TPWD adopts, on an emergency basis, new §65.100, concerning Emergency Provisions CWD TSE PRION
TPWD adopts, on an emergency basis, new §65.100, concerning Emergency Provisions CWD TSE PRION
TITLE 31. NATURAL RESOURCES AND CONSERVATION
PART 2. TEXAS PARKS AND WILDLIFE DEPARTMENT
CHAPTER 65. WILDLIFE
SUBCHAPTER B. DISEASE DETECTION AND RESPONSE
DIVISION 2. CHRONIC WASTING DISEASE - MOVEMENT OF DEER
The Texas Parks and Wildlife Department adopts, on an emergency basis, new §65.100, concerning Emergency Provisions. The emergency action replaces the emergency rule filed on July 19, 2021, and published in the August 6, 2021, issue of the Texas Register (46 TexReg 4759). The effective period of the emergency rule was extended through December 18, 2021, as published in the October 22, 2021, issue of the Texas Register (46 TexReg 7113). This action is necessary to alter the current emergency rule to address the impacts of a national shortage of the chemical reagent used in disease testing required by the rule.
The emergency rule was adopted in response to the threat of chronic wasting disease (CWD), a fatal neurodegenerative disorder that affects cervid species such as white-tailed deer, mule deer, elk, red deer, sika, and others (susceptible species). The department, along with the Texas Animal Health Commission (TAHC), has been engaged in an ongoing battle with CWD in Texas since 2002. White-tailed deer and mule deer are species authorized to be regulated by the department under the Parks and Wildlife Code. TAHC is the state agency charged with disease management in livestock and exotic livestock, including exotic livestock known to be susceptible to CWD. The recent detections of CWD in breeding facilities created an unprecedented situation because they occurred at a scale that is orders of magnitude greater than earlier instances of detection encountered by the department.
The department has determined that if the regulated community is unable to comply with the disease testing requirements of the rule there could be significant unforeseen consequences that further threaten deer populations in the state.
The department has specified an expiration date of December 18, 2021, for the expiration of this replacement emergency adoption in order to preserve the maximum 180-day period of effectiveness established by statute for emergency filings.
The rule is adopted on an emergency basis under Parks and Wildlife Code, Chapter 43, Subchapter L, which authorizes the Parks and Wildlife Commission to establish regulations governing the possession of white-tailed and mule deer under a deer breeders permit; Parks and Wildlife Code, §12.027, which authorizes the Texas Parks and Wildlife Commission and the department's executive director to adopt emergency rules if there is an immediate danger to a species authorized to be regulated by the department, and under Government Code, §2001.034, which authorizes a state agency to adopt such emergency rules without prior notice or hearing.
§65.100.Emergency Provisions.
(a) Effectiveness.
(1) To the extent that any provision of this section conflicts with any provision of this division, the provisions of this section prevail.
(2) The provisions of Division 1 of this subchapter apply to any facility designated by the department as a Category A, Category B, or Tier 1 breeding facility subject to the provisions of this section.
(b) Definitions. The following words and terms shall have the following meanings, unless the context clearly indicates otherwise. All other words and terms used in this section shall have the meanings assigned by the Parks and Wildlife Code and §65.90 of this title (relating to Definitions).
(1) Exposed deer--A deer that meets any of the following criteria:
(A) the deer is or has been in a breeding facility where a CWD-positive deer has been kept following the date the facility was first exposed to CWD (if known);
(B) the deer is or has been in a breeding facility within the five-year period preceding the death date of any CWD-positive deer that was in the facility (or the date of a positive ante-mortem test result); or
(C) the deer is in a breeding facility on or after the date that the facility received a deer under the circumstances described in subparagraph (A) or (B) of this paragraph.
(2) Exposure--The period of time that has elapsed following the introduction of an exposed deer to a breeding facility.
(3) "Insufficient follicles"--A test result indicating that a tonsil or rectal biopsy sample contained an insufficient number of lymphoid follicles to produce a valid test result.
(4) Last known exposure--the last date a deer in a trace-out breeding facility was exposed to a trace deer prior to the death or transfer of that trace deer, or the last date an exposed deer entered a Tier 1 facility.
(5) Test-eligible deer--A deer at least nine months of age.
(6) Tier 1 facility--A breeding facility that has received an exposed deer that was in a trace-out breeding facility.
(7) Trace deer--A deer that the department has determined had been in a CWD-positive deer breeding facility on or after the date the facility was first exposed to CWD, if known; otherwise, within the previous five years from the reported mortality date of the CWD-positive deer, or the date of the ante-mortem test result.
(8) Trace-out breeding facility--A breeding facility that has received an exposed deer that was in a CWD-positive deer breeding facility.
(c) General provisions.
(1) Deer required to be reported to the department under §65.605 of this title (relating to Holding Facility Standards and Care of Deer) are considered to be mortalities for the purposes of this subchapter until lawfully recaptured. A deer that is not recaptured will be treated as a mortality that occurred within the facility from which the escape is required to be reported.
(2) Deer that according to department records should be present in a breeding facility but cannot be accounted for to the satisfaction of the department are considered to be mortalities for the purposes of this subchapter.
(3) For facilities required to test ten or more deer, the department will not accept inconclusive ante-mortem test results, including but not limited to "insufficient follicles," for more than 10 percent of the total number of deer tested. For facilities required to test less than ten deer, inconclusive ante-mortem test results, including but not limited to "insufficient follicles," will not be accepted.
(4) Fawns in any Category A, Category B, and or Tier 1 facility may be transferred to a registered nursing facility, provided:
(A) the originating facility was MQ at the time the facility was designated Category A, Category B, or Tier 1 ; and
(B) no fawns from any other breeding facility are or have been present in the nursing facility during the current permit year.
(5) Nursing facilities may not possess fawns that are older than 120 days of age.
(d) Category A trace-out breeding facility.
(1) A Category A facility is a trace-out breeding facility:
(A) in which all trace deer are alive in the facility; or
(B) for which post-mortem test results of "not detected" have been returned for trace deer that have died and all other trace deer are alive and present in the facility.
(2) Except as provided in paragraph (3) of this subsection, a permittee shall, upon notification by the department of Category A status:
(A) within seven days euthanize all trace deer in the breeding facility and submit test samples for each of those deer for post-mortem testing within one business day;
(B) inspect the facility daily for mortalities;
(C) immediately report all test-eligible mortalities that occur within the facility; and
(D) immediately collect test samples from all test-eligible mortalities that occur within the facility and submit the samples for post-mortem testing within one business day of collection.
(3) In lieu of the testing requirements prescribed in paragraph (2)(A) of this subsection, a permittee may request the development of a custom testing plan as provided in subsection (g) of this section; provided however, the permittee must comply with the requirements of paragraph (2)(B) - (D) of this subsection.
(4) The department in consultation with TAHC may decline to authorize a custom testing plan under subsection (g) of this section if an epidemiological assessment determines that a custom testing plan is inappropriate.
(5) The department will not restore MQ status unless CWD "not detected" test results are obtained for all required sample submissions and the permittee has complied with all applicable requirements of this subsection and this division.
(e) Category B trace-out breeding facility.
(1) A Category B facility is a trace-out breeding facility in which less than 100% of the trace deer that department records indicate were received by the facility are for whatever reason (including but not limited to transfer, release, or escape) available for testing.
(2) Upon notification by the department of Category B status, a permittee shall:
(A) within seven days euthanize all trace deer in the breeding facility and submit test samples for each of those deer for post-mortem testing within one business day;
(B) inspect the facility daily for mortalities;
(C) immediately report all test-eligible mortalities that occur within the facility;
(D) immediately collect test samples from all test-eligible mortalities that occur within the facility and submit the samples for post-mortem testing within one business day of collection; and
(E) conduct ante-mortem testing of all test-eligible deer in the facility as specified in the following:
(i) for a facility for which the date of last known exposure is within the immediately preceding 18 months:
(I) submit rectal or tonsil biopsy samples collected on or after April 1, 2021; and
(II) submit tonsil biopsy samples collected no earlier than 24 months from the date of last known exposure;
(ii) for a facility for which the date of last known exposure is not within the immediately preceding 18 months and not at a time prior to the immediately preceding 36 months: collect and submit tonsil biopsy samples no earlier than 24 months from the date of last known exposure; and
(iii) for a facility for which the date of last known exposure occurred at a time after the immediately preceding 36 months: collect and submit rectal or tonsil biopsy samples collected no earlier than 36 months from the date of last known exposure.
(3) In lieu of the testing requirements prescribed by paragraph (2)(A) and (2)(E) of this subsection, a permittee may request the development of a custom testing plan as provided in subsection (g) of this section; provided, however, the permittee must comply with subparagraphs (B) - (D) of this paragraph.
(4) Samples required by paragraph (2)(E) of this subsection shall be submitted no later than 45 days after the applicable last known exposure period as determined by the department.
(5) The department in consultation with TAHC may decline to authorize a custom testing plan under subsection (g) of this section if an epidemiological assessment determines that a custom testing plan is inappropriate.
(6) The department will not restore MQ status unless CWD "not detected" test results are obtained for all required sample submissions and the permittee has complied with all applicable requirements of this subsection and this division.
(f) Tier 1 facility.
(1) Upon notification by the department of Tier 1 status, a facility is automatically NMQ and the permittee shall:
(A) inspect the facility daily for mortalities;
(B) immediately report all test-eligible deer mortalities that occur within the facility; and
(C) immediately collect test samples from all test-eligible deer mortalities that occur within the facility and submit for post-mortem testing within one business day of collection.
(2) A permittee may request the development of a custom testing plan as provided in subsection (g) of this section; provided, however, the permittee must comply with the provisions of paragraph (1)(A) - (C) of this subsection.
(3) The department will not restore MQ status unless the permittee has complied with all applicable requirements of this subsection and this division, and any one of the following:
(A) post-mortem results of "not detected" have been submitted for every exposed deer received from a trace facility; or
(B) the department has restored MQ status to all trace facilities from which deer were received; or
(C) the permittee has conducted ante-mortem testing as specified in subsection (e)(2)(E) of this section; or
(D) the permittee has conducted testing as specified in compliance with the provisions of a custom testing plan under the provisions of subsection (g) of this section to the satisfaction of the department and TAHC.
(4) The department in consultation with TAHC may decline to authorize a custom testing plan under subsection (g) of this section if an epidemiological assessment determines that a custom testing plan is inappropriate.
(g) Custom Testing Plan. Within seven days of being notified by the department that a breeding facility has been designated a Category A, Category B, or Tier 1 facility, a permittee may, in lieu of meeting the applicable testing requirements of subsections (d) - (f) of this subsection, request the development of a custom testing plan by the department in consultation with TAHC based upon an epidemiological assessment conducted by the department and TAHC. A custom testing plan under this subsection is not valid unless it has been approved by the department and TAHC.
(1) The department shall temporarily suspend the applicable testing provisions of subsections (d)(2)(A) and (e)(2)(A) and (E) of this section while the epidemiological assessment and custom testing plan development under this subsection take place.
(2) Upon the development of a custom testing plan under the provisions of this subsection, the department shall provide the permittee with a copy of the custom testing plan and the permittee shall, within seven days:
(A) agree in writing to comply with the provisions of the custom testing plan; or
(B) notify the department in writing that the permittee declines to participate in the custom testing plan.
(C) If a permittee chooses to decline participation in a custom testing plan under this subsection, the provisions of subsections (d)(2)(A) and (e)(2)(A) and (E) of this section take effect as of the date of the notification required by subparagraph (B) of this paragraph and all time-dependent calculations of those subsections begin.
(D) If a permittee agrees in writing to comply with the provisions of a custom testing plan under this subsection, the custom testing plan replaces the testing provisions of subsections (d)(2)(A) and (e)(2)(A) and (E) of this section.
(3) A breeding facility designated by the department as Category A, Category B, or Tier 1 is NMQ as of the date of such notification and remains NMQ until the provisions of the custom testing plan under this subsection have been satisfied.
(4) If for any reason the permittee does not comply with the provisions of a custom testing plan under this subsection, the provisions of subsections (d) - (f) of this section resume applicability.
(5) The terms of a custom testing plan under this subsection are non-negotiable and final.
(h) Release of breeder deer.
(1) No person may transfer a test-eligible breeder deer to a release facility or cause or allow a breeder deer to be transferred to a release facility unless an ante-mortem test on rectal or tonsil tissue collected from the deer within the six months immediately preceding the release has been returned with test results of "not detected."
(2) Upon notification of the department by the Texas Veterinary Medical Diagnostic Laboratory (TVMDL) that a national shortage of the chemical reagent used in immunohistochemistry testing for CWD prevents TVMDL from performing the ante-mortem testing required by this section, the department will notify permittees that test-eligible breeder deer may be transferred to a release facility; provided, however no deer may be transferred under the provisions of this paragraph unless the permittee has submitted and TVMDL has received a valid ante-mortem test sample collected from each deer within six months immediately preceding the release.
(3) Upon notification of the department by TVMDL that sufficient chemical reagent is available to perform the ante-mortem testing required by this section, the department will notify permittees that the provisions of paragraph (2) of this subsection have ceased effect.
(4) A facility from which deer are transferred in violation of paragraph (1) or (2) of this subsection becomes automatically NMQ and any further transfers are prohibited until the permittee has conducted ante-mortem testing as specified in writing by the department.
(i) Violations and Penalties. In addition to any other conduct punishable as a violation of this subchapter or the Parks and Wildlife Code, it is an offense for any person to fail to abide by any provision of this section, a permit provision, a herd plan provision, or a provision of a custom testing plan developed under subsection (g) of this section.
The agency certifies that legal counsel has reviewed the emergency adoption and found it to be within the state agency's legal authority to adopt.
Filed with the Office of the Secretary of State on November 30, 2021.
TRD-202104772
James Murphy
General Counsel
Texas Parks and Wildlife Department
Effective date: November 30, 2021
Expiration date: December 18, 2021
For further information, please call: (512) 389-4775
TAHC National Shortage of Prion Testing Reagents Utilized for CWD Testing
November 17, 2021
On Friday, November 5, 2021, Texas A&M Veterinary Medical Diagnostic Laboratory (TVMDL) made a formal announcement regarding the National Animal Health Laboratory Network (NAHLN) national shortage of prion testing reagents utilized to complete immunohistochemistry (IHC) testing for Chronic Wasting Disease (CWD).
At that time, TVMDL engaged NAHLN, USDA- National Veterinary Services Laboratory (USDA/NVSL), other CWD testing labs in the U.S. and Canada, and the Texas Parks and Wildlife Department (TPWD) in daily communications to explore expedient solutions.
As of Friday, November 12, 2021, TVMDL exhausted their supply of prion kits and are unable to perform the IHC test. As all CWD testing labs have been affected by the shortage, there are no other labs available to assist TVMDL with IHC testing. The estimated timeframe for getting more IHC testing kits is mid-December.
USDA Cervid staff have determined that deer in the CWD Herd Certification Program (HCP) administered by the Texas Animal Health Commission (TAHC) are not eligible to be tested by ELISA. While antemortem samples are not eligible for the ELISA test, postmortem samples from penned deer not in the CWD HCP are eligible. The ELISA test requires fresh, not formalin-fixed, samples submitted within seven (7) days of collection.
The TAHC advises deer breeders enrolled in the CWD HCP to continue to collect the required postmortem samples and fix them in formalin. All samples collected must be submitted to TVMDL within seven days of collection and will be IHC tested upon the availability of test kits.
TVMDL staff continue to prepare all CWD antemortem test samples, a process which takes two days, so that they may be stained as soon as the reagent is made available. TVMDL will continue communications with the reagent supplier and NVSL/USDA to maintain an up-to-date timeline of when reagents will be available. TVMDL and TPWD have indicated they will continue to update permitted deer breeders as to the status of this situation on a regular basis.
Please direct any questions that you may have regarding the reagent shortage to TVMDL. Please contact TPWD or your TAHC Region Office regarding CWD sample collecting.
Thank you,
Texas Animal Health Commission
TPWD CWD TSE PRION TRACKER UPDATE TEXAS 270 CONFIRMED TO DATE POSTIVE CAPTIVE AND WILD
2021-11-18 Free Range Medina N/A White-tailed Deer M 3.5
2021-11-04 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 8.189041096
2021-10-12 Breeder Deer Uvalde Facility #8 White-tailed Deer M 1.208219178
2021-10-12 Breeder Deer Uvalde Facility #8 White-tailed Deer M 1.21369863
2021-10-12 Breeder Deer Uvalde Facility #8 White-tailed Deer M 1.205479452
2021-10-12 Breeder Deer Uvalde Facility #8 White-tailed Deer M 2.208219178
2021-10-12 Breeder Deer Uvalde Facility #8 White-tailed Deer M 2.117808219
2021-10-08 Breeder Deer Duval Facility #13 White-tailed Deer F 3.238356164
2021-10-08 Breeder Deer Medina Facility #4 White-tailed Deer F 2.260273973
2021-09-14 Breeder Deer Medina Facility #4 White-tailed Deer F 6.205479452
SNIP...SEE ALL;
“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
Oh, Deer, CWD, Heading Off a Wildlife Epidemic Texas Real Estate Research Center TAMU
Texas A & M University
Texas Real Estate Research Center
Oh, Deer
Heading Off a Wildlife Epidemic
Charles E. Gilliland (Aug 18, 2021)
The Takeaway
Landowners in certain parts of the state need to be aware of chronic wasting disease, which can greatly reduce the number of deer. While there are no known cures or ways to eradicate the disease, the Texas Parks and Wildlife Department is taking measures to reduce its spread.
snip...
Because the spread of CWD is evolving, regulations can change quickly. Therefore, anyone involved in hunting activity should consult the most recent Outdoor Annual for the latest regulations. To reduce the chances of spreading the disease, TPWD regulations also restrict the movement of live deer from CWD zones.
Impact on Rural Landowners CWD poses a significant threat to the future of hunting in Texas. Deer population declines of 45 and 50 percent have been documented in Colorado and Wyoming. A broad infection of Texas deer populations resulting in similar population impacts would inflict severe economic damage to rural communities and could negatively impact land markets. Specifically, those landowners seeking to establish a thriving herd of deer could avoid buying in areas with confirmed CWD infections.
As they do with anthrax-susceptible properties, land brokers may find it advisable to inquire about the status of CWD infections on properties that they present for sale. Prospective buyers should also investigate the status of the wildlife on prospective properties. In addition, existing landowners should monitor developments as TPWD crafts management strategies to identify and contain this deadly disease.
____________________
Dr. Gilliland (c-gilliland@tamu.edu) is a research economist with the Texas Real Estate Research Center at Texas A&M University.
TERRIBLE NEWS for Texas for sure, and the good Doctor brings much needed attention to a topic no one wants to talk about, and i have been trying to bring awareness to this very topic for decades, 5 or 6 years quarantine is NOT LONG ENOUGH FOR CWD TSE PRION !!!
QUARANTINE NEEDS TO BE 21 YEARS FOR CWD TSE PRION !
3. INDEMNITY, NO MORE Federal indemnity program, or what i call, ENTITLEMENT PROGRAM for game farm industry. NO MORE BAIL OUTS FROM TAX PAYERS. if the captive industry can't buy insurance to protect not only themselves, but also their customers, and especially the STATE, from Chronic Wasting Disease CWD TSE Prion or what some call mad deer disease and harm therefrom, IF they can't afford to buy that insurance that will cover all of it, then they DO NOT GET A PERMIT to have a game farm for anything. This CWD TSE Prion can/could/has caused property values to fall from some reports in some places. roll the dice, how much is a state willing to lose?
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)
Texas adopts new management rules for chronic wasting disease in deer Nov 6, 2021
Texas adopts new management rules for chronic wasting disease in deer
Matt Wyatt
Staff writer
Nov. 6, 2021
A white-tailed buck photographed by Shannon Tompkins.
Shannon Tompkins/Houston Chronicle
AUSTIN — The Texas Parks and Wildlife Commission adopted a new chronic wasting disease management rule package Thursday, regulations mostly geared toward the state’s deer breeding industry.
Texas Parks and Wildlife Department staff believe the update was necessary because the previous CWD rules were deemed inadequate to prevent the transmission of the always-deadly disease in the wake of a recent outbreak in more than 30 CWD-positive deer at seven facilities across the state.
The most significant aspects of the new rule package include a requirement that breeders ante-mortum (live deer) test every deer 12 months and older at least eight months prior to release, 100 percent testing of mortalities and a temporary suspension of the Trap, Transport and Transplant permit program (TTT). TPWD staff and the commission will re-examine TTT over the next weeks and months and will discuss avenues to bring the program back.
The commission put a three-year sunset on the 100 percent ante-mortum testing requirement. Continuing that mandate after three years will be the subject of a future commission.
TPWD initially implemented requisite ante-mortum testing with emergency orders in June as a response to the outbreak.
That particular rule change drew the ire of the multimillion-dollar deer breeding industry. Breeders believe live testing every deer is an undue burden on the community and does significant damage to how they do business.
“Despite countless efforts to come to the table with TPWD commissioners to find an effective solution that encompasses all stakeholder concerns, TDA is disappointed that deer breeders are still forced to comply with excessive live-testing regulations that place unfair requirements on our industry and put our animals at unnecessary risk,” Texas Deer Association president John True said in a statement after the rules were adopted.
Deer breeding organizations believe the added cost of live testing will drive the smaller breeders out of business. That sentiment was shared by several breeders who provided comment at the meeting.
Deer breeder Grant Evridge said he may have to shut down his operation because of the live-testing requirement. He told the commission that he’d recently had 16 of his deer live tested for a nearly $5,800 sum. He said if he was to test all of his 89 adult deer, the cost would be $32,000 based on that bill.
“We go through with these rules … we will be out of business,” Evridge said.
"We've lost 112 breeders since the emergency rules went into effect in June,” True said at Thursday’s meeting.
Some of the other rule changes: The minimum expected post-mortum testing requirement was increased to 5 percent from 3.6. Mortalities will be reported and submitted within seven days, reduced from 14. Both the medial retropharyngeal lymph nodes and obex are to be required for post-mortum testing, instead of either. Escaped deer are considered dead deer for the purpose of testing requirements. Breeders were previously allowed to make up for mortality testing with ante-mortum testing at a 3:1 ratio. That’s been raised to 5:1, acknowledging that 3:1 was insufficient. Nursing facilities can only take fawns from a single facility in a season.
The proposals were supported by numerous hunter, landowner and conservation groups, including the Texas Wildlife Association.
“We’ve heard many times over the past few weeks about the economic concerns from those who will be directly impacted by the new rules. And while those concerns may be valid, they must be balanced by the concerns of the much larger number that stand to be affected by the continued spread of the disease,” TWA president Sarah Biedenharn said.
“With just 850 registered deer breeders and 70,000 captive deer, the deer breeding industry makes up a very small piece of the overall hunting economy in Texas. The decisions made today will impact the health of the state’s 5.4 million wild deer that are cared for and relied on by 1.3 million hunters and over 250,000 landowners. Not to mention the many generations of hunters and landowners who will likely experience the bulk of the consequences from further spread of the disease. CWD threatens the future of hunting for all Texans and will burden thousands of hunting-related businesses, which will consequently impact many rural economies.”
Approximately 260 deer have tested positive in the state; two-thirds are linked to breeding facilities. So far, CWD prevalence is low in Texas. Wildlife officials are working to keep it that way and prevent the type of proliferation that has occurred in states like Wyoming, Colorado and Wisconsin. The Centers for Disease Control and Prevention’s CWD heat map nearly engulfs Wyoming. Colorado Parks and Wildlife has acknowledged that as of February 2020, CWD exists in 33 of the state’s 54 deer herds, 14 of 43 elk herds and two of the nine moose herds. Wisconsin has detected over 8,000 positives.
CWD is insidious. The disease has a protracted latency period that can prevent it from being detected for months or years. It is a neurological disease caused by misfolded proteins called prions that can spread through bodily fluids, environmental contamination and other unknown vectors.
Once it becomes established in an environment, it is believed to be impossible to eradicate. And it has no cure.
"I completely support Texas Parks and Wildlife in their efforts to protect our native deer herd. My least favorite words in the English language are ‘would've,’ ‘could've,’ ‘should've,’” Bernadine Dittmar said while imploring the commission to act on behalf of future generations of Texas hunters and landowners, including her grandchildren.
Evridge concluded: “What about my grandkids? My grandkids want to raise deer, too. Do they not count?”
TEXAS LEGISLATING CHRONIC WASTING DISEASE CWD TSE PRION SPREAD?
listening in on November 4, after presentation, the QA session,
FRIDAY, NOVEMBER 05, 2021
Texas Parks and Wildlife Commission TPWD CWD TSE Prion November 3-4, 2021
i picked up on something that was said, there were several folks complaining that the breeders were getting picked on, and someone said something about trying to 'legislate' there way out of this. folks, this is terrible, i have seen this in other states, and it just spreads cwd even more. hell, it happened right here in Texas in the early days, that's why we are where were at now, you cannot let a bunch of Austin Legislative Socialites regulate CWD, just look what happened in Wisconsin. but i bet this attempted swaying of regulatory power shift from TPWD et al to the Texas Legislature in Austin is happening as we speak. we can't let this happen...
SUNDAY, JANUARY 22, 2017
Texas 85th Legislative Session 2017 Chronic Wasting Disease CWD TSE Prion Cervid Captive Breeder Industry
FRIDAY, JANUARY 27, 2017
TEXAS, Politicians, TAHC, TPWD, and the spread of CWD TSE Prion in Texas
SUNDAY, MAY 14, 2017
85th Legislative Session 2017 AND THE TEXAS TWO STEP Chronic Wasting Disease CWD TSE Prion, and paying to play $$$
Powerful Abbott appointee's lobbying sparks blowback in Legislature
In an ironic twist for Gov. Greg Abbott, who has made ethics reform an urgent political priority, the Texas House is taking aim at what critics call a "pay to play" culture among his appointees.
BY JAY ROOT MAY 12, 2017 12 AM
Houston billionaire Dan Friedkin is chairman of the Texas Parks and Wildlife Commission.
Texas Parks and Wildlife Commission
When Gov. Greg Abbott tapped one of his top campaign donors to become chairman of the Texas Parks and Wildlife Commission, he didn’t get a part-time appointee who would merely draft rules and implement conservation laws passed by the Legislature.
In Dan Friedkin, the governor got a Houston billionaire — with a team of privately funded lobbyists — willing to use his influence to ensure his wildlife interests are taken into account by the Legislature before they pass those laws, interviews and records show.
On the receiving end of that influence, and not in a happy way, is state Rep. Chris Paddie, R-Marshall. Paddie said a lobbyist working for Friedkin’s business empire, which includes a massive South Texas hunting ranch, has been working against his deer breeder management bill, which many large ranchers oppose. The state Parks and Wildlife Department oversees deer breeding regulations in Texas.
“Many times these appointees are well-heeled, very influential people,” Paddie said. “Overall, I feel that it’s inappropriate for an appointee of a board or commission to have personal lobbyists lobbying on issues related to that board or commission.”
Under Texas law, state agencies are barred from lobbying the Legislature. But the powerful people who oversee them aren’t.
If Paddie and dozens of his colleagues get their way, that practice soon will be a Class A misdemeanor.
Last weekend, Paddie attached a ban on appointee lobbying — which would apply to any issues intersecting with their state responsibilities — to an ethics bill that already had powerful friends of the governor in its crosshairs. The provision was adopted unanimously and the bill sailed out of the Texas House on a 91-48 vote Saturday.
The ethics bill, authored by Rep. Lyle Larson, R-San Antonio, would bar big campaign donors from getting appointed by governors in the first place. Anyone who contributed over $2,500 would be barred from serving on state boards and commissions.
Larson pointed to news articles documenting the amount of campaign money appointees have collectively given governors. Last year the San Antonio Express-News calculated that Abbott had received nearly $9 million from people he’s picked for appointed office; before that, a widely cited report from Texans for Public Justice found former Gov. Rick Perry had received $17 million from his own appointees.
Larson said 20 years from now, Texans will be reading the same stories about a future governor unless the Legislature does something about it now.
“We’ve read that article for the last three decades,” Larson said during a brief floor speech. “This is your opportunity to say, 'We need to stop this.' The most egregious ethics violation we’ve got in the state is the pay to play in the governor’s office.”
A prodigious fundraiser, Abbott has put plenty of big donors on prestigious boards and commissions. On the Parks and Wildlife Commission alone, he has installed three mega-donors — pipeline mogul Kelcy Warren, who’s given Abbott more than $800,000 over his statewide political career; Houston businessman S. Reed Morian, who has given $600,000; and Friedkin, who personally donated more than $700,000 — while his Gulf States Toyota PAC gave Abbott another $100,000, according to Ethics Commission records.
Passage of Larson’s HB 3305 represents an ironic twist for Abbott, who for the second session in a row has made ethics reform an urgent political priority — resulting in a bill that's now taking aim at his gubernatorial appointments. Abbott, who has made a habit of ignoring tough questions, hasn't made any public statements about the bill, and his office did not respond to multiple requests for comment.
Friedkin — whose wealth is estimated at $3.4 billion by Forbes — is the owner and CEO of Gulf States Toyota, founded in 1969, which has had the exclusive rights to distribute new Toyotas in Texas and four nearby states. He’d also been a mega-donor to former Gov. Rick Perry, who first appointed Friedkin to the Parks and Wildlife Commission in 2005. Abbott made Friedkin chairman of the commission in 2015.
Requests for comment from Friedkin's office went unanswered.
In addition to his public role as parks and wildlife chairman, a perch that gives him significant influence over deer management issues, Friedkin has private wildlife interests. He owns the sprawling Comanche Ranch in South Texas, according to published news accounts.
The January 2014 edition of Texas Wildlife, published by the Texas Wildlife Association, described Friedkin’s Comanche Ranch as “privately owned and privately hunted” and said it’s “in the business to produce as many trophy bucks as possible, without damaging the native habitat.”
The association, which advocates for private landowners and hunting rights, has locked horns with deer breeding interests at Parks and Wildlife and the Capitol. They compete against each other in the lucrative trophy deer hunting market — and the battle between them perennially spills into the rule-making process at the Parks and Wildlife Commission.
One of their battles centers on how captive deer are tagged so that game wardens and others can distinguish them from native deer. Current law requires a combination of tags and tattoos, and the ranchers and large landowners want to keep it that way. The breeders, meanwhile, favor tagging deer with microchips, which they contend are more accurate and foolproof.
The Wildlife Association said in a Facebook post that removing visible tag or tattoo requirements and allowing microchip tracking “creates real biosecurity risks and blurs ethical lines in the hunting community, as captive deer breeders are allowed to transport and release these animals to be co-mingled with pasture-born deer.” Proponents of the current system say tough rules on breeders are needed to keep out imported deer that may carry Chronic Wasting Disease, which has been found in Texas.
On the other side of the issue is the Texas Deer Association, which represents breeder interests. Executive Director Patrick Tarlton said opposition to his $1.6 billion industry stems less from environmental and health concerns and more from wealthy ranch owners who want to boost profits from trophy-seeking hunters. He notes that Chronic Wasting Disease has been found in both free range and captive deer.
Paddie sided with the breeders by filing House Bill 2855, which would allow breeders to track their deer with microchips instead of relying on physical tags that they say can be torn off.
No one identifying themselves as a Friedkin corporate lobbyist opposed the deer breeding bills during public hearings, according to House and Senate committee records published online.
Behind the scenes, it was a different story.
Paddie said his chief of staff reached out to Laird Doran, one of several lobbyists for Friedkin’s Gulf States Toyota, after hearing that he was trying to convince other legislators to help defeat Paddie's deer microchip bill.
“My chief called him and said, 'Hey, if you’ve got a problem with our bill why aren’t you talking to us?’ ” Paddie said. “He said he represented the Friedkin Group when that happened.”
According to an email from an aide to Sen. Craig Estes, R-Wichita Falls, who is carrying the deer breeding bill in the Senate, Doran also identified himself as a representative of the “Friedkin Group.” That’s the name of the consortium that contains Friedkin's Gulf States Toyota, according to the company’s Linked-In page. He told Estes’ aide that the Friedkin group was opposed to any bill that would “remove requirements for (deer) ear tags,” the senator’s office confirmed.
It’s not clear exactly which Friedkin interests Doran was advancing. Doran is registered at the Texas Ethics Commission with a single entity — Gulf States Toyota — and the agency has no record of a lobbyist working for an entity or individual with the name Friedkin in it, the commission confirmed Wednesday afternoon.
However, Doran checked a variety of non-automotive subject areas in which he is lobbying during this legislative session on behalf of Friedkin’s lucrative distributorship, including “animals,” “parks & wildlife,” “state agencies, boards & commissions,” “environment” and more, his detailed lobby disclosures show.
Doran, director of government relations and senior counsel at the Friedkin Group, did not return phone and email messages left by The Texas Tribune.
Estes said he didn’t have a problem with a governor's appointee engaging in lobbying on issues that affected their private interests, as long as they keep that separate from their state roles.
“I don’t think they should be barred from expressing their views as long as they’re careful to say these are my views, not the views of the agency I’m representing,” Estes said.
But Tarlton, the deer association director, said Friedkin’s use of lobbyists to oppose deer breeders in the Legislature gives the breeders' opponents a huge advantage.
“I think that if the commissioner of Texas Parks and Wildlife is actively lobbying against an industry which his department directly oversees, it absolutely sets up an unfair and closed system of government,” Tarlton said. “The commission is supposed to be the unbiased and equitable oversight for everything wildlife.”
Paddie hopes his amendment to Larsen's ethics bill will even the playing field. He referred to the wealthy Parks and Wildlife chairman (see the 2:29:00 mark in this recorded exchange) when he tacked the appointee-lobbying provision onto Larson’s bill.
Paddie said he’s not singling out anyone. He said it would apply to other powerful gubernatorial appointees in a position to do the same.
“I could have named any number of examples as far as the agencies in particular,” Paddie said. “I want to stop it if anyone serving on any agency is doing this.”
Ryan Murphy contributed to this report.
Disclosure: The Texas Wildlife Association, Texas Parks and Wildlife Department and Gulf States Toyota have been financial supporters of The Texas Tribune. A complete list of Tribune donors and sponsors is available here.
TUESDAY, AUGUST 02, 2016
TEXAS TPWD Sets Public Hearings on Deer Movement Rule Proposals in Areas with CWD Rule Terry S. Singeltary Sr. comment submission
SUNDAY, MAY 22, 2016
TEXAS CWD DEER BREEDERS PLEA TO GOVERNOR ABBOTT TO CIRCUMVENT TPWD SOUND SCIENCE TO LET DISEASE SPREAD
Wednesday, May 04, 2016
TPWD proposes the repeal of §§65.90 -65.94 and new §§65.90 -65.99 Concerning Chronic Wasting Disease - Movement of Deer Singeltary Comment Submission
Terry S. Singeltary Sr. Your opinions and comments have been submitted successfully. Thank you for participating in the TPWD regulatory process.
Wednesday, October 28, 2015
Interim Chronic Wasting Disease Response Rules Comment online through 07:00 a.m. November 5, 2015
Texas 84th Legislative Session Sunday, December 14, 2014
*** TEXAS 84th Legislature commencing this January, deer breeders are expected to advocate for bills that will seek to further deregulate their industry
TUESDAY, DECEMBER 16, 2014
Texas 84th Legislature 2015 H.R. No. 2597 Kuempel Deer Breeding Industry TAHC TPWD CWD TSE PRION
SUNDAY, FEBRUARY 16, 2020
***> Jerking for Dollars, Are Texas Politicians and Legislators Masturbating Deer For Money, and likely spreading CWD TSE Prion?
TEXAS CWD
''CWD has been detected in 261 captive or free ranging cervids in 14 counties, including white-tailed deer, mule deer, red deer and elk. To date, 168 of those of those positives are from captive breeding facilities or associated release sites and 68 are from free-ranging populations.''
Hunters taking advantage of Texas Public Hunting Lands must also have the Annual Public Hunting Permit. It’s also important for public land hunters to consult the Public Hunting Lands Map Booklet to review regulations that may apply to specific areas. The My Texas Hunt Harvest app can be used to complete on-site registration electronically at a public hunting area.
The discovery of new cases of Chronic Wasting Disease (CWD) has prompted TPWD to establish new containment and surveillance zones to mitigate the potential spread of CWD. TPWD recommends hunters review information about testing requirements and carcass movement restrictions in the CWD zones for the 2021-22 season before heading out to the field.
CWD is slow, progressive and fatal neurological disease found in certain cervids, including deer, elk, moose and other members of the deer family. Due to long incubation periods, affected cervids do not show visible signs of illness until years after they are infected.
CWD was first discovered in Texas in 2012 in free-ranging mule deer along a remote area of the Hueco Mountains near the Texas-New Mexico border. Since then, it has been detected in 261 captive or free ranging cervids in 14 counties, including white-tailed deer, mule deer, red deer and elk. To date, 168 of those of those positives are from captive breeding facilities or associated release sites and 68 are from free-ranging populations.
Landowners and hunters play a critical role in managing CWD. The most effective way for them to help slow the spread of CWD is to report sick deer to a TPWD biologist, properly dispose of inedible carcass parts, and to voluntarily test their harvests by taking them to a local check station or contacting a TPWD biologist in their area.
By adhering to CWD regulations and recommendations, hunters, landowners, and communities are helping to ensure that native deer populations remain healthy and plentiful for years to come, allowing for the conservation of the species and preservation of Texas’ hunting heritage and traditions.
TAHC Chapter 40, Chronic Wasting Disease Terry Singeltary Comment Submission
***> 1st and foremost your biggest problem is 'VOLUNTARY'! AS with the BSE 589.2001 FEED REGULATIONS, especially since it is still voluntary with cervid, knowing full well that cwd and scrapie will transmit to pigs by oral route. VOLUNTARY DOES NOT WORK! all animal products should be banned and be made mandatory, and the herd certification program should be mandatory, or you don't move cervid. IF THE CWD HERD CERTIFICATION IS NOT MANDATORY, it will be another colossal tse prion failure from the start.
***> 2nd USA should declare a Declaration of Extraordinary Emergency due to CWD, and all exports of cervid and cervid products must be stopped internationally, and there should be a ban of interstate movement of cervid, until a live cwd test is available.
***> 3rd Captive Farmed cervid ESCAPEES should be made mandatory to report immediately, and strict regulations for those suspect cwd deer that just happen to disappear. IF a cervid escapes and is not found, that farm should be indefinitely shut down, all movement, until aid MIA cervid is found, and if not ever found, that farm shut down permanently.
***> 4th Captive Farmed Cervid, INDEMNITY, NO MORE Federal indemnity program, or what i call, ENTITLEMENT PROGRAM for game farm industry. NO MORE BAIL OUTS FROM TAX PAYERS. if the captive industry can't buy insurance to protect not only themselves, but also their customers, and especially the STATE, from Chronic Wasting Disease CWD TSE Prion or what some call mad deer disease and harm therefrom, IF they can't afford to buy that insurance that will cover all of it, then they DO NOT GET A PERMIT to have a game farm for anything. This CWD TSE Prion can/could/has caused property values to fall from some reports in some places. roll the dice, how much is a state willing to lose?
***> 5th QUARANTINE OF ALL FARMED CAPTIVE, BREEDERS, URINE, ANTLER, VELVET, SPERM, OR ANY FACILITY, AND THEIR PRODUCTS, that has been confirmed to have Chronic Wasting Disease CWD TSE Prion, the QUARANTINE should be for 21 years due to science showing what scrapie can do. 5 years is NOT near long enough. see; Infectious agent of sheep scrapie may persist in the environment for at least 16 to 21 years.
***> 6th America BSE 589.2001 FEED REGULATIONS CWD TSE Prion
***> 7TH TRUCKING TRANSPORTING CERVID CHRONIC WASTING DISEASE TSE PRION VIOLATING THE LACEY ACT
***> 8TH ALL CAPTIVE FARMING CERVID OPERATIONS MUST BE INSURED TO PAY FOR ANY CLEAN UP OF CWD AND QUARANTINE THERE FROM FOR THE STATE, NO MORE ENTITLEMENT PROGRAM FOR CERVID GAME FARMING PAY TO PLAY FOR CWD TSE PRION OFF THE TAX PAYERS BACK.
***> 9TH ANY STATE WITH DOCUMENTED CWD, INTERSTATE, NATIONAL, AND INTERNATIONAL MOVEMENT OF ALL CERVID, AND ALL CERVID PRODUCTS MUST BE HALTED!
***> 10TH BAN THE SALE OF STRAW BRED BUCKS AND ALL CERVID SEMEN AND URINE PRODUCTS
***> 11th ALL CAPTIVE FARMED CERVID AND THEIR PRODUCTS MUST BE CWD TSE PRION TESTED ANNUALLY AND BEFORE SALE FOR CWD TSE PRION
SEE FULL SCIENCE REFERENCES AND REASONINGS
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
“Regrettably, the gravity of this situation continues to mount with these new CWD positive discoveries, as well as with the full understanding of just how many other facilities and release sites across Texas were connected to the CWD positive sites in Uvalde and Hunt Counties,” said Carter Smith, Executive Director of TPWD.
TAHC Chapter 40, Chronic Wasting Disease Terry Singeltary Comment Submission
Texas Parks and Wildlife Commission TPWD CWD TSE Prion November 3-4, 2021
Texas Parks and Wildlife Commission
Schedule for November 3-4, 2021
ACTION – Chronic Wasting Disease - Disease Detection and Response – Recommended Adoption of Proposed Changes – Mitch Lockwood
Comment on Proposed New Rule for Proof of Sex for Deer
Comment on Proposed Amendments to Rules Governing Chronic Wasting Disease Management
Comment on Proposed Amendment to Deer Management Permit Rules
''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).''
Commission Meeting Agenda Item No. 5
Presenter: Mitch Lockwood
Action
Chronic Wasting Disease - Disease Detection and Response
Recommended Adoption of Proposed Changes
November 4, 2021
I. Executive Summary: Staff seeks adoption of proposed amendments to the comprehensive Chronic Wasting Disease (CWD) rules.
II. Discussion: CWD, a fatal neurodegenerative disorder that affects cervid species such as white-tailed deer, mule deer, elk, red deer, sika, and others (which will be referred to as susceptible species), has been detected in seven permitted deer breeding facilities since March 23, 2021. Texas Parks and Wildlife Department (TPWD), along with Texas Animal Health Commission (TAHC), has been engaged in an ongoing battle with CWD in Texas since 2002. 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). Emergency rules filed on June 22, 2021 were intended to address significant concerns for CWD being transferred from deer breeding facilities where the disease may exist undetected, however those rules expire after 180 days, and amendments to the comprehensive rules are necessary to mitigate risks not addressed in the current rules.
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. Vigilance is crucial to minimizing the severity of biological and economic impacts that could result from the current situation. Therefore, TPWD believes that amendments to the comprehensive CWD rules including enhanced CWD-testing requirements for deer breeding facilities as well as antemortem testing of breeder deer prior to any release represent a wise and responsible course of action.
At the Texas Parks and Wildlife Commission (Commission) special meeting on September 15, 2021, staff was authorized to publish the proposed rules in the Texas Register for public comment. The proposed rules appeared in the October 1, 2021 issue of the Texas Register (46 TexReg 6506, 6507, 6528). A summary of public comment on the proposed rules will be presented at the time of the hearing.
III. Recommendation: The staff recommends that the Commission adopt the proposed motion:
“The Texas Parks and Wildlife Commission adopts new 31 TAC, §65.4, concerning Proof of Sex for Deer, the repeal of §65.99, amendments to §§65.80-65.83, 65.88 and 65.90-65.98, and new §65.99 and §65.100, concerning Disease Detection and Response, and an amendment to §65.133, concerning Deer Management Permit (DMP), with changes as necessary to the proposed text as published in the October 1, 2021 issue of the Texas Register (46 TexReg 6506, 6507, 6528).”
Attachments – 3
Exhibit A – Proposed Proof of Sex Rule for Deer
Exhibit B – Proposed Disease Detection and Response Rules
Exhibit C – Proposed Deer Management Permit Rule
Commission Agenda Item No. 5
Exhibit A
CHRONIC WASTING DISEASE MANAGEMENT
PROOF OF SEX REQUIREMENTS FOR DEER
PROPOSAL PREAMBLE
1. Introduction.
The Texas Parks and Wildlife Department proposes new §65.4, concerning Proof of Sex for Deer. The proposed new section would replace the provisions of current §65.10(e) with respect to deer for the upcoming hunting season. Section 65.10 cannot be amended at the present time because of pending rule action relating to the implementation of rules regarding digital hunting and fishing licenses. The department will comport the provisions of the two sections at a future date.
The proposed new section is in response to the threat to free-ranging deer populations posed by chronic wasting disease (CWD). CWD is a fatal neurodegenerative disorder that affects some cervid species, including white-tailed deer, mule deer, elk, red deer, sika, and their hybrids (referred to collectively as susceptible species). It is classified as a TSE (transmissible spongiform encephalopathy), a family of diseases that includes scrapie (found in sheep), bovine spongiform encephalopathy (BSE, found in cattle and commonly known as "Mad Cow Disease"), and variant Creutzfeldt-Jakob Disease (vCJD) in humans. CWD can be transmitted both directly (through animal-to-animal contact) and indirectly (through environmental contamination). CWD has been detected in multiple locations in Texas, primarily in deer breeding facilities but also in free-ranging populations in several counties. The department, along with the Texas Animal Health Commission, has been engaged in a long-term battle to detect and contain CWD. If CWD is not contained and controlled, the implications of the disease for Texas and its multi-billion-dollar ranching, hunting, wildlife management, and real estate economies could be significant.
The movement, and ultimately, the improper disposal of carcasses and carcass parts, particularly skulls, brains, and spinal cords, increases the risk of spreading CWD. Under current rule, proof-of-sex for deer is the head of the deer, which must accompany the carcass until a final destination is reached. The proposed new rule would provide an alternative to the current rules regarding proof of sex for female deer by allowing certain gender-related anatomical parts to accompany the carcass in lieu of the head. This would provide hunters an option to leave the head of a female deer at the site of harvest to reduce risk for the potential spread of CWD from that site.
2. Fiscal Note.
Mitch Lockwood, Big Game Program Director, has determined that for each of the first five years that the rule as proposed is in effect, there will be no fiscal implications to state or local governments as a result of administering or enforcing the rule.
3. Public Benefit/Cost Note.
Mr. Lockwood also has determined that for each of the first five years that the rule as proposed is in effect:
(A) The public benefit anticipated as a result of enforcing or administering the proposed rule will be the protection of indigenous wildlife resources for public use and enjoyment.
(B) Under the provisions of Government Code, Chapter 2006, a state agency must prepare an economic impact statement and a regulatory flexibility analysis for a rule that may have an adverse economic effect on small businesses, micro-businesses, or rural communities. As required by Government Code, §2006.002(g), the Office of the Attorney General has prepared guidelines to assist state agencies in determining a proposed rule’s potential adverse economic impacts to small businesses, micro-businesses, or rural communities. Those guidelines state that an agency need only consider a proposed rule’s “direct adverse economic impacts” to small businesses and micro-businesses to determine if any further analysis is required. For that purpose, the department considers “direct economic impact“ to mean a requirement that would directly impose recordkeeping or reporting requirements; impose taxes or fees; result in lost sales or profits; adversely affect market competition; or require the purchase or modification of equipment or services.
The department has determined that the proposed rule will not result in direct adverse impacts on small businesses, micro-businesses, or rural communities because the proposed rule regulates various aspects of recreational license privileges that allow individual persons to pursue and harvest public wildlife resources in this state and therefore does not directly affect small businesses, micro-businesses, or rural communities. Therefore, neither the economic impact statement nor the regulatory flexibility analysis described in Government Code, Chapter 2006, is required.
(C) The department has not drafted a local employment impact statement under the Administrative Procedures Act, §2001.022, as the agency has determined that the rule as proposed will not impact local economies.
(D) The department has determined that Government Code, §2001.0225 (Regulatory Analysis of Major Environmental Rules), does not apply to the proposed rule.
(E) The department has determined that there will not be a taking of private real property, as defined by Government Code, Chapter 2007, as a result of the proposed rule.
(F) In compliance with the requirements of Government Code, §2001.0221, the department has prepared the following Government Growth Impact Statement (GGIS). The rule as proposed, if adopted, will:
(1) neither create nor eliminate a government program;
(2) not result in an increase or decrease in the number of full-time equivalent employee needs;
(3) not result in a need for additional General Revenue funding;
(4) not affect the amount of any fee;
(5) not create a new regulation (but will augment an existing regulations);
(6) not repeal, expand, or limit a regulation;
(7) neither increase nor decrease the number of individuals subject to regulation; and
(8) not positively or adversely affect the state’s economy.
4. Request for Public Comment.
Comments on the proposal may be submitted to Mitch Lockwood at (830) 792-9677, e-mail: mitch.lockwood@tpwd.texas.gov. Comments also may be submitted via the department’s website at http://www.tpwd.texas.gov/business/feedback/public_comment/.
5. Statutory Authority.
The new section is proposed under the authority of Parks and Wildlife Code, Chapter 61, which requires the commission to regulate the periods of time when it is lawful to hunt, take, or possess game animals, game birds, or aquatic animal life in this state; the means, methods, and places in which it is lawful to hunt, take, or possess game animals, game birds, or aquatic animal life in this state; the species, quantity, age or size, and, to the extent possible, the sex of the game animals, game birds, or aquatic animal life authorized to be hunted, taken, or possessed; and the region, county, area, body of water, or portion of a county where game animals, game birds, or aquatic animal life may be hunted, taken, or possessed.
The proposed new rule affects Parks and Wildlife Code, Chapter 61.
6. Rule Text.
§65.4. Proof of Sex for Deer.
(a) Until repealed, the provisions of this section replace the provisions of §65.10(e) of this title (relating to Possession of Wildlife Resources) that apply to deer.
(b) All other provisions of §65.10 continue in force and effect.
(c) Proof of sex for deer must remain with the carcass until tagging requirements cease.
(d) Proof of sex for deer consists of:
(1) buck: the head, with antlers still attached; and
(2) female antlerless (“doe”):
(A) the head; or
(B) the mammary organ (udder) or vulva, and tail; and
(3) male antlerless (“nubbin,” “button,” “shed-antlered” buck): the head.
This agency hereby certifies that the proposal has been reviewed by legal counsel and found to be within the agency’s authority to adopt.
Issued in Austin, Texas, on
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
For Immediate Release
November 5, 2021
TAHC Requirements for Harvesting
Exotic CWD Susceptible Species in Texas
AUSTIN, TX – The Texas Animal Health Commission (TAHC) reminds Texas landowners of statewide exotic chronic wasting disease (CWD) susceptible species requirements for the 2021-22 hunting season.
Exotic susceptible species include North American elk or wapiti, black tailed deer, red deer, reindeer, sika deer, moose and/or any associated subspecies and hybrids. Axis deer are not classified as a susceptible species.
“The TAHC and Texas Parks and Wildlife Department (TPWD) have worked diligently to develop and adopt rules to protect CWD susceptible species in Texas,” said Dr. Andy Schwartz, TAHC Executive Director. “The new CWD rules that went into effect October 14, 2021 are important steps to enhance surveillance and movement requirements to prevent the spread of CWD.”
Hunters Harvesting Exotic CWD Susceptible Species
In addition to the TAHC’s statewide surveillance and movement requirements for exotic CWD susceptible species, hunters should be aware of Texas’ CWD Containment and Surveillance Zones.
All exotic CWD susceptible species, 16 months of age or older, that are hunter harvested in a zone shall be tested for CWD. In addition, no part of a CWD susceptible species carcass may be removed from the property unless additional carcass requirements are met. Furthermore, no carcass may be moved from a zone unless accompanied by a TPWD-issued-check-station receipt, which is required during the operation of the mandatory TPWD check stations. As an alternative to the TPWD check stations, you may contact a TAHC Certified CWD Post Mortem Sample Collector.
Properties where Exotic CWD Susceptible Species are Hunter Harvested
Every calendar year, landowners must have eligible mortalities CWD tested until such time that three animals are tested. An eligible mortality is a death from any cause of an exotic CWD susceptible species that is 16 months of age or older. This includes hunter harvested, herd culling, and natural mortalities on the premises, and animals moved directly to slaughter. The owner of the premises shall ensure that the CWD samples are properly collected and submitted for testing. The owner must also report to the TAHC within 30 days of receiving the test results by writing to Texas Animal Health Commission, CWD Susceptible Species Reporting, P.O. Box 12966, Austin, Texas 78711-2966; by fax to (512) 719-0729; or by email to CWD_reports@tahc.texas.gov.
The owners of high, low, or no fenced properties where exotic CWD susceptible species, at least 16 months of age, are harvested must submit a mortality record to the TAHC each calendar year. Mortality record forms are due to the TAHC on or before April 1 of each year, and shall be retained for one year from the date of submission.
Owners Moving or Transporting Live Exotic CWD Susceptible Species
To move live exotic CWD susceptible species to or from a premises, the owner must obtain a Premises Identification Number (PIN) or Location Identification Number (LID) from the TAHC or Media Contact: TAHC Communications
512.719.0750
United States Department of Agriculture (USDA). All live exotic CWD susceptible species moved or transported within the state must have an official identification device (ID). For more information on PINs, LIDs, and official ID, contact the TAHC Animal Disease Traceability (ADT) Department at 512- 719-0733..
An owner of a premises where exotic CWD susceptible species are located within a high fence shall keep herd records that include an annual inventory and mortality records for all exotic CWD susceptible species. The inventory shall be reconciled and submitted to the TAHC on or before April 1 of each year. Annual inventory records shall be retained for one year following submission. A complete movement record for all live exotic CWD susceptible species moved onto or off of a premises shall be submitted to the TAHC. The person moving the exotic CWD susceptible species must have documentation with the exotic CWD susceptible species being moved. This record shall be submitted within 48 hours of the movement and be directed to the TAHC by writing the Texas Animal Health Commission, CWD Susceptible Species Reporting, P.O. Box 12966, Austin, Texas 78711-2966; by fax to (512)-719-0729; or by email to CWD_reports@tahc.texas.gov.
Dealer Record Keeping Requirements for Exotic CWD Susceptible Species
A dealer shall maintain records for all exotic CWD susceptible species transported within the state or where there is a transfer of ownership, and provide these to a TAHC representative upon request. Records required to be kept under the provisions of this section shall be maintained for not less than five years.
For more information on CWD, CWD zones, and requirements:
• TAHC Exotic CWD Susceptible Species Page: https://www.tahc.texas.gov/animal_health/elkdeer/#cwdexotic
• TPWD CWD Page: https://tpwd.texas.gov/huntwild/wild/diseases/cwd/#navTop
This is an unofficial summary of TAHC Exotic CWD Susceptible Species requirements. Visit Title 4, Part 2 of the Texas Administrative Code for official requirements:
###
TAHC Did you know that axis and fallow deer are not classified as exotic CWD susceptible species?
Fallow deer and Axis deer are susceptible to chronic wasting disease cwd tse prion, and to make believe that they are not, is not scientific, and you are just playing prion poker again, and that is a lose, lose, game...terry
FREQUENTLY ASKED QUESTIONS Exotic CWD Susceptible Species WWW.TAHC.TEXAS.GOV 02.20 Updated as of December 2020
Find out more about exotic CWD susceptible species and requirements here: https://bit.ly/3kGi82O.
FREQUENTLY ASKED QUESTIONS Exotic CWD Susceptible Species
Updated as of December 2020
1. What are exotic chronic wasting disease (CWD) susceptible species?
Exotic CWD susceptible species are cervid species that are non-native to Texas and are determined to be susceptible to CWD. Exotic CWD susceptible species include North American elk or wapiti, black tailed deer, red deer, reindeer, Sika deer, moose, and any associated subspecies and hybrids. Axis and fallow deer are not classified as an exotic CWD susceptible species.
2. When were the TAHC surveillance and movement requirements for exotic CWD susceptible species adopted?
On May 30, 2017, the Texas Animal Health Commission (TAHC) adopted amendments to §40.5 of the Texas Administrative Code to add surveillance, movement reporting, identification, and mortality record-keeping requirements for exotic CWD susceptible species.
3. Where can I find the TAHC rules?
The TAHC rules can be found at
OWNERS OF CAPTIVE, EXOTIC CWD SUSCEPTIBLE SPECIES
The following questions and answers only apply to owners of captive exotic CWD susceptible species located within a high fence.
MOVEMENT REQUIREMENTS
Snip...
TAHC-Axis and fallow deer are not classified as an exotic CWD susceptible species.
please see;
''In Texas, coordinated CWD testing for axis deer might be important within previously established CWD surveillance and containment zones, followed by surveillance in areas where CWD may be a concern but not yet detected.''
2021, VOL. 15, NO. 1, 44–52 https://doi.org/10.1080/19336896.2021.1910177
SHORT COMMUNICATIONS
Characterization of the prion protein gene in axis deer (Axis axis) and implications for susceptibility to chronic wasting disease
Matthew J. Buchholz a, Emily A. Wrightb, Blake A. Grishama, Robert D. Bradleyb,c, Thomas L. Arsuffid, and Warren C. Conwaya
aDepartment of Natural Resources Management, Texas Tech University,Lubbock, TX USA; bDepartment of Biological Sciences, Texas Tech University, Lubbock, TX USA; cNatural Science Research Laboratory, Museum of Texas Tech University, Lubbock, TX USA; dLlano River Field Station, Texas Tech University, Junction, TX USA
ABSTRACT
Axis deer (Axis axis) occur both in captivity and free-ranging populations in portions of North America, but to-date, no data exist pertaining to the species’ susceptibility to CWD. We sequenced the prion protein gene (PRNP) from axis deer. We then compared axis deer PrPC sequences and amino acid polymorphisms to those of CWD susceptible species. A single PRNP allele with no evidence of intraspecies variation was identified in axis deer that indicates axis deer PRNP is most similar to North American elk (Cervus canadensis) PRNP. Therefore, axis deer may be susceptible to CWD. We recommend proactively increasing CWD surveillance for axis deer, particularly where CWD has been detected and axis deer are sympatric with native North American CWD susceptible species.
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Discussion
The entire PRNP exon 3 was sequenced from free- ranging axis deer in Texas and Hawaii. Out of the other species with available PRNP sequences on GenBank, axis deer were most similar to elk in PrPC amino acid sequence. The complete lack of PRNP sequence diversity among all axis deer individuals sequenced in this study from Texas and Hawaii was unexpected given known PRNP diversity in other spe- cies closely related to axis deer (e.g., 6/771 nucleotide sites are variable in elk, 11/771 in red deer, and 4/771 in sika deer) [1] and the number of individuals sequenced.
However, the highly conserved nature of PRNP within and among taxa may contribute to this finding [1,26]. Furthermore, a previous assessment of PRNP found PRNP to be monomorphic in roe deer (Capreolus capreolus, n = 297) and fallow deer (n = 66) [19].
Axis deer displayed none of the amino acid substitu- tions known to result in reduced susceptibility to CWD between individuals with the substitution compared to those without of other cervid species, but did show two amino acid substitutions. The first amino acid substitu- tion (Q226E) is consistent with the majority of known sequences from the subfamily Cervinae which may confer decreased susceptibility to CWD in elk and other species in Cervinae compared to species in the subfamily Capreolinae [1,27]. The second amino acid substitution (F249V) previously has not been identified in any other Cervidae species. Given the introduced nature of axis deer populations in Texas and Hawaii, it is possible that other unidentified nucleotide substi- tutions and amino acid polymorphisms exist in PrPC in axis deer in their native range that are not represented in free-ranging populations in Texas and Hawaii as an artefact of a founder effect of limited founding indivi- duals of these populations. However, the lack of any PRNP sequence diversity within axis deer in Texas and Hawaii, and common amino acid sequence of PrPC to species that are susceptible to CWD (e.g., elk) suggests axis deer in Texas and Hawaii may be susceptible to CWD.
The identification of a novel amino acid substitu- tion at residue 249 in axis deer poses the question of whether this substitution has an effect on the suscept- ibility of PrPC to misfolding into PrPCWD. However, the mature protein (i.e., the portion of PrPC that misfolds after contact with PrPCWD) that results after the terminal signals are removed during post- translational editing is from amino acid residues 23–231 [28]. Residue 249 is located in the C-terminal signal and therefore is outside of the mature protein (Figure 4), and is unlikely to have an effect on the conformation of mature PrPC or PrPCWD. Similar findings have been documented with amino acid sub- stitutions outside of the mature protein in other cervid species [29].
Axis deer have the amino acid substitution Q226E that is characteristic of elk and other members of Cervinae from white-tailed deer and other members of Capreolinae [1]. Furthermore, after the amino acid substitution at residue 249 in axis deer is removed during post-translational editing of PrPC, axis deer have the same amino acid sequence as the wild type genotype of elk (M132; ~63% of elk; Figure 4), which also is the elk genotype that is most susceptible to CWD [1,10,28]. There was a lack of continued support for differentiation of PRNP between known cervid sequences, including the sequence obtained for axis deer from this study. The lack of significant differentia- tion of PRNP within Cervidae supports that many, if not all, cervids potentially are susceptible to CWD, including axis deer, because their ensuing PrPC amino acid sequences likely do not have sufficient diversity to prevent misfolding [30], making them susceptible to CWD infection.
Definitive evidence such as a positive ELISA or IHC test or a protein misfolding cyclic amplification (PMCA) study of axis deer PrPC is needed to conclu- sively demonstrate axis deer are capable of contracting CWD. However, this research in combination with other work indicating a wider range of susceptible species than previously known [13,19], suggests axis deer in Texas and Hawaii may be susceptible to CWD, and should be managed as an at-risk species for CWD through the implementation of more formalized CWD surveillance. The proactive establishment of a CWD testing programme in axis deer wherever CWD has been detected in other species may be justified. Areas where axis deer coexist with native North American, CWD susceptible species, namely white-tailed deer, may also be justified. In Texas, coordinated CWD test- ing for axis deer might be important within previously established CWD surveillance and containment zones, followed by surveillance in areas where CWD may be a concern but not yet detected. Due to geographic isolation from areas where CWD occurs, axis deer populations in Hawaii are likely not high risk for CWD occurrence. However, awareness of the possibility and care should be taken to ensure CWD-infected material/animals does not arrive on the islands.
''In Texas, coordinated CWD test- ing for axis deer might be important within previously established CWD surveillance and containment zones, followed by surveillance in areas where CWD may be a concern but not yet detected.''
Title: Experimental Transmission of Chronic Wasting Disease (CWD) from Elk (Cervus elaphus nelsoni) and White-tailed Deer (Odocoileus virginianus) to Fallow Deer (Dama dama) by Intracerebral Route: Final Report
Author item Hamir, Amirali item Greenlee, Justin item Nicholson, Eric item Kunkle, Robert item Richt, Juergen item Miller, Janice
item HALL, S - Animal And Plant Health Inspection Service (APHIS) Submitted to: Canadian Journal of Veterinary Research Publication Type: Peer Reviewed Journal Publication Acceptance Date: 5/10/2010
Publication Date: 4/1/2011
Citation: Hamir, A.N., Greenlee, J.J., Nicholson, E.M., Kunkle, R.A., Richt, J.A., Miller, J.M., Hall, M. 2011.
Experimental transmission of chronic wasting disease (CWD) from elk and white-tailed deer to fallow deer by intracerebral route: final report.
Canadian Journal of Veterinary Research. 75(2):152-156.
Interpretive Summary: In this communication we report final observations on experimental transmission of chronic wasting disease (CWD) from elk and white-tailed deer to fallow deer. The study was terminated 5 years after it was initiated. Thirteen fawns were inoculated intracerebrally with CWD-infected brain material from white-tailed deer (n = 7) or elk (n = 6) and 3 other fawns were kept as uninoculated controls. This study demonstrates that brain-inoculated fallow deer do amplify CWD prions from white tailed-deer and elk and that there may be some differences in these two inocula.
Technical Abstract: In this communication we report final observations on experimental transmission of chronic wasting disease (CWD) from elk (Cervus elaphus nelsoni) and white tailed deer (Odocoileus virginianus) to fallow deer (Dama dama). The study was terminated 5 years after it was initiated. Thirteen fawns were inoculated intracerebrally with CWD infected brain material from white tailed deer (n = 7) or elk (n = 6) and 3 other fawns were kept as uninoculated controls. Three CWD inoculated deer were euthanized at 7.6 months post inoculation (MPI). None revealed presence of abnormal prion protein (PrP**d) in their tissues. At 24 and 26 MPI one sick deer died and one non clinical deer was euthanized, respectively. Both animals had a small focal accumulation of PrP**d in their midbrains. Between 29 and 37 MPI, three other deer became sick and were euthanized. All had shown gradual decrease in appetite and some loss of body weight. The five remaining deer became sick and were euthanized between 51 and 60 MPI. Microscopic lesions of spongiform encephalopathy (SE) were observed in only five animals that were euthanized after 51 MPI. However, PrP**d was detected in tissues of the central nervous system by immunohistochemistry, Western blot and by commercial rapid test in all animals that survived beyond 24 MPI. This study demonstrates that intracerebrally inoculated fallow deer do amplify CWD prions from white tailed deer and elk and that there may be some differences in these two inocula.
Title: Experimental chronic wasting disease (CWD) in fallow deer
Author item Hamir, Amirali item Kunkle, Robert item Nicholson, Eric item MILLER, JANICE item HALL, S item Schonenbrucher, Holger item Richt, Juergen
Submitted to: Meeting Abstract Publication Type: Abstract Only Publication Acceptance Date: 6/21/2007 Publication Date: 9/26/2007
Citation: Hamir, A.N., Kunkle, R.A., Nicholson, E.M., Miller, J.M., Hall, S.M., Schonenbrucher, H.H., Richt, J.A. 2007. Preliminary observations on the experimental transmission of chronic wasting disease (CWD) from elk and white-tailed deet to fallow deer [abstract].
Prion 2007. Paper No. PO2.43.
Interpretive Summary:
Technical Abstract: To determine the transmissibility of chronic wasting disease (CWD) to fallow deer (Cervus dama) and to provide information about clinical course, lesions and suitability of currently used diagnostic procedures for detection of CWD in this species, 13 fawns were inoculated intracerebrally with CWD brain suspension from elk (n = 6) or white-tailed deer (n = 7). Three other fawns were kept as uninfected controls. This communication documents preliminary observations from a currently in-progress experiment. Three CWD-inoculated deer were euthanized at 7.6 months post inoculation (MPI). None revealed presence of abnormal prion protein (PrP**d) in their tissues. At 24 and 26 MPI one sick deer died and one non-clinical deer was euthanized, respectively. Both animals had a small focal accumulation of PrP**d in their midbrains. Between 29 and 37 MPI, three other deer became sick and were euthanized. All had shown gradual decrease in appetite and some loss of body weight. Microscopic lesions of spongiform encephalopathy were not observed but PrP**d was detected in tissues of the central nervous system by immunohistochemistry, the OIE recommended enrichment Western blot and by two commercial rapid tests. This study demonstrates that intracerebrally inoculated fallow deer amplified CWD PrP**d from white tailed-deer and elk in absence of SE lesions. Similar observations have also been shown to occur in cattle inoculated with the scrapie and CWD agents; however, PrP**d amplification in fallow deer was minimal in comparison to scrapie- and CWD-affected cattle. Four years after the CWD inoculation, the remaining five inoculated and two control deer are alive and apparently healthy. Although these preliminary findings demonstrate that it is possible to transmit CWD to fallow deer by intracerebral inoculation, past experience with TSE cross-species transmission studies indicate a low probability for oral transmission of CWD to fallow deer in the species' normal life span.
Title: Preliminary observations on the experimental transmission of chronic wasting disease (CWD) from elk and white-tailed deer to fallow deer
Author item Hamir, Amirali item Kunkle, Robert item Nicholson, Eric item MILLER, JANICE item HALL, S item Schonenbrucher, Holger item Brunelle, Brian item Richt, Juergen
Submitted to: Journal of Comparative Pathology Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 12/5/2007
Publication Date: 2/1/2008
Citation: Hamir, A.N., Kunkle, R.A., Nicholson, E.M., Miller, J.M., Hall, S.M., Schonenbrucher, H., Brunelle, B.W., Richt, J.A. 2008.
Preliminary observations on the experimental transmission of chronic wasting disease (CWD) from elk and white-tailed deer to fallow deer.
Journal of Comparative Pathology. 138(2-3):121-130.
Interpretive Summary: To determine the transmissibility of chronic wasting disease (CWD) to fallow deer 13 fawns were inoculated into the brain with CWD suspension from elk or white-tailed deer with CWD. Between 7.6 and 37 months after inoculation, 8 deer were euthanized and were examined by various laboratory tests. Five deer (all euthanized after 7.6 months) were positive for CWD. Four years after the CWD inoculation, the remaining five inoculated deer are alive and apparently healthy. These preliminary findings demonstrate that it is possible to transmit CWD to fallow deer by inoculation into the brain. However, it is not likely that the oral transmission of CWD to fallow deer will result in clinical CWD during the species' normal life span.
Technical Abstract: To determine the transmissibility of chronic wasting disease (CWD) to fallow deer (Dama dama) and to provide information about clinical course, lesions and suitability of currently used diagnostic procedures for detection of CWD in this species, 13 fawns were inoculated intracerebrally with CWD brain suspension from elk (n = 6) or white-tailed deer (n = 7). Three other fawns were kept as uninfected controls. This communication documents 4 years into the experiment. Three CWD-inoculated deer were euthanized at 7.6 months post inoculation (MPI). None revealed presence of abnormal prion protein (PrP**d) in their tissues. At 24 and 26 MPI one sick deer died and one non-clinical deer was euthanized, respectively. Both animals had a small focal accumulation of PrP**d in their midbrains. Between 29 and 37 MPI, three other deer became sick and were euthanized. All had shown gradual decrease in appetite and some loss of body weight. Microscopic lesions of spongiform encephalopathy were not observed but PrP**d was detected in tissues of the central nervous system by immunohistochemistry, Western blot and by two commercial rapid tests. This study demonstrates that intracerebrally inoculated fallow deer amplified CWD PrP**d from white tailed-deer and elk in absence of SE lesions. Similar observations have also been shown to occur in cattle inoculated with the scrapie and CWD agents; however, PrP**d amplification in fallow deer was minimal in comparison to scrapie- and CWD-affected cattle. Four years after the CWD inoculation, the remaining five inoculated and two control deer are alive and apparently healthy. Although these preliminary findings demonstrate that it is possible to transmit CWD to fallow deer by intracerebral inoculation, past experience with TSE cross-species transmission studies indicate a low probability for CWD to develop following oral transmission to fallow deer in the species’ normal life span.
3.2.1. North American isolates
3.2.1.1. Natural hosts
Naturally infected species in North America include all the indigenous wild cervid species: whitetailed deer, mule deer, moose and elk/wapiti. Natural CWD infection has been also detected in captive red deer in the United States (Schwabenlander et al., 2013) and Canada (Walther et al., 2019) and in a farmed reindeer in Illinois.6 Other cervid species are susceptible to CWD following experimental challenge. These include muntjac and fallow deer. Muntjac deer were susceptible to oral challenge with a NA CWD source and have been proposed as a suitable experimental species for modelling natural transmission routes of CWD (Nalls et al., 2013). Finally, fallow deer were susceptible to IC inoculation with CWD from white-tailed deer and mule deer (Hamir et al., 2011).
BSE TSE Prion in zoo animals, exotic ruminants, domestic cats, and CPD Camel Prion Disease, a review 2020
FRIDAY, OCTOBER 15, 2021
TAHC Did you know that axis and fallow deer are not classified as exotic CWD susceptible species?
Fallow deer and Axis deer are susceptible to chronic wasting disease cwd tse prion, and to make believe that they are not, is not scientific, and you are just playing prion poker again, and that is a lose, lose, game...terry
THURSDAY, DECEMBER 19, 2019
TSE surveillance statistics exotic species and domestic cats Update December 2019
FRIDAY, OCTOBER 18, 2019
TAHC Exotic CWD Susceptible Species Rules, Regulations, TSE PRION, WHEAT, GRAINS, HAY, STRAY, GLOBAL CONCERNS GROW, UPDATE, October 17, 2019
WEDNESDAY, MAY 31, 2017
Texas New Exotic CWD Susceptible Species Rules Now in Effect
***> TEXAS HISTORY OF CWD <***
Singeltary telling TAHC, that CWD was waltzing into Texas from WSMR around Trans Pecos region, starting around 2001, 2002, and every year, there after, until New Mexico finally shamed TAHC et al to test where i had been telling them to test for a decade. 2012 cwd was detected first right there where i had been trying to tell TAHC for 10 years.
***> Singeltary on Texas Chronic Wasting Disease CWD TSE Prion History <***
Scrapie Field Trial Experiments Mission, Texas, The Moore Air Force Base Scrapie Experiment 1964
How Did CWD Get Way Down In Medina County, Texas?
Confucius ponders...
Could the Scrapie experiments back around 1964 at Moore Air Force near Mission, Texas, could this area have been ground zero for CWD TSE Prion (besides the CWD cases that have waltzed across the Texas, New Mexico border near WSMR Trans Pecos region since around 2001)?
Epidemiology of Scrapie in the United States 1977
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Scrapie Field Trial Experiments Mission, Texas A Scrapie Field Trial was developed at Mission, Texas, to provide additional information for the eradication program on the epidemiology of natural scrapie. The Mission Field Trial Station is located on 450 acres of pastureland, part of the former Moore Air Force Base, near Mission, Texas.
It was designed to bring previously exposed, and later also unexposed, sheep or goats to the Station and maintain and breed them under close observation for extended periods to determine which animals would develop scrapie and define more closely the natural spread and other epidemiological aspects of the disease.
The 547 previously exposed sheep brought to the Mission Station beginning in 1964 were of the Cheviot, Hampshire, Montadale, or Suffolk breeds.
They were purchased as field outbreaks occurred, and represented 21 bloodlines in which scrapie had been diagnosed.
Upon arrival at the Station, the sheep were maintained on pasture, with supplemental feeding as necessary.
The station was divided into 2 areas:
(1) a series of pastures and-pens occupied by male animals only, and
(2) a series of pastures and pens occupied by females and young progeny of both sexes.
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see full text ;
TEXAS CWD TSE Prion Urgent Letter to Honorable Arch H. Aplin, III from Officials and Land Owners
''the high rate of “lost” deer, and other inadequacies and loopholes in the current rules have put our state’s susceptible cervid herds at significant risk''
June 14, 2021
The Honorable Arch H. Aplin, III
Chairman, Texas Parks and Wildlife Commission
4200 Smith School Road
Austin, Texas 78744
Dear Chairman Aplin,
In light of the recent discovery of CWD in captive deer herds, the undersigned encourage the Commission to take swift and decisive action to protect our captive and wild deer herds, even up to an immediate partial or complete shut-down of deer movement. It is imperative that the response be focused not only on uncovering the sources of the infections, but also in promptly conducting all necessary trace-outs to determine the extent of disease spread.
We appreciate and value the efforts of the Commission and the Department staff to rapidly and effectively deal with this CWD outbreak, but as you are aware, and as staff at the Texas Parks and Wildlife Department (Department) have stated, the modeling used in establishing the current testing requirements has proven insufficient to detect CWD at any reasonable probability and degree of confidence. It is likely that CWD was present in the Uvalde County index facility for a year or more prior to detection, and over a hundred deer were transported to other breeders and release sites in the interim. Additionally, the combined effects of insufficient reporting, testing, and other non-compliance issues with current rules, the high rate of “lost” deer, and other inadequacies and loopholes in the current rules have put our state’s susceptible cervid herds at significant risk.
By the rights and privileges conveyed in the permitting process, deer breeders have accepted and taken calculated risks, for which they are ultimately responsible. While the Department has operated in good faith, it is also the Department’s responsibility to take any and all necessary actions required by their mission statement. The time has come for deer breeders and the Department to accept the necessity that additional steps must be taken to protect this incredibly valuable resource for the public good.
The undersigned strongly urge that the Commission promote enforcement of existing rules and regulations, including revocation, suspension, or non-renewal of non-compliant deer breeders, pursuant to Sunset recommendations. It is also imperative that the Commission promptly engage all appropriate stakeholders (CWD Taskforce, White-tailed Deer Advisory Committee, and Deer Breeder User Group) to review and bolster existing rules that have clearly proven insufficient to identify and contain this disease. In addition, we urge the Department to work closely with Texas Animal Health Commission (TAHC) and other regulatory agencies in expediting the trace-out process, strengthening the oversight of carcass disposal and transport, as well as strengthening the rules and testing related to exotics as a highest priority.
In closing, we express our strong support for tightening any loopholes that exist in current rules associated with CWD detection and containment. We also ask that the Department revisit all assessments made for probability of detection and correct deficits that might currently exist. It is imperative that our response to CWD in Texas move from a reactive to a proactive posture that more effectively protects this precious resource.
Again, we whole-heartedly support and value the Commission and the Department staff as you rapidly and effectively deal with this CWD outbreak, and we stand ready to assist and support you in any manner necessary.
Respectfully,
Terry Anderson – Nacogdoches County Landowner
Ernest Angelo Jr. - Former TPWD Commissioner
John Barrett – Mason County Landowner
Giovana L. Benitez, South Texans’ Property Rights Association Director, Hidalgo
County Landowner
George Bristol – Texas Foundation for Conservation
Dr. Fred C. Bryant – Texas Foundation for Conservation; Past President, Texas Chapter of The
Wildlife Society; Former Board Member, Rocky Mountain Elk Foundation; Professional
Member, Boone & Crockett Club
Rene Barrientos – South Texas Landowner
Emry Birdwell - Partner, Birdwell & Clark Ranch, Lone Star Land Steward Award Recipient
Rory Burroughs – Fisher County Landowner
Gus T. Canales – South Texas Landowner
Linda Campbell – Certified Wildlife Biologist; Past President, Texas Chapter of The Wildlife
Society
Dr. Jim Cathey – Past President – Texas Chapter of The Wildlife Society
Ken Cearley – Certified Wildlife Biologist, Cornerstone Ranching Solutions LLC
Michael J. Cherry - Wildlife Biologist
Deborah Clark - Partner, Birdwell & Clark Ranch, Lone Star Land Steward Award Recipient
Charles A. DeYoung - Ph D, Wildlife Biologist
Dr. Randy DeYoung - PhD, Fellow, The Wildlife Society
Don Dietz – Certified Wildlife Biologist
Cary Dietzmann – Washington County Landowner
Alice East – South Texans’ Property Rights Association, South Texas Landowner
Dr. Bill Eikenhorst – Veterinarian, Washington County Landowner
Jay C. Evans –Texas Landowner
Richard Guerra - Starr County landowner
Henry Hamman, South Texas Landowner
Trey Henderson – Angelina County Landowner
Dr. David G. Hewitt; Past President of the Texas Chapter of The Wildlife Society; Professional
Member, Boone and Crockett Club
Dr. Clayton D. Hilton – Veterinarian; Professional Member, Boone and Crockett Club
Gail & Bruce Hoffman - Jim Wells County Landowners
Anson B. Howard, Dimmit, Tom Green, and Coleman County Landowner
A.C. “Dick” Jones, IV - Jim Hogg County Landowner
W.W “Whit” Jones III - Jim Hogg County Landowner
David Kelly – Brooks County Ranch Manager, Leopold Award Recipient
Tio Kleberg – South Texas Landowner
Whitney Marion Klenzendorf – Frio County Landowner
Dr. Wallace Klussmann – Retired Head, Department of Wildlife and Fisheries Sciences, Texas
A&M University; Past President, Texas Chapter of The Wildlife Society; Founder, Texas
Youth Hunting Program
Jim Kolkhorst – Conservationist, Washington and Freestone County Landowner
Keith Lake – Wildlife Biologist
David K. Langford – Kendall County Landowner; Retired CEO, Texas Wildlife Association;
Lone Star Land Steward Award Recipient, Emeritus Member, Boone & Crockett Club
Berdon Lawrence – South Texans’ Property Rights Director, South Texas Landowner
Ken Leonard – South Texas Landowner
Roy Leslie – Low fence, no lease Kendall County Landowner; Lone Star Land Steward Award
Recipient
Dr. Roel Lopez – Past President – Texas Chapter of The Wildlife Society, Texas Foundation for
Conservation, Professional Member – Boone & Crockett Club
Chancey Lewis - Wildlife Biologist, Milam County Landowner
Steve C. Lewis – Kendall & Medina Landowner; Past President, Texas Wildlife Association
Ben Masters - Conservation Filmmaker, Writer
T. Nyle Maxwell – McCulloch and Hudspeth County Landowner
Coley Means – Culberson & Jeff Davis County Landowner
Jon Means – Culberson & Jeff Davis County Landowner; Past President, Texas & Southwestern
Cattle Raisers Association
Dr. Dan McBride – Veterinarian; Regular Member, Boone and Crockett Club, Burnet and
Hudspeth County Landowner
Robert F. McFarlane M.D. – Anderson County Landowner, Leopold Conservation Award
Recipient
Dr. James E. Miller - Past-President, The Wildlife Society; Honorary Member of The Wildlife
Society; Aldo Leopold Memorial Award Recipient
Brian Murphy – Certified Wildlife Biologist; Former CEO, Quality Deer Management
Association
Steve Nelle – Consulting Biologist
Eric Opiela, South Texans’ Property Rights Association President; Karnes, Bee and Live Oak
County Landowner
Dr. J. Alfonso “Poncho” Ortega, President of the Society for Range Management
Ellen Randall – South Texans’ Property Rights Association Director, Medina County Landowner
Jenny Sanders – Conservationist, Trinity County Landowner
Robert Sanders – Wildlife Biologist, Trinity County Landowner
Andrew Sansom - Professor of Practice in Geography and Executive Director; The Meadows
Center for Water and the Environment
Neil Shelton – Hartley & Oldham County Landowner
John Shepperd, Texas Foundation for Conservation
Dr. Nova J. Silvy - Fellow and Past President, The Wildlife Society; Aldo Leopold Memorial
Award Recipient
Greg Simons – Wildlife Biologist, Liberty, Jasper, Brazoria and Johnson County Landowner
South Texans’ Property Rights Association
Dr. Don Steinbach – Certified Wildlife Biologist, Executive Director – Texas Chapter of The
Wildlife Society, Washington County Landowner
Tye Stephens - Wildlife Biologist, Ranch Broker
Romey Swanson – Certified Wildlife Biologist; President, Texas Chapter of The Wildlife
Society
Ellen Temple – East Texas Landowner, Leopold Conservation Award Recipient
Tamara Trail – Conservationist, Shackelford County Landowner, Lone Star Land Steward
Award Recipient
Gary Valentine
Dr. Matt Wagner, Certified Wildlife Biologist
Larry Weishuhn – Wildlife Biologist; Co-Founder, Texas Wildlife Association
Irvin Welch – Wildlife Biologist, Landowner
Dr. Neal Wilkins – Certified Wildlife Biologist; South Texans’ Property Rights Association
Director; Professional Member, Boone & Crockett Club
Charlie Williams – Bandera and Medina County Landowner
Simon Winston – Trinity, Angelina, and Nacogdoches County Landowner; Leopold
Conservation Award Recipient
Carl Young - Williamson, Travis, and Brewster County Landowner
CC: The Honorable Greg Abbott, Governor of Texas
The Honorable Dan Patrick, Lieutenant Governor of Texas
The Honorable Dade Phelan, Speaker – Texas House of Representatives
The Honorable Ken King, Chair – House Culture, Recreation & Tourism Committee
The Honorable Tracy King, Chair – House Agriculture & Livestock Committee
The Honorable Charles Perry, Chair – Senate Agriculture, Water & Rural Affairs
Committee
The Honorable James E. Abell, TPW Commissioner
The Honorable Oliver J. Bell, TPW Commissioner
The Honorable Paul L. Foster, TPW Commissioner
The Honorable Anna B. Gallo, TPW Commissioner
The Honorable Jeffery D. Hildebrand, TPW Commissioner
The Honorable Robert L. “Bobby” Patton, Jr., TPW Commissioner
The Honorable Travis B. “Blake” Rowling, TPW Commissioner
The Honorable Richard “Dick” Scott, TPW Commissioner
The Honorable Lee M. Bass, Chairman-Emeritus – TPW Commission
The Honorable T. Dan Friedkin, Chairman-Emeritus – TPW Commission
The Honorable Coleman Locke, Chair - TAHC Commission
The Honorable Jim Eggleston, TAHC Commissioner
The Honorable Jimmie Ruth Evans, TAHC Commissioner
The Honorable Melanie Johnson, TAHC Commissioner
The Honorable Kenneth “Ken” Jordan, TAHC Commissioner
The Honorable Barret J. Klein, TAHC Commissioner
The Honorable Wendee C. Langdon, TAHC Commissioner
The Honorable Joe Leathers, TAHC Commissioner
The Honorable Thomas “Tommy” Oates, TAHC Commissioner
The Honorable Joseph “Joe” Osterkamp, TAHC Commissioner
The Honorable Keith M. Staggs, TAHC Commissioner
The Honorable Leo Vermedahl, TAHC Commissioner
The Honorable Michael L. Vickers, TAHC Commissioner
The Honorable Jimmie Ruth Evans, Chair, TPWD Private Lands Advisory Committee
Mr. Carter Smith, TPWD Executive Director
Dr. Andy Schwartz, DVM, TAHC Executive Director
=====end=====
MONDAY, NOVEMBER 29, 2021
Experimental Oronasal Transmission of Chronic Wasting Disease Agent from White-Tailed Deer to Suffolk Sheep Volume 27, Number 12—December 2021 Dispatch
MONDAY, NOVEMBER 29, 2021
HOW MANY DEER DIE FROM CWD TSE PRION?
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
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Voluntary Chronic Wasting Disease Herd Certification Program Annual Update, FY2020
SUNDAY, OCTOBER 24, 2021
Voluntary Chronic Wasting Disease Herd Certification Program Annual Update, FY2020
Cervids: CWD Voluntary Herd Certification Program
Last Modified: Jun 29, 2021
CWD status of captive herds
SATURDAY, OCTOBER 23, 2021
USDA APHIS Farmed Cervid Chronic Wasting Disease Management and Response Activities 2021 and other Cooperative Agreements 2021 Spending Plans
MONDAY, OCTOBER 04, 2021
APHIS Provides $5.7 Million in Funding to Control and Prevent Chronic Wasting Disease
WEDNESDAY, OCTOBER 13, 2021
Continuing Enhanced National Surveillance for Prion Diseases in the U.S.
The estimated total program funding for this effort is $17,500,000.
***> Confidential!!!!
***> As early as 1992-3 there had been long studies conducted on small pastures containing scrapie infected sheep at the sheep research station associated with the Neuropathogenesis Unit in Edinburgh, Scotland. Whether these are documented...I don't know. But personal recounts both heard and recorded in a daily journal indicate that leaving the pastures free and replacing the topsoil completely at least 2 feet of thickness each year for SEVEN years....and then when very clean (proven scrapie free) sheep were placed on these small pastures.... the new sheep also broke out with scrapie and passed it to offspring. I am not sure that TSE contaminated ground could ever be free of the agent!! A very frightening revelation!!!
---end personal email---end...tss
and so it seems...
Scrapie Agent (Strain 263K) Can Transmit Disease via the Oral Route after Persistence in Soil over Years
Published: May 9, 2007
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Our results showed that 263K scrapie agent can persist in soil at least over 29 months. Strikingly, not only the contaminated soil itself retained high levels of infectivity, as evidenced by oral administration to Syrian hamsters, but also feeding of aqueous soil extracts was able to induce disease in the reporter animals. We could also demonstrate that PrPSc in soil, extracted after 21 months, provides a catalytically active seed in the protein misfolding cyclic amplification (PMCA) reaction. PMCA opens therefore a perspective for considerably improving the detectability of prions in soil samples from the field.
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***> 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.
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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
***> 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
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.
=========================
***>>> 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.
========================
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 been mostly 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.
COMMODITIES SUCH AS HAY, STRAW, GROWN IN CWD TSE PRION ENDEMIC AREAS HAVE BEEN BANNED IN SOME COUNTRIES
NOW, let's take this a step further, with concerns about CWD TSE Prion and Plants, Grains, Hay, Straw, etc. Some countries have already started taking action on imports of some commodities of said products, from being grown in CWD TSE Prion endemic areas,
Regulation concerning additional requirements for imported hay and straw for animal feed
Legal basis: Adopted by The Norwegian Ministry of Agriculture and Food 22 October 2018 on the basis of Law 19 December 2003 No 124 relating to Food Production and Food Safety (Food Act) §§ 12, 15, 17 and 19, cf. Delegation Decision 19 December 2003 No 1790.
§ 1 Objective
The objective of this regulation is to prevent the spread of contagious animal disease with the import of hay and straw for feed from countries that are not part of the European Economic Area.
§ 2 Scope
This regulation applies to the import of hay and straw for feed from countries that are not part of the European Economic Area.
§ 3 Additional requirements
Hay and straw for feed that is imported to Norway must:
a) be accompanied by a declaration from the producer that the product has been stored for two months in the country of origin and that it was harvested from farms where manure has not been used as fertilizer for the past two years, and
b) be accompanied by attestation from an official veterinarian in the country of origin certifying that the product was harvested from farms where there are no restrictions because of contagious animal disease.
Hay and straw from USA and Canada must also be accompanied by attestation from an official veterinarian certifying that the product was harvested in a state or province where Chronic Wasting Disease has not been detected.
§ 4 Controll and decisions
The Norwegian Food Safety Authority may carry out controls and make necessary (individual) decisions, cf. Food Act § 23, to ensure compliance with provisions given in this regulation or in accordance with it. The Norwegian Food Safety Authority may also make decisions in accordance with Food Act § 24 to § 26.
§ 5 Penalties
The breach of provisions in this regulation, or a decision taken pursuant to this regulation, is a criminal offence pursuant to Food Act § 28.
§ 6 Dispensation
The Norwegian Food Safety Authority may grant a dispensation from provisions in this regulation in exceptional circumstances.
§ 7 Entry into force
This regulation enters into force immediately
§ 8 Amendments to other regulations
On the date of entry into force of this regulation Regulation 31 August 1991 No 507 om the prohibition of import of animals and articles which may transmit disease is amended as follows:
In § 3 Definition of product the first indent shall read:
- Raw material of animal origin for the production of pharmaceutical products or technical products.
In § 3 Definition of product the seventh indent shall read:
- Grass, hay, straw etc. that will not be used for animal feed.
Indent 11 in § 3 Definition of product is deleted.
In § 8 point 3 and 4 the word «animal feed» is deleted
Prions can also bind to or be taken up into plant tissues and spread disease. Experimental food crops testing positive thus far include alfalfa, wheat, corn, and tomatoes. These findings present a potential route of prion exposure for wildlife, domestic animals, and humans following consumption of these plants. Additionally, there is concern that other countries may ban export of crops from areas with CWD. Agricultural commodities, such as hay and straw, in CWDaffected areas may be baled with infected feces and moved inter-state or internationally. The European Food Safety Authority recognized this risk in their assessment of CWD in Norway. Consequently, Norway banned hay and straw imports from North America that do not have an accompanying veterinary statement verifying the products originated from a CWD-free zone.
P.157: Uptake of prions into plants
Christopher Johnson1, Christina Carlson1, Matthew Keating1,2, Nicole Gibbs1, Haeyoon Chang1, Jamie Wiepz1, and Joel Pedersen1 1USGS National Wildlife Health Center; Madison, WI USA; 2University of Wisconsin - Madison; Madison, WI USA
Soil may preserve chronic wasting disease (CWD) and scrapie infectivity in the environment, making consumption or inhalation of soil particles a plausible mechanism whereby na€ıve animals can be exposed to prions. Plants are known to absorb a variety of substances from soil, including whole proteins, yet the potential for plants to take up abnormal prion protein (PrPTSE) and preserve prion infectivity is not known. In this study, we assessed PrPTSE uptake into roots using laser scanning confocal microscopy with fluorescently tagged PrPTSE and we used serial protein misfolding cyclic amplification (sPMCA) and detect and quantify PrPTSE levels in plant aerial tissues. Fluorescence was identified in the root hairs of the model plant Arabidopsis thaliana, as well as the crop plants alfalfa (Medicago sativa), barley (Hordeum vulgare) and tomato (Solanum lycopersicum) upon exposure to tagged PrPTSE but not a tagged control preparation. Using sPMCA, we found evidence of PrPTSE in aerial tissues of A. thaliana, alfalfa and maize (Zea mays) grown in hydroponic cultures in which only roots were exposed to PrPTSE. Levels of PrPTSE in plant aerial tissues ranged from approximately 4 £ 10 ¡10 to 1 £ 10 ¡9 g PrPTSE g ¡1 plant dry weight or 2 £ 105 to 7 £ 106 intracerebral ID50 units g ¡1 plant dry weight. Both stems and leaves of A. thaliana grown in culture media containing prions are infectious when intracerebrally-injected into mice.
***Our results suggest that prions can be taken up by plants and that contaminated plants may represent a previously unrecognized risk of human, domestic species and wildlife exposure to prions.
===========
***Our results suggest that prions can be taken up by plants and that contaminated plants may represent a previously unrecognized risk of human, domestic species and wildlife exposure to prions.
*** SEE ; Friday, May 15, 2015 Grass Plants Bind, Retain, Uptake, and Transport Infectious Prions Report
PRION UPDATE VIA VEGETABLE PLANTS FROM THE SOIL
56. Members considered that there is no evidence that crops grown on the land which received composted excreta from BSE-challenged animals pose a TSE risk to humans or animals. One member suggested that, as some of these animals are orally challenged with high doses of BSE-infected materials, and the distribution of infectivity in the digestive system is not completely understood, it might be premature to conclude that there is no infective agent in the manure.
Furthermore, an unpublished study had indicated low level absorption of PrP from soil by tomato plants although it should be noted that this study had not been repeated. Details of this work would be sent to the SEAC Secretary. Dr Matthews explained that most of the manure from animals challenged with high doses of BSE had already been composted and used for coppicing. Members agreed that the risks from disposal of residual manure from experimental animals would be much less than historic risks of on farm contamination from naturally infected animals at the height of the BSE epidemic. ...SNIP...END
Trucking CWD TSE Prion
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
CHRONIC WASTING DISEASE CWD TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHY TSE PRION
***> 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.
MONDAY, NOVEMBER 29, 2021
Experimental Oronasal Transmission of Chronic Wasting Disease Agent from White-Tailed Deer to Suffolk Sheep Volume 27, Number 12—December 2021 Dispatch
TAHC National Shortage of Prion Testing Reagents Utilized for CWD Testing
November 17, 2021
On Friday, November 5, 2021, Texas A&M Veterinary Medical Diagnostic Laboratory (TVMDL) made a formal announcement regarding the National Animal Health Laboratory Network (NAHLN) national shortage of prion testing reagents utilized to complete immunohistochemistry (IHC) testing for Chronic Wasting Disease (CWD).
At that time, TVMDL engaged NAHLN, USDA- National Veterinary Services Laboratory (USDA/NVSL), other CWD testing labs in the U.S. and Canada, and the Texas Parks and Wildlife Department (TPWD) in daily communications to explore expedient solutions.
As of Friday, November 12, 2021, TVMDL exhausted their supply of prion kits and are unable to perform the IHC test. As all CWD testing labs have been affected by the shortage, there are no other labs available to assist TVMDL with IHC testing. The estimated timeframe for getting more IHC testing kits is mid-December.
USDA Cervid staff have determined that deer in the CWD Herd Certification Program (HCP) administered by the Texas Animal Health Commission (TAHC) are not eligible to be tested by ELISA. While antemortem samples are not eligible for the ELISA test, postmortem samples from penned deer not in the CWD HCP are eligible. The ELISA test requires fresh, not formalin-fixed, samples submitted within seven (7) days of collection.
The TAHC advises deer breeders enrolled in the CWD HCP to continue to collect the required postmortem samples and fix them in formalin. All samples collected must be submitted to TVMDL within seven days of collection and will be IHC tested upon the availability of test kits.
TVMDL staff continue to prepare all CWD antemortem test samples, a process which takes two days, so that they may be stained as soon as the reagent is made available. TVMDL will continue communications with the reagent supplier and NVSL/USDA to maintain an up-to-date timeline of when reagents will be available. TVMDL and TPWD have indicated they will continue to update permitted deer breeders as to the status of this situation on a regular basis.
Please direct any questions that you may have regarding the reagent shortage to TVMDL. Please contact TPWD or your TAHC Region Office regarding CWD sample collecting.
Thank you,
Texas Animal Health Commission
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Update: National Shortage of Prion Testing Reagents Utilized for CWD Testing
December 2, 2021
The Texas A&M Veterinary Medical Diagnostic Laboratory (TVMDL) received information from the National Veterinary Services Laboratories (NVSL) that an alternative immunohistochemistry (IHC) staining protocol for CWD has been validated and approved, by the USDA, using the latest generation of Roche IHC instruments, the Roche Ventana Discovery ULTRA.
Additionally, NVSL is in the process of approving the protocol for the use of the previous model of Roche IHC instruments, the Roche Ventana Discovery XT. When that approval is complete, TVMDL will be able to utilize all five Ventana stainer models and perform testing at full capacity.
On November 22, 2021, TVMDL placed an order for the alternative staining kits and confirmed with Roche that the kits should be delivered to TVMDL on December 3, 2021. Once the staining kits have been received, TVMDL has indicated they will run quality control slides to ensure the staining kits’ performance are within specified parameters, and then resume IHC testing of CWD samples.
In consistency with previous messaging regarding this topic, and assuming delivery of a new supply of staining kits on December 3, the Texas Parks and Wildlife Department (TPWD) will consider the submission of a valid antemortem test sample to TVMDL sufficient for a “Not Detected” test result for the purpose of liberation of breeder deer that occur on December 1 and 2.
The requirement for a “Not Detected” test result for breeder deer liberations will resume on December 3; however, since it will take several weeks for TVMDL to work through the case backlog, TPWD will be working with deer breeders and TVMDL to prioritize sample processing to address the most urgent needs of those who have already submitted samples to the lab.
If you submitted antemortem CWD samples to TVMDL by November 30, and you have an urgent need to release those deer in the month of December, you are asked to contact TPWD Wildlife Permitting staff at 512-389-4585 or deer.breeder@tpwd.texas.gov to explain your need.
For cervid herds in the TAHC Herd Certification Program (HCP), please keep in mind the CWD testing requirements:
Test all deaths aged 12 months or older, including but not limited to, animals killed on premises maintained for hunting and animals sent to slaughter.
The samples may be collected by a state or federal animal health official, an accredited veterinarian, or a TAHC Postmortem Sample Collector.
Alternatively, owners may remove and submit the entire head with all attached identification devices to an approved CWD laboratory for tissue collection.
Test samples shall be collected and submitted to an approved laboratory within 7 days of collection.
A positive IHC or ELISA test result on any sample submitted to the approved laboratory will be considered a CWD-suspect test result to be confirmed by IHC at the appropriate federal laboratory.
Thank you,
Texas Animal Health Commission
***> CHRONIC WASTING DISEASE TSE PRP HUMANS ZOONOSIS ZOONOTIC <***
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.
Snip...
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 ;
==================
''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
snip...
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:
snip...
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 Gerstmann Sträussler-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) <***
Terry S. Singeltary Sr.
posted by Terry S. Singeltary Sr. at
12:10 PM
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