H.R.5608 - Chronic Wasting Disease Research and Management Act 117th Congress (2021-2022) Singeltary Submission
H.R.5608 - Chronic Wasting Disease Research and Management Act 117th Congress (2021-2022) Singeltary Submission
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From: Terry Singeltary <flounder9@verizon.net>To: ron.kind@mail.house.gov <ron.kind@mail.house.gov>; president@whitehouse.gov <president@whitehouse.gov>
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Sent: Sat, Apr 30, 2022 12:30 pm
Subject: H.R.5608 - Chronic Wasting Disease Research and Management Act 117th Congress (2021-2022)
Greetings Honorable Government Officials,
with great urgency, i must submit the following updated science on chronic wasting disease cwd transmissible spongiform encephalopathy tse prion disease. my comments follows ;
H.R.5608 - Chronic Wasting Disease Research and Management Act 117th Congress (2021-2022)
Sponsor: Rep. Kind, Ron [D-WI-3] (Introduced 10/19/2021)
Committees: House - Agriculture | Senate - Agriculture, Nutrition, and Forestry
Committee Meetings: 10/21/21 10:00AM
Committee Reports: H. Rept. 117-202
Latest Action: Senate - 12/09/2021 Received in the Senate and Read twice and referred to the Committee on Agriculture, Nutrition, and Forestry. (All Actions)
Roll Call Votes: There has been 1 roll call vote
Shown Here: Passed House (12/08/2021) Chronic Wasting Disease Research and Management Act
This bill directs the Department of Agriculture (USDA) to address chronic wasting disease afflicting deer, elk, and moose populations.
Specifically, the bill directs USDA to establish a program to research and manage the disease. Under the program, USDA must offer to enter into agreements with state or tribal wildlife agencies and departments of agriculture, institutions of higher education, and research centers to support research on the transmission of, resistance to, and diagnosis of the disease. In addition, USDA must offer to enter into agreements with such agencies and departments to support state and tribal efforts to develop and implement management strategies that address the disease.
USDA must also develop and maintain materials to inform the public on chronic wasting disease and techniques to help prevent the spread of the disease.
In addition, USDA must solicit public feedback on potential updates and improvements to standards of the chronic wasting disease herd certification program.
117TH CONGRESS REPORT " !
HOUSE OF REPRESENTATIVES 1st Session 117–202
CHRONIC WASTING DISEASE RESEARCH AND MANAGEMENT ACT DECEMBER 7, 2021.—Committed to the Committee of the Whole House on the State of the Union and ordered to be printed Mr. DAVID SCOTT of Georgia, from the Committee on Agriculture, submitted the following R E P O R T [To accompany H.R. 5608] The Committee on Agriculture, to whom was referred the bill (H.R. 5608) to support research and state management efforts on chronic wasting disease, having considered the same, reports favorably thereon without amendment and recommends that the bill do pass.
BRIEF EXPLANATION
This legislation authorizes $70 million annually from Fiscal Year 2022 through Fiscal Year 2028 to be divided equally between research and management projects regarding chronic wasting disease (CWD). USDA will administer the funds through cooperative agreements. The bill also requires the development of educational materials to inform the public on CWD and directs USDA to review its CWD herd certification program (HCP) standards within 18 months.
PURPOSE AND NEED FOR LEGISLATION
CWD is a contagious neurological disease affecting cervids (deer, elk and moose). Since first being documented in 1967, CWD has spread to 27 states throughout the U.S. CWD is in the family of diseases known as transmissible spongiform encephalopathies (TSE). Unlike other infectious diseases, TSEs are not caused by bacteria or viruses, but rather by a naturally occurring protein, that when folded incorrectly, becomes both infectious and deadly. The exact mechanism of disease transmission is unclear, although evidence suggests CWD is transmitted directly from one animal to another through bodily fluids and tissues. Unfortunately, there is currently no cure or preventative measure, such as a vaccine, available for CWD. Because other diseases may present in a similar manner, post mortem testing is required to verify the disease. CWD is of increasing concern for wildlife managers, sportsmen, and captive cervid farmers across the country.
The bill is designed to help address these concerns by promoting a better scientific understanding of CWD, the development of improved diagnostic tools, and other mitigation and management strategies to help combat the disease. More specifically, the research section of the bill authorizes funds to be spent on: (1) methods to effectively detect CWD in live cervids and the environment; (2) testing methods on non-live cervids; (3) genetic resistance to CWD; (4) sustainable cervid harvest management practices to reduce CWD occurrence; and (5) factors contributing to local emergence of CWD. The management section authorizes funding for State or Tribal wildlife agencies and departments of agriculture with the following funding priorities: (1) areas with the highest incidence of CWD; (2) jurisdictions demonstrating the greatest financial commitment to managing, monitoring, surveying, and researching chronic CWD; (3) efforts to develop comprehensive policies and programs focused on CWD management; (4) areas showing the greatest risk of an initial occurrence of CWD; and (5) areas responding to new outbreaks of CWD.
H.R. 5608, CHRONIC WASTING DISEASE RESEARCH AND MANAGEMENT ACT
SECTION-BY-SECTION
Section 1. Short title
Section 1 provides the short title of the bill as the ‘‘Chronic Wasting Disease Research and Management Act.’’
Section 2. Findings
Section 2 describes a series of findings of Congress related to chronic wasting disease.
Section 3. Chronic wasting disease research and management program
Subsection (a) paragraph (1) requires the Secretary of Agriculture to establish a program to enter into cooperative agreements with eligible entities to conduct research on the transmission of, resistance to, and diagnosis of chronic wasting disease. Paragraph (2) describes the type of research that the Secretary shall give priority to when entering into cooperative agreements with eligible entities.
Paragraph (3) requires, to the maximum extent practicable, that the funds awarded to individual cooperative agreements shall be at least two percent and not more than 10 percent of the funds appropriated. Paragraph (4) allows the eligible entities to use not more than 10 percent of funds awarded for administrative costs.
Subsection (b) paragraph (1) requires the Secretary to enter into cooperative agreements with State or Tribal wildlife agencies and departments of agriculture to provide direct financial assistance in support of their effort to develop and implement strategies to address chronic wasting disease, subject to the availability of appropriations. Paragraph (2) requires State or Tribal wildlife agency or department of agriculture to submit an application to receive financial assistance. Paragraph (3) requires the Secretary to give priority to States and Indian Tribes that have: (1) the highest occurrence of chronic wasting disease; (2) shown the greatest financial commitment to managing, monitoring, surveying, and researching chronic wasting disease; (3) policies and programs focused on chronic wasting disease management and integrated them with all involved agencies; (4) the greatest risk of initial occurrence of chronic wasting disease originating from surrounding areas; or (5) the greatest need for response to new outbreaks of chronic wasting disease. Paragraph (4) allows the Secretary to immediately issue funds to a State or Indian Tribe that was not previously infected. Paragraph (5) requires the Secretary, in consultation with State and Tribal departments of agriculture and wildlife agencies, to develop and maintain materials based on the latest scientific knowledge to educate the public on chronic wasting disease.
Subsection (c) defines the term ‘‘chronic wasting disease’’ as the animal disease affecting deer, elk, and moose populations that is a transmissible disease of the nervous system resulting in distinctive lesions in the brain and belongs to the group of diseases known as transmissible spongiform encephalopathies, which includes scrapie, bovine spongiform encephalopathy, and Creutzfeldt-Jakob disease. The subsection also defines ‘‘eligible entity’’ as a State or Tribal department of agriculture, a State or Tribal wildlife agency, a Tribal research facility, an institution of higher education, and a research center conducting or qualified to conduct scientific research on chronic wasting disease.
Subsection (d) requires the Secretary to publish a notice in the Federal Register within 18 months of the date of enactment to solicit public feedback on potential updates and improvements to the chronic wasting disease heard certificate program standards. Subsection (e) authorizes $70 million for each of Fiscal Years 2022 through 2028 to be allocated evenly between research programs and management programs. Not less than 75 percent of management program funding shall be made available to State or Tribal wildlife agencies.
Subsection (f) requires that not more than 10 percent of funds be for administrative costs.
Subsection (g) requires that nothing in this section be construed as interfering with the authority of the Federal Government or States to manage wildlife and livestock on land within their jurisdiction.
Section 4. Technical amendment
Section 4 provides a technical amendment to section 10403(8) of the Animal Health Protection Act.
COMMITTEE CONSIDERATION
I. FULL COMMITTEE
On October 21, 2021, the Committee on Agriculture met pursuant to notice, with a quorum present, to consider H.R. 5608, the Chronic Wasting Disease Research and Management Act. Chairman Scott made an opening statement as did Ranking Member Thompson. Chairman Scott requested other Members submit their opening statements for the record. Without objection, H.R. 5608 was placed before the Committee for consideration, a first reading of the bill was waived, and it was opened for amendment at any point.
Chairman Scott recognized Ranking Member Thompson, the bill’s sponsor to speak on the bill. Discussion occurred and without objection, the Committee considered the bill. There being no amendments, a voice vote was conducted, and the bill was reported favorably from the Committee.
At the conclusion of the meeting, Chairman Scott advised Members that pursuant to the Rules of the House of Representatives, Members had until October 28, 2021, to file any supplemental, additional, dissenting, or minority views with the Committee. Without objection, staff was given permission to make any necessary technical, clarifying, or conforming changes to reflect the intent of the Committee. Chairman Scott thanked all the Members and adjourned the meeting.
COMMITTEE VOTES
In compliance with clause 3(b) of rule XIII of the House of Representatives, H.R. 5608 was reported by voice vote with a majority quorum present. There was no request for a recorded vote.
COMMITTEE OVERSIGHT FINDINGS
In compliance with clause 3(c)(1) of rule XIII and clause 2(b)(1) of rule X of the Rules of the House of Representatives, the Committee’s oversight findings and recommendations are reflected in the descriptive portions of this report.
COST OF LEGISLATION AND THE CONGRESSIONAL BUDGET ACT
With respect to the requirements of clause 3(c)(2) of rule XIII of the Rules of the House of Representatives and section 308(a) of the Congressional Budget Act of 1974 and with respect to requirements of clause (3)(c)(3) of rule XIII of the Rules of the House of Representatives and section 402 of the Congressional Budget Act of 1974, the Committee has requested but not received a cost estimate for this bill from the Director of the Congressional Budget Office. The Committee adopts as its own cost estimate the forthcoming cost estimate of the Director of the Congressional Budget Office, should such cost estimate be made available before House passage of the bill.
The Committee has requested but not received from the Director of the Congressional Budget Office a statement as to whether this bill contains any new budget authority, spending authority, credit authority, or an increase or decrease in revenues or tax expenditures. Congressional Budget Office staff has informed the Committee on a preliminary, informal, nonbinding basis that there does not appear to be any direct spending associated with the bill.
CONSTITUTIONAL AUTHORITY STATEMENT
The Committee finds the Constitutional authority for this legislation in Article I, section 8, clause 18, that grants Congress the power to make all laws necessary and proper for carrying out the powers vested by Congress in the consideration of the United States or in any department or officer thereof. The Committee further finds the Constitutional authority for the legislation in Article, section 8, clause 1, that grants Congress the authority to provide for the general welfare of the United States.
PERFORMANCE GOALS AND OBJECTIVES
Pursuant to clause 3(c)(4) of rule XIII of the House of Representatives, the performance goals and objectives of this measure are to support research and state management efforts on chronic wasting disease.
ADVISORY COMMITTEE STATEMENT
No advisory committee within the meaning of section 5(b) of the Federal Advisory Committee Act was created by this legislation.
APPLICABILITY TO THE LEGISLATIVE BRANCH
The Committee finds that the legislation does not relate to the terms and conditions of employment or access to public services or accommodations within the meaning of section 102(b)(3) of the Congressional Accountability Act (Public Law 104–1).
FEDERAL MANDATES STATEMENT
An estimate of Federal mandates prepared by the Director of the
Congressional Budget Office pursuant to section 423 of the Unfunded Mandates Reform Act was not made available to the Committee in time for the filing of this report. The Chair of the Committee shall cause such estimate to be printed in the Congressional Record upon its receipt by the Committee.
EARMARK STATEMENT
This measure does not contain any congressional earmarks, limited tax benefits, or limited tariff benefits as defined in clause 9(e), 9(f), or 9(g) of rule XXI of the House of Representatives.
DUPLICATION OF FEDERAL PROGRAMS
This measure does not establish or reauthorize a program of the Federal Government known to be duplicative of another Federal program, a program that was included in any report from Government Accountability Office to Congress pursuant to section 21 of Public Law 111–139, or a program related to a program in the most recent Catalog of Federal Domestic Assistance.
DISCLOSURE OF DIRECTED RULE MAKINGS
The Committee does not believe that the legislation directs an Executive Branch official to conduct any specific rule making proceedings within the meaning of 5 U.S.C. 551.
CHANGES IN EXISTING LAW MADE BY THE BILL, AS REPORTED
In compliance with clause 3(e) of rule XIII of the Rules of the House of Representatives, changes in existing law made by the bill, as reported, are shown as follows (existing law proposed to be omitted is enclosed in black brackets, new matter is printed in italics, and existing law in which no change is proposed is shown in roman):
TITLE X—MISCELLANEOUS
* * * * * * *
Subtitle E—Animal Health Protection
* * * * * * *
SEC. 10403. DEFINITIONS.
In this subtitle:
(1) ANIMAL.—The term ‘‘animal’’ means any member of the animal kingdom (except a human).
(2) ARTICLE.—The term ‘‘article’’ means any pest or disease or any material or tangible object that could harbor a pest or disease.
(3) DISEASE.—The term ‘‘disease’’ has the meaning given the term by the Secretary.
(4) ENTER.—The term ‘‘enter’’ means to move into the commerce of the United States.
(5) EXPORT.—The term ‘‘export’’ means to move from a place within the territorial limits of the United States to a place outside the territorial limits of the United States.
(6) FACILITY.—The term ‘‘facility’’ means any structure.
(7) IMPORT.—The term ‘‘import’’ means to move from a place outside the territorial limits of the United States to a place within the territorial limits of the United States.
(8) INDIAN TRIBE.—The term ‘‘Indian tribe’’ has the meaning given the term in section 4 of the Indian Self-Determination and Education Assistance Act ø(25 U.S.C. 450b)¿ (25 U.S.C. 5304).
(9) INTERSTATE COMMERCE.—The term ‘‘interstate commerce’’ means trade, traffic, or other commerce—
(A) between a place in a State and a place in another State, or between places within the same State but through any place outside that State; or
(B) within the District of Columbia or any territory or possession of the United States.
(10) LIVESTOCK.—The term ‘‘livestock’’ means all farm-raised animals.
(11) MEANS OF CONVEYANCE.—The term ‘‘means of conveyance’’ means any personal property used for or intended for use for the movement of any other personal property.
(12) MOVE.—The term ‘‘move’’ means—
(A) to carry, enter, import, mail, ship, or transport;
(B) to aid, abet, cause, or induce carrying, entering, importing, mailing, shipping, or transporting;
(C) to offer to carry, enter, import, mail, ship, or transport;
(D) to receive in order to carry, enter, import, mail, ship, or transport;
(E) to release into the environment; or
(F) to allow any of the activities described in this paragraph.
(13) PEST.—The term ‘‘pest’’ means any of the following that can directly or indirectly injure, cause damage to, or cause disease in livestock:
(A) A protozoan.
(B) A plant.
(C) A bacteria.
(D) A fungus.
(E) A virus or viroid.
(F) An infectious agent or other pathogen.
(G) An arthropod.
(H) A parasite.
(I) A prion.
(J) A vector.
(K) Any organism similar to or allied with any of the organisms described in this paragraph.
(14) SECRETARY.—The term ‘‘Secretary’’ means the Secretary of Agriculture.
(15) STATE.—The term ‘‘State’’ means any of the States, the District of Columbia, the Commonwealth of Puerto Rico, Guam, the Commonwealth of the Northern Mariana Islands, the Virgin Islands of the United States, or any territory or possession of the United States.
(16) THIS SUBTITLE.—Except when used in this section, the term ‘‘this subtitle’’ includes any regulation or order issued by the Secretary under the authority of this subtitle.
(17) UNITED STATES.—The term ‘‘United States’’ means all of the States.
(18) VETERINARY COUNTERMEASURE.—The term ‘‘veterinary countermeasure’’ means any biological product (including an animal vaccine or diagnostic), pharmaceutical product (including a therapeutic), non-pharmaceutical product (including a disinfectant), or other product or equipment to prevent, detect, respond to, or mitigate harm to public or animal health resulting from, animal pests or diseases.
* * * * * * *
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THE CAPTIVE DEER FARMING AND CHRONIC WASTING DISEASE CWD TSE PRP, HAVE GOTTEN COMPLETELY OUT OF HAND.
THE RELEASE OF CWD INFECTED CERVID BY BREEDER RELEASE HAS GOT TO STOP.
THE TRANSPORTATION OF CAPTIVE CERVID MUST STOP IMMEDIATLEY.
A DECLRATION OF EMERGENCY MUST BE ADDRESSED FOR CWD TSE PRION DISEASE.
THE tse prion aka mad cow type disease is not your normal pathogen.
The TSE prion disease survives ashing to 600 degrees celsius, that’s around 1112 degrees farenheit.
you cannot cook the TSE prion disease out of meat.
you can take the ash and mix it with saline and inject that ash into a mouse, and the mouse will go down with TSE.
Prion Infected Meat-and-Bone Meal Is Still Infectious after Biodiesel Production as well.
the TSE prion agent also survives Simulated Wastewater Treatment Processes.
IN fact, you should also know that the TSE Prion agent will survive in the environment for years, if not decades.
you can bury it and it will not go away.
The TSE agent is capable of infected your water table i.e. Detection of protease-resistant cervid prion protein in water from a CWD-endemic area.
it’s not your ordinary pathogen you can just cook it out and be done with.
***> that’s what’s so worrisome about Iatrogenic mode of transmission, a simple autoclave will not kill this TSE prion agent.
1: J Neurol Neurosurg Psychiatry 1994 Jun;57(6):757-8
***> Transmission of Creutzfeldt-Jakob disease to a chimpanzee by electrodes contaminated during neurosurgery.
Gibbs CJ Jr, Asher DM, Kobrine A, Amyx HL, Sulima MP, Gajdusek DC.
Laboratory of Central Nervous System Studies, National Institute of
Neurological Disorders and Stroke, National Institutes of Health,
Bethesda, MD 20892.
Stereotactic multicontact electrodes used to probe the cerebral cortex of a middle aged woman with progressive dementia were previously implicated in the accidental transmission of Creutzfeldt-Jakob disease (CJD) to two younger patients. The diagnoses of CJD have been confirmed for all three cases. More than two years after their last use in humans, after three cleanings and repeated sterilisation in ethanol and formaldehyde vapour, the electrodes were implanted in the cortex of a chimpanzee. Eighteen months later the animal became ill with CJD. This finding serves to re-emphasise the potential danger posed by reuse of instruments contaminated with the agents of spongiform encephalopathies, even after scrupulous attempts to clean them.
PMID: 8006664 [PubMed - indexed for MEDLINE]
New studies on the heat resistance of hamster-adapted scrapie agent: Threshold survival after ashing at 600°C suggests an inorganic template of replication
Prion Infected Meat-and-Bone Meal Is Still Infectious after Biodiesel Production
MONDAY, APRIL 19, 2021
Evaluation of the application for new alternative biodiesel production process for rendered fat including Category 1 animal by-products (BDI-RepCat® process, AT) ???
Detection of protease-resistant cervid prion protein in water from a CWD-endemic area
A Quantitative Assessment of the Amount of Prion Diverted to Category 1 Materials and Wastewater During Processing
Rapid assessment of bovine spongiform encephalopathy prion inactivation by heat treatment in yellow grease produced in the industrial manufacturing process of meat and bone meals
THURSDAY, FEBRUARY 28, 2019
BSE infectivity survives burial for five years with only limited spread
5 or 6 years quarantine is NOT LONG ENOUGH FOR CWD TSE PRION !!!
QUARANTINE NEEDS TO BE 21 YEARS FOR CWD TSE PRION !
FRIDAY, APRIL 30, 2021
Should Property Evaluations Contain Scrapie, CWD, TSE PRION Environmental Contamination of the land?
***> Confidential!!!!
***> As early as 1992-3 there had been long studies conducted on small pastures containing scrapie infected sheep at the sheep research station associated with the Neuropathogenesis Unit in Edinburgh, Scotland. Whether these are documented...I don't know. But personal recounts both heard and recorded in a daily journal indicate that leaving the pastures free and replacing the topsoil completely at least 2 feet of thickness each year for SEVEN years....and then when very clean (proven scrapie free) sheep were placed on these small pastures.... the new sheep also broke out with scrapie and passed it to offspring. I am not sure that TSE contaminated ground could ever be free of the agent!! A very frightening revelation!!!
---end personal email---end...tss
and so it seems...
Scrapie Agent (Strain 263K) Can Transmit Disease via the Oral Route after Persistence in Soil over Years
Published: May 9, 2007
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Our results showed that 263K scrapie agent can persist in soil at least over 29 months. Strikingly, not only the contaminated soil itself retained high levels of infectivity, as evidenced by oral administration to Syrian hamsters, but also feeding of aqueous soil extracts was able to induce disease in the reporter animals. We could also demonstrate that PrPSc in soil, extracted after 21 months, provides a catalytically active seed in the protein misfolding cyclic amplification (PMCA) reaction. PMCA opens therefore a perspective for considerably improving the detectability of prions in soil samples from the field.
snip...
***> This is very likely to have parallels with control efforts for CWD in cervids. <***
Paper
Rapid recontamination of a farm building occurs after attempted prion removal
Kevin Christopher Gough BSc (Hons), PhD Claire Alison Baker BSc (Hons) Steve Hawkins MIBiol Hugh Simmons BVSc, MRCVS, MBA, MA Timm Konold DrMedVet, PhD, MRCVS … See all authors
First published: 19 January 2019 https://doi.org/10.1136/vr.105054
Abstract
The transmissible spongiform encephalopathy scrapie of sheep/goats and chronic wasting disease of cervids are associated with environmental reservoirs of infectivity. Preventing environmental prions acting as a source of infectivity to healthy animals is of major concern to farms that have had outbreaks of scrapie and also to the health management of wild and farmed cervids. Here, an efficient scrapie decontamination protocol was applied to a farm with high levels of environmental contamination with the scrapie agent. Post‐decontamination, no prion material was detected within samples taken from the farm buildings as determined using a sensitive in vitro replication assay (sPMCA). A bioassay consisting of 25 newborn lambs of highly susceptible prion protein genotype VRQ/VRQ introduced into this decontaminated barn was carried out in addition to sampling and analysis of dust samples that were collected during the bioassay. Twenty‐four of the animals examined by immunohistochemical analysis of lymphatic tissues were scrapie‐positive during the bioassay, samples of dust collected within the barn were positive by month 3. The data illustrates the difficulty in decontaminating farm buildings from scrapie, and demonstrates the likely contribution of farm dust to the recontamination of these environments to levels that are capable of causing disease.
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This study clearly demonstrates the difficulty in removing scrapie infectivity from the farm environment. Practical and effective prion decontamination methods are still urgently required for decontamination of scrapie infectivity from farms that have had cases of scrapie and this is particularly relevant for scrapiepositive goatherds, which currently have limited genetic resistance to scrapie within commercial breeds.24 This is very likely to have parallels with control efforts for CWD in cervids.
***>This is very likely to have parallels with control efforts for CWD in cervids.
***> Infectious agent of sheep scrapie may persist in the environment for at least 16 years
***> Nine of these recurrences occurred 14–21 years after culling, apparently as the result of environmental contamination, but outside entry could not always be absolutely excluded.
JOURNAL OF GENERAL VIROLOGY Volume 87, Issue 12
Infectious agent of sheep scrapie may persist in the environment for at least 16 years Free
Gudmundur Georgsson1, Sigurdur Sigurdarson2, Paul Brown3
Front. Vet. Sci., 14 September 2015 | https://doi.org/10.3389/fvets.2015.00032
Objects in contact with classical scrapie sheep act as a reservoir for scrapie transmission
imageTimm Konold1*, imageStephen A. C. Hawkins2, imageLisa C. Thurston3, imageBen C. Maddison4, imageKevin C. Gough5, imageAnthony Duarte1 and imageHugh A. Simmons1
1Animal Sciences Unit, Animal and Plant Health Agency Weybridge, Addlestone, UK
2Pathology Department, Animal and Plant Health Agency Weybridge, Addlestone, UK
3Surveillance and Laboratory Services, Animal and Plant Health Agency Penrith, Penrith, UK
4ADAS UK, School of Veterinary Medicine and Science, University of Nottingham, Sutton Bonington, UK
5School of Veterinary Medicine and Science, University of Nottingham, Sutton Bonington, UK
Classical scrapie is an environmentally transmissible prion disease of sheep and goats. Prions can persist and remain potentially infectious in the environment for many years and thus pose a risk of infecting animals after re-stocking. In vitro studies using serial protein misfolding cyclic amplification (sPMCA) have suggested that objects on a scrapie-affected sheep farm could contribute to disease transmission. This in vivo study aimed to determine the role of field furniture (water troughs, feeding troughs, fencing, and other objects that sheep may rub against) used by a scrapie-infected sheep flock as a vector for disease transmission to scrapie-free lambs with the prion protein genotype VRQ/VRQ, which is associated with high susceptibility to classical scrapie. When the field furniture was placed in clean accommodation, sheep became infected when exposed to either a water trough (four out of five) or to objects used for rubbing (four out of seven). This field furniture had been used by the scrapie-infected flock 8 weeks earlier and had previously been shown to harbor scrapie prions by sPMCA. Sheep also became infected (20 out of 23) through exposure to contaminated field furniture placed within pasture not used by scrapie-infected sheep for 40 months, even though swabs from this furniture tested negative by PMCA. This infection rate decreased (1 out of 12) on the same paddock after replacement with clean field furniture. Twelve grazing sheep exposed to field furniture not in contact with scrapie-infected sheep for 18 months remained scrapie free. The findings of this study highlight the role of field furniture used by scrapie-infected sheep to act as a reservoir for disease re-introduction although infectivity declines considerably if the field furniture has not been in contact with scrapie-infected sheep for several months. PMCA may not be as sensitive as VRQ/VRQ sheep to test for environmental contamination.
snip...
Discussion
Classical scrapie is an environmentally transmissible disease because it has been reported in naïve, supposedly previously unexposed sheep placed in pastures formerly occupied by scrapie-infected sheep (4, 19, 20).
Although the vector for disease transmission is not known, soil is likely to be an important reservoir for prions (2) where – based on studies in rodents – prions can adhere to minerals as a biologically active form (21) and remain infectious for more than 2 years (22).
Similarly, chronic wasting disease (CWD) has re-occurred in mule deer housed in paddocks used by infected deer 2 years earlier, which was assumed to be through foraging and soil consumption (23).
Our study suggested that the risk of acquiring scrapie infection was greater through exposure to contaminated wooden, plastic, and metal surfaces via water or food troughs, fencing, and hurdles than through grazing.
Drinking from a water trough used by the scrapie flock was sufficient to cause infection in sheep in a clean building.
Exposure to fences and other objects used for rubbing also led to infection, which supported the hypothesis that skin may be a vector for disease transmission (9).
The risk of these objects to cause infection was further demonstrated when 87% of 23 sheep presented with PrPSc in lymphoid tissue after grazing on one of the paddocks, which contained metal hurdles, a metal lamb creep and a water trough in contact with the scrapie flock up to 8 weeks earlier, whereas no infection had been demonstrated previously in sheep grazing on this paddock, when equipped with new fencing and field furniture.
When the contaminated furniture and fencing were removed, the infection rate dropped significantly to 8% of 12 sheep, with soil of the paddock as the most likely source of infection caused by shedding of prions from the scrapie-infected sheep in this paddock up to a week earlier.
This study also indicated that the level of contamination of field furniture sufficient to cause infection was dependent on two factors: stage of incubation period and time of last use by scrapie-infected sheep.
Drinking from a water trough that had been used by scrapie sheep in the predominantly pre-clinical phase did not appear to cause infection, whereas infection was shown in sheep drinking from the water trough used by scrapie sheep in the later stage of the disease.
It is possible that contamination occurred through shedding of prions in saliva, which may have contaminated the surface of the water trough and subsequently the water when it was refilled.
Contamination appeared to be sufficient to cause infection only if the trough was in contact with sheep that included clinical cases.
Indeed, there is an increased risk of bodily fluid infectivity with disease progression in scrapie (24) and CWD (25) based on PrPSc detection by sPMCA.
Although ultraviolet light and heat under natural conditions do not inactivate prions (26), furniture in contact with the scrapie flock, which was assumed to be sufficiently contaminated to cause infection, did not act as vector for disease if not used for 18 months, which suggest that the weathering process alone was sufficient to inactivate prions.
PrPSc detection by sPMCA is increasingly used as a surrogate for infectivity measurements by bioassay in sheep or mice.
In this reported study, however, the levels of PrPSc present in the environment were below the limit of detection of the sPMCA method, yet were still sufficient to cause infection of in-contact animals.
In the present study, the outdoor objects were removed from the infected flock 8 weeks prior to sampling and were positive by sPMCA at very low levels (2 out of 37 reactions).
As this sPMCA assay also yielded 2 positive reactions out of 139 in samples from the scrapie-free farm, the sPMCA assay could not detect PrPSc on any of the objects above the background of the assay.
False positive reactions with sPMCA at a low frequency associated with de novo formation of infectious prions have been reported (27, 28).
This is in contrast to our previous study where we demonstrated that outdoor objects that had been in contact with the scrapie-infected flock up to 20 days prior to sampling harbored PrPSc that was detectable by sPMCA analysis [4 out of 15 reactions (12)] and was significantly more positive by the assay compared to analogous samples from the scrapie-free farm.
This discrepancy could be due to the use of a different sPMCA substrate between the studies that may alter the efficiency of amplification of the environmental PrPSc.
In addition, the present study had a longer timeframe between the objects being in contact with the infected flock and sampling, which may affect the levels of extractable PrPSc.
Alternatively, there may be potentially patchy contamination of this furniture with PrPSc, which may have been missed by swabbing.
The failure of sPMCA to detect CWD-associated PrP in saliva from clinically affected deer despite confirmation of infectivity in saliva-inoculated transgenic mice was associated with as yet unidentified inhibitors in saliva (29), and it is possible that the sensitivity of sPMCA is affected by other substances in the tested material.
In addition, sampling of amplifiable PrPSc and subsequent detection by sPMCA may be more difficult from furniture exposed to weather, which is supported by the observation that PrPSc was detected by sPMCA more frequently in indoor than outdoor furniture (12).
A recent experimental study has demonstrated that repeated cycles of drying and wetting of prion-contaminated soil, equivalent to what is expected under natural weathering conditions, could reduce PMCA amplification efficiency and extend the incubation period in hamsters inoculated with soil samples (30).
This seems to apply also to this study even though the reduction in infectivity was more dramatic in the sPMCA assays than in the sheep model.
Sheep were not kept until clinical end-point, which would have enabled us to compare incubation periods, but the lack of infection in sheep exposed to furniture that had not been in contact with scrapie sheep for a longer time period supports the hypothesis that prion degradation and subsequent loss of infectivity occurs even under natural conditions.
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.
These results suggest that the VRQ/VRQ sheep model may be more sensitive than sPMCA for the detection of environmentally associated scrapie, and suggest that extremely low levels of scrapie contamination are able to cause infection in susceptible sheep genotypes.
Keywords: classical scrapie, prion, transmissible spongiform encephalopathy, sheep, field furniture, reservoir, serial protein misfolding cyclic amplification
***> 172. Establishment of PrPCWD extraction and detection methods in the farm soil
Kyung Je Park, Hoo Chang Park, In Soon Roh, Hyo Jin Kim, Hae-Eun Kang and Hyun Joo Sohn
Foreign Animal Disease Division, Animal and Plant Quarantine Agency, Gimcheon, Gyeongsangbuk-do, Korea
Conclusions: Our studies showed that PrPCWD persist in 0.001% CWD contaminated soil for at least 4 year and natural CWD-affected farm soil. When cervid reintroduced into CWD outbreak farm, the strict decontamination procedures of the infectious agent should be performed in the environment of CWD-affected cervid habitat.
***> CONGRESSIONAL ABSTRACTS PRION CONFERENCE 2018
P69 Experimental transmission of CWD from white-tailed deer to co-housed reindeer
Mitchell G (1), Walther I (1), Staskevicius A (1), Soutyrine A (1), Balachandran A (1)
(1) National & OIE Reference Laboratory for Scrapie and CWD, Canadian Food Inspection Agency, Ottawa, Ontario, Canada.
Chronic wasting disease (CWD) continues to be detected in wild and farmed cervid populations of North America, affecting predominantly white-tailed deer, mule deer and elk. Extensive herds of wild caribou exist in northern regions of Canada, although surveillance has not detected the presence of CWD in this population. Oral experimental transmission has demonstrated that reindeer, a species closely related to caribou, are susceptible to CWD. Recently, CWD was detected for the first time in Europe, in wild Norwegian reindeer, advancing the possibility that caribou in North America could also become infected. Given the potential overlap in habitat between wild CWD-infected cervids and wild caribou herds in Canada, we sought to investigate the horizontal transmissibility of CWD from white-tailed deer to reindeer.
Two white-tailed deer were orally inoculated with a brain homogenate prepared from a farmed Canadian white-tailed deer previously diagnosed with CWD. Two reindeer, with no history of exposure to CWD, were housed in the same enclosure as the white-tailed deer, 3.5 months after the deer were orally inoculated. The white-tailed deer developed clinical signs consistent with CWD beginning at 15.2 and 21 months post-inoculation (mpi), and were euthanized at 18.7 and 23.1 mpi, respectively. Confirmatory testing by immunohistochemistry (IHC) and western blot demonstrated widespread aggregates of pathological prion protein (PrPCWD) in the central nervous system and lymphoid tissues of both inoculated white-tailed deer. Both reindeer were subjected to recto-anal mucosal associated lymphoid tissue (RAMALT) biopsy at 20 months post-exposure (mpe) to the white-tailed deer. The biopsy from one reindeer contained PrPCWD confirmed by IHC. This reindeer displayed only subtle clinical evidence of disease prior to a rapid decline in condition requiring euthanasia at 22.5 mpe. Analysis of tissues from this reindeer by IHC revealed widespread PrPCWD deposition, predominantly in central nervous system and lymphoreticular tissues. Western blot molecular profiles were similar between both orally inoculated white-tailed deer and the CWD positive reindeer. Despite sharing the same enclosure, the other reindeer was RAMALT negative at 20 mpe, and PrPCWD was not detected in brainstem and lymphoid tissues following necropsy at 35 mpe. Sequencing of the prion protein gene from both reindeer revealed differences at several codons, which may have influenced susceptibility to infection.
Natural transmission of CWD occurs relatively efficiently amongst cervids, supporting the expanding geographic distribution of disease and the potential for transmission to previously naive populations. The efficient horizontal transmission of CWD from white-tailed deer to reindeer observed here highlights the potential for reindeer to become infected if exposed to other cervids or environments infected with CWD.
SOURCE REFERENCE 2018 PRION CONFERENCE ABSTRACT
Research Project: TRANSMISSION, DIFFERENTIATION, AND PATHOBIOLOGY OF TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES Location: Virus and Prion Research
Title: Horizontal transmission of chronic wasting disease in reindeer
Author
item MOORE, SARAH - ORISE FELLOW item KUNKLE, ROBERT item WEST GREENLEE, MARY - IOWA STATE UNIVERSITY item Nicholson, Eric item RICHT, JUERGEN item HAMIR, AMIRALI item WATERS, WADE item Greenlee, Justin
Submitted to: Emerging Infectious Diseases
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 8/29/2016
Publication Date: 12/1/2016
Citation: Moore, S., Kunkle, R., Greenlee, M., Nicholson, E., Richt, J., Hamir, A., Waters, W., Greenlee, J. 2016. Horizontal transmission of chronic wasting disease in reindeer. Emerging Infectious Diseases. 22(12):2142-2145. doi:10.3201/eid2212.160635.
Interpretive Summary: Chronic wasting disease (CWD) is a fatal neurodegenerative disease that occurs in farmed and wild cervids (deer and elk) of North America and was recently diagnosed in a single free-ranging reindeer (Rangifer tarandus tarandus) in Norway. CWD is a transmissible spongiform encephalopathy (TSE) that is caused by infectious proteins called prions that are resistant to various methods of decontamination and environmental degradation. Little is known about the susceptibility of or potential for transmission amongst reindeer. In this experiment, we tested the susceptibility of reindeer to CWD from various sources (elk, mule deer, or white-tailed deer) after intracranial inoculation and tested the potential for infected reindeer to transmit to non-inoculated animals by co-housing or housing in adjacent pens. Reindeer were susceptible to CWD from elk, mule deer, or white-tailed deer sources after experimental inoculation. Most importantly, non-inoculated reindeer that were co-housed with infected reindeer or housed in pens adjacent to infected reindeer but without the potential for nose-to-nose contact also developed evidence of CWD infection. This is a major new finding that may have a great impact on the recently diagnosed case of CWD in the only remaining free-ranging reindeer population in Europe as our findings imply that horizontal transmission to other reindeer within that herd has already occurred. Further, this information will help regulatory and wildlife officials developing plans to reduce or eliminate CWD and cervid farmers that want to ensure that their herd remains CWD-free, but were previously unsure of the potential for reindeer to transmit CWD.
Technical Abstract: Chronic wasting disease (CWD) is a naturally-occurring, fatal prion disease of cervids. Reindeer (Rangifer tarandus tarandus) are susceptible to CWD following oral challenge, and CWD was recently reported in a free-ranging reindeer of Norway. Potential contact between CWD-affected cervids and Rangifer species that are free-ranging or co-housed on farms presents a potential risk of CWD transmission. The aims of this study were to 1) investigate the transmission of CWD from white-tailed deer (Odocoileus virginianus; CWDwtd), mule deer (Odocoileus hemionus; CWDmd), or elk (Cervus elaphus nelsoni; CWDelk) to reindeer via the intracranial route, and 2) to assess for direct and indirect horizontal transmission to non-inoculated sentinels. Three groups of 5 reindeer fawns were challenged intracranially with CWDwtd, CWDmd, or CWDelk. Two years after challenge of inoculated reindeer, non-inoculated negative control reindeer were introduced into the same pen as the CWDwtd inoculated reindeer (direct contact; n=4) or into a pen adjacent to the CWDmd inoculated reindeer (indirect contact; n=2). Experimentally inoculated reindeer were allowed to develop clinical disease. At death/euthanasia a complete necropsy examination was performed, including immunohistochemical testing of tissues for disease-associated CWD prion protein (PrPcwd). Intracranially challenged reindeer developed clinical disease from 21 months post-inoculation (months PI). PrPcwd was detected in 5 out of 6 sentinel reindeer although only 2 out of 6 developed clinical disease during the study period (< 57 months PI). We have shown that reindeer are susceptible to CWD from various cervid sources and can transmit CWD to naïve reindeer both directly and indirectly.
Infectivity surviving ashing to 600*C is (in my opinion) degradable but infective. based on Bown & Gajdusek, (1991), landfill and burial may be assumed to have a reduction factor of 98% (i.e. a factor of 50) over 3 years. CJD-infected brain-tissue remained infectious after storing at room-temperature for 22 months (Tateishi et al, 1988). Scrapie agent is known to remain viable after at least 30 months of desiccation (Wilson et al, 1950). and pastures that had been grazed by scrapie-infected sheep still appeared to be contaminated with scrapie agent three years after they were last occupied by sheep (Palsson, 1979).
Dr. Paul Brown Scrapie Soil Test BSE Inquiry Document
Pathogens. 2020 Apr; 9(4): 311.
Published online 2020 Apr 23. doi: 10.3390/pathogens9040311
PMCID: PMC7238116
PMID: 32340296
Long-Term Incubation PrPCWD with Soils Affects Prion Recovery but Not Infectivity
Alsu Kuznetsova,1 Debbie McKenzie,2 Catherine Cullingham,3 and Judd M. Aiken1,*
Abstract
Chronic wasting disease (CWD) is a contagious prion disease of cervids. The infectious agent is shed from animals at the preclinical and clinical stages of disease where it persists in the environment as a reservoir of CWD infectivity. In this study, we demonstrate that long-term incubation of CWD prions (generated from tg-mice infected with deer or elk prions) with illite, montmorillonite (Mte) and whole soils results in decreased recovery of PrPCWD, suggesting that binding becomes more avid and irreversible with time. This continual decline of immunoblot PrPCWD detection did not correlate with prion infectivity levels. Bioassay showed no significant differences in incubation periods between mice inoculated with 1% CWD brain homogenate (BH) and with the CWD-BH pre-incubated with quartz or Luvisolic Ae horizon for 1 or 30 weeks. After 55 weeks incubation with Chernozem and Luvisol, bound PrPCWD was not detectable by immunoblotting but remained infectious. This study shows that although recovery of PrPCWD bound to soil minerals and whole soils with time become more difficult, prion infectivity is not significantly altered. Detection of prions in soil is, therefore, not only affected by soil type but also by length of time of the prion–soil interaction.
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4. Conclusions
The binding of prions to soil minerals and other soil constituents impacts PrPCWD recovery. During extended incubation with soils, PrP signal on immunoblots continuously declined until it was no longer detectable after 25 weeks in soils with loamy-clay texture and Mte minerology. PrPCWD infectivity did not, however, decrease after 30 weeks incubation with quartz and the Luvisolic Ae soil horizon. At 55 weeks incubation in Chernozem and Luvisol, CWD-BH remained infectious. We studied a wide variety of soil types (from prairie, mountain and boreal regions) and showed decreased PrPCWD signal recovery (as measured by immunoblotting) with retention of infectivity. The decrease in PrPCWD recovery was particularly dramatic in soils from the prairie region. Regardless of soil minerology, texture and humus content, detection of PrPCWD in environmental soil samples is a challenge after long-term incubation. These findings provide important information on the behavior of prions in natural environments, but complicate analysis of environmental samples.
Keywords: prion protein, soil, CWD, prolonged incubation, CWD infectivity, prion detection
Prion. 2012 Jul 1; 6(3): 302–308. doi: 10.4161/pri.20025 PMCID: PMC3399538 PMID: 22561162
Temperature influences the interaction of ruminant PrPTSE with soil
Ben C. Maddison, 1 Jonathan P. Owen, 1 Maged A. Taema, 2 George Shaw, 3 and Kevin C. Gough 2 , *
Abstract
Ovine scrapie and cervid chronic wasting disease can be transmitted in the absence of animal-to-animal contact, and environmental reservoirs of infectivity have been implicated in their spread and persistence. Investigating environmental factors that influence the interaction of disease-associated PrP with soils is imperative to understanding what is likely to be the complex role of soil in disease transmission. Here, we describe the effects of soil temperature on the binding/desorption and persistence of both ovine scrapie- and bovine BSE-PrPTSE. Binding of PrPTSE to a sandy loam soil at temperatures of 4°C, 8–12°C and 25–30°C demonstrated that an increase in temperature resulted in (1) a decrease in the amount of PrPTSE recovered after 24 h of interaction with soil, (2) an increase in the amount of N-terminal cleavage of the prion protein over 11 d and (3) a decrease in the persistence of PrPTSE on soil over an 18 mo period.
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In the present study we investigated the effects of soil temperature in the range 4°C to 30°C on the interaction of BSE- and scrapie-PrPTSE with a complex soil matrix. Lower soil temperatures resulted in increased levels of PrPTSE recovery and persistence over an 18-mo incubation period. A low soil temperature also resulted in less cleavage of the N-terminal domain of PrPTSE after an 11-d interaction. These effects of temperature on PrPTSE-soil interaction were likely to be exerted through both microbial activity and abiotic cleavage mechanisms. Together, the data indicate that for the recoverable fraction of PrPTSE, soils at lower temperature may release increased levels of PrPTSE.
A recent study using transmissible mink encephalopathy reported a correlation between the level of desorption of PrPTSE from soil and the infectivity titer of the sample.25 If such a correlation is also true for ovine scrapie and bovine BSE, the data presented here indicate that the bioavailability of prions in soil for the environmental transmission of scrapie or BSE may be influenced by the temperature of the soil. However, it remains to be seen whether the reported influence of temperature on prion interaction with a sandy-loam soil is consistent with other soil types. Of course, it should also be considered that temperature would be just one of a range of factors influencing the bioavailability of prions from soil; other factors would likely include soil type, prion strain and the biological matrix of the prion source. Scrapie and CWD are known to be spread by environmental routes and therefore understanding the range of factors that influence the persistence of environmental prions is vital in developing eradication programmes.
Keywords: BSE, environment, prion, scrapie, soil, transmission
Using in vitro Prion replication for high sensitive detection of prions and prionlike proteins and for understanding mechanisms of transmission.
Claudio Soto Mitchell Center for Alzheimer's diseases and related Brain disorders, Department of Neurology, University of Texas Medical School at Houston.
Prion and prion-like proteins are misfolded protein aggregates with the ability to selfpropagate to spread disease between cells, organs and in some cases across individuals. I n T r a n s m i s s i b l e s p o n g i f o r m encephalopathies (TSEs), prions are mostly composed by a misfolded form of the prion protein (PrPSc), which propagates by transmitting its misfolding to the normal prion protein (PrPC). The availability of a procedure to replicate prions in the laboratory may be important to study the mechanism of prion and prion-like spreading and to develop high sensitive detection of small quantities of misfolded proteins in biological fluids, tissues and environmental samples. Protein Misfolding Cyclic Amplification (PMCA) is a simple, fast and efficient methodology to mimic prion replication in the test tube. PMCA is a platform technology that may enable amplification of any prion-like misfolded protein aggregating through a seeding/nucleation process. In TSEs, PMCA is able to detect the equivalent of one single molecule of infectious PrPSc and propagate prions that maintain high infectivity, strain properties and species specificity. Using PMCA we have been able to detect PrPSc in blood and urine of experimentally infected animals and humans affected by vCJD with high sensitivity and specificity. Recently, we have expanded the principles of PMCA to amplify amyloid-beta (Aβ) and alphasynuclein (α-syn) aggregates implicated in Alzheimer's and Parkinson's diseases, respectively. Experiments are ongoing to study the utility of this technology to detect Aβ and α-syn aggregates in samples of CSF and blood from patients affected by these diseases.
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***>>> Recently, we have been using PMCA to study the role of environmental prion contamination on the horizontal spreading of TSEs. These experiments have focused on the study of the interaction of prions with plants and environmentally relevant surfaces. Our results show that plants (both leaves and roots) bind tightly to prions present in brain extracts and excreta (urine and feces) and retain even small quantities of PrPSc for long periods of time. Strikingly, ingestion of prioncontaminated leaves and roots produced disease with a 100% attack rate and an incubation period not substantially longer than feeding animals directly with scrapie brain homogenate. Furthermore, plants can uptake prions from contaminated soil and transport them to different parts of the plant tissue (stem and leaves). Similarly, prions bind tightly to a variety of environmentally relevant surfaces, including stones, wood, metals, plastic, glass, cement, etc. Prion contaminated surfaces efficiently transmit prion disease when these materials were directly injected into the brain of animals and strikingly when the contaminated surfaces were just placed in the animal cage. These findings demonstrate that environmental materials can efficiently bind infectious prions and act as carriers of infectivity, suggesting that they may play an important role in the horizontal transmission of the disease.
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Since its invention 13 years ago, PMCA has helped to answer fundamental questions of prion propagation and has broad applications in research areas including the food industry, blood bank safety and human and veterinary disease diagnosis.
source reference Prion Conference 2015 abstract book
Grass Plants Bind, Retain, Uptake, and Transport Infectious Prions
Sandra Pritzkow,1 Rodrigo Morales,1 Fabio Moda,1,3 Uffaf Khan,1 Glenn C. Telling,2 Edward Hoover,2 and Claudio Soto1, * 1Mitchell Center for Alzheimer’s Disease and Related Brain Disorders, Department of Neurology, University of Texas Medical School at Houston, 6431 Fannin Street, Houston, TX 77030, USA
2Prion Research Center, Department of Microbiology, Immunology, and Pathology, College of Veterinary Medicine and Biomedical Sciences, Colorado State University, Fort Collins, CO 80523, USA
3Present address: IRCCS Foundation Carlo Besta Neurological Institute, 20133 Milan, Italy *Correspondence: claudio.soto@uth.tmc.edu http://dx.doi.org/10.1016/j.celrep.2015.04.036
SUMMARY
Prions are the protein-based infectious agents responsible for prion diseases. Environmental prion contamination has been implicated in disease transmission. Here, we analyzed the binding and retention of infectious prion protein (PrPSc) to plants. Small quantities of PrPSc contained in diluted brain homogenate or in excretory materials (urine and feces) can bind to wheat grass roots and leaves. Wild-type hamsters were efficiently infected by ingestion of prion-contaminated plants. The prion-plant interaction occurs with prions from diverse origins, including chronic wasting disease. Furthermore, leaves contaminated by spraying with a prion-containing preparation retained PrPSc for several weeks in the living plant. Finally, plants can uptake prions from contaminated soil and transport them to aerial parts of the plant (stem and leaves). These findings demonstrate that plants can efficiently bind infectious prions and act as carriers of infectivity, suggesting a possible role of environmental prion contamination in the horizontal transmission of the disease.
INTRODUCTION
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DISCUSSION
This study shows that plants can efficiently bind prions contained in brain extracts from diverse prion infected animals, including CWD-affected cervids. PrPSc attached to leaves and roots from wheat grass plants remains capable of seeding prion replication in vitro. Surprisingly, the small quantity of PrPSc naturally excreted in urine and feces from sick hamster or cervids was enough to efficiently contaminate plant tissue. Indeed, our results suggest that the majority of excreted PrPSc is efficiently captured by plants’ leaves and roots. Moreover, leaves can be contaminated by spraying them with a prion-containing extract, and PrPSc remains detectable in living plants for as long as the study was performed (several weeks). Remarkably, prion contaminated plants transmit prion disease to animals upon ingestion, producing a 100% attack rate and incubation periods not substantially longer than direct oral administration of sick brain homogenates.
Finally, an unexpected but exciting result was that plants were able to uptake prions from contaminated soil and transport them to aerial parts of the plant tissue. Although it may seem farfetched that plants can uptake proteins from the soil and transport it to the parts above the ground, there are already published reports of this phenomenon (McLaren et al., 1960; Jensen and McLaren, 1960;Paungfoo-Lonhienne et al., 2008). The high resistance of prions to degradation and their ability to efficiently cross biological barriers may play a role in this process. The mechanism by which plants bind, retain, uptake, and transport prions is unknown. We are currently studying the way in which prions interact with plants using purified, radioactively labeled PrPSc to determine specificity of the interaction, association constant, reversibility, saturation, movement, etc.
Epidemiological studies have shown numerous instances of scrapie or CWD recurrence upon reintroduction of animals on pastures previously exposed to prion-infected animals. Indeed, reappearance of scrapie has been documented following fallow periods of up to 16 years (Georgsson et al., 2006), and pastures were shown to retain infectious CWD prions for at least 2 years after exposure (Miller et al., 2004). It is likely that the environmentally mediated transmission of prion diseases depends upon the interaction of prions with diverse elements, including soil, water, environmental surfaces, various invertebrate animals, and plants.
However, since plants are such an important component of the environment and also a major source of food for many animal species, including humans, our results may have far-reaching implications for animal and human health. Currently, the perception of the riskfor animal-to-human prion transmission has beenmostly limited to consumption or exposure to contaminated meat; our results indicate that plants might also be an important vector of transmission that needs to be considered in risk assessment.
Published: 07 October 2021
Review on PRNP genetics and susceptibility to chronic wasting disease of Cervidae
Katayoun Moazami-Goudarzi, Olivier Andréoletti, Jean-Luc Vilotte & Vincent Béringue
Veterinary Research volume 52, Article number: 128 (2021) Cite this article
Abstract
To date, chronic wasting disease (CWD) is the most infectious form of prion disease affecting several captive, free ranging and wild cervid species. Responsible for marked population declines in North America, its geographical spread is now becoming a major concern in Europe. Polymorphisms in the prion protein gene (PRNP) are an important factor influencing the susceptibility to prions and their rate of propagation. All reported cervid PRNP genotypes are affected by CWD. However, in each species, some polymorphisms are associated with lower attack rates and slower progression of the disease. This has potential consequences in terms of genetic selection, CWD diffusion and strain evolution. CWD also presents a zoonotic risk due to prions capacity to cross species barriers. This review summarizes our current understanding of CWD control, focusing on PRNP genetic, strain diversity and capacity to infect other animal species, including humans.
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CWD positive animals with extended time before they succumb to disease likely represent a source of chronic prion shedding within populations and may contribute to environmental contamination.
***> CWD positive animals with extended time before they succumb to disease likely represent a source of chronic prion shedding within populations and may contribute to environmental contamination. <***
Genes (Basel) . 2021 Sep 10;12(9):1396. doi: 10.3390/genes12091396.
Selective Breeding for Disease-Resistant PRNP Variants to Manage Chronic Wasting Disease in Farmed Whitetail Deer
Nicholas Haley 1, Rozalyn Donner 1, Kahla Merrett 1, Matthew Miller 1, Kristen Senior 1
Affiliations expand
PMID: 34573378 DOI: 10.3390/genes12091396
Abstract
Chronic wasting disease (CWD) is a fatal transmissible spongiform encephalopathy (TSE) of cervids caused by a misfolded variant of the normal cellular prion protein, and it is closely related to sheep scrapie. Variations in a host's prion gene, PRNP, and its primary protein structure dramatically affect susceptibility to specific prion disorders, and breeding for PRNP variants that prevent scrapie infection has led to steep declines in the disease in North American and European sheep. While resistant alleles have been identified in cervids, a PRNP variant that completely prevents CWD has not yet been identified. Thus, control of the disease in farmed herds traditionally relies on quarantine and depopulation. In CWD-endemic areas, depopulation of private herds becomes challenging to justify, leading to opportunities to manage the disease in situ. We developed a selective breeding program for farmed white-tailed deer in a high-prevalence CWD-endemic area which focused on reducing frequencies of highly susceptible PRNP variants and introducing animals with less susceptible variants. With the use of newly developed primers, we found that breeding followed predictable Mendelian inheritance, and early data support our project's utility in reducing CWD prevalence. This project represents a novel approach to CWD management, with future efforts building on these findings.
Keywords: CWD; PRNP; deer; prion; resistance; selective breeding; susceptibility.
***> While resistant alleles have been identified in cervids, a PRNP variant that completely prevents CWD has not yet been identified.
In Moore et al., reindeer carrying allele E had longer survival-times following intracranial exposure [24]. In the same experiment, a reindeer with a genotype carrier of E, found dead without showing clinical signs ~13 months post-intracranial inoculation, had no histopathological lesions or PrPSc deposition at post-mortem examination.
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Our data support the notion that PRNP genetic variation modulates CWD susceptibility rather than conferring complete resistance. This is in agreement with experimental observations of reindeer-developing CWD after intracranial inoculation regardless of PRNP genotype [24].
***> Our data support the notion that PRNP genetic variation modulates CWD susceptibility rather than conferring complete resistance.
Published: 27 May 2021
White-tailed deer S96 prion protein does not support stable in vitro propagation of most common CWD strains
Alicia Otero, Camilo Duque Velásquez, Judd Aiken & Debbie McKenzie
Scientific Reports volume 11, Article number: 11193 (2021) Cite this article
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Abstract
PrPC variation at residue 96 (G/S) plays an important role in the epidemiology of chronic wasting disease (CWD) in exposed white-tailed deer populations. In vivo studies have demonstrated the protective effect of serine at codon 96, which hinders the propagation of common CWD strains when expressed in homozygosis and increases the survival period of S96/wt heterozygous deer after challenge with CWD. Previous in vitro studies of the transmission barrier suggested that following a single amplification step, wt and S96 PrPC were equally susceptible to misfolding when seeded with various CWD prions. When we performed serial prion amplification in vitro using S96-PrPC, we observed a reduction in the efficiency of propagation with the Wisc-1 or CWD2 strains, suggesting these strains cannot stably template their conformations on this PrPC once the primary sequence has changed after the first round of replication. Our data shows the S96-PrPC polymorphism is detrimental to prion conversion of some CWD strains. These data suggests that deer homozygous for S96-PrPC may not sustain prion transmission as compared to a deer expressing G96-PrPC.
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The protective effect of S96 and H95 alleles was further demonstrated by experimental oral infection in white-tailed deer expressing these amino acid substitutions19. Among the alleles of the PRNP gene associated with a lower CWD incidence and extended preclinical phase, S96 has the highest allelic frequency (~ 25%) after the wt allele in several white-tailed deer populations from the United States and Canada26,27,31. Subsequent independent transmission and epidemiological studies have demonstrated that deer homozygous and heterozygous for S96-PrPC are, compared to wt/wt deer, less susceptible to CWD infection, present prolonged survival times, show delayed prion accumulation and are generally at a significantly earlier stage of disease when deer herds are depopulated23,31,32,33.
***> Subsequent independent transmission and epidemiological studies have demonstrated that deer homozygous and heterozygous for S96-PrPC are, compared to wt/wt deer, less susceptible to CWD infection, present prolonged survival times,
Prion protein polymorphisms associated with reduced CWD susceptibility limit peripheral PrPCWD deposition in orally infected white-tailed deer
Alicia Otero1 , Camilo Duque Velásquez4,5, Chad Johnson3 , Allen Herbst2,5, Rosa Bolea1 , Juan José Badiola1 , Judd Aiken2,5 and Debbie McKenzie4,5*
Abstract
Background: Chronic wasting disease (CWD) is a prion disease affecting members of the Cervidae family. PrPC primary structures play a key role in CWD susceptibility resulting in extended incubation periods and regulating the propagation of CWD strains. We analyzed the distribution of abnormal prion protein (PrPCWD) aggregates in brain and peripheral organs from orally inoculated white-tailed deer expressing four different PRNP genotypes: Q95G96/ Q95G96 (wt/wt), S96/wt, H95/wt and H95/S96 to determine if there are substantial differences in the deposition pattern of PrPCWD between different PRNP genotypes.
Results: Although we detected differences in certain brain areas, globally, the different genotypes showed similar PrPCWD deposition patterns in the brain. However, we found that clinically affected deer expressing H95 PrPC , despite having the longest survival periods, presented less PrPCWD immunoreactivity in particular peripheral organs. In addition, no PrPCWD was detected in skeletal muscle of any of the deer.
Conclusions: Our data suggest that expression of H95-PrPC limits peripheral accumulation of PrPCWD as detected by immunohistochemistry. Conversely, infected S96/wt and wt/wt deer presented with similar PrPCWD peripheral distribution at terminal stage of disease, suggesting that the S96-PrPC allele, although delaying CWD progression, does not completely limit the peripheral accumulation of the infectious agent.
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The significantly longer incubation periods observed in deer with H95-PRNP alleles may not impact secretion of CWD (i.e., less CWD secreted over longer time periods). The emergence of new CWD strains could implicate a zoonotic potential [20].
Keywords: Prions, Prion diseases, Chronic wasting disease, CWD, PrPCWD, Peripheral tissues, Polymorphisms, Deer
***> Selective Breeding
***> less susceptible to CWD infection, present prolonged survival times...
this is very disturbing. with all the hype about selective breeding with different alleles, and presenting longer survival times with cwd, this would only allow the spreading of the cwd tse prion to last longer in the given environment imo., and as such has been stated in scientific literature...terry
With cervids, however, resistance based on the PRNP allele alone is not absolute, and is better characterized as a delayed progression [18,25]
Volume 23, Number 9—September 2017 Research Letter
Chronic Wasting Disease Prion Strain Emergence and Host Range Expansion
Allen Herbst1, Camilo Duque Velásquez1, Elizabeth Triscott, Judd M. Aiken, and Debbie McKenzieComments to Author Author affiliations: University of Alberta, Edmonton, Alberta, Canada
Abstract
Human and mouse prion proteins share a structural motif that regulates resistance to common chronic wasting disease (CWD) prion strains. Successful transmission of an emergent strain of CWD prion, H95+, into mice resulted in infection. Thus, emergent CWD prion strains may have higher zoonotic potential than common strains.
P-145 Estimating chronic wasting disease resistance in cervids using real time quaking- induced conversion
Nicholas J Haley1, Rachel Rielinqer2, Kristen A Davenport3, W. David Walter4, Katherine I O'Rourke5, Gordon Mitchell6, Juergen A Richt2 1 Department of Microbiology and Immunology, Midwestern University, United States; 2Department of Diagnostic Medicine and Pathobiology, Kansas State University; 3Prion Research Center; Colorado State University; 4U.S. Geological Survey, Pennsylvania Cooperative Fish and Wildlife Research Unit; 5Agricultural Research Service, United States Department of Agriculture; 6Canadian Food Inspection Agency, National and OlE Reference Laboratory for Scrapie and CWD
In mammalian species, the susceptibility to prion diseases is affected, in part, by the sequence of the host's prion protein (PrP). In sheep, a gradation from scrapie susceptible to resistant has been established both in vivo and in vitro based on the amino acids present at PrP positions 136, 154, and 171, which has led to global breeding programs to reduce the prevalence of scrapie in domestic sheep. In cervids, resistance is commonly characterized as a delayed progression of chronic wasting disease (CWD); at present, no cervid PrP allele conferring absolute resistance to prion infection has been identified. To model the susceptibility of various naturally-occurring and hypothetical cervid PrP alleles in vitro, we compared the amplification rates and efficiency of various CWD isolates in recombinant PrPC using real time quaking-induced conversion. We hypothesized that amplification metrics of these isolates in cervid PrP substrates would correlate to in vivo susceptibility - allowing susceptibility prediction for alleles found at 10 frequency in nature, and that there would be an additive effect of multiple resistant codons in hypothetical alleles. Our studies demonstrate that in vitro amplification metrics predict in vivo susceptibility, and that alleles with multiple codons, each influencing resistance independently, do not necessarily contribute additively to resistance. Importantly, we found that the white-tailed deer 226K substrate exhibited the slowest amplification rate among those evaluated, suggesting that further investigation of this allele and its resistance in vivo are warranted to determine if absolute resistance to CWD is possible.
***at present, no cervid PrP allele conferring absolute resistance to prion infection has been identified.
PRION 2016 CONFERENCE TOKYO
''There are no known familial or genetic TSEs of animals, although polymorphisms in the PRNP gene of some species (sheep for example) may influence the length of the incubation period and occurrence of disease.'' c) The commonest form of CJD occurs as a sporadic disease, the cause of which is unknown, although genetic factors (particularly the codon 129 polymorphism in the prion protein gene (PRNP)) influence disease susceptibility. The familial forms of human TSEs (see Box 1) appear to have a solely genetic origin and are closely associated with mutations or insertions in the PRNP gene. Most, but not all, of the familial forms of human TSEs have been transmitted experimentally to animals. There are no known familial or genetic TSEs of animals, although polymorphisms in the PRNP gene of some species (sheep for example) may influence the length of the incubation period and occurrence of disease.
''There are no known familial or genetic TSEs of animals, although polymorphisms in the PRNP gene of some species (sheep for example) may influence the length of the incubation period and occurrence of disease.''
c) The commonest form of CJD occurs as a sporadic disease, the cause of which is unknown, although genetic factors (particularly the codon 129 polymorphism in the prion protein gene (PRNP)) influence disease susceptibility. The familial forms of human TSEs (see Box 1) appear to have a solely genetic origin and are closely associated with mutations or insertions in the PRNP gene. Most, but not all, of the familial forms of human TSEs have been transmitted experimentally to animals. There are no known familial or genetic TSEs of animals, although polymorphisms in the PRNP gene of some species (sheep for example) may influence the length of the incubation period and occurrence of disease.
Genetic susceptibility to chronic wasting disease in free-ranging white-tailed deer: Complement component C1q and Prnp polymorphisms§
Julie A. Blanchong a, *, Dennis M. Heisey b , Kim T. Scribner c , Scot V. Libants d , Chad Johnson e , Judd M. Aiken e , Julia A. Langenberg f , Michael D. Samuel g
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Identifying the genetic basis for heterogeneity in disease susceptibility or progression can improve our understanding of individual variation in disease susceptibility in both free-ranging and captive populations. What this individual variation in disease susceptibility means for the trajectory of disease in a population, however, is not straightforward. For example, the greater, but not complete, resistance to CWD in deer with at least one Serine (S) at amino acid 96 of the Prnp gene appears to be associated with slower progression of disease (e.g., Johnson et al., 2006; Keane et al., 2008a). If slower disease progression results in longer-lived, infected deer with longer periods of infectiousness, resistance may lead to increased disease transmission rates, higher prion concentrations in the environment, and increased prevalence, as has been observed in some captive deer herds (Miller et al., 2006; Keane et al., 2008a). Alternatively, if the slower progression of disease in resistant deer is not associated with longer periods of infectiousness, but might instead indicate a higher dose of PrPCWD is required for infection, transmission rates in the population could decline especially if, as in Wisconsin, deer suffer high rates of mortality from other sources (e.g., hunting). Clearly, determining the relationship between genetic susceptibility to infection, dose requirements, disease progression, and the period of PrPCWD infectiousness are key components for understanding the consequences of CWD to free-ranging populations.
THURSDAY, DECEMBER 16, 2021
Detection of CWD prions in naturally infected white‑tailed deer fetuses and gestational tissues by PMCA
THURSDAY, DECEMBER 16, 2021
RT‑QuIC detection of CWD prion seeding activity in white‑tailed deer muscle tissues
Transmission of Cervid Prions to Humanized Mice Demonstrates the Zoonotic Potential of CWD
Samia Hannaoui, Irina Zemlyankina, Sheng Chun Chang, Maria Immaculata Arifin, Vincent Beringue, Debbie McKEnzie, Hermann M Schatzl, Sabine Gilch
Affiliations:
1 Department of Comparative Biology and Experimental Medicine, Faculty of Veterinary
Medicine; Hotchkiss Brain Institute; University of Calgary, Calgary, Canada
2 Université Paris-Saclay, INRAE, UVSQ, VIM, 78 350 Jouy-en-Josas, France
3 Department of Biological Sciences, Center for Prions and Protein Folding Diseases, University
of Alberta, Edmonton, Canada
*Corresponding author. Email: sgilch@ucalgary.ca
This article is a preprint and has not been certified by peer review [what does this mean?].
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 the strongest evidence to date supporting the zoonotic potential of CWD prions, and their probable materialization in humans using mice expressing human prion protein (PrP) as an infection model. Inoculation of these mice with deer CWD isolates resulted in atypical clinical manifestations, with prion seeding activity and efficient transmissible infectivity in the brain and, remarkably, in feces. 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 are the first evidence that CWD can infect humans with a distinctive clinical presentation, signature, and tropism, and 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.
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Discussion
Our findings strongly suggest that CWD is 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.
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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 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 48-51. 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 (Figure 2 and 4) are very similar to that of GSS, both in terms of migration profile and the N-terminal cleavage site.
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CWD in humans might remain subclinical but with PrPSc deposits in the brain (e.g., mouse #328; Figure 3), clinical with untraceable abnormal PrP (e.g., mouse #327) but still transmissible and uncovered upon subsequent passage (e.g., mouse #3063), 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.
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Taking this into consideration, our study is the strongest proof-of-principal that CWD is transmissible to humans. Using humanized mice, we demonstrated the zoonotic potential of CWD. Furthermore, our findings provide striking insights into how CWD might manifest in humans and the impact it may have on human health. We have used Wisc-1/CWD1, one of the most common CWD strains, notably WTD prions, which have been shown to be more prone to generate human prions in vitro 43. This implies a high risk of exposure to this strain, e.g., through consumption or handling of infected carcasses, in contrast to rarer CWD strains, and therefore, an actual risk for human health. In addition, CWD surveillance in humans should encompass a wider spectrum of tissues/organs tested and include new criteria in the diagnosis of potential patients.
EFSA Panel on Biological Hazards (BIOHAZ) Antonia Ricci Ana Allende Declan Bolton Marianne Chemaly Robert Davies Pablo Salvador Fernández Escámez ... See all authors
First published: 17 January 2018 https://doi.org/10.2903/j.efsa.2018.5132 ;
also, see;
8. Even though human TSE‐exposure risk through consumption of game from European cervids can be assumed to be minor, if at all existing, no final conclusion can be drawn due to the overall lack of scientific data.
***> In particular the US data do not clearly exclude the possibility of human (sporadic or familial) TSE development due to consumption of venison.
The Working Group thus recognizes a potential risk to consumers if a TSE would be present in European cervids. It might be prudent considering appropriate measures to reduce such a risk, e.g. excluding tissues such as CNS and lymphoid tissues from the human food chain, which would greatly reduce any potential risk for consumers.. However, it is stressed that currently, no data regarding a risk of TSE infections from cervid products are available.
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The tissue distribution of infectivity in CWD‐infected cervids is now known to extend beyond CNS and lymphoid tissues. While the removal of these specific tissues from the food chain would reduce human dietary exposure to infectivity, exclusion from the food chain of the whole carcass of any infected animal would be required to eliminate human dietary exposure.
ARS RESEARCH Generation of human chronic wasting disease in transgenic mice
Publication Acceptance Date: 9/8/2021
Research Project: Pathobiology, Genetics, and Detection of Transmissible Spongiform Encephalopathies Location: Virus and Prion Research
Title: Generation of human chronic wasting disease in transgenic mice
Author item WANG, ZERUI - Case Western Reserve University (CWRU) item QIN, KEFENG - University Of Chicago item CAMACHO, MANUEL - Case Western Reserve University (CWRU) item SHEN, PINGPING - Case Western Reserve University (CWRU) item YUAN, JUE - Case Western Reserve University (CWRU) item Greenlee, Justin item CUI, LI - Jilin University item KONG, QINGZHONG - Case Western Reserve University (CWRU) item MASTRIANNI, JAMES - University Of Chicago item ZOU, WEN-QUAN - Case Western Reserve University (CWRU)
Submitted to: Acta Neuropathologica Publication Type: Peer Reviewed Journal Publication Acceptance Date: 9/8/2021 Publication Date: N/A Citation: N/A
Interpretive Summary: Prion diseases are invariably fatal neurologic diseases for which there is no known prevention or cure. Chronic wasting disease (CWD) is the prion disease of deer and elk and is present in farmed and free ranging herds throughout North America. To date there is no clear evidence that the CWD agent could be transmitted to humans. This manuscript describes the use of an in vitro technique, cell-free serial protein misfolding cyclic amplification (sPMCA), to generate a CWD prion that is infectious to transgenic mice expressing the human prion protein. This study provides the first evidence that CWD prions may be able to cause misfolding in the human prion protein. This information will impact medical experts and those involved in making policy for farmed cervids and wildlife.
Technical Abstract: Chronic wasting disease (CWD) is a cervid spongiform encephalopathy or prion disease caused by the infectious prion or PrPSc, a misfolded conformer of cellular prion protein (PrPC). It has rapidly spread in North America and also has been found in Asia and Europe. In contrast to the zoonotic mad cow disease that is the first animal prion disease found transmissible to humans, the transmissibility of CWD to humans remains uncertain although most previous studies have suggested that humans may not be susceptible to CWD. Here we report the generation of an infectious human PrPSc by seeding CWD PrPSc in normal human brain PrPC through the in vitro cell-free serial protein misfolding cyclic amplification (sPMCA). Western blotting confirms that the sPMCA-induced proteinase K-resistant PrPSc is a human form, evidenced by a PrP-specific antibody that recognizes human but not cervid PrP. Remarkably, two lines of humanized transgenic (Tg) mice expressing human PrP-129Val/Val (VV) or -129Met/Met (MM) polymorphism develop prion disease at 233 ± 6 (mean ± SE) days post-inoculation (dpi) and 552 ± 27 dpi, respectively, upon intracerebral inoculation with the sPMCA-generated PrPSc. The brain of diseased Tg mice reveals the electrophoretic profile of PrPSc similar to sporadic Creutzfeldt-Jakob disease (sCJD) MM1 or VV2 subtype but different neuropathological patterns. We believe that our study provides the first evidence that CWD PrPSc is able to convert human PrPC into PrPSc in vitro and the CWD-derived human PrPSc mimics atypical sCJD subtypes in humanized Tg mice.
''The brain of diseased Tg mice reveals the electrophoretic profile of PrPSc similar to sporadic Creutzfeldt-Jakob disease (sCJD) MM1 or VV2 subtype but different neuropathological patterns.''
''We believe that our study provides the first evidence that CWD PrPSc is able to convert human PrPC into PrPSc in vitro and the CWD-derived human PrPSc mimics atypical sCJD subtypes in humanized Tg mice.''
Published: 26 September 2021
Generation of human chronic wasting disease in transgenic mice
Zerui Wang, Kefeng Qin, Manuel V. Camacho, Ignazio Cali, Jue Yuan, Pingping Shen, Justin Greenlee, Qingzhong Kong, James A. Mastrianni & Wen-Quan Zou
Acta Neuropathologica Communications volume 9, Article number: 158 (2021)
Abstract
Chronic wasting disease (CWD) is a cervid prion disease caused by the accumulation of an infectious misfolded conformer (PrPSc) of cellular prion protein (PrPC). It has been spreading rapidly in North America and also found in Asia and Europe. Although bovine spongiform encephalopathy (i.e. mad cow disease) is the only animal prion disease known to be zoonotic, the transmissibility of CWD to humans remains uncertain. Here we report the generation of the first CWD-derived infectious human PrPSc by elk CWD PrPSc-seeded conversion of PrPC in normal human brain homogenates using in vitro protein misfolding cyclic amplification (PMCA). Western blotting with human PrP selective antibody confirmed that the PMCA-generated protease-resistant PrPSc was derived from the human PrPC substrate. Two lines of humanized transgenic mice expressing human PrP with either Val or Met at the polymorphic codon 129 developed clinical prion disease following intracerebral inoculation with the PMCA-generated CWD-derived human PrPSc. Diseased mice exhibited distinct PrPSc patterns and neuropathological changes in the brain. Our study, using PMCA and animal bioassays, provides the first evidence that CWD PrPSc can cross the species barrier to convert human PrPC into infectious PrPSc that can produce bona fide prion disease when inoculated into humanized transgenic mice.
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It is worth noting that the annual number of sporadic CJD (sCJD) cases in the USA has increased, with the total number of suspected and confirmed sCJD cases rising from 284 in 2003 to 511 in 2017 (https://www.cdc.gov/prions/cjd/occurrence-transmission.html). The greatly enhanced CJD surveillance and an aging population in the USA certainly contributed to the observed increase in annual sCJD case numbers in recent years, but the possibility cannot be excluded that some of the increased sCJD prevalence is linked to CWD exposure.
In the present study, using serial protein misfolding cyclic amplification (sPMCA) assay we generate PrPSc by seeding CWD prions in normal human brain homogenates. Importantly, we reveal that two lines of humanized Tg mice expressing human PrP-129VV and 129MM develop prion diseases upon intracerebral inoculation of the abnormal PrP generated by sPMCA. We believe that our study provides the first opportunity to dissect the clinical, pathological and biochemical features of the CWD-derived human prion disease in two lines of humanized Tg mice expressing two major human PrP genotypes, respectively.
i thought i might share some news about cwd zoonosis that i got, that i cannot share or post to the public yet, i promised for various reasons, one that it will cause a shit storm for sure, but it was something i really already knew from previous studies, but, i was told that ;
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https://www.nature.com/articles/srep11573
PRION 2016 TOKYO
Saturday, April 23, 2016
SCRAPIE WS-01: Prion diseases in animals and zoonotic potential 2016
Prion. 10:S15-S21. 2016 ISSN: 1933-6896 printl 1933-690X online
Taylor & Francis
Prion 2016 Animal Prion Disease Workshop Abstracts
WS-01: Prion diseases in animals and zoonotic potential
Transmission of the different scrapie isolates in these mice leads to the emergence of prion strain phenotypes that showed similar characteristics to those displayed by MM1 or VV2 sCJD prion.
These results demonstrate that scrapie prions have a zoonotic potential and raise new questions about the possible link between animal and human prions.
http://www.tandfonline.com/doi/abs/10.1080/19336896.2016.1163048?journalCode=kprn20
Title: Transmission of scrapie prions to primate after an extended silent incubation period)
*** In complement to the recent demonstration that humanized mice are susceptible to scrapie, we report here the first observation of direct transmission of a natural classical scrapie isolate to a macaque after a 10-year incubation period. Neuropathologic examination revealed all of the features of a prion disease: spongiform change, neuronal loss, and accumulation of PrPres throughout the CNS.
*** This observation strengthens the questioning of the harmlessness of scrapie to humans, at a time when protective measures for human and animal health are being dismantled and reduced as c-BSE is considered controlled and being eradicated.
*** Our results underscore the importance of precautionary and protective measures and the necessity for long-term experimental transmission studies to assess the zoonotic potential of other animal prion strains.
http://www.ars.usda.gov/research/publications/publications.htm?SEQ_NO_115=313160
''As you can imagine, 2 and 5 (especially 5) may raise alarms. The evidence we have for 4 are not as strong or tight as I would like to have. At this point, please do not post any of the points publicly yet, but you can refer to points 1-3 in private discussions and all 5 points when discussing with relevant public officials to highlight the long-term risks of CWD zoonosis.''
====================
so, i figure your as about as official as it gets, and i think this science is extremely important for you to know and to converse about with your officials. it's about to burn a whole in my pocket. this is about as close as it will ever get for cwd zoonosis to be proven in my time, this and what Canada Czub et al found with the Macaques, plus an old study from cjd surveillance unit back that showed cjd and a 9% increase in risk from folks that eat venison, i will post all this below for your files Sir. i remember back in the BSE nvCJD days, from when the first BSE case in bovine was confirmed around 1984 maybe 83, i forget the good vets named that screwed it up first, Carol something, but from 83ish to 95 96 when nvCJD was linked to humans from BSE in cattle, so that took 10 to 15 years. hell, at that rate, especially with Texas and cwd zoonsis, hell, i'll be dead before it's official, if ever, so here ya go Sir. there was a grant study on cwd zoonosis that had been going on for some time, i followed it over the years, then the grant date for said study had expired, so, i thought i would write the good Professor about said study i.e. Professor Kong, CWRU et al. i will post the grant study abstract first, and then after that, what reply i got back, about said study that i was told not to post/publish...
CWD ZOONOSIS GRANT FIRST;
===============
Cervid to human prion transmission
Kong, Qingzhong
Case Western Reserve University, Cleveland, OH, United States
Abstract Prion disease is transmissible and invariably fatal. Chronic wasting disease (CWD) is the prion disease affecting deer, elk and moose, and it is a widespread and expanding epidemic affecting 22 US States and 2 Canadian provinces so far. CWD poses the most serious zoonotic prion transmission risks in North America because of huge venison consumption (>6 million deer/elk hunted and consumed annually in the USA alone), significant prion infectivity in muscles and other tissues/fluids from CWD-affected cervids, and usually high levels of individual exposure to CWD resulting from consumption of the affected animal among often just family and friends. However, we still do not know whether CWD prions can infect humans in the brain or peripheral tissues or whether clinical/asymptomatic CWD zoonosis has already occurred, and we have no essays to reliably detect CWD infection in humans. We hypothesize that: (1) The classic CWD prion strain can infect humans at low levels in the brain and peripheral lymphoid tissues; (2) The cervid-to-human transmission barrier is dependent on the cervid prion strain and influenced by the host (human) prion protein (PrP) primary sequence; (3) Reliable essays can be established to detect CWD infection in humans; and (4) CWD transmission to humans has already occurred. We will test these hypotheses in 4 Aims using transgenic (Tg) mouse models and complementary in vitro approaches.
Aim 1 will prove that the classical CWD strain may infect humans in brain or peripheral lymphoid tissues at low levels by conducting systemic bioassays in a set of humanized Tg mouse lines expressing common human PrP variants using a number of CWD isolates at varying doses and routes. Experimental human CWD samples will also be generated for Aim 3.
Aim 2 will test the hypothesis that the cervid-to-human prion transmission barrier is dependent on prion strain and influenced by the host (human) PrP sequence by examining and comparing the transmission efficiency and phenotypes of several atypical/unusual CWD isolates/strains as well as a few prion strains from other species that have adapted to cervid PrP sequence, utilizing the same panel of humanized Tg mouse lines as in Aim 1.
Aim 3 will establish reliable essays for detection and surveillance of CWD infection in humans by examining in details the clinical, pathological, biochemical and in vitro seeding properties of existing and future experimental human CWD samples generated from Aims 1-2 and compare them with those of common sporadic human Creutzfeldt-Jakob disease (sCJD) prions.
Aim 4 will attempt to detect clinical CWD-affected human cases by examining a significant number of brain samples from prion-affected human subjects in the USA and Canada who have consumed venison from CWD-endemic areas utilizing the criteria and essays established in Aim 3. The findings from this proposal will greatly advance our understandings on the potential and characteristics of cervid prion transmission in humans, establish reliable essays for CWD zoonosis and potentially discover the first case(s) of CWD infection in humans.
Public Health Relevance There are significant and increasing human exposure to cervid prions because chronic wasting disease (CWD, a widespread and highly infectious prion disease among deer and elk in North America) continues spreading and consumption of venison remains popular, but our understanding on cervid-to-human prion transmission is still very limited, raising public health concerns. This proposal aims to define the zoonotic risks of cervid prions and set up and apply essays to detect CWD zoonosis using mouse models and in vitro methods. The findings will greatly expand our knowledge on the potentials and characteristics of cervid prion transmission in humans, establish reliable essays for such infections and may discover the first case(s) of CWD infection in humans.
Funding Agency Agency National Institute of Health (NIH) Institute National Institute of Neurological Disorders and Stroke (NINDS) Type Research Project (R01) Project # 1R01NS088604-01A1 Application # 9037884 Study Section Cellular and Molecular Biology of Neurodegeneration Study Section (CMND) Program Officer Wong, May Project Start 2015-09-30 Project End 2019-07-31 Budget Start 2015-09-30 Budget End 2016-07-31 Support Year 1 Fiscal Year 2015 Total Cost $337,507 Indirect Cost $118,756
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Professor Kongs reply to me just this month about above grant study that has NOT been published in peer reveiw yet...
=================================
Here is a brief summary of our findings:
snip...can't post, made a promise...tss
On Sat, Apr 3, 2021 at 12:19 PM Terry Singeltary <flounder9@verizon.net> wrote:
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end...tss
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CWD ZOONOSIS THE FULL MONTY TO DATE
International Conference on Emerging Diseases, Outbreaks & Case Studies & 16th Annual Meeting on Influenza March 28-29, 2018 | Orlando, USA
Qingzhong Kong
Case Western Reserve University School of Medicine, USA
Zoonotic potential of chronic wasting disease prions from cervids
Chronic wasting disease (CWD) is the prion disease in cervids (mule deer, white-tailed deer, American elk, moose, and reindeer). It has become an epidemic in North America, and it has been detected in the Europe (Norway) since 2016. The widespread CWD and popular hunting and consumption of cervid meat and other products raise serious public health concerns, but questions remain on human susceptibility to CWD prions, especially on the potential difference in zoonotic potential among the various CWD prion strains. We have been working to address this critical question for well over a decade. We used CWD samples from various cervid species to inoculate transgenic mice expressing human or elk prion protein (PrP). We found infectious prions in the spleen or brain in a small fraction of CWD-inoculated transgenic mice expressing human PrP, indicating that humans are not completely resistant to CWD prions; this finding has significant ramifications on the public health impact of CWD prions. The influence of cervid PrP polymorphisms, the prion strain dependence of CWD-to-human transmission barrier, and the characterization of experimental human CWD prions will be discussed.
Speaker Biography Qingzhong Kong has completed his PhD from the University of Massachusetts at Amherst and Post-doctoral studies at Yale University. He is currently an Associate Professor of Pathology, Neurology and Regenerative Medicine. He has published over 50 original research papers in reputable journals (including Science Translational Medicine, JCI, PNAS and Cell Reports) and has been serving as an Editorial Board Member on seven scientific journals. He has multiple research interests, including public health risks of animal prions (CWD of cervids and atypical BSE of cattle), animal modeling of human prion diseases, mechanisms of prion replication and pathogenesis, etiology of sporadic Creutzfeldt-Jacob disease (CJD) in humans, normal cellular PrP in the biology and pathology of multiple brain and peripheral diseases, proteins responsible for the α-cleavage of cellular PrP, as well as gene therapy and DNA vaccination.
SUNDAY, JULY 25, 2021
North American and Norwegian Chronic Wasting Disease prions exhibit different potential for interspecies transmission and zoonotic risk
''Our data suggest that reindeer and red deer from Norway could be the most transmissible CWD prions to other mammals, whereas North American CWD prions were more prone to generate human prions in vitro.''
MONDAY, JULY 19, 2021
***> U Calgary researchers at work on a vaccine against a fatal infectious disease affecting deer and potentially people
Prion Conference 2018 Abstracts
BSE aka MAD COW DISEASE, was first discovered in 1984, and it took until 1995 to finally admit that BSE was causing nvCJD, the rest there is history, but that science is still evolving i.e. science now shows that indeed atypical L-type BSE, atypical Nor-98 Scrapie, and typical Scrapie are all zoonosis, zoonotic for humans, there from.
HOW long are we going to wait for Chronic Wasting Disease, CWD TSE Prion of Cervid, and zoonosis, zoonotic tranmission to humans there from?
Studies have shown since 1994 that humans are susceptible to CWD TSE Prion, so, what's the hold up with making CWD a zoonotic zoonosis disease, the iatrogenic transmissions there from is not waiting for someone to make a decision.
Prion Conference 2018 Abstracts
P190 Human prion disease mortality rates by occurrence of chronic wasting disease in freeranging cervids, United States
Abrams JY (1), Maddox RA (1), Schonberger LB (1), Person MK (1), Appleby BS (2), Belay ED (1)
(1) Centers for Disease Control and Prevention (CDC), National Center for Emerging and Zoonotic Infectious Diseases, Atlanta, GA, USA (2) Case Western Reserve University, National Prion Disease Pathology Surveillance Center (NPDPSC), Cleveland, OH, USA.
Background
Chronic wasting disease (CWD) is a prion disease of deer and elk that has been identified in freeranging cervids in 23 US states. While there is currently no epidemiological evidence for zoonotic transmission through the consumption of contaminated venison, studies suggest the CWD agent can cross the species barrier in experimental models designed to closely mimic humans. We compared rates of human prion disease in states with and without CWD to examine the possibility of undetermined zoonotic transmission.
Methods
Death records from the National Center for Health Statistics, case records from the National Prion Disease Pathology Surveillance Center, and additional state case reports were combined to create a database of human prion disease cases from 2003-2015. Identification of CWD in each state was determined through reports of positive CWD tests by state wildlife agencies. Age- and race-adjusted mortality rates for human prion disease, excluding cases with known etiology, were determined for four categories of states based on CWD occurrence: highly endemic (>16 counties with CWD identified in free-ranging cervids); moderately endemic (3-10 counties with CWD); low endemic (1-2 counties with CWD); and no CWD states. States were counted as having no CWD until the year CWD was first identified. Analyses stratified by age, sex, and time period were also conducted to focus on subgroups for which zoonotic transmission would be more likely to be detected: cases <55 years old, male sex, and the latter half of the study (2010-2015).
Results
Highly endemic states had a higher rate of prion disease mortality compared to non-CWD states (rate ratio [RR]: 1.12, 95% confidence interval [CI] = 1.01 - 1.23), as did low endemic states (RR: 1.15, 95% CI = 1.04 - 1.27). Moderately endemic states did not have an elevated mortality rate (RR: 1.05, 95% CI = 0.93 - 1.17). In age-stratified analyses, prion disease mortality rates among the <55 year old population were elevated for moderately endemic states (RR: 1.57, 95% CI = 1.10 – 2.24) while mortality rates were elevated among those ≥55 for highly endemic states (RR: 1.13, 95% CI = 1.02 - 1.26) and low endemic states (RR: 1.16, 95% CI = 1.04 - 1.29). In other stratified analyses, prion disease mortality rates for males were only elevated for low endemic states (RR: 1.27, 95% CI = 1.10 - 1.48), and none of the categories of CWD-endemic states had elevated mortality rates for the latter time period (2010-2015).
Conclusions
While higher prion disease mortality rates in certain categories of states with CWD in free-ranging cervids were noted, additional stratified analyses did not reveal markedly elevated rates for potentially sensitive subgroups that would be suggestive of zoonotic transmission. Unknown confounding factors or other biases may explain state-by-state differences in prion disease mortality.
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P172 Peripheral Neuropathy in Patients with Prion Disease
Wang H(1), Cohen M(1), Appleby BS(1,2)
(1) University Hospitals Cleveland Medical Center, Cleveland, Ohio (2) National Prion Disease Pathology Surveillance Center, Cleveland, Ohio.
Prion disease is a fatal progressive neurodegenerative disease due to deposition of an abnormal protease-resistant isoform of prion protein. Typical symptoms include rapidly progressive dementia, myoclonus, visual disturbance and hallucinations. Interestingly, in patients with prion disease, the abnormal protein canould also be found in the peripheral nervous system. Case reports of prion deposition in peripheral nerves have been reported. Peripheral nerve involvement is thought to be uncommon; however, little is known about the exact prevalence and features of peripheral neuropathy in patients with prion disease.
We reviewed autopsy-proven prion cases from the National Prion Disease Pathology Surveillance Center that were diagnosed between September 2016 to March 2017. We collected information regarding prion protein diagnosis, demographics, comorbidities, clinical symptoms, physical exam, neuropathology, molecular subtype, genetics lab, brain MRI, image and EMG reports. Our study included 104 patients. Thirteen (12.5%) patients had either subjective symptoms or objective signs of peripheral neuropathy. Among these 13 patients, 3 had other known potential etiologies of peripheral neuropathy such as vitamin B12 deficiency or prior chemotherapy. Among 10 patients that had no other clear etiology, 3 (30%) had familial CJD. The most common sCJD subtype was MV1-2 (30%), followed by MM1-2 (20%). The Majority of cases wasere male (60%). Half of them had exposure to wild game. The most common subjective symptoms were tingling and/or numbness of distal extremities. The most common objective finding was diminished vibratory sensation in the feet. Half of them had an EMG with the findings ranging from fasciculations to axonal polyneuropathy or demyelinating polyneuropathy.
Our study provides an overview of the pattern of peripheral neuropathy in patients with prion disease. Among patients with peripheral neuropathy symptoms or signs, majority has polyneuropathy. It is important to document the baseline frequency of peripheral neuropathy in prion diseases as these symptoms may become important when conducting surveillance for potential novel zoonotic prion diseases.
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P177 PrP plaques in methionine homozygous Creutzfeldt-Jakob disease patients as a potential marker of iatrogenic transmission
Abrams JY (1), Schonberger LB (1), Cali I (2), Cohen Y (2), Blevins JE (2), Maddox RA (1), Belay ED (1), Appleby BS (2), Cohen ML (2)
(1) Centers for Disease Control and Prevention (CDC), National Center for Emerging and Zoonotic Infectious Diseases, Atlanta, GA, USA (2) Case Western Reserve University, National Prion Disease Pathology Surveillance Center (NPDPSC), Cleveland, OH, USA.
Background
Sporadic Creutzfeldt-Jakob disease (CJD) is widely believed to originate from de novo spontaneous conversion of normal prion protein (PrP) to its pathogenic form, but concern remains that some reported sporadic CJD cases may actually be caused by disease transmission via iatrogenic processes. For cases with methionine homozygosity (CJD-MM) at codon 129 of the PRNP gene, recent research has pointed to plaque-like PrP deposition as a potential marker of iatrogenic transmission for a subset of cases. This phenotype is theorized to originate from specific iatrogenic source CJD types that comprise roughly a quarter of known CJD cases.
Methods
We reviewed scientific literature for studies which described PrP plaques among CJD patients with known epidemiological links to iatrogenic transmission (receipt of cadaveric human grown hormone or dura mater), as well as in cases of reported sporadic CJD. The presence and description of plaques, along with CJD classification type and other contextual factors, were used to summarize the current evidence regarding plaques as a potential marker of iatrogenic transmission. In addition, 523 cases of reported sporadic CJD cases in the US from January 2013 through September 2017 were assessed for presence of PrP plaques.
Results
We identified four studies describing 52 total cases of CJD-MM among either dura mater recipients or growth hormone recipients, of which 30 were identified as having PrP plaques. While sporadic cases were not generally described as having plaques, we did identify case reports which described plaques among sporadic MM2 cases as well as case reports of plaques exclusively in white matter among sporadic MM1 cases. Among the 523 reported sporadic CJD cases, 0 of 366 MM1 cases had plaques, 2 of 48 MM2 cases had kuru plaques, and 4 of 109 MM1+2 cases had either kuru plaques or both kuru and florid plaques. Medical chart review of the six reported sporadic CJD cases with plaques did not reveal clinical histories suggestive of potential iatrogenic transmission.
Conclusions
PrP plaques occur much more frequently for iatrogenic CJD-MM cases compared to sporadic CJDMM cases. Plaques may indicate iatrogenic transmission for CJD-MM cases without a type 2 Western blot fragment. The study results suggest the absence of significant misclassifications of iatrogenic CJD as sporadic. To our knowledge, this study is the first to describe grey matter kuru plaques in apparently sporadic CJD-MM patients with a type 2 Western blot fragment.
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P180 Clinico-pathological analysis of human prion diseases in a brain bank series
Ximelis T (1), Aldecoa I (1,2), Molina-Porcel L (1,3), Grau-Rivera O (4), Ferrer I (5), Nos C (6), Gelpi E (1,7), Sánchez-Valle R (1,4)
(1) Neurological Tissue Bank of the Biobanc-Hospital ClÃnic-IDIBAPS, Barcelona, Spain (2) Pathological Service of Hospital ClÃnic de Barcelona, Barcelona, Spain (3) EAIA Trastorns Cognitius, Centre Emili Mira, Parc de Salut Mar, Barcelona, Spain (4) Department of Neurology of Hospital ClÃnic de Barcelona, Barcelona, Spain (5) Institute of Neuropathology, Hospital Universitari de Bellvitge, Hospitalet de Llobregat, Barcelona (6) General subdirectorate of Surveillance and Response to Emergencies in Public Health, Department of Public Health in Catalonia, Barcelona, Spain (7) Institute of Neurology, Medical University of Vienna, Vienna, Austria.
Background and objective:
The Neurological Tissue Bank (NTB) of the Hospital Clínic-Institut d‘Investigacions Biomèdiques August Pi i Sunyer, Barcelona, Spain is the reference center in Catalonia for the neuropathological study of prion diseases in the region since 2001. The aim of this study is to analyse the characteristics of the confirmed prion diseases registered at the NTB during the last 15 years.
Methods:
We reviewed retrospectively all neuropathologically confirmed cases registered during the period January 2001 to December 2016.
Results:
176 cases (54,3% female, mean age: 67,5 years and age range: 25-86 years) of neuropathological confirmed prion diseases have been studied at the NTB. 152 cases corresponded to sporadic Creutzfeldt-Jakob disease (sCJD), 10 to genetic CJD, 10 to Fatal Familial Insomnia, 2 to GerstmannSträussler-Scheinker disease, and 2 cases to variably protease-sensitive prionopathy (VPSPr). Within sCJD subtypes the MM1 subtype was the most frequent, followed by the VV2 histotype.
Clinical and neuropathological diagnoses agreed in 166 cases (94%). The clinical diagnosis was not accurate in 10 patients with definite prion disease: 1 had a clinical diagnosis of Fronto-temporal dementia (FTD), 1 Niemann-Pick‘s disease, 1 Lewy Body‘s Disease, 2 Alzheimer‘s disease, 1 Cortico-basal syndrome and 2 undetermined dementia. Among patients with VPSPr, 1 had a clinical diagnosis of Amyotrophic lateral sclerosis (ALS) and the other one with FTD.
Concomitant pathologies are frequent in older age groups, mainly AD neuropathological changes were observed in these subjects.
Discussion:
A wide spectrum of human prion diseases have been identified in the NTB being the relative frequencies and main characteristics like other published series. There is a high rate of agreement between clinical and neuropathological diagnoses with prion diseases. These findings show the importance that public health has given to prion diseases during the past 15 years. Continuous surveillance of human prion disease allows identification of new emerging phenotypes. Brain tissue samples from these donors are available to the scientific community. For more information please visit:
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P192 Prion amplification techniques for the rapid evaluation of surface decontamination procedures
Bruyere-Ostells L (1), Mayran C (1), Belondrade M (1), Boublik Y (2), Haïk S (3), Fournier-Wirth C (1), Nicot S (1), Bougard D (1)
(1) Pathogenesis and control of chronic infections, Etablissement Français du Sang, Inserm, Université de Montpellier, Montpellier, France. (2) Centre de Recherche en Biologie cellulaire de Montpellier, CNRS, Université de Montpellier, Montpellier, France. (3) Inserm U 1127, CNRS UMR 7225, Sorbonne Universités, UPMC Université Paris 06 UMR S 1127, Institut du Cerveau et de la Moelle épinière, ICM, Paris, France.
Aims:
Transmissible Spongiform Encephalopathies (TSE) or prion diseases are a group of incurable and always fatal neurodegenerative disorders including Creutzfeldt-Jakob diseases (CJD) in humans. These pathologies include sporadic (sCJD), genetic and acquired (variant CJD) forms. By the past, sCJD and vCJD were transmitted by different prion contaminated biological materials to patients resulting in more than 400 iatrogenic cases (iCJD). The atypical nature and the biochemical properties of the infectious agent, formed by abnormal prion protein or PrPTSE, make it particularly resistant to conventional decontamination procedures. In addition, PrPTSE is widely distributed throughout the organism before clinical onset in vCJD and can also be detected in some peripheral tissues in sporadic CJD. Risk of iatrogenic transmission of CJD by contaminated medical device remains thus a concern for healthcare facilities. Bioassay is the gold standard method to evaluate the efficacy of prion decontamination procedures but is time-consuming and expensive. Here, we propose to compare in vitro prion amplification techniques: Protein Misfolding Cyclic Amplification (PMCA) and Real-Time Quaking Induced Conversion (RT-QuIC) for the detection of residual prions on surface after decontamination.
Methods:
Stainless steel wires, by mimicking the surface of surgical instruments, were proposed as a carrier model of prions for inactivation studies. To determine the sensitivity of the two amplification techniques on wires (Surf-PMCA and Surf-QuIC), steel wires were therefore contaminated with serial dilutions of brain homogenates (BH) from a 263k infected hamster and from a patient with sCJD (MM1 subtype). We then compared the different standard decontamination procedures including partially and fully efficient treatments by detecting the residual seeding activity on 263K and sCJD contaminated wires. We completed our study by the evaluation of marketed reagents endorsed for prion decontamination.
Results:
The two amplification techniques can detect minute quantities of PrPTSE adsorbed onto a single wire. 8/8 wires contaminated with a 10-6 dilution of 263k BH and 1/6 with the 10-8 dilution are positive with Surf-PMCA. Similar performances were obtained with Surf-QuIC on 263K: 10/16 wires contaminated with 10-6 dilution and 1/8 wires contaminated with 10-8 dilution are positive. Regarding the human sCJD-MM1 prion, Surf-QuIC allows us to detect 16/16 wires contaminated with 10-6 dilutions and 14/16 with 10-7 . Results obtained after decontamination treatments are very similar between 263K and sCJD prions. Efficiency of marketed treatments to remove prions is lower than expected.
Conclusions:
Surf-PMCA and Surf-QuIC are very sensitive methods for the detection of prions on wires and could be applied to prion decontamination studies for rapid evaluation of new treatments. Sodium hypochlorite is the only product to efficiently remove seeding activity of both 263K and sCJD prions.
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WA2 Oral transmission of CWD into Cynomolgus macaques: signs of atypical disease, prion conversion and infectivity in macaques and bio-assayed transgenic mice
Schatzl HM (1, 2), Hannaoui S (1, 2), Cheng Y-C (1, 2), Gilch S (1, 2), Beekes M (3), SchulzSchaeffer W (4), Stahl-Hennig C (5) and Czub S (2, 6)
(1) University of Calgary, Calgary Prion Research Unit, Calgary, Canada (2) University of Calgary, Faculty of Veterinary Medicine, Calgary, Canada, (3) Robert Koch Institute, Berlin, Germany, (4) University of Homburg/Saar, Homburg, Germany, (5) German Primate Center, Goettingen, Germany, (6) Canadian Food Inspection Agency (CFIA), Lethbridge, Canada.
To date, BSE is the only example of interspecies transmission of an animal prion disease into humans. The potential zoonotic transmission of CWD is an alarming issue and was addressed by many groups using a variety of in vitro and in vivo experimental systems. Evidence from these studies indicated a substantial, if not absolute, species barrier, aligning with the absence of epidemiological evidence suggesting transmission into humans. Studies in non-human primates were not conclusive so far, with oral transmission into new-world monkeys and no transmission into old-world monkeys. Our consortium has challenged 18 Cynomolgus macaques with characterized CWD material, focusing on oral transmission with muscle tissue. Some macaques have orally received a total of 5 kg of muscle material over a period of 2 years. After 5-7 years of incubation time some animals showed clinical symptoms indicative of prion disease, and prion neuropathology and PrPSc deposition were found in spinal cord and brain of euthanized animals. PrPSc in immunoblot was weakly detected in some spinal cord materials and various tissues tested positive in RT-QuIC, including lymph node and spleen homogenates. To prove prion infectivity in the macaque tissues, we have intracerebrally inoculated 2 lines of transgenic mice, expressing either elk or human PrP. At least 3 TgElk mice, receiving tissues from 2 different macaques, showed clinical signs of a progressive prion disease and brains were positive in immunoblot and RT-QuIC. Tissues (brain, spinal cord and spleen) from these and preclinical mice are currently tested using various read-outs and by second passage in mice. Transgenic mice expressing human PrP were so far negative for clear clinical prion disease (some mice >300 days p.i.). In parallel, the same macaque materials are inoculated into bank voles. Taken together, there is strong evidence of transmissibility of CWD orally into macaques and from macaque tissues into transgenic mouse models, although with an incomplete attack rate. The clinical and pathological presentation in macaques was mostly atypical, with a strong emphasis on spinal cord pathology. Our ongoing studies will show whether the transmission of CWD into macaques and passage in transgenic mice represents a form of non-adaptive prion amplification, and whether macaque-adapted prions have the potential to infect mice expressing human PrP. The notion that CWD can be transmitted orally into both new-world and old-world non-human primates asks for a careful reevaluation of the zoonotic risk of CWD.
See also poster P103
***> The notion that CWD can be transmitted orally into both new-world and old-world non-human primates asks for a careful reevaluation of the zoonotic risk of CWD.
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WA16 Monitoring Potential CWD Transmission to Humans
Belay ED
Centers for Disease Control and Prevention (CDC), National Center for Emerging and Zoonotic Infectious Diseases, Atlanta, GA, USA.
The spread of chronic wasting disease (CWD) in animals has raised concerns about increasing human exposure to the CWD agent via hunting and venison consumption, potentially facilitating CWD transmission to humans. Several studies have explored this possibility, including limited epidemiologic studies, in vitro experiments, and laboratory studies using various types of animal models. Most human exposures to the CWD agent in the United States would be expected to occur in association with deer and elk hunting in CWD-endemic areas. The Centers for Disease Control and Prevention (CDC) collaborated with state health departments in Colorado, Wisconsin, and Wyoming to identify persons at risk of CWD exposure and to monitor their vital status over time. Databases were established of persons who hunted in Colorado and Wyoming and those who reported consumption of venison from deer that later tested positive in Wisconsin. Information from the databases is periodically cross-checked with mortality data to determine the vital status and causes of death for deceased persons. Long-term follow-up of these hunters is needed to assess their risk of development of a prion disease linked to CWD exposure.
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P166 Characterization of CJD strain profiles in venison consumers and non-consumers from Alberta and Saskatchewan
Stephanie Booth (1,2), Lise Lamoureux (1), Debra Sorensen (1), Jennifer L. Myskiw (1,2), Megan Klassen (1,2), Michael Coulthart (3), Valerie Sim (4)
(1) Zoonotic Diseases and Special Pathogens, National Microbiology Laboratory, Public Health Agency of Canada, Winnipeg (2) Department of Medical Microbiology and Infectious Diseases, University of Manitoba, Winnipeg (3) Canadian CJD Surveillance System, Public Health Agency of Canada, Ottawa (4) Division of Neurology, Department of Medicine Centre for Prions and Protein Folding Diseases, University of Alberta, Edmonton.
Chronic wasting disease (CWD) is spreading rapidly through wild cervid populations in the Canadian provinces of Alberta and Saskatchewan. While this has implications for tourism and hunting, there is also concern over possible zoonotic transmission to humans who eat venison from infected deer. Whilst there is no evidence of any human cases of CWD to date, the Canadian CJD Surveillance System (CJDSS) in Canada is staying vigilant. When variant CJD occurred following exposure to BSE, the unique biochemical fingerprint of the pathologic PrP enabled a causal link to be confirmed. However, we cannot be sure what phenotype human CWD prions would present with, or indeed, whether this would be distinct from that see in sporadic CJD. Therefore we are undertaking a systematic analysis of the molecular diversity of CJD cases of individuals who resided in Alberta and Saskatchewan at their time of death comparing venison consumers and non-consumers, using a variety of clinical, imaging, pathological and biochemical markers. Our initial objective is to develop novel biochemical methodologies that will extend the baseline glycoform and genetic polymorphism typing that is already completed by the CJDSS. Firstly, we are reviewing MRI, EEG and pathology information from over 40 cases of CJD to select clinically affected areas for further investigation. Biochemical analysis will include assessment of the levels of protease sensitive and resistant prion protein, glycoform typing using 2D gel electrophoresis, testing seeding capabilities and kinetics of aggregation by quaking-induced conversion, and determining prion oligomer size distributions with asymmetric flow field fractionation with in-line light scattering. Progress and preliminary data will be presented. Ultimately, we intend to further define the relationship between PrP structure and disease phenotype and establish a baseline for the identification of future atypical CJD cases that may arise as a result of exposure to CWD.
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Source Prion Conference 2018 Abstracts
Volume 24, Number 8—August 2018 Research Susceptibility of Human Prion Protein to Conversion by Chronic Wasting Disease Prions
Marcelo A. BarriaComments to Author , Adriana Libori, Gordon Mitchell, and Mark W. Head Author affiliations: National CJD Research and Surveillance Unit, University of Edinburgh, Edinburgh, Scotland, UK (M.A. Barria, A. Libori, M.W. Head); National and OIE Reference Laboratory for Scrapie and CWD, Canadian Food Inspection Agency, Ottawa, Ontario, Canada (G. Mitchell)
Abstract Chronic wasting disease (CWD) is a contagious and fatal neurodegenerative disease and a serious animal health issue for deer and elk in North America. The identification of the first cases of CWD among free-ranging reindeer and moose in Europe brings back into focus the unresolved issue of whether CWD can be zoonotic like bovine spongiform encephalopathy. We used a cell-free seeded protein misfolding assay to determine whether CWD prions from elk, white-tailed deer, and reindeer in North America can convert the human prion protein to the disease-associated form. We found that prions can convert, but the efficiency of conversion is affected by polymorphic variation in the cervid and human prion protein genes. In view of the similarity of reindeer, elk, and white-tailed deer in North America to reindeer, red deer, and roe deer, respectively, in Europe, a more comprehensive and thorough assessment of the zoonotic potential of CWD might be warranted.
snip...
Discussion Characterization of the transmission properties of CWD and evaluation of their zoonotic potential are important for public health purposes. Given that CWD affects several members of the family Cervidae, it seems reasonable to consider whether the zoonotic potential of CWD prions could be affected by factors such as CWD strain, cervid species, geographic location, and Prnp–PRNP polymorphic variation. We have previously used an in vitro conversion assay (PMCA) to investigate the susceptibility of the human PrP to conversion to its disease-associated form by several animal prion diseases, including CWD (15,16,22). The sensitivity of our molecular model for the detection of zoonotic conversion depends on the combination of 1) the action of proteinase K to degrade the abundant human PrPC that constitutes the substrate while only N terminally truncating any human PrPres produced and 2) the presence of the 3F4 epitope on human but not cervid PrP. In effect, this degree of sensitivity means that any human PrPres formed during the PMCA reaction can be detected down to the limit of Western blot sensitivity. In contrast, if other antibodies that detect both cervid and human PrP are used, such as 6H4, then newly formed human PrPres must be detected as a measurable increase in PrPres over the amount remaining in the reaction product from the cervid seed. Although best known for the efficient amplification of prions in research and diagnostic contexts, the variation of the PMCA method employed in our study is optimized for the definitive detection of zoonotic reaction products of inherently inefficient conversion reactions conducted across species barriers. By using this system, we previously made and reported the novel observation that elk CWD prions could convert human PrPC from human brain and could also convert recombinant human PrPC expressed in transgenic mice and eukaryotic cell cultures (15).
A previous publication suggested that mule deer PrPSc was unable to convert humanized transgenic substrate in PMCA assays (23) and required a further step of in vitro conditioning in deer substrate PMCA before it was able to cross the deer–human molecular barrier (24). However, prions from other species, such as elk (15) and reindeer affected by CWD, appear to be compatible with the human protein in a single round of amplification (as shown in our study). These observations suggest that different deer species affected by CWD could present differing degrees of the olecular compatibility with the normal form of human PrP.
The contribution of the polymorphism at codon 129 of the human PrP gene has been extensively studied and is recognized as a risk factor for Creutzfeldt-Jakob disease (4). In cervids, the equivalent codon corresponds to the position 132 encoding methionine or leucine. This polymorphism in the elk gene has been shown to play an important role in CWD susceptibility (25,26). We have investigated the effect of this cervid Prnp polymorphism on the conversion of the humanized transgenic substrate according to the variation in the equivalent PRNP codon 129 polymorphism. Interestingly, only the homologs methionine homozygous seed–substrate reactions could readily convert the human PrP, whereas the heterozygous elk PrPSc was unable to do so, even though comparable amounts of PrPres were used to seed the reaction. In addition, we observed only low levels of human PrPres formation in the reactions seeded with the homozygous methionine (132 MM) and the heterozygous (132 ML) seeds incubated with the other 2 human polymorphic substrates (129 MV and 129 VV). The presence of the amino acid leucine at position 132 of the elk Prnp gene has been attributed to a lower degree of prion conversion compared with methionine on the basis of experiments in mice made transgenic for these polymorphic variants (26). Considering the differences observed for the amplification of the homozygous human methionine substrate by the 2 polymorphic elk seeds (MM and ML), reappraisal of the susceptibility of human PrPC by the full range of cervid polymorphic variants affected by CWD would be warranted.
In light of the recent identification of the first cases of CWD in Europe in a free-ranging reindeer (R. tarandus) in Norway (2), we also decided to evaluate the in vitro conversion potential of CWD in 2 experimentally infected reindeer (18). Formation of human PrPres was readily detectable after a single round of PMCA, and in all 3 humanized polymorphic substrates (MM, MV, and VV). This finding suggests that CWD prions from reindeer could be more compatible with human PrPC generally and might therefore present a greater risk for zoonosis than, for example, CWD prions from white-tailed deer. A more comprehensive comparison of CWD in the affected species, coupled with the polymorphic variations in the human and deer PRNP–Prnp genes, in vivo and in vitro, will be required before firm conclusions can be drawn. Analysis of the Prnp sequence of the CWD reindeer in Norway was reported to be identical to the specimens used in our study (2). This finding raises the possibility of a direct comparison of zoonotic potential between CWD acquired in the wild and that produced in a controlled laboratory setting. (Table).
The prion hypothesis proposes that direct molecular interaction between PrPSc and PrPC is necessary for conversion and prion replication. Accordingly, polymorphic variants of the PrP of host and agent might play a role in determining compatibility and potential zoonotic risk. In this study, we have examined the capacity of the human PrPC to support in vitro conversion by elk, white-tailed deer, and reindeer CWD PrPSc. Our data confirm that elk CWD prions can convert the human PrPC, at least in vitro, and show that the homologous PRNP polymorphisms at codon 129 and 132 in humans and cervids affect conversion efficiency. Other species affected by CWD, particularly caribou or reindeer, also seem able to convert the human PrP. It will be important to determine whether other polymorphic variants found in other CWD-affected Cervidae or perhaps other factors (17) exert similar effects on the ability to convert human PrP and thus affect their zoonotic potential.
Dr. Barria is a research scientist working at the National CJD Research and Surveillance Unit, University of Edinburgh. His research has focused on understanding the molecular basis of a group of fatal neurologic disorders called prion diseases.
Acknowledgments We thank Aru Balachandran for originally providing cervid brain tissues, Abigail Diack and Jean Manson for providing mouse brain tissue, and James Ironside for his critical reading of the manuscript at an early stage.
This report is independent research commissioned and funded by the United Kingdom’s Department of Health Policy Research Programme and the Government of Scotland. The views expressed in this publication are those of the authors and not necessarily those of the Department of Health or the Government of Scotland.
Author contributions: The study was conceived and designed by M.A.B. and M.W.H. The experiments were conducted by M.A.B. and A.L. Chronic wasting disease brain specimens were provided by G.M. The manuscript was written by M.A.B. and M.W.H. All authors contributed to the editing and revision of the manuscript.
Prion 2017 Conference Abstracts
First evidence of intracranial and peroral transmission of Chronic Wasting Disease (CWD) into Cynomolgus macaques: a work in progress Stefanie Czub1, Walter Schulz-Schaeffer2, Christiane Stahl-Hennig3, Michael Beekes4, Hermann Schaetzl5 and Dirk Motzkus6 1
University of Calgary Faculty of Veterinary Medicine/Canadian Food Inspection Agency; 2Universitatsklinikum des Saarlandes und Medizinische Fakultat der Universitat des Saarlandes; 3 Deutsches Primaten Zentrum/Goettingen; 4 Robert-Koch-Institut Berlin; 5 University of Calgary Faculty of Veterinary Medicine; 6 presently: Boehringer Ingelheim Veterinary Research Center; previously: Deutsches Primaten Zentrum/Goettingen
This is a progress report of a project which started in 2009.
21 cynomolgus macaques were challenged with characterized CWD material from white-tailed deer (WTD) or elk by intracerebral (ic), oral, and skin exposure routes. Additional blood transfusion experiments are supposed to assess the CWD contamination risk of human blood product. Challenge materials originated from symptomatic cervids for ic, skin scarification and partially per oral routes (WTD brain). Challenge material for feeding of muscle derived from preclinical WTD and from preclinical macaques for blood transfusion experiments. We have confirmed that the CWD challenge material contained at least two different CWD agents (brain material) as well as CWD prions in muscle-associated nerves.
Here we present first data on a group of animals either challenged ic with steel wires or per orally and sacrificed with incubation times ranging from 4.5 to 6.9 years at postmortem. Three animals displayed signs of mild clinical disease, including anxiety, apathy, ataxia and/or tremor. In four animals wasting was observed, two of those had confirmed diabetes. All animals have variable signs of prion neuropathology in spinal cords and brains and by supersensitive IHC, reaction was detected in spinal cord segments of all animals. Protein misfolding cyclic amplification (PMCA), real-time quaking-induced conversion (RT-QuiC) and PET-blot assays to further substantiate these findings are on the way, as well as bioassays in bank voles and transgenic mice.
At present, a total of 10 animals are sacrificed and read-outs are ongoing. Preclinical incubation of the remaining macaques covers a range from 6.4 to 7.10 years. Based on the species barrier and an incubation time of > 5 years for BSE in macaques and about 10 years for scrapie in macaques, we expected an onset of clinical disease beyond 6 years post inoculation.
PRION 2017 DECIPHERING NEURODEGENERATIVE DISORDERS ABSTRACTS REFERENCE
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.
SATURDAY, FEBRUARY 23, 2019
Chronic Wasting Disease CWD TSE Prion and THE FEAST 2003 CDC an updated review of the science 2019
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. "
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....
Prion Infectivity in Fat of Deer with Chronic Wasting Disease▿
Brent Race#, Kimberly Meade-White#, Richard Race and Bruce Chesebro* + Author Affiliations
In mice, prion infectivity was recently detected in fat. Since ruminant fat is consumed by humans and fed to animals, we determined infectivity titers in fat from two CWD-infected deer. Deer fat devoid of muscle contained low levels of CWD infectivity and might be a risk factor for prion infection of other species.
Prions in Skeletal Muscles of Deer with Chronic Wasting Disease
Here bioassays in transgenic mice expressing cervid prion protein revealed the presence of infectious prions in skeletal muscles of CWD-infected deer, demonstrating that humans consuming or handling meat from CWD-infected deer are at risk to prion exposure.
*** now, let’s see what the authors said about this casual link, personal communications years ago, and then the latest on the zoonotic potential from CWD to humans from the TOKYO PRION 2016 CONFERENCE.
see where it is stated NO STRONG evidence. so, does this mean there IS casual evidence ???? “Our conclusion stating that we found no strong evidence of CWD transmission to humans”
From: TSS
Subject: CWD aka MAD DEER/ELK TO HUMANS ???
Date: September 30, 2002 at 7:06 am PST
From: "Belay, Ermias"
To: Cc: "Race, Richard (NIH)" ; ; "Belay, Ermias"
Sent: Monday, September 30, 2002 9:22 AM
Subject: RE: TO CDC AND NIH - PUB MED- 3 MORE DEATHS - CWD - YOUNG HUNTERS
Dear Sir/Madam,
In the Archives of Neurology you quoted (the abstract of which was attached to your email), we did not say CWD in humans will present like variant CJD.. That assumption would be wrong. I encourage you to read the whole article and call me if you have questions or need more clarification (phone: 404-639-3091). Also, we do not claim that "no-one has ever been infected with prion disease from eating venison." Our conclusion stating that we found no strong evidence of CWD transmission to humans in the article you quoted or in any other forum is limited to the patients we investigated.
Ermias Belay, M.D. Centers for Disease Control and Prevention
-----Original Message-----
From: Sent: Sunday, September 29, 2002 10:15 AM
Subject: TO CDC AND NIH - PUB MED- 3 MORE DEATHS - CWD - YOUNG HUNTERS
Sunday, November 10, 2002 6:26 PM .......snip........end..............TSS
Thursday, April 03, 2008
A prion disease of cervids: Chronic wasting disease 2008 1: Vet Res. 2008 Apr 3;39(4):41 A prion disease of cervids: Chronic wasting disease Sigurdson CJ.
snip...
*** twenty-seven CJD patients who regularly consumed venison were reported to the Surveillance Center***,
snip... full text ;
> However, to date, no CWD infections have been reported in people.
sporadic, spontaneous CJD, 85%+ of all human TSE, did not just happen. never in scientific literature has this been proven.
if one looks up the word sporadic or spontaneous at pubmed, you will get a laundry list of disease that are classified in such a way;
sporadic = 54,983 hits https://www.ncbi.nlm.nih.gov/pubmed/?term=sporadic
spontaneous = 325,650 hits https://www.ncbi.nlm.nih.gov/pubmed/?term=spontaneous
key word here is 'reported'. science has shown that CWD in humans will look like sporadic CJD. SO, how can one assume that CWD has not already transmitted to humans? they can't, and it's as simple as that. from all recorded science to date, CWD has already transmitted to humans, and it's being misdiagnosed as sporadic CJD. ...terry
*** LOOKING FOR CWD IN HUMANS AS nvCJD or as an ATYPICAL CJD, LOOKING IN ALL THE WRONG PLACES $$$ ***
> However, to date, no CWD infections have been reported in people.
key word here is ‘reported’. science has shown that CWD in humans will look like sporadic CJD. SO, how can one assume that CWD has not already transmitted to humans? they can’t, and it’s as simple as that. from all recorded science to date, CWD has already transmitted to humans, and it’s being misdiagnosed as sporadic CJD. …terry
*** LOOKING FOR CWD IN HUMANS AS nvCJD or as an ATYPICAL CJD, LOOKING IN ALL THE WRONG PLACES $$$ ***
*** These results would seem to suggest that CWD does indeed have zoonotic potential, at least as judged by the compatibility of CWD prions and their human PrPC target. Furthermore, extrapolation from this simple in vitro assay suggests that if zoonotic CWD occurred, it would most likely effect those of the PRNP codon 129-MM genotype and that the PrPres type would be similar to that found in the most common subtype of sCJD (MM1).***
CWD TSE PRION AND ZOONOTIC, ZOONOSIS, POTENTIAL
Subject: Re: DEER SPONGIFORM ENCEPHALOPATHY SURVEY & HOUND STUDY
Date: Fri, 18 Oct 2002 23:12:22 +0100
From: Steve Dealler
Reply-To: Bovine Spongiform Encephalopathy Organization: Netscape Online member
To: BSE-L@ References: <3daf5023 .4080804="" wt.net="">
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 ===============
''The association between venison eating and risk of CJD shows similar pattern, with regular venison eating associated with a 9 FOLD INCREASE IN RISK OF CJD (p = 0.04).''
CREUTZFELDT JAKOB DISEASE SURVEILLANCE IN THE UNITED KINGDOM THIRD ANNUAL REPORT AUGUST 1994
Consumption of venison and veal was much less widespread among both cases and controls. For both of these meats there was evidence of a trend with increasing frequency of consumption being associated with increasing risk of CJD. (not nvCJD, but sporadic CJD...tss) These associations were largely unchanged when attention was restricted to pairs with data obtained from relatives. ...
Table 9 presents the results of an analysis of these data.
There is STRONG evidence of an association between ‘’regular’’ veal eating and risk of CJD (p = .0.01).
Individuals reported to eat veal on average at least once a year appear to be at 13 TIMES THE RISK of individuals who have never eaten veal.
There is, however, a very wide confidence interval around this estimate. There is no strong evidence that eating veal less than once per year is associated with increased risk of CJD (p = 0.51).
The association between venison eating and risk of CJD shows similar pattern, with regular venison eating associated with a 9 FOLD INCREASE IN RISK OF CJD (p = 0.04).
There is some evidence that risk of CJD INCREASES WITH INCREASING FREQUENCY OF LAMB EATING (p = 0.02).
The evidence for such an association between beef eating and CJD is weaker (p = 0.14). When only controls for whom a relative was interviewed are included, this evidence becomes a little STRONGER (p = 0.08).
snip...
It was found that when veal was included in the model with another exposure, the association between veal and CJD remained statistically significant (p = < 0.05 for all exposures), while the other exposures ceased to be statistically significant (p = > 0.05).
snip...
In conclusion, an analysis of dietary histories revealed statistical associations between various meats/animal products and INCREASED RISK OF CJD. When some account was taken of possible confounding, the association between VEAL EATING AND RISK OF CJD EMERGED AS THE STRONGEST OF THESE ASSOCIATIONS STATISTICALLY. ...
snip...
In the study in the USA, a range of foodstuffs were associated with an increased risk of CJD, including liver consumption which was associated with an apparent SIX-FOLD INCREASE IN THE RISK OF CJD. By comparing the data from 3 studies in relation to this particular dietary factor, the risk of liver consumption became non-significant with an odds ratio of 1.2 (PERSONAL COMMUNICATION, PROFESSOR A. HOFMAN. ERASMUS UNIVERSITY, ROTTERDAM). (???...TSS)
snip...see full report ;
http://web.archive.org/web/20090506050043/http://www.bseinquiry.gov.uk/files/yb/1994/08/00004001.pdf
http://web.archive.org/web/20090506050244/http://www.bseinquiry.gov.uk/files/yb/1994/07/00001001.pdf
BSE Inquiry Steve Dealler
Management In Confidence
BSE: Private Submission of Bovine Brain Dealler
snip...see full text;
MONDAY, FEBRUARY 25, 2019
***> MAD DOGS AND ENGLISHMEN BSE, SCRAPIE, CWD, CJD, TSE PRION A REVIEW 2019
***> ''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).''
***> In conclusion, sensory symptoms and loss of reflexes in Gerstmann-Sträussler-Scheinker syndrome can be explained by neuropathological changes in the spinal cord. We conclude that the sensory symptoms and loss of lower limb reflexes in Gerstmann-Sträussler-Scheinker syndrome is due to pathology in the caudal spinal cord. <***
***> The clinical and pathological presentation in macaques was mostly atypical, with a strong emphasis on spinal cord pathology.<***
***> The notion that CWD can be transmitted orally into both new-world and old-world non-human primates asks for a careful reevaluation of the zoonotic risk of CWD. <***
***> All animals have variable signs of prion neuropathology in spinal cords and brains and by supersensitive IHC, reaction was detected in spinal cord segments of all animals.<***
***> 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.'' Scientific opinion on chronic wasting disease (II) <***
***Moreover, sporadic disease has never been observed in breeding colonies or primate research laboratories, most notably among hundreds of animals over several decades of study at the National Institutes of Health25, and in nearly twenty older animals continuously housed in our own facility.***
Even if the prevailing view is that sporadic CJD is due to the spontaneous formation of CJD prions, it remains possible that its apparent sporadic nature may, at least in part, result from our limited capacity to identify an environmental origin.
https://www.nature.com/articles/srep11573
O.05: Transmission of prions to primates after extended silent incubation periods: Implications for BSE and scrapie risk assessment in human populations
Emmanuel Comoy, Jacqueline Mikol, Valerie Durand, Sophie Luccantoni, Evelyne Correia, Nathalie Lescoutra, Capucine Dehen, and Jean-Philippe Deslys Atomic Energy Commission; Fontenay-aux-Roses, France
Prion diseases (PD) are the unique neurodegenerative proteinopathies reputed to be transmissible under field conditions since decades. The transmission of Bovine Spongiform Encephalopathy (BSE) to humans evidenced that an animal PD might be zoonotic under appropriate conditions. Contrarily, in the absence of obvious (epidemiological or experimental) elements supporting a transmission or genetic predispositions, PD, like the other proteinopathies, are reputed to occur spontaneously (atpical animal prion strains, sporadic CJD summing 80% of human prion cases).
Non-human primate models provided the first evidences supporting the transmissibiity of human prion strains and the zoonotic potential of BSE. Among them, cynomolgus macaques brought major information for BSE risk assessment for human health (Chen, 2014), according to their phylogenetic proximity to humans and extended lifetime. We used this model to assess the zoonotic potential of other animal PD from bovine, ovine and cervid origins even after very long silent incubation periods.
*** We recently observed the direct transmission of a natural classical scrapie isolate to macaque after a 10-year silent incubation period,
***with features similar to some reported for human cases of sporadic CJD, albeit requiring fourfold long incubation than BSE. Scrapie, as recently evoked in humanized mice (Cassard, 2014),
***is the third potentially zoonotic PD (with BSE and L-type BSE),
***thus questioning the origin of human sporadic cases.
We will present an updated panorama of our different transmission studies and discuss the implications of such extended incubation periods on risk assessment of animal PD for human health.
===============
***thus questioning the origin of human sporadic cases***
===============
***our findings suggest that possible transmission risk of H-type BSE to sheep and human. Bioassay will be required to determine whether the PMCA products are infectious to these animals.
==============
https://prion2015.files.wordpress.com/2015/05/prion2015abstracts.pdf
***Transmission data also revealed that several scrapie prions propagate in HuPrP-Tg mice with efficiency comparable to that of cattle BSE. While the efficiency of transmission at primary passage was low, subsequent passages resulted in a highly virulent prion disease in both Met129 and Val129 mice.
***Transmission of the different scrapie isolates in these mice leads to the emergence of prion strain phenotypes that showed similar characteristics to those displayed by MM1 or VV2 sCJD prion.
***These results demonstrate that scrapie prions have a zoonotic potential and raise new questions about the possible link between animal and human prions.
http://www.tandfonline.com/doi/abs/10.1080/19336896.2016.1163048?journalCode=kprn20
Prion diseases (PD) are the unique neurodegenerative proteinopathies reputed to be transmissible under field conditions since decades. The transmission of Bovine Spongiform Encephalopathy (BSE) to humans evidenced that an animal PD might be zoonotic under appropriate conditions. Contrarily, in the absence of obvious (epidemiological or experimental) elements supporting a transmission or genetic predispositions, PD, like the other proteinopathies, are reputed to occur spontaneously (atpical animal prion strains, sporadic CJD summing 80% of human prion cases).
Non-human primate models provided the first evidences supporting the transmissibiity of human prion strains and the zoonotic potential of BSE. Among them, cynomolgus macaques brought major information for BSE risk assessment for human health (Chen, 2014), according to their phylogenetic proximity to humans and extended lifetime. We used this model to assess the zoonotic potential of other animal PD from bovine, ovine and cervid origins even after very long silent incubation periods.
*** We recently observed the direct transmission of a natural classical scrapie isolate to macaque after a 10-year silent incubation period,
***with features similar to some reported for human cases of sporadic CJD, albeit requiring fourfold long incubation than BSE. Scrapie, as recently evoked in humanized mice (Cassard, 2014),
***is the third potentially zoonotic PD (with BSE and L-type BSE),
***thus questioning the origin of human sporadic cases.
We will present an updated panorama of our different transmission studies and discuss the implications of such extended incubation periods on risk assessment of animal PD for human health.
===============
***thus questioning the origin of human sporadic cases***
===============
***our findings suggest that possible transmission risk of H-type BSE to sheep and human. Bioassay will be required to determine whether the PMCA products are infectious to these animals.
==============
https://prion2015.files.wordpress.com/2015/05/prion2015abstracts.pdf
***Transmission data also revealed that several scrapie prions propagate in HuPrP-Tg mice with efficiency comparable to that of cattle BSE. While the efficiency of transmission at primary passage was low, subsequent passages resulted in a highly virulent prion disease in both Met129 and Val129 mice.
***Transmission of the different scrapie isolates in these mice leads to the emergence of prion strain phenotypes that showed similar characteristics to those displayed by MM1 or VV2 sCJD prion.
***These results demonstrate that scrapie prions have a zoonotic potential and raise new questions about the possible link between animal and human prions.
http://www.tandfonline.com/doi/abs/10.1080/19336896.2016.1163048?journalCode=kprn20
PRION 2016 TOKYO
Saturday, April 23, 2016
SCRAPIE WS-01: Prion diseases in animals and zoonotic potential 2016
Prion. 10:S15-S21. 2016 ISSN: 1933-6896 printl 1933-690X online
Taylor & Francis
Prion 2016 Animal Prion Disease Workshop Abstracts
WS-01: Prion diseases in animals and zoonotic potential
Transmission of the different scrapie isolates in these mice leads to the emergence of prion strain phenotypes that showed similar characteristics to those displayed by MM1 or VV2 sCJD prion.
These results demonstrate that scrapie prions have a zoonotic potential and raise new questions about the possible link between animal and human prions.
http://www.tandfonline.com/doi/abs/10.1080/19336896.2016.1163048?journalCode=kprn20
Title: Transmission of scrapie prions to primate after an extended silent incubation period)
*** In complement to the recent demonstration that humanized mice are susceptible to scrapie, we report here the first observation of direct transmission of a natural classical scrapie isolate to a macaque after a 10-year incubation period. Neuropathologic examination revealed all of the features of a prion disease: spongiform change, neuronal loss, and accumulation of PrPres throughout the CNS.
*** This observation strengthens the questioning of the harmlessness of scrapie to humans, at a time when protective measures for human and animal health are being dismantled and reduced as c-BSE is considered controlled and being eradicated.
*** Our results underscore the importance of precautionary and protective measures and the necessity for long-term experimental transmission studies to assess the zoonotic potential of other animal prion strains.
http://www.ars.usda.gov/research/publications/publications.htm?SEQ_NO_115=313160
GAME FARM INDUSTRY WANTS TO COVER UP FINDINGS OF INCREASE RISK TO CJD FROM CERVID
BSE INQUIRY
CJD9/10022
October 1994
Mr R.N. Elmhirst Chairman British Deer Farmers Association Holly Lodge Spencers Lane
BerksWell Coventry CV7 7BZ
Dear Mr Elmhirst,
CREUTZFELDT-JAKOB DISEASE (CJD) SURVEILLANCE UNIT REPORT
Thank you for your recent letter concerning the publication of the third annual report from the CJD Surveillance Unit. I am sorry that you are dissatisfied with the way in which this report was published.
The Surveillance Unit is a completely independant outside body and the Department of Health is committed to publishing their reports as soon as they become available. In the circumstances it is not the practice to circulate the report for comment since the findings of the report would not be amended.. In future we can ensure that the British Deer Farmers Association receives a copy of the report in advance of publication.
The Chief Medical Officer has undertaken to keep the public fully informed of the results of any research in respect of CJD. This report was entirely the work of the unit and was produced completely independantly of the the Department.
The statistical results regarding the consumption of venison was put into perspective in the body of the report and was not mentioned at all in the press release. Media attention regarding this report was low key but gave a realistic presentation of the statistical findings of the Unit. This approach to publication was successful in that consumption of venison was highlighted only once by the media ie. in the News at one television proqramme.
I believe that a further statement about the report, or indeed statistical links between CJD and consumption of venison, would increase, and quite possibly give damaging credence, to the whole issue. From the low key media reports of which I am aware it seems unlikely that venison consumption will suffer adversely, if at all.
http://web.archive.org/web/20030511010117/http://www.bseinquiry.gov.uk/files/yb/1994/10/00003001.pdf
Recently the question has again been brought up as to whether scrapie is transmissible to man. This has followed reports that the disease has been transmitted to primates. One particularly lurid speculation (Gajdusek 1977) conjectures that the agents of scrapie, kuru, Creutzfeldt-Jakob disease and transmissible encephalopathy of mink are varieties of a single "virus". The U.S. Department of Agriculture concluded that it could "no longer justify or permit scrapie-blood line and scrapie-exposed sheep and goats to be processed for human or animal food at slaughter or rendering plants" (ARC 84/77)" The problem is emphasized by the finding that some strains of scrapie produce lesions identical to the once which characterize the human dementias"
Whether true or not. the hypothesis that these agents might be transmissible to man raises two considerations. First, the safety of laboratory personnel requires prompt attention. Second, action such as the "scorched meat" policy of USDA makes the solution of the scrapie problem urgent if the sheep industry is not to suffer grievously.
snip...
76/10.12/4.6
IN CONFIDENCE
SCRAPIE TRANSMISSION TO CHIMPANZEES
IN CONFIDENCE
reference...
RB3.20
TRANSMISSION TO CHIMPANZEES
1. Kuru and CJD have been successfully transmitted to chimpanzees but scrapie and TME have not.
2. We cannot say that scrapie will not transmit to chimpanzees. There are several scrapie strains and I am not aware that all have been tried (that would have to be from mouse passaged material). Nor has a wide enough range of field isolates subsequently strain typed in mice been inoculated by the appropriate routes (i/c, ilp and i/v) :
3. I believe the proposed experiment to determine transmissibility, if conducted, would only show the susceptibility or resistance of the chimpanzee to infection/disease by the routes used and the result could not be interpreted for the predictability of the susceptibility for man. Proposals for prolonged oral exposure of chimpanzees to milk from cattle were suggested a long while ago and rejected.
4. In view of Dr Gibbs' probable use of chimpazees Mr Wells' comments (enclosed) are pertinent. I have yet to receive a direct communication from Dr Schellekers but before any collaboration or provision of material we should identify the Gibbs' proposals and objectives.
5. A positive result from a chimpanzee challenged severely would likely create alarm in some circles even if the result could not be interpreted for man. I have a view that all these agents could be transmitted provided a large enough dose by appropriate routes was given and the animals kept long enough. Until the mechanisms of the species barrier are more clearly understood it might be best to retain that hypothesis.
6. A negative result would take a lifetime to determine but that would be a shorter period than might be available for human exposure and it would still not answer the question regarding mans' susceptibility. In the meantime no doubt the negativity would be used defensively. It would however be counterproductive if the experiment finally became positive. We may learn more about public reactions following next Monday' s meeting.
R. Bradley
23 September 1990
CVO (+Mr Wells' comments)
Dr T W A Little
Dr B J Shreeve
90/9.23/1.1.
http://web.archive.org/web/20090506041740/http://www.bseinquiry.gov.uk/files/yb/1990/09/23001001.pdf
IN CONFIDENCE CHIMPANZEES
CODE 18-77 Reference RB3.46
Some further information that may assist in decision making has been gained by discussion with Dr Rosalind Ridley.
She says that careful study of Gajdusek's work shows no increased susceptibility of chimpanzees over New World Monkeys such as Squirrel Monkeys. She does not think it would tell you anything about the susceptibility to man. Also Gajdusek did not, she believes, challenge chimpanzees with scrapie as severely as we did pigs and we know little of that source of scrapie. Comparisons would be difficult. She also would not expect the Home Office to sanction such experiments here unless there was a very clear and important objective that would be important for human health protection. She doubted such a case could be made. If this is the case she thought it would be unethical to do an experiment abroad because we could not do it in our own country.
Retrospectively she feels they should have put up more marmosets than they did. They all remain healthy. They would normally regard the transmission as negative if no disease resulted in five years.
We are not being asked for a decision but I think that before we made one we should gain as much knowledge as we can. If we decided to proceed we would have to bear any criticisms for many years if there was an adverse view by scientists or media. This should not be undertaken lightly. There is already some adverse comment here, I gather, on the pig experiment though that will subside.
The Gibbs' (as' distinct from Schellekers') study is somewhat different. We are merely supplying material for comparative studies in a laboratory with the greatest experience of human SEs in the world and it has been sanctioned by USDA (though we do not know for certain yet if chimpanzees specifically will be used). This would keep it at a lower profile than if we conducted such an experiment in the UK or Europe.
I consider we must have very powerful and defendable objectives to go beyond Gibbs' proposed experiments and should not initiate others just because an offer has been made.
Scientists have a responsibility to seek other methods of investigative research other than animal experimentation. At present no objective has convinced me we need to do research using Chimpanzees - a species in need of protection. Resisting such proposals would enable us to communicate that information to the scientist and the public should the need arise. A line would have been drawn.
CVO cc Dr T Dr B W A Little Dr B J Shreeve
R Bradley
26 September 1990
90/9.26/3.2
http://web.archive.org/web/20090506041605/http://www.bseinquiry.gov.uk/files/yb/1990/09/26003001.pdf
this is tse prion political theater here, i.e. what i call TSE PRION POKER...tss
3. Prof. A. Robertson gave a brief account of BSE. The US approach was to accord it a very low profile indeed. Dr. A Thiermann showed the picture in the ''Independent'' with cattle being incinerated and thought this was a fanatical incident to be avoided in the US at all costs.
snip...
PAGE 26
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.
The occurrence of CWD must be viewed against the contest of the locations in which it occurred. It was an incidental and unwelcome complication of the respective wildlife research programmes. Despite its subsequent recognition as a new disease of cervids, therefore justifying direct investigation, no specific research funding was forthcoming. The USDA viewed it as a wildlife problem and consequently not their province! ...page 26.
snip...see;
IN CONFIDENCE
PERCEPTIONS OF UNCONVENTIONAL SLOW VIRUS DISEASE OF ANIMALS IN THE USA
GAH WELLS
REPORT OF A VISIT TO THE USA
APRIL-MAY 1989
why do we not want to do TSE transmission studies on chimpanzees $
5. A positive result from a chimpanzee challenged severly would likely create alarm in some circles even if the result could not be interpreted for man.
***> I have a view that all these agents could be transmitted provided a large enough dose by appropriate routes was given and the animals kept long enough.
***> Until the mechanisms of the species barrier are more clearly understood it might be best to retain that hypothesis.
snip...
MONDAY, FEBRUARY 25, 2019
***> MAD DOGS AND ENGLISHMEN BSE, SCRAPIE, CWD, CJD, TSE PRION A REVIEW 2019
*** The potential impact of prion diseases on human health was greatly magnified by the recognition that interspecies transfer of BSE to humans by beef ingestion resulted in vCJD. While changes in animal feed constituents and slaughter practices appear to have curtailed vCJD, there is concern that CWD of free-ranging deer and elk in the U.S. might also cross the species barrier. Thus, consuming venison could be a source of human prion disease. Whether BSE and CWD represent interspecies scrapie transfer or are newly arisen prion diseases is unknown. Therefore, the possibility of transmission of prion disease through other food animals cannot be ruled out. There is evidence that vCJD can be transmitted through blood transfusion. There is likely a pool of unknown size of asymptomatic individuals infected with vCJD, and there may be asymptomatic individuals infected with the CWD equivalent. ***These circumstances represent a potential threat to blood, blood products, and plasma supplies.
MONDAY, FEBRUARY 14, 2022
Atypical Nor98 Scrapie, Atypical BSE, CWD, Can Emerge As Different TSE PrP In Cross Species Transmission, A Volatile Situation For Human and Animal Health
FRIDAY, JANUARY 31, 2020
CJD TSE Prion Blood Products, iatrogenic transmission, Confucius is confused again, WHAT IF? Docket Number: FDA-2012-D-0307
Thursday, October 28, 2021
Chronic Wasting Disease (CWD) TSE Prion Zoonosis, friendly fire, iatrogenic transmission, blood products, sporadic CJD, what if?
Thursday, July 29, 2021
TSE PRION OCCUPATIONAL EXPOSURE VIA ANIMAL OR HUMAN, iatrogenic transmission, nvCJD or sCJD, what if?
Saturday, February 2, 2019
CWD GSS TSE PRION SPINAL CORD, Confucius Ponders, What if?
snip...
***> 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.'' Scientific opinion on chronic wasting disease (II) <***
REVIEW
***> In conclusion, sensory symptoms and loss of reflexes in Gerstmann-Sträussler-Scheinker syndrome can be explained by neuropathological changes in the spinal cord. We conclude that the sensory symptoms and loss of lower limb reflexes in Gerstmann-Sträussler-Scheinker syndrome is due to pathology in the caudal spinal cord. <***
***> The clinical and pathological presentation in macaques was mostly atypical, with a strong emphasis on spinal cord pathology.<***
***> The notion that CWD can be transmitted orally into both new-world and old-world non-human primates asks for a careful reevaluation of the zoonotic risk of CWD. <***
***> All animals have variable signs of prion neuropathology in spinal cords and brains and by supersensitive IHC, reaction was detected in spinal cord segments of all animals.<***
***> 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.'' Scientific opinion on chronic wasting disease (II) <***
Thursday, March 8, 2018
Familial human prion diseases associated with prion protein mutations Y226X and G131V are transmissible to transgenic mice expressing human prion protein
TUESDAY, MAY 11, 2021
***> A Unique Presentation of Creutzfeldt-Jakob Disease in a Patient Consuming Deer Antler Velvet <***
Conclusion
We believe that our patient’s case of CJD is highly suspicious for cervid etiology given the circumstances of the case as well as the strong evidence of plausibility reported in published literature. This is the first known case of CJD in a patient who had consumed deer antler velvet. Despite the confirmed diagnosis of CJD, a causal relationship between the patient’s disease and his consumption of deer antler velvet cannot be definitively concluded.
Supplemental data including molecular tissue sample analysis and autopsy findings could yield further supporting evidence. Given this patient’s clinical resemblance to CBD and the known histological similarities of CBD with CJD, clinicians should consider both diseases in the differential diagnosis of patients with a similarly esoteric presentation. Regardless of the origin of this patient’s disease, it is clear that the potential for prion transmission from cervids to humans should be further investigated by the academic community with considerable urgency.
''We believe that our patient’s case of CJD is highly suspicious for cervid etiology given the circumstances of the case as well as the strong evidence of plausibility reported in published literature. This is the first known case of CJD in a patient who had consumed deer antler velvet. Despite the confirmed diagnosis of CJD, a causal relationship between the patient’s disease and his consumption of deer antler velvet cannot be definitively concluded.''
cwd consumption, exposure, friendly fire there from, iatrogenic, what if?
Friday, March 11, 2022
Prevalence of Surgical Procedures at Symptomatic Onset of Prion Disease
Saturday, April 9, 2022
EFSA EU Request for a scientific opinion on the monitoring of Chronic Wasting Disease (CWD) EFSA-Q-2022-00114 M-2022-00040 Singeltary Submission
***> Please send relevant new references and proposed modifications to the OIE Science Department (scientific.dept@oie.int). <***
TUESDAY, MARCH 29, 2022
***> OIE Agent causing chronic wasting disease (CWD) TSE Prion of Cervid <***
TUESDAY, APRIL 26, 2022
Chronic Wasting Disease (CWD) in Cervids and the Consequences of a Mutable Protein Conformation
KOREA CWD UPDATE
FRIDAY, MARCH 18, 2022
Korea Chronic Wasting Disease CWD TSE PrP Update Increase of Positive Cases and Polymorphisms of the prion-related protein gene
IN 235 elks, 22 elks (9.4%) were infected with CWD.
IN 257 red deer, 78 red deer (30.4%) were infected with CWD.
IN 150 sika deer, 16 sika deer (10.7%) were infected with CWD.
THURSDAY, FEBRUARY 17, 2022
Captive Cervids and their Contribution to CWD
Published: 06 September 2021
***> Chronic wasting disease: a cervid prion infection looming to spillover
Alicia Otero, Camilo Duque Velásquez, Judd Aiken & Debbie McKenzie
Veterinary Research volume 52, Article number: 115 (2021)
FRIDAY, FEBRUARY 11, 2022
Passage of the CWD agent through meadow voles results in increased attack rates and decreased incubation periods in raccoons
TUESDAY, APRIL 26, 2022
Susceptibility of Beavers to Chronic Wasting Disease
SATURDAY, APRIL 23, 2022
Texas Parks and Wildlife threatens to euthanize deer at North Texas ranch over chronic wasting disease
SUNDAY, MARCH 20, 2022
CHRONIC WASTING DISEASE CASES CWD STATUS OF CAPTIVE HERDS AS OF February 2022
SUNDAY, JANUARY 23, 2022
Pennsylvania Chronic Wasting Disease CWD TSE PrP Surveillance 2021 2022 Update
THURSDAY, MARCH 31, 2022
PENNSYLVANIA CWD SURVEILLANCE
USDA TO PGC ONCE CAPTIVES ESCAPE
*** "it‘s no longer its business.”
http://chronic-wasting-disease.blogspot.com/2013/01/usda-to-pgc-once-captives-escape-its-no.html
EFSA ONE Conference 2022 Chronic Wasting Disease CWD TSE PrP of Cervid and Zoonosis Zoonotic Transmission Singeltary Submission
TUESDAY, MARCH 29, 2022
OIE Agent causing chronic wasting disease (CWD) TSE Prion of Cervid
Saturday, April 9, 2022
EFSA EU Request for a scientific opinion on the monitoring of Chronic Wasting Disease (CWD) EFSA-Q-2022-00114 M-2022-00040 Singeltary Submission
PENNSYLVANIA HISTORY CWD TSE PrP AND GAME FARMS
PENNSYLVANIA NEWLY DETECTED CWD-POSITIVE LEADS TO DMA3 EXPANSION AND A NEW DMA
NEWLY DETECTED CWD-POSITIVE LEADS TO DMA3 EXPANSION AND A NEW DMA
10/22/2021
HARRISBURG, PA - A CWD-positive deer recently detected in Jefferson County has led to new regulations to reduce the risk of the disease spreading.
The Pennsylvania Game Commission today announced the expansion of Disease Management Area 3 (DMA 3) and the creation of a new DMA (DMA 6).
Detection of Chronic Wasting Disease (CWD) in a road-killed deer on the northern boundary of DMA3 prompted these changes. The adult male was collected as part of ongoing CWD surveillance efforts.
CWD affects deer, elk, and other members of the deer family. The disease is fatal to any deer or elk infected with it, and CWD has no treatment or cure.
When a new CWD-positive is detected in either a wild or captive deer or elk in Pennsylvania, a Disease Management Area (DMA) is established. DMAs are created to reduce risk of human-assisted spread of CWD.
This new CWD detection is within 2 miles of Pennsylvania’s elk management area. The short distance to the elk management area required creating DMA 6 within the elk management area. DMA 6 will prevent high-risk parts from the entirety of DMA 3 being moved into the elk management area.
“If a CWD-positive animal is found within any elk hunt zone, all elk hunt zones will become a DMA due to the behavior and longer distance movements of elk,” said Andrea Korman, Game Commission CWD wildlife biologist. “If this were to occur, the impact on deer and elk populations, hunters, and the public will be significant. Although this has not occurred yet, this newly found positive deer shows how close it is.”
DMA 6 was created to restrict movement of high-risk parts into the elk management area and to restrict human activities known to increase disease risk.
Within all DMAs, it is unlawful to:
Remove or export any deer or elk high-risk parts (e.g., head, spinal column, and spleen) from a DMA. This also prevents movement of high-risk parts between adjacent DMAs
Use or possess deer or elk urine-based attractants
Directly or indirectly feed wild, free-ranging deer. It is already illegal to feed elk regardless of DMA location
Rehabilitate wild, free-ranging deer or elk
To increase surveillance around the detection, a new DMAP Unit (#4760) was also created. Over 1,300 permits have been made available for this unit and allow hunters to take up to two additional antlerless deer. Hunters can get DMAP permits by providing the unit number (4760) online or at license-issuing agents.
In conjunction with the additional hunting opportunities, hunters are asked to provide samples for CWD testing. Submitting harvested deer heads for CWD testing helps determine the extent of CWD infection.
The Game Commission offers free CWD testing within the DMAs. Hunters should deposit the heads of deer they harvest with properly filled out and legible harvest tags in one of the head-collection containers the Game Commission provides within DMAs. Locations of head-collection containers can be found at http://bit.ly/PGC-CWDMapOpens In A New Window. Antlers should be removed from bucks before the double-bagged head is placed in a collection container. Hunters can check for their test results online or by calling the CWD hotline (1-833-INFOCWD).
For deer hunters in DMAs – especially those who live outside the DMA – it’s important to plan their hunt and know ahead of time what they will do with any deer harvested. Since high-risk cervid parts can’t be removed from any DMA, even if they share a boundary like DMAs 3 and 6, successful hunters cannot transport whole deer outside the DMA.
Hunters can take deer they harvest to a processor within the DMA or on the list of approved processors for the DMA where they harvested the deer. The list of approved processors and taxidermists is available at www.pgc.pa.gov/CWD. Approved processors properly dispose of the high-risk parts. Hunters can also dispose of high-risk parts in trash that is destined for a landfill or quarter the animal and leave the high-risk parts at the kill site. The meat, antlers (free of brain material) and other low-risk parts then can be transported outside the DMA.
Deer hunters getting taxidermy mounts also must take their harvests to a taxidermist within the DMA or on the list of approved processors and taxidermists for the DMA in which they harvested the deer available at www.pgc.pa.gov/CWD.
Although CWD has not been documented in humans, the Centers for Disease Control and Prevention recommends never eating the meat of a CWD-positive deer.
Much more information on CWD is available at www.pgc.pa.gov/CWD.
DMA 3 boundary has been expanded and is as follows:
Beginning at the southernmost point at the intersection of State Highway 403 and State Highway 286 in the town of Clymer, proceed east on State Highway 286 for 4.9 miles to State Highway 240. Follow in State Highway 240 east for 8.5 miles to the intersection of US Highway 219. Follow US Highway 219 north for 2.4 miles to Sylvis Road. Follow Sylvis Road east for 5.8 miles to the intersection of State Highway 36. Follow State Highway 36 east for 8.8 miles to the intersection of La Jose Road (SR-3016) in Newburg. Follow La Jose Road east for 3.6 miles becoming Cherry Corner Road (SR-3005) for another .3 mile to the intersection of Marron Road (SR-3016). Turn left onto Marron Road and follow northeast for 2.7 miles to the intersection of State Road 729. Follow State Road 729 east for .9 miles to the intersection of Old Station Road. Follow Old Station Road (SR-2012) east for 2.4 miles to the intersection of Douglas Road (SR-3007). Continue east on Douglas Road for .3 miles to the intersection of Zion Road (SR-2012) near New Millport. Follow Zion Road east for 4.5 miles to the intersection of Faunce Road (SR-2012). Turn right and follow Faunce Road east for 3.1 miles becoming Sanborn Road (SR-2012) in Woodward Township. Continue east on Sanborn Road for 2.5 miles to the intersection of State Highway 153. Follow State Highway 153 north for 5 miles to the intersection of Valley Road (SR-2027). Follow Valley Road north for 2.1 miles becoming Hogback Hill Road (SR-2027). Continue north on Hogback Hill Road for 1 mile to the intersection of Main Street in Mineral Springs. Turn right on Main Street for .2 miles to the intersection of Bigler Cutoff Road. Turn left on Bigler Cutoff Road for .1 miles to the intersection of US Highway 322. Follow US Highway 322 east for .7 miles to the intersection of State Highway 970. Follow State Highway 970 north for 1.5 miles to the intersection of Interstate Highway 80. Follow I-80 west for 26.4 miles to the exit for State Highway 219 north. Follow State Highway 219 north for 21.2 miles to Boot Jack becoming State Route 948. Follow State Route 948 for 4.2 miles to the Clarion River in Ridgway. Follow the Clarion River for 28.3 miles to Bridge Road. Continue south on Bridge Road for 0.05 mile to the intersection of State Highway 949. Turn right on State Highway 949 and continue west for 16.3 miles to the intersection of US Highway 322 in Corsica. Follow US Highway 322 east for 0.3 miles to the intersection of State Highway 949. Follow State Highway 949 south for 4.2 miles to the intersection of State Highway 28. Follow State Highway 28 south for 13.2 miles to the intersection of State Highway 839 in New Bethlehem. Follow State Highway 839 south for 21 miles to State Highway 85. Follow State Highway 85 south for 11.7 miles to the intersection of US Highway 119 in the town of Home. Turn left on US Highway 119 and follow 3.4 miles to the intersection of State Highway 403 in Marion Center. Follow State Highway 403 south for 8.5 miles to Clymer at the place of beginning.
DMA 6 is in portions of Clearfield, Elk, and Jefferson Counties and its exact boundary is as follows:
Beginning at the northeast corner at the intersection of Chicken Hill Road and State Route 948 in the town of Kersey, proceed south on Chicken Hill Road for 0.9 mile becoming South Kersey Road. Follow South Kersey Road south for 1.4 miles. Continue straight onto Boone Mountain Road for 6.5 miles to the intersection with State Route 153. Turn left onto State Route 153 and continue south 4.9 miles to State Route 255. Turn right on State Route 255 and continue south for 9.5 miles to Interstate Highway 80. Turn right on Interstate Highway 80 and continue west 4.4 miles to State Highway 219. Turn right on State Highway 219 and continue north 21.1 miles to State Route 948. Turn right on State Route 948 and proceed east for 5.3 miles to Kersey at the place of beginning.
MEDIA CONTACT: Travis Lau - 717-705-6541
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SATURDAY, OCTOBER 23, 2021
PENNSYLVANIA NEWLY DETECTED CWD-POSITIVE LEADS TO DMA3 EXPANSION AND A NEW DMA
Wednesday, May 26, 2021
Pennsylvania Department of Agriculture today announced a confirmed positive for CWD in a white-tailed deer on a Warren County hunting preserve
TUESDAY, MARCH 09, 2021
Pennsylvania 2020 Annual Report Updated CWD samples collected so far this year 196 were positive
THURSDAY, APRIL 08, 2021
Pennsylvania 2020 2021 had 162 CWD Violations with 196 Positive for the year
The Department of Agriculture never did have any interest in stopping cwd in the captive farms, and history shows this.
THEY as much as said so back in 2013;
USDA TO PGC ONCE CAPTIVES ESCAPE "it‘s no longer its business.”
SUNDAY, JANUARY 06, 2013
USDA TO PGC ONCE CAPTIVES ESCAPE "it‘s no longer its business.”
Commission, sportsmen pay for fences around deer farm
Published: Saturday, January 5, 2013, 8:54 p.m. Updated 12 hours ago
Sportsmen have paid to keep wild deer from accessing a farm connected to the discovery of chronic wasting disease this past fall.
The bill, to rebuild fences, was not theirs to pay. But pay it they did, through the Pennsylvania Game Commission.
The farm is located in York County. No wasting disease was found there. But it was one of the first four put under quarantine by the Pennsylvania Department of Agriculture because of its connection to an Adams County farm where the disease was discovered. The quarantine means, among other things, that fences are to be maintained so that wild deer cannot move onto the property and perhaps contract the disease.
The department of agriculture — in response to questions in a letter from the Pennsylvania federation of Sportsmen‘s Clubs — indicated re-fencing should occur. It said its quarantine order allows for criminal and civil penalties against deer farmers who don‘t live up to its mandates.
“This provides a very strong incentive to re-fence such areas,” its letter to the Federation reads.
But with no fences rebuilt months after the disease‘s discovery and no indication that they would be any time soon, the Game Commission decided it couldn‘t wait any longer. It paid to re-fence the farm in an attempt to protect wild deer.
“We would have waited a long, long time ... putting free-roaming deer at risk,” said Cal DuBrock, director of the commission‘s bureau of wildlife management. “It was an investment worth making.”
Commission executive director Carl Roe did not say how much money the agency spent, but said “it was an expense.”
In the meantime, the commission is taking a more aggressive approach to dealing with escaped deer.
