Thursday, August 25, 2016

TPWD Action Disease Detection and Response – Chronic Wasting Disease TPW Commission Adopts New CWD Zones, Deer Movement Rules August 25, 2016

News Release Media Contact: TPWD News, news@tpwd.texas.gov, 512-389-8030
 
Aug. 25, 2016
 
TPW Commission Adopts New CWD Zones, Deer Movement Rules
 
AUSTIN – The Texas Parks and Wildlife Commission today approved new rules establishing chronic wasting disease (CWD) zones and restricting live deer movement authorized under permits to or from properties within those areas.
 
In addition, the commission adopted regulations banning importation of certain deer carcass parts from states where the disease has been detected and restricting carcass movement from CWD zones within Texas. The steps are part of the state’s comprehensive CWD management plan, which calls for measures to determine the prevalence and geographic extent of the disease where it exists and to reduce the risk of CWD being spread via permitted live deer relocation and movement of harvested deer carcasses.
 
Since CWD prions are known to be present in tissues of infected animals (especially brain, spinal cord and viscera), the new deer carcass movement restrictions establish the conditions under which certain parts of a harvested white-tailed deer or mule deer could be lawfully transported from those same zones or from a state, province or other place outside Texas where CWD has been detected among free-ranging or captive herds.
 
Hunters will be allowed to transport boned or packaged venison, cut quarters with the brain stem and spinal tissue removed, caped hides with skull not attached, the skull plate with antlers attached and cleaned of all soft tissue or finished taxidermy products. Hunters wishing to preserve a head for mounting can obtain a waiver to transport the skinned or unskinned head of a susceptible species to a taxidermist, provided all brain material, soft tissue, spinal column and any unused portions of the head are disposed of in a landfill in Texas permitted by the Texas Commission on Environmental Quality. These waivers can be obtained at CWD check stations where TPWD staff will collect CWD samples. Texans hunting out of state can obtain releases online at www.tpwd.texas.gov/cwd .
 
The commission also revised the CWD zone structure by reducing the number of tiers from three to two — Containment Zones (CZ) and Surveillance Zones (SZ) — to more appropriately characterize areas where the disease has been detected.
 
The new rules shrink the current CWD zones in Culberson, El Paso, Hudspeth and Reeves counties based on the department’s CWD surveillance efforts over the past four hunting seasons, establish a new CZ and SZ in the western Panhandle around Hartley County and create a SZ in portions of Bandera, Medina and Uvalde counties.
 
Since the disease has only been associated with permitted deer breeding facilities and an enclosed release site within the Medina area SZ, the new rules do not require hunters in this particular zone to submit harvested deer for sampling. However, a grassroots effort to generate voluntary samples from hunter harvests will be necessary to establish sufficient confidence that the disease will be detected if present at a low prevalence. The Texas Parks and Wildlife Department encourages all hunters who harvest deer in Bandera, Medina and Uvalde counties to assist in this voluntary effort by presenting their harvested deer at a department-run voluntary check station for CWD testing. Check station locations and additional information can be found at www.tpwd.texas.gov/cwd.
 
 2016-08-25
 
 
TPWD Action Disease Detection and Response – Chronic Wasting Disease August 25, 2016 (More Catering to the Industry imo)
 
Commission Agenda Item No. 3 Presenter: Mitch Lockwood
 
Action Disease Detection and Response – Chronic Wasting Disease August 25, 2016
 
I. Executive Summary: This item presents for adoption proposed changes to the department’s rules governing the department’s management efforts in response to the detection or expected detection of chronic wasting disease (CWD) in Texas. The proposed changes would:
 
•Eliminate the Buffer Zone concept;
 
•Replace the High Risk Zone (HRZ) designation with a Surveillance Zone (SZ) designation;
 
•Reduce the extent of the initial Containment Zone (CZ) and Surveillance Zone in far west Texas;
 
•Designate a new CZ and SZ to address the discovery of CWD in the Panhandle during the 2015-16 hunting season;
 
•Prescribe carcass movement restrictions designed to prevent/retard the inadvertent spread of CWD via the interstate and intrastate movement of dead deer; and
 
•Designate an SZ without mandatory check stations or carcass movement restrictions in portions of Bandera, Medina, and Uvalde counties in response to the discovery of CWD in multiple deer breeding facilities in that area.
 
II. Discussion: In July of 2012, the department surveillance efforts in the Hueco Mountains of far west Texas resulted in the discovery of chronic wasting disease (CWD) in two free-ranging mule deer. In response, the Commission promulgated rules to establish zones in which the movement of deer under department permits is restricted to varying degrees, and to implement mandatory check stations in certain areas in order to assess the extent and prevalence of CWD. Department surveillance efforts indicate that CWD has not increased in extent or prevalence in the area of these zones since discovery. In addition, rules governing permitted deer movement reduce the risk of moving the disease out of or within those populations. Thus, staff have determined that the CZ and the SZ in that area can be reduced in size. Unfortunately, during the last hunting season, a hunter-harvested mule deer in the Panhandle was confirmed positive for CWD, necessitating the designation of a CZ and SZ around that location.
 
On June 30, 2015, the department received confirmation that a two-year-old white-tailed deer held in a deer breeding facility in Medina County had tested positive for CWD. Heightened testing requirements resulted in additional discoveries. A total of 20 white-tailed breeder deer have now been confirmed positive at three deer breeding facilities in Medina County, necessitating the designation of a SZ surrounding those locations. Because local officials have committed to a voluntary effort, mandatory sampling and carcass movement restrictions will not be imposed in this zone at this time. At this time staff do not believe the designation of a CZ in this area is warranted because the breeding facilities where CWD has been discovered are under a TAHC Hold Order and Herd Plan that have equal or greater limits on permitted deer movement than department rules.
 
Additionally, because prions (the infectious causal agent of CWD) in the tissues of infected animals can be spread from carcasses, causing environmental contamination and a potential infection pathway to free-ranging deer, staff believe prudent restrictions on the transportation of carcasses from states where CWD has been confirmed and from CZs and SZs is warranted.
 
At the May, 2016 Work Session of the Commission, staff was authorized to publish the proposed rules in the Texas Register for public comment. The proposed rules appeared in the July 22, 2016, issue of the Texas Register (41 TexReg 5391). A summary of public comment on the proposed rules will be presented at the time of the hearing.
 
III. Recommendation: Staff recommends that the Commission adopt the proposed motion:
 
“The Texas Parks and Wildlife Commission adopts the repeal of §65.83 and §65.88, amendments to §§65.80-65.82 and 65.84-65.86, and new §65.88 and §65.89, concerning Disease Detection and Response, with changes as necessary to the proposed text as published in the July 22, 2016, issue of the Texas Register (41 TexReg 5391).”
 
Attachments – 1 1.Exhibit A – Proposed Rules
 
Commission Agenda Item No. 3 Exhibit A
 
DISEASE DETECTION AND RESPONSE RULES
 
CWD CONTAINMENT AND SURVEILLANCE/CARCASS MOVEMENT RESTRICTIONS
 
PROPOSAL PREAMBLE
 
1. Introduction
 
 The Texas Parks and Wildlife Department (the department) proposes the repeal of §65.83 and §65.88, amendments to §§65.80-65.82 and 65.84-65.86, and new §65.88 and §65.89, concerning Chronic Wasting Disease.
 
 On July 10, 2012, the department confirmed the first known cases of Texas wildlife infected with chronic wasting disease (CWD) in two free-ranging mule deer in the Hueco Mountains of far west Texas. With that discovery, Texas joined 20 other states and two Canadian provinces where CWD has been detected in free-ranging or captive environments. In response, the department adopted §§65.80-65.88 (37 TexReg 10231), effective January 2, 2013, to establish zones in which the permitted movement of deer is more restricted in order to impede or prevent the spread of CWD, and to implement mandatory check stations in certain areas to determine the geographic extent and prevalence of the disease.
 
 On June 30, 2015, the department received confirmation that a two-year-old white-tailed deer held in a permitted deer breeding facility in Medina County had tested positive for CWD, which was followed by positive test results for white-tailed deer in three additional deer breeding facilities. In addition, a hunter-harvested free-ranging mule deer in Hartley County in the Texas Panhandle tested positive for CWD in the past year. In response, the department first adopted emergency rules (40 TexReg 5566) to respond immediately to the threat, then developed interim rules (41 TexReg 815) intended to function through the 2015-2016 hunting season until permanent rules could be implemented. Working closely with the Texas Animal Health Commission (TAHC), the regulated community, and key stakeholders, and with the assistance of the Center for Public Policy Dispute Resolution of the University of Texas School of Law, the department developed a rule package to implement a comprehensive CWD management strategy associated with permitted deer management practices involving the permitted movement of live deer (41 TexReg 815). Those rules were approved for adoption by the Parks and Wildlife Commission, with changes, on June 20, 2016 (referred to herein as “comprehensive CWD management rules”). The notice of adoption for the comprehensive CWD management rules will be published in the Texas Register in August of this year. The repeal, amendments, and new section are necessary to harmonize the current rules in Chapter 65, Subchapter B, Division 1 with the rules in Chapter 65, Subchapter B, Division 2, which implement the comprehensive CWD management strategy and to modify types and extent of the zones in which the permitted movement of deer and the movement of deer carcasses are restricted.
 
 The proposed rules are a result of cooperation between the department, TAHC, and the department’s CWD Task Force, comprised of wildlife-health professionals and cervid producers and are intended to protect susceptible species of exotic and native wildlife from 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 (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 variant Creutzfeldt-Jakob Disease (vCJD) in humans.
 
 Much remains unknown about CWD. The peculiarities of its transmission (how it is passed from animal to animal), infection rate (the frequency of occurrence through time or other comparative standard), incubation period (the time from exposure to clinical manifestation), and potential for transmission to other species are still being investigated. There is no scientific evidence to indicate that CWD is transmissible to humans. What is known is that CWD is invariably fatal to cervids, and is transmitted both directly (through deer-to-deer contact) and indirectly (through environmental contamination). Moreover, a high prevalence of the disease correlates with deer population decline in at least one free-ranging population, and human dimensions research suggests that hunters will avoid areas of high CWD prevalence. Additionally, the apparent persistence of CWD in contaminated environments represents a significant obstacle to eradication of CWD from either farmed or free-ranging cervid populations. The potential implications of CWD for Texas and its annual, multi-billion dollar ranching, hunting, real estate, tourism, and wildlife management-related economies could be significant, unless it is contained and controlled.
 
 The department has been concerned for over a decade about the possible emergence of CWD in free-ranging and captive deer populations in Texas. Since 2002, more than 40,000 “not detected” CWD test results have been obtained from free-ranging (i.e., not breeder) deer in Texas, and deer breeders have submitted approximately 20,000 “not detected” test results as well. The intent of the proposed rules is to reduce the probability of CWD being spread from areas and deer breeding facilities where it might exist and to increase the probability of detecting and containing CWD if it does exist.
 
 Under Parks and Wildlife Code, Chapter 43, Subchapters C, E, L, R, and R-1, the department regulates the possession of white-tailed deer and mule deer for various purposes. Subchapter C governs permits for scientific research, zoological collection, rehabilitation, and educational display of protected wildlife, which includes deer. Subchapter E governs Triple T activities (trap, transport, and transplant), in which game animals or game birds are captured and relocated to adjust populations. Subchapter E also governs Urban White-tailed Deer Removal Permits and Permits to Trap, Transport, and Process Surplus White-tailed Deer (TTP). Unless otherwise stated, the permits issued under authority of Subchapter E are collectively referred to herein as “Triple T” permits. Subchapter L governs deer breeder permit activities, which include, among other things, possession of captive-raised deer within a facility for breeding purposes and release of such deer. Subchapters R and R-1 govern Deer Management Permit (DMP) activities for white-tailed deer and mule deer, respectively, in which free-ranging deer may be captured and temporarily retained for breeding purposes. The department notes that although DMPs for mule deer were authorized by the legislature in 2011, no DMPs for mule deer have been issued because the department has deferred promulgation of regulations pending acquisition of requisite data to develop biologically defensible rules and address disease threats, including CWD.
 
 Triple T, deer breeder permits, and DMP all authorize release of deer under certain circumstances. Additionally, the permits governed by Parks and Wildlife Code, Chapter 43, Subchapter C, can also include permit conditions for release.
 
 From an epidemiological point of view, the higher the density of susceptible organisms, the more likely disease transmission is to occur, if it exists in a population. Obviously, deer kept in circumstances (facilities, pens, trailers, etc.) in which densities are many times higher than what occurs naturally are more likely to both manifest and spread communicable diseases at a higher rate or in greater numbers than would occur in a free-ranging populations. Therefore, the proposed rules are designed and intended to provide reasonable assurance that once CWD is detected it is quickly isolated and not spread as a result of increased concentration of deer, the movement of live deer under permits issued by the department, or the movement of carcasses of harvested deer.
 
 The proposed repeal of §65.83, concerning Buffer Zones, is necessary because buffer zones are being eliminated. The current rules impose a three-tiered cordon approach to address the possibility of CWD being spread via permitted deer movements (deer breeder, Triple T, and DMP activities often involve the physical translocation of animals at distances that are far beyond what is possible by free-ranging animals). Currently, the three cordons are the Containment Zone (the area immediately surrounding the location where a CWD-positive animal has been found), the High-Risk Zone (the area surrounding or adjoining the Containment Zone), and the Buffer Zone (an area surrounding or adjoining the High-Risk Zone). The rules governing permitted deer movement are the most rigorous in the Containment Zone and become successively less rigorous as distance from where the disease was discovered increases. The comprehensive CWD management rules (to be contained in Chapter 65, Subchapter B, Division 2) previously referenced in this preamble impose increased CWD-testing requirements for breeder deer, Triple T trap sites, and DMP sites where breeder are introduced on a statewide basis, which makes the concept of the buffer zone superfluous.
 
 The proposed amendment to §65.80, concerning Definitions, would eliminate the definition for “buffer zone” for the reasons discussed in the proposed repeal of §65.83. The proposed amendment also would alter current paragraph (4) to eliminate the term “High-Risk Zone” and replace it with “Surveillance Zone,” and to remove the language defining such zones as surrounding or being adjacent to a Containment Zone (CZ). The department has determined that the term “high-risk” could inadvertently and unnecessarily stigmatize an area, so a term that more accurately describes the function of the zone has been selected. Additionally, for reasons discussed in the proposed amendment to §65.82, concerning Surveillance Zones; Restrictions, the proposed amendment would eliminate the phrase “adjacent to or surrounding a CZ” from the definition. The proposed amendment also would alter the definition of “susceptible species” in current paragraph (6) to clarify that the term includes parts of animals and is not restricted to a whole animal.
 
 The proposed amendment to §65.81, concerning Containment Zones; Restrictions, would redefine the boundaries of the CZ currently in effect and create a new CZ in the Texas Panhandle to address the discovery of CWD in Hartley County. The proposal would modify the current CZ by decreasing its current geographical extent in Culberson, El Paso, and Hudspeth counties. The contraction of the CZ in those counties is possible because the department’s surveillance efforts indicate that CWD has not likely spread beyond the Hueco Mountains. Several factors (e.g., cervid population parameters, cervid behavior and life history, historical surveillance intensity, clear boundaries, etc.) are considered when determining the appropriate extent of a CZ or SZ. For example, when CWD was detected just across the New Mexico border in 2012, there was more than a strong possibility that infected mule deer were present in Texas, since the movement of desert mule deer can be as much as 25-30 linear miles.
 
 The proposed amendment to §65.81 would alter the provisions of paragraph (2)(C) by adding language to allow the recapture of deer that have escaped from a deer breeding facility within a CZ if specifically authorized under a hold order or herd plan issued by TAHC. The department has determined that escaped breeder deer may be epidemiologically significant in some instances and that recapture should be permitted if authorized by TAHC.
 
 Under current §65.81(2)(A), the movement of deer into, out of, or within a CZ is prohibited, except for department-authorized research. The proposed amendment to §65.81 would add new paragraph (2)(D) to allow TC 1 deer breeding facilities within a CZ to release breeder deer to immediately adjoining acreage (provided the release site and the breeding facility share the same ownership and the release site is high-fenced as required by the comprehensive CWD rules alluded to previously in this preamble). Because TC 1 breeding facilities (more thoroughly described in the comprehensive CWD management rules) represent the lowest risk of spreading CWD, the department considers the release of such breeder deer to adjoining acreage under the same ownership to present a very low risk, but all other movement of breeder deer would continue to be prohibited.
 
 The proposed amendment to §65.81 also changes the term “deer breeder facility” to “deer breeding facility” for purposes of consistency.
 
 The proposed amendment to §65.82, concerning High-Risk Zones; Restrictions, would change the title of the section to Surveillance Zones: Restrictions, as previously noted in this preamble, shrink the current zone in effect for far west Texas, create two new zones (one to address the additional CWD discovery in the Texas Panhandle and one to address the discovery of CWD in deer breeding facilities in Medina County), and allow the permitted movement of deer within a SZ under certain circumstances. A Surveillance Zone (SZ) is a geographic area within which the department has determined, using the best available science and data, that the presence of CWD could reasonably be expected. With respect to proposed new paragraph (1)(C), the department is creating a Surveillance Zone in portions of Bandera, Medina, and Uvalde counties, but not a CZ. The reason for not creating a CZ is two-fold. First, the CWD discovery in this part of the state occurred in breeder deer and deer breeding facilities, which are required by law to be designed and built to both prevent the free movement of deer and contact with free-ranging deer, which coincidentally is imperative for the control and management of CWD. Second, the facilities where CWD was discovered are operating under TAHC herd plans, which restrict deer movement and require CWD testing at an equal or higher level to what is required in a CZ.
 
 Under the current provisions of §65.82, the permitted movement of deer was restricted to breeder deer being transferred to or from a deer breeding facility that had achieved “Certified” status in the TAHC Herd Certification Program. With the adoption of the comprehensive CWD management rules alluded to earlier in this preamble, the testing, TAHC herd status, and herd inventory requirements of current §65.82 with respect to breeder deer are no longer necessary in §65.82; however, because the comprehensive CWD management rules create a classification system that identifies breeding facilities and prospective DMP and Triple T trap sites that are epidemiologically determined to present limited risk of CWD transfer, the proposed amendment would add new subparagraphs (B)-(D) to paragraph (2) to address that fact and prescribe the criteria under which those activities would be allowed.
 
 Proposed new §65.82(2)(B) would address deer breeding facilities and provide that except as provided by the provisions of Division 2 of Subchapter B (the comprehensive CWD management rules), TC 1 breeding facilities within a SZ may transfer, receive, or liberate breeder deer within or beyond the SZ, because they represent a low risk of CWD. Similarly, the proposed amendment would allow TC 2 breeding facilities to receive deer from any deer breeder in the state authorized to transfer deer and to transfer, receive, or liberate deer within the SZ, but not beyond the SZ. TC 2 breeding facilities are those facilities that are not directly linked to a CWD-positive facility but at the same time cannot provide sufficient epidemiological data to achieve TC 1 status; therefore, because breeder deer transferred from breeding facility to breeding facility are always within a high-fenced area, which the comprehensive CWD management rules also require for release sites, these activities can be allowed within the SZ without increasing the chance of spreading CWD beyond the SZ in the event the disease does occur within the SZ. The proposed amendment to §65.82 also would add new subparagraph (B)(ii) to allow the recapture of deer that have escaped from a deer breeding facility within a SZ if specifically authorized under a hold order or herd plan issued by TAHC. As stated previously in this preamble, the department has determined that escaped breeder deer may be epidemiologically significant in some instances and that recapture should be permitted only if authorized by TAHC.
 
 Proposed new §65.82(2)(C) would address the movement of deer pursuant to Triple T permits and would provide for the approval of Triple T releases in a SZ, but prohibit trapping for Triple T purposes within a SZ. From an epidemiological standpoint, the release of deer within a SZ does not present a significant risk of spreading or accelerating the spread of CWD, and in any case, the department will not approve a release that would result in deer densities greater than the habitat conditions and deer populations at the release site can sustain, which would be the major concern in evaluating disease propagation potential. Conversely, the trapping of deer from within a SZ, because the source population’s disease potential is unknown, represents an unacceptable risk of disease propagation in the absence of adequate sampling data to provide sufficient confidence that CWD does not exist within that area.
 
 Proposed new §65.82(2)(D) would address the movement of deer pursuant to a DMP and would provide for the issuance of DMPs in SZs with the proviso that any breeder deer introduced to a DMP must be released to the designated release site and cannot be returned to a deer breeding facility. A DMP authorizes the trapping and temporary detention of free-ranging deer at the trap site for breeding purposes. Breeder deer may be introduced to a DMP pen as well, but since the epidemiological status of free-ranging deer within high-fenced enclosures is unknown, it is problematic to allow breeder deer exposed to such deer to be returned to a breeding facility.
 
 The proposed amendment to §65.84, concerning Powers and Duties of the Executive Director, would alter the terminology used in the section in order to conform the terminology with the changes proposed elsewhere in this rulemaking.
 
 The proposed amendment to §65.85, concerning Mandatory Check Stations, would make nonsubstantive changes to terminology to comport the section with amendments being made to other sections.
 
 The proposed amendment to §65.86, concerning Preemption, would create an exception for the comprehensive CWD management rules contained in Division 2 of the subchapter. The current provision allows Division 1 to control in instances of conflict with other provisions of Chapter 65, but in order for the proposed amendments to function as intended, the current rule must be amended to allow regulatory primacy for the provisions of Division 2 in the event of conflicts.
 
 Proposed new §65.88, concerning Deer Carcass Movement Restrictions, would set forth the conditions under which certain parts of a susceptible species harvested within a CZ or SZ could be lawfully transported from the CZ or SZ where the harvest occurred.
 
 Proposed new §65.88(a) would prohibit the possession or transport of certain parts of a susceptible species (white-tailed deer or mule deer) taken in a state, province, or other place outside Texas where CWD has been detected in free-ranging or captive herds. CWD prions are known to be present in tissues of infected animals, especially brain, spinal cord and viscera; thus, carcasses with these tissues entering Texas from other states and countries where CWD has been confirmed represent a source of environmental contamination and a potential infection pathway to free-ranging and farmed deer in Texas. For the same reason, proposed new subsection (a)(2) would prohibit the transport of any part of a susceptible species from within a CZ or SZ, except in compliance with the proposed new section.
 
 Proposed new §65.88(b) would establish exceptions to subsection (a), consisting of various types of processing that would have to take place in order to lawfully transport susceptible species from the place of harvest. The exceptions consist of meat that has been cut up and packaged (boned or filleted); a carcass that has been reduced to quarters with no brain or spinal tissue present; a cleaned hide (skull and soft tissue must not be attached or present); whole skull (or skull plate) with antlers attached, provided the skull or skull plate has been completely cleaned of all soft tissue; finished taxidermy products; cleaned teeth; or tissue prepared and packaged for delivery to and use by a diagnostic or research laboratory. In general, these types of processing reflect the removal of the types of tissues that are known to concentrate CWD prions.
 
 Proposed new §65.88(c) would provide that the exceptions created by subsection (b) apply if the susceptible species is processed within the CZ or SZ where it was harvested. In order to minimize the potential that brain or spinal tissue potentially infected with CWD could be transported beyond a CZ or SZ and present a risk of environmental contamination, the processing of the susceptible species must occur within the CZ or SZ where the animal is killed. The only exceptions are the transport of the head to a check station for tissue extraction and the transport of a head to a taxidermist.
 
 Proposed new §65.88(d) would allow a susceptible species harvested in a CZ or SZ and processed in accordance with the provisions of subsections (b) and (c) to be transported from the CZ or SZ, provided it is accompanied by a department-issued check-station receipt, which must remain with the susceptible species until it reaches a final destination. At the current time, the only mandatory check stations in Texas are located in the one CZ that has been established in west Texas; however, additional mandatory check stations will be designated in the Panhandle area in Dallam, Deaf Smith, Hartley, Moore, Parmer, Potter, Randall, Oldham, and Sherman counties. Therefore, the proposed provision would allow the transport of susceptible species only if the required processing has occurred and the head has been presented at a check station.
 
 Proposed new §65.88(e) would allow susceptible species harvested from a CZ or SZ, other state, Canadian province, or other place outside of Texas to be transported to a taxidermist for taxidermy purposes; however, in order to minimize the potential for environmental contamination, all brain material, soft tissue, spinal column and any unused portions of the head would be required to be disposed of in a landfill permitted by the Texas Commission on Environmental Quality (TCEQ). The proposed new subsection does not exempt hunters within a CZ or SZ from the requirement, except as specifically authorized by the department, to submit the head of a susceptible species harvested within a CZ or SZ to a check station for tissue collection.
 
 Proposed new §65.88(f) would exempt deer harvested in Surveillance Zone 3 from the mandatory check station requirement and documentation requirements of the section. The department was approached by concerned county officials and landowners in Medina County who committed to organizing a volunteer hunter and landowner effort to provide the department with a sufficient number of valid “not detected” CWD test results, which would allow the department to make an epidemiologically sound determination about the prevalence (if any) of CWD within Surveillance Zone 3.
 
 Proposed new §65.89, concerning Penalties, would state the statutory penalties for violations of the proposed new rules for ease of reference.
 
2. Fiscal Note.
 
 Mr. Mitch Lockwood, Big Game Program Director, has determined that for each of the first five years that the rules as proposed are in effect, there will be no fiscal implications to state and local governments as a result of enforcing or administering the rules as proposed, as department personnel currently allocated to the administration and enforcement of the affected department programs will administer and enforce the rules as part of their current job duties and testing costs associated with the rules will be absorbed within current budgetary resources.
 
3. Cost/Benefit Note.
 
 Mr. Lockwood also has determined that for each of the first five years the rules as proposed are in effect:
 
 (A) The public benefit anticipated as a result of enforcing or administering the rules as proposed will be the protection of free-ranging, native deer from communicable diseases, thus ensuring the public of continued enjoyment of the resource and also ensuring the continued beneficial economic impacts of hunting in Texas. Additionally, the protection of free-ranging deer herds will have the simultaneous collateral benefit of protecting captive herds, and maintaining the economic viability of deer breeding operations.
 
 (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 and micro-businesses. As required by Government Code, §2006.002(g), in April 2008, the Office of the Attorney General issued guidelines to assist state agencies in determining a proposed rule’s potential adverse economic impact on small businesses. These guidelines state that “[g]enerally, there is no need to examine the indirect effects of a proposed rule on entities outside of an agency’s regulatory jurisdiction.” The 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. The guidelines also list examples of the types of costs that may result in a “direct economic impact.” Such costs may include costs associated with additional recordkeeping or reporting requirements; new taxes or fees; lost sales or profits; changes in market competition; or the need to purchase or modify equipment or services. As explained in more detail below, the department has determined that except for deer breeders, the proposed rules will not have an adverse impact on small or micro-businesses.
 
 The department recognizes that Triple T and DMP holders in many cases obtain such permits as part of an effort to enhance the antler quality or increase the density of a deer herd located on a specific property. In turn, such landowners may seek to obtain a higher fee for hunting opportunities based on the perception of a higher-quality hunting experience. However, adverse economic impacts to the pricing structure of hunting opportunity as a result of the proposed new rules, if they occur, are indirect at best. The rules do not directly impact a landowner’s ability to charge a fee for a hunting opportunity on the landowner’s property. In addition, any deer that are introduced to a property as a result of Triple T or DMP activities continue to be a public resource.
 
Scientific Educational, Zoological, and Rehabilitation Permits
 
 There will be no adverse economic impacts to persons holding permits issued under Parks and Wildlife Code, Chapter 43, Subchapter C (permits for rehabilitation, scientific collection, educational display, and zoological display). Current rules (31 TAC §69.44(b) and §69.302) prohibit the sale of protected wildlife held under those permits. Since persons possessing these permits undertake permitted activities on a non-profit basis, any person or entity involved in permitted activities would not be engaged in such activities for the purpose of making a profit and would thus not be considered a small or micro-business as defined in Government Code, §2006.001.
 
Triple T Permits
 
 There will be no adverse economic effects to holders of Triple T permits. Triple T permits authorize only the trapping, transporting, and transplantation of a public resource, and wildlife trapped under a Triple T may not be sold, bartered, or exchanged for anything of value (Parks and Wildlife Code, §1.011; 31 TAC §69.117(a)(6)). Therefore, persons engaged in such activities would not suffer a direct adverse economic impact from the proposed rules. Current department rules governing Triple T permit issuance provide for the denial of a permit if the department determines that release of a game animal or game bird may detrimentally affect existing populations or systems (31 TAC §65.103(c)(3)). The rules as proposed would further clarify this authority by prohibiting the trapping of susceptible species from within a CZ or SZ since trapping and moving susceptible species from within a CZ or SZ would have the potential to detrimentally affect other populations of deer by exposure to animals possibly infected with CWD.
 
Deer Management Permits
 
 There will be no adverse economic impact to holders of DMPs. As noted previously, the department has not promulgated rules governing DMPs for mule deer; therefore, the only DMP activities affected by the proposed new rules would be DMPs issued for white-tailed deer in SZ 2 or 3. A DMP authorizes the permittee to temporarily detain free-ranging white-tailed deer for breeding purposes, including deer introduced to the DMP pen via Triple T permit and/or deer breeder permit. Except for breeder deer, which under normal circumstances may be returned to a breeding facility, deer held pursuant to a DMP must be released following breeding activities in a DMP pen and may not be sold (Parks and Wildlife Code, §§1.011, 43.621; 31 TAC §65.133(g)). As a result, persons engaged in such activities would not suffer a direct small or micro-business adverse economic effect from the proposed rules.
 
Deer Breeder Permits
 
 Parks and Wildlife Code, §43.357(a), authorizes a person to whom a breeder permit has been issued to “engage in the business of breeding breeder deer in the immediate locality for which the permit was issued” and to “sell, transfer to another person, or hold in captivity live breeder deer for the purpose of propagation.” As a result, unlike the other permits impacted by the proposed rules, breeder permits authorize persons to engage in business activities.
 
 Government Code, §2006.001(1), defines a small or micro-business as a legal entity “formed for the purpose of making a profit” and “independently owned and operated.” A micro-business is a business with 20 or fewer employees. A small business is defined as a business with fewer than 100 employees, or less than $6 million in annual gross receipts. Although the department does not require holders of breeder permits to provide financial information to the department, the department believes that many if not all persons holding deer breeder permits would qualify as a small or micro-business. Since the rules as proposed would impact the ability of a deer breeder to engage in certain activities undertaken to generate a profit, the proposed rules may have an adverse impact on persons holding a deer breeder permit.
 
 The proposed new rules would result in potential adverse economic impacts to one deer breeder with a breeding facility in proposed SZ 2 and 12 deer breeders with breeding facilities in proposed SZ 3. There are no breeding facilities located in any existing or proposed CZ. Of the 13 breeding facilities directly affected by the rules as proposed, six are designated as TC 3 breeding facilities. Under the comprehensive CWD management rules alluded to previously in this rulemaking, TC 3 breeding facilities are prohibited from or limited in transferring or releasing deer. The department notes that when the comprehensive CWD management rules become effective, many TC 3 breeding facilities will become TC 2 breeding facilities, although those under a TAHC hold order will remain at TC 3 status. Thus, the amendments as proposed do not impose any direct economic impact on TC 3 breeding facilities because those facilities are already prevented by other rules from engaging in deer movement and are under hold orders and herd plans issued by TAHC, which remain in effect until epidemiological confidence can be established that CWD is not present in those facilities. The remaining breeding facilities directly affected by the proposed rules are TC 2 breeding facilities in Medina, Bandera, and Uvalde counties and none of the facilities are under a TAHC hold order. The proposed rules allow TC 2 facilities to transfer breeder deer to and from other breeding facilities and release sites with a SZ, but prohibit any activity that would result in the movement of deer beyond the SZ. Thus, these 13 breeding facilities could experience adverse economic impacts. The extent of such adverse economic impact would consist of loss of revenue as a result of being unable to move deer into or beyond the SZ. The dollar value of the adverse economic impact is dependent on the volume of deer produced or acquired by any given permittee, which can vary from a few deer to hundreds of deer, and upon the cost of the deer, which can vary from hundreds of dollars to many thousands of dollars. The department does not require deer breeders to report the sale or purchase prices of breeder deer; however, publicly available information indicates that sale prices, especially for buck deer, may be significant. The sale price for a single deer may range from hundreds of dollars to many thousands of dollars.
 
 Although a deer breeder permit confers the privilege to buy and sell breeder deer and many deer breeders participate in a market for breeder deer, other deer breeders are interested only in breeding and liberating deer on their own properties for hunting opportunity. Once a breeder deer is liberated, it cannot be returned to a breeding facility. Thus, if a deer breeder is engaged primarily in buying and selling deer, the potential adverse economic impact is greater than that for a deer breeder who engages in deer breeding activities primarily for purposes of release onto that person’s property. The department notes that the designation of a SZ is not necessarily permanent and that the department can change the size and shape of a SZ depending on assessments of prevalence and extent of CWD within a CZ as epidemiological certainty is resolved. The department also notes that the comprehensive CWD management rules alluded to elsewhere in this preamble provide a pathway for all TC 2 breeding facilities to attain TC 1 status within three years. (Under the proposed rules, TC 1 facilities in a SZ may transfer deer anywhere for any purpose, provided there is compliance with the department’s regulations regarding transfer of deer.) Therefore, any adverse economic impacts to deer breeders as a result of CZ designations could be temporary. The estimated costs of performing tests necessary to reach TC 1 status are as set out in the proposal for the comprehensive CWD management rules (41 TexReg 2853).
 
 No other small or microbusinesses or persons required to comply would incur any immediate direct adverse economic impacts.
 
 The department notes that because CWD has been proven to be transmissible by direct contact (including through fences) and via environmental contamination, there may be adverse economic impacts unrelated to the proposed rules in the event that CWD is confirmed near a breeding facility due to the possible reluctance of potential customers to purchase deer from a facility in an area where CWD has been confirmed. Additionally, if CWD is detected within a breeding facility, there could be lost revenue to the permittee since potential purchasers who are aware of the potential of CWD would likely refrain from purchasing deer from such a facility. Thus, the proposed rules, by providing a mechanism to minimize the spread of CWD, could also protect the economic interests of the regulated community.
 
 The department considered several alternatives to achieve the goals of the proposed new rules while reducing potential adverse impacts on small and micro-businesses and persons required to comply. The department considered proposing no rules. This alternative was rejected because a regulation that clearly sets out the restrictions on the regulated community is necessary to stem the spread of CWD. The department concluded that the need to protect the wildlife resources that sustain the state’s multi-billion-dollar hunting industry outweighs the temporary adverse impacts to small and micro-businesses and persons required to comply.
 
 The department also considered CZs and SZs that are more narrowly drawn. This alternative was rejected because the size of a CZ or SZ is biologically determined by using the best science and data available, correlated to the susceptible species. If the department chose to implement smaller CZs and SZs, it would increase the risk of spreading CWD and introduce regulatory confusion.
 
 (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 rules as proposed will not impact local economies.
 
 (D) 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. Any impacts resulting from the discovery of CWD in or near private real property would be the result of the discovery of CWD and not the proposed rules.
 
4. Request for Public Comment.
 
 Comments on the proposed rule may be submitted to Mitch Lockwood, Texas Parks and Wildlife Department, 4200 Smith School Road, Austin, Texas, 78744; (830) 792-9677 (e-mail: mitch.lockwood@tpwd.state.tx.us); or via the department’s website at www.tpwd.state.tx.us.
 
5. Statutory Authority.
 
 The amendments and new rules are proposed under the authority of Parks and Wildlife Code, Chapter 43, Subchapter C, which requires the commission to adopt rules to govern the collecting, holding, possession, propagation, release, display, or transport of protected wildlife for scientific research, educational display, zoological collection, or rehabilitation; Subchapter E, which requires the commission to adopt rules for the trapping, transporting, and transplanting of game animals and game birds, urban white-tailed deer removal, and trapping and transporting surplus white-tailed deer; Subchapter L, which authorizes the commission to make regulations governing the possession of breeder deer held under the authority of the subchapter; Subchapter R, which authorizes the commission to establish the conditions of a deer management permit, including the number, type, and length of time that white-tailed deer may be temporarily detained in an enclosure; Subchapter R-1, which authorizes the commission to establish the conditions of a deer management permit, including the number, type, and length of time that mule deer may be temporarily detained in an enclosure (although as noted previously, the department has not yet established the DMP program for mule deer authorized by Subchapter R-1); and §61.021, which provides that no person may possess a game animal at any time or in any place except as permitted under a proclamation of the commission.
 
 The proposed amendments and new rules affect Parks and Wildlife Code, Chapter 43, Subchapters C, E, L, R, and R-1 and Chapter 61.
 
6. Rule Text.
 
 §65.80. Definitions. The following words and terms, when used in this subchapter, shall have the following meanings, unless the context clearly indicates otherwise. All other words in this subchapter shall have the meanings assigned by Parks and Wildlife Code.
 
 (1) Adult deer — A white-tailed deer or mule deer that is 16 months of age or older.
 
 [(2) Buffer Zone (BZ) — A department-defined geographic area in this state adjacent to or surrounding a HRZ, within which the department, using the best available science and data, has determined that an elevated probability of discovering CWD exists.]
 
 (2)[(3)] Containment Zone (CZ) — A department-defined geographic area in this state within which CWD has been detected or the department has determined, using the best available science and data, CWD detection is probable.
 
 (3)[(4)] Eligible mortality — Any lawfully possessed adult deer that has died.
 
 (4)[(5)] Surveillance Zone (SZ)[High-Risk Zone (HRZ)] — A department-defined geographic area in this state [adjacent to or surrounding a CZ,] within which the department has determined, using the best available science and data, that the presence of CWD could reasonably be expected.
 
 (5)[(6)] Susceptible species — Any species or part of a species of wildlife resource that is susceptible to CWD.
 
 §65.81. Containment Zones; Restrictions. The areas described in paragraph (1) of this section are CZs.
 
 (1) Containment Zones.
 
 (A) Containment Zone 1: That portion of the state within the boundaries of a line beginning in Culberson County where U.S. Highway (U.S.) 62-180 enters from the State of New Mexico; thence southwest along U.S. 62-180 to F.M. 1111 in Hudspeth County; thence south on F.M. 1111 to I.H. 10[the intersection with State Highway (S.H.) 54; thence south along S.H. 54 to Interstate Highway (I.H.) 10;] thence west along I.H. 10 to S.H. 20; thence northwest along [to] S.H. 20 to Farm-to Market Road (F.M.) 1088; thence south along F.M. 1088 to the Rio Grande; thence northwest along the Rio Grande to the Texas-New Mexico border.
 
 (B) Containment Zone 2: That portion of the state within the boundaries of a line beginning where I.H. 40 enters from the State of New Mexico in Deaf Smith County; thence east along I.H. 40 to U.S. 385 in Oldham County; thence north along U.S. 385 to the Oklahoma state line.
 
 (C)[(B)] Existing CZs may be modified and additional CZs may be designated as necessary by the executive director as provided in §65.84 of this title (relating to Powers and Duties of the Executive Director).
 
 (2) Restrictions.
 
 (A) Except as provided in this section or §65.87 of this title (relating to Exception), no person within a CZ shall conduct, authorize or cause any activity involving the movement of a susceptible species under a permit issued pursuant to Parks and Wildlife Code, Chapter 43, Subchapter C, E, L, R, or R-1. Such prohibited activity, includes, but is not limited to transportation, introduction, removal, authorizing the transportation, introduction or removal of, or causing the transportation, introduction or removal of a live susceptible species into, out of, or within a CZ.
 
 (B) If the department receives an application for a deer breeder permit for a new facility that is to be located within an area designated as a CZ, the department will issue the permit but will not authorize the possession of susceptible species within the facility so long as the CZ designation exists.
 
 (C) Deer that escape from a deer breeding[breeder] facility within a CZ may not be recaptured unless specifically authorized under a hold order or herd plan issued by the Texas Animal Health Commission.
 
 (D) A TC 1 deer breeding facility located in a CZ may release breeder deer to immediately adjoining acreage if the release site and the breeding facility share the same ownership, but may not transfer deer to or from any other location. Breeder deer may not be transferred to or from a TC 2 or TC 3 deer breeding facility located within a CZ.
 
 §65.82. Surveillance Zones; Restrictions[High Risk Zones; Restrictions]. The areas described in paragraph (1) of this section are SZs[HRZs].
 
 (1) Surveillance Zones[High Risk Zones].
 
 (A) Surveillance[High-Risk] Zone 1: That portion of the state lying within a line beginning where U.S. 285 enters from the State of New Mexico in Reeves County; thence southeast along U.S. 285 to R.M. 652; thence west along R.M. 652 to Rustler Springs Rd./FM 3541 in Culberson County; thence south along Rustler Springs Rd./F.M. 3541 to F.M. 2185; thence south along F.M. 2185 to Nevel Road; thence west along Nevel Road to County Road 501; thence south along County Road 501 to Weatherby Road; thence south along Weatherby Road to F.M. 2185; thence southwest along to F.M. 2185 to S.H. 54; thence south on S.H. 54 to U.S. 90; thence south along U.S. 90 to the Culberson County line; thence southwest along the Culberson County line to the Rio Grande River in Hudspeth County; thence north along the Rio Grande to F.M. 1088; thence northeast along F.M. 1088 to S.H. 20; thence southeast along S.H. 20 to I.H. 10; thence southeast along I.H. 10 to F.M 1111; thence north on F.M. 1111 to U.S. 62/180; thence east and north along U.S. 62/180 to the New Mexico state line in Culberson County[in Reeves County where the Pecos River enters from New Mexico; thence southeast along the Pecos River to Interstate Highway (I.H.) 20; thence west along I.H. 20 to I.H. 10; thence west along I.H. 10 to the Culberson County line; thence southwest along the Culberson County line to the Rio Grande; thence northwest along the Rio Grande to F.M. 192 in Hudspeth County; thence northeast along F.M. 192 to S.H. 20; thence southeast along S.H. 20 to I.H. 10; thence east along I.H. 10 to S.H. 54 in Hudspeth County; thence north along S.H. 54 to U.S. 62-180; thence northwest along U.S. 62-180 to the Texas-New Mexico border].
 
 (B) Surveillance Zone 2. That portion of the state lying within a line beginning at the New Mexico state line where U.S. 60 enters Texas; thence northeast along U.S. 60 to U.S. 87 in Randall County; thence north along U.S. 87 to I.H. 27; thence north along U.S. 87/I.H. 27 to U.S. 287 in Moore County; thence north along US 287 to the Oklahoma state line.
 
 (C) Surveillance Zone 3. That portion of the state lying within a line beginning at U. S. 90 in Hondo in Medina County; thence west along U.S. Highway 90 to F.M. 187 in Uvalde County; thence north along F.M. 187 to F. M. 470 in Bandera County; thence east along F.M. 470 to Tarpley in Bandera County; thence south along F.M. 462 to U.S. 90 in Hondo.
 
 (D)[(B)]Existing SZs[HRZs] may be modified and additional SZs[HRZs] may be designated as necessary by the executive director as provided in §65.84 of this title (relating to Powers and Duties of the Executive Director).
 
 (2) Restrictions.
 
 (A) Except as provided in §65.87 of this title (relating to Exception) and subparagraph (B) of this paragraph, no person within a SZ [an HRZ] may conduct, authorize or cause any activity involving the movement of a susceptible species, into, out of, or within a SZ [an HRZ] under a permit issued pursuant to Parks and Wildlife Code, Chapter 43, Subchapter C, E, L, R, or R-1. Such prohibited activity, includes, but is not limited to transportation, introduction, removal, authorizing the transportation, introduction or removal, or causing the transportation, introduction or removal of a live susceptible species into, out of, or within a SZ [an HRZ].
 
 (B) Breeder Deer.
 
 (i) Except as provided in Division 2 of this subchapter, a breeding facility that is within a SZ and designated as a:
 
 (I) TC 1 breeding facility may:
 
 (-a-) transfer to or receive breeder deer from any other deer breeding facility in this state; and
 
 (-b-) transfer breeder deer anywhere in this state for purposes of liberation, including to release sites within the SZ.
 
 (II) TC 2 breeding facility may:
 
 (-a-) receive deer from any facility in the state that is authorized to transfer deer; and
 
 (-b-) transfer deer to a breeding facility or release site that is within the same SZ; but
 
 (-c-) is prohibited from transferring deer to any facility outside of the SZ.
 
 (ii) Deer that escape from a breeding facility within a SZ may not be recaptured unless specifically authorized under a hold order or herd plan issued by the Texas Animal Health Commission.
 
 [(B) No person shall:]
 
 [(i) introduce, remove, authorize the introduction or removal, or cause the introduction or removal of a live susceptible species into or from a deer breeder facility permitted under the provisions of Parks and Wildlife Code, Chapter 43, Subchapter L, that is located in a HRZ unless:]
 
 [(I) CWD test results of "not detected" have been returned from an accredited test facility on all eligible mortalities that occurred within the facility within the preceding five-year period;]
 
 [(II) the facility has obtained Level "C" status as defined by 4 TAC §40.3 (relating to Herd Status Plans for Cervidae); and]
 
 [(III) the department has confirmed that the herd inventory record maintained by the department is accurate; or]
 
 [(ii) transport, authorize the transport, or cause the transport of a susceptible species into a HRZ unless:]
 
 [(I) the requirements of clause (i)(I) — (III) of this subparagraph have been met; and]
 
 [(II) the susceptible species are transported to a deer breeder facility permitted under Parks and Wildlife Code, Chapter 43, Subchapter L.]
 
 (C) Permits to Transplant Game Animals and Game Birds (Triple T permit). The department may authorize the release of susceptible species in a SZ under the provisions of a Triple T permit issued by the department under the authority of Parks and Wildlife Code, Chapter 43, Subchapter E and the provisions of Subchapter C of this chapter, but the department will not authorize the trapping of deer within a SZ for purposes of a Triple T permit.
 
 [(C) No person shall liberate a susceptible species within an HRZ.]
 
 (D) Deer Management Permit (DMP). The department may issue a DMP for a facility in a SZ; however, any breeder deer introduced to a DMP facility must be released and may not be transferred to any deer breeding facility.
 
 [(D) Deer that escape from a deer breeder facility within HRZ may not be recaptured.]
 
 §65.84. Powers and Duties of the Executive Director.
 
 (a) The executive director may designate any geographic area in this state a CZ or SZ[, HRZ, or BZ] if the area meets the applicable definition set forth in §65.80 of this title (relating to Definitions).
 
 (b) The executive director shall notify the presiding officer of the commission prior to taking any action under the provisions of subsection (a) of this section.
 
 (c) The executive director shall ensure that the department makes a reasonable effort to provide public notice in the event that a CZ or SZ[, HRZ, or BZ] is declared.
 
 (d) The designation of a CZ or SZ[, HRZ, or BZ] under the provisions of subsection (a) of this section is:
 
 (1) effective immediately; and
 
 (2) applicable to all permits issued under the provisions of Parks and Wildlife Code, Chapter 43, Subchapters C, E, L, R, and R-1.
 
 (e) The department shall initiate rulemaking to adopt any CZ or SZ[, HRZ, or BZ] designated by the executive director as soon as practicable.
 
 §65.85. Mandatory Check Stations.
 
 (a) The department may establish mandatory check stations in any CZ or SZ or portion of a CZ or SZ[CZ, HRZ, or BZ] for the purpose of collecting biological information on susceptible species taken within a CZ or SZ[CZ, HRZ, or BZ].
 
 (b) In a CZ or SZ[CZ, HRZ, or BZ] where mandatory check stations have been established, the intact, unfrozen head of any susceptible species that has been killed must be presented to a designated check station within 24 hours of take by the person or representative of the person who killed the susceptible species, unless otherwise authorized in writing by department personnel.
 
 (c) The department will issue documentation for each specimen of a susceptible species that is presented at a check station. The department-issued documentation must remain with the specimen until it reaches the possessor’s final destination.
 
 (d) A person who fails or refuses to comply with this section commits an offense.
 
 §65.86. Preemption. Except as provided in Division 2 of this subchapter, to[To] the extent a provision of this subchapter conflicts with a provision of another subchapter of this chapter, this subchapter controls.
 
 §65.88. Deer Carcass Movement Restrictions.
 
 (a) Except as provided in this section, no person may:
 
 (1) transport into this state or possess any part of a susceptible species from a state, Canadian province, or other place outside of Texas where CWD has been detected in free-ranging or captive herds; or
 
 (2) transport or cause the transport of any part of a susceptible species from a property within a CZ or SZ.
 
 (b) Subsection (a) of this section does not apply to susceptible species processed in accordance with this subsection, provided the applicable requirements of subsections (c) — (e) of this section have been met:
 
 (1) meat that has been cut up and packaged (boned or filleted);
 
 (2) a carcass that has been reduced to quarters with no brain or spinal tissue present;
 
 (3) a cleaned hide (skull and soft tissue must not be attached or present);
 
 (4) a whole skull (or skull plate) with antlers attached, provided the skull plate has been completely cleaned of all soft tissue;
 
 (5) finished taxidermy products;
 
 (6) cleaned teeth; or
 
 (7) tissue prepared and packaged for delivery to and use by a diagnostic or research laboratory.
 
 (c) For susceptible species harvested in a CZ or SZ, the provisions of subsection (b) of this section are applicable only if the susceptible species is processed within the CZ or SZ where the susceptible species was harvested, except for the transport of an intact head to a designated check station.
 
 (d) A susceptible species harvested in a CZ or SZ and processed in accordance with the provisions of subsections (b) and (c) of this section may be transported from the CZ or SZ, provided it is accompanied by a department-issued check-station receipt, which shall remain with the susceptible species until it reaches a final destination.
 
 (e) The skinned or unskinned head of a susceptible species from a CZ or SZ, other state, Canadian province, or other place outside of Texas where CWD has been detected in free-ranging or captive herds may be transported to a taxidermist for taxidermy purposes, provided all brain material, soft tissue, spinal column and any unused portions of the head are disposed of in a landfill in Texas permitted by the Texas Commission on Environmental Quality (TCEQ).
 
 (f) The provisions of subsections (a)(2) and (b)–(d) of this section do not apply to deer harvested in Surveillance Zone 3 as described in §65.82 of this title (relating to Surveillance Zones; Restrictions).
 
 §65.89. Penalties. A person who violates any provision of this subchapter commits an offense and is subject to the penalties prescribed by Parks and Wildlife Code, Chapter 43, Subchapter C, E, L, R or R-1, and Chapter 61, as applicable.
 
 This agency hereby certifies that the proposal has been reviewed by legal counsel and found to be within the agency’s authority to adopt.
 
 Issued in Austin, Texas, on
 
 The repeals are proposed under the authority of Parks and Wildlife Code, Chapter 43, Subchapter C, which requires the commission to adopt rules to govern the collecting, holding, possession, propagation, release, display, or transport of protected wildlife for scientific research, educational display, zoological collection, or rehabilitation; Subchapter E, which requires the commission to adopt rules for the trapping, transporting, and transplanting of game animals and game birds, urban white-tailed deer removal, and trapping and transporting surplus white-tailed deer; Subchapter L, which authorizes the commission to make regulations governing the possession of breeder deer held under the authority of the subchapter; Subchapter R, which authorizes the commission to establish the conditions of a deer management permit, including the number, type, and length of time that white-tailed deer may be temporarily detained in an enclosure; Subchapter R-1, which authorizes the commission to establish the conditions of a deer management permit, including the number, type, and length of time that mule deer may be temporarily detained in an enclosure (although as noted previously, the department has not yet established the DMP program for mule deer authorized by Subchapter R-1); and §61.021, which provides that no person may possess a game animal at any time or in any place except as permitted under a proclamation of the commission.
 
 The proposed repeals affect Parks and Wildlife Code, Chapter 43, Subchapters C, E, L, R, and R-1 and Chapter 61.
 
 §65.83. Buffer Zones.
 
 §65.88. Penalties.
 
 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
 
 
TPWD Action Disease Detection and Response – Chronic Wasting Disease August 25, 2016 Catering to the Industry
 
 
 
Executive Session
 
Wednesday, August 24, 2016 9:00 a.m.
 
Texas Parks and Wildlife Department Executive Office Conference Room 4200 Smith School Road, Austin, TX 78744
 
T. Dan Friedkin, Commission Chair Carter Smith, Executive Director
 
1.Update on Regulatory Litigation – Ann Bright (Executive Session Only) ◦Chronic Wasting Disease – Deer Breeder Litigation
 
 
 
 
This map shows the recently imposed Surveillance Zone for CWD in portions of Bandera, Medina and Uvalde counties.
 
 
 
 
 Administrators with Texas Parks and Wildlife Department have outlined a proposed voluntary Chronic Wasting Disease (CWD) reporting Surveillance Zone for portions of Bandera, Medina and Uvalde counties.
 
The proposed 400 square mile area is bounded by FM 462 from Tarpley to Hondo, west on Highway 90 to Sabinal and north to Utopia along Highway 83 and back to Tarpley on FM 470. CWD infecting deer has spread from the Four Corners area to New Mexico and isolated portions of Texas. The proposed Tarpley area Surveillance Zone (SZ) will add a surveillance area to the two Texas mandatory compliance-surveillance areas that already exist in the Trans Pecos area and the Panhandle.
 
This proposed zone will remain until the carcass tissue count reaches 1,749 tests and presenters encouraged early compliance from landowners and hunters. If the CWD samples are statistically negative, then the SZ will be removed. Among other issues, the proposed regulations concern the disposal of carcass “soft tissue,” which is key to containing the disease. Proposed CWD rules have been published by the TPWD at the tpwd.texas.gov/business/feedback/publiccomment. TPWD representatives introduced the proposed rules at a special meeting in Hondo on August 17 and will repeat the same information in Tarpley at 7 pm, Thursday, Sept. 15, in the old school house.
 
Chronic Wasting Disease is held in the soil for many years and is very difficult to eradicate. It affects cervids, including white-tail dear. This fatal neurological disease is spread via animal to animal or through contact with contaminated soil and vegetation. Additionally, there is some controversy that CWD might be transmissible to humans if infected deer meat is consumed. Most of the investigators deny that it is transmissible, but at the same time warn against eating the meat of a contaminated animal. CWD was first noted locally on a deer-breeding ranch on the boundary between Bandera and Medina Counties about six miles south of Tarpley. It has subsequently been found at two other ranches in northwest Medina County.
 
Ranchers and hunters have recently noted a perceived decrease in the deer population in this area. This dwindling deer count could be related to several factors such as high game fences, hunting, CWD or better than average range conditions resulting a more disperse pattern.
 
 
 
TEXAS REGISTER
 
Volume 41 Number 30 July 22, 2016 Pages 5277 – 5476
 
skip to PAGE 115;
 
CHAPTER 65. WILDLIFE SUBCHAPTER B. DISEASE DETECTION AND RESPONSE DIVISION 1. CHRONIC WASTING DISEASE (CWD) The Texas Parks and Wildlife Department (the department) proposes the repeal of §65.83 and §65.88, amendments to §§65.80 -65.82 and 65.84 -65.86, and new §65.88 and §65.89, concerning Chronic Wasting Disease.
 
 
‘’VERY HOPEFUL ABOUT VOLUNTARY EFFORTS’’
 
LMAO!!!
 
good old boy system alive and well in Texas.
 
only fooling yourselves folks, only fooling yourselves. any voluntary efforts, just to cater to the industry, will only spread CWD TSE Prion, because the industry still does not get it. ...TSS
 
Saturday, August 20, 2016
 
TPWD alerts deer breeders TVMDL is USDA live testing approved. Faster ELISA testing now available
 
 
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
 
 
Monday, July 18, 2016
 
Texas Parks Wildlife Dept TPWD HIDING TSE (CWD) in Deer Herds, Farmers Sampling Own Herds, Rapid Testing, False Negatives, a Recipe for Disaster
 
 
Saturday, July 09, 2016
 
Texas Intrastate – within state movement of all Cervid or Trucking Chronic Wasting Disease CWD TSE Prion Moratorium
 
 
Friday, July 01, 2016
 
*** TEXAS Thirteen new cases of chronic wasting disease (CWD) were confirmed at a Medina County captive white-tailed deer breeding facility on June 29, 2016***
 
 
*** How Did CWD Get Way Down In Medina County, Texas?
 
DISCUSSION Observations of natural outbreaks of scrapie indicated that the disease spread from flock to flock by the movement of infected, but apparently normal, sheep which were incubating the disease.
 
There was no evidence that the disease spread to adjacent flocks in the absent of such movements or that vectors or other host species were involved in the spread of scrapie to sheep or goats; however, these possibilities should be kept open...
 
 
 
 
Friday, February 26, 2016
 
TEXAS Hartley County Mule Deer Tests Positive for Chronic Wasting Disease CWD TSE Prion
 
 
NEWS RELEASE
 
April 22, 2016
 
Scrapie Confirmed in a Hartley County Sheep
 
AUSTIN - Texas Animal Health Commission (TAHC) officials have confirmed scrapie in a Hartley County ewe. The ewe was tested by TAHC after the owner reported signs of weight loss and lack of coordination to their local veterinarian. The premises was quarantined and a flock plan for monitoring is being developed by the TAHC and USDA.
 
"The TAHC is working closely with the flock owner, sharing all of the options for disease eradication," said Dr. David Finch, TAl-lC Region 1 Director. ‘We are thankful the producer was proactive in identifying a problem and seeking veterinary help immediately.”
 
Texas leads the nation in sheep and goat production. Since 2003, there have been no confirmed cases of scrapie in Texas. The last big spike in Texas scrapie cases was in 2006 when nine infected herds were identified and the last herd was released from restrictions in 2013.
 
According to USDA regulations, Texas must conduct adequate scrapie surveillance by collecting a minimum of 598 sheep samples annually. Since USDA slaughter surveillance started in FY 2003, the percent of cull sheep found positive for scrapie at slaughter (once adjusted for face color) has decreased 90 percent.
 
Scrapie is the oldest known transmissible spongiform encephalopathies, and under natural conditions only sheep and goats are known to be affected by scrapie. It is a fatal disease that affects the central nervous system of sheep and goats. It is not completely understood how scrapie is passed from one animal to the next and apparently healthy sheep infected with scrapie can spread the disease. Sheep and goats are typically infected as young lambs or kids, though adult sheep and goats can become infected.
 
The most effective method of scrapie prevention is to maintain a closed flock. Raising replacement ewes, purchasing genetically resistant rams and ewes, or buying from a certified-free scrapie flock are other options to reduce the risk of scrapie. At this time the resistant genetic markers in goats have not been identified, therefore it is important to maintain your sheep and goat herds separately.
 
The incubation period for scrapie is typically two to five years. Producers should record individual identification numbers and the seller's premise identification number on purchase and sales records. These records must be maintained for a minimum of five years.
 
 
 
Tuesday, June 07, 2016
 
*** Comparison of two US sheep scrapie isolates supports identification as separate strains ***
 
Research Project: TRANSMISSION, DIFFERENTIATION, AND PATHOBIOLOGY OF TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES
 
 
Thursday, August 18, 2016
 
PROCEEDINGS ONE HUNDRED AND Nineteenth ANNUAL MEETING of the USAHA BSE, CWD, SCRAPIE, PORCINE TSE PRION October 22 28, 2015
 
 
Saturday, May 28, 2016
 
*** Infection and detection of PrPCWD in soil from CWD infected farm in Korea Prion 2016 Tokyo ***
 
 
Thursday, August 04, 2016
 
MEETING ON THE FEASIBILITY OF CARRYING OUT EPIDEMIOLOGICAL STUDIES ON CREUTZFELDT JAKOB DISEASE 1978 THE SCRAPIE FILES IN CONFIDENCE CONFIDENTIAL SCJD
 
 
Monday, May 02, 2016
 
*** Zoonotic Potential of CWD Prions: An Update Prion 2016 Tokyo ***
 
 
‘’The differences between samples, tonsil versus rectal lymphoid biopsies, is largely affected by two factors, the relative number of lymphoid follicles in each tissue (tonsil > rectal) ***and the skill of the person taking the biopsy.’’
 
Wednesday, July 22, 2015
 
Texas Certified Chronic Wasting Disease CWD Sample Collector, like the Wolf Guarding the Henhouse
 
Just got off the phone with TAHC, and I wanted to confirm this. but it seems true, that in the state of Texas, even if you are a Captive game farmer, breeder, part of the captive industry at all, if you want to sample your own cervid for cwd, instead of the TAHC, TPWD, or Doctor, all you have to do is pass the Certified CWD Sample Collector course, and bingo, you sample your own herd. ...tss
 
 
Friday, August 14, 2015
 
Carcass Management During a Mass Animal Health Emergency Draft Programmatic Environmental Impact Statement—August 2015
 
 
Thursday, May 02, 2013
 
*** Chronic Wasting Disease (CWD) Texas Important Update on OBEX ONLY TEXTING
 
 
Saturday, February 04, 2012
 
Wisconsin 16 age limit on testing dead deer Game Farm CWD Testing Protocol Needs To Be Revised
 
 
Thursday, June 09, 2016
 
Scrapie Field Trial Experiments Mission, Texas, The Moore Air Force Base Scrapie TSE Prion Experiment 1964
 
How Did CWD Get Way Down In Medina County, Texas?
 
 
Tuesday, June 21, 2016
 
TPW Commission Adopts Amended Deer Movement Rules and Some Deer breeders walk out of hearing on chronic wasting disease CWD TSE Prion
 
 
Thursday, June 16, 2016
 
Help fight this fatal disease CWD TSE PRION threat to Texas wild deer herd
 
 
Tuesday, June 07, 2016
 
*** Comparison of two US sheep scrapie isolates supports identification as separate strains ***
 
Research Project: TRANSMISSION, DIFFERENTIATION, AND PATHOBIOLOGY OF TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES
 
 
Friday, June 03, 2016
 
Chronic Wasting Disease CWD TSE Prion Surveillance and Testing in Texas, a very concerning situation
 
 
Saturday, May 28, 2016
 
TPWD gives in to Breeders again and postponed their decision regarding proposed changes to state regulations for managing CWD allowing the TSE Prion to spread further
 
 
Sunday, May 22, 2016
 
TEXAS CWD DEER BREEDERS PLEA TO GOVERNOR ABBOTT TO CIRCUMVENT TPWD SOUND SCIENCE TO LET DISEASE SPREAD
 
 
Sunday, June 12, 2016
 
TPWD Special Meeting Chronic Wasting Disease Response Rules June 20, 2016
 
 
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
 
 
Friday, April 22, 2016
 
*** Texas Scrapie Confirmed in a Hartley County Sheep where CWD was detected in a Mule Deer
 
 
Monday, April 25, 2016
 
TEXAS Nilgai Exotic Antelope Let Loose for Trophy Hunts Blamed for Spreading Cattle Tick Fever, and what about CWD TSE Prion Disease ?
 
 
Saturday, April 02, 2016
 
TEXAS TAHC BREAKS IT'S SILENCE WITH TWO MORE CASES CWD CAPTIVE DEER BRINGING TOTAL TO 10 CAPTIVES REPORTED TO DATE
 
 
Friday, February 26, 2016
 
TEXAS Hartley County Mule Deer Tests Positive for Chronic Wasting Disease CWD TSE Prion
 
 
Friday, February 05, 2016
 
TEXAS NEW CHRONIC WASTING DISEASE CWD CASE DISCOVERD AT CAPTIVE DEER RELEASE SITE
 
 
Saturday, January 23, 2016
 
Texas new interim rule governing Deer Management Permit (DMP) activities as part of the state’s response to the detection of chronic wasting disease (CWD) in captive deer populations
 
 
Sunday, January 17, 2016
 
Texas 10,000 deer in Texas tested for deadly disease CWD TSE, but not tested much in the most logical place, the five-mile radius around the Medina County captive-deer facility where it was discovered
 
 
Friday, January 15, 2016
 
TEXAS PARKS & WILDLIFE CWD Ante-Mortem Testing Symposium Texas Disposal Systems Events Pavilion January 12, 2016
 
 
Sunday, January 10, 2016
 
TEXAS MEDIA REPORTING A BIT OF GOOD NEWS ON CWD TESTING SO FAR INSTEAD OF TAHC which is still mum, still refusing timely updates to the public TSE PRION DISEASE
 
 
Tuesday, December 29, 2015
 
*** TEXAS MONTHLY CHRONIC WASTING DISEASE CWD JANUARY 2016 DEER BREEDERS STILL DON'T GET IT $
 
Chronic Wasting Unease
 
*** The emergence of a deadly disease has wildlife officials and deer breeders eyeing each other suspiciously. ***
 
 
Monday, November 16, 2015
 
*** TEXAS PARKS AND WILDLIFE DEPARTMENT EXECUTIVE DIRECTOR ORDER NO. 015-006
 
*** Chronic Wasting Disease (CWD) immediate danger to the white-tailed deer and mule deer resources of Texas
 
 
Saturday, November 14, 2015
 
TEXAS CAPTIVE BREEDER CHRONIC WASTING DISEASE CWD 2 MORE SUSPECTS DECTECTED BRINGING NUMBER TO 7 DETECTED IN CAPTIVE BREEDER (if/when the last two are confirmed).
 
 
Thursday, November 05, 2015
 
*** TPW Commission Adopts Interim Deer Breeder Movement Rules
 
 
Friday, October 09, 2015
 
Texas TWA Chronic Wasting Disease TSE Prion Webinars and Meeting October 2015
 
 
Saturday, October 03, 2015
 
TEXAS CHRONIC WASTING DISEASE CWD TSE PRION GOD MUST NOT BE A TEXAN 2002 TO 2015
 
 
Thursday, September 24, 2015
 
TEXAS Hunters Asked to Submit Samples for Chronic Wasting Disease CWD TSE Prion Testing
 
*** I cannot stress enough to all of you, for the sake of your family and mine, before putting anything in the freezer, have those deer tested for CWD. ...terry
 
 
***raw and uncut
 
Sunday, August 23, 2015
 
TAHC Chronic Wasting Disease CWD TSE Prion and how to put lipstick on a pig and take her to the dance in Texas
 
 
Friday, August 07, 2015
 
*** Texas CWD Captive, and then there were 4 ?
 
 
Thursday, August 06, 2015
 
*** WE HAVE LOST TEXAS TO CWD TASK FORCE CATERING TO INDUSTRY
 
 
Tuesday, July 21, 2015
 
*** Texas CWD Medina County Herd Investigation Update July 16, 2015 ***
 
 
Thursday, July 09, 2015
 
TEXAS Chronic Wasting Disease (CWD) Herd Plan for Trace-Forward Exposed Herd with Testing of Exposed Animals
 
 
Wednesday, July 01, 2015
 
TEXAS Chronic Wasting Disease Detected in Medina County Captive Deer
 
 
Wednesday, March 18, 2015
 
Chronic Wasting Disease CWD Confirmed Texas Trans Pecos March 18, 2015
 
 
Wednesday, March 25, 2015
 
Chronic Wasting Disease CWD Cases Confirmed In New Mexico 2013 and 2014 UPDATE 2015
 
 
*** I understand that the 84th Legislation might have made some terrible mistakes with regards to Chronic Wasting Disease CWD TSE Prion aka mad cow type disease, by weakening CWD rules for breeders.
 
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
 
 
Monday, February 11, 2013
 
TEXAS CHRONIC WASTING DISEASE CWD Four New Positives Found in Trans Pecos
 
 
Tuesday, July 10, 2012
 
Chronic Wasting Disease Detected in Far West Texas
 
 
Monday, March 26, 2012
 
Texas Prepares for Chronic Wasting Disease CWD Possibility in Far West Texas
 
 
2011 – 2012
 
Friday, October 28, 2011
 
CWD Herd Monitoring Program to be Enforced Jan. 2012 TEXAS
 
Greetings TAHC et al,
 
A kind greetings from Bacliff, Texas.
 
In reply to ;
 
Texas Animal Health Commission (TAHC) Announcement October 27, 2011
 
I kindly submit the following ;
 
 
 
Wednesday, March 25, 2015
 
Chronic Wasting Disease CWD Cases Confirmed In New Mexico 2013 and 2014 UPDATE 2015
 
 
***for anyone interested, here is some history of CWD along the Texas, New Mexico border, and my attempt to keep up with it...terry
 
snip...
 
see history CWD Texas, New Mexico Border ;
 
Monday, March 26, 2012
 
3 CASES OF CWD FOUND NEW MEXICO MULE DEER SEVERAL MILES FROM TEXAS BORDER
 
 
Sunday, October 04, 2009
 
CWD NEW MEXICO SPREADING SOUTH TO TEXAS 2009 2009 Summary of Chronic Wasting Disease in New Mexico New Mexico Department of Game and Fish
 
 
Thursday, August 20, 2015
 
TEXAS CAPTIVE Deer Industry, Pens, Breeding, Big Business, Invites Crooks and CWD
 
a review of sorts ;
 
 
Sunday, July 17, 2016
 
*** CHRONIC WASTING DISEASE CWD TSE PRION GLOBAL REPORT UPDATE JULY 17 2016
 
 
Thursday, April 07, 2016
 
*** What is the risk of chronic wasting disease being introduced into Great Britain? An updated Qualitative Risk Assessment March 2016 ***
 
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, however, suggests that human susceptibility to CWD is low and there may be a robust species barrier for CWD transmission to humans (Sigurdson, 2008). It is apparent, though, that CWD is affecting wild and farmed cervid populations in endemic areas with some deer populations decreasing as a result.
 
snip...
 
For the purpose of the qualitative risk assessment developed here it is necessary to estimate the probability that a 30-ml bottle of lure contains urine from an infected deer. This requires an estimate of the proportion of deer herds in the USA which are infected with CWD together with the within herd prevalence.
 
The distribution map of CWD in US shows it is present mainly in central states (Figure 1). However, Virginia in the east of the country has recorded seven recent cases of CWD (Anon 2015a). Some US manufacturers claim to take steps to prevent urine being taken from infected animals eg by sourcing from farms where the deer are randomly tested for CWD (Anon 2015a). However, if disease is already present and testing is not carried out regularly, captive populations are not necessarily disease free (Strausser 2014). Urine-based deer lures have been known to be collected from domestic white-tailed deer herds and therefore there is a recognised risk. This is reflected by 6 US States which have
 
14
 
banned the use of natural deer urine for lures, as the deer urine may be sourced from CWD-endemic areas in the USA as well as from areas free of CWD. For example, the US State of Virginia is banning the use of urine-based deer lures on July 2015 and Vermont from 2016 due to the risk of spread of CWD. Alaska banned their use in 2012 (Anon 2015a). Pennsylvania Game Commission has banned urine-based deer lures and acknowledged that there is no way to detect their use (Strausser 2014). On the basis of unpublished data (J. Manson, Pers. Comm.) it appears that up to 50% of deer herds can be infected with 80-90% of animals infected within some herds.
 
*** It is therefore assumed that probability that a 30-ml bottle of deer urine lure imported from the USA is sources from an infected deer is medium.
 
SNIP...
 
In the USA, under the Food and Drug Administration’s BSE Feed Regulation (21 CFR 589.2000) most material (exceptions include milk, tallow, and gelatin) from deer and elk is prohibited for use in feed for ruminant animals. With regards to feed for non-ruminant animals, under FDA law, CWD positive deer may not be used for any animal feed or feed ingredients. ***For elk and deer considered at high risk for CWD, the FDA recommends that these animals do not enter the animal feed system. ***However, this recommendation is guidance and not a requirement by law.
 
***Animals considered at high risk for CWD include:
 
***1) animals from areas declared to be endemic for CWD and/or to be CWD eradication zones and
 
***2) deer and elk that at some time during the 60-month period prior to slaughter were in a captive herd that contained a CWD-positive animal.
 
***Therefore, in the USA, materials from cervids other than CWD positive animals may be used in animal feed and feed ingredients for non-ruminants. The amount of animal PAP that is of deer and/or elk origin imported from the USA to GB cannot be determined, however, as it is not specified in TRACES. It may constitute a small percentage of the very low tonnage of non-fish origin processed animal proteins that were imported from US into GB.
 
*** Overall, therefore, it is considered there is a greater than negligible risk that (non-ruminant) animal feed and pet food containing deer and/or elk protein is imported into GB. There is uncertainty associated with this estimate given the lack of data on the amount of deer and/or elk protein possibly being imported in these products.
 
SNIP...
 
 
Summary and MORE HERE ;
 
What is the risk of chronic wasting disease being introduced into Great Britain? An updated Qualitative Risk Assessment March 2016
 
 
I strenuously once again urge the FDA and its industry constituents, to make it MANDATORY that all ruminant feed be banned to all ruminants, and this should include all cervids, as well as non-ruminants such as cats and dogs as well, as soon as possible for the following reasons...
 
31 Jan 2015 at 20:14 GMT
 
*** Ruminant feed ban for cervids in the United States? ***
 
31 Jan 2015 at 20:14 GMT
 
see Singeltary comment ;
 
 
*** PLEASE SEE THIS URGENT UPDATE ON CWD AND FEED ANIMAL PROTEIN ***
 
Sunday, March 20, 2016
 
Docket No. FDA-2003-D-0432 (formerly 03D-0186) Use of Material from Deer and Elk in Animal Feed ***UPDATED MARCH 2016*** Singeltary Submission
 
 
Docket No. FDA-2003-D-0432 (formerly 03D-0186) Use of Material from Deer and Elk in Animal Feed Singeltary Submission
 
 
 
 
*** Docket No. APHIS-2007-0127 Scrapie in Sheep and Goats Terry Singeltary Sr. Submission ***
 
Monday, November 16, 2015
 
*** Docket No. APHIS-2007-0127 Scrapie in Sheep and Goats Terry Singeltary Sr. Submission ***
 
 
Draft Guidance for Industry on Ensuring Safety of Animal Feed Maintained and Fed On-Farm; Availability
 
# 203 entitled “Ensuring Safety of Animal Feed Maintained and Fed On-Farm.”
 
 
Terry S. Singeltary Sr. submission ;
 
 
Docket No. APHIS-2014-0107 Bovine Spongiform Encephalopathy; Importation of Animals and Animal Products Singeltary Submission
 
Posted: 12/30/2014ID: APHIS-2014-0107-0001
 
 
Notice: Environmental Impact Statements; Availability, etc.: Animal Carcass Management
 
Document ID: APHIS-2013-0044-0001 Docket ID: APHIS-2013-0044 Comment ID: APHIS-2013-0044-0002
 
 
(APHIS) Notice: Agency Information Collection Activities; Proposals, Submissions, and Approvals: Chronic Wasting Disease Herd Certification Program Agency Information Collection Activities; Proposals, Submissions, and Approvals: Chronic Wasting Disease Herd Certification Program (Document ID APHIS-2011-0032-0001)
 
 
*** Infectious agent of sheep scrapie may persist in the environment for at least 16 years ***
 
Gudmundur Georgsson1, Sigurdur Sigurdarson2 and Paul Brown3
 
 
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.
 
 
see ;
 
with CWD TSE Prions, I am not sure there is any absolute yet, other than what we know with transmission studies, and we know tse prion kill, and tse prion are bad. science shows to date, that indeed soil, dirt, some better than others, can act as a carrier. same with objects, farm furniture. take it with how ever many grains of salt you wish, or not. if load factor plays a role in the end formula, then everything should be on the table, in my opinion. see ;
 
***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.
 
 
see ;
 
 
Oral Transmissibility of Prion Disease Is Enhanced by Binding to Soil Particles
 
Author Summary
 
Transmissible spongiform encephalopathies (TSEs) are a group of incurable neurological diseases likely caused by a misfolded form of the prion protein. TSEs include scrapie in sheep, bovine spongiform encephalopathy (‘‘mad cow’’ disease) in cattle, chronic wasting disease in deer and elk, and Creutzfeldt-Jakob disease in humans. Scrapie and chronic wasting disease are unique among TSEs because they can be transmitted between animals, and the disease agents appear to persist in environments previously inhabited by infected animals. Soil has been hypothesized to act as a reservoir of infectivity and to bind the infectious agent. In the current study, we orally dosed experimental animals with a common clay mineral, montmorillonite, or whole soils laden with infectious prions, and compared the transmissibility to unbound agent. We found that prions bound to montmorillonite and whole soils remained orally infectious, and, in most cases, increased the oral transmission of disease compared to the unbound agent. The results presented in this study suggest that soil may contribute to environmental spread of TSEs by increasing the transmissibility of small amounts of infectious agent in the environment.
 
 
tse prion soil
 
 
 
 
 
Wednesday, December 16, 2015
 
Objects in contact with classical scrapie sheep act as a reservoir for scrapie transmission
 
 
The sources of dust borne prions are unknown but it seems reasonable to assume that faecal, urine, skin, parturient material and saliva-derived prions may contribute to this mobile environmental reservoir of infectivity. This work highlights a possible transmission route for scrapie within the farm environment, and this is likely to be paralleled in CWD which shows strong similarities with scrapie in terms of prion dissemination and disease transmission. The data indicate that the presence of scrapie prions in dust is likely to make the control of these diseases a considerable challenge.
 
 
>>>Particle-associated PrPTSE molecules may migrate from locations of deposition via transport processes affecting soil particles, including entrainment in and movement with air and overland flow. <<<
 
Fate of Prions in Soil: A Review
 
Christen B. Smith, Clarissa J. Booth, and Joel A. Pedersen*
 
Several reports have shown that prions can persist in soil for several years. Significant interest remains in developing methods that could be applied to degrade PrPTSE in naturally contaminated soils. Preliminary research suggests that serine proteases and the microbial consortia in stimulated soils and compost may partially degrade PrPTSE. Transition metal oxides in soil (viz. manganese oxide) may also mediate prion inactivation. Overall, the effect of prion attachment to soil particles on its persistence in the environment is not well understood, and additional study is needed to determine its implications on the environmental transmission of scrapie and CWD.
 
 
P.161: Prion soil binding may explain efficient horizontal CWD transmission
 
Conclusion. Silty clay loam exhibits highly efficient prion binding, inferring a durable environmental reservoir, and an efficient mechanism for indirect horizontal CWD transmission.
 
 
>>>Another alternative would be an absolute prohibition on the movement of deer within the state for any purpose. While this alternative would significantly reduce the potential spread of CWD, it would also have the simultaneous effect of preventing landowners and land managers from implementing popular management strategies involving the movement of deer, and would deprive deer breeders of the ability to engage in the business of buying and selling breeder deer. Therefore, this alternative was rejected because the department determined that it placed an avoidable burden on the regulated community.<<<
 
Wednesday, December 16, 2015
 
Objects in contact with classical scrapie sheep act as a reservoir for scrapie transmission
 
Objects in contact with classical scrapie sheep act as a reservoir for scrapie transmission
 
Timm Konold1*, Stephen A. C. Hawkins2, Lisa C. Thurston3, Ben C. Maddison4, Kevin C. Gough5, Anthony Duarte1 and Hugh A. Simmons1
 
1 Animal Sciences Unit, Animal and Plant Health Agency Weybridge, Addlestone, UK, 2 Pathology Department, Animal and Plant Health Agency Weybridge, Addlestone, UK, 3 Surveillance and Laboratory Services, Animal and Plant Health Agency Penrith, Penrith, UK, 4 ADAS UK, School of Veterinary Medicine and Science, University of Nottingham, Sutton Bonington, UK, 5 School of Veterinary Medicine and Science, University of Nottingham, Sutton Bonington, UK
 
Classical scrapie is an environmentally transmissible prion disease of sheep and goats. Prions can persist and remain potentially infectious in the environment for many years and thus pose a risk of infecting animals after re-stocking. In vitro studies using serial protein misfolding cyclic amplification (sPMCA) have suggested that objects on a scrapie affected sheep farm could contribute to disease transmission. This in vivo study aimed to determine the role of field furniture (water troughs, feeding troughs, fencing, and other objects that sheep may rub against) used by a scrapie-infected sheep flock as a vector for disease transmission to scrapie-free lambs with the prion protein genotype VRQ/VRQ, which is associated with high susceptibility to classical scrapie. When the field furniture was placed in clean accommodation, sheep became infected when exposed to either a water trough (four out of five) or to objects used for rubbing (four out of seven). This field furniture had been used by the scrapie-infected flock 8 weeks earlier and had previously been shown to harbor scrapie prions by sPMCA. Sheep also became infected (20 out of 23) through exposure to contaminated field furniture placed within pasture not used by scrapie-infected sheep for 40 months, even though swabs from this furniture tested negative by PMCA. This infection rate decreased (1 out of 12) on the same paddock after replacement with clean field furniture. Twelve grazing sheep exposed to field furniture not in contact with scrapie-infected sheep for 18 months remained scrapie free. The findings of this study highlight the role of field furniture used by scrapie-infected sheep to act as a reservoir for disease re-introduction although infectivity declines considerably if the field furniture has not been in contact with scrapie-infected sheep for several months. PMCA may not be as sensitive as VRQ/VRQ sheep to test for environmental contamination.
 
snip...
 
Discussion
 
Classical scrapie is an environmentally transmissible disease because it has been reported in naïve, supposedly previously unexposed sheep placed in pastures formerly occupied by scrapie-infected sheep (4, 19, 20). Although the vector for disease transmission is not known, soil is likely to be an important reservoir for prions (2) where – based on studies in rodents – prions can adhere to minerals as a biologically active form (21) and remain infectious for more than 2 years (22). Similarly, chronic wasting disease (CWD) has re-occurred in mule deer housed in paddocks used by infected deer 2 years earlier, which was assumed to be through foraging and soil consumption (23).
 
Our study suggested that the risk of acquiring scrapie infection was greater through exposure to contaminated wooden, plastic, and metal surfaces via water or food troughs, fencing, and hurdles than through grazing. Drinking from a water trough used by the scrapie flock was sufficient to cause infection in sheep in a clean building. Exposure to fences and other objects used for rubbing also led to infection, which supported the hypothesis that skin may be a vector for disease transmission (9). The risk of these objects to cause infection was further demonstrated when 87% of 23 sheep presented with PrPSc in lymphoid tissue after grazing on one of the paddocks, which contained metal hurdles, a metal lamb creep and a water trough in contact with the scrapie flock up to 8 weeks earlier, whereas no infection had been demonstrated previously in sheep grazing on this paddock, when equipped with new fencing and field furniture. When the contaminated furniture and fencing were removed, the infection rate dropped significantly to 8% of 12 sheep, with soil of the paddock as the most likely source of infection caused by shedding of prions from the scrapie-infected sheep in this paddock up to a week earlier.
 
This study also indicated that the level of contamination of field furniture sufficient to cause infection was dependent on two factors: stage of incubation period and time of last use by scrapie-infected sheep. Drinking from a water trough that had been used by scrapie sheep in the predominantly pre-clinical phase did not appear to cause infection, whereas infection was shown in sheep drinking from the water trough used by scrapie sheep in the later stage of the disease. It is possible that contamination occurred through shedding of prions in saliva, which may have contaminated the surface of the water trough and subsequently the water when it was refilled. Contamination appeared to be sufficient to cause infection only if the trough was in contact with sheep that included clinical cases. Indeed, there is an increased risk of bodily fluid infectivity with disease progression in scrapie (24) and CWD (25) based on PrPSc detection by sPMCA. Although ultraviolet light and heat under natural conditions do not inactivate prions (26), furniture in contact with the scrapie flock, which was assumed to be sufficiently contaminated to cause infection, did not act as vector for disease if not used for 18 months, which suggest that the weathering process alone was sufficient to inactivate prions.
 
PrPSc detection by sPMCA is increasingly used as a surrogate for infectivity measurements by bioassay in sheep or mice. In this reported study, however, the levels of PrPSc present in the environment were below the limit of detection of the sPMCA method, yet were still sufficient to cause infection of in-contact animals. In the present study, the outdoor objects were removed from the infected flock 8 weeks prior to sampling and were positive by sPMCA at very low levels (2 out of 37 reactions). As this sPMCA assay also yielded 2 positive reactions out of 139 in samples from the scrapie-free farm, the sPMCA assay could not detect PrPSc on any of the objects above the background of the assay. False positive reactions with sPMCA at a low frequency associated with de novo formation of infectious prions have been reported (27, 28). This is in contrast to our previous study where we demonstrated that outdoor objects that had been in contact with the scrapie-infected flock up to 20 days prior to sampling harbored PrPSc that was detectable by sPMCA analysis [4 out of 15 reactions (12)] and was significantly more positive by the assay compared to analogous samples from the scrapie-free farm. This discrepancy could be due to the use of a different sPMCA substrate between the studies that may alter the efficiency of amplification of the environmental PrPSc. In addition, the present study had a longer timeframe between the objects being in contact with the infected flock and sampling, which may affect the levels of extractable PrPSc. Alternatively, there may be potentially patchy contamination of this furniture with PrPSc, which may have been missed by swabbing. The failure of sPMCA to detect CWD-associated PrP in saliva from clinically affected deer despite confirmation of infectivity in saliva-inoculated transgenic mice was associated with as yet unidentified inhibitors in saliva (29), and it is possible that the sensitivity of sPMCA is affected by other substances in the tested material. In addition, sampling of amplifiable PrPSc and subsequent detection by sPMCA may be more difficult from furniture exposed to weather, which is supported by the observation that PrPSc was detected by sPMCA more frequently in indoor than outdoor furniture (12). A recent experimental study has demonstrated that repeated cycles of drying and wetting of prion-contaminated soil, equivalent to what is expected under natural weathering conditions, could reduce PMCA amplification efficiency and extend the incubation period in hamsters inoculated with soil samples (30). This seems to apply also to this study even though the reduction in infectivity was more dramatic in the sPMCA assays than in the sheep model. Sheep were not kept until clinical end-point, which would have enabled us to compare incubation periods, but the lack of infection in sheep exposed to furniture that had not been in contact with scrapie sheep for a longer time period supports the hypothesis that prion degradation and subsequent loss of infectivity occurs even under natural conditions.
 
In conclusion, the results in the current study indicate that removal of furniture that had been in contact with scrapie-infected animals should be recommended, particularly since cleaning and decontamination may not effectively remove scrapie infectivity (31), even though infectivity declines considerably if the pasture and the field furniture have not been in contact with scrapie-infected sheep for several months. As sPMCA failed to detect PrPSc in furniture that was subjected to weathering, even though exposure led to infection in sheep, this method may not always be reliable in predicting the risk of scrapie infection through environmental contamination. These results suggest that the VRQ/VRQ sheep model may be more sensitive than sPMCA for the detection of environmentally associated scrapie, and suggest that extremely low levels of scrapie contamination are able to cause infection in susceptible sheep genotypes.
 
Keywords: classical scrapie, prion, transmissible spongiform encephalopathy, sheep, field furniture, reservoir, serial protein misfolding cyclic amplification
 
 
Wednesday, December 16, 2015
 
*** Objects in contact with classical scrapie sheep act as a reservoir for scrapie transmission ***
 
 
*** Infectious agent of sheep scrapie may persist in the environment for at least 16 years ***
 
Gudmundur Georgsson1, Sigurdur Sigurdarson2 and Paul Brown3
 
 
Circulation of prions within dust on a scrapie affected farm
 
Kevin C Gough1, Claire A Baker2, Hugh A Simmons3, Steve A Hawkins3 and Ben C Maddison2*
 
Abstract
 
Prion diseases are fatal neurological disorders that affect humans and animals. Scrapie of sheep/goats and Chronic Wasting Disease (CWD) of deer/elk are contagious prion diseases where environmental reservoirs have a direct link to the transmission of disease. Using protein misfolding cyclic amplification we demonstrate that scrapie PrPSc can be detected within circulating dusts that are present on a farm that is naturally contaminated with sheep scrapie. The presence of infectious scrapie within airborne dusts may represent a possible route of infection and illustrates the difficulties that may be associated with the effective decontamination of such scrapie affected premises.
 
snip...
 
Discussion
 
We present biochemical data illustrating the airborne movement of scrapie containing material within a contaminated farm environment. We were able to detect scrapie PrPSc within extracts from dusts collected over a 70 day period, in the absence of any sheep activity. We were also able to detect scrapie PrPSc within dusts collected within pasture at 30 m but not at 60 m distance away from the scrapie contaminated buildings, suggesting that the chance of contamination of pasture by scrapie contaminated dusts decreases with distance from contaminated farm buildings. PrPSc amplification by sPMCA has been shown to correlate with infectivity and amplified products have been shown to be infectious [14,15]. These experiments illustrate the potential for low dose scrapie infectivity to be present within such samples. We estimate low ng levels of scrapie positive brain equivalent were deposited per m2 over 70 days, in a barn previously occupied by sheep affected with scrapie. This movement of dusts and the accumulation of low levels of scrapie infectivity within this environment may in part explain previous observations where despite stringent pen decontamination regimens healthy lambs still became scrapie infected after apparent exposure from their environment alone [16]. The presence of sPMCA seeding activity and by inference, infectious prions within dusts, and their potential for airborne dissemination is highly novel and may have implications for the spread of scrapie within infected premises. The low level circulation and accumulation of scrapie prion containing dust material within the farm environment will likely impede the efficient decontamination of such scrapie contaminated buildings unless all possible reservoirs of dust are removed. Scrapie containing dusts could possibly infect animals during feeding and drinking, and respiratory and conjunctival routes may also be involved. It has been demonstrated that scrapie can be efficiently transmitted via the nasal route in sheep [17], as is also the case for CWD in both murine models and in white tailed deer [18-20].
 
The sources of dust borne prions are unknown but it seems reasonable to assume that faecal, urine, skin, parturient material and saliva-derived prions may contribute to this mobile environmental reservoir of infectivity. This work highlights a possible transmission route for scrapie within the farm environment, and this is likely to be paralleled in CWD which shows strong similarities with scrapie in terms of prion dissemination and disease transmission. The data indicate that the presence of scrapie prions in dust is likely to make the control of these diseases a considerable challenge.
 
 
Saturday, May 28, 2016
 
*** Infection and detection of PrPCWD in soil from CWD infected farm in Korea Prion 2016 Tokyo ***
 
 
CHRONIC WASTING DISEASE TSE PRION
 
PRION 2016 TOKYO
 
Zoonotic Potential of CWD Prions: An Update
 
Ignazio Cali1, Liuting Qing1, Jue Yuan1, Shenghai Huang2, Diane Kofskey1,3, Nicholas Maurer1, Debbie McKenzie4, Jiri Safar1,3,5, Wenquan Zou1,3,5,6, Pierluigi Gambetti1, Qingzhong Kong1,5,6
 
1Department of Pathology, 3National Prion Disease Pathology Surveillance Center, 5Department of Neurology, 6National Center for Regenerative Medicine, Case Western Reserve University, Cleveland, OH 44106, USA.
 
4Department of Biological Sciences and Center for Prions and Protein Folding Diseases, University of Alberta, Edmonton, Alberta, Canada,
 
2Encore Health Resources, 1331 Lamar St, Houston, TX 77010
 
Chronic wasting disease (CWD) is a widespread and highly transmissible prion disease in free-ranging and captive cervid species in North America. The zoonotic potential of CWD prions is a serious public health concern, but the susceptibility of human CNS and peripheral organs to CWD prions remains largely unresolved. We reported earlier that peripheral and CNS infections were detected in transgenic mice expressing human PrP129M or PrP129V. Here we will present an update on this project, including evidence for strain dependence and influence of cervid PrP polymorphisms on CWD zoonosis as well as the characteristics of experimental human CWD prions.
 
PRION 2016 TOKYO
 
In Conjunction with Asia Pacific Prion Symposium 2016
 
PRION 2016 Tokyo
 
Prion 2016
 
 
Prion 2016
 
Purchase options Price * Issue Purchase USD 198.00
 
 
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
 
Institution
 
Name Case Western Reserve University
 
Department Pathology
 
Type Schools of Medicine
 
DUNS # 077758407
 
City Cleveland
 
State OH
 
Country United States
 
Zip Code 44106
 
 
===========================================================
 
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.
 
============================================================
 
Key Molecular Mechanisms of TSEs
 
Zabel, Mark D.
 
Colorado State University-Fort Collins, Fort Collins, CO, United States Abstract Prion diseases, or transmissible spongiform encephalopathies (TSEs), are fatal neurodegenerative diseases affecting humans, cervids, bovids, and ovids. The absolute requirement of PrPC expression to generate prion diseases and the lack of instructional nucleic acid define prions as unique infectious agents. Prions exhibit species-specific tropism, inferring that unique prion strains exist that preferentially infct certain host species and confront transmission barriers to heterologous host species. However, transmission barriers are not absolute. Scientific consensus agrees that the sheep TSE scrapie probably breached the transmission barrier to cattle causing bovine spongiform encephalopathy that subsequently breached the human transmission barrier and likely caused several hundred deaths by a new-variant form of the human TSE Creutzfeldt-Jakob disease in the UK and Europe. The impact to human health, emotion and economies can still be felt in areas like farming, blood and organ donations and the threat of a latent TSE epidemic. This precedent raises the real possibility of other TSEs, like chronic wasting disease of cervids, overcoming similar human transmission barriers. A groundbreaking discovery made last year revealed that mice infected with heterologous prion strains facing significant transmission barriers replicated prions far more readily in spleens than brains6. Furthermore, these splenic prions exhibited weakened transmission barriers and expanded host ranges compared to neurogenic prions. These data question conventional wisdom of avoiding neural tissue to avoid prion xenotransmission, when more promiscuous prions may lurk in extraneural tissues. Data derived from work previously funded by NIH demonstrate that Complement receptors CD21/35 bind prions and high density PrPC and differentially impact prion disease depending on the prion isolate or strain used. Recent advances in live animal and whole organ imaging have led us to generate preliminary data to support novel, innovative approaches to assessing prion capture and transport. We plan to test our unifying hypothesis for this proposal that CD21/35 control the processes of peripheral prion capture, transport, strain selection and xenotransmission in the following specific aims.
 
1. Assess the role of CD21/35 in splenic prion strain selection and host range expansion.
 
2. Determine whether CD21/35 and C1q differentially bind distinct prion strains
 
3. Monitor the effects of CD21/35 on prion trafficking in real time and space
 
4. Assess the role of CD21/35 in incunabular prion trafficking
 
Public Health Relevance Transmissible spongiform encephalopathies, or prion diseases, are devastating illnesses that greatly impact public health, agriculture and wildlife in North America and around the world. The impact to human health, emotion and economies can still be felt in areas like farming, blood and organ donations and the threat of a latent TSE epidemic. This precedent raises the real possibility of other TSEs, like chronic wasting disease (CWD) of cervids, overcoming similar human transmission barriers. Early this year Canada reported its first case of BSE in over a decade audits first case of CWD in farmed elk in three years, underscoring the need for continued vigilance and research. Identifying mechanisms of transmission and zoonoses remains an extremely important and intense area of research that will benefit human and other animal populations.
 
Funding Agency Agency National Institute of Health (NIH)
 
Institute National Institute of Allergy and Infectious Diseases (NIAID)
 
Type High Priority, Short Term Project Award (R56)
 
Project # 1R56AI122273-01A1
 
Application # 9211114
 
Study Section Cellular and Molecular Biology of Neurodegeneration Study Section (CMND)
 
Program Officer Beisel, Christopher E
 
Project Start 2016-02-16
 
Project End 2017-01-31
 
Budget Start 2016-02-16
 
Budget End 2017-01-31
 
Support Year 1
 
Fiscal Year 2016
 
Total Cost
 
Indirect Cost Institution Name Colorado State University-Fort Collins
 
Department Microbiology/Immun/Virology
 
Type Schools of Veterinary Medicine
 
DUNS # 785979618 City Fort Collins
 
State CO
 
Country United States
 
Zip Code 80523
 
 
PMCA Detection of CWD Infection in Cervid and Non-Cervid Species
 
Hoover, Edward Arthur
 
Colorado State University-Fort Collins, Fort Collins, CO, United States Abstract Chronic wasting disease (CWD) of deer and elk is an emerging highly transmissible prion disease now recognized in 18 States, 2 Canadian provinces, and Korea. We have shown that Infected deer harbor and shed high levels of infectious prions in saliva, blood, urine, and feces, and in the tissues generating those body fluids and excreta, thereby leading to facile transmission by direct contact and environmental contamination. We have also shown that CWD can infect some non-cervid species, thus the potential risk CWD represents to domestic animal species and to humans remains unknown. Whether prions borne in blood, saliva, nasal fluids, milk, or excreta are generated or modified in the proximate peripheral tissue sites, may differ in subtle ways from those generated in brain, or may be adapted for mucosal infection remain open questions. The increasing parallels in the pathogenesis between prion diseases and human neurodegenerative conditions, such as Alzheimer's and Parkinson's diseases, add relevance to CWD as a transmissible protein misfolding disease. The overall goal of this work is to elucidate the process of CWD prion transmission from mucosal secretory and excretory tissue sites by addressing these questions: (a) What are the kinetics and magnitude of CWD prion shedding post-exposure? (b) Are excreted prions biochemically distinct, or not, from those in the CNS? (c) Are peripheral epithelial or CNS tissues, or both, the source of excreted prions? and (d) Are excreted prions adapted for horizontal transmission via natural/trans-mucosal routes? The specific aims of this proposal are: (1) To determine the onset and consistency of CWD prion shedding in deer and cervidized mice; (2); To compare the biochemical and biophysical properties of excretory vs. CNS prions; (3) To determine the capacity of peripheral tissues to support replication of CWD prions; (4) To determine the protease- sensitive infectious fraction of excreted vs. CNS prions; and (5) To compare the mucosal infectivity of excretory vs. CNS prions. Understanding the mechanisms that enable efficient prion dissemination and shedding will help elucidate how horizontally transmissible prions evolve and succeed, and is the basis of this proposal. Understanding how infectious misfolded proteins (prions) are generated, trafficked, shed, and transmitted will aid in preventing, treating, and managing the risks associated with these agents and the diseases they cause.
 
Public Health Relevance Chronic wasting disease (CWD) of deer and elk is an emergent highly transmissible prion disease now recognized throughout the USA as well as in Canada and Korea. We have shown that infected deer harbor and shed high levels of infectious prions in saliva, blood, urine, and feces thereby leading to transmission by direct contact and environmental contamination. In that our studies have also shown that CWD can infect some non-cervid species, the potential risk CWD may represents to domestic animal species and humans remains unknown. The increasing parallels in the development of major human neurodegenerative conditions, such as Alzheimer's and Parkinson's diseases, and prion diseases add relevance to CWD as a model of a transmissible protein misfolding disease. Understanding how infectious misfolded proteins (prions) are generated and transmitted will aid in interrupting, treating, and managing the risks associated with these agents and the diseases they cause.
 
Funding Agency Agency National Institute of Health (NIH)
 
Institute National Institute of Neurological Disorders and Stroke (NINDS)
 
Type Research Project (R01)
 
Project # 4R01NS061902-07
 
Application # 9010980
 
Study Section Cellular and Molecular Biology of Neurodegeneration Study Section (CMND)
 
Program Officer Wong, May Project Start 2009-09-30
 
Project End 2018-02-28
 
Budget Start 2016-03-01
 
Budget End 2017-02-28
 
Support Year 7
 
Fiscal Year 2016
 
Total Cost $409,868
 
Indirect Cost $134,234 Institution Name Colorado State University-Fort Collins
 
Department Microbiology/Immun/Virology
 
Type Schools of Veterinary Medicine
 
DUNS # 785979618 City Fort Collins
 
State CO
 
Country United States
 
Zip Code 80523
 
 
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).***
 
 
PRION 2015 CONFERENCE FT. COLLINS CWD RISK FACTORS TO HUMANS
 
*** LATE-BREAKING ABSTRACTS PRION 2015 CONFERENCE ***
 
O18
 
Zoonotic Potential of CWD Prions
 
Liuting Qing1, Ignazio Cali1,2, Jue Yuan1, Shenghai Huang3, Diane Kofskey1, Pierluigi Gambetti1, Wenquan Zou1, Qingzhong Kong1 1Case Western Reserve University, Cleveland, Ohio, USA, 2Second University of Naples, Naples, Italy, 3Encore Health Resources, Houston, Texas, USA
 
*** These results indicate that the CWD prion has the potential to infect human CNS and peripheral lymphoid tissues and that there might be asymptomatic human carriers of CWD infection.
 
==================
 
***These results indicate that the CWD prion has the potential to infect human CNS and peripheral lymphoid tissues and that there might be asymptomatic human carriers of CWD infection.***
 
==================
 
P.105: RT-QuIC models trans-species prion transmission
 
Kristen Davenport, Davin Henderson, Candace Mathiason, and Edward Hoover Prion Research Center; Colorado State University; Fort Collins, CO USA
 
Conversely, FSE maintained sufficient BSE characteristics to more efficiently convert bovine rPrP than feline rPrP. Additionally, human rPrP was competent for conversion by CWD and fCWD.
 
***This insinuates that, at the level of protein:protein interactions, the barrier preventing transmission of CWD to humans is less robust than previously estimated.
 
================
 
***This insinuates that, at the level of protein:protein interactions, the barrier preventing transmission of CWD to humans is less robust than previously estimated.***
 
================
 
 
*** PRICE OF CWD TSE PRION POKER GOES UP 2014 ***
 
Transmissible Spongiform Encephalopathy TSE PRION update January 2, 2014
 
*** chronic wasting disease, there was no absolute barrier to conversion of the human prion protein.
 
*** Furthermore, the form of human PrPres produced in this in vitro assay when seeded with CWD, resembles that found in the most common human prion disease, namely sCJD of the MM1 subtype.
 
 
 
*** 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).***
 
 
*** The potential impact of prion diseases on human health was greatly magnified by the recognition that interspecies transfer of BSE to humans by beef ingestion resulted in vCJD. While changes in animal feed constituents and slaughter practices appear to have curtailed vCJD, there is concern that CWD of free-ranging deer and elk in the U.S. might also cross the species barrier. Thus, consuming venison could be a source of human prion disease. Whether BSE and CWD represent interspecies scrapie transfer or are newly arisen prion diseases is unknown. Therefore, the possibility of transmission of prion disease through other food animals cannot be ruled out. There is evidence that vCJD can be transmitted through blood transfusion. There is likely a pool of unknown size of asymptomatic individuals infected with vCJD, and there may be asymptomatic individuals infected with the CWD equivalent. These circumstances represent a potential threat to blood, blood products, and plasma supplies.
 
 
***********CJD REPORT 1994 increased risk for consumption of veal and venison and lamb***********
 
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 ;
 
 
CJD9/10022
 
October 1994
 
Mr R.N. Elmhirst Chairman British Deer Farmers Association Holly Lodge Spencers Lane BerksWell Coventry CV7 7BZ
 
Dear Mr Elmhirst,
 
CREUTZFELDT-JAKOB DISEASE (CJD) SURVEILLANCE UNIT REPORT
 
Thank you for your recent letter concerning the publication of the third annual report from the CJD Surveillance Unit. I am sorry that you are dissatisfied with the way in which this report was published.
 
The Surveillance Unit is a completely independant outside body and the Department of Health is committed to publishing their reports as soon as they become available. In the circumstances it is not the practice to circulate the report for comment since the findings of the report would not be amended. In future we can ensure that the British Deer Farmers Association receives a copy of the report in advance of publication.
 
The Chief Medical Officer has undertaken to keep the public fully informed of the results of any research in respect of CJD. This report was entirely the work of the unit and was produced completely independantly of the the Department.
 
The statistical results reqarding the consumption of venison was put into perspective in the body of the report and was not mentioned at all in the press release. Media attention regarding this report was low key but gave a realistic presentation of the statistical findings of the Unit. This approach to publication was successful in that consumption of venison was highlighted only once by the media ie. in the News at one television proqramme.
 
I believe that a further statement about the report, or indeed statistical links between CJD and consumption of venison, would increase, and quite possibly give damaging credence, to the whole issue. From the low key media reports of which I am aware it seems unlikely that venison consumption will suffer adversely, if at all.
 
 
Monday, May 02, 2016
 
*** Zoonotic Potential of CWD Prions: An Update Prion 2016 Tokyo ***
 
 
*** PRION 2014 CONFERENCE CHRONIC WASTING DISEASE CWD
 
 
*** PPo3-7: Prion Transmission from Cervids to Humans is Strain-dependent
 
*** Here we report that a human prion strain that had adopted the cervid prion protein (PrP) sequence through passage in cervidized transgenic mice efficiently infected transgenic mice expressing human PrP,
 
*** indicating that the species barrier from cervid to humans is prion strain-dependent and humans can be vulnerable to novel cervid prion strains.
 
PPo2-27:
 
Generation of a Novel form of Human PrPSc by Inter-species Transmission of Cervid Prions
 
*** Our findings suggest that CWD prions have the capability to infect humans, and that this ability depends on CWD strain adaptation, implying that the risk for human health progressively increases with the spread of CWD among cervids.
 
PPo2-7:
 
Biochemical and Biophysical Characterization of Different CWD Isolates
 
*** The data presented here substantiate and expand previous reports on the existence of different CWD strains.
 
 
Envt.07:
 
Pathological Prion Protein (PrPTSE) in Skeletal Muscles of Farmed and Free Ranging White-Tailed Deer Infected with Chronic Wasting Disease
 
***The presence and seeding activity of PrPTSE in skeletal muscle from CWD-infected cervids suggests prevention of such tissue in the human diet as a precautionary measure for food safety, pending on further clarification of whether CWD may be transmissible to humans.
 
 
>>>CHRONIC WASTING DISEASE , THERE WAS NO ABSOLUTE BARRIER TO CONVERSION OF THE HUMAN PRION PROTEIN<<<
 
*** PRICE OF CWD TSE PRION POKER GOES UP 2014 ***
 
Transmissible Spongiform Encephalopathy TSE PRION update January 2, 2014
 
Wednesday, January 01, 2014
 
Molecular Barriers to Zoonotic Transmission of Prions
 
*** chronic wasting disease, there was no absolute barrier to conversion of the human prion protein.
 
*** Furthermore, the form of human PrPres produced in this in vitro assay when seeded with CWD, resembles that found in the most common human prion disease, namely sCJD of the MM1 subtype.
 
 
 
*** 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 (216-119-163-189.ipset45.wt.net)
 
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
 
To: rr26k@nih.gov; rrace@niaid.nih.gov; ebb8@CDC.GOV
 
Subject: TO CDC AND NIH - PUB MED- 3 MORE DEATHS - CWD - YOUNG HUNTERS
 
Sunday, November 10, 2002 6:26 PM ......snip........end..............TSS
 
Thursday, April 03, 2008
 
A prion disease of cervids: Chronic wasting disease 2008 1: Vet Res. 2008 Apr 3;39(4):41 A prion disease of cervids: Chronic wasting disease Sigurdson CJ.
 
snip...
 
*** twenty-seven CJD patients who regularly consumed venison were reported to the Surveillance Center***,
 
snip... full text ;
 
 
Monday, May 02, 2016
 
*** Zoonotic Potential of CWD Prions: An Update Prion 2016 Tokyo ***
 
 
*** NIH awards $11 million to UTHealth researchers to study deadly CWD prion diseases Claudio Soto, Ph.D. ***
 
Public Release: 29-Jun-2016
 
 
I urge everyone to watch this video closely...terry
 
*** you can see video here and interview with Jeff's Mom, and scientist telling you to test everything and potential risk factors for humans ***
 
 
Tuesday, July 12, 2016
 
Chronic Wasting Disease CWD, Scrapie, Bovine Spongiform Encephalopathy BSE, TSE, Prion Zoonosis Science History
 
see history of NIH may destroy human brain collection
 
 
Monday, August 22, 2016
 
CREUTZFELDT JAKOB DISEASE USA 2015 SPORADIC CJD TOTAL FIGURES REACHES HIGHEST ANNUAL COUNT TO DATE AT 239 CONFIRMED CASES
 
 
Prion. 10:S15-S21. 2016 ISSN: 1933-6896 printl 1933-690X online
 
Taylor & Francis
 
Prion 2016 Animal Prion Disease Workshop Abstracts
 
WS-01: Prion diseases in animals and zoonotic potential
 
Juan Maria Torres a, Olivier Andreoletti b, J uan-Carlos Espinosa a. Vincent Beringue c. Patricia Aguilar a,
 
Natalia Fernandez-Borges a. and Alba Marin-Moreno a
 
"Centro de Investigacion en Sanidad Animal ( CISA-INIA ). Valdeolmos, Madrid. Spain; b UMR INRA -ENVT 1225 Interactions Holes Agents Pathogenes. ENVT. Toulouse. France: "UR892. Virologie lmmunologie MolécuIaires, Jouy-en-Josas. France
 
Dietary exposure to bovine spongiform encephalopathy (BSE) contaminated bovine tissues is considered as the origin of variant Creutzfeldt Jakob (vCJD) disease in human. To date, BSE agent is the only recognized zoonotic prion. Despite the variety of Transmissible Spongiform Encephalopathy (TSE) agents that have been circulating for centuries in farmed ruminants there is no apparent epidemiological link between exposure to ruminant products and the occurrence of other form of TSE in human like sporadic Creutzfeldt Jakob Disease (sCJD). However, the zoonotic potential of the diversity of circulating TSE agents has never been systematically assessed. The major issue in experimental assessment of TSEs zoonotic potential lies in the modeling of the ‘species barrier‘, the biological phenomenon that limits TSE agents’ propagation from a species to another. In the last decade, mice genetically engineered to express normal forms of the human prion protein has proved essential in studying human prions pathogenesis and modeling the capacity of TSEs to cross the human species barrier.
 
To assess the zoonotic potential of prions circulating in farmed ruminants, we study their transmission ability in transgenic mice expressing human PrPC (HuPrP-Tg). Two lines of mice expressing different forms of the human PrPC (129Met or 129Val) are used to determine the role of the Met129Val dimorphism in susceptibility/resistance to the different agents.
 
These transmission experiments confirm the ability of BSE prions to propagate in 129M- HuPrP-Tg mice and demonstrate that Met129 homozygotes may be susceptible to BSE in sheep or goat to a greater degree than the BSE agent in cattle and that these agents can convey molecular properties and neuropathological indistinguishable from vCJD. However homozygous 129V mice are resistant to all tested BSE derived prions independently of the originating species suggesting a higher transmission barrier for 129V-PrP variant.
 
Transmission data also revealed that several scrapie prions propagate in HuPrP-Tg mice with efficiency comparable to that of cattle BSE. While the efficiency of transmission at primary passage was low, subsequent passages resulted in a highly virulent prion disease in both Met129 and Val129 mice. Transmission of the different scrapie isolates in these mice leads to the emergence of prion strain phenotypes that showed similar characteristics to those displayed by MM1 or VV2 sCJD prion. These results demonstrate that scrapie prions have a zoonotic potential and raise new questions about the possible link between animal and human prions.
 
 
 
SCRAPIE AND CWