. Bioassay of material from additional animals is currently underway. This study demonstrates that pigs can serve as potential hosts for CWD, although with low attack rates and scant PrPcwd accumulation. Detection of infectivity in orally challenged pigs using mouse bioassay raises the possibility that naturally exposed pigs act as a reservoir of CWD infectivity, even though affected pigs do not develop overt clinical signs or readily detectable PrPcwd.
https://www.ars.usda.gov/research/publications/publication/?seqNo115=326166
cwd scrapie pigs oral routes
***> However, at 51 months of incubation or greater, 5 animals were positive by one or more diagnostic methods. Furthermore, positive bioassay results were obtained from all inoculated groups (oral and intracranial; market weight and end of study) suggesting that swine are potential hosts for the agent of scrapie. <***
*** Although the current U.S. feed ban is based on keeping tissues from TSE infected cattle from contaminating animal feed, swine rations in the U.S. could contain animal derived components including materials from scrapie infected sheep and goats. These results indicating the susceptibility of pigs to sheep scrapie, coupled with the limitations of the current feed ban, indicates that a revision of the feed ban may be necessary to protect swine production and potentially human health. <***
***> 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 month group was positive by EIA. PrPSc was detected by QuIC in at least one of the lymphoid tissues examined in 5/6 pigs in the intracranial <6 months group, 6/7 intracranial >6 months group, 5/6 pigs in the oral <6 months group, and 4/6 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.
https://www.ars.usda.gov/research/publications/publication/?seqNo115=353091
https://www.ars.usda.gov/research/project/?accnNo=432011&fy=2017
https://www.ars.usda.gov/research/publications/publication/?seqNo115=337105
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.
https://www.ars.usda.gov/research/publications/publication/?seqNo115=337105
Component 6: Transmissible Spongiform Encephalopathies
Sheep scrapie agent can infect white-tailed deer after oronasal exposure.
The origin of chronic wasting disease (CWD) is not known, but it has many similarities to the sheep prion disease called scrapie. It has long been hypothesized that CWD arose through transmission of sheep scrapie to deer. ARS researchers in Ames, Iowa, conducted research to determine if scrapie derived from sheep could be transmitted to white-tailed deer. The deer inoculated with sheep scrapie developed clinical signs and the abnormal prion protein could be detected in a wide range of tissues. These results indicate that deer may be susceptible to sheep scrapie if exposed to the disease in natural or agricultural settings. In addition, several strong similarities between CWD in white-tailed deer and the experimental cases of scrapie in white-tailed deer suggests that it would be difficult to distinguish scrapie from CWD in deer or identify scrapie if a case occurs. This information should be considered by deer farmers for keeping their herds free from prion diseases.
https://www.ars.usda.gov/ARSUserFiles/np103/AnnualReports/NP103%20FY2023%20Annual%20Report_Final.pdf
The chronic wasting disease agent from white-tailed deer is highly infectious to humanized mice after passage through raccoons
https://www.ars.usda.gov/research/publications/publication/?seqNo115=400777
Docket No. FDA-2003-D-0432 (formerly 03D-0186) Use of Material from Deer and Elk in Animal Feed
PUBLIC SUBMISSION
Comment from Terry Singeltary Sr.
Posted by the Food and Drug Administration on May 17, 2016 Comment
Docket No. FDA-2003-D-0432 (formerly 03D-0186) Use of Material from Deer and Elk in Animal Feed Singeltary Submission
https://www.regulations.gov/comment/FDA-2003-D-0432-0011
https://www.regulations.gov/docket/FDA-2003-D-0432
WHO IS GETTING PAID OFF CWD, IS IT DNR, INSURANCE COMPANIES, GOVERNMENT, CONSPIRACY, OR COULD IT BE…indemnity for captive Cervid industry?
USDA EXPLANATORY NOTES ANIMAL AND PLANT HEALTH INSPECTION SERVICE 2025-2014 CHRONIC WASTING DISEASE CWD TSE CERVID
https://chronic-wasting-disease.blogspot.com/2025/09/usda-explanatory-notes-animal-and-plant.html
TUESDAY, NOVEMBER 11, 2025
USAHA 128th Annual Meeting October 2024 CWD, TSE, Prion Update
https://chronic-wasting-disease.blogspot.com/2025/11/usaha-128th-annual-meeting-october-2024.html
FRIDAY, OCTOBER 31, 2025
Captive Cervid and the Economic Burden of Chronic Wasting Disease CWD TSE Prion?
The economic burden of ignoring CWD would be far greater, imo, with time, if no cervid were left, or just a select few, if the environment/property was so exposed and saturated with CWD, that you couldn’t sell it, you couldn’t grow crops because of the soil saturation of the CWD, water tables saturated with CWD, saturation of hay, grains, from crops uptake on said property, cervid meat saturated from Cervid CWD, remember, You cannot cook the TSE prion disease out of meat, In fact new data now shows that exposure to high temperatures used to cook the meat increased the availability of prions for in vitro amplification. So, what Do we do, how many humans and animals do we continue to expose, continue to saturate with the CWD TSE Prion, …
https://chronic-wasting-disease.blogspot.com/2025/10/captive-cervid-and-economic-burden-of.html
https://prpsc.proboards.com/thread/183/captive-cervid-economic-burden-prion
CWD Status Captive Herds
https://www.aphis.usda.gov/sites/default/files/status-of-captive-herds.pdf
https://www.thewildlifenews.com/2025/12/03/elk-feedlots-and-chronic-wasting-disease/
Human CWD TSE PrP, what if?
the problem is, to date, there is NO diagnostic criteria set in stone that would confirm a case of human Cwd, like there was with nvCJD (my Mom died from confirmed hvCJD a rare strain of the infamous sporadic CJDs with new strains mounting, sporadic CJD simply means ‘unknown’, IT DOES NOT MEAN 85%+ SPORADIC CJD IS ALL SPONTANEOUS, that’s all iatrogenic CJD is sporadic CJD, until the iatrogenic event is detected, confirmed, traced back, confirmed, put I to the academic domain, and finally, if your lucky, finally published to the media, and finally the public domain.) sorry, I got off course…but let me perfectly clear here, all science to date shows, Human CWD will not look like New Variant Creutzfeldt Jakob disease nvCJD. CWD to humans will look like some variant of sporadic Creutzfeldt Jakob Disease. And here me out very clearly, and this is from the to TSE Prion Gods themselves, old correspondence from way back during my investigations early BSE nvCJD days…2002
“Also, we do not claim that "no-one has ever been infected with prion disease from eating venison." Our conclusion stating that we found no strong evidence of CWD transmission to humans in the article you quoted or in any other forum is limited to the patients we investigated.”
*** now, let’s see what the authors said about this casual link, personal communications years ago, and then the latest on the zoonotic potential from CWD to humans from the TOKYO PRION 2016 CONFERENCE.
see where it is stated NO STRONG evidence. so, does this mean there IS casual evidence ????
“Our conclusion stating that we found no strong evidence of CWD transmission to humans”
Subject: CWD aka MAD DEER/ELK TO HUMANS ??? Date: September 30, 2002 at 7:06 am PST From: "Belay, Ermias" To: Cc: "Race, Richard (NIH)" ; ; "Belay, Ermias"
Sent: Monday, September 30, 2002 9:22 AM
Subject: RE: TO CDC AND NIH - PUB MED- 3 MORE DEATHS - CWD - YOUNG HUNTERS
Dear Sir/Madam, In the Archives of Neurology you quoted (the abstract of which was attached to your email), we did not say CWD in humans will present like variant CJD.. That assumption would be wrong. I encourage you to read the whole article and call me if you have questions or need more clarification (phone: 404-639-3091).
Also, we do not claim that "no-one has ever been infected with prion disease from eating venison." Our conclusion stating that we found no strong evidence of CWD transmission to humans in the article you quoted or in any other forum is limited to the patients we investigated.
Ermias Belay, M.D. Centers for Disease Control and Prevention
Subject: TO CDC AND NIH - PUB MED- 3 MORE DEATHS - CWD - YOUNG HUNTERS
Sunday, November 10, 2002 6:26 PM .......snip........end..............TSS
-----Original Message-----
From: Sent: Sunday, September 29, 2002 10:15 AM
To: rr26k@nih.gov; rrace@niaid.nih.gov; ebb8@CDC.GOV
Subject: TO CDC AND NIH - PUB MED- 3 MORE DEATHS - CWD - YOUNG HUNTERS
Sunday, November 10, 2002 6:26 PM .......snip........end..............TSS
Thursday, April 03, 2008
A prion disease of cervids: Chronic wasting disease 2008 1: Vet Res. 2008 Apr 3;39(4):41 A prion disease of cervids: Chronic wasting disease Sigurdson CJ.
snip...
*** twenty-seven CJD patients who regularly consumed venison were reported to the Surveillance Center, however there have been no unusual or novel prion subtypes that might indicate the appearance of a new prion strain [7, 41].
snip... full text ;
https://www.vetres.org/articles/vetres/abs/2008/04/v08092/v08092.html
https://chronic-wasting-disease.blogspot.com/2008/04/prion-disease-of-cervids-chronic.html
“regular venison eating associated with a 9 FOLD INCREASE IN RISK OF CJD”
Subject: Re: DEER SPONGIFORM ENCEPHALOPATHY SURVEY & HOUND STUDY Date: Fri, 18 Oct 2002 23:12:22 +0100 From: Steve Dealler Reply-To: Bovine Spongiform Encephalopathy Organization: Netscape Online member
To: BSE-L@ …
######## Bovine Spongiform Encephalopathy <BSE-L@UNI-KARLSRUHE.DE> #########
Dear Terry,
An excellent piece of review as this literature is desparately difficult to get back from Government sites. What happened with the deer was that an association between deer meat eating and sporadic CJD was found in about 1993. The evidence was not great but did not disappear after several years of asking CJD cases what they had eaten. I think that the work into deer disease largely stopped because it was not helpful to the UK industry...and no specific cases were reported.
Well, if you dont look adequately like they are in USA currenly then you wont find any!
Steve Dealler
########### http://mailhost.rz.uni-karlsruhe.de/warc/bse-l.html ############
Subject: DEER SPONGIFORM ENCEPHALOPATHY SURVEY & HOUND STUDY From: "Terry S. Singeltary Sr." <flounder@WT.NET> Reply To: Bovine Spongiform Encephalopathy <BSE-L@UNI-KARLSRUHE.DE> Date: Thu, 17 Oct 2002 17:04:51 -0700
snip...
''The association between venison eating and risk of CJD shows similar pattern, with regular venison eating associated with a 9 FOLD INCREASE IN RISK OF CJD (p = 0.04).''
CREUTZFELDT JAKOB DISEASE SURVEILLANCE IN THE UNITED KINGDOM THIRD ANNUAL REPORT AUGUST 1994
snip...see full report ;
http://web.archive.org/web/20090506050043/http://www.bseinquiry.gov.uk/files/yb/1994/08/00004001.pdf
http://web.archive.org/web/20090506050007/http://www.bseinquiry.gov.uk/files/yb/1994/10/00003001.pdf
http://web.archive.org/web/20090506050244/http://www.bseinquiry.gov.uk/files/yb/1994/07/00001001.pdf
Stephen Dealler is a consultant medical microbiologist deal@airtime.co.uk BSE Inquiry Steve Dealler Management In Confidence BSE: Private Submission of Bovine Brain Dealler
snip...end
########### http://mailhost.rz.uni-karlsruhe.de/warc/bse-l.html ############
*** 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).***
http://www.tandfonline.com/doi/full/10.4161/pri.28124?src=recsys
http://www.tandfonline.com/doi/pdf/10.4161/pri.28124?needAccess=true
https://wwwnc.cdc.gov/eid/article/20/1/13-0858_article
So, this is what we leave our children and grandchildren?
What does CDC say?
CDC CWD TSE Prion Update 2025
KEY POINTS
Chronic wasting disease affects deer, elk and similar animals in the United States and a few other countries.
The disease hasn't been shown to infect people.
However, it might be a risk to people if they have contact with or eat meat from animals infected with CWD.
https://www.cdc.gov/chronic-wasting/about/index.html
Prions in Muscles of Cervids with Chronic Wasting Disease, Norway
Volume 31, Number 2—February 2025
Research
Prions in Muscles of Cervids with Chronic Wasting Disease, Norway
Snip…
In summary, the results of our study indicate that prions are widely distributed in peripheral and edible tissues of cervids in Norway, including muscles. This finding highlights the risk of human exposure to small amounts of prions through handling and consuming infected cervids. Nevertheless, we note that this study did not investigate the zoonotic potential of the Norway CWD prions. In North America, humans have historically consumed meat from CWD-infected animals, which has been documented to harbor prions (35,44–47). Despite the potential exposure to prions, no epidemiologic evidence indicates a correlation between the occurrence of CWD cases in animals and the prevalence of human prion diseases (48). A recent bioassay study reported no transmissions from 3 Nordic isolates into transgenic mice expressing human PrP (49). Therefore, our findings should be interpreted with caution in terms of human health implications, and further research is required to determine the zoonotic potential of these CWD strains.
The presence of prions in peripheral tissues indicates that CWD may have a systemic nature in all Norwegian cervid species, challenging the view that prions are exclusively localized in the CNS in sporadic CWD of moose and red deer. Our findings expand the notion of just how widely distributed prions can be in cervids affected with CWD and call into question the capability of emerging CWD strains in terms of infectivity to other species, including humans.
Appendix
https://wwwnc.cdc.gov/eid/article/31/2/24-0903-app1.pdf
https://wwwnc.cdc.gov/eid/article/31/2/24-0903_article
Volume 31, Number 2—February 2025
Dispatch
Detection of Chronic Wasting Disease Prions in Raw, Processed, and Cooked Elk Meat, Texas, USA
Rebeca Benavente, Fraser Brydon, Francisca Bravo-Risi, Paulina Soto, J. Hunter Reed, Mitch Lockwood, Glenn Telling, Marcelo A. Barria, and Rodrigo MoralesComments to Author
Snip…
CWD prions have been detected in the muscle of both farmed and wild deer (10), and at concentrations relevant to sustain disease transmission (11). CWD prions have also been identified across several cervid species and in multiple tissues, including lymph nodes, spleen, tongue, intestines, adrenal gland, eyes, reproductive tissues, ears, lungs, and liver, among others (12–14). Those findings raise concerns about the safety of ingesting processed meats that contain tissues other than skeletal muscle (15) (Appendix). https://wwwnc.cdc.gov/eid/article/31/2/24-0906-app1.pdf
In addition, those findings highlight the need for continued vigilance and research on the transmission risks of prion diseases and for development of new preventative and detection measures to ensure the safety of the human food supply.
Snip…
Overall, our study results confirm previous reports describing the presence of CWD prions in elk muscles (13). The data also demonstrated CWD prion persistence in food products even after processing through different procedures, including the addition of salts, spices, and other edible elements. Of note, our data show that exposure to high temperatures used to cook the meat increased the availability of prions for in vitro amplification. Considering the potential implications in food safety and public health, we believe that the findings described in this study warrant further research. Our results suggest that although the elk meat used in this study resisted different manipulations involved in subsequent consumption by humans, their zoonotic potential was limited. Nevertheless, even though no cases of CWD transmission to human have been reported, the potential for human infection is still unclear and continued monitoring for zoonotic potential is warranted.
https://wwwnc.cdc.gov/eid/article/31/2/24-0906_article
The detection and decontamination of chronic wasting disease prions during venison processing
Aims: There is a growing concern that chronic wasting disease (CWD) prions in venison pose a risk to human health. CWD prions accumulate in infected deer tissues that commonly enter the human food chain through meat processing and consumption. The United States (US) Food and Drug Administration and US Department of Agriculture now formally consider CWD-positive venison unfit for human and animal consumption. Yet, the degree to which prion contamination occurs during routine venison processing is unknown. Here, we use environmental surface swab methods to:
a) experimentally test meat processing equipment (i.e., stainless steel knives and polyethylene cutting boards) before and after processing CWD-positive venison and
b) test the efficacy of five different disinfectant types (i.e., Dawn dish soap, Virkon-S, Briotech, 10% bleach, and 40% bleach) to determine prion decontamination efficacy.
Materials and Methods: We used a real-time quaking-induced conversion (RT-QuIC) assay to determine CWD infection status of venison and to detect CWD prions in the swabs. We collected three swabs per surface and ran eight technical replicates on RT-QuIC.
Results: CWD prions were detected on all cutting boards (n= 3; replicates= 8/8, 8/8, 8/8 and knives (n= 3; replicates= 8/8, 8/8, 8/8) used in processing CWD-positive venison, but not on those used for CWD-negative venison. After processing CWD-positive venison, allowing the surfaces to dry, and washing the cutting board with Dawn dish soap, we detected CWD prions on the cutting board surface (n= 3; replicates= 8/8, 8/8, 8/8) but not on the knife (n= 3, replicates = 0/8, 0/8, 0/8). Similar patterns were observed with Briotech (cutting board: n= 3; replicates= 7/8, 1/8, 0/8; knife: n= 3; replicates = 0/8, 0/8, 0/8). We did not detect CWD prions on the knives or cutting boards after disinfecting with Virkon-S, 10% bleach, and 40% bleach.
Conclusions: These preliminary results suggest that Dawn dish soap and Briotech do not reliably decontaminate CWD prions from these surfaces. Our data suggest that Virkon-S and various bleach concentrations are more effective in reducing prion contamination of meat processing surfaces; however, surface type may also influence the ability of prions to adsorb to surfaces, preventing complete decontamination. Our results will directly inform best practices to prevent the introduction of CWD prions into the human food chain during venison processing.
Prion 2023 Abstracts
https://prion2023.org/wp-content/uploads/2023/10/Meeting-book-final-version2.pdf
DETECTION OF CHRONIC WASTING DISEASE PRIONS IN PROCESSED MEATS.
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.
https://intcwdsympo.files.wordpress.com/2023/06/final-agenda-with-abstracts.pdf?force_download=true
Detection of chronic wasting disease prions in processed meats
Results: Our results show positive prion detection in all the samples analyzed using deer and elk substrates. Surprisingly, cooked meats displayed increased seeding activities. This data suggests that CWD-prions are available to people even after meats are processed and cooked.
Conclusions: These results suggest CWD prions are accessible to humans through meats, even after processing and cooking. Considering the fact that these samples were collected from already processed specimens, the availability of CWD prions to humans is probably underestimated.
"Our results show positive prion detection in all the samples analyzed using deer and elk substrates. Surprisingly, cooked meats displayed increased seeding activities."
https://prion2023.org/wp-content/uploads/2023/10/Meeting-book-final-version2.pdf
Aims: Whether CWD prions can infect humans remains unclear despite the very substantial scale and long history of human exposure of CWD in many states or provinces of USA and Canada. Multiple in vitro conversion experiments and in vivo animal studies indicate that the CWD-to-human transmission barrier is not unbreakable. A major long-term 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.
Materials and Methods: We inoculated several sCJD brain samples into cervidized transgenic mice (Tg12), which were intended as negative controls for bioassays of brain tissues from sCJD cases who had potentially been exposed to CWD. Some of the Tg12mice became infected and their brain tissues were further examined by Western blot as well as 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 the original CJDElkPrP in transgenic mice expressing human PrP. We passaged CJDElkPrP two more times in the Tg12mice. We found that such second and third passage CJDElkPrP prions retained 100% transmission rate in the humanized mice, despite that the natural elk CWD isolates and CJDElkPrP share the same elk PrP sequence. In contrast, we and others found zero or poor transmission of natural elk CWD isolates in humanized mice.
Conclusions: Our data indicate that highly zoonotic cervid prion strains are not only possible but also can retain zoonotic potential after serial passages in cervids, suggesting a very significant and serious long-term risk of CWD zoonosis given that the broad and continuing spread of CWD prions will provide fertile grounds for the emergence of zoonotic CWD strains over time.
https://prion2023.org/wp-content/uploads/2023/10/Meeting-book-final-version2.pdf
Samia Hannaoui1 · Irina Zemlyankina1 · Sheng Chun Chang1 · Maria Immaculata Arifn1 · Vincent Béringue2 · Debbie McKenzie3 · Hermann M. Schatzl1 · Sabine Gilch1
Received: 24 May 2022 / Revised: 5 August 2022 / Accepted: 7 August 2022
© The Author(s) 2022
Abstract
Prions cause infectious and fatal neurodegenerative diseases in mammals. Chronic wasting disease (CWD), a prion disease of cervids, spreads efficiently among wild and farmed animals. Potential transmission to humans of CWD is a growing concern due to its increasing prevalence. Here, we provide evidence for a zoonotic potential of CWD prions, and its probable signature using mice expressing human prion protein (PrP) as an infection model. Inoculation of these mice with deer CWD isolates resulted in atypical clinical manifestation with prion seeding activity and efficient transmissible infectivity in the brain and, remarkably, in feces, but without classical neuropathological or Western blot appearances of prion diseases. Intriguingly, the protease-resistant PrP in the brain resembled that found in a familial human prion disease and was transmissible upon second passage. Our results suggest that CWD might infect humans, although the transmission barrier is likely higher compared to zoonotic transmission of cattle prions. Notably, our data suggest a different clinical presentation, prion signature, and tissue tropism, which causes challenges for detection by current diagnostic assays. Furthermore, the presence of infectious prions in feces is concerning because if this occurs in humans, it is a source for human-to-human transmission. These findings have strong implications for public health and CWD management.
Keywords Chronic wasting disease · CWD · Zoonotic potential · Prion strains · Zoonotic prions
HIGHLIGHTS OF THIS STUDY
================================
Our results suggest that CWD might infect humans, although the transmission barrier is likely higher compared to zoonotic transmission of cattle prions. Notably, our data suggest a different clinical presentation, prion signature, and tissue tropism, which causes challenges for detection by current diagnostic assays. Furthermore, the presence of infectious prions in feces is concerning because if this occurs in humans, it is a source for human-to-human transmission. These findings have strong implications for public health and CWD management.
In this study, we evaluated the zoonotic potential of CWD using a transgenic mouse model overexpressing human M129-PrPC (tg650 [12]). We inoculated tg650mice intracerebrally with two deer CWD isolates, Wisc-1 and 116AG [22, 23, 27, 29]. We demonstrate that this transgenic line was susceptible to infection with CWD prions and displayed a distinct leading clinical sign, an atypical PrPSc signature and unusual fecal shedding of infectious prions. Importantly, these prions generated by the human PrP transgenic mice were transmissible upon passage. Our results are the first evidence of a zoonotic risk of CWD when using one of the most common CWD strains, Wisc-1/CWD1 for infection. We demonstrated in a human transgenic mouse model that the species barrier for transmission of CWD to humans is not absolute. The fact that its signature was not typical raises the questions whether CWD would manifest in humans as a subclinical infection, whether it would arise through direct or indirect transmission including an intermediate host, or a silent to uncovered human-to-human transmission, and whether current detection techniques will be suffcient to unveil its presence.
Our findings strongly suggest that CWD should be regarded as an actual public health risk. Here, we use humanized mice to show that CWD prions can cross the species barrier to humans, and remarkably, infectious prions can be excreted in feces.
Our results indicate that if CWD crosses the species-barrier to humans, it is unlikely to resemble the most common forms of human prion diseases with respect to clinical signs, tissue tropism and PrPSc signature. For instance, PrPSc in variable protease-sensitive prionopathy (VPSPr), a sporadic form of human prion disease, and in the genetic form Gerstmann-Sträussler-Scheinker syndrome (GSS) is defined by an atypical PK-resistant PrPSc fragment that is non-glycosylated and truncated at both C- and N-termini, with a molecular weight between 6 and 8 kDa [24, 44–46]. These biochemical features are unique and distinctive from PrPSc (PrP27-30) found in most other human or animal prion disease. The atypical PrPSc signature detected in brain homogenate of tg650 mice #321 (1st passage) and #3063 (2nd passage), and the 7–8 kDa fragment (Figs. 2, 4) are very similar to that of GSS, both in terms of migration profile and the N-terminal cleavage site.
CWD in humans might remain subclinical but with PrPSc deposits in the brain with an unusual morphology that does not resemble the patterns usually seen in different prion diseases (e.g., mouse #328; Fig. 3), clinical with untraceable abnormal PrP (e.g., mouse #327) but still transmissible and uncovered upon subsequent passage (e.g., mouse #3063; Fig. 4), or prions have other reservoirs than the usual ones, hence the presence of infectivity in feces (e.g., mouse #327) suggesting a potential for human-to-human transmission and a real iatrogenic risk that might be unrecognizable.
“suggesting a potential for human-to-human transmission and a real iatrogenic risk that might be unrecognizable.”
=================================
Supplementary Information The online version contains supplementary material available at
https://doi.org/10.1007/s00401-022-02482-9
snip...see full text;
https://link.springer.com/article/10.1007/s00401-022-02482-9
https://link.springer.com/content/pdf/10.1007/s00401-022-02482-9.pdf
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
Snip…
***> Further passage to cervidized mice revealed transmission with a 100% attack rate.
***> Our findings demonstrate that macaques, considered the best model for the zoonotic potential of prions, were infected upon CWD challenge, including the oral one.
****> The disease manifested as atypical in macaques and initial transgenic mouse transmissions, but with infectivity present at all times, as unveiled in the bank vole model with an unusual tissue tropism.
***> Epidemiologic surveillance of prion disease among cervid hunters and people likely to have consumed venison contaminated with chronic wasting disease
=====
https://intcwdsympo.files.wordpress.com/2023/06/final-agenda-with-abstracts.pdf?force_download=true
Transmission of Cervid Prions to Humanized Mice Demonstrates the Zoonotic Potential of CWD
Samia Hannaouia, Irina Zemlyankinaa, Sheng Chun Changa, Maria Immaculata Arifina, Vincent Béringueb, Debbie McKenziec, Hermann M. Schatzla, and Sabine Gilcha
Results: Here, we provide the strongest evidence supporting the zoonotic potential of CWD prions, and their possible phenotype in humans. Inoculation of mice expressing human PrPCwith deer CWD isolates (strains Wisc-1 and 116AG) resulted in atypical clinical manifestations in > 75% of the mice, with myoclonus as leading clinical sign. Most of tg650brain homogenates were positive for seeding activity in RT-QuIC. Clinical disease and presentation was transmissible to tg650mice and bank voles. Intriguingly, protease-resistant PrP in the brain of tg650 mice resembled that found in a familial human prion disease and was transmissible upon passage. Abnormal PrP aggregates upon infection with Wisc-1 were detectable in thalamus, hypothalamus, and midbrain/pons regions.
Unprecedented in human prion disease, feces of CWD-inoculated tg650 mice harbored prion seeding activity and infectious prions, as shown by inoculation of bank voles and tg650 with fecal homogenates.
Conclusions: This is the first evidence that CWD can infect humans and cause disease with a distinctive clinical presentation, signature, and tropism, which might be transmissible between humans while current diagnostic assays might fail to detect it. These findings have major implications for public health and CWD-management.
https://www.tandfonline.com/doi/full/10.1080/19336896.2022.2091286
18. Zoonotic potential of moose-derived chronic wasting disease prions after adaptation in intermediate species
Tomás Barrioa, Jean-Yves Doueta, Alvina Huora, Séverine Lugana, Naïma Arona, Hervé Cassarda, Sylvie L. Benestadb, Juan Carlos Espinosac, Juan María Torresc, Olivier Andréolettia
aUnité Mixte de Recherche de l’Institut National de Recherche pour l’Agriculture, l’Alimentation et l’Environnement 1225 Interactions Hôtes-Agents Pathogènes, École Nationale Vétérinaire de Toulouse, 31076 Toulouse, France; bNorwegian Veterinary Institute, P.O. Box 64, NO-1431 Ås, Norway; cCentro de Investigación en Sanidad Animal (CISA-INIA), 28130, Valdeolmos, Madrid, Spain
Aims: Chronic wasting disease (CWD) is an emerging prion disease in Europe. To date, cases have been reported in three Nordic countries and in several species, including reindeer (Rangifer tarandus), moose (Alces alces) and red deer (Cervus elaphus). Cumulating data suggest that the prion strains responsible for the European cases are distinct from those circulating in North America. The biological properties of CWD prions are still poorly documented, in particular their spillover and zoonotic capacities. In this study, we aimed at characterizing the interspecies transmission potential of Norwegian moose CWD isolates.
Materials and Methods: For that purpose, we performed experimental transmissions in a panel of transgenic models expressing the PrPC sequence of various species.
Results: On first passage, one moose isolate propagated in the ovine PrPC-expressing model (Tg338). After adaptation in this host, moose CWD prions were able to transmit in mice expressing either bovine or human PrPC with high efficacy.
Conclusions: These results suggest that CWD prions can acquire enhanced zoonotic properties following adaptation in an intermediate species.
Funding
Grant number: AAPG2020 EU-CWD, ICRAD2020 TCWDE, NRC2022 NorCWD
Acknowledgement
https://www.tandfonline.com/doi/full/10.1080/19336896.2024.2424058
“ After adaptation in this host, moose CWD prions were able to transmit in mice expressing either bovine or human PrPC with high efficacy.”
While no one was watching: Tenuous status of CDC prion unit, risk of CWD to people worry scientists
Mary Van Beusekom, MS Today at 9:15 a.m.
Chronic Wasting Disease BSE CWD zone deer disposal site Lorie Shaull / Flickr cc
Nine months ago, Janie Johnston, 73, left her home in the Chicago suburbs to drive to her doctor's office for routine care. She made it as far as the side of the street opposite the clinic but couldn't figure out how to get there, so she returned home, where she struggled to remember the abbreviation "GPS."
That was the first sign that something was seriously wrong. Soon, the semi-retired geologist couldn't speak in full sentences or feed herself. Within 2 months, the woman who had been reviewing proposals for the National Science Foundation in the weeks leading up to symptom onset was dead of a terrifying neurological disease her family had never heard of: Creutzfeldt-Jakob disease (CJD).
CWD may cause CJD-like disease if it infects people Rather than being genetic or acquired, Johnston's CJD developed when normal prions in her brain spontaneously began misfolding. The abnormal prions accumulated rather than being shed, triggering confusion and fatigue that doctors initially mistook for stroke, meningitis, or alcohol withdrawal. The disease usually occurs in older adults.
Seeing what my mom went through, I do not want anyone else to have to experience that, nor their family members. Kristal Enter
While no one is certain, experts think that another always-fatal prion disease—this one currently known to occur only in cervids such as deer, moose, and elk—may behave the same way if it should jump the species barrier and infect people.
Chronic wasting disease (CWD) has been decimating cervid populations throughout North America since it was first diagnosed in a captive Colorado mule deer in 1967. While mitigation measures such as hunting may help slow its spread, it can't be stopped.
This is because cervids are ubiquitous and free ranging, the interval from infection to symptom onset can take years, and prions spread easily from animal to animal and through environmental contamination, which can persist for years.
Johnston's daughter, Kristal Enter, 39, a fundraiser in Boston, is familiar with CWD and its potential implications for human health. "Seeing what my mom went through, I do not want anyone else to have to experience that, nor their family members," she told CIDRAP News. "The more we're on top of chronic wasting disease and thinking about it, the better."
But the frightening thing is that, for well over a month during the recent US government shutdown, no one was watching the human disease landscape for CWD, a highly infectious disease with no treatment or cure.
If cases slip by, it will be too late Nine days after the government shutdown began, all four staff members of the Centers for Disease Control and Prevention's (CDC's) National Center for Emerging and Zoonotic Infectious Diseases Prion and Public Health Office were sent home after receiving reduction-in-force (RIF) notices. While the end of the shutdown led all four to be reinstated through at least January, layoffs after that time are possible.
Within the past few months, two other researchers who had been part of the team also had to be let go after their fellowship contracts weren't renewed, per the administration's policy of blocking contract renewals.
The prion unit, which monitors the nation for human prion diseases, is part of the Division of High-Consequence Pathogens and Pathology. It launched in the mid-1990s in response to the outbreak of bovine spongiform encephalopathy (BSE, or "mad cow disease") in UK cattle. BSE prions were inadvertently consumed by people who ate contaminated beef, causing the human form of BSE, variant CJD (vCJD). All infected people—more than 230—died.
The initial goal of the Prion and Public Health Office was to watch for any cases of vCJD in the US population. Since then, its focus has expanded to include advising hospitals on how to prevent and respond to prion contamination of instruments used in neurosurgery (prions are resistant to many usual sterilization methods), as well as working with state health departments on disease surveillance. Unit members also answer questions from the public.
Today, as CWD continues its inexorable march across the landscape, exposing more and more people, the prion unit's priority is conducting surveillance for signs of a CWD species jump into high-risk people such as hunters. Without this expertise, no one will be able to evaluate whether a suspected case of CWD prion transmission to humans is likely from an animal.
The prion unit has launched several epidemiologic studies in collaboration with multiple states to look at whether more hunters are dying of prion diseases than would be expected.
Janie Johnston Janie Johnston / Courtesy of Kristal Enter As an example of the unit's work, last spring, a cluster of CJD cases in Oregon was widely conjectured to be linked to CWD. Such cases require autopsy and an epidemiologic investigation to determine whether CWD was involved and, if so, what kind of public health measures are needed. The prion unit shared ideas and strategy with the Oregon state health department in this investigation, which, thankfully, found no link.
But experts say that without anyone looking for these deviations from normal—particularly given that signs of illness may take years to appear—cases could easily go unnoticed, and it will be too late to implement public health measures that could mitigate some of these consequences.
Lawrence Schonberger, MD, MPH, retired chief of the Prion and Public Health Office, said that, as was the situation with BSE, CWD containment efforts must continue. "Unlike with mad cow disease, however, these efforts to date have not been successful," he said. Surveillance and research "should continue to help people recognize any emerging risk to humans from this agent now and in the future, when this agent's pathogenicity [ability to cause disease] may change."
'Worst time to get rid of such a division' Brian Appleby, MD, is director of the National Prion Disease Pathology Surveillance Center at Case Western University, which conducts diagnostic testing for human prion diseases and conducted Johnston's autopsy. The CDC funds the center, which collaborates with the Prion and Public Health Office on public health efforts and research projects.
When you don't have a neutral party investigating these things or doing neuropathology to confirm or refute those things, you really have no idea what's going on in the public health space. Brian Appleby, MD
If the CDC prion unit were eliminated, "no one would be looking at prion disease," Appleby said. "We wouldn't be able to tell if we have an increase in cases or where they're going or coming from. And when you don't have a neutral party investigating these things or doing neuropathology to confirm or refute those things, you really have no idea what's going on in the public health space."
And with the threat of CWD, "this is probably the worst time to get rid of such a division," he added.
While there have been no stated plans to eliminate the unit, history hints that its continued existence may be in jeopardy. In fact, it was removed from President Donald Trump's budget during both of his administrations, before the House of Representatives and Senate reinstated it, Appleby said.
In the first Trump administration, report language stated that human prion surveillance is redundant because cattle are now screened for BSE, and the National Institutes of Health cover research, said Appleby, who refuted the assertions.
"Part of the reason why we are a safe export country for beef is not just the cattle surveillance for BSE, but the human surveillance for variant CJD," he said, adding that monitoring is a separate function from research. "When we were removed from the president's budget this time around, there was no report language, so we have no signal to know why."
Always 'one step behind' Debbie Yobs, president and executive director of the CJD Foundation, a patient-advocacy organization that works with Appleby's center to provide medical lectures, support groups, and other programs, emphasized the importance of sustained surveillance. "You can't have gaps in monitoring a deadly disease like prion disease," she said.
It's like combining symptoms of Alzheimer's, Parkinson's, and ALS [amyotrophic lateral sclerosis, or Lou Gehrig's disease] and then speeding it all up. Debbie Yobs
CJD is devastating for patients and families, said Yobs, whose husband, Patrick, died at age 45 of the less common, genetic form of the disease. "It's like combining symptoms of Alzheimer's, Parkinson's, and ALS [amyotrophic lateral sclerosis, or Lou Gehrig's disease] and then speeding it all up," she added. "There's no definitive diagnosis except through autopsy."
Indeed, Enter called her family's ordeal "unreal," because although Johnston's case was typical of a sporadic case, CJD affects only about 500 to 600 people in the United States each year, per the CDC. At the same time as the family was grieving, they were trying to learn how hospice staff could best manage Johnston's symptoms, which none of them had dealt with before.
"It becomes incumbent upon the family members to become the experts to guide the care," she said. "What they say about CJD is that every day is another new symptom or new complication to have to try to address. And you always feel like you're one step behind."
https://www.cidrap.umn.edu/chronic-wasting-disease/while-no-one-was-watching-tenuous-status-cdc-prion-unit-risk-cwd-people
“While no one was watching: Tenuous status of CDC prion unit, risk of CWD to people worry scientists”
FRIDAY, NOVEMBER 21, 2025
While no one was watching: Tenuous status of CDC prion unit, risk of CWD to people worry scientists
https://chronic-wasting-disease.blogspot.com/2025/11/while-no-one-was-watching-tenuous.html
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
https://histodb15.usz.ch/pages/Images/videos/video-004/video-004.html
2004
April 22, 2004, 10:30 AM CDT Guests: Patrick Singh, Terry Schwan, Janet Skarbek, Bill Fielding (BEGIN VIDEOTAPE) ANNOUNCER: DEBORAH NORVILLE TONIGHT.
https://www.nbcnews.com/id/wbna4806886
1997-11-10: Panorama - The British disease
https://histodb15.usz.ch/pages/Images/videos/video-009/video-009.html
Two Hunters from the Same Lodge Afflicted with Sporadic CJD: Is Chronic Wasting Disease to Blame?
(P7-13.002) Jonathan Trout, Matthew Roberts, Michel Tabet, Eithan Kotkowski, and Sarah HornAUTHORS INFO & AFFILIATIONS April 9, 2024 issue 102 (17_supplement_1) https://doi.org/10.1212/WNL.0000000000204407
Abstract Publication History Information & Authors Metrics & Citations Share Abstract
Objective:
This study presents a cluster of Creutzfeldt-Jakob disease (CJD) cases after exposure to chronic wasting disease (CWD)-infected deer, suggestive of potential prion transmission from CWD-infected deer to humans.
Background:
CJD is a rapidly progressive central nervous system disorder caused by misfolded prion proteins. CWD, a prion disease prevalent in North American deer, has raised concerns due to its possible link to CJD. Although no conclusive evidence of cross-species prion transmission exists, vigilance for such cases is crucial for public health.
Design/Methods:
Not applicable.
Results:
In 2022, a 72-year-old man with a history of consuming meat from a CWD-infected deer population presented with rapid-onset confusion and aggression. His friend, who had also eaten venison from the same deer population, recently died of CJD, raising concerns about a potential link between CWD and human prion disease. Despite aggressive symptomatic treatment of seizures and agitation, the patient’s condition deteriorated and he died within a month of initial presentation. The diagnosis was confirmed postmortem as sporadic CJD with homozygous methionine at codon 129 (sCJDMM1). The patient’s history, including a similar case in his social group, suggests a possible novel animal-to-human transmission of CWD. Based on non-human primate and mouse models, cross-species transmission of CJD is plausible. Due to the challenge of distinguishing sCJDMM1 from CWD without detailed prion protein characterization, it is not possible to definitively rule out CWD in these cases. Although causation remains unproven, this cluster emphasizes the need for further investigation into the potential risks of consuming CWD-infected deer and its implications for public health.
Conclusions:
Clusters of sporadic CJD cases may occur in regions with CWD-confirmed deer populations, hinting at potential cross-species prion transmission. Surveillance and further research are essential to better understand this possible association.
Disclosure: Mr. Trout has nothing to disclose. Dr. Roberts has nothing to disclose. Dr. Tabet has nothing to disclose. Dr. Kotkowski has nothing to disclose. Dr. Horn has received personal compensation in the range of $500-$4,999 for serving as a Consultant for Cala Trio. The institution of Dr. Horn has received research support from Alzheimer's Association.
https://www.neurology.org/doi/abs/10.1212/WNL.0000000000204407
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.
https://thescipub.com/pdf/ajidsp.2021.43.48.pdf
''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.''
https://thescipub.com/pdf/ajidsp.2021.43.48.pdf
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.netRef: 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
https://creutzfeldt-jakob-disease.blogspot.com/2021/05/a-unique-presentation-of-creutzfeldt.html
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.
https://efsa.onlinelibrary.wiley.com/doi/full/10.2903/j.efsa.2018.5132
SATURDAY, FEBRUARY 23, 2019
Chronic Wasting Disease CWD TSE Prion and THE FEAST 2003 CDC an updated review of the science 2019
https://chronic-wasting-disease.blogspot.com/2019/02/chronic-wasting-disease-cwd-tse-prion.html
TUESDAY, NOVEMBER 04, 2014
Six-year follow-up of a point-source exposure to CWD contaminated venison in an Upstate New York community: risk behaviours and health outcomes 2005–2011 Authors, though, acknowledged the study was limited in geography and sample size and so it couldn't draw a conclusion about the risk to humans. They recommended more study. Dr. Ermias Belay was the report's principal author but he said New York and Oneida County officials are following the proper course by not launching a study. "There's really nothing to monitor presently. No one's sick," Belay said, noting the disease's incubation period in deer and elk is measured in years. "
http://chronic-wasting-disease.blogspot.com/2014/11/six-year-follow-up-of-point-source.html
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....
https://web.archive.org/web/20090506002237/http://www..bseinquiry.gov.uk/files/mb/m11b/tab01.pdf
Docket No. FDA-2003-D-0432 (formerly 03D-0186) Use of Material from Deer and Elk in Animal Feed
PUBLIC SUBMISSION Comment from Terry Singeltary Sr.
Posted by the Food and Drug Administration on May 17, 2016
Comment Docket No. FDA-2003-D-0432 (formerly 03D-0186) Use of Material from Deer and Elk in Animal Feed Singeltary Submission
https://www.regulations.gov/comment/FDA-2003-D-0432-0011
https://www.regulations.gov/docket/FDA-2003-D-0432
Control of Chronic Wasting Disease OMB Control Number: 0579-0189APHIS-2021-0004 Singeltary Submission
https://www.regulations.gov/comment/APHIS-2021-0004-0002
https://downloads.regulations.gov/APHIS-2021-0004-0002/attachment_1.pdf
Docket No. APHIS-2018-0011 Chronic Wasting Disease Herd Certification
https://www.regulations.gov/document/APHIS-2018-0011-0003
https://downloads.regulations.gov/APHIS-2018-0011-0003/attachment_1.pdf
APHIS Indemnity Regulations [Docket No. APHIS-2021-0010] RIN 0579-AE65 Singeltary Comment Submission
Comment from Singeltary Sr., Terry
Posted by the Animal and Plant Health Inspection Service on Sep 8, 2022
https://www.regulations.gov/comment/APHIS-2021-0010-0003
https://downloads.regulations.gov/APHIS-2021-0010-0003/attachment_1.pdf
Chronic Wasting Disease CWD TSE Prion Environmental Factors Update
https://chronic-wasting-disease.blogspot.com/2025/09/chronic-wasting-disease-cwd-tse-prion.html
While no one was watching: Tenuous status of CDC prion unit, risk of CWD to people worry scientists
https://chronic-wasting-disease.blogspot.com/2025/11/while-no-one-was-watching-tenuous.html
posted by Terry S. Singeltary Sr. at
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