Two such animals got loose from deer farms this fall. The department of agriculture — again, to the consternation of the Federation — did not notify the public of the escapes. It explained its silence by saying that once a deer is outside a fence, whether it got there intentionally or not, it‘s no longer its business.
“The department … defers to the Game Commission once a deer is considered wild or free ranging,” reads its letter to the Federation. Because such escapes are “numerous” in any given year, DuBrock said, the commission has asked the agriculture department to immediately notify executive director Carl Roe, DuBrock and veterinarian Walt Cottrell of them. From there, wildlife conservation officers have the green light to shoot those deer as soon as safely possible “and figure out the ownership later,” DuBrock said.
Bob Frye is a staff writer for Trib Total Media. Reach him at bfrye@tribweb.com or via Twitter @bobfryeoutdoors.
ALSO;
”The occurrence of CWD must be viewed against the contest of the locations in which it occurred. It was an incidental and unwelcome complication of the respective wildlife research programmes. Despite it’s subsequent recognition as a new disease of cervids, therefore justifying direct investigation, no specific research funding was forthcoming. The USDA viewed it as a wildlife problem and consequently not their province!” page 26.
the movement of captive cervid is absolutely one of the greatest risk imo for cwd. especially breeder release.
THEY CALL IT TRUCKING CWD TSE PRP!
SCIENCE SHOWS THIS!
SEE;
CHRONIC WASTING DISEASE CASES CWD STATUS OF CAPTIVE HERDS AS OF February 2022
2/23/2022 4.5 Y Male PA Lancaster WTD Shooter No No 93 Quarantine
1/5/2022 4.5 Y Female PA Lycoming WTD Shooter No No 177 Quarantine
10/14/2021 11.5 Y Female PA Fulton WTD Hobby No No 1 Quarantine
10/14/2021 2.5 Y Male PA Bedford WTD Breeder No No 70 Quarantine
10/12/2021 4.5 Y Female PA Indiana Red Deer Shooter No No 14 Quarantine
10/5/2021 1.5 Y Male PA Bedford WTD Shooter No No 50 Quarantine 9/27/2021 Y Male WI Vilas WTD Shooter No No Quarantine
9/27/2021 4.5 Y Male PA Huntingdon WTD Breeder No No 137 Quarantine
9/21/2021 1 Y Male PA Blair WTD Breeder No No 26 Quarantine
9/9/2021 3.5 Y Male PA Bedford WTD Breeder No No 36 Quarantine
8/26/2021 4 Y Male PA Bedford WTD Shooter No No >200 Quarantine
5/28/2021 9 Y Female PA Bedford WTD Breeder No No 29 Quarantine
5/12/2021 2.5 Y Male PA Warren WTD Shooter No No 19 Depopulated
4/20/2021 Six positives PA Bedford WTD Breeder Traceback No No 87 Depopulated
3/29/2021 4 Y Female PA Blair WTD Breeder No NA 11 Quarantine
3/19/2021 3.75 Y Male PA Bedford WTD Hobby No NA 8 Quarantine
2/8/2021 3.5 Y Male PA Blair WTD Shooter No NA 19 Quarantine
12/30/2020 Ukn Y Female PA Bedford WTD Shooter No NA 51 Quarantine
12/15/2020 2.5 Y Female PA Fulton WTD Hobby No NA 19 Quarantine
10/29/2020 2 Y Male PA Somerset WTD Shooter No No 0 Depopulated
snip...see full text;
CHRONIC WASTING DISEASE CASES CWD STATUS OF CAPTIVE HERDS AS OF February 2022
CHRONIC WASTING DISEASE CASES CWD STATUS OF CAPTIVE HERDS
Date of Index Case Confirmation Index Case State County Species Herd Type HCP Enrolled HCP Certified Number of Animals Herd Status
2/23/2022 4.5 Y Male PA Lancaster WTD Shooter No No 93 Quarantine
1/12/2022 6.5 Y Female WV Hardy WTD Shooter Yes Yes 18 Quarantine
1/5/2022 4.5 Y Female PA Lycoming WTD Shooter No No 177 Quarantine
11/8/2021 3 Y Male WI Waukesha WTD/ Elk Breeder Yes Yes 22 Quarantine
11/4/2021 2, 3 Y Male MI Kent Elk Breeder Yes Yes 0 Depopulated
10/18/2021 9 Y Female WI Portage WTD Shooter No No 370 Quarantine
10/14/2021 11.5 Y Female PA Fulton WTD Hobby No No 1 Quarantine
10/14/2021 2.5 Y Male PA Bedford WTD Breeder No No 70 Quarantine
10/12/2021 4.5 Y Female PA Indiana Red Deer Shooter No No 14 Quarantine
10/5/2021 1.5 Y Male PA Bedford WTD Shooter No No 50 Quarantine 9/27/2021 Y Male WI Vilas WTD Shooter No No Quarantine
9/27/2021 4.5 Y Male PA Huntingdon WTD Breeder No No 137 Quarantine
9/21/2021 1 Y Male PA Blair WTD Breeder No No 26 Quarantine
9/9/2021 3.5 Y Male PA Bedford WTD Breeder No No 36 Quarantine
9/2/2021 11 Y Female WI Outagamie WTD Breeder Yes Yes 31 Quarantine
8/31/2021 1 Y Female WI Langlade WTD Breeder Yes Yes 58 Quarantine
8/31/2021 2 Y Male WV Hampshire WTD Breeder Yes Yes 23 Quarantine
8/26/2021 4 Y Male PA Bedford WTD Shooter No No >200 Quarantine
8/24/2021 3Y Female TX Duval WTD Breeder No No 188 Quarantine
8/11/2021 6 Y Female WI Taylor WTD Breeder Yes Yes 220 Quarantine
8/9/2021 9 Y Male WI Sauk WTD Hobby No No 1 Quarantine
7/15/2021 4 Y Female MI Montcalm WTD Breeder No No 109 Quarantine
6/15/2021 4 Y Female TX Uvalde WTD Breeder & Shooter No No 1000+ Quarantine
5/28/2021 9 Y Female PA Bedford WTD Breeder No No 29 Quarantine
5/12/2021 2.5 Y Male PA Warren WTD Shooter No No 19 Depopulated
5/10/2021 3 Y Female MN Beltrami WTD Breeder No No 61 Depopulated
4/20/2021 Six positives PA Bedford WTD Breeder Traceback No No 87 Depopulated
4/20/2021 1.5 Y Male TX Mason WTD Breeder Traceback Yes Yes 93 Depopulated
4/20/2021 1.5 Y Male TX Matagorda WTD Breeder Traceback Yes No 221 Depopulated
4/18/2021 2.5 Y Male MI WTD Shooter No No ukn Quarantine
3/30/2021 3.5 Y, 2.5 Y, 3.5Y TX Uvalde WTD Breeder Yes Yes 61 Quarantine
3/30/2021 2.5 Y & 1.5 Y TX Uvalde WTD Breeder Yes No 318 Quarantine
3/29/2021 3Y Female TX Hunt WTD Breeder Yes No 381 Quarantine
3/29/2021 4 Y Female PA Blair WTD Breeder No NA 11 Quarantine
3/19/2021 3.75 Y Male PA Bedford WTD Hobby No NA 8 Quarantine
3/3/2021 4 Y Male MI Montcalm WTD Shooter No NA 14 Quarantine
2/8/2021 3.5 Y Male PA Blair WTD Shooter No NA 19 Quarantine
12/30/2020 Ukn Y Female PA Bedford WTD Shooter No NA 51 Quarantine
12/15/2020 2.5 Y Female PA Fulton WTD Hobby No NA 19 Quarantine
11/18/2020 2.5 Y Female KS Rawlins MD Breeder Yes Yes 70 Quarantine
10/29/2020 2 Y Male PA Somerset WTD Shooter No No 0 Depopulated
10/14/2020 2 Y Male SD Custer Elk Breeder/Hobby No NA 6 Quarantine
10/14/2020 2.5 Y Female MN Houston WTD Breeder Yes yes 49 Quarantine
10/1/2020 MT WTD Breeder No NA 17 Depopulated
10/1/2020 4 Y Male WI Washburn WTD Breeder Yes No 21 Quarantine
9/23/2020 6 Y Female UT Duchesne Elk Breeder No NA 55 Partial Depopulation/ Quarantine
7/2/2020 3 Y Female KS Osage Elk Breeder Yes Yes 20+ Depopulated
Updated February 2022
snip...see full list ;
***> Pennsylvania Chronic Wasting Disease CWD TSE PrP Surveillance 2021-22 PA Hunting & Trapping Digest
The Game Commission began monitoring CWD in 1998, more than 10 years prior to the state’s first CWD detection.
As of March 2021, more than 100,000 deer had been tested for CWD in Pennsylvania.
Surveillance efforts include testing road-killed deer, hunterharvested deer, escaped captive deer, and deer showing clinical signs of CWD.
In addition, all hunter-harvested elk are tested for CWD.
As of March 2021, a total of 689 free-ranging deer had tested positive for CWD in Pennsylvania, 679 of them within DMA 2 and the remaining 10 in DMA 3. CWD only has been detected in captive deer in DMA 4.
ESTABLISHED AREA
An Established Area (EA) is a portion of a DMA where CWD detections occur contiguously and consistently from year to year.
In an EA, CWD is considered to be established within the deer population and, coupled with environmental contamination, poses a long-term threat to neighboring areas.
Pennsylvania has one EA, located within the larger boundaries of DMA 2. It includes all or parts of Blair, Bedford, Franklin, Fulton and Huntingdon counties. That’s all of WMU 4A and a portion of WMU 2C.
CWD sample prevalence rates in Pennsylvania’s Established Area (EA) have been climbing and, as of March 2021, stood at roughly 14 percent in hunterharvested adult deer. That means nearly one in seven hunter-harvested adult deer that were sampled for CWD tested positive for the disease.
Experiences from other states suggest that, with no change, CWD prevalence among deer in Pennsylvania’s Established Area (EA) will continue to increase without deer population reductions.
There are regulations in place within the EA to reduce the risk of human-assisted spread of CWD. Within an EA it is unlawful to:
• Remove or export any cervid high-risk parts from an EA.
• Use or possess cervid urine-based attractants.
• Directly or indirectly feed any wild, free- ranging cervids.
• Rehabilitate wild, free-ranging cervids.
***> As of March 2021, a total of 689 free-ranging deer had tested positive for CWD in Pennsylvania
Pennsylvania Map Captive Dashboard
Pennsylvania: Eight new CWD positive herds
Breeding herd of 33 WTD, HCP certified, depopulated with Federal indemnity
Breeding herd of 6 WTD, not in HCP, depopulated with Federal indemnity
Breeding herd of 15 WTD, not in HCP, depopulated by owner\
Hunt preserve of 58 WTD, not in HCP, populated and under quarantine
Breeding herd of 75 WTD, not in HCP, populated and under quarantine
Breeding herd of WTD, not in HCP, populated and under quarantine
Breeding herd of 90 WTD, not in HCP, populated and under quarantine
Breeding herd of 4 WTD, not in HCP, populated and under quarantine
snip...see full text;
Voluntary Chronic Wasting Disease Herd Certification Program Annual Update, FY2020
Last Modified: Feb 9, 2021
U.S. Department of Agriculture
Animal and Plant Health Inspection Service (APHIS) Veterinary Services
Annual Update from the Cervid Health Team
Voluntary Chronic Wasting Disease Herd Certification Program (HCP)
The APHIS National CWD Herd Certification Program (HCP) was implemented in 2014. It is a voluntary Federal-State-industry cooperative program administered by APHIS and implemented by participating States. The program provides uniform national herd certification standards that minimize the risk of spreading CWD in farmed cervid populations. Participating States and herd owners must comply with requirements for animal identification, fencing, recordkeeping, inspections/inventories, as well as animal mortality testing and response to any CWD-exposed, suspect, and positive herds. APHIS monitors the Approved State HCPs to ensure consistency with Federal standards through annual reporting by the States.
With each year of successful surveillance, herds participating in the HCP will advance in status until reaching five years with no evidence of CWD, at which time herds are certified as being low risk for CWD. Only farmed cervids from enrolled herds certified as low risk for CWD may move interstate. FY 2020 marks the eighth year that Approved States have submitted their CWD HCP annual reports to APHIS.
The current Cervid Health Program staff officers are as follows: Dr. Mark Lyons, Dr. Jennifer Siembieda, and Dr. Tracy Nichols
Voluntary Herd Certification Participation Summary
Currently, 28 States participate in the voluntary CWD Herd Certification Program encompassing 2,145 enrolled herds, of which, 1,723 had the certified status in the program.
1,616 enrolled deer herds, of which, 1,297 were certified
371 enrolled elk herds, of which, 328 were certified
147 enrolled mixed species herds, of which, 98 were certified CWD in Farmed Cervids Summary of CW Detections
There were 22 newly identified CWD positive herds in FY20
13 of these herds were not participants in the Federal HCP
2 herds were considered enrolled in the HCP
7 herds were certified in the HCP
Half of the herds were located within 20 miles of identified CWD in the wild, half were not CWD Herds by State
Pennsylvania: Eight new CWD positive herds
Breeding herd of 33 WTD, HCP certified, depopulated with Federal indemnity
Breeding herd of 6 WTD, not in HCP, depopulated with Federal indemnity
Breeding herd of 15 WTD, not in HCP, depopulated by owner\
Hunt preserve of 58 WTD, not in HCP, populated and under quarantine
Breeding herd of 75 WTD, not in HCP, populated and under quarantine
Breeding herd of WTD, not in HCP, populated and under quarantine
Breeding herd of 90 WTD, not in HCP, populated and under quarantine
Breeding herd of 4 WTD, not in HCP, populated and under quarantine
Iowa: Two new CWD positive herds
Breeding herd of 23 WTD, HCP certified, depopulated with Federal indemnity
Breeding herd of 13 WTD, HCP certified, depopulated with Federal indemnity
Minnesota: Two new CWD positive herds
Breeding herd of 3 WTD, enrolled in HCP, not certified, depopulated by owner
Breeding herd of 6 WTD, enrolled in HCP, not certified, depopulated with Federal indemnity
Colorado: Two new CWD positive herds
Breeding herd/hunt preserve of 9 elk, HCP certified, depopulated by owner
Breeding herd of 8 elk, HCP certified, populated and under quarantine
Utah: Two new CWD positive herds
Breeding herd of 465 elk, not in HCP, partial depopulation with Federal indemnity- removed purchased animals, populated-quarantine
Breeding herd of 103 elk, not in HCP, partial depopulation with Federal indemnity- removed purchased animals, populated-quarantine
Michigan: One new CWD positive herd
Hunt preserve of >600 WTD, not in HCP, populated and under quarantine Montana: One new CWD positive herd
Breeding herd of 3 elk, not in HCP, populated and under quarantine
Texas: one new CWD positive herd
Breeding herd of 59 WTD, not in HCP, depopulated with Federal indemnity
Kansas: One new CWD positive herd
Breeding herd of 20 elk, HCP certified, depopulated with Federal indemnity
Ohio: Eight new CWD positive herd
Breeding herd of 138 WTD, HCP certified, depopulated with Federal indemnity
Research
Whole genome study investigating the association of genetics with CWD susceptibility has been published.
Blinded validation of the genetic predicative model is almost complete
A standardized protocol has been developed, in partnership with ARS, USGS, University of WI, and NIH for tissue sample testing using RT-QuIC
A study is starting shortly to determine the sensitivity and specify of RT-QuIC utilizing the standardized protocol
Cervid Tuberculosis
snip...
USDA Animal and Plant Health Inspection Service 2020 IMPACT REPORT
Collected 916 samples for chronic wasting disease (CWD) testing and removed 1,863 cervids for CWD management/sampling with $685,400 in State cooperative funding to help combat this fatal animal disease
U.S. Department of Agriculture Animal and Plant Health Inspection Service (APHIS) Veterinary Services Annual Update from the Cervid Health Team Fiscal Year (FY) 2019
Voluntary Chronic Wasting Disease (CWD) Herd Certification Program
The APHIS National CWD Herd Certification Program (HCP) was implemented in 2014. It is a voluntary Federal-State-industry cooperative program administered by APHIS and implemented by participating States. The program provides uniform national herd certification standards that minimize the risk of spreading CWD in farmed cervid populations. Participating States and herd owners must comply with requirements for animal identification, fencing, recordkeeping, inspections/inventories, as well as animal mortality testing and response to any CWD-exposed, suspect, and positive herds. APHIS monitors the Approved State HCPs to ensure consistency with Federal standards through annual reporting by the States.
With each year of successful surveillance, herds participating in the HCP will advance in status until reaching five years with no evidence of CWD, at which time herds are certified as being low risk for CWD. Only farmed cervids from enrolled herds certified as low risk for CWD may move interstate. Currently, 28 States participate in the voluntary CWD Herd Certification Program and have Approved HCPs. FY 2019 marks the seventh year that Approved States have submitted their CWD HCP annual reports to APHIS. In FY 2019 there were 2,192 enrolled cervidae herds: 1,696 deer, 361 elk and 135 mixed species herds. Of those, there were 1,748 certified cervidae herds: 1,337 deer, 314 elk and 97 mixed species herds.
CWD in Farmed Cervids
Summary of CWD detections. As of September 30, 2019, CWD has been confirmed in wild deer and elk in 23 U.S. States, and in farmed cervids in 17 States. In total, 26 States have identified CWD in wild and/or farmed cervids. CWD has been reported in 117 farmed cervid herds in the United States.
FY 2019 CWD Detections in Farmed Cervids: Seventeen newly-identified CWD positive farmed cervid herds were identified in FY 2019 (9 white-tailed deer, 6 elk, and 2 mixed herds). Twelve herds were within 20 miles of confirmed CWD positives in the wild.
Pennsylvania: November, 2018: NVSL confirmed CWD in a three and a half year old white-tailed doe in Fulton County. The doe was a natural addition to the 23 head breeding deer herd that sits within a half mile of where CWD has been identified in the wild. This herd was not enrolled in the HCP and was depopulated with Federal funds in April of 2019. All 23 depopulated animals were found to be CWD positive.
2
January, 2019: NVSL confirmed CWD in a three and a half year old white-tailed buck in Clearfield County. The buck was a purchased addition to a hunt preserve of 12 whitetailed deer that was not a participant in the Federal HCP. This animal resided on the preserve four days before being hunted. The animal was traced back to an HCP-certified breeding herd in Fulton County within a CWD-endemic area. This breeding herd consisted of 137 white-tailed deer and was depopulated in May, 2019 with Federal indemnity. There were 27 additional positives identified at depopulation.
April, 2019: NVSL confirmed CWD in one three and one four year old white-tailed doe in a breeding herd in Fulton County in a CWD-endemic area. The herd consists of 12 whitetailed deer and is not enrolled in the Federal HCP. The herd is under quarantine and the owner will depopulate.
May, 2019: NVSL confirmed CWD in a two and a half year old white-tailed buck in Fulton County. The buck was a natural addition to the 320 head breeding deer herd that lies within a CWD-endemic area. This herd was not enrolled in the Federal HCP and is under quarantine. To date, eight additional CWD-positive animals have been identified from this herd.
June, 2019: NVSL confirmed CWD in a six year old white-tailed doe in Perry County. The doe was a natural addition to the 222 head breeding deer herd that lies within a CWD endemic area. This herd was double fenced and certified in the Federal HCP. It is currently under quarantine.
Wisconsin:
January, 2019: NVSL confirmed CWD in a six year old white-tailed buck in a Forrest County hunt preserve. This herd was already under a trace quarantine from a breeding facility in Marinette County in FY18 and is not enrolled in the Federal HCP. This hunt preserve consists of approximately 399 animals, is not in a CWD endemic area, and remains under quarantine.
June, 2019: NVSL confirmed CWD in a two and a half year old white-tailed buck in Portage County. The buck was a purchased addition to a hunt preserve of 151 white-tailed deer not enrolled in the Federal HCP. CWD has been detected 11 miles from this site. The index animal resided there for five days prior to being harvested. This herd was depopulated with State indemnity and no additional positive cases were found. The source herd for the index animal was a double-fenced, federally certified HCP breeding herd within a CWD-endemic area consisting of 42 white-tailed deer. The herd was depopulated with Federal funds. An additional six CWD-positive animals were identified at depopulation.
August, 2019: NVSL confirmed CWD in a six year old elk bull in in Burnette County. The bull was a purchased addition to a small breeding herd of five elk five years prior to CWD detection. The herd is certified in the Federal HCP, within an area endemic for CWD, and is currently under quarantine.
3
South Dakota:
January, 2019: NVSL confirmed CWD in a two year old elk cow in Clark County. The cow was a purchased addition to the herd, which was certified in the Federal HCP. The herd consisted of 18 animals and was depopulated with Federal funds in October, 2019. CWD test results are pending. CWD has not been identified in the wild in this area. The source herd for this animal was in Meade County certified in the Federal HCP. CWD was identified in a seven year old bull and an eight year old cow elk in September, 2019. This herd consisted of five animals, was not in a CWD-endemic area, and was depopulated with Federal funds in October, 2019. CWD test results are pending.
Colorado:
October, 2018: NVSL confirmed CWD in a seven year old cow elk from a hunt preserve in Mesa County. The bull was a purchased addition and was moved into a pasture that had previously contained CWD-positive animals. This herd is certified in the Federal HCP certified, consists of 191 animals, and remains under quarantine.
November, 2018: NVSL confirmed CWD in a one and a half year old elk bull in Jackson County. The bull was a natural addition to the herd which is certified in the Federal HCP and consists of 42 animals within a CWD-endemic area. This herd is under quarantine.
Michigan:
September, 2019: NVSL confirmed CWD in a two year old female white-tailed deer in Montcalm County. The doe was a natural addition to the breeding herd which consists of 50 white-tailed deer. This herd is not enrolled in the Federal HCP, is within a CWDendemic area, and is under quarantine.
Nebraska: September, 2019: NVSL confirmed CWD in a five year old elk cow in Buffalo County. The cow was a purchase addition to the herd in 2018. This is a breeding herd of 48 elk and it is not enrolled in the Federal HCP. The herd is currently under quarantine and is not in an area where CWD has been identified. The source herd of this animal was an HCPcertified herd in Lincoln County, Oklahoma.
Oklahoma: April, 2019: NVSL confirmed CWD in a two year old elk bull in and in a two year old elk cow in May, 2019 in Lincoln County. Both were natural additions to the herd. This herd was certified in the Federal HCP and consisted of 246 elk in the breeding area, and more than 50 in the hunt preserve. Animals in the breeding facility and hunt preserve were depopulated with Federal funds in August and September, 2019. No additional CWD positive animals were identified.
4
Cervid Health Program Staffing
The USDA APHIS Cervid Health Program (CHP) has undergone some organizational and staffing changes in FY19. Small ruminant health programs including CHP are now a part of the Ruminant Health Center under the direction of Dr. Alecia Naugle. Dr. Diane Sutton is the Ruminant Health Center Assistant Director for small ruminant health programs. Dr. Nancy Hannaway is no longer with the CHP and Drs. Byron Schick and Tracy Nichols are the current CHP points of contact. Dr. Nichols is primary for CWD policy, research coordination and tissue archive. Dr. Schick is primary for cervid indemnity, cervid TB and brucellosis policy, and CWD annual reporting.
CWD Program Standards
The CWD Program Standards were published and took effect in May, 2019. A webinar highlighting the most significant changes was presented to State Animal Health officials to clarify important aspects of the standards such as consequences of poor quality and missing samples, ante mortem diagnostics, sample collection and submission, epidemiological investigations, indemnity, and biosecurity. This webinar, and others related to the revised Program Standards, can be found on the Cervid Health Webpage (www.aphis.usda.gov/animalhealth/cervid) on the CWD Herd Certification Program page linked from the CWD Section. Additionally, the Cervid Health Program continues to address topics related to the changes in the Program Standards on monthly calls with State Animal Health officials to allow for questions and clarifications.
CWD Research and the Cervid Health Program
Determination of the predictive value of whole genome markers: USDA APHIS initiated, and then collaborated with Texas Parks and Wildlife, on a study with Texas A&M University geneticist Dr. Christopher Seabury to evaluate the white-tailed deer genome for genetic markers that might influence susceptibility to CWD. Dr. Seabury identified a suite of genes (inside and outside of the prion gene) that appear to predict the susceptibility of WTD to CWD with greater than 80% accuracy. The study will be submitted for scientific peer review shortly. Based on the preliminary findings from this initial study, APHIS and Texas Parks and Wildlife have provided funding to validate the predictive model and will provide additional samples to better inform the model for potential use in the future.
Evaluation of RT-QuIC assay on targeted ante and post mortem tissue samples: The RT-QuIC amplification assay has been demonstrated by numerous scientific studies to be a highly sensitive tool for the detection of CWD. There is increased interest by both the cervid industry and wildlife managers to develop more sensitive ante and post mortem CWD diagnostic tools. This topic was also identified as one of the top five most important CWD research targets at the 2019 CWD Research Consortium hosted by Michigan State University. Dr. Nichols from the APHIS Cervid Health Program is a member of this consortium and is collaborating with the USDA Agricultural Research Service (ARS) in Pullman, WA, and USGS National Wildlife Health Center in Madison, WI to evaluate RT-QuIC CWD detection sensitivity and specificity on retropharyngeal lymph node, as tonsil and rectal biopsy.
5
TB in Farmed Cervids
Annual TB Surveillance Summary
snip...
PENNSYLVANIA NEWLY DETECTED CWD-POSITIVE LEADS TO DMA3 EXPANSION AND A NEW DMA
NEWLY DETECTED CWD-POSITIVE LEADS TO DMA3 EXPANSION AND A NEW DMA
10/22/2021
HARRISBURG, PA - A CWD-positive deer recently detected in Jefferson County has led to new regulations to reduce the risk of the disease spreading.
The Pennsylvania Game Commission today announced the expansion of Disease Management Area 3 (DMA 3) and the creation of a new DMA (DMA 6).
Detection of Chronic Wasting Disease (CWD) in a road-killed deer on the northern boundary of DMA3 prompted these changes. The adult male was collected as part of ongoing CWD surveillance efforts.
CWD affects deer, elk, and other members of the deer family. The disease is fatal to any deer or elk infected with it, and CWD has no treatment or cure.
When a new CWD-positive is detected in either a wild or captive deer or elk in Pennsylvania, a Disease Management Area (DMA) is established. DMAs are created to reduce risk of human-assisted spread of CWD.
This new CWD detection is within 2 miles of Pennsylvania’s elk management area. The short distance to the elk management area required creating DMA 6 within the elk management area. DMA 6 will prevent high-risk parts from the entirety of DMA 3 being moved into the elk management area.
“If a CWD-positive animal is found within any elk hunt zone, all elk hunt zones will become a DMA due to the behavior and longer distance movements of elk,” said Andrea Korman, Game Commission CWD wildlife biologist. “If this were to occur, the impact on deer and elk populations, hunters, and the public will be significant. Although this has not occurred yet, this newly found positive deer shows how close it is.”
DMA 6 was created to restrict movement of high-risk parts into the elk management area and to restrict human activities known to increase disease risk.
Within all DMAs, it is unlawful to:
Remove or export any deer or elk high-risk parts (e.g., head, spinal column, and spleen) from a DMA. This also prevents movement of high-risk parts between adjacent DMAs
Use or possess deer or elk urine-based attractants
Directly or indirectly feed wild, free-ranging deer. It is already illegal to feed elk regardless of DMA location
Rehabilitate wild, free-ranging deer or elk
To increase surveillance around the detection, a new DMAP Unit (#4760) was also created. Over 1,300 permits have been made available for this unit and allow hunters to take up to two additional antlerless deer. Hunters can get DMAP permits by providing the unit number (4760) online or at license-issuing agents.
In conjunction with the additional hunting opportunities, hunters are asked to provide samples for CWD testing. Submitting harvested deer heads for CWD testing helps determine the extent of CWD infection.
The Game Commission offers free CWD testing within the DMAs. Hunters should deposit the heads of deer they harvest with properly filled out and legible harvest tags in one of the head-collection containers the Game Commission provides within DMAs. Locations of head-collection containers can be found at http://bit.ly/PGC-CWDMapOpens In A New Window. Antlers should be removed from bucks before the double-bagged head is placed in a collection container. Hunters can check for their test results online or by calling the CWD hotline (1-833-INFOCWD).
For deer hunters in DMAs – especially those who live outside the DMA – it’s important to plan their hunt and know ahead of time what they will do with any deer harvested. Since high-risk cervid parts can’t be removed from any DMA, even if they share a boundary like DMAs 3 and 6, successful hunters cannot transport whole deer outside the DMA.
Hunters can take deer they harvest to a processor within the DMA or on the list of approved processors for the DMA where they harvested the deer. The list of approved processors and taxidermists is available at www.pgc.pa.gov/CWD. Approved processors properly dispose of the high-risk parts. Hunters can also dispose of high-risk parts in trash that is destined for a landfill or quarter the animal and leave the high-risk parts at the kill site. The meat, antlers (free of brain material) and other low-risk parts then can be transported outside the DMA.
Deer hunters getting taxidermy mounts also must take their harvests to a taxidermist within the DMA or on the list of approved processors and taxidermists for the DMA in which they harvested the deer available at www.pgc.pa.gov/CWD.
Although CWD has not been documented in humans, the Centers for Disease Control and Prevention recommends never eating the meat of a CWD-positive deer.
Much more information on CWD is available at www.pgc.pa.gov/CWD.
DMA 3 boundary has been expanded and is as follows:
Beginning at the southernmost point at the intersection of State Highway 403 and State Highway 286 in the town of Clymer, proceed east on State Highway 286 for 4.9 miles to State Highway 240. Follow in State Highway 240 east for 8.5 miles to the intersection of US Highway 219. Follow US Highway 219 north for 2.4 miles to Sylvis Road. Follow Sylvis Road east for 5.8 miles to the intersection of State Highway 36. Follow State Highway 36 east for 8.8 miles to the intersection of La Jose Road (SR-3016) in Newburg. Follow La Jose Road east for 3.6 miles becoming Cherry Corner Road (SR-3005) for another .3 mile to the intersection of Marron Road (SR-3016). Turn left onto Marron Road and follow northeast for 2.7 miles to the intersection of State Road 729. Follow State Road 729 east for .9 miles to the intersection of Old Station Road. Follow Old Station Road (SR-2012) east for 2.4 miles to the intersection of Douglas Road (SR-3007). Continue east on Douglas Road for .3 miles to the intersection of Zion Road (SR-2012) near New Millport. Follow Zion Road east for 4.5 miles to the intersection of Faunce Road (SR-2012). Turn right and follow Faunce Road east for 3.1 miles becoming Sanborn Road (SR-2012) in Woodward Township. Continue east on Sanborn Road for 2.5 miles to the intersection of State Highway 153. Follow State Highway 153 north for 5 miles to the intersection of Valley Road (SR-2027). Follow Valley Road north for 2.1 miles becoming Hogback Hill Road (SR-2027). Continue north on Hogback Hill Road for 1 mile to the intersection of Main Street in Mineral Springs. Turn right on Main Street for .2 miles to the intersection of Bigler Cutoff Road. Turn left on Bigler Cutoff Road for .1 miles to the intersection of US Highway 322. Follow US Highway 322 east for .7 miles to the intersection of State Highway 970. Follow State Highway 970 north for 1.5 miles to the intersection of Interstate Highway 80. Follow I-80 west for 26.4 miles to the exit for State Highway 219 north. Follow State Highway 219 north for 21.2 miles to Boot Jack becoming State Route 948. Follow State Route 948 for 4.2 miles to the Clarion River in Ridgway. Follow the Clarion River for 28.3 miles to Bridge Road. Continue south on Bridge Road for 0.05 mile to the intersection of State Highway 949. Turn right on State Highway 949 and continue west for 16.3 miles to the intersection of US Highway 322 in Corsica. Follow US Highway 322 east for 0.3 miles to the intersection of State Highway 949. Follow State Highway 949 south for 4.2 miles to the intersection of State Highway 28. Follow State Highway 28 south for 13.2 miles to the intersection of State Highway 839 in New Bethlehem. Follow State Highway 839 south for 21 miles to State Highway 85. Follow State Highway 85 south for 11.7 miles to the intersection of US Highway 119 in the town of Home. Turn left on US Highway 119 and follow 3.4 miles to the intersection of State Highway 403 in Marion Center. Follow State Highway 403 south for 8.5 miles to Clymer at the place of beginning.
DMA 6 is in portions of Clearfield, Elk, and Jefferson Counties and its exact boundary is as follows:
Beginning at the northeast corner at the intersection of Chicken Hill Road and State Route 948 in the town of Kersey, proceed south on Chicken Hill Road for 0.9 mile becoming South Kersey Road. Follow South Kersey Road south for 1.4 miles. Continue straight onto Boone Mountain Road for 6.5 miles to the intersection with State Route 153. Turn left onto State Route 153 and continue south 4.9 miles to State Route 255. Turn right on State Route 255 and continue south for 9.5 miles to Interstate Highway 80. Turn right on Interstate Highway 80 and continue west 4.4 miles to State Highway 219. Turn right on State Highway 219 and continue north 21.1 miles to State Route 948. Turn right on State Route 948 and proceed east for 5.3 miles to Kersey at the place of beginning.
MEDIA CONTACT: Travis Lau - 717-705-6541
# # #
SUNDAY, JANUARY 23, 2022
Pennsylvania Chronic Wasting Disease CWD TSE PrP Surveillance 2021 2022 Update
***>WARNING!!!
WARNING, WARNED, PENNSYLVANIA AND STATE REP. DAVID MALONEY, R-BERKS, THROWING TAXPAYERS MONEY AWAY FOR GAME FOR INDUSTRY AND JUNK SCIENCE!
FRIDAY, MARCH 06, 2020
Pennsylvania CWD TSE Prion deer and State Rep. David Maloney, R-Berks
THURSDAY, MARCH 05, 2020
PGC Audit Reeks of Politics Research Representative Maloney Wants To Gut wildlife management and hunting and help spread CWD in Pennsylvania
WEDNESDAY, MARCH 04, 2020
Politicians State Rep. David Maloney, R-Berks Helping to Spread Chronic Wasting Disease CWD TSE Prion
MONDAY, NOVEMBER 04, 2019
Legislators legislating, or throwing away your money for battling cwd tse prion, State Rep. Steve Green, R-Fosston more money to deer farms for antibiotics?
POLITICIANS AND LEGISLATORS THERE FROM, ARE HELPING SPREAD CWD TSE PRION AKA MAD DEER DISEASE...imo...terry
I TRIED TO TELL YOU!
BMC Genomics. 2022 Jan 21;23(1):69. doi: 10.1186/s12864-022-08306-0.
Neural transcriptomic signature of chronic wasting disease in white-tailed deer
Eóin O'Hara 1 2, Allen Herbst 1, Arun Kommadath 3, Judd M Aiken 1, Debbie McKenzie 4, Negin Goodarzi 5, Pamela Skinner 5, Paul Stothard 6 Affiliations expand
*** > An association between CWD and spiroplasma infection was not found.
***> we mined our data to address the speculative hypothesis that specific bacteria are the etiological agent of CWD, but found no evidence to support this hypothesis.
Maloney to Join Press Conference on Chronic Wasting Disease JAN. 25, 2019
WHAT: After decades of intensive research, Dr. Frank Bastian at Louisiana State University believes he has discovered the true cause of chronic wasting disease (CWD) and the press event will detail an agreement between Unified Sportsmen of Pennsylvania and LSU toward raising funding to eradicate CWD from Pennsylvania and throughout America.
WHO: Maloney, other concerned state legislators, LSU research scientist Dr. Frank Bastian and Unified Sportsmen of Pennsylvania.
WHEN: Monday, Feb. 4, 10:30 a.m.
WHERE: Main Rotunda state Capitol
LIVE WEBSTREAMING: RepMaloney.com
Media contact: Charles Lardner, 717.260.6443, clardner@pahousegop.com
http://www.repmaloney.com/News/8187/Press-Releases/Maloney-to-Join-Press-Conference-on-Chronic-Wasting-Disease
All Efforts to Cure CWD are Welcome, Maloney Says FEB. 05, 2019
HARRISBURG – Rep. David Maloney (R-Berks) applauded the public-private partnership that was announced yesterday between Unified Sportsmen of Pennsylvania and Louisiana State University (LSU) scientist Frank Bastian aimed at curing chronic wasting disease (CWD) in white-tailed deer and other animals.
At a Capitol press conference on Monday, leadership members of the Unified Sportsmen of Pennsylvania announced they were self-funding the research partnership with Dr. Bastian because his research thus far on CWD shows more promise than previous years of state-funded research that have so far yielded no results.
After decades of intensive research, Bastian, an LSU AgCenter animal scientist, believes he has isolated the cause of CWD. He believes it is a bacterium called a spiroplasma. It is this spiroplasma that causes the CWD proteins known as “prions.”
“For years, the Game Commission and the Department of Agriculture have been telling us that prions are the cause of chronic wasting disease,” Maloney said. “Yet, despite decades of efforts, we are no further along to finding a cure than we were when CWD was first discovered some 30 years ago. It seems to me we should welcome a different approach while current efforts continue to be pursued. A closed mind has never solved anything.”
The entire press conference can be viewed here.
Maloney’s remarks following the press conference can be viewed here.
Representative David Maloney 130th District Pennsylvania House of Representatives Media Contact: Charles Lardner 717.260.6443 clardner@pahousegop.com RepMaloney.com
NEWS FLASH ON MALONEY'S FAKE NEWS ABOUT BASTIAN'S CWD CURE;
to date, there is no vaccine that will cure or stop cwd tse prion, and for the ones that might come into play once validated, if validated, that slows the progression of the cwd tse prion in the brain and throughout the body, it would only give that cervid longer to spread the cwd tse prion throughout the environment...it's just science...terry
FRIDAY, JANUARY 03, 2020
Ground-breaking study could reveal true cause of fatal chronic wasting disease CWD TSE Prion...NOT!
YOU CANNOT LEGISLATE CHRONIC WASTING DISEASE CWD TSE PRION WITH JUNK SCIENCE, just like i said back in 2020, what i said years before, Bastian and his spiroplasma theory has never ever been proven, and i tried to warn that Pennsylvania et al were just throwing more cwd research money down the drain in a chase for spiroplasma, but no, legislators like Representative David Maloney 130th District Pennsylvania House of Representatives just love to throw money away and something he knows nothing about, and it's what you get when you chase junk science down a rabbit hole, just to please the cervid captive game farm industry...imo.
I TRIED TO TELL YOU!
BMC Genomics. 2022 Jan 21;23(1):69. doi: 10.1186/s12864-022-08306-0.
Neural transcriptomic signature of chronic wasting disease in white-tailed deer
Eóin O'Hara 1 2, Allen Herbst 1, Arun Kommadath 3, Judd M Aiken 1, Debbie McKenzie 4, Negin Goodarzi 5, Pamela Skinner 5, Paul Stothard 6 Affiliations expand
*** > An association between CWD and spiroplasma infection was not found.
***> we mined our data to address the speculative hypothesis that specific bacteria are the etiological agent of CWD, but found no evidence to support this hypothesis.
SUNDAY, APRIL 12, 2020
PENNSYLVANIA REVISED CWD RESPONSE PLAN DRAFT AVAILABLE FOR REVIEW
WEDNESDAY, MARCH 04, 2020
Pennsylvania YOUR STATE WILDLIFE AGENCY 2019 ANNUAL REPORT CWD TSE Prion 123 tested positive
SATURDAY, JANUARY 04, 2020
Pennsylvania 2020 CWD Response Plan Proposal
My submission to Pennsylvania Draft CWD Response Plan: Public Comment will be the same as my recent submission to Texas and other states, with a few additions, and is as follows;
SUNDAY, DECEMBER 22, 2019
Pennsylvania Steady Climb of CWD TSE Prion Confirms 250 Positive To Date In Wild Cervid As At September 12, 2019
Pennsylvania Captive Cervid Industry Total CWD TSE Prion ??? anyone's guess...
THURSDAY, FEBRUARY 21, 2019
Pennsylvania More CWD Bethel Township, Fulton County breeding farm
SATURDAY, NOVEMBER 10, 2018
Pennsylvania Thirty-Eight Deer Test Positive for Chronic Wasting Disease on Fulton and Bedford County Deer Farms
FRIDAY, FEBRUARY 23, 2018
Pennsylvania NEW CWD MANAGEMENT AREA TO BE ANNOUNCED
MONDAY, FEBRUARY 12, 2018
Pennsylvania CWD TSE Prion has been found in captive deer in Huntingdon and Lancaster counties
FRIDAY, JUNE 15, 2018
Pennsylvania CWD Cases Triple in One Year
THURSDAY, OCTOBER 24, 2019
Pennsylvania NEWLY DETECTED CWD-POSITIVE DEER CAPTIVE-RAISED WILL EXPAND DMA 4 IN 2020
SATURDAY, NOVEMBER 10, 2018
***> Pennsylvania Thirty-Eight Deer Test Positive for Chronic Wasting Disease on Fulton and Bedford County Deer Farms
WEDNESDAY, APRIL 04, 2018 2017
Annual Report | Pennsylvania Game Commission Chronic Wasting Disease CWD TSE Prion
MONDAY, FEBRUARY 12, 2018
Pennsylvania CWD TSE Prion has been found in captive deer in Huntingdon and Lancaster counties
MONDAY, FEBRUARY 12, 2018
Pennsylvania Deer found near Jefferson County elementary school tests positive for CWD TSE Prion
SATURDAY, JANUARY 20, 2018
Pennsylvania CWD TSE Prion Cases Explodes 51 deer from the 2017-18 hunting seasons have tested positive for CWD majority of samples collected still are being analyzed
FRIDAY, DECEMBER 15, 2017
Pennsylvania Four Deer Test Positive for Chronic Wasting Disease on Franklin, Fulton County Quarantined Hunting Preserves
THURSDAY, SEPTEMBER 28, 2017
Pennsylvania GAME COMMISSION OFFERS FREE CWD TESTS FOR DMA-HARVESTED DEER
THURSDAY, SEPTEMBER 21, 2017
Pennsylvania Game Commission has scheduled a series of public meetings to ensure Pennsylvanians remain informed about chronic wasting disease CWD TSE Prion
SATURDAY, AUGUST 12, 2017
*** Pennsylvania 27 deer from Bedford County farm test positive for chronic wasting disease ***
WEDNESDAY, JULY 12, 2017
PENNSYLVANIA CWD FOUND IN THE WILD IN CLEARFIELD COUNTY
THURSDAY, JUNE 01, 2017
PENNSYLVANIA Third Case of CWD Discovered in a Captive Deer Farm in Four Months
MONDAY, MAY 15, 2017
Pennsylvania 25 more deer test positive for CWD TSE PRION in the wild
WEDNESDAY, MARCH 01, 2017
South central Pennsylvania Captive Deer Tests Positive for Chronic Wasting Disease
FRIDAY, JANUARY 13, 2017
Pennsylvania Deer Tests Positive for Chronic Wasting Disease four-year-old white-tailed deer Franklin County Hunting Preserve
Wednesday, May 11, 2016
PENNSYLVANIA TWELVE MORE CASES OF CWD FOUND: STATE GEARS UP FOR ADDITIONAL CONTROL MEASURES
Saturday, November 07, 2015
PENNSYLVANIA CHRONIC WASTING DISEASE CWD TSE PRION RULES EXPAND
Saturday, November 07, 2015
Pennsylvania 2015 September Minutes CWD Urine Scents
Sunday, October 18, 2015
*** Pennsylvania Game Commission Law and Law Makers CWD TSE PRION Bans Singeltary 2002 from speaking A smelly situation UPDATED 2015
Tuesday, May 05, 2015
Pennsylvania CWD DETECTED IN SIX MORE FREE-RANGING DEER Disease Management Area 2 again expanded due to new cases Release #030-15
Sunday, July 13, 2014
Louisiana deer mystery unleashes litigation 6 does still missing from CWD index herd in Pennsylvania Great Escape
Saturday, June 29, 2013
PENNSYLVANIA CAPTIVE CWD INDEX HERD MATE YELLOW *47 STILL RUNNING LOOSE IN INDIANA, YELLOW NUMBER 2 STILL MISSING, AND OTHERS ON THE RUN STILL IN LOUISIANA
Tuesday, June 11, 2013
*** CWD GONE WILD, More cervid escapees from more shooting pens on the loose in Pennsylvania
Tuesday, May 28, 2013
Chronic Wasting Disease CWD quarantine Louisiana via CWD index herd Pennsylvania Update May 28, 2013
*** 6 doe from Pennsylvania CWD index herd still on the loose in Louisiana, quarantine began on October 18, 2012, still ongoing, Lake Charles premises.
Sunday, January 06, 2013
USDA TO PGC ONCE CAPTIVES ESCAPE
*** "it‘s no longer its business.”
http://chronic-wasting-disease.blogspot.com/2013/01/usda-to-pgc-once-captives-escape-its-no.html
”The occurrence of CWD must be viewed against the contest of the locations in which it occurred. It was an incidental and unwelcome complication of the respective wildlife research programmes. Despite it’s subsequent recognition as a new disease of cervids, therefore justifying direct investigation, no specific research funding was forthcoming. The USDA viewed it as a wildlife problem and consequently not their province!” page 26.
Wednesday, November 14, 2012
PENNSYLVANIA 2012 THE GREAT ESCAPE OF CWD INVESTIGATION MOVES INTO LOUISIANA and INDIANA
Tuesday, October 23, 2012
PA Captive deer from CWD-positive farm roaming free
Thursday, October 11, 2012
Pennsylvania Confirms First Case CWD Adams County Captive Deer Tests Positive
Pennsylvania Has Confirmed 3 Cases Of Atypical Nor-98 TSE Prion To Date
THURSDAY, JANUARY 7, 2021
Atypical Nor-98 Scrapie TSE Prion USA State by State Update January 2021
Subject: Pennsylvania Scrapie Outbreak August 2018
Ag Secretary, State Veterinarian: New Animal ID Rules Help Track Disease, Prevent Outbreaks
09/18/2020
Harrisburg, PA - Agriculture Secretary Russell Redding and State Veterinarian Dr. Kevin Brightbill today reminded small-ruminant producers that new requirements for scrapie tags and premises IDs will help ensure better, faster disease tracing and control. Adhering to new federal requirements will help keep scrapie instances from becoming full-blown outbreaks, ultimately saving producers from devastating livestock and financial losses.
“We have made significant progress in eradicating this costly and fatal disease,” said Redding. “Our commonwealth must continue efforts to ensure the protection of our herds and flocks from scrapie as it threatens Pennsylvania agriculture. Establish a premises identification number for your herd or flock.”
Scrapie is known to be transmissible from infected to uninfected sheep and goats through exposure from birthing fluids and tissues. Clinical signs may be noticed 18 months to 5 years after exposure and include progressive weight loss despite no decrease in appetite, difficulty walking, fine tremors/shaking of ears and head and, most notably, extreme itching. At this time, there is no vaccine to protect animals against scrapie, and there is no known cure or treatment for the disease.
“Scrapie is a fatal infectious and progressive disease affecting the brain and spinal cord of sheep and goats and belongs to a group of diseases called transmissible spongiform encephalopathies (TSEs),” said Brightbill. “There is no evidence humans have ever been infected with scrapie.”
In August 2018, a Pennsylvania goat sampled at slaughter in July 2018, was confirmed positive for classical scrapie. The goat was traced to a Pennsylvania herd that has both sheep and goats. The herd was designated as a source flock by the United States Department of Agriculture (USDA). An additional five sheep and one goat were confirmed positive for classical scrapie within that herd at the time of partial herd depopulation. Only sheep and goats shown to be genetically susceptible to scrapie were depopulated.
To establish a premises identification number (PIN) for your herd or flock please visit the Pennsylvania Department of Agriculture Premises Registration Form to enroll your premises.
After a PIN has been established, dial USDA’s toll-free tag line at (866) 873-2824 to order scrapie tags for your herd or flock. The Pennsylvania Veterinary Diagnostic Laboratory (PVL) is offering genetic screening for owners interested in identifying scrapie resistant animals in their flocks. To find out more ask your veterinarian or call PVL at (717) 787-8808. Additionally, USDA APHIS offers free scrapie testing for deceased animals over the age of 14 months.
All sheep and goats born in Pennsylvania must be identified with a PDA-approved form of official individual identification, prior to being transported live off the birth premises. No sheep or goat, of any age, shall be imported or shipped into the Commonwealth of Pennsylvania without a department-approved form of individual identification. Additionally, per the Final Rule of the National Scrapie Eradication ProgramOpens In A New Window, all sheep and goats must be accompanied in transit by either a valid Interstate Health Certificate or owner shipper statement if the animals are moving in slaughter channels.
Up until January 1, 2021 the department will offer educational outreach and written notices of violation to gently prompt compliance. After January 1, 2021, entities failing to comply will be subject to enforcement and penalties as are allowed under the provisions of Pennsylvania’s Domestic Animal Law, including revocation of license, criminal prosecution and/or civil penalties of up to $10,000 per violation and injunctive.
Additional questions may be addressed by calling the Bureau of Animal Health and Diagnostic Services at 717-772-2852 or RA-ahds@pa.gov. Questions directed toward USDA APHIS may be addressed by calling Dr. Stephanie Ringler at 717-599-9957.
MEDIA CONTACT: Shannon Powers - 717.783.2628
# # #
https://d1cqrq366w3ike.cloudfront.net/http/DOCUMENT/SheepUSA/March%202019%20Scrapie%20Newsletter.pdf
NOTICES DEPARTMENT OF AGRICULTURE General Quarantine Order; Scrapie [50 Pa.B. 675] [Saturday, February 1, 2020]
MONDAY, APRIL 11, 2022
Pennsylvania new DMA 7 created when CWD recently was detected at a captive facility in Lycoming County
CWD Quarantines equal CWD time bomb waiting to go off...terry
***> Texas Chronic Wasting Disease CWD TSE Prion Confirmed Positive Jumps By 91 Total To Date 361 Cases
TEXAS CWD TRACKING
CWD Positive
Confirmation Date Free Range/Captive County Source Species Sex Age
Pending Breeder Deer Kimble Facility #6 White-tailed Deer Unknown 3.5
Pending Breeder Deer Hunt Facility #9 White-tailed Deer M 1.9
N/A Free Range Hartley N/A Mule Deer M 5.5
2022-01-25 Free Range Medina N/A White-tailed Deer F 5.5
2022-01-12 Breeder Deer Hunt Facility #9 White-tailed Deer M 1.5
2022-01-12 Breeder Deer Hunt Facility #9 White-tailed Deer F 3.5
2022-01-12 Breeder Release Site Medina Facility #3 Red Deer F 4.5
2022-01-12 Free Range Hartley N/A White-tailed Deer M 3.5
2022-01-12 Free Range Hartley N/A Mule Deer M 5.5
2022-01-12 Free Range Hartley N/A Mule Deer M 4.5
2022-01-12 Free Range Hartley N/A Mule Deer M 5.5
2022-01-12 Free Range Hartley N/A Mule Deer F 3.5
2022-01-12 Breeder Deer Kimble Facility #6 White-tailed Deer Unknown 5.5
2022-01-12 Free Range Hartley N/A Mule Deer M 3.5
2022-01-12 Free Range Hartley N/A Mule Deer M 7.5
2022-01-10 Free Range Medina N/A White-tailed Deer M 4.5
2022-01-10 Breeder Deer Uvalde Facilities #7 & 8 White-tailed Deer M 1.3
2022-01-10 Breeder Deer Uvalde Facilities #7 & 8 White-tailed Deer M 1.4
2022-01-07 Breeder Deer Uvalde Facilities #7 & 8 White-tailed Deer M 2.4
2022-01-07 Breeder Deer Uvalde Facilities #7 & 8 White-tailed Deer F 1.4
2022-01-07 Breeder Deer Uvalde Facilities #7 & 8 White-tailed Deer M 1.4
2022-01-07 Breeder Deer Uvalde Facilities #7 & 8 White-tailed Deer M 1.4
2022-01-07 Breeder Deer Uvalde Facilities #7 & 8 White-tailed Deer M 1.4
2022-01-07 Breeder Deer Uvalde Facilities #7 & 8 White-tailed Deer M 1.4
2022-01-07 Breeder Deer Uvalde Facilities #7 & 8 White-tailed Deer M 1.4
2022-01-07 Breeder Deer Uvalde Facilities #7 & 8 White-tailed Deer M 1.4
2022-01-07 Breeder Deer Uvalde Facilities #7 & 8 White-tailed Deer M 1.4
2022-01-07 Breeder Deer Uvalde Facilities #7 & 8 White-tailed Deer M 1.4
2022-01-07 Breeder Deer Uvalde Facilities #7 & 8 White-tailed Deer M 1.4
2022-01-07 Breeder Deer Uvalde Facilities #7 & 8 White-tailed Deer M 1.4
2022-01-07 Breeder Deer Uvalde Facilities #7 & 8 White-tailed Deer M 1.4
2022-01-07 Breeder Deer Uvalde Facilities #7 & 8 White-tailed Deer M 2.4
2022-01-07 Breeder Deer Uvalde Facilities #7 & 8 White-tailed Deer F 1.4
2022-01-07 Breeder Deer Uvalde Facilities #7 & 8 White-tailed Deer M 1.4
2022-01-07 Breeder Deer Uvalde Facilities #7 & 8 White-tailed Deer M 2.4
2022-01-07 Breeder Deer Uvalde Facilities #7 & 8 White-tailed Deer F 1.4
2022-01-07 Breeder Deer Uvalde Facilities #7 & 8 White-tailed Deer F 1.4
2022-01-07 Breeder Deer Uvalde Facilities #7 & 8 White-tailed Deer M 5.4
2022-01-07 Breeder Deer Uvalde Facilities #7 & 8 White-tailed Deer F 1.4
2022-01-07 Breeder Deer Uvalde Facilities #7 & 8 White-tailed Deer F 1.4
2022-01-07 Breeder Deer Uvalde Facilities #7 & 8 White-tailed Deer F 1.4
2022-01-07 Breeder Deer Uvalde Facilities #7 & 8 White-tailed Deer F 1.4
2022-01-07 Breeder Deer Uvalde Facilities #7 & 8 White-tailed Deer F 1.4
2022-01-07 Breeder Deer Uvalde Facilities #7 & 8 White-tailed Deer F 1.4
2022-01-07 Breeder Deer Uvalde Facilities #7 & 8 White-tailed Deer M 2.4
2022-01-07 Breeder Deer Uvalde Facilities #7 & 8 White-tailed Deer M 2.4
2022-01-07 Breeder Deer Uvalde Facilities #7 & 8 White-tailed Deer M 2.4
2022-01-07 Breeder Deer Uvalde Facilities #7 & 8 White-tailed Deer M 1.4
2022-01-07 Breeder Deer Uvalde Facilities #7 & 8 White-tailed Deer M 2.4
2022-01-07 Breeder Deer Uvalde Facilities #7 & 8 White-tailed Deer M 2.4
2022-01-07 Breeder Deer Uvalde Facilities #7 & 8 White-tailed Deer M 3.4
2022-01-07 Breeder Deer Uvalde Facilities #7 & 8 White-tailed Deer M 3.4
2022-01-07 Breeder Deer Uvalde Facilities #7 & 8 White-tailed Deer M 3.4
2022-01-07 Breeder Deer Uvalde Facilities #7 & 8 White-tailed Deer M 3.4
2022-01-07 Breeder Deer Uvalde Facilities #7 & 8 White-tailed Deer M 2.4
2022-01-07 Breeder Deer Uvalde Facilities #7 & 8 White-tailed Deer M 2.4
2022-01-07 Breeder Deer Uvalde Facilities #7 & 8 White-tailed Deer M 2.4
2022-01-07 Breeder Deer Uvalde Facilities #7 & 8 White-tailed Deer M 2.4
2022-01-07 Breeder Deer Uvalde Facilities #7 & 8 White-tailed Deer F 1.4
2022-01-07 Breeder Deer Uvalde Facilities #7 & 8 White-tailed Deer F 1.4
2022-01-07 Breeder Deer Uvalde Facilities #7 & 8 White-tailed Deer F 1.4
2022-01-07 Breeder Deer Uvalde Facilities #7 & 8 White-tailed Deer M 1.4
2022-01-07 Breeder Deer Uvalde Facilities #7 & 8 White-tailed Deer M 1.4
2022-01-07 Breeder Deer Uvalde Facilities #7 & 8 White-tailed Deer F 1.4
2022-01-07 Breeder Deer Uvalde Facilities #7 & 8 White-tailed Deer F 1.4
2022-01-07 Breeder Deer Uvalde Facilities #7 & 8 White-tailed Deer M 3.4
2022-01-07 Breeder Deer Uvalde Facilities #7 & 8 White-tailed Deer F 2.4
2022-01-07 Breeder Deer Uvalde Facilities #7 & 8 White-tailed Deer F 1.4
2022-01-07 Breeder Deer Uvalde Facilities #7 & 8 White-tailed Deer F 1.4
2022-01-07 Breeder Deer Uvalde Facilities #7 & 8 White-tailed Deer M 1.4
2022-01-07 Breeder Deer Uvalde Facilities #7 & 8 White-tailed Deer M 2.4
2022-01-07 Breeder Deer Uvalde Facilities #7 & 8 White-tailed Deer F 1.4
2022-01-07 Breeder Deer Uvalde Facilities #7 & 8 White-tailed Deer F 1.4
2022-01-07 Breeder Deer Uvalde Facilities #7 & 8 White-tailed Deer F 1.4
2022-01-07 Breeder Deer Uvalde Facilities #7 & 8 White-tailed Deer M 1.4
2022-01-07 Breeder Deer Uvalde Facilities #7 & 8 White-tailed Deer M 1.4
2022-01-07 Breeder Deer Uvalde Facilities #7 & 8 White-tailed Deer M 1.4
2022-01-07 Breeder Deer Uvalde Facilities #7 & 8 White-tailed Deer M 1.4
2022-01-07 Breeder Deer Uvalde Facilities #7 & 8 White-tailed Deer M 1.4
2022-01-07 Breeder Deer Uvalde Facilities #7 & 8 White-tailed Deer M 1.4
2022-01-07 Breeder Deer Uvalde Facilities #7 & 8 White-tailed Deer M 2.4
2022-01-07 Breeder Deer Uvalde Facilities #7 & 8 White-tailed Deer M 2.4
2022-01-07 Breeder Deer Uvalde Facilities #7 & 8 White-tailed Deer M 2.4
2022-01-07 Breeder Deer Uvalde Facilities #7 & 8 White-tailed Deer M 2.4
2022-01-07 Breeder Deer Uvalde Facilities #7 & 8 White-tailed Deer F 1.4
2022-01-07 Breeder Deer Uvalde Facilities #7 & 8 White-tailed Deer F 1.4
2022-01-07 Breeder Deer Uvalde Facilities #7 & 8 White-tailed Deer M 5.4
2022-01-06 Free Range Medina N/A White-tailed Deer M 2.5
2021-12-28 Breeder Deer Uvalde Facilities #7 & 8 White-tailed Deer M 3.4
2021-12-28 Breeder Deer Uvalde Facilities #7 & 8 White-tailed Deer M 3.4
2021-12-13 Free Range Medina N/A White-tailed Deer M 3.5
2021-12-13 Breeder Deer Duval Facility #13 White-tailed Deer F 4.4
2021-12-13 Free Range El Paso N/A Mule Deer F 4.5
2021-10-18 Breeder Deer Medina Facility #4 White-tailed Deer M 4
2021-10-12 Breeder Deer Hunt Facility #9 White-tailed Deer F 8.2
2021-10-12 Breeder Deer Uvalde Facilities #7 & 8 White-tailed Deer M 1.2
2021-10-12 Breeder Deer Uvalde Facilities #7 & 8 White-tailed Deer M 1.2
2021-10-12 Breeder Deer Uvalde Facilities #7 & 8 White-tailed Deer M 1.2
2021-10-12 Breeder Deer Uvalde Facilities #7 & 8 White-tailed Deer M 2.2
2021-10-12 Breeder Deer Uvalde Facilities #7 & 8 White-tailed Deer M 2.1
Showing 1 to 100 of 361 entries Previous Next
National CWD Tracking Map
“Regarding the current situation involving CWD in permitted deer breeding facilities, TPWD records indicate that within the last five years, the seven CWD-positive facilities transferred a total of 2,530 deer to 270 locations in 102 counties and eight locations in Mexico (the destinations included 139 deer breeding facilities, 118 release sites, five Deer Management Permit sites, and three nursing facilities).'' ...
It is apparent that prior to the recent emergency rules, the CWD detection rules were ineffective at detecting CWD earlier in the deer breeding facilities where it was eventually discovered and had been present for some time; this creates additional concern regarding adequate mitigation of the risk of transferring CWD-positive breeder deer to release sites where released breeder deer come into contact with free-ranging deer...
Commission Agenda Item No. 5 Exhibit B
DISEASE DETECTION AND RESPONSE RULES
PROPOSAL PREAMBLE
1. Introduction.
snip...
A third issue is the accuracy of mortality reporting. Department records indicate that for each of the last five years an average of 26 deer breeders have reported a shared total of 159 escapes. Department records for the same time period indicate an average of 31 breeding facilities reported a shared total of 825 missing deer (deer that department records indicate should be present in the facility, but cannot be located or verified).
Listen here;
Nov 3, 2021
Nov 4, 2021
Counties where CWD Exposed Deer were Released, September 2021
Number of CWD Exposed Deer Released by County, September 2021
Control of Chronic Wasting Disease OMB Control Number: 0579-0189 APHIS-2021-0004 Singeltary Submission
Docket No. APHIS-2018-0011 Chronic Wasting Disease Herd Certification
SATURDAY, FEBRUARY 26, 2022
Texas Chronic Wasting Disease CWD TSE Prion Confirmed Positive Jumps By 91 Total To Date 361 Cases
FRIDAY, APRIL 30, 2021
Should Property Evaluations Contain Scrapie, CWD, TSE PRION Environmental Contamination of the land?
WEDNESDAY, MAY 17, 2017
*** Chronic Wasting Disease CWD TSE Prion aka Mad Deer Disease and the Real Estate Market Land Values ***
WEDNESDAY, DECEMBER 04, 2013
Chronic Wasting Disease CWD and Land Value concerns?
TUESDAY, APRIL 13, 2021
Implications of farmed-cervid movements on the transmission of chronic wasting disease
TRUCKING TRANSPORTING CERVID CHRONIC WASTING DISEASE TSE PRION VIOLATING THE LACEY ACT
MONDAY, MARCH 05, 2018
TRUCKING AROUND AND SPREADING CHRONIC WASTING DISEASE CWD TSE PRION VIA MOVEMENT OF CERVID AND TRANSPORTATION VEHICLES
SATURDAY, JULY 09, 2016
Texas Intrastate – within state movement of all Cervid or Trucking Chronic Wasting Disease CWD TSE Prion Moratorium
THURSDAY, AUGUST 20, 2015
TEXAS CAPTIVE Deer Industry, Pens, Breeding, Big Business, Invites Crooks and CWD
MONDAY, AUGUST 14, 2017
***> Texas Chronic Wasting Disease CWD TSE Prion History
***> Michigan 2021 Wildlife Division Annual Report Deer Farms and CWD
Celebrating 100 Years of Caring for Michigan's Wildlife and Wild Places
January 25, 2022
Private Owned Cervidae
Privately Owned Cervidae
Raising deer and elk in captivity is jointly regulated by the DNR and the Michigan Department of Agriculture and Rural Development. The DNR oversees the registration of facilities containing farmed cervids and performs inspections of these operations. MDARD manages the disease programs for the state’s POC facilities. Participation in disease surveillance programs - such as those for chronic wasting disease (CWD) and the bovine tuberculosis (TB) - ensures for a robust industry by increasing the marketability of these animals by decreasing their potential for carrying disease. There are nearly 300 licensed facilities in 76 Michigan counties totaling over 63,000 fenced acres. The division conducts about 95 facility inspections per year to ensure that fencing and recordkeeping meet industry standards.
2021 Wildlife Health Section Accomplishments
Tested 2,500 heads for chronic wasting disease.
Michigan Chronic Wasting Disease CWD TSE Prion Update
CWD in Michigan
Since May 2015 when the first CWD deer was found in Michigan, CWD has been confirmed in a number of townships in the Lower Peninsula. As of October 2018, a CWD positive deer was found in the Upper Peninsula in Dickinson County. CWD was also found in August 2008 at a Kent County deer farm facility and in January 2017 in two captive deer that were from a deer farm facility in Mecosta County.
CWD TESTING RESULTS
Desperado Deer: The Persistent Problem of Captive Deer Running Wild
by Editor | May 8, 2018 | Conservation, Hunting
Cervid Escapees – Measuring the Problem
For starters, no one knows for sure how many deer escape from high-fence facilities each year. Neither the DNR nor the Michigan Department of Agriculture and Rural Development keep accurate, complete records of the number of escapees reported by citizens and/or investigated by DNR conservation officers. Only in 2017 did the DNR first begin using an electronic database to monitor escaped cervids.
Currently, there are 333 licensed captive cervid facilities in the state, most of which are breeding farms (161) or hunting ranches (132), holding over 21,000 whitetail deer, fallow deer, red deer, Sitka deer and elk. While the number of deer escapees voluntarily reported has declined over recent years, the numbers do not include escapees that are never reported.
Chronic wasting disease (CWD) is a transmissible neurological disease found in deer and elk populations that produces small lesions in brains of infected animals. As a result, CWD causes weight loss and a decline in body control. It is a species-specific disease, and there have been no cases in humans or other animals.
Currently, to determine the presence of CWD, brain and lymph node samples are taken by an accredited veterinarian after an animal dies. These samples are then submitted for testing.
As part of their operations, all privately-owned cervid (POC) facilities in Michigan are required to submit samples. The number of samples that must be submitted depends on what specific program that a producer participates in: the Chronic Wasting Disease Herd Certification Program (CWD HCP) or the Surveillance Program.
First, for the CWD HCP, all cervids 12 months of age and older that die for any reason must be tested for CWD.
Second, all facilities that are not a part of the CWD HCP must participate in the Surveillance Program. The Surveillance Program requires that all animals 12 months of age and older that die from illness, injury, or euthanasia due to disease must be tested for CWD. In addition, 25% of cervids slaughtered, hunted, or culled must be tested. This number is calculated on an annual basis. In general, all facilities that have at least one death must test at least this one animal.
Samples for either of these programs can be submitted to a private veterinarian, the Michigan State University Veterinary Diagnostic Lab, or an MDARD drop off location.
For more information, contact the MDARD Cervid Program.
General Questions/Concerns: MDARD-Cervid@Michigan.gov
Cervid Program Manager:
Dr. Jennifer Calogero CalogeroJ@Michigan.gov 517-284-5692
Cervid Program Secretary: Melanie Hart HartM1@Michigan.gov 517-284-5679
Privately Owned Cervidae
Raising deer and elk in captivity is jointly regulated by the DNR and the Michigan Department of Agriculture and Rural Development. The DNR oversees the registration of facilities containing farmed cervids and performs inspections of these operations. MDARD manages the disease programs for the state’s POC facilities. Participation in disease surveillance programs - such as those for chronic wasting disease (CWD) and the bovine tuberculosis (TB) - ensures for a robust industry by increasing the marketability of these animals by decreasing their potential for carrying disease. There are nearly 300 licensed facilities in 76 Michigan counties totaling over 63,000 fenced acres. The division conducts about 95 facility inspections per year to ensure that fencing and recordkeeping meet industry standards.
2021 Wildlife Health Section Accomplishments
Tested over 8,000 deer heads for bovine tuberculosis and
2,500 heads for chronic wasting disease.
While CWD is not known to be zoonotic, bTB can infect humans, domestic animals and wild animals beyond white-tailed deer.
***> Tested ...and 2,500 heads for chronic wasting disease.
MDNR estimates put the Michigan deer population around 1.75 million for 2019. Dec 25, 2019
Issues Pros and Cons Despite federal, state, and local regulations and other measures intended to prevent the spread or reduce CWD prevalence, the disease continues to be identified in captive cervid facilities certified as “low risk” through the United States Department of Agriculture (USDA) Herd Certification Program and the CFIA (Canadian Food Inspection Agency) Voluntary Herd Certification Programs (participating in a federally-approved CWD program was a measure of the ATA program). According to the USDA data reports, there were 22 new CWD-positive captive cervid facilities identified in FY2020; 41 percent of those were either enrolled or certified in the federal HCP program. There are a variety of unregulated processes used to collect urine, and they often result in the accumulation of a mixture of secretions, therefore providing concurrent contaminated risks. In addition, urine products are frequently batched/combined from multiple locations and distributed across the country, which increases the likelihood of CWDinfected urine entering the market. There are currently no standard regulations to ensure that urine collected for lures and attractants are disease-free.
snip...
Biological
Nationally, CWD continues to be found in captive cervid facilities.
From the years 2012 to 2021, there have been 66 privately owned cervid facilities nationally where CWD has been identified.
Of those 66 facilities, 39 were enrolled in the HCP, and 32 of those facilities were HCP-certified (meaning there had been at least five years of disease monitoring and no rule violations) indicating low risk for CWD.
This national USDA CWD HCP is not mandatory, and more importantly, recent CWD events show that it does not and cannot guarantee that captive deer herds are CWD free.
To date, CWD has been found in more than 140 captive deer herds in 16 states and two Canadian provinces.
Front. Vet. Sci., 18 January 2022 | https://doi.org/10.3389/fvets.2021.824815
Evaluation of Real-Time Quaking-Induced Conversion, ELISA, and Immunohistochemistry for Chronic Wasting Disease Diagnosis
All, except one, CWD positive RLNs analyzed were from ten Counties geographically located in the West Michigan region of the Lower Peninsula. Taken together, we show evidence that the RT-QuIC assay is comparable to ELISA and IHC and could be helpful for routine CWD detection in surveillance programs. RT-QuIC also demonstrated that CWD prions are distributed across lymph nodes in a variety of anatomic locations.
MICHIGAN CWD CAPTIVE
11/4/2021 2, 3 Y Male MI Kent Elk Breeder Yes Yes 0 Depopulated
7/15/2021 4 Y Female MI Montcalm WTD Breeder No No 109 Quarantine
4/18/2021 2.5 Y Male MI WTD Shooter No No ukn Quarantine
3/3/2021 4 Y Male MI Montcalm WTD Shooter No NA 14 Quarantine
12/2019 3, 4.5 Y Males MI Newaygo WTD Shooter No No >600 Quarantine
4/2019 2.5 Y Female MI Montcalm WTD Breeder No NA 113 Depopulated
12/2017 1.5 Y Female MI Mecosta WTD Breeder Yes Yes 525 Quarantined
1/2017 2Y Female MI Mecosta WTD & Sika deer Shooter No NA 71 Depopulated
Michigan:
September, 2019: NVSL confirmed CWD in a two year old female white-tailed deer in Montcalm County. The doe was a natural addition to the breeding herd which consists of 50 white-tailed deer. This herd is not enrolled in the Federal HCP, is within a CWDendemic area, and is under quarantine.
Michigan: One new CWD positive herd
Hunt preserve of >600 WTD, not in HCP, populated and under quarantine
Farmed Cervid Chronic Wasting Disease Management and Response Activities 2021 Cooperative Agreements
APHIS also conducts monitoring and surveillance activities to detect diseases that affect cervids, including chronic wasting disease (CWD) and tuberculosis (TB). APHIS’ voluntary national CWD Herd Certification Plan (HCP) works with States, Tribes, and the cervid industry to control CWD in farmed cervids by allowing the interstate movement only from certified herds.
Currently, 28 States participate in the national CWD HCP. In FY 2019 APHIS tested more than 11,000 farmed cervids for CWD.
As a result, APHIS identified 17 new CWD positive farmed cervid herds.
FRIDAY, FEBRUARY 18, 2022
Michigan Chronic Wasting Disease CWD TSE Prion Update February 2022
***> Wisconsin 2022 WCC Spring Hearing Questions Deer Farms and CWD
Deer and Elk Committee
Due to an increase in the number of counties where CWD positive deer have been detected, some believe it is necessary for the Wisconsin Conservation Congress to gather statewide opinions concerning captive cervid operations (deer farms and shooting preserves) in Wisconsin. Recently CWD positive deer were found on captive cervid operations in Taylor, Langlade, and Outagamie counties, which were all associated with one source. Additionally, deer farms in Sauk and Vilas County have recently been found with CWD positive deer. In late May an adult deer which tested positive for CWD was found dead in Green Lake County.
As of 10-20-2021 there are 44 Wisconsin counties with CWD positive detections. Of those, there are 31 counties with wild CWD detections, 26 with CWD captive detections, and 13 which have both wild and captive CWD positive detections within them. At this time, there are 301 registered deer premises in Wisconsin with 68 of those being hunting ranches. There have been 34 farms with a CWD positive test since 2001, and 19 herds depopulated as a result of a CWD positive on them.
10. Do you support or oppose the presence of captive cervid operations (game farms and shooting preserves) in Wisconsin?
Wisconsin two white-tailed deer at a Waukesha County farm have tested positive for chronic wasting disease (CWD)
Waukesha County Deer Farm Tests Positive for CWD
FOR IMMEDIATE RELEASE: February 10, 2022
Contact: Kevin Hoffman, Public Information Officer, (608) 224-5005, kevin.hoffman@wisconsin.gov
Download PDF
MADISON, Wis. – The Wisconsin Department of Agriculture, Trade and Consumer Protection (DATCP) has confirmed that two white-tailed deer at a Waukesha County farm have tested positive for chronic wasting disease (CWD). The samples were confirmed by the National Veterinary Services Laboratories in Ames, Iowa.
Both affected animals were 3-year-old bucks. The 9-acre farm had been under quarantine since November 2021 after white-tailed deer moved from its herd tested positive at an Eau Claire County ranch. It will remain under quarantine while DATCP and the U.S. Department of Agriculture (USDA) veterinarians and staff conduct the epidemiological investigation.
CWD is a fatal, neurological disease of deer, elk and moose caused by an infectious protein called a prion that affects the animal's brain, and testing for CWD is typically only performed after the animal's death. DATCP regulates deer farms for registration, recordkeeping, disease testing, movement, and permit requirements.
More information
DATCP's http://farm-raised deer program: https://datcp.wi.gov/Pages/Programs_Services/FarmRaisedDeer.aspx
###
Wisconsin Lawmakers should end their frolic with ‘Hunter Nation’
Kevin Wilson
CWD hunters
It’s time for Wisconsin lawmakers to work with hunters, anglers and trappers to address chronic wasting disease and other challenges to the state’s natural resources.
Patrick Durkin
Wisconsin this month fortified its standing as the capital of the world for chronic wasting disease by verifying the plague in wild deer in 38 of the state’s 72 counties.
Yep, Wisconsin now has more counties with CWD in free-ranging deer than it does counties without. We passed the halfway mark Jan. 11 when the Department of Natural Resources reported two adult bucks in Monroe County and one deer in Oconto County tested positive for the always-fatal disease.
We started the 2021 hunting seasons with CWD in 34 counties but made it 35 when the DNR confirmed a sick adult doe Oct. 29 in Fond du Lac County. We then reached the halfway point Dec. 12 when the DNR confirmed a sick yearling (18 months old) buck in Vilas County.
And just think what we’d find if we searched aggressively for CWD. All four newly christened CWD counties found their first cases despite modest sampling efforts. Hunters in Monroe County have provided a respectable 373 samples during the current testing year, but hunters in Oconto provided only 162; Vilas, 161; and Fond du Lac, 105.
The 2021 sampling year ends March 31, but it’s safe to report that 25 Wisconsin counties will end the year with less than 100 samples tested, given the hunt is largely over.
As of Jan.15, Wisconsin has confirmed 9,450 CWD cases since discovering the disease in three deer shot west of Madison in November 2001. The DNR has documented 1,283 cases statewide so far this year after testing 16,165 samples. That’s 8% of all tests, which is similar to 2020’s rate.
CWD sampling declined this past fall, with 2,749 fewer samples (-14.5%) statewide than in 2020 (18,914). Most samples come from the DNR’s southern farmland zone, where sampling fell 22% from 9,3892 a year ago to 7,277.
Despite the decline, 1,234 deer (17%) have tested positive so far in that zone, which is 4 percentage points lower than the 2020 total. For perspective, when the DNR tested similar numbers (7,097 deer) in the Southern farmlands in 2010, it found 219 (3%) CWD cases, or 5.6 times fewer doomed deer.
Elsewhere, CWD cases more than doubled from 19 to 39 in central Wisconsin’s farmlands this year, accounting for 40% of the zone’s historical total of 98 cases. In addition, deer baiting is now banned in 58 Wisconsin counties. The 14 counties where the controversial practice remains are Douglas, Bayfield, Ashland, Iron, Sawyer, Rusk, Price, St. Croix, Pierce, Lincoln, Brown, Manitowoc, Kewaunee and Door.
Iowa County again leads the state with 315 cases this year, or 31% of the 1,026 samples provided. Next was Richland, 270 cases (21% positive); Sauk, 222 (25%); Dane, 151 (17%); Grant, 80 (14%); and Columbia, 72 (15%).
Cooperation from hunters remains poor as indifference reigns. In Sauk County, hunters tested only 15% of the 6,002 deer they registered during the 2021 gun, crossbow and archery seasons. Further, Dane County hunters tested 23.5% of 3,833 registered deer; Richland County, 24% of 5,228; Iowa County, 28% of 3,607; Grant County, 0.09% of 6,176; and Columbia County, 0.08% of 6,007.
A soon-to-be released DNR survey from 2019 also found that 70% of Wisconsin hunters have never submitted a deer for CWD testing. The survey also found that 33% of hunters who get their deer tested don’t wait for results before eating it.
Despite such dismal numbers, GOP lawmakers are ignoring the mess by distracting everyone with the Wisconsin Sporting Freedom Act. This bag of stale air from the Kansas-based group Hunter Nation doesn’t even mention CWD.
We pause here to ask, “Sporting Freedom Act”? What is that? Do politicians think they can just insert “freedom” in a bill’s title, and we’ll snap to attention and salute? As silly as “freedom fries” sounded in February 2003, at least the word choice made sense. You’ll recall folks were mad at France for not supporting the war in Iraq, and urged restaurants to purge “French” from their menus.
Again I ask: Sporting Freedom Act? Freedom from what? Science? Biology? A future for deer hunting in Wisconsin?
If you think that’s harsh, explain how mandating the annual raising and releasing of 200,000 pheasants and 100,000 brook trout is relevant to liberty and freedom, or wise fish and wildlife management?
And how about the act’s “turkey hunting simplification” bill? Luke Hilgemann, CEO/president of Hunter Nation, recently wrote that our current spring turkey season confuses Wisconsin hunters. Really? Name someone who’s puzzled. True, our current season of six weeklong hunting periods might baffle your average lobbyist, state senator, assembly-creature, and Gov. Scott Walker’s four appointees to the Natural Resources Board. But Wisconsin’s spring season wins praise from 70% to 80% of turkey hunters surveyed annually.
Another bill in the “Freedom Act” infuriates many retired conservation wardens and the Wisconsin Hunter Education Instructor Association. The Mentored Hunt Bill (SB-611 and AB-670) would allow beginning hunters to earn their hunter-education certificate by simply taking an online course and then going afield with a licensed adult hunter, not a certified instructor.
Yes, that shortcut was allowed the past year because of COVID-19, and it sounded OK the first time I read it, but I was wrong. It doesn’t deserve our Legislature’s permanent blessing.
Hilgemann also recently wrote: “Hunting … in Wisconsin is a sacred tradition (and the Freedom Act sends) a strong message about our heritage and way of life. Not only does the Wisconsin Sporting Freedom Act reform rules for hunters and anglers, it helps ensure that future generations still have access to the resources that help these sacred traditions thrive through proactive resource management.”
Huh? You’ll find more substance in a bag of cheetos. Hunter Nation and its GOP backers insult Wisconsin’s hunting heritage by ignoring all the work of recent decades that made hunting so safe.
The WHEIA notes that conservation wardens annually investigated 174 hunting accidents, including 17 deaths, from 1956 to 1966 in Wisconsin. The state’s hunter education program began in 1967. Since then, over 17,000 volunteer instructors helped reduce those numbers to an annual average of 21 accidents and 1.8 deaths.
Y’know, we don’t need Hunter Nation messing with our programs. It’s time GOP lawmakers stop frolicking with these amateurs and get serious about addressing CWD and other obvious challenges to our natural resources.
That won’t happen, however, if hunters, anglers and trappers don’t hold lawmakers accountable with emails, letters, phone calls and votes.
Hunter Nation exposed this Legislature’s scarcity of thinkers and leaders. They must be told what to do.
— Patrick Durkin is a free-lance writer who covers outdoors recreation in Wisconsin. Contact him at patrickdurkin56@gmail.com, or at @patrickdurkinoutdoors.com on Facebook and Instagram.
Kevin Wilson
very sad, indeed very sad...
Wisconsin CWD TSE Prion Spreads To More Wild Deer In New Counties of Monroe and Oconto
FOR IMMEDIATE RELEASE: 2022-01-11
Contact: Scott Roepke, DNR Area Wildlife Supervisor
Scott.Roepke@wisconsin.gov or 715-284-1403
DNR CONFIRMS CWD IN WILD DEER HARVESTED IN MONROE COUNTY
BAITING AND FEEDING BANS RENEWED FOR MONROE COUNTY
MADISON, Wis. – The Wisconsin Department of Natural Resources (DNR) confirms two wild deer tested positive for chronic wasting disease (CWD) in Monroe County during the fall 2021 hunting season. The two deer were adult bucks harvested in the towns of Ridgeville and Glendale. These are the first confirmed wild positive cases of CWD in Monroe County.
As required by state law, the DNR enacts three-year baiting and feeding bans in counties where CWD has been detected and two-year bans in adjoining counties that lie within 10 miles of a CWD detection. Following state law, the DNR will renew a three-year baiting and feeding ban in Monroe County.
Baiting or feeding deer encourages them to congregate unnaturally around a shared food source where sick deer can spread CWD through direct contact with healthy deer or by leaving behind infectious prions in their bodily secretions.
More information regarding baiting and feeding regulations and CWD in Wisconsin is available here.
The DNR asks deer hunters in Monroe county to assist with efforts to identify where CWD occurs. Those harvesting deer within 10 miles of the newly detected positive case are especially encouraged to have their harvested adult deer tested for CWD. Collecting CWD samples is essential for assessing where and to what extent CWD occurs in deer across the state.
Information on how to have deer tested during the 2021-2022 hunting seasons is available here.
The DNR will hold a virtual informational meeting on Thursday, Feb. 3 from 6-8 p.m. to discuss CWD in Monroe County. Members of the public are invited to attend this meeting and will have the opportunity to provide input.
CWD is a fatal, infectious nervous system disease of deer, moose, elk and reindeer/caribou. It belongs to the family of diseases known as transmissible spongiform encephalopathies (TSEs) or prion diseases. The Wisconsin DNR began monitoring the state's wild white-tailed deer population for CWD in 1999. The first positives were found in 2002.
MEETING DETAILS
WHAT: CWD In Monroe County
WHEN: 6-8 p.m. Feb. 3, 2022
WHERE: Join by Zoom here.
Join by phone: 833-548-0282, Meeting ID: 818 9196 0967
FOR IMMEDIATE RELEASE: 2022-01-11
Contact: Janet Brehm, Peshtigo Area Wildlife Supervisor
Janet.Brehm@wisconsin.gov or 715-409-3277
DNR CONFIRMS CWD IN WILD DEER HARVESTED IN OCONTO COUNTY
BAITING AND FEEDING BANS RENEWED FOR OCONTO AND MENOMINEE COUNTIES, ONGOING FOR SHAWANO COUNTY
Wisconsin DNR news release
The Wisconsin DNR confirms CWD in a wild deer harvested in Oconto County. Baiting and feeding bans are renewed for Oconto and Menominee Counties and remain in effect for Shawano County.
Photo credit: Wisconsin DNR
MADISON, Wis. – The Wisconsin Department of Natural Resources (DNR) confirms a wild deer tested positive for chronic wasting disease (CWD) in the Town of Underhill in Oconto County. The deer was a one-year-old hunter-harvested buck taken during the 2021 gun deer season. This is the first confirmed wild positive case of CWD in Oconto County.
Following state law, the DNR will renew a three-year baiting and feeding ban in Oconto County as well as a two-year ban in Menominee County, as the deer was harvested within 10 miles of the county line. Shawano County is also within 10 miles of the Oconto positive’s harvest location, but is already under a longer three-year baiting and feeding ban due to a positive CWD detection at a captive deer farm earlier this year.
Baiting or feeding deer encourages them to congregate unnaturally around a shared food source where sick deer can spread CWD through direct contact with healthy deer or by leaving behind infectious prions in their bodily secretions.
More information regarding baiting and feeding regulations and CWD in Wisconsin is available here.
Those harvesting deer within 10 miles of the newly detected positive case are especially encouraged to have their harvested adult deer tested for CWD. The Farmland Zone of Oconto County has an either-sex extended archery and crossbow deer hunt through Jan. 31, 2022; harvest authorizations are still available for purchase with your license. Collecting CWD samples is essential for assessing where and to what extent CWD occurs in deer across the state.
Information on how to have deer tested during the 2021-22 hunting seasons is available here.
Successful CWD management depends in part on citizen involvement in the decision-making process through local County Deer Advisory Councils (CDAC). The DNR and the Oconto and Shawano CDACs will hold a public meeting on the status of CWD and a response plan for sampling wild deer in Oconto and Shawano County. The virtual meeting is open to all members of the public and will take place on Tuesday, Feb. 1 from 6-8 p.m. via Zoom. The public may also call in to the meeting by dialing 888-475-4499, meeting ID 871 6740 0821.
CWD is a fatal, infectious nervous system disease of deer, moose, elk and reindeer/caribou. It belongs to the family of diseases known as transmissible spongiform encephalopathies (TSEs) or prion diseases. The Wisconsin DNR began monitoring the state's wild white-tailed deer population for CWD in 1999. The first positives were found in 2002.
MEETING DETAILS:
WHAT: CWD In Oconto County
WHEN: 6-8 p.m. Feb. 1, 2022
WHERE: Join by Zoom here.
Join by phone: 888-475-4499, Meeting ID: 871 6740 0821
FOR IMMEDIATE RELEASE: 2022-01-07
Contact: DNR Office of Communications
VIRTUAL CWD RESPONSE PLAN REVIEW COMMITTEE MEETING JAN. 12
MADISON, Wis. – The Wisconsin Department of Natural Resources (DNR) today announced it will host the Chronic Wasting Disease Response Plan Review Committee meeting on Wednesday, Jan. 12 from 9 a.m. to 1:30 p.m.
The DNR’s 15-year CWD Response Plan, in effect through 2025, helps guide the department’s approach to addressing CWD in Wisconsin. The plan was developed to fulfill its public trust responsibility to manage wildlife and ensure the health of Wisconsin’s wildlife populations. As part of the plan’s implementation, the department will review progress toward meeting its goals and objectives every five years.
The committee is comprised of a group of stakeholders representing conservation, business and hunting organizations and tribal governments. During its meetings, the committee will develop input on the plan’s implementation and actions to consider as it completes this second five-year review.
Chronic wasting disease is a fatal, infectious nervous system disease of deer, moose, elk and reindeer/caribou. The Wisconsin DNR began monitoring the state's wild white-tailed deer population for CWD in 1999. The first positives were found in 2002.
More information on CWD is available on the DNR's CWD webpage.
Additional information on the DNR’s CWD Response Plan is available on the DNR’s website.
WHAT: CWD Response Plan Review Committee Meeting
WHEN: 9 a.m. – 1:30 p.m. Jan. 12, 2022
WHERE: The public is invited to watch live on the DNR’s YouTube channel here.
There is no registration required to attend, and a recording of the meeting will be posted to the DNR website.
WISCONSIN DNR CONFIRMS CWD IN WILD DEER HARVESTED IN VILAS COUNTY WITH A TOTAL OF 9,040 POSITIVE WILD CASES TO DATE
FOR IMMEDIATE RELEASE: 2021-12-17
Contact: DNR Office of Communications
DNR CONFIRMS CWD IN WILD DEER HARVESTED IN VILAS COUNTY
BAITING AND FEEDING BANS RENEWED FOR VILAS AND FOREST COUNTIES AND REMAIN IN EFFECT FOR ONEIDA COUNTY
The Wisconsin DNR confirms CWD in wild deer harvested in Vilas County. Baiting and feeding bans renewed for Vilas and Forest Counties and remain in effect for Oneida County. MADISON, Wis. – The Wisconsin Department of Natural Resources (DNR) confirms a wild deer tested positive for chronic wasting disease (CWD) in the Town of Lincoln in Vilas County. This is the first confirmed wild positive case of CWD in Vilas County.
As required by state law, the DNR enacts three-year baiting and feeding bans in counties where CWD has been detected and two-year bans in adjoining counties that lie within 10 miles of a CWD detection.
Following state law, the DNR will renew a three-year baiting and feeding ban in Vilas County as well as a two-year ban in Forest county, as the deer was harvested within 10 miles of the county line. Oneida County is also within 10 miles of the Vilas positive’s harvest location but is already under a longer three-year baiting and feeding ban due to a positive CWD detection at a game farm earlier this year.
Baiting or feeding deer encourages them to congregate unnaturally around a shared food source where sick deer can spread CWD through direct contact with healthy deer or by leaving behind infectious prions in their bodily secretions.
More information regarding baiting and feeding regulations and CWD in Wisconsin is available here.
The DNR asks deer hunters in Vilas, Forest and Oneida counties to assist with efforts to identify where CWD occurs. Those harvesting deer within 10 miles of the newly detected positive case are especially encouraged to have their harvested adult deer tested for CWD. Collecting CWD samples is essential for assessing where and to what extent CWD occurs in deer across the state.
The DNR will work with Vilas County Deer Advisory Council members to schedule a meeting in January to discuss response actions. Members of the public will be invited to attend this meeting and will have the opportunity to provide input.
CWD is a fatal, infectious nervous system disease of deer, moose, elk and reindeer/caribou. It belongs to the family of diseases known as transmissible spongiform encephalopathies (TSEs) or prion diseases. The Wisconsin DNR began monitoring the state's wild white-tailed deer population for CWD in 1999. The first positives were found in 2002.
Information on how to have deer tested during the 2020-21 hunting seasons is available here.
Wisconsin Portage County Deer Farm Tests Positive for CWD
Portage County Deer Farm Tests Positive for CWD
FOR IMMEDIATE RELEASE: December 17, 2021
Contact: Kevin Hoffman, Public Information Officer, (608) 224-5005, kevin.hoffman@wisconsin.gov
MADISON, Wis. – The Wisconsin Department of Agriculture, Trade and Consumer Protection (DATCP) confirms that two white-tailed deer at a Portage County hunt ranch have tested positive for chronic wasting disease (CWD). Positive samples were confirmed by the National Veterinary Services Laboratories in Ames, Iowa.
The 200-acre farm and its herd of approximately 370 deer are under quarantine while an epidemiological investigation is conducted by DATCP and U.S. Department of Agriculture (USDA) veterinarians and staff.
CWD is a fatal, neurological disease of deer, elk and moose caused by an infectious protein called a prion that affects the animal's brain, and testing for CWD is typically only performed after the animal’s death. DATCP regulates deer farms for registration, recordkeeping, disease testing, movement, and permit requirements.
More information
About CWD:
DATCP’s farm-raised deer program:
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This table shows available CWD test results for the selected year for each of DNR's four zones statewide. Results for an individual year are for the CWD year, which runs from April 1st through March 31st. For example, the results for the 2021 CWD year would be April 1st, 2021 through March 31st, 2022. Deer will not have full data until the datasheet is entered.
DNR Zone # Sampled # Analyzed Positive for CWD
Central Farmland Zone 5669 3231 19
Central Forest Zone 509 284 3
Northern Forest Zone 1977 1024 0
Southern Farmland Zone 6864 4919 849
Unknown Zone 162 54 2
Totals: 15181 9512 873
This table shows available CWD test results for each of DNR's four zones statewide. It includes data released through December 16, 2021. Deer will not have full data until the datasheet is entered.
DNR Zone # Sampled # Analyzed Positive for CWD
Central Farmland Zone 54182 51724 78
Central Forest Zone 7028 6801 47
Northern Forest Zone 29498 28539 6
Southern Farmland Zone 186740 184763 8904
Unknown Zone 3049 2933 5
Statewide Totals: 280497 274760 9040
Wisconsin Eau Claire County Deer Farm Tests Positive for CWD
Eau Claire County Deer Farm Tests Positive for CWD
FOR IMMEDIATE RELEASE: November 9, 2021
Contact: Kevin Hoffman, Public Information Officer, (608) 224-5005,
MADISON, Wis. – The Wisconsin Department of Agriculture, Trade and Consumer Protection (DATCP) confirms that a white-tailed deer from an Eau Claire County hunt ranch has tested positive for chronic wasting disease (CWD). Positive samples from a 3-year-old buck were confirmed by the National Veterinary Services Laboratories in Ames, Iowa.
The herd of approximately 15 deer is under quarantine while an epidemiological investigation is conducted by DATCP and U.S. Department of Agriculture (USDA) veterinarians and staff. The ranch was confirmed to have received the deer from a Waukesha County deer farm, which also has been placed under quarantine.
CWD is a fatal, neurological disease of deer, elk and moose caused by an infectious protein called a prion that affects the animal's brain, and testing for CWD is typically only performed after the animal’s death. DATCP regulates deer farms for registration, recordkeeping, disease testing, movement, and permit requirements.
More information
About CWD:
DATCP’s farm-raised deer program:
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Wisconsin Outagamie County Deer Farm Tests Positive for CWD
Outagamie County Deer Farm Tests Positive for CWD
FOR IMMEDIATE RELEASE: September 2, 2021
Contact: Kevin Hoffman, Public Information Officer, (608) 224-5005, kevin.hoffman@wisconsin.gov
Download PDF
MADISON, Wis. – The Wisconsin Department of Agriculture, Trade and Consumer Protection (DATCP) confirms that a deer farm in Outagamie County has tested positive for chronic wasting disease (CWD). Positive samples were confirmed by the National Veterinary Services Laboratories in Ames, Iowa.
The farm was already under quarantine after receiving animals from a CWD affected farm. The herd of approximately 30 deer will remain under quarantine while an epidemiological investigation is conducted by DATCP and U.S. Department of Agriculture (USDA) veterinarians and staff.
CWD is a fatal, neurological disease of deer, elk and moose caused by an infectious protein called a prion that affects the animal's brain, and testing for CWD is typically only performed after the animal's death. DATCP regulates deer farms for registration, recordkeeping, disease testing, movement and permit requirements.
More information
DATCP's farm-raised deer program: https://datcp.wi.gov/Pages/Programs_Services/FarmRaisedDeer.aspx
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CARCASS MOVEMENT, PROCESSING AND DISPOSAL
The movement of dead or alive CWD positive deer, moose, elk or reindeer/caribou (natural or human-assisted) is a key pathway in the spread of CWD. The infectious nature of the CWD prion contributes to an increased risk of introduction and spread of CWD if dead carcasses are brought to new areas and not disposed of properly.
FIND CWD SAMPLING AND CARCASS DISPOSAL LOCATIONS NEAR YOU
Wisconsin Langlade County Deer Farm Tests Positive for CWD
Langlade County Deer Farm Tests Positive for CWD
FOR IMMEDIATE RELEASE: September 1, 2021
Contact: Kevin Hoffman, Public Information Officer, (608) 224-5005, kevin.hoffman@wisconsin.gov
Download PDF
MADISON, Wis. – The Wisconsin Department of Agriculture, Trade and Consumer Protection (DATCP) confirms that a deer farm in Langlade County has tested positive for chronic wasting disease (CWD).
A positive sample from a 1-year-old doe was confirmed by the National Veterinary Services Laboratory in Ames, Iowa. All 57 deer at the 6-acre farm were already under quarantine after receiving animals from a CWD-affected farm. The herd will remain under quarantine while an epidemiological investigation is conducted by DATCP and U.S. Department of Agriculture (USDA) veterinarians and staff.
CWD is a fatal, neurological disease of deer, elk and moose caused by an infectious protein called a prion that affects the animal's brain, and testing for CWD is typically only performed after the animal's death. DATCP regulates deer farms for registration, recordkeeping, disease testing, movement and permit requirements.
More information
DATCP's farm-raised deer program: https://datcp.wi.gov/Pages/Programs_Services/FarmRaisedDeer.aspx
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Deer Farms in Sauk, Taylor Counties Test Positive for CWD
Release Date: August 11, 2021
Media Contact: Kevin Hoffman, Public Information Officer, (608) 224-5005, kevin.hoffman@wi.gov
MADISON — The Wisconsin Department of Agriculture, Trade and Consumer Protection (DATCP) confirms that deer farms in Sauk and Taylor counties have tested positive for chronic wasting disease (CWD). Results were confirmed by the National Veterinary Services Laboratory in Ames, Iowa.
Positive samples were taken from a 6-year-old doe in Taylor County and a 9-year-old buck in Sauk County. There is no connection between the two locations. The 227 whitetail deer at the 22-acre double-fenced Taylor County farm and the two whitetail deer at the 1-acre singlefenced Sauk County farm have been quarantined, meaning no live animals or whole carcasses are permitted to leave the property. The herds will remain under quarantine while an epidemiological investigation is conducted by DATCP and U.S. Department of Agriculture (USDA) veterinarians and staff.
CWD is a fatal, neurological disease of deer, elk and moose caused by an infectious protein called a prion that affects the animal's brain, and testing for CWD is typically only performed after the animal’s death. DATCP regulates deer farms for registration, recordkeeping, disease testing, movement and permit requirements.
More information
About CWD:
DATCP’s farm-raised deer program:
Title: Chronic wasting disease in a Wisconsin white-tailed deer farm
Author item KEANE, DELWYN item BARR, DANIEL item BOCHSLER, PHILIP item HALL, S item GIDLEWSKI, THOMAS item O'Rourke, Katherine item SPRAKER, TERRY item SAMUEL, MICHAEL
Submitted to: Journal of Veterinary Diagnostic Investigation Publication Type: Peer Reviewed Journal Publication Acceptance Date: 5/5/2008 Publication Date: 9/2/2008
Citation: Keane, D.P., Barr, D.J., Bochsler, P.N., Hall, S.M., Gidlewski, T.E., O'Rourke, K.I., Spraker, T.R., Samuel, M.D. 2008. Chronic wasting disease in a Wisconsin white-tailed deer farm. Journal of Veterinary Diagnostic Investigation. 20(5):698-703. Interpretive Summary: Chronic wasting disease is a fatal disease of deer and elk. Clinical signs, including weight loss, frequent urination, excessive thirst, and changes in behavior and gait, have been reported in mule deer and elk with this disorder. Clinical signs in captive white tailed deer are less well understood. In a previous study, a captive facility housed 200 deer, of which half were positive for the disease with no clinical signs reported. In this study, we examined 78 white tailed deer from a captive facility with a history of chronic wasting disease and no animals with clinical signs. Examination of the brain and lymph nodes demonstrated that the abnormal prion protein, a marker for disease, was observed in 60 of the deer. Biopsy of the rectal mucosa, a test that can be performed on live deer, detected 83% of the infected animals. The prion genetics of the deer was strongly linked to the rate of infection and to disease progression. The results demonstrate that clinical signs are a poor indicator of the disease in captive white tailed deer and that routine testing of live deer and comprehensive necropsy surveillance may be needed to identify infected herds.
Technical Abstract: Chronic wasting disease CWD is a transmissible spongiform encephalopathy or prion disease of deer and elk in North America. All diseases in this family are characterized by long preclinical incubation periods following by a relatively short clinical course. Endpoint disease is characterized by extensive deposits of aggregates of the abnormal prion protein in the central nervous system,. In deer, the abnormal prion proteins accumulate in some peripheral lymphoid tissues early in disease and are therefore suitable for antemortem and preclinical postmortem diagnostics and for determining disease progression in infected deer. In this study, a herd of deer with previous CWD diagnoses was depopulated. No clinical suspects were identified at that time. Examination of the brain and nodes demonstrated that 79% of the deer were infected. Of the deer with abnormal prion in the peripheral lymphoid system, the retropharyngeal lymph node was the most reliable diagnostic tissue. Biopsy of the rectal mucosal tissue, a site readily sampled in the restrained or chemically immobilized deer, provided an accurate diagnosis in 83% of the infected deer. The retina in the eye of the deer was positive only in late stage cases. This study demonstrated that clinical signs are a poor indicator of disease, supports the use of the retropharyngeal lymph node as the most appropriate postmortem sample, and supports a further evaluation of the rectal mucosal tissue biopsy as an antemortem test on a herd basis.
Chronic Wasting Disease Positives in Farm-raised Deer
Revised: 3/1/2021
County (Premises #) Sample Collection Date of First CWD Positive in Farmraised Deer Sample Collection Date of Last CWD Positive in Farmraised Deer Total CWD Positive in Farm-raised Deer
Portage(1) 9/4/2002 1/18/2006 82
Walworth(1) 9/20/2002 12/13/2002 6
Manitowoc 3/5/2003 3/5/2003 1
Sauk(1) 10/3/2003 10/3/2003 1
Racine 5/1/2004 5/1/2004 1
Walworth(2) 7/28/2004 11/3/2004 3
Crawford 1/19/2005 1/25/2007 2
Portage(2) 9/22/2008 11/18/2008 2
Jefferson 12/1/2008 12/1/2008 1
Marathon 11/7/2013 11/9/2020 113
Richland(1) 9/13/2014 11/19/2014 8
Eau Claire 6/8/2015 11/24/2015 34
Oneida 11/4/2015 12/8/2020 23
Iowa(1) 1/22/2016 11/19/2020 5
Oconto 9/4/2016 1/15/2021 215
Shawano 9/18/2017 1/10/2021 63
Waupaca 9/21/2017 12/7/2017 12
Washington 2/18/2018 11/15/2018 12
Richland(2) 5/11/2018 5/11/2018 1
Dane 5/16/2018 5/16/2018 1
Iowa(2) 5/18/2018 5/18/2018 21
Marinette 5/19/2018 12/4/2020 2
Sauk(2) 6/4/2018 11/28/2018 2
Portage(3) 10/23/2018 10/23/2018 1
Portage(4) 11/16/2018 5/1/2019 8
Forest 1/8/2019 12/7/2020 8
Burnett(1) 7/30/2019 7/30/2019 1
Trempealeau 11/7/2019 11/4/2020 3
Burnett(2) 9/3/2020 9/3/2020 1
Registered Deer Farms and Past/Current CWD Farms
^_ Hunting Ranches Infected with CWD Currently in Operation
^_ Deer Farm Infected with CWD Currently in Operation
!( Past Positive CWD Farms, Depopulated
!( Currently Registered Farm-Raised Deer Farms
CWD Affected Counties March 2021
Wisconsin Buckhorn Flats CWD
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.
see;
Title, Baiting and Feeding
Baiting and feeding deer brings a greater number of deer into close contact with each other. This increases the chances of Chronic Wasting Disease (CWD) being transmitted from deer to deer. One of the ways this can be done is nose to nose contact. Deer droppings and urine are also concentrated at bait sites or feeding station. That also increases the chances for a healthy deer to pick up the prions that cause CWD.
Outdoor News, Feb. 23, 2018 Pg. 9
The state's worst site remains the former Buckhorn Flats Game Farm near Almond in Portage County, where 80 deer tested positive for CWD from 2002 to 2006. When the U.S. Department of Agriculture shot out the 70 acer pen in January 2006, 60 of the remaining deer 76 deer carried CWD, a nearly 80 percent infection rate.
This proves that concentrating deer increases the spread of CWD.
Solution, ban baiting and feeding
BE IT RESOLVED, that the Conservation Congress, DNR and Legislative Bodies work together to write a law that puts a moratorium on baiting and feeding until a cure is found for wild deer in Wisconsin.
Harold Halverson
Private Citizen W12431 820th Ave. River Falls, Wi. 54022 PH 715-781-6804
Chronic wasting disease in a Wisconsin white-tailed deer farm
THURSDAY, FEBRUARY 10, 2022
Wisconsin two white-tailed deer at a Waukesha County farm have tested positive for chronic wasting disease (CWD)
***> Minnesota Board of Animal Health Report Concurrent Authority Regulating Farmed White-tailed Deer and CWD TSE Prion
Minnesota Board of Animal Health
Report: Concurrent Authority Regulating Farmed
White-tailed Deer
As required by Minnesota Session Law 2021, 1st Special Session, Chapter 6 02/01/2001
Report to the Minnesota Legislature Minnesota Department of Natural Resources
500 Lafayette Road Saint Paul, MN 55155 (Phone) 651-296-6157 info.dnr@state.mn.us dnr.state.mn.us
As requested by Minnesota Statute 3.197: This report cost approximately $37,368 to prepare, including staff time and contracting expenses.
Upon request, this material will be made available in an alternative format such as large print, Braille or audio recording. Printed on recycled paper.
Contents
Background 1
Work Accomplished to Date 2
Inspections of Farmed White-tailed Deer Facilities 2
Data Sharing and Analysis - Animal Health Information System 3
Internal Communications 3 Concurrent Authority Implementation Challenges 3
Ongoing Challenges to Managing CWD 5
Compliance Inspections and Enforcement 5
Movement 6
Costs of CWD Surveillance in Wild and Farmed White-tailed Deer 6
Recommendations 7
Roles and Responsibilities 7
Communication 7
Recommendations for Rule and Statute Changes to Address CWD Challenges 7
Appendix A: DNR Project Plan-Captive Cervid Facilities Co-Management 9
Background
The 2021 Minnesota State Legislature, in a special session ending in July 2021, issued direction to the Minnesota Department of Natural Resources (DNR) and the Board of Animal Health (BAH) by amending Chapter 35.155 as follows:
2021 Minn. Laws 1st Sp. Sess. Chap. 6 Art. 2 Sec. 17
Subd. 14. Concurrent authority; regulating farmed white-tailed deer.
(a) The commissioner of natural resources and the Board of Animal Health possess concurrent authority to regulate farmed white-tailed deer under this section, sections 35.92 to 35.96, and any administrative rules adopted pursuant to this section or sections 35.92 to 35.96. This does not confer to the commissioner any additional authorities under chapter 35, other than those set forth in sections 35.155 and 35.92 to 35.96, and any administrative rules adopted thereto.
(b) By February 1, 2022, the commissioner of natural resources, in conjunction with the Board of Animal Health, must submit a report to the chairs and ranking minority members of the legislative committees and divisions with jurisdiction over the environment and natural resources and agriculture on the implementation of the concurrent authority under this section. The report must include:
(1) a summary of how the agencies worked together under this section, including identification of any challenges;
(2) an assessment of ongoing challenges to managing chronic wasting disease in this state; and
(3) recommendations for statutory and programmatic changes to help the state better manage the disease.
In the 2005 legislative special session, the Legislature amended the farmed cervid program statutes to give authority over farmed cervids to the BAH; prior to this change, the DNR had managed the state’s farmed cervid program. The DNR continues to manage regulation of other similar commercial activities, including taxidermies, commercial minnow/fish harvest, logging, and commercial decorative forest products.
This report fulfills the requirements to report to the Legislature by February 1, 2022, summarizing how the agencies worked together under concurrent authority, describing ongoing challenges to managing chronic wasting disease (CWD) and providing recommendations for moving forward.
Work Accomplished to Date
Upon enactment of 2021 Min. Laws 1st Sp. Session, Chapter 6 Art. 2 Sec. 17, the DNR created a farmed cervid project plan entitled Captive Cervid Facilities Co-Management Project Plan (see Appendix A) and assembled a project team. The project team’s plan contains deliverables including completion of an early set of at least 40 inspections of white-tailed deer facilities with BAH staff, development and implementation of data management and protocols, and engagement with the BAH on recommendations for policy and programmatic changes to reduce the spread of CWD. In October 2021, the BAH’s internal cervid program staff organized a similar farmed cervid project team and established a weekly interagency meeting with the DNR project team to discuss the activities taking place under concurrent authority.
Inspections of Farmed White-tailed Deer Facilities
Immediately upon passage of concurrent authority legislation, the BAH engaged with the DNR to provide structured training on program management, conducting epidemiological investigations, and monitoring whitetailed deer movement. This education progressed into real-time field training during joint BAH and DNR farm inspections. Additionally, BAH staff provided guidance and instruction to the DNR in email communications, reference documents and written processes. This training was initially provided to support BAH inspectors during field activities, with an eventual goal of DNR staff conducting inspections independently in the future.
DNR and BAH staff conducted joint inspections of white-tailed deer farms. Initially, BAH served as the lead inspector while the DNR took an active learning role. As inspections progressed into the late fall and early winter, the DNR took a more active role, offering suggestions to mitigate interaction between farmed and wild white-tailed deer and helping BAH inspectors determine compliance. From the end of August to December 2021, DNR and BAH inspectors jointly inspected 50 registered Cervidae farms and identified 17 compliance infractions:
• 10 farms with inadequate fencing;
• 2 farms with inadequate redundant gating;
• 2 herd owners’ failure to submit death reports within the required timeline;
• 1 herd owner’s failure to submit samples for CWD testing;
• 1 farm where inspectors could not visualize official ID, and
• 1 farm with official identification missing.
During the inspections, DNR staff closely evaluated the potential for farmed and wild deer to interact near fence lines, since this is a potential risk for the spread of CWD. DNR found:
• Good deer cover or habitat at the fence line on 35 farms.
• Close or direct contact potential between farmed and wild deer on 22 farms. Evidence included feces, rubs/scrapes, tracks, and wild deer sightings in the vicinity of the fence.
• At least one water, feed, or mineral station within 10 feet of the perimeter fence on 23 farms; 17 farms had at least one feeder within 10 feet of the fence.
This new information shows that wild and farmed deer have the potential to interact at fence lines; given that, it reinforces the need for strong fencing requirements and compliance. Further, it highlights the potential for exclusionary fencing to offer additional safeguards for separation of wild and farmed deer.
Data Sharing and Analysis - Animal Health Information System
The BAH uses CoreOne by Trace First as its animal health information system. This system contains data for animals regulated by the BAH, including farmed white-tailed deer herds and mixed-species herds. The DNR and BAH considered multiple options to determine how the DNR could access needed data from the BAH database. The most important factors were data privacy and cost. Minnesota Government Data Practices statutes regulate access to data the BAH maintains. Ultimately, to provide DNR staff with only the data necessary for concurrent management, the BAH, DNR and Minnesota IT Services (MNIT) staff worked with CoreOne by Trace First to create a second, separate database that contained only data related to farmed white-tailed deer herds. The vendor copied farms with mixed-species herds data, and permanently moved data related to farms with only white-tailed deer herds, from the BAH system into the DNR database.
The DNR just recently obtained access to view data in this separate system. However, access is limited to a readonly testing phase through the end of January 2022. Because of this limitation, and the desire to limit duplicate data entry, the DNR has been unable to enter data into the new database. Given this, the DNR has not yet assigned dedicated staff to enter or manage this system. There will be a final migration of white-tailed deer farm data into the new DNR database on Feb. 1, 2022. This process will solidify the new DNR CoreOne database as the system of record for farmed white-tailed deer moving forward; however, both agencies will maintain access to this database.
Internal Communications
Both agencies have internal teams working on the white-tailed deer program. The DNR project team meets weekly with a standing agenda to discuss topics surrounding farmed white-tailed deer and concurrent authority. The agenda covers farm inspections, data management, communications, and emergent issues such as escapes, movement bans and compliance issues. The BAH also holds an internal weekly meeting and supplies meeting notes to the DNR.
In addition, the DNR and BAH staff hold weekly joint meetings that include similar agendas as the internal meetings but also cover interagency communication topics, training and education, and stakeholder communications. These meetings keep the agencies informed on current activities under the concurrent authority.
Concurrent Authority Implementation Challenges
One significant challenge has been establishing a mutual understanding of what concurrent authority looks like operationally. Although BAH and DNR have different skills and mandates, both agencies agree CWD is a common threat for farmed and wild white-tailed deer and other cervids, and that joint management offers strategic benefits. The agencies are engaging in discussions on how to optimize concurrent authority to contain and manage CWD.
The challenges related to farm inspections, data documentation, and communications identified thus far are:
• Farm inspections: Up to three DNR and BAH staff members have participated in each of the 50 inspections conducted since concurrent authority was enacted. Training and educating DNR staff is necessary during this transition period. To date, DNR staff have not taken the lead in any part of the inspection process. There is a need to clarify roles and scope for BAH and DNR inspectors in the farminspection process. Additionally, concurrent authority in general, and DNR staff presence on farms in particular, has caused concern among some herd owners. There have been at least two incidents of strong resistance to these changes by herd owners. BAH anticipated this response and developed a policy that it would not conduct an inspection unless a producer allowed DNR staff on premises.
• Data sharing and analysis. In addition to continued training for DNR staff on the CoreOne system, and the potential hiring of additional data entry staff, maintaining two systems for mixed species farms will be an ongoing challenge. Since the BAH currently maintains the exclusive regulation and data ownership of farmed non-white-tailed deer species, including those in mixed species herds, there will be a continued need for BAH staff to manage data in both systems. Some duplication of data will be required in certain cases: for example, maintaining a current list of certified CWD sample collectors. Due to the complex nature of certain program data, such as inventories, a go-live date of Feb. 1, 2022 means some 2021 data will still need to be entered. As a result, BAH staff will have to duplicate that remaining data in both systems. Reporting activities will be more complicated now that data are split between two databases. Not only will new platforms with reporting criteria need to be developed and connected to the DNR system, there also will be a significant amount of data-combining needed for reports involving multiple species of farmed cervids. Additional protocols will need to be determined in the future as the new system moves into a live phase.
• Internal communication. Significant progress has been made to improve communication between agencies since concurrent authority was granted. Prior to October 2021, each agency worked fairly independently to develop plans. Since then, the DNR and BAH have been addressing the challenges of consistent flow and clarity between the two agencies and developing a mutually agreed-upon vision for concurrent authority and its implementation.
• Public communication. Coordination between the DNR and BAH surrounding public communication is a work in progress. In January 2019 (prior to concurrent authority), a Memorandum of Understanding (MOU) was finalized between the DNR and BAH that contained protocols for sharing information between agencies and communicating with the public. These protocols must be reviewed to make this agreement operational under concurrent authority.
Ongoing Challenges to Managing CWD
CWD is a fatal, neurologic disease that affects cervids including white-tailed deer, mule deer, elk, moose, reindeer, and others. Minnesota is home to approximately 1 million free-ranging white-tailed deer, about 3,000 moose, and several hundred free-ranging elk. The discovery of CWD in Minnesota in either free-ranging or farmed cervid populations represents a risk to all susceptible species.
The primary risk factors facilitating the introduction of CWD into Minnesota—or its spread within the state—are the movement of live cervids and high-risk carcass parts (e.g., brain, spinal column). In wild populations, live cervid movements are typically limited to their distinct home ranges and migratory patterns attributed to each species. In the farmed cervid industry, movement of live cervids through sales and exchanges can cover hundreds of miles. Cervid carcasses can also move long distances, from harvest locations to homes, taxidermists or meat processors. Both types of movements can contribute to CWD spread through direct contact or environmental contamination.
Minnesota has addressed the risk of hunter-mediated interstate carcass movements with a blanket ban that restricts the import of any whole cervid carcass from anywhere outside of Minnesota, including Canada, regardless of chronic wasting disease status. Successful out-of-state hunters may only bring back quarters, deboned meat, cleaned skull plates, and finished taxidermy mounts. Similarly, Minnesota imposes intrastate carcass movements of cervids harvested within CWD management zones until CWD test results are received, with the exception of quarters or deboned meat, and provides dumpsters to reduce the instances of carcasses left on the landscape in high-risk areas. For farmed cervid carcasses, Minnesota does not allow cervid carcass movement from a CWD endemic area, except for cut and wrapped meat, quarters or other portions of meat with no part of the spinal column or head attached. Carcasses may not be imported into Minnesota from a herd infected with or exposed to CWD.
It is understood that the concurrent authority granted and referred to in this report is limited to white-tailed deer. Because chronic wasting disease affects additional cervid species, the following sections refer to the ongoing challenges in managing CWD risk to all susceptible animals in the state.
Compliance Inspections and Enforcement
An important component of managing CWD is the regulation of cervid farms. There have been inconsistencies noted in compliance inspections and enforcement activities. Communication with herd owners regarding regulations and other contributing factors to disease spread between wild and farmed herds, such as methods to evaluate the potential for wild and farmed deer interactions near the fence, will aid in managing overall risk. Consistent and firm enforcement of statutes and rules must take place, regardless of which agency has the authority.
Movement
Interstate Movement
Current Minnesota Rules prohibit the import of live cervids from herds infected or exposed to CWD, as well as herds existing in counties where CWD has been detected in free-ranging cervid populations. Interstate movement of live cervids is permitted if the originating herd participates in a federal CWD certification program; however, most of the herds discovered to have CWD in the United States in the past 5 years have been Level 6 (highest level of certification) at the time of disease discovery. This suggests the certification program does not adequately address disease risk. The lack of a validated ante-mortem test for CWD, which would indicate illness or infection sustained before death, allows movement of infected live cervids early in the incubation period of the disease, often months or years before the disease is identified on the source premises. This built-in delay in disease discovery exposes other cervid herds receiving these infected animals, as well as the free-ranging cervid populations that exist in the surrounding area, to increased risk of CWD.
Intrastate Movement
Movement within states (intrastate) holds similar CWD risks as movement between states (interstate). CWD certification status has not proven to be an accurate indicator of a facility’s disease status. Of the 12 farmed cervid herds confirmed with CWD in Minnesota, all but one were at a Level 6 certification status at the time of disease discovery. Further, spread of CWD among farmed herds through intrastate movements has spread the disease hundreds of miles across Minnesota, increasing risk to wild populations through fence-line contact and mechanical movement of prions.
Currently, the BAH defines “CWD Endemic Areas” as 15-mile radius circles around wild CWD-positive deer, and farmed herds within these areas have movement restrictions. However, any movement of deer from CWD endemic areas increases the risk of disease spread.
Costs of CWD Surveillance in Wild and Farmed White-tailed Deer
The State of Minnesota covers the cost of CWD testing of all farmed Cervidae over 12 months of age that die or are killed. In addition, testing is required of newborns over six months of age that die or are killed in herds that are quarantined with CWD-exposed animals in the herd. In 2021, Minnesota spent $55,176 on CWD testing of farmed cervids.
Additionally, Minnesota spent approximately $2.9M in fiscal year 2021 on additional CWD-related activities such as sampling and testing hunter-harvested deer, conducting targeted culling, CWD surveillance planning and deer movement studies.
Each new CWD-positive farmed herd results in a minimum of 3 years of wild deer surveillance at a cost to Minnesota of $300,000 to $500,000. The cost increases if the disease has migrated into the wild population and mitigation and management efforts must continue.
Recommendations
As concurrent authority for farmed white-tailed deer continues, the DNR and BAH recommend the responsibilities that fall under Minnesota statutes 35.155, 35.92 to 35.96, and any administrative rules adopted, be assigned to agencies and acted on in a predictable, coordinated way. DNR and BAH will develop a new interagency MOU to create a shared vision, address all responsibilities, and create a transition plan to implement agreed upon actions and roles. The agencies will continue planning to assess the benefit of revising statutes and rules related to the division of responsibilities between themselves.
Roles and Responsibilities
The DNR and BAH have defined a list of activities involved in the regulation of farmed white-tailed deer and further clarified which activities best fit the skills and mandates of each agency. Examples of activities include inspections and follow up, tracking white-tailed deer movement, data entry and management, and rule development. The agencies will continue to refine roles and responsibilities and will formalize this in an interagency MOU.
Communication
Coordinated communication with Minnesotans and specific stakeholder groups, such as deer farmers and deer hunters, is critically important.
While the 2019 MOU between the DNR and BAH related to roles and responsibilities around cervid management provides a strong foundation, the agencies agree that a coordinated effort must continue to address this important priority.
Recommendations for Rule and Statute Changes to Address CWD Challenges
The BAH has been pursuing changes to Minnesota Rules Chapter 1721 for cervid program rules modifications for approximately two years. The agency has enlisted the assistance of a rules advisory team, held numerous virtual listening sessions for many diverse groups and communicated publicly during the process. The change to concurrent authority occurred during this rules process. The BAH paused its rules process after the legislative change, intending to pick up the important and imperative work with DNR rule writing staff for the white-tailed deer portion of the rules. The BAH recommends the DNR provide designated staff to continue this work in cooperation with the BAH.
The DNR has identified areas of CWD transmission risk it believes can be mitigated through changes to rule and statute. These changes have the potential to benefit both wild cervids and the farmed cervid industry. • Fence deficiencies: Perimeter fences are the last line of defense in keeping farmed deer secure inside the enclosure and keeping wild deer out. Fences must meet specifications and be free of defects to promote animal containment and reduce escapes.
o DNR recommends reducing the time allowed for repair of fence deficiencies from 45 days to 14 days (Statute 35.155, Subd. 4). This change would be further supported in Rule 1721.0380 General Requirements: Subp. 3. Inspections B with a reduction in time allowed for repair from 45 to 14 days. Further, a change to Inspections A to reduce the window for reinspection from 3 months to 30 days will help ensure fence deficiencies are corrected in a timely manner.
• Spread of CWD through interstate and intrastate movement: We must minimize the risk of deer moving between herds spreading disease. To accomplish this, we must be able to account for all animals in a herd, ensure they are properly identified, and inventories are accurate.
o DNR recommends statutory and rule changes that require all white-tailed deer fawns be tagged within 14 days of birth, physical inventories occur on 2-year intervals to verify ID of all animals in the herd, and record keeping that includes age, sex, species, date of birth/acquisition, and parentage (Statute 35.155 Farmed Cervidae, Subd 6, 7; Rules 1721.0390 Animal Identification, 1721.0380, Subp. 10. Record Keeping, 1721.0380 General Requirements).
o DNR recommends prohibiting import of cervids from any herd originating from a state or province where CWD has been detected in either farmed or wild deer. This would also prohibit all movement of live cervids that originate from a herd within a CWD Management Zone, except direct to slaughter (Statute 35.155 Farmed Cervidae, Subd 12; Rules 1721.0400 Importation of Farmed Cervidae, 1721.0410. Intrastate Movement of Farmed Cervidae).
• Rapid detection of CWD within a herd, timely depopulations, and containment of prions in the environment: To increase the opportunity to detect CWD early within a herd, it’s important to test all animals upon death.
o DNR recommends requiring CWD testing upon death for all deer ≥6 months, reporting the death within 7 days, and submitting all collected tissue samples within 7 days to an appropriate laboratory (Statute 35.155 Farmed Cervidae, Subd 11, Rules 1721.0420 CWD).
o DNR recommends that herd owners who fail to test all dead deer for CWD have movement restrictions on their herd.
o DNR recommends that herds confirmed with CWD be required to be depopulated within 30 days by the owner if an indemnification application is not submitted (Rule 1721.0420 CWD). Also, all herd depopulation plans will be required to include perimeter fencing requirements maintained for 20 years to reduce risk of spread to wild cervids (Statute 35.155 Farmed Cervidae, Subd 11, Rules 1721.0420 Subp. 2, CWD).
Appendix A: DNR Project Plan-Captive Cervid Facilities Co-Management
Project Plan
Captive Cervid Facilities Co-Management
DRAFT as of July 22, 2021
Background (Why We’re Doing This)
During the 2021 special legislative session, the state legislature passed a law directing the MN Department of Natural Resources (DNR) and the Board of Animal Health (BAH) to concurrently manage farmed cervid facilities containing whitetailed deer. Part of this concurrent authority provision requires a report to the legislature by February 1, 2022, detailing how the agencies have worked together, an assessment of ongoing challenges to managing Chronic Wasting Disease (CWD) in the state, and recommendations for further statutory and programmatic changes to address the disease. The report and associated activities require focused effort by both agencies to ensure appropriate response. The Commissioner’s Office has established this high-priority project within the DNR’s Enforcement (ENF) and Fish and Wildlife (FAW) divisions to ensure our own agency’s capabilities to work as an effective partner toward that end, and to do our part alongside BAH to make tangible progress.
The current political and operating environment both pose numerous risks, given the high profile of CWD within the state, concerns about the disease’s spread, and the inherent challenges of two state agencies with overlapping but different missions working together quickly and effectively. Nevertheless, the Commissioner’s Office and project team are confident that our work can reflect the best values of the agency and state work: science-driven and fact-based decision-making; accountability to taxpayers and legislature for activities undertaken; and strong partnership with and respect for BAH, captive cervid facility owners, and other stakeholders.
Goals and Deliverables (What We’ll Do Together)
We want to achieve the following broad goals as a project team and agency:
• Prevent the spread of CWD in both farmed and wild cervid populations;
• Ensure compliance of all farmed cervid facilities with relevant state laws and rules;
• Fulfill the legislative requirements for farmed cervid facilities containing white-tailed deer;
• Identify deficiencies of existing laws and rules, provide recommendations in the February report, and keep working beyond that report to make thoughtful changes to those laws and rules; and
• Demonstrate a strong, effective relationship between DNR and BAH.
• Biosecurity Compliance – biosecurity rules must be adhered to by field staff or others going on farmed cervid premises for inspections, enforcement, or other types of site visits to prevent the spread and introduction of disease to and from the premises.
To make progress toward these goals, we will focus on the following specific deliverables during the timeline of this project:
• Immediate rules progress. Engage the current rules package under consideration by the BAH and seek tangible, positive changes regarding farmed cervid facility management that will demonstrate early engagement with the state legislature’s directives.
• Staff capacity. Hire, designate, develop, and/or train staff within the FAW and ENF divisions to establish long-term capacity for inspections, compliance assurance, and related ongoing statutory obligations.
• Data capacity. Engage BAH and Minnesota IT Services (MNIT) to develop and implement the data governance, management, and equitable sharing processes required for effective concurrent authority over farmed cervid facilities containing white-tailed deer.
• Early set of inspections. 40 white-tailed deer facilities would be inspected prior to the legislative report. Facilities inspections would be targeted to get an equitable cross section of facilities of all types and sizes across the state. This would represent a clear, tangible mark of progress that, like the data capacity and immediate rules progress, would improve the quality of the mandated report. At least one representative from FAW and ENF Divisions will be on every inspection. BAH and DNR would be completing inspections together to ensure the inspection process is done in a consistent manner. However, FAW and ENF Divisions would complete inspections without BAH if they are otherwise unable to complete inspections as needed or in the timeline provided within the project plan.
• Communications plan. As we release the report to the legislature, the project will have a communications plan ready to ensure legislators, conservation organizations, the media and public are aware of the work and understand its context and importance. Part of the message should also indicate what next steps may happen, and how to engage future process. The DNR will solicit comments from BAH on the communications.
• Mandated report. Submit a report by February 1, 2022, to the appropriate legislative authority on the implementation of the concurrent authority, as required by the recent law. This report will detail how the agencies have worked together, an assessment of ongoing challenges to managing Chronic Wasting Disease (CWD) in the state, and recommendations for further statutory and programmatic changes to address the disease.
In Scope (What We’ll Do and Discuss to Get the Deliverables)
Analysis of existing policies and rules, and proposals for changes. The fundamental driver of this project is the state legislature’s desire to see things change, to improve outcomes on CWD disease spread. All relevant policies, procedures, and rules are on the table. A science-driven, fact-based approach to policy analysis is essential.
Partnership with the BAH and MNIT. While this project contains deliverables and activities that DNR has some control over, we cannot succeed without our colleagues in BAH and MNIT. This project’s initial focus is on the internal activities we need to conduct immediately, to ensure success. The team’s priority will be to transition to the concurrent inspection, enforcement, and investigation authority implementation in collaboration with the BAH. After completion of the report and draft rules, the project’s leadership will shift the focus toward the more collaborative and longer-term activities required for ultimate success. The activities related to data are particularly complex and will require close partnership, early on.
Engagement with farmed cervid facilities’ owners and other key stakeholders. Effective and thoughtful communication and outreach strategies will be crucial to early and long-term success. The best compliance outcomes are from parties who are informed, engaged, and educated on the regulations’ purpose. We can and should seek their input at appropriate points in the rulemaking and policy analysis process, during and after this project. An initial list of such stakeholders is below.
Out of Scope (What We’ll Set Aside So We Can Focus on the Deliverables)
Wild and farmed cervid species beyond white-tailed deer. While the report and policy components of this project may point out known/discovered interactions between farmed white-tailed deer and other cervid species, the primary focus should be on farmed white-tailed deer. In addition, any enforcement or compliance activities will focus only on what the legislation directs.
Activities beyond winter 2022. For the sake of project focus, this outline is only for those activities that will lead up to the generation, submission, and presentation of a successful legislative report. Certainly, those activities (e.g., hiring staff) will set us up for long term success. New deliverables we design, for which we cannot complete a tangible milestone by February 2022, whether on our own as an agency or in partnership with BAH, will have their own project definition developed and dedicated resources to work on.
Roles and Responsibilities (Who Will Do What)
Most of the project’s roles and responsibilities fall to staff within the ENF and FAW divisions; there are also resources assigned from Operations Services Division (OSD) and MNIT at DNR. As noted above, as the project progresses, project leadership may either adjust this work or generate a new project that would express partnership roles for BAH staff, with their consent and full participation.
snip...
Again, there will be multiple activities that can and must continue beyond the scope of this project. Executive and managing sponsors should consider developing a longer-term planning framework that tracks additional necessary work, such as the development of an advisory group, additional staffing needs, ongoing policy-making processes, long-run enforcement and compliance activities, and how the agency will pursue the recommendations generated by the report. Logistics (Where and How We’ll Do All of This)
Given the multiple deliverables that are part of this project, there will be multiple “sub-teams”:
• Immediate rules changes. Led by Michelle Carstensen.
• Report generation. Led by the project managers.
• Policy analysis (including the interagency consulting team). Led by [TBD].
• First set of early inspections. FAW and ENF will conduct facility inspections. Led by project managers or TBD designees.
• Data protocols. Led by Bruce Anderson.
• Others as needed
The logistics for each team will be a bit different, given the wide differences in timeline and product. Common risks for each sub-team to consider while progressing: Coordination with BAH. Interagency collaboration can be challenging even under the best of circumstances. Here, the time pressures, staffing pressures, and political visibility of the issue all contribute to very high risk of process failure.
In particular, a team from BAH consisting of Linda Glaser, Annie Balghiti and Courtney Wheeler and DNR staff consisting of Michelle Carstensen, Robert Gorecki and Chris Balzer immediately will be assigned to the project. Project managers and managing sponsors should consider how to coordinate these contacts. Closer collaboration on this project, and inclusion of key BAH personnel on the full project team, should be an early consideration. This will help efficiency with communication and logistics for all moving parts.
• Issue complexity. CWD spread is well-recognized as a complex public policy issue involving multiple state and federal agencies; a wide range of stakeholder groups with strongly differing opinions; and natural limits to what testing and observation can tell us in a timely manner.
• COVID-19 protocols. While some staff may be returning from telework (or never did), a large portion of relevant staff should still be presumed teleworking for at least some of the time, early in the project timeline. Sub-teams should carefully consider the safety of all colleagues and partners when scheduling meetings, inspections, and other project activities.
• Public perception and political pressure. The entire project faces the well-known risk of misperceptions or mischaracterization by some members of the public as to what the DNR (or any state agency) can reasonably accomplish, as well as what enforcement activities may be reasonable. Project team members can minimize these risks and their impact by committing to themselves and each other an approach of mutual respect toward differing
perspectives, and a collaborative approach to colleagues who may disagree. Whatever the final product, all project team members must stand behind it.
• Data Collection and Dissemination Protocols. All staff must adhere to data practices regulations under MN Statute: 13.643 Subd. 6. Animal premises data: There are implications for the public (or not public) status of certain data that will require training and careful practice. Close coordination with both agencies’ Data Practices Compliance Officials will be a key strategy in minimizing the risk of inappropriate data use. Data collection will benefit from a data management plan.
The full project team should check in at least monthly. Sub-teams should check in at least weekly. Project managers should consult with managing sponsors (and if desired, the project facilitator) at their discretion, but no less frequently than biweekly.
March 7, 2022 4:39 PM
Proposed moratorium on new deer farms moves on to environment committee
By Rob Hubbard
How widespread are chronic wasting disease and COVID-19 in deer that live on Minnesota farms?
We don’t really know.
A comprehensive study hasn’t been undertaken on the farmed deer of Minnesota, but an Iowa study completed in 2021 found 80% of the sampled deer on farms there tested positive for COVID-19, according to Kevin Dupuis, chairman of the Fond du Lac Band of Lake Superior Chippewa.
That’s one reason Rep. Rick Hansen (DFL-South St. Paul) is sponsoring HF3273, a bill that would prohibit the Board of Animal Health from approving new registrations for the possession of farmed white-tailed deer.
On Monday, the House Agriculture Finance and Policy Committee voted 8-4 along party lines to refer the bill to the House Environment and Natural Resources Finance and Policy Committee.
The bill’s companion, SF3169, sponsored by Sen. John Marty (DFL-Roseville), awaits action by the Senate Agriculture and Rural Development Finance and Policy Committee.
“The first step is to stop the bleeding, and that is to issue no new registrations,” Hansen said. “There is precedence for this, about 20 years ago, with registrations for commercial turtle harvesting. … Last fall, we had testimony that there had been six to 10 new registrations per year.”
Craig Engwall, executive director of the Minnesota Deer Hunters Association, said his approximately 20,000-member organization supported the bill’s proposed moratorium at its recent annual meeting.
“Chronic wasting disease is a strong focus [for the organization], and we virtually unanimously supported a moratorium on new registrations as a means of protecting the wild deer herd,” he said. “On Feb. 1, the DNR and the Board of Animal Health issued their joint report finding that there was about a 34% infraction rate on their inspected farms. These included inadequate fencing, inadequate gates, refusing inspection. We believe we’ve reached the point where the wild deer herd is under significant threat.”
Representing the Minnesota Deer Farmers Association, Tim Spreck said the bill would do “irreparable damage” to the deer-farming industry. “We’re trying to drive the deer-farming industry into oblivion, one cut at a time. We don’t want to be bought out. We don’t want to go away.”
Rep. Rob Ecklund (DFL-International Falls) noted it was the first time he’d heard committee discussion of the state “buying out” the deer farming industry.
“Let’s clean up this industry,” Ecklund said. “I’ve never said let’s eliminate it. I think it has value. I’ve just been trying to protect the wild deer herd.”
When Rep. Paul Anderson (R-Starbuck) asked Hansen if he would support a buyout, Hansen replied, “No, because it would just turn into a publicly funded auction.”
“I think the mistakes have been delicate ones,” Anderson said. “And I think this takes a sledgehammer to things. I think this is too severe and strict on the deer farmers.”
Feb 14 2022 4:05PM
Deer farmers could face more requirements to safeguard against chronic wasting disease
By Brian Hall
In a continuing effort to eradicate and control the spread of chronic wasting disease, Minnesota deer farmers could be forced to test their entire herd.
Sponsored by Rep. Rob Ecklund (DFL-International Falls), HF2814 would require owners of farmed white-tailed deer to test their animals for the disease by October. Additional testing would be required for animals who test positive for chronic wasting disease.
The bill includes a $250,000 appropriation to the Board of Animal Health for the testing and would establish a requirement for a soil test before sale or transfer of land where the disease was detected while farming cervids, including deer, moose and elk.
Following a 9-3 vote by the House Agriculture Finance and Policy Committee Monday, the bill was sent to the House Environment and Natural Resources Finance and Policy Committee without recommendation, in part, due to questions surrounding the testing used for the deer and soil.
The real-time quaking-induced conversion test has not been approved by the U.S. Department of Agriculture.
Rep. Rob Ecklund
“Approval is expected in the near future,” Ecklund said. “We go to great lengths and take all precautions in protecting our meat and food supply. The RTQuIC test is one more tool that we have available to protect the industry.”
Several Republicans felt the bill was being considered too early given the test hasn’t been approved by the USDA.
Rep. Paul Anderson (R-Starbuck) said that the bill was originally going to be laid over before a late addition recommended it be moved on. Because of the time, Anderson said members didn’t feel an urgency in putting amendments forward.
“Given what we’ve heard today, we do need to slow down,” said Rep. John Burkel (R-Badger).
Ecklund said there’s approximately 3,500 captive white-tailed deer in the state.
“If we do find any problems through the use of this technology, then we would know the areas in the state that need the most attention,” he said.
The companion, SF3037, is sponsored by Sen. John Marty (DFL-Roseville) and awaiting action by the Senate Agriculture and Rural Development Finance and Policy Committee.
“We’ve been fighting CWD for five years,” Ecklund said. “I’d like to get to the bottom of what’s going on here.”
He later added: “If we had something in our swine population, if we had something in our turkey population, if we had something in our cattle population, it would be all hands on deck to make sure that we were addressing this.”
''Several Republicans felt the bill was being considered too early given the test hasn’t been approved by the USDA.''
''Rep. Paul Anderson (R-Starbuck) said that the bill was originally going to be laid over before a late addition recommended it be moved on. Because of the time, Anderson said members didn’t feel an urgency in putting amendments forward.''
“Given what we’ve heard today, we do need to slow down,” said Rep. John Burkel (R-Badger).''
''Ecklund said there’s approximately 3,500 captive white-tailed deer in the state.''
“We’ve been fighting CWD for five years, ” Ecklund said. “I’d like to get to the bottom of what’s going on here.”
END
***> WHILE republicans and captive lobbyist continue to flounder, CWD continues to spread, it's the name of the game...terry
SATURDAY, JANUARY 29, 2022
Minnesota Chronic Wasting Disease CWD PrP 146 WILD Positive To Date
Minnesota captive cwd to date???
TUESDAY, MARCH 08, 2022
Minnesota Board of Animal Health Report Concurrent Authority Regulating Farmed White-tailed Deer and CWD TSE Prion
***> OHIO CHRONIC WASTING DISEASE CWD TSE PrP in two wild white-tailed deer harvested during the 2020-21 hunting season
CHRONIC WASTING DISEASE (DEER) Deer Hunters in Marion, Hardin, and Wyandot Counties
The Ohio Department of Natural Resources (ODNR) Division of Wildlife announced in June that it has enacted a disease surveillance area (DSA) in three north-central counties following the discovery of Chronic Wasting Disease (CWD) in two wild white-tailed deer harvested during the 2020-21 hunting season (see map below).
Testing thus far has confirmed five additional CWD-positive deer, including an adult doe harvested in Marion county, 4 miles south of the Wyandot county line. In response to this we are strongly encouraging hunters in central and southern Marion county to have their deer tested using one of our convenient self-serve testing locations (see map below). Testing is voluntary but strongly encouraged and greatly appreciated. Testing will continue throughout the Disease Surveillance Area through the end of the season.
The DSA (2021-01) includes:
Wyandot County (all 13 townships)
Hardin County (Jackson, Goshen, and Dudley townships)
Marion County (Grand, Grand Prairie, Salt Rock, Montgomery, Big Island, and Marion townships)
The following regulations apply within the DSA:
Successful hunters must bring either the head or complete carcasses of all deer harvested within the DSA to either a staffed sampling station or use a self-serve kiosk during the following days: Nov. 6-7 and Nov. 13-14, 2021 and Nov. 29 – Dec. 5, 2021. Division of Wildlife staff will only be on hand Monday, Tuesday, and Saturday of Ohio’s 7-day gun season. Self-serve options must be used the other four days.
Beginning immediately, prohibits the placement of or use of salt, mineral supplement, grain, fruit, vegetables, or other feed to attract or feed deer within the disease surveillance area;
Beginning immediately, prohibits hunting of deer by the aid of salt, mineral supplement, grain, fruit, vegetables, or other feed within the disease surveillance area;
Prohibits the removal of a complete carcass or high-risk parts from the disease surveillance area, unless the carcass complies with deer carcass regulations or the carcass is delivered to a certified taxidermist or processor within 24 hours of leaving the disease surveillance area.
If you harvest a deer within the DSA but outside of the mandatory sampling days, or harvest a deer in Hardin or Marion counties but outside of the DSA, we encourage you to voluntarily submit your deer head for testing at one of the 17 conveniently located self-serve kiosks (see map below). These self-serve locations will be available Oct. 1, 2021 - Jan. 14, 2022.
Additional information on carcass regulations and a complete list of certified processors and taxidermists can be found below.
Disease Surveillance Area Regulations & Sampling Locations [pdf]
Map of Sampling Locations in Wyandot, Hardin, and Marion Counties.Click map to enlarge
ID Name County Street City
1 Wyandot Wildlife Area Wyandot 4191 County Hwy 97 Carey
2 Johnson's Hunting and Fishing Wyandot 8501 County Hwy 16 McCutchenville
3 Mickey Mart Wyandot 103 W Saffell Ave Sycamore
4 Richland Township Fire Dept Wyandot 200 W. Franklin St Wharton
5 Salem Township Building Wyandot Wyandot 13077 County Hwy 47 Upper Sandusky
6 Wyandot County Fairgrounds Wyandot 10191 OH 53 Upper Sandusky
7 The Sportsman's Stop Wyandot 2733 County Hwy 330 Nevada
8 Bull Pen Auction Wyandot 104 E. Hillcrest St Nevada
9 Andreoff Wildlife Area Hardin 3373 County Rd 215 Forest
10 Mifflin Township Building Wyandot 14991 Township Hwy 103 Upper Sandusky
11 Marseilles Township Building Wyandot 20461 State Route 37 LaRue
12 Killdeer Plains Wildlife Area HQ Wyandot 19100 County Hwy 115 Harpster
13 Grand Prairie Township Building Marion 5071 Marion-Upper Sandusky Rd Marion
14 Meeker Community Center Marion Marion 6400 Harding Highway W Marion
15 Hardin County Coon Hunters Club Hardin 21623 County Rd 144 Kenton
16 Big Island Wildlife Area Marion 3600 Marion-Agosta Rd Marion
17 Big Island Wildlife Area HQ Marion 5389 Larue-Prospect Rd W New Bloomington
18 Scioto Valley Fire Dept Marion 100 N Front St LaRue
19 Ridgeway Hardware & General Store Hardin 119 Main St Ridgeway
20 Green Camp Fire Dept Marion 217 Main St Green Camp
21 Pleasant Township Fire Dept Marion 1035 Owens Rd W Marion
CWD Testing Results (2021-2022) click to expand
Sampling Locations Announced for Disease Surveillance Area 2021-01 click to expand
2021-01 Disease Surveillance Area Established (Effective June 15, 2021) click to expand
Deer Carcass Possession and Movement Restrictions click to expand
Processor and Taxidermist Training and Certification click to expand
Disease Surveillance Areas & Regulations click to expand
CWD News Archive
OHIO history of Chronic Wasting Disease CWD TSE Prion Disease Wild and Captive to date
In 2020, the Ohio Department of Natural Resources (ODNR) Division of Wildlife identified Ohio's first positive test for CWD in a wild Ohio white-tailed deer in Wyandot County.
A second positive test was identified in January 2021 during a controlled hunt on the Killdeer Plains Wildlife Area refuge, within 2 miles of the first positive location.
How to collect samples for CWD testing
Watch our YouTube video for proper collection techniques for CWD sampling
Chronic Wasting Disease Detected on Wayne County Farm
Chronic Wasting Disease (CWD) has been detected at a farm in Wayne County.
OHIO CWD TSE Prion expands to wild with 2 confirmed positive cases and 26 confirmed positive cases in captive farmed cervid to date
Effective SEPTEMBER 1, 2021 to AUGUST 31, 2022 HUNTING AND TRAPPING REGULATIONS 2021-22
CHRONIC WASTING DISEASE
KNOW THE FACTS
Chronic Wasting Disease (CWD) is a fatal neurological disease of white-tailed deer. There is no strong evidence that CWD is transmissible to humans. The first confirmed case of CWD in Ohio was at a hunting preserve in Holmes County in 2014. Since then, 25 deer, from four captive facilities in Holmes and Wayne counties have tested positive for CWD.
In December of 2020, Ohio confirmed its first CWD-positive wild deer. The mature buck, harvested in late October in Wyandot County, was taken to a local taxidermist as part of routine CWD surveillance. In January of 2021, a positive yearling doe was harvested during a controlled hunt on the Killdeer Plains Refuge. A Disease Surveillance Area (DSA) has been established, and intensive monitoring will continue for at least three years in all of Wyandot and parts of Hardin and Marion Counties.
PROTECT OHIO’S DEER HERD
Properly dispose of a deer carcass. Be sure to double-bag all high-risk parts (brain, spinal cord, eyes, and lymphoid tissues) and dispose of them with your household trash.
It is illegal to bring high-risk carcass parts into Ohio from anywhere outside the state , unless the animal is delivered to a Division of Wildlife certified processor or taxidermist within 24 hours.
Contact a Division of Wildlife district office or state wildlife officer if you see a deer that appears sick, is acting abnormally, or has a visible ear tag.
The Division of Wildlife has a Disease Surveillance Area (DSA), 2021-01, which includes all of Wyandot County, Jackson, Goshen, Dudley townships in Hardin County and Grand, Salt Rock, Grand Prairie, Montgomery, Big Island, and Marion townships in Marion County.
PRECAUTIONS FOR HUNTERS
A deer infected with CWD typically does not immediately show signs of the disease. As the disease progresses, the animal begins to lose body condition and stagger, carry its head and ears lowered, drool excessively, and show little fear of humans. They will eventually lose body condition and appear weak and emaciated.
Wear rubber gloves when field-dressing and thoroughly wash your hands and instruments after field-dressing and butchering.
Bone out the meat from your animal and minimize the handling of brain and spinal tissues.
Do not eat the brain, spinal cord, eyes, spleen, tonsils, and lymph nodes.
Do not consume meat from any animal that tests positive for CWD.
Hunters may have a harvested deer tested at the Ohio Department of Agriculture’s Animal Disease Diagnostic Laboratory. Call (614) 728-6220 for more information.
DSA RULES INCLUDE:
The placement of or use of bait (salt, minerals, or any food) to attract or feed deer within the Disease Surveillance Area (DSA) boundaries is prohibited, as is the hunting of deer by the aid of bait.
Normal agricultural activities, including feeding domestic animals, as well as hunting deer over food plots, naturally occurring or cultivated plants, and agricultural crops are not prohibited in the DSA.
MANDATORY SAMPLING FOR DEER HARVESTED WITHIN THE DISEASE SURVEILLANCE AREA (DSA)
Mandatory sampling is required for ALL deer harvested Nov. 6-7, and 13-14 as well as the entire seven-day gun season (Nov. 29 – Dec. 5).
In-person sampling is available on Nov. 6-7, 13-14, and Monday (Nov. 29), Tuesday (Nov. 30), and Saturday (Dec. 5) of gun season. To avoid lengthy delays, hunters are encouraged to complete the game check process before presenting their deer for sampling. Staff is available from 8 a.m. to 8 p.m. at the following locations:
BIG ISLAND Wildlife Area Headquarters 5389 Larue-Prospect Rd West, New Bloomington, OH 43341
KILLDEER PLAINS Wildlife Area Headquarters 19100 CH 115 Harpster, OH 43323
WYANDOT COUNTY Fairgrounds 10191 OH 53 Upper Sandusky, OH 43351
Hunters who find it more convenient to use the self-serve kiosks may do so. For hunter convenience, self-serve kiosks are available October 1 through the close of the statewide muzzleloader season (January 11, 2022). Participation is voluntary outside the 11 mandatory days noted above. Instructions for sample submission are provided at the kiosk. Kiosk locations and instructions are available at wildohio.gov.
INCREASED CWD SURVEILLANCE PLANNED FOR WYANDOT, HARDIN, AND MARION COUNTIES
October 26, 2021
Increased CWD Surveillance Planned for Wyandot, Hardin, and Marion Counties
COLUMBUS, Ohio – Testing for Chronic Wasting Disease (CWD) in Ohio’s white-tailed deer population will continue during the 2021-22 hunting season, according to the Ohio Department of Natural Resources (ODNR) Division of Wildlife.
CWD is a fatal neurological disease that affects white-tailed deer and other similar species, including mule deer, elk, and moose. According to the Centers for Disease Control and Prevention, there is no strong evidence that CWD is transmissible to humans.
Two CWD-positive wild deer were confirmed during the 2020-21 hunting season in Wyandot County. A disease surveillance area has been established in response to the confirmed cases, and intensive monitoring will continue for at least three years in Wyandot County as well as portions of Hardin and Marion counties.
Specific regulations apply to hunters who harvest a deer in this location, including mandatory testing on Nov. 6-7, Nov. 13-14, and the seven-day gun season, Nov. 29 – Dec. 5. In-person sampling is available at the Big Island Wildlife Area Headquarters, Killdeer Plains Wildlife Area Headquarters, and the Wyandot County Fairgrounds on those dates. Self-serve kiosks are also available. A list of kiosk locations and instructions can be found at ohiodnr.gov/cwd.
In addition to mandatory testing, the following regulations apply within the disease surveillance area:
Prohibits the placement of or use of salt, mineral supplement, grain, fruit, vegetables, or other feed to attract or feed deer
Prohibits hunting of deer by the aid of salt, mineral supplement, grain, fruit, vegetables, or other feed
Prohibits the removal of a complete carcass or high-risk parts from the disease surveillance area, unless the carcass complies with deer carcass regulations or the carcass is delivered to a certified taxidermist or processor within 24 hours of leaving the area. Additional information on carcass regulations and a complete list of certified processors and taxidermists can be found at wildohio.gov.
Normal agricultural activities, including feeding of domestic animals, as well as hunting deer over food plots, naturally occurring or cultivated plants, and agriculture crops are not prohibited.
To help protect Ohio’s deer herd from CWD, hunters should properly dispose of their deer carcasses by double-bagging all high-risk parts (brain, spinal cord, eyes, and lymphoid tissue) and setting it out with their household garbage for trash pickup. Those without trash pickup can double bag the carcass and take it to a municipal solid waste landfill or bury the carcass at least 3 feet deep on the property of harvest. The proper handling of carcasses, trims, and parts dramatically decreases the odds of spreading CWD.
The Division of Wildlife has conducted routine surveillance for CWD since 2002, with more than 30,000 deer tested. CWD has previously been detected at captive deer breeding facilities in Ohio. CWD has been detected in 26 states and four Canadian provinces.
Hunters may test a harvested deer at the Ohio Department of Agriculture’s Animal Disease Diagnostic Laboratory for a fee. Call (614) 728-6220 for more information.
The mission of the Division of Wildlife is to conserve and improve fish and wildlife resources and their habitats for sustainable use and appreciation by all. Visit wildohio.gov to find out more.
ODNR ensures a balance between wise use and protection of our natural resources for the benefit of all. Visit the ODNR website at ohiodnr.gov.
Editor’s Note: A map of the disease surveillance area is included with this release.
Ohio CWD TSE Prion
FRIDAY, AUGUST 13, 2021
Ohio Annual Deer Program Summary Spring 2021 CWD TSE Prion Update
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In December 2020, routine surveillance detected the first case of CWD in Ohio’s wild deer population.
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Chronic Wasting Disease Chronic Wasting Disease (CWD) is a fatal disease of the central nervous system of mule deer, white-tailed deer, elk, moose, and reindeer. CWD is caused by abnormal proteins, or prions (not a bacteria or virus), that ultimately destroy brain tissue. CWD can be spread through direct animal-to-animal contact or by contact with saliva, urine, feces, carcass parts of an infected animal, or contaminated materials in the environment (plants and soil). Prions released into the environment through bodily fluids or diseased carcasses are extremely resistant to degradation and can remain infectious for years. CWD is known as a transmissible spongiform encephalopathy, a family of diseases that includes bovine spongiform encephalopathy (mad cow disease), scrapie in sheep, and Creutzfeldt-Jakob Disease in humans.
Since 2002, the Division of Wildlife has conducted statewide CWD surveillance, testing 28,613 deer. In 2020, a record 4,654 deer were submitted for CWD testing. Division of Wildlife staff collected 853 road-killed deer from all 88 counties and hunters submitted 3,176 deer via cooperating taxidermists and processors. An additional 287 deer were submitted by hunters at collection and inspection stations. Additional deer (338) were collected and tested through various means (deer displaying abnormal behavior and/or poor physical condition, found dead under suspicious circumstances, removed in conflict or culling situations, etc.). For the first time ever, CWD was detected in a wild Ohio deer.
Positive Detections in the Wild Population
In December 2020, the Division of Wildlife received test results that a mature buck harvested in southern Wyandot County tested positive for CWD. The buck was presented to a cooperating taxidermist who was aiding the Division of Wildlife with tissue collections as part of our routine disease surveillance. Given the significant delay between the time the deer was shot and when it was ultimately recovered (9 days), only the head was delivered to the taxidermist. Division of Wildlife staff visited the site of the harvest, collected and properly disposed of the carcass, and removed the top layer of soil in an effort to reduce environmental contamination. Upon detection, a 15-township area surrounding the positive location was designated for enhanced surveillance (Figure 11) where hunters were encouraged to submit deer for testing throughout the remainder of the deer season, particularly during the 2-day bonus gun and muzzleloader seasons. Additionally, given the proximity to Killdeer Plains Wildlife Area and Refuge, all deer harvested on the remaining controlled hunts were submitted for testing (n = 171). This additional surveillance produced a second positive, a yearling doe that was harvested during a controlled hunt on the Killdeer Plains refuge.
Additional culling efforts were implemented on the refuge and surrounding area following the deer season to 1) obtain more information about the prevalence and distribution of the disease, 2) reduce population density (aerial surveys revealed an abnormally high deer density within and surrounding the refuge), and 3) potentially remove additional CWD-positive deer from the herd. In three nights of operations, Division of Wildlife staff removed and tested 72 deer with no additional positive detections.
Disease Surveillance Area
In October 2014, a mature buck from a shooting preserve in Holmes County tested positive for CWD, becoming the first-ever CWD-positive deer in Ohio. The shooting preserve was depopulated in April 2015, and testing revealed no additional CWD-positive animals. Subsequent testing of nearly 300 free-ranging deer in an eight-township area around the shooting preserve failed to detect any CWD-positive deer as well. However, in spring of 2015, two more CWD positive deer were reported from a captive white-tailed deer breeding pen in Holmes County. This herd was depopulated in June 2015, and 16 additional deer tested positive for the disease. In response to these findings, the Division of Wildlife conducted targeted surveillance in the immediate vicinity of the infected facility during the summer of 2015, collecting 18 deer (including two that had escaped from captive facilities), with none testing positive for CWD.
Additionally, the focus area in 2015 was expanded to include two townships in southern Wayne County, and the 10- township focus area was declared a Disease Surveillance Area (DSA, visit wildohio.gov for specific regulations pertaining to a DSA). The 10-township DSA in central Holmes and southern Wayne counties expired on July 31, 2018 after three seasons of intensive surveillance revealed no CWD-positive animals in the wild herd. However, due to the early 2018 discovery of three additional CWD-positives in an eastern Holmes County captive facility, a new, 7-township DSA was established (Figure 12). During the 2020-21 season, 175 hunter harvested deer from DSA 2018-01 were collected at inspection stations during Ohio’s 7-day gun season. Again, CWD was not detected in any of the deer tested.
In April 2020, a female mule deer on a farm in southeastern Wayne County tested positive for CWD. A second mule deer doe tested positive in June 2020, and, following depopulation of the herd in August 2020, one additional whitetailed deer buck tested positive. These additional positives bring the total number of positive detections in captive herds to 25. Given the low prevalence of disease in the facility, low deer densities in the surrounding area, and history of surveillance in the area, no additional action was taken in response to this event.
Figure 11. Enhanced surveillance area covering 15 townships in portions of Wyandot, Marion, and Hardin counties.
Figure 12. Disease Surveillance Area 2018-01 (DSA)
FRIDAY, JUNE 11, 2021
Ohio Confirms 2 CWD Positive Wild Cervid 2020-2021 With Additional 25 deer from four captive deer facilities confirmed positive to date
THURSDAY, JANUARY 20, 2022
OHIO CHRONIC WASTING DISEASE CWD TSE PrP in five additional CWD-positive deer
February 14, 2001
Diagnosis and Reporting of Creutzfeldt-Jakob Disease
Terry S. Singeltary, Sr
Author Affiliations
JAMA. 2001;285(6):733-734. doi:10-1001/pubs.JAMA-ISSN-0098-7484-285-6-jlt0214 To the Editor: In their Research Letter, Dr Gibbons and colleagues1 reported that the annual US death rate due to Creutzfeldt-Jakob disease (CJD) has been stable since 1985. These estimates, however, are based only on reported cases, and do not include misdiagnosed or preclinical cases. It seems to me that misdiagnosis alone would drastically change these figures. An unknown number of persons with a diagnosis of Alzheimer disease in fact may have CJD, although only a small number of these patients receive the postmortem examination necessary to make this diagnosis. Furthermore, only a few states have made CJD reportable. Human and animal transmissible spongiform encephalopathies should be reportable nationwide and internationally.
Terry S. Singeltary, Bacliff, Texas USA, 77518, Galveston Bay flounder9@verizon.net on the bottom!
posted by Terry S. Singeltary Sr. at
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