Texas Kimble County Farm Chronic Wasting Disease CWD TSE Prion Approximate Herd Prevalence 12%

Texas Kimble County Farm Chronic Wasting Disease CWD TSE Prion Approximate Herd Prevalence 12%

Texas Kimble County Farm Chronic Wasting Disease CWD TSE Prion Approximate Herd Prevalence 12%
SUMMARY MINUTES OF THE 407th COMMISSION MEETING Texas Animal Health Commission
September 22, 2020
Chronic Wasting Disease (CWD):
A new CWD positive breeding herd was disclosed in February 2020 in Kimble County. This herd depopulation was completed in July 2020. Including the two index positive deer, an additional eight more positive deer were disclosed (approximate herd prevalence 12%). Since July 2015 and prior to this discovery, five positive captive breeder herds have been disclosed and four of those are in Medina County. One herd in Lavaca and three herds in Medina County were depopulated leaving one large herd in Medina County that is managed on a herd plan. A new zone was established in Val Verde County in December 2019 as a result of a positive free-ranging White-tailed Deer (WTD). A second positive WTD was also disclosed in February 2020 in the same area.
Item 17 – Consideration of and Possible Action on Regulation ADOPTION Regarding Ms. Mary Luedeker provided the background and overview of the regulation proposal.
(a) Chapter 40, Chronic Wasting Disease
On December 18, 2019, the commission received confirmation that a free ranging 5.5-year-old female white-tailed deer killed in Val Verde County tested positive for CWD. The Executive Director issued an order declaring a high-risk containment zone for portions of Val Verde County on December 20, 2019. This proposed rulemaking would replace the Executive Order and establish a Containment Zone (CZ) 4 in §40.6(b)(1)(D) and Surveillance Zone (SZ) 4 in §40.6(b)(2)(D) for Val Verde County.
40.6(b)(1)(D) Containment Zone 4. That portion of the state lying within the boundaries of a line beginning in Val Verde County at the International Bridge and proceeding northeast along Spur 239 to U.S. 90; thence north along U.S. 90 to the intersection of U.S. 277/377, thence north along U.S. 277/377 to the U.S. 277/377 bridge at Lake Amistad (29.496183°, -100.913355°), thence west along the southern shoreline of Lake Amistad to International Boundary at Lake Amistad dam, thence south along the Rio Grande River to the International Bridge on Spur 239. 40.6(b)(2)(D) Surveillance Zone 4. That portion of the state lying within a line beginning in Val Verde County at the confluence of Sycamore Creek and the Rio Grande River (29.242341°, – 100.793906°); thence northeast along Sycamore Creek to U.S. 277; thence northwest on U.S. 277 to Loop 79; thence north along Loop 79 to the Union Pacific Railroad; thence east along the Union Pacific Railroad to Liberty Drive (north entrance to Laughlin Air Force Base); thence north along Liberty Drive to U.S. 90; thence west along U.S. 90 to Loop 79; thence north along Loop 79 to the American Electric Power (AEP) Ft. Lancaster-to-Hamilton Road 138kV transmission line (29.415542°, -100.847993°); thence north along the AEP Ft. Lancaster-to-Hamilton Road 138kV transmission line to a point where the AEP Ft. Lancaster-to-Hamilton Road 138kV transmission line turns northwest (29.528552°, -100.871618°); thence northwest along the AEP Ft. Lancasterto-Hamilton Road 138kV transmission line to the AEP Ft. Lancaster-to-Hamilton Road maintenance road (29.569259°, -100.984758°); thence along the AEP Ft. Lancaster-to-Hamilton Road maintenance road to Spur 406; thence northwest along Spur 406 to U.S. 90; thence south along U.S. 90 to Box Canyon Drive; thence west along Box Canyon Drive to Bluebonnet Drive; thence southwest along Bluebonnet Drive to Lake Drive; thence south along Lake Drive to Lake Amistad (29.513298°, -101.172454°), thence southeast along the International Boundary to the International Boundary at the Lake Amistad dam; thence southeast along the Rio Grande River to the confluence of Sycamore Creek (29.242341°, -100.793906°).
On January 28, 2020, the commission received confirmation that a 4.5-year-old male white-tailed deer and a 3.5-year-old female white-tailed deer killed in Medina County tested positive for CWD. The proposed amendment takes the location of these mortalities into consideration and establishes Containment Zone 3 boundaries in §40.6(b)(1)(C) for Medina and Uvalde counties. The proposed
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SUMMARY MINUTES OF THE 407th COMMISSION MEETING – 9/22/2020
change to §40.6(b)(2)(C) extends the surveillance zone boundaries from F.M. 187 to the Sabinal River in Uvalde County.
40.6(b)(1)(C) Containment Zone 3. That portion of the state lying within Bandera, Medina and Uvalde counties and depicted in the following figure and more specifically described by the following latitude-longitude coordinate pairs:
Boundaries consist of properties under the same ownership or management for facilities operating under a herd plan due to a positive result in a CWD susceptible species in Medina and Uvalde counties.
40.6(b)(2)(C) Surveillance Zone 3. That portion of the state within the boundaries of a line beginning at U.S. 90 in Hondo in Medina County; thence west along U.S. 90 to the Sabinal River F.M. 187 in Uvalde County; thence north along F.M. 187 to F.M. 470 in Bandera County; thence east along F.M. 470 to Tarpley in Bandera County; thence south along F.M. 462 to U.S. 90 in Hondo.
On February 26, 2020, the commission received confirmation that a 5.5-year-old female white-tailed deer held in a deer breeding facility in Kimble County tested positive for CWD. The proposed amendment would establish Surveillance Zone 5 in Kimble County in §40.6(b)(2)(E). This proposal does not create a CZ in Kimble County because the detection was in a breeder deer facility, which is required by law to be designed and built to both prevent the free movement of deer and contact with freeranging deer. Second, the facility where CWD was discovered is operating under a commission herd plan, which restricts deer movement and requires CWD testing at an equal or higher level to what is required in a CZ.
40.6(b)(2)(E) Surveillance Zone 5. That portion of the state lying within the boundaries of a line beginning on U.S. 83 at the Kerr/Kimble County line; thence north along U.S. 83 to I.H. 10; thence northwest along on I.H. 10 to F.M. 2169; thence east along F.M. 2169 to County Road (C.R.) 410; thence east along C.R. 410 to C.R. 412; thence south along C.R. 412 to C.R. 470; thence east along C.R. 470 to C.R. 420; thence south along C.R. 420 to F.M. 479; thence east along F.M. 479 to C.R. 433; thence south along C.R. 433 to U.S. 290; thence west along U.S. 290 to I.H. 10; thence southeast along I.H. 10 to the Kerr/Kimble County line; thence west along the Kerr/Kimble County line to U.S. 83.
An opportunity for public comment was offered and instructions for unmuting lines and for the speaker to identify themselves was detailed. There was no public comment concerning the Rule Adoption. The motion to ADOPT the amendments to Chapter 40, Chronic Wasting Disease passed.
SUMMARY MINUTES OF THE 407th COMMISSION MEETING – 9/22/2020
Scrapie: The flock identified in April 2016 remains under quarantine in Hartley County.
https://www.tahc.texas.gov/agency/meetings/minutes/SummaryMinutes_CommMtg_2020-09-22.pdf
WEDNESDAY, SEPTEMBER 09, 2020 TEXAS TAHC CWD TSE Prion SUMMARY MINUTES OF THE 406th COMMISSION MEETING https://chronic-wasting-disease.blogspot.com/2020/09/texas-tahc-cwd-tse-prion-summary.html
FRIDAY, OCTOBER 16, 2020 TAHC Rules and Resources for Harvesting Exotic CWD Susceptible Species this 2020-21 Hunting Season https://chronic-wasting-disease.blogspot.com/2020/10/tahc-rules-and-resources-for-harvesting.html
Sent: Sun, Aug 30, 2020 10:37 am Subject: Texas CWD TSE Prion 3 More Documented, 185 Cases To Date Texas CWD TSE Prion 3 More Documented, 185 Cases To Date CWD Positives in Texas CWD Positive Confirmation Date Free Range/Captive County Source Species Sex Age 2020-07-30 Breeder Deer Kimble Facility #6 White-tailed Deer M 3 2020-07-29 Free Range El Paso N/A Mule Deer M 2.5 2020-06-25 Free Range El Paso N/A Mule Deer F 5.5 https://tpwd.texas.gov/huntwild/wild/diseases/cwd/tracking/ SUNDAY, AUGUST 30, 2020 Texas CWD TSE Prion 3 More Documented, 185 Cases To Date https://chronic-wasting-disease.blogspot.com/2020/08/texas-cwd-tse-prion-3-more-documented.html Sent: Thu, Jul 9, 2020 10:00 am Subject: Texas CWD TSE Prion Jumps BY 13 To 182 Confirmed Cases To Date Texas CWD TSE Prion Jumps To 182 Confirmed Cases 2020-06-25 Free Range El Paso N/A Mule Deer F 5.5 2020-06-16 Free Range El Paso N/A Mule Deer M 5.5 2020-06-10 Breeder Release Site Medina Facility #3 White-tailed Deer F 5.5 2020-06-10 Breeder Release Site Medina Facility #3 White-tailed Deer M 3.5 2020-06-10 Breeder Release Site Uvalde Facility #3 White-tailed Deer F 5.5 2020-06-09 Breeder Release Site Uvalde Facility #3 White-tailed Deer F 2.5 2020-06-09 Breeder Release Site Uvalde Facility #3 White-tailed Deer F 4.5 2020-05-22 Free Range Hartley N/A Mule Deer M 4.5 2020-05-22 Free Range Hartley N/A Mule Deer F 5.5 2020-05-22 Free Range Hartley N/A Mule Deer M 4.5 2020-05-22 Free Range Dallam N/A Mule Deer M 2.5 2020-05-22 Free Range Hartley N/A Mule Deer M 5.5 2020-05-22 Free Range Hartley N/A Mule Deer M 5.5 SUNDAY, MARCH 08, 2020 Texas CWD TSE Prion Confirms 169 Positive To Date https://chronic-wasting-disease.blogspot.com/2020/03/texas-cwd-tse-prion-confirms-169.html THURSDAY, JULY 09, 2020 Texas CWD TSE Prion Jumps BY 13 To 182 Confirmed Cases To Date https://chronic-wasting-disease.blogspot.com/2020/07/texas-cwd-tse-prion-jumps-by-13-to-182.html SATURDAY, JULY 04, 2020 TAHC CHAPTER 40 CHRONIC WASTING DISEASE 406th COMMISSION MEETING AGENDA June 23, 2020 8:30 A.M. https://chronic-wasting-disease.blogspot.com/2020/07/tahc-chapter-40-chronic-wasting-disease.html TUESDAY, JANUARY 28, 2020 Mississippi MDWFP North MS CWD Management Zone Since October 2019, 25 CWD-positive deer have been detected from this zone https://chronic-wasting-disease.blogspot.com/2020/01/mississippi-mdwfp-north-ms-cwd.html CWD WEBINAR CWD YESTERDAY! December 11, 2019 Dr. Mckenzie and CIDRAP on CWD TSE Prion https://www.youtube.com/watch?v=xzYcnmc3Xh0 122: Prions and Chronic Wasting Disease with Jason Bartz https://www.asm.org/Podcasts/MTM/Episodes/Prions-and-Chronic-Wasting-Disease-with-Jason-Bart Texas CWD Symposium: Transmission by Saliva, Feces, Urine & Blood the other part, these tissues and things in the body then shed or secrete prions which then are the route to other animals into the environment, so in particular, the things, the secretions that are infectious are salvia, feces, blood and urine. so pretty much anything that comes out of a deer is going to be infectious and potential for transmitting disease. https://www.youtube.com/watch?v=bItnEElzuKo&index=6&list=PL7ZG8MkruQh3wI96XQ8_EymytO828rGxj ”On January 21, 2017 a tornado took down thousands of feet of fence for a 420-acre illegal deer enclosure in Lamar County that had been subject to federal and state investigation for illegally importing white-tailed deer into Mississippi from Texas (a CWD positive state). Native deer were free to move on and off the property before all of the deer were able to be tested for CWD. Testing will be made available for a period of three years for CWD on the property and will be available for deer killed within a 5-mile radius of the property on a voluntary basis. ” Texas Chronic Wasting Disease CWD TSE Prion Symposium 2018 posted January 2019 VIDEO SET 18 CLIPS See Wisconsin update…terrible news, right after Texas updated map around 5 minute mark… https://www.youtube.com/watch?v=JAK_YBZh2tA&feature=youtu.be&list=PL7ZG8MkruQh3wI96XQ8_EymytO828rGxj&t=299 WISCONSIN CWD CAPTIVE CWD UPDATE VIDEO https://www.youtube.com/watch?v=JAK_YBZh2tA&feature=youtu.be&t=602&fbclid=IwAR04yvki5GDJqjAeNOeP3QETcUOmWHRNRrGXzRUTnsxvcLUO50kSDsBzHTs cwd update on Wisconsin from Tammy Ryan… https://www.youtube.com/watch?v=hvy2SMGQt6o&index=11&list=PL7ZG8MkruQh3wI96XQ8_EymytO828rGxj Wyoming CWD Dr. Mary Wood ”first step is admitting you have a problem” ”Wyoming was behind the curve” wyoming has a problem… https://www.youtube.com/watch?v=y1bsK4Igt1o&index=10&list=PL7ZG8MkruQh3wI96XQ8_EymytO828rGxj TEXAS BREEDER DEER ESCAPEE WITH CWD IN THE WILD, or so the genetics would show? OH NO, please tell me i heard this wrong, a potential Texas captive escapee with cwd in the wild, in an area with positive captive cwd herd? apparently, no ID though. tell me it ain’t so please… 23:00 minute mark ”Free Ranging Deer, Dr. Deyoung looked at Genetics of this free ranging deer and what he found was, that the genetics on this deer were more similar to captive deer, than the free ranging population, but he did not see a significant connection to any one captive facility that he analyzed, so we believe, A , this animal had some captive ahhh, whatnot.” https://youtu.be/aoPDeGL6mpQ?t=1384 Wyoming CWD Dr. Mary Wood ”first step is admitting you have a problem” ”Wyoming was behind the curve” wyoming has a problem… https://www.youtube.com/watch?v=y1bsK4Igt1o&index=10&list=PL7ZG8MkruQh3wI96XQ8_EymytO828rGxj the other part, these tissues and things in the body then shed or secrete prions which then are the route to other animals into the environment, so in particular, the things, the secretions that are infectious are salvia, feces, blood and urine. so pretty much anything that comes out of a deer is going to be infectious and potential for transmitting disease. https://www.youtube.com/watch?v=bItnEElzuKo&index=6&list=PL7ZG8MkruQh3wI96XQ8_EymytO828rGxj Texas Chronic Wasting Disease CWD TSE Prion Symposium 2018 posted January 2019 VIDEO SET 18 CLIPS See Wisconsin update…terrible news, right after Texas updated map around 5 minute mark… https://www.youtube.com/watch?v=JAK_YBZh2tA&feature=youtu.be&list=PL7ZG8MkruQh3wI96XQ8_EymytO828rGxj&t=299 SATURDAY, JANUARY 19, 2019 Texas Chronic Wasting Disease CWD TSE Prion Symposium 2018 posted January 2019 VIDEO SET 18 CLIPS https://chronic-wasting-disease.blogspot.com/2019/01/texas-chronic-wasting-disease-cwd-tse.html FRIDAY, DECEMBER 20, 2019 TEXAS ANIMAL HEALTH COMMISSION EXECUTIVE DIRECTOR ORDER DECLARING A CHRONIC WASTING DISEASE HIGH RISK AREA CONTAINMENT ZONE FOR PORTIONS OF VAL VERDE COUNTY https://chronic-wasting-disease.blogspot.com/2019/12/texas-animal-health-commission.html TUESDAY, DECEMBER 31, 2019 In Vitro detection of Chronic Wasting Disease (CWD) prions in semen and reproductive tissues of white tailed deer bucks (Odocoileus virginianus SUNDAY, AUGUST 02, 2015 TEXAS CWD, Have you been ThunderStruck, deer semen, straw bred bucks, super ovulation, and the potential TSE Prion connection, what if? https://chronic-wasting-disease.blogspot.com/2019/12/in-vitro-detection-of-chronic-wasting.html SUNDAY, FEBRUARY 16, 2020 ***> Jerking for Dollars, Are Texas Politicians and Legislators Masturbating Deer For Money, and likely spreading CWD TSE Prion? https://chronic-wasting-disease.blogspot.com/2020/02/jerking-for-dollars-are-texas.html TUESDAY, FEBRUARY 04, 2020 TEXAS REPORTS 20 NEW CWD TSE PRION CASES 3 WILD 17 BREEDER 166 POSITIVE TO DATE https://chronic-wasting-disease.blogspot.com/2020/02/texas-reports-20-new-cwd-tse-prion.html FRIDAY, MAY 22, 2020 TPW Commission has adopted rules establishing Chronic Wasting Disease (CWD) management zones to further detection and response efforts among WTD https://chronic-wasting-disease.blogspot.com/2020/05/tpw-commission-has-adopted-rules.html SUNDAY, MARCH 01, 2020 Texas As one CWD investigation continues, another launches…THE FULL MONTY! https://chronic-wasting-disease.blogspot.com/2020/03/texas-as-one-cwd-investigation.html SATURDAY, DECEMBER 02, 2017 TEXAS TAHC CWD TSE PRION Trace Herds INs and OUTs Summary Minutes of the 399th and 398th Commission Meeting – 8/22/2017 5/9/2017 http://chronic-wasting-disease.blogspot.com/2017/12/texas-tahc-cwd-tse-prion-trace-herds.html SUNDAY, MAY 14, 2017 85th Legislative Session 2017 AND THE TEXAS TWO STEP Chronic Wasting Disease CWD TSE Prion, and paying to play http://chronic-wasting-disease.blogspot.com/2017/05/85th-legislative-session-2017-and-texas.html SUNDAY, JANUARY 22, 2017 Texas 85th Legislative Session 2017 Chronic Wasting Disease CWD TSE Prion Cervid Captive Breeder Industry http://chronic-wasting-disease.blogspot.com/2017/01/texas-85th-legislative-session-2017.html *** TEXAS TAHC OLD STATISTICS BELOW FOR PAST CWD TESTING *** CWD TEXAS TAHC OLD FILE HISTORY updated from some of my old files, some of the links will not work. *** Subject: CWD testing in Texas *** Date: Sun, 25 Aug 2002 19:45:14 –0500 From: Kenneth Waldrup To: flounder@wt.net snip…see ; http://chronic-wasting-disease.blogspot.com/2012/07/texas-animal-health-commission.html MONDAY, AUGUST 14, 2017 *** Texas Chronic Wasting Disease CWD TSE Prion History *** http://chronic-wasting-disease.blogspot.com/2017/08/texas-chronic-wasting-disease-cwd-tse.html
FRIDAY, OCTOBER 23, 2020
Scrapie TSE Prion Zoonosis Zoonotic, what if?
https://transmissiblespongiformencephalopathy.blogspot.com/2020/10/scrapie-tse-prion-zoonosis-zoonotic.html
THURSDAY, SEPTEMBER 24, 2020 ***> The emergence of classical BSE from atypical/ Nor98 scrapie 1st up BSE 589.2001 FEED REGULATIONS https://bse-atypical.blogspot.com/2020/06/radical-change-in-zoonotic-abilities-of.html
SUNDAY, OCTOBER 11, 2020 Bovine adapted transmissible mink encephalopathy is similar to L-BSE after passage through sheep with the VRQ/VRQ genotype but not VRQ/ARQ https://transmissible-mink-encephalopathy.blogspot.com/2020/10/bovine-adapted-transmissible-mink.html
H.R.925 America’s Conservation Enhancement Act 116th Congress 2019-2020 SEC 104 CHRONIC WASTING DISEASE TASK FORCE Greetings Congressman Mike Thompson et al @ TASK FORCE, I tried to submit some information and history to the ‘TASK FORCE’ on chronic wasting disease cwd tse prion to Congressman Mike Thompson, i called his office in Washington, but unfortunately, they were not interested in it. for anybody else that might be interested, the following is some history on cwd tse prion in cervid, state by state, and the latest science…kind regards, terry H.R.925 – America’s Conservation Enhancement Act 116th Congress (2019-2020) BILL Overview Sponsor: Rep. Thompson, Mike [D-CA-5] (Introduced 01/30/2019) Committees: House – Natural Resources Committee Meetings: 09/25/19 10:00AM Committee Reports: H. Rept. 116-284 Latest Action: House – 09/30/2020 Rule H. Res. 1161 passed House. (All Actions) Tracker: This bill has the status Passed Senate Here are the steps for Status of Legislation: Introduced Passed House Snip… SEC. 104. CHRONIC WASTING DISEASE TASK FORCE. (a) Definition Of Chronic Wasting Disease.—In this section, the term “chronic wasting disease” means the animal disease afflicting deer, elk, and moose populations that— (1) is a transmissible disease of the nervous system resulting in distinctive lesions in the brain; and (2) belongs to the group of diseases known as transmissible spongiform encephalopathies, which group includes scrapie, bovine spongiform encephalopathy, and Creutzfeldt-Jakob disease. (b) Establishment.— (1) IN GENERAL.—There is established within the United States Fish and Wildlife Service a task force, to be known as the “Chronic Wasting Disease Task Force” (referred to in this subsection as the “Task Force”). (2) DUTIES.—The Task Force shall— (A) collaborate with foreign governments to share research, coordinate efforts, and discuss best management practices to reduce, minimize, prevent, or eliminate chronic wasting disease in the United States; (B) develop recommendations, including recommendations based on findings of the study conducted under subsection (c), and a set of best practices regarding— (i) the interstate coordination of practices to prevent the new introduction of chronic wasting disease; (ii) the prioritization and coordination of the future study of chronic wasting disease, based on everything ng research needs; (iii) ways to leverage the collective resources of Federal, State, and local agencies, Indian Tribes, and foreign governments, and resources from private, nongovernmental entities, to address chronic wasting disease in the United States and along the borders of the United States; and (iv) any other area where containment or management efforts relating to chronic wasting disease may differ across jurisdictions; (C) draw from existing and future academic and management recommendations to develop an interstate action plan under which States and the United States Fish and Wildlife Service agree to enact consistent management, educational, and research practices relating to chronic wasting disease; and (D) facilitate the creation of a cooperative agreement by which States and relevant Federal agencies agree to commit funds to implement best practices described in the interstate action plan developed under subparagraph (C). (3) MEMBERSHIP.— (A) IN GENERAL.—The Task Force shall be composed of— (i) 1 representative of the United States Fish and Wildlife Service with experience in chronic wasting disease, to be appointed by the Secretary of the Interior (referred to in this subsection as the “Secretary”); (ii) 1 representative of the United States Geological Survey; (iii) 2 representatives of the Department of Agriculture with experience in chronic wasting disease, to be appointed by the Secretary of Agriculture— (I) 1 of whom shall have expertise in research; and (II) 1 of whom shall have expertise in wildlife management; (iv) in the case of each State in which chronic wasting disease among elk, mule deer, white-tailed deer, or moose has been reported to the appropriate State agency, not more than 2 representatives, to be nominated by the Governor of the State— (I) not more than 1 of whom shall be a representative of the State agency with jurisdiction over wildlife management or wildlife disease in the State; and (II) in the case of a State with a farmed cervid program or economy, not more than 1 of whom shall be a representative of the State agency with jurisdiction over farmed cervid regulation in the State; (v) in the case of each State in which chronic wasting disease among elk, mule deer, white-tailed deer, or moose has not been documented, but that has carried out measures to prevent the introduction of chronic wasting disease among those species, not more than 2 representatives, to be nominated by the Governor of the State; (vi) not more than 2 representatives from an Indian tribe or tribal organization chosen in a process determined, in consultation with Indian tribes, by the Secretary; and (vii) not more than 5 nongovernmental members with relevant expertise appointed, after the date on which the members are first appointed under clauses (i) through (vi), by a majority vote of the State representatives appointed under clause (iv). (B) EFFECT.—Nothing in this paragraph requires a State to participate in the Task Force. (4) CO-CHAIRS.—The Co-Chairs of the Task Force shall be— (A) the Federal representative described in paragraph (3)(A)(i); and (B) 1 State representative appointed under paragraph (3)(A)(iv), to be selected by a majority vote of those State representatives. (5) DATE OF INITIAL APPOINTMENT.— (A) IN GENERAL.—The members of the Task Force shall be appointed not later than 180 days after the date on which the study is completed under subsection (c). (B) NOTIFICATION.—On appointment of the members of the Task Force, the Co-Chairs of the Task Force shall notify the Chairs and Ranking Members of the Committees on Environment and Public Works of the Senate and Natural Resources of the House of Representatives. (6) VACANCIES.—Any vacancy in the members appointed to the Task Force— (A) shall not affect the power or duty of the Task Force; and (B) shall be filled not later than 30 days after the date of the vacancy. (7) MEETINGS.—The Task Force shall convene— (A) not less frequently than twice each year; and (B) at such time and place, and by such means, as the Co-Chairs of the Task Force determine to be appropriate, which may include the use of remote conference technology. (8) INTERSTATE ACTION PLAN.— (A) IN GENERAL.—Not later than 1 year after the date on which the members of the Task Force are appointed, the Task Force shall submit to the Secretary, and the heads of the State agencies with jurisdiction over wildlife disease and farmed cervid regulation of each State with a representative on the Task Force, the interstate action plan developed by the Task Force under paragraph (2)(C). (B) COOPERATIVE AGREEMENTS.— (i) IN GENERAL.—To the maximum extent practicable, the Secretary, any other applicable Federal agency, and each applicable State shall enter into a cooperative agreement to fund necessary actions under the interstate action plan submitted under subparagraph (A). (ii) TARGET DATE.—The Secretary shall make the best effort of the Secretary to enter into any cooperative agreement under clause (i) not later than 180 days after the date of submission of the interstate action plan under subparagraph (A). (C) MATCHING FUNDS.— (i) IN GENERAL.—Subject to clause (ii), for each fiscal year, the United States Fish and Wildlife Service shall provide funds to carry out an interstate action plan through a cooperative agreement under subparagraph (B) in the amount of funds provided by the applicable States. (ii) LIMITATION.—The amount provided by the United State Fish and Wildlife Service under clause (i) for a fiscal year shall be not greater than $5,000,000. (9) REPORTS.—Not later than September 30 of the first full fiscal year after the date on which the first members of the Task Force are appointed, and each September 30 thereafter, the Task Force shall submit to the Secretary, and the heads of the State agencies with jurisdiction over wildlife disease and farmed cervid regulation of each State with a representatives on the Task Force, a report describing— (A) progress on the implementation of actions identified in the interstate action plan submitted under paragraph (8)(A), including the efficacy of funding under the cooperative agreement entered into under paragraph (8)(B); (B) updated resource requirements that are needed to reduce and eliminate chronic wasting disease in the United States; (C) any relevant updates to the recommended best management practices included in the interstate action plan submitted under paragraph (8)(B) to reduce or eliminate chronic wasting disease; (D) new research findings and emerging research needs relating to chronic wasting disease; and (E) any other relevant information. (c) Chronic Wasting Disease Transmission In Cervidae Resource Study.— (1) DEFINITIONS.—In this subsection: (A) ACADEMY.—The term “Academy” means the National Academy of Sciences. (B) CERVID.—The term “cervid” means any species within the family Cervidae. (C) SECRETARIES.—The term “Secretaries” means the Secretary of Agriculture, acting through the Administrator of the Animal and Plant Health Inspection Service, and the Secretary of the Interior, acting through the Director of the United States Geological Survey, acting jointly. (2) STUDY.— (A) IN GENERAL.—The Secretaries shall enter into an arrangement with the Academy under which the Academy shall conduct, and submit to the Secretaries a report describing the findings of, a special resource study to identify the predominant pathways and mechanisms of the transmission of chronic wasting disease in wild, captive, and farmed populations of cervids in the United States. (B) REQUIREMENTS.—The arrangement under subparagraph (A) shall provide that the actual expenses incurred by the Academy in conducting the study under subparagraph (A) shall be paid by the Secretaries, subject to the availability of appropriations. (3) CONTENTS OF THE STUDY.—The study under paragraph (2) shall— (A) with respect to wild, captive, and farmed populations of cervids in the United States, identify— (i) (I) the pathways and mechanisms for the transmission of chronic wasting disease within live cervid populations and cervid products, which may include pathways and mechanisms for transmission from Canada; (II) the infection rates for each pathway and mechanism identified under subclause (I); and (III) the relative frequency of transmission of each pathway and mechanism identified under subclause (I); (ii) (I) anthropogenic and environmental factors contributing to new chronic wasting disease emergence events; (II) the development of geographical areas with increased chronic wasting disease prevalence; and (III) the overall geographical patterns of chronic wasting disease distribution; (iii) significant gaps in current scientific knowledge regarding the transmission pathways and mechanisms identified under clause (i)(I) and potential prevention, detection, and control methods identified under clause (v); (iv) for prioritization the scientific research projects that will address the knowledge gaps identified under clause (iii), based on the likelihood that a project will contribute significantly to the prevention or control of chronic wasting disease; and (v) potential prevention, detection, or control measures, practices, or technologies to be used to mitigate the transmission and spread of chronic wasting disease in wild, captive, and farmed populations of cervids in the United States; (B) assess the effectiveness of the potential prevention, detection, or control measures, practices, or technologies identified under subparagraph (A)(v); and (C) review and compare science-based best practices, standards, and guidance regarding the prevention, detection, and management of chronic wasting disease in wild, captive, and farmed populations of cervids in the United States that have been developed by— (i) the National Chronic Wasting Disease Herd Certification Program of the Animal and Plant Health Inspection Service; (ii) the United States Geological Survey; (iii) State wildlife and agricultural agencies, in the case of practices, standards, and guidance that provide practical, science-based recommendations to State and Federal agencies for minimizing or eliminating the risk of transmission of chronic wasting disease in the United States; and (iv) industry or academia, in the case of any published guidance on practices that provide practical, science-based recommendations to cervid producers for minimizing or eliminating the risk of transmission of chronic wasting disease within or between herds. (4) DEADLINE.—The study under paragraph (2) shall be completed not later than 180 days after the date on which funds are first made available for the study. (5) DATA SHARING.—The Secretaries shall share with the Academy, as necessary to conduct the study under paragraph (2), subject to the avoidance of a violation of a privacy or confidentiality requirement and the protection of confidential or privileged commercial, financial, or proprietary information, data and access to databases on chronic wasting disease under the jurisdiction of— (A) the Veterinary Services Program of the Animal and Plant Health Inspection Service; and (B) the United States Geological Survey. (6) REPORT.—Not later than 60 days after the date of completion of the study, the Secretaries shall submit to the Committee on Agriculture, Nutrition, and Forestry, the Committee on Energy and Natural Resources, and the Committee on Environment and Public Works of the Senate and the Committee on Agriculture and the Committee on Natural Resources of the House of Representatives a report that describes— (A) the findings of the study; and (B) any conclusions and recommendations that the Secretaries determine to be appropriate. (d) Authorization Of Appropriations.—There are authorized to be appropriated to carry out this section— (1) for the period of fiscal years 2021 through 2025, $5,000,000 to the Secretary of the Interior, acting through the Director of the United States Fish and Wildlife Service, to carry out administrative activities under subsection (b); (2) for fiscal year 2021, $1,200,000 to the Secretary of the Interior, acting through the Director of the United States Geological Survey, to carry out activities to fund research under subsection (c); and (3) for fiscal year 2021, $1,200,000 to the Secretary of Agriculture, acting through the Administrator of the Animal and Plant Health Inspection Service, to carry out activities to fund research under subsection (c). https://www.congress.gov/bill/116th-congress/house-bill/925/text https://www.congress.gov/116/bills/hr925/BILLS-116hr925eas.pdf MONDAY, DECEMBER 16, 2019 Chronic Wasting Disease CWD TSE Prion aka mad cow type disease in cervid Zoonosis Update ***> ”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) 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).*** http://www.tandfonline.com/doi/full/10.4161/pri.28124?src=recsys http://www.tandfonline.com/doi/pdf/10.4161/pri.28124?needAccess=true https://wwwnc.cdc.gov/eid/article/20/1/13-0858_article Chronic Wasting Disease CWD TSE Prion aka mad deer disease zoonosis 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. http://grantome.com/grant/NIH/R01-NS088604-04 ZOONOTIC CHRONIC WASTING DISEASE CWD TSE PRION UPDATE Prion 2017 Conference 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 PRION 2018 CONFERENCE Oral transmission of CWD into Cynomolgus macaques: signs of atypical disease, prion conversion and infectivity in macaques and bio-assayed transgenic mice Hermann M. Schatzl, Samia Hannaoui, Yo-Ching Cheng, Sabine Gilch (Calgary Prion Research Unit, University of Calgary, Calgary, Canada) Michael Beekes (RKI Berlin), Walter Schulz-Schaeffer (University of Homburg/Saar, Germany), Christiane Stahl-Hennig (German Primate Center) & Stefanie Czub (CFIA Lethbridge). To date, BSE is the only example of interspecies transmission of an animal prion disease into humans. The potential zoonotic transmission of CWD is an alarming issue and was addressed by many groups using a variety of in vitro and in vivo experimental systems. Evidence from these studies indicated a substantial, if not absolute, species barrier, aligning with the absence of epidemiological evidence suggesting transmission into humans. Studies in non-human primates were not conclusive so far, with oral transmission into new-world monkeys and no transmission into old-world monkeys. Our consortium has challenged 18 Cynomolgus macaques with characterized CWD material, focusing on oral transmission with muscle tissue. Some macaques have orally received a total of 5 kg of muscle material over a period of 2 years. After 5-7 years of incubation time some animals showed clinical symptoms indicative of prion disease, and prion neuropathology and PrPSc deposition were detected in spinal cord and brain of some euthanized animals. PrPSc in immunoblot was weakly detected in some spinal cord materials and various tissues tested positive in RT-QuIC, including lymph node and spleen homogenates. To prove prion infectivity in the macaque tissues, we have intracerebrally inoculated 2 lines of transgenic mice, expressing either elk or human PrP. At least 3 TgElk mice, receiving tissues from 2 different macaques, showed clinical signs of a progressive prion disease and brains were positive in immunoblot and RT-QuIC. Tissues (brain, spinal cord and spleen) from these and pre-clinical mice are currently tested using various read-outs and by second passage in mice. Transgenic mice expressing human PrP were so far negative for clear clinical prion disease (some mice >300 days p.i.). In parallel, the same macaque materials are inoculated into bank voles. Taken together, there is strong evidence of transmissibility of CWD orally into macaques and from macaque tissues into transgenic mouse models, although with an incomplete attack rate. The clinical and pathological presentation in macaques was mostly atypical, with a strong emphasis on spinal cord pathology. Our ongoing studies will show whether the transmission of CWD into macaques and passage in transgenic mice represents a form of non-adaptive prion amplification, and whether macaque-adapted prions have the potential to infect mice expressing human PrP. The notion that CWD can be transmitted orally into both new-world and old-world non-human primates asks for a careful reevaluation of the zoonotic risk of CWD.. ***> The notion that CWD can be transmitted orally into both new-world and old-world non-human primates asks for a careful reevaluation of the zoonotic risk of CWD. However, to date, no CWD infections have been reported in people. sporadic, spontaneous CJD, 85%+ of all human TSE, just 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 $$$ *** *** These results would seem to suggest that CWD does indeed have zoonotic potential, at least as judged by the compatibility of CWD prions and their human PrPC target. Furthermore, extrapolation from this simple in vitro assay suggests that if zoonotic CWD occurred, it would most likely effect those of the PRNP codon 129-MM genotype and that the PrPres type would be similar to that found in the most common subtype of sCJD (MM1).*** http://www.tandfonline.com/doi/full/10.4161/pri.28124?src=recsys http://www.tandfonline.com/doi/pdf/10.4161/pri.28124?needAccess=true https://wwwnc.cdc.gov/eid/article/20/1/13-0858_article FRIDAY, JULY 26, 2019 Chronic Wasting Disease in Cervids: Implications for Prion Transmission to Humans and Other Animal Species https://chronic-wasting-disease.blogspot.com/2019/07/chronic-wasting-disease-in-cervids.html TUESDAY, JANUARY 21, 2020 ***> 2004 European Commission Chronic wasting disease AND TISSUES THAT MIGHT CARRY A RISK FOR HUMAN FOOD AND ANIMAL FEED CHAINS REPORT UPDATED 2020 https://chronic-wasting-disease.blogspot.com/2020/01/2004-european-commission-chronic.html ***> 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) <*** https://familialcjdtseprion.blogspot.com/2019/02/cwd-gss-tse-prion-spinal-cord-confucius.html FRIDAY, OCTOBER 25, 2019 Experts testify United States is underprepared for bioterrorism threats Transmissible Spongiform Encephalopathy TSE Prion disease https://usdameatexport.blogspot.com/2019/10/experts-testify-united-states-is.html ***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 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 1: J Infect Dis 1980 Aug;142(2):205-8 Oral transmission of kuru, Creutzfeldt-Jakob disease, and scrapie to nonhuman primates. Gibbs CJ Jr, Amyx HL, Bacote A, Masters CL, Gajdusek DC. Kuru and Creutzfeldt-Jakob disease of humans and scrapie disease of sheep and goats were transmitted to squirrel monkeys (Saimiri sciureus) that were exposed to the infectious agents only by their nonforced consumption of known infectious tissues. The asymptomatic incubation period in the one monkey exposed to the virus of kuru was 36 months; that in the two monkeys exposed to the virus of Creutzfeldt-Jakob disease was 23 and 27 months, respectively; and that in the two monkeys exposed to the virus of scrapie was 25 and 32 months, respectively. Careful physical examination of the buccal cavities of all of the monkeys failed to reveal signs or oral lesions. One additional monkey similarly exposed to kuru has remained asymptomatic during the 39 months that it has been under observation. snip… The successful transmission of kuru, Creutzfeldt-Jakob disease, and scrapie by natural feeding to squirrel monkeys that we have reported provides further grounds for concern that scrapie-infected meat may occasionally give rise in humans to Creutzfeldt-Jakob disease. PMID: 6997404 http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=6997404&dopt=Abstract 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 emphasised by the finding that some strains of scrapie produce lesions identical to the once which characterise 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 acrapie problem urgent if the sheep industry is not to suffer grievously. snip… 76/10.12/4.6 http://web.archive.org/web/20010305223125/www.bseinquiry.gov.uk/files/yb/1976/10/12004001.pdf Nature. 1972 Mar 10;236(5341):73-4. Transmission of scrapie to the cynomolgus monkey (Macaca fascicularis). Gibbs CJ Jr, Gajdusek DC. Nature 236, 73 – 74 (10 March 1972); doi:10.1038/236073a0 Transmission of Scrapie to the Cynomolgus Monkey (Macaca fascicularis) C. J. GIBBS jun. & D. C. GAJDUSEK National Institute of Neurological Diseases and Stroke, National Institutes of Health, Bethesda, Maryland SCRAPIE has been transmitted to the cynomolgus, or crab-eating, monkey (Macaca fascicularis) with an incubation period of more than 5 yr from the time of intracerebral inoculation of scrapie-infected mouse brain. The animal developed a chronic central nervous system degeneration, with ataxia, tremor and myoclonus with associated severe scrapie-like pathology of intensive astroglial hypertrophy and proliferation, neuronal vacuolation and status spongiosus of grey matter. The strain of scrapie virus used was the eighth passage in Swiss mice (NIH) of a Compton strain of scrapie obtained as ninth intracerebral passage of the agent in goat brain, from Dr R. L. Chandler (ARC, Compton, Berkshire). http://www.nature.com/nature/journal/v236/n5341/abs/236073a0.html http://scrapie-usa.blogspot.com/2010/04/scrapie-and-atypical-scrapie.html Wednesday, February 16, 2011 IN CONFIDENCE SCRAPIE TRANSMISSION TO CHIMPANZEES IN CONFIDENCE http://scrapie-usa.blogspot.com/2011/02/in-confidence-scrapie-transmission-to.html Subject: Re: DEER SPONGIFORM ENCEPHALOPATHY SURVEY & HOUND STUDY Date: Fri, 18 Oct 2002 23:12:22 +0100 From: Steve Dealler Reply-To: Bovine Spongiform Encephalopathy Organization: Netscape Online member To: BSE-L@ References: Dear Terry, An excellent piece of review as this literature is 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 https://caninespongiformencephalopathy.blogspot.com/2010/03/canine-spongiform-encephalopathy-aka.html Stephen Dealler is a consultant medical microbiologist deal@airtime.co.uk BSE Inquiry Steve Dealler Management In Confidence BSE: Private Submission of Bovine Brain Dealler snip…see full text; MONDAY, FEBRUARY 25, 2019 ***> MAD DOGS AND ENGLISHMEN BSE, SCRAPIE, CWD, CJD, TSE PRION A REVIEW 2019 https://bseinquiry.blogspot.com/2019/02/mad-dogs-and-englishmen-bse-scrapie-cwd.html WEDNESDAY, AUGUST 5, 2020 1996-12-04: BBC – Horizon BSE1 – BSE2 The Invisible Enemy, The British Disease, CWD, sporadic CJD https://transmissiblespongiformencephalopathy.blogspot.com/2020/08/1996-12-04-bbc-horizon-bse1-bse2.html Mad Camel Disease CPD TSE Prion dromedary camels (Camelus dromedarius) is spreading In 2018 prion disease was detected in camels at an abattoir in Algeria for the first time. Prion disease has recently been confirmed in three dromedary camels (Camelus dromedarius) from an Algerian slaughterhouse (Babelhadj et al., 2018) after clinical signs compatible with those of TSEs in other species were observed ante mortem. Disease associated pathological changes or prion protein were found in brain by Western blotting, histology, immunohistochemistry (IHC) and paraffin-embedded tissue blot; PrPSc was also detected in the lymph nodes of the one camel tested by IHC. Information gathered from breeders and slaughterhouse personnel suggests that similar clinical signs had been observed since the 1980s (Babelhadj et al., 2018). Subsequently, the disease has also been reported in a single case of a 12 year old dromedary camel from the region of Tataouine, Tunisia (Agrimi, 2019; OIE bulletin 2019). There are many knowledge gaps about the biological characteristics of this new TSE, termed camel prion disease (CPD). Detection of infection in lymph nodes of one animal suggests extra-neural pathogenesis and, therefore, potential transmission of CPD between animals similar to that of classical scrapie and CWD. Such transmission of CPD could be facilitated over long distances by the traditional nomadic herding practices of dromedaries and the trade patterns between Algeria and other countries in North Africa and the Middle East (Bouslikhane, 2015). In light of the devastation caused by BSE, and its subsequent zoonotic transmission, CPD was used here to assess the probability of entry of a novel prion disease agent into the UK via livestock and livestock products. The approach used was to assess the aggregated probability, using the number of imports per year to avoid potential under-estimation as has previously been described (Kelly et al., 2018). Of note, the zoonotic potential of the disease is unknown and this assessment is of the probability of introduction of the CPD agent into the UK only, not of any onward transmission to humans or animals. snip… 3. Results 3.1. Risk assessment 3.1.1. Probability camel is infected with camel prion disease in exporting country (p1) Detection of abnormal neurological signs since the 1980s within a restricted geographical area of Algeria suggests that the expansion of CPD to other areas (and countries) may be restricted or that the disease can remain largely undiagnosed. According to a recent presentation of the Mediterranean Animal Health Network, the disease was also reported in Tunisia and the incidence in the initial region of Algeria was described as ‘rapidly and progressively increasing’ (Agrimi, 2019). It is, therefore, possible that movement of camels has allowed infected animals to enter other countries. Asides from the legal trade of camels, approximately 268 million people in Africa practice some form of pastoralism (Luizza, 2017). For example, over 95% of cross-border trade within the Horn of Africa is unofficial and carried out by nomadic pastoralists trading livestock. Given that disease was first noticed in the 1980s and the nomadic way of life in this area, exporting countries were therefore considered as those making up the regions of North Africa and the Middle East for the purpose of this assessment. Twenty of 937 camels in 2015 and 51 of 1,322 in 2016 showed neurologic signs at slaughter giving an overall estimated apparent prevalence of 3.1% in dromedaries brought for slaughter (Babelhadj et al., 2018). In the absence of further information including confirmatory testing, an assumption was made that the prevalence of CPD in live camels in the regions of interest was high with high uncertainty because of the lack of testing data from countries other than Algeria and in only 3 camels in Algeria itself. see full report; Assessing the aggregated probability of entry of a novel prion disease agent into the United Kingdom https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7428426/pdf/main.pdf Monday, September 14, 2020 Assessing the aggregated probability of entry of a novel prion disease agent into the United Kingdom https://camelusprp.blogspot.com/2020/09/assessing-aggregated-probability-of.html Camel prion disease: a possible emerging disease in dromedary camel populations? The identification of a new prion disease in dromedary camels in Algeria and Tunisia, called camel prion disease (CPD), extends the spectrum of animal species naturally susceptible to prion diseases and opens up new research areas for investigation. Camel prion disease was identified in 2018 in adult camels showing clinical signs at the ante mortem inspection at slaughterhouses in the region of Ouargla (Algeria), and in 2019 in the region of Tataouine (Tunisia). It adds to the group of existing animal prion diseases, including scrapie in sheep and goats, chronic wasting disease (CWD) in cervids and BSE (mainly in bovines). The detection of a new prion disease in the dromedary population requires attention and investigation needs to be carried out to assess the risks of this disease to animal and public health. As of today, very limited epidemiological information is available to assess the prevalence, geographical distribution and dynamic of the transmission of the disease. Based on the clinical signs suggesting prion disease, CPD seems to have occurred in 3.1% of the dromedaries brought to the abattoir in Ouargla. Pathognomonic neurodegeneration and diseasespecific prion protein (PrPSc) were detected in brain tissue from three symptomatic animals (source: CDC article wwwnc.cdc.gov/eid/article/24/6/17-2007_article). ; In May 2019, the OIE received a report from Tunisia on a single case of a 12-year-old slaughtered dromedary camel showing neurological signs confirmed as CPD by the Istituto Superiore di Sanità (ISS) based in Italy. ©B. Babelhadj/University Kasdi Merbah, Algeria www.oiebulletin.com 2 Is camel prion disease transmissible in natural conditions? The involvement of lymphoid tissue in prion replication, observed both in the Algeria and Tunisia cases, is suggestive of a peripheral pathogenesis, which is thought to be a prerequisite for prion shedding into the environment. As with other animal prion diseases, such as scrapie and CWD, in which lymphoid tissues are extensively involved and horizontal transmission occurs efficiently under natural conditions, the detection of prion proteins in lymph nodes is suggestive of the infectious nature of CPD and concurs to hypothesise the potential impact of CPD on animal health. No evidence is currently available with which to argue for the relevance of CPD for human health. However, no absolute species barrier exists in prion diseases and minimising the exposure of humans to prion-infected animal products is an essential aspect of public health protection. As for the relationship between CPD and other animal prion diseases, preliminary analyses suggest that CPD prions have a different molecular signature from scrapie and BSE. Actions on the follow up of CPD Since the first description of CPD, the OIE promoted discussions on the impact of this new disease through the OIE Scientific Commission for Animal Diseases (Scientific Commission). The Scientific Commission consulted two OIE ad hoc Groups, one on BSE risk status evaluation of Members and the other on camelids. It analysed the information available from the Algeria and Tunisia cases to evaluate if CPD should be considered an ‘emerging disease’ based on the criteria listed in the Terrestrial Animal Health Code1 . The OIE Scientific Commission noted that limited surveillance data were available on the prevalence of CPD and that the evidence was not sufficient to measure, at that time, the impact of the disease on animal or public health. Therefore, it was concluded that, with the current knowledge, CPD did not currently meet the criteria to be considered an emerging disease. Nonetheless, it was emphasised that CPD should be considered as a new disease not to be overlooked and called for the collection of further scientific evidence through research and surveillance in the affected countries and in countries with dromedary camel populations to measure the impact of the disease. As new scientific evidence becomes available,the OIE Scientific Commission will reassess whether this disease should be considered as an emerging disease. The worldwide camel population is ~35 million head (FAO, 2019), 88% of which is found in Africa. The camel farming system is evolving rapidly, and these animals represent vital sources of meat, milk and transportation for millions of people living in the most arid regions of the world. This makes it necessary to assess the risk for animal and human health and to develop evidence-based policies to control and limit the spread of the disease in animals, and to minimise human exposure. As a first step, the awareness of Veterinary Services about CPD and its diagnostic capacity needs to be improved in all countries where dromedaries are part of the domestic livestock. At the regional level, CPD was first discussed in the 18th Joint Permanent Committee of the Mediterranean Animal Health Network (REMESA) held in Cairo, Egypt, in June 2019 where an expert 1 a new occurrence in an animal of a disease, infection or infestation, causing a significant impact on animal or public health resulting from a) a change of a known pathogenic agent or its spread to a new geographic area or species, or b) a previously unrecognised pathogenic agent or disease diagnosed for the first time www.oiebulletin.com 3 from ISS, Italy, shared the knowledge available on the new disease with the 15 REMESA Member Countries. The discussion highlighted the need to strengthen surveillance systems in order to collect epidemiological data to inform the risk assessments. The results of these risk assessments will support the implementation of evidence-based policies to manage the risks in both animals and humans. CPD was recently discussed at the 15thConference of the OIE Regional Commission for the Middle East in November. During this conference, the CAMENET (Camel Middle East Network) launched a wideranging proposal for training, coordinated surveillance and research on CPD. In addition, the ERFAN (Enhancing Research forAfrica Network), a platform aimed at enhancing scientific cooperation between Africa and Italy, during its 2nd ERFAN meeting for North Africa, presented a project on CPD with the objective of increasing CPD coordinated surveillance in North Africa. The OIE, through its Reference Laboratories for prion diseases, and by involving the above scientific initiatives, is keeping a close watch on the evolution of the disease to gather scientific evidence and to allow a proper and more thorough assessment of the risk associated with this novel disease. ◼ December 2019 https://oiebulletin.com/wp-content/uploads/2019/12/OIE-News-December-2019-Camel-prion-disease.pdf Tuesday, September 15, 2020 Mad Camel Disease CPD TSE Prion dromedary camels (Camelus dromedarius) is spreading https://camelusprp.blogspot.com/2020/09/mad-camel-disease-cpd-tse-prion.html THURSDAY, AUGUST 06, 2020 Scrapie Documented in Tunisia https://scrapie-usa.blogspot.com/2020/08/scrapie-documented-in-tunisia.html Thursday, August 1, 2019 Camel prion disease detected in Tunisian camels Camel prion disease detected in Tunisian camels A novel prion disease first reported in three dromedary camels in Algeria in 2018 has now been detected in dromedaries in Tunisia, the second country to be affected within a year, ProMED Mail, the online reporting system of the International Society for Infectious Diseases, reported yesterday. The Tunisian detection and the latest information about the disease, called camel prion disease (CPD) and sometimes referred to as “mad camel disease”, came from a presentation at the Mediterranean Animal Health Network meeting, held in Cairo on Jun 26 and 27. According to the meeting presentation, CPD is spreading rapidly in the Ouargla region of Algeria where the disease was first identified in older camels at a slaughterhouse. The scientists who presented at the meeting also said preliminary results suggest that the CPD prion is different from scrapie and bovine spongiform encephalitis (BSE, or “mad cow disease”). A comment from the ProMED Mail moderator Arnon Shimshony, DVM, associate professor of veterinary medicine at Hebrew University of Jerusalem, notes that the area where CPD was first found in Algeria is about 174 miles from the Tunisian border. In the initial report on the first detection in Algerian camels, published in April 2018 in Emerging Infectious Diseases, described disease-specific prion protein in brain tissues from symptomatic camels, including positive samples in lymph nodes, suggesting infection. The moderator also requested more details about the detections in Tunisia, including location, clinical signs, and ages and origins of affected camels. Jul 29 ProMED Mail post Apr 18, 2018, CIDRAP News story “‘Mad camel’ disease? New prion infection causes alarm” http://www.cidrap.umn.edu/news-perspective/2019/07/news-scan-jul-30-2019 https://camelusprp.blogspot.com/2019/08/camel-prion-disease-detected-in.html ***> NEW TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHY TSE PRION DISEASE (MAD CAMEL DISEASE) IN A NEW SPECIES IMPORTS AND EXPORTS SEE MASSIVE AMOUNTS OF BANNED ANIMAL PROTEIN AKA MAD COW FEED IN COMMERCE USA DECADES AFTER POST BAN Saturday, April 14, 2018 Dromedary Camels Algeria Prion (Mad Camel Disease) TSE BSE MRR Import Export Risk Factors Excluding Grains and Plants Dromedary Camels Algeria Prion (Mad Camel Disease) TSE BSE MRR Import Export Risk Factors Excluding Grains and Plants (Grains and Plants Materials Could Harbor the Transmissible Spongiform Encephalopathy TSE Prion agent…TSS) Dromedary Camels Algeria Prion (Mad Camel Disease) TSE BSE MRR Import Export Risk Factors Excluding Grains and Plants http://camelusprp.blogspot.com/2018/04/dromedary-camels-algeria-prion-mad.html http://camelusprp.blogspot.com/ America BSE 589.2001 FEED REGULATIONS, BSE SURVEILLANCE, BSE TESTING, and CJD TSE Prion so far, we have been lucky. to date, with the science at hand, no cwd transmitted to cattle, that has been documented, TO DATE, WITH THE SCIENCE AT HAND, it’s not to say it has not already happened, just like with zoonosis of cwd i.e. molecular transmission studies have shown that cwd transmission to humans would look like sporadic cjd, NOT nvCJD or what they call now vCJD. the other thing is virulence and or horizontal transmission. this is very concerning with the recent fact of what seems to be a large outbreak of a new tse prion disease in camels in Africa. there is much concern now with hay, straw, grains, and such, with the cwd tse prion endemic countries USA, Canada. what is of greatest concern is the different strains of cwd, and the virulence there from? this thing (cwd) keeps mutating to different strains, and to different species, the bigger the chance of one of these strains that WILL TRANSMIT TO CATTLE OR HUMANS, and that it is documented (i believe both has already occured imo with scienct to date). with that said, a few things to ponder, and i am still very concerned with, the animal feed. we now know from transmission studies that cwd and scrapie will transmit to pigs by oral routes. the atypical bse strains will transmit by oral routes. i don’t mean to keep kicking a mad cow, just look at the science; ***> cattle, pigs, sheep, cwd, tse, prion, oh my! ***> In contrast, cattle are highly susceptible to white-tailed deer CWD and mule deer CWD in experimental conditions but no natural CWD infections in cattle have been reported (Sigurdson, 2008; Hamir et al., 2006). Sheep and cattle may be exposed to CWD via common grazing areas with affected deer but so far, appear to be poorly susceptible to mule deer CWD (Sigurdson, 2008). In contrast, cattle are highly susceptible to white-tailed deer CWD and mule deer CWD in experimental conditions but no natural CWD infections in cattle have been reported (Sigurdson, 2008; Hamir et al., 2006). It is not known how susceptible humans are to CWD but given that the prion can be present in muscle, it is likely that humans have been exposed to the agent via consumption of venison (Sigurdson, 2008). Initial experimental research suggests that human susceptibility to CWD is low and there may be a robust species barrier for CWD transmission to humans (Sigurdson, 2008), however the risk appetite for a public health threat may still find this level unacceptable. https://assets.publishing.service.gov.uk/government/uploads/system/uploads/attachment_data/file/733407/DEFRA_QRA_TSE_in_cervids_June2018_v1.pdf http://chronic-wasting-disease.blogspot.com/2012/08/susceptibility-of-cattle-to-agent-of.html cwd scrapie pigs oral routes ***> However, at 51 months of incubation or greater, 5 animals were positive by one or more diagnostic methods. Furthermore, positive bioassay results were obtained from all inoculated groups (oral and intracranial; market weight and end of study) suggesting that swine are potential hosts for the agent of scrapie. *** Although the current U.S. feed ban is based on keeping tissues from TSE infected cattle from contaminating animal feed, swine rations in the U.S. could contain animal derived components including materials from scrapie infected sheep and goats. These results indicating the susceptibility of pigs to sheep scrapie, coupled with the limitations of the current feed ban, indicates that a revision of the feed ban may be necessary to protect swine production and potentially human health. Results: PrPSc was not detected by EIA and IHC in any RPLNs. All tonsils and MLNs were negative by IHC, though the MLN from one pig in the oral <6 month group was positive by EIA. PrPSc was detected by QuIC in at least one of the lymphoid tissues examined in 5/6 pigs in the intracranial 6 months group, 5/6 pigs in the oral 6 months group. Overall, the MLN was positive in 14/19 (74%) of samples examined, the RPLN in 8/18 (44%), and the tonsil in 10/25 (40%). ***> Conclusions: This study demonstrates that PrPSc accumulates in lymphoid tissues from pigs challenged intracranially or orally with the CWD agent, and can be detected as early as 4 months after challenge. CWD-infected pigs rarely develop clinical disease and if they do, they do so after a long incubation period. This raises the possibility that CWD-infected pigs could shed prions into their environment long before they develop clinical disease. Furthermore, lymphoid tissues from CWD-infected pigs could present a potential source of CWD infectivity in the animal and human food chains. https://www.ars.usda.gov/research/publications/publication/?seqNo115=353091 https://www.ars.usda.gov/research/project/?accnNo=432011&fy=2017 https://www.ars.usda.gov/research/publications/publication/?seqNo115=337105 Friday, December 14, 2012 DEFRA U.K. What is the risk of Chronic Wasting Disease CWD being introduced into Great Britain? A Qualitative Risk Assessment October 2012 snip In the USA, under the Food and Drug Administration’s BSE Feed Regulation (21 CFR 589.2000) most material (exceptions include milk, tallow, and gelatin) from deer and elk is prohibited for use in feed for ruminant animals. With regards to feed for non-ruminant animals, under FDA law, CWD positive deer may not be used for any animal feed or feed ingredients. For elk and deer considered at high risk for CWD, the FDA recommends that these animals do not enter the animal feed system. However, this recommendation is guidance and not a requirement by law. Animals considered at high risk for CWD include: 1) animals from areas declared to be endemic for CWD and/or to be CWD eradication zones and 2) deer and elk that at some time during the 60-month period prior to slaughter were in a captive herd that contained a CWD-positive animal. Therefore, in the USA, materials from cervids other than CWD positive animals may be used in animal feed and feed ingredients for non-ruminants. The amount of animal PAP that is of deer and/or elk origin imported from the USA to GB can not be determined, however, as it is not specified in TRACES. It may constitute a small percentage of the 8412 kilos of non-fish origin processed animal proteins that were imported from US into GB in 2011. Overall, therefore, it is considered there is a __greater than negligible risk___ that (nonruminant) animal feed and pet food containing deer and/or elk protein is imported into GB. There is uncertainty associated with this estimate given the lack of data on the amount of deer and/or elk protein possibly being imported in these products. snip 36% in 2007 (Almberg et al., 2011). In such areas, population declines of deer of up to 30 to 50% have been observed (Almberg et al., 2011). In areas of Colorado, the prevalence can be as high as 30% (EFSA, 2011). The clinical signs of CWD in affected adults are weight loss and behavioural changes that can span weeks or months (Williams, 2005). In addition, signs might include excessive salivation, behavioural alterations including a fixed stare and changes in interaction with other animals in the herd, and an altered stance (Williams, 2005). These signs are indistinguishable from cervids experimentally infected with bovine spongiform encephalopathy (BSE). Given this, if CWD was to be introduced into countries with BSE such as GB, for example, infected deer populations would need to be tested to differentiate if they were infected with CWD or BSE to minimise the risk of BSE entering the human food-chain via affected venison. snip The rate of transmission of CWD has been reported to be as high as 30% and can approach 100% among captive animals in endemic areas (Safar et al., 2008). snip In summary, in endemic areas, there is a medium probability that the soil and surrounding environment is contaminated with CWD prions and in a bioavailable form. In rural areas where CWD has not been reported and deer are present, there is a greater than negligible risk the soil is contaminated with CWD prion. snip In summary, given the volume of tourists, hunters and servicemen moving between GB and North America, the probability of at least one person travelling to/from a CWD affected area and, in doing so, contaminating their clothing, footwear and/or equipment prior to arriving in GB is greater than negligible… For deer hunters, specifically, the risk is likely to be greater given the increased contact with deer and their environment. However, there is significant uncertainty associated with these estimates. snip Therefore, it is considered that farmed and park deer may have a higher probability of exposure to CWD transferred to the environment than wild deer given the restricted habitat range and higher frequency of contact with tourists and returning GB residents. s nip https://web.archive.org/web/20170404125557/http://webarchive.nationalarchives.gov.uk/20130822084033/http://www.defra.gov.uk/animal-diseases/files/qra_chronic-wasting-disease-121029.pdf ***> READ THIS VERY, VERY, CAREFULLY, AUGUST 1997 MAD COW FEED BAN WAS A SHAM, AS I HAVE STATED SINCE 1997! 3 FAILSAFES THE FDA ET AL PREACHED AS IF IT WERE THE GOSPEL, IN TERMS OF MAD COW BSE DISEASE IN USA, AND WHY IT IS/WAS/NOT A PROBLEM FOR THE USA, and those are; BSE TESTING (failed terribly and proven to be a sham) BSE SURVEILLANCE (failed terribly and proven to be a sham) BSE 589.2001 FEED REGULATIONS (another colossal failure, and proven to be a sham) these are facts folks. trump et al just admitted it with the feed ban. see; FDA Reports on VFD Compliance John Maday August 30, 2019 09:46 AM VFD-Form 007 (640×427) Before and after the current Veterinary Feed Directive rules took full effect in January, 2017, the FDA focused primarily on education and outreach. ( John Maday ) Before and after the current Veterinary Feed Directive (VFD) rules took full effect in January, 2017, the FDA focused primarily on education and outreach to help feed mills, veterinarians and producers understand and comply with the requirements. Since then, FDA has gradually increased the number of VFD inspections and initiated enforcement actions when necessary. On August 29, FDA released its first report on inspection and compliance activities. The report, titled “Summary Assessment of Veterinary Feed Directive Compliance Activities Conducted in Fiscal Years 2016 – 2018,” is available online. https://www.fda.gov/media/130382/download SUNDAY, SEPTEMBER 1, 2019 ***> FDA Reports on VFD Compliance https://bovineprp.blogspot.com/2019/09/fda-reports-on-vfd-compliance.html ***> cattle, pigs, sheep, cwd, tse, prion, oh my! ***> In contrast, cattle are highly susceptible to white-tailed deer CWD and mule deer CWD in experimental conditions but no natural CWD infections in cattle have been reported (Sigurdson, 2008; Hamir et al., 2006). Sheep and cattle may be exposed to CWD via common grazing areas with affected deer but so far, appear to be poorly susceptible to mule deer CWD (Sigurdson, 2008). In contrast, cattle are highly susceptible to white-tailed deer CWD and mule deer CWD in experimental conditions but no natural CWD infections in cattle have been reported (Sigurdson, 2008; Hamir et al., 2006). It is not known how susceptible humans are to CWD but given that the prion can be present in muscle, it is likely that humans have been exposed to the agent via consumption of venison (Sigurdson, 2008). Initial experimental research suggests that human susceptibility to CWD is low and there may be a robust species barrier for CWD transmission to humans (Sigurdson, 2008), however the risk appetite for a public health threat may still find this level unacceptable. https://assets.publishing.service.gov.uk/government/uploads/system/uploads/attachment_data/file/733407/DEFRA_QRA_TSE_in_cervids_June2018_v1.pdf http://chronic-wasting-disease.blogspot.com/2012/08/susceptibility-of-cattle-to-agent-of.html FRIDAY, OCTOBER 04, 2019 Inactivation of chronic wasting disease prions using sodium hypochlorite i think some hunters that don’t read this carefully are going to think this is a cure all for cwd tse contamination. IT’S NOT! first off, it would take a strong bleach type sodium hypochlorite, that is NOT your moms bleach she uses in her clothes, and store bought stuff. Concentrated bleach is an 8.25 percent solution of sodium hypochlorite, up from the “regular bleach ” concentration of 5.25 percent .Nov 1, 2013 https://waterandhealth.org/disinfect/high-strength-bleach-2/ second off, the study states plainly; ”We found that a five-minute treatment with a 40% dilution of household bleach was effective at inactivating CWD seeding activity from stainless-steel wires and CWD-infected brain homogenates. However, bleach was not able to inactivate CWD seeding activity from solid tissues in our studies.” ”We initially tested brains from two CWD-infected mice and one uninfected mouse using 40% bleach for 5 minutes. The results from these experiments showed almost no elimination of prion seeding activity ( Table 4 ). We then increased the treatment time to 30 minutes and tested 40% and 100% bleach treatments. Again, the results were disappointing and showed less than a 10-fold decrease in CWD-seeding activity ( Table 4 ). Clearly, bleach is not able to inactivate prions effectively from small brain pieces under the conditions tested here.” ”We found that both the concentration of bleach and the time of treatment are critical for inactivation of CWD prions. A 40% bleach treatment for 5 minutes successfully eliminated detectable prion seeding activity from both CWD-positive brain homogenate and stainless-steel wires bound with CWD. However, even small solid pieces of CWD-infected brain were not successfully decontaminated with the use of bleach.” https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0223659 https://chronic-wasting-disease.blogspot.com/2019/10/inactivation-of-chronic-wasting-disease.html i think with all the fear from recent studies, and there are many, of potential, or likelihood of zoonosis, if it has not already happened as scjd, i think this study came out to help out on some of that fear, that maybe something will help, but the study plainly states it’s for sure not a cure all for exposure and contamination of the cwd tse prion on surface materials. imo…terry HUNTERS, CWD TSE PRION, THIS SHOULD A WAKE UP CALL TO ALL OF YOU GUTTING AND BONING OUT YOUR KILL IN THE FIELD, AND YOUR TOOLS YOU USE… * 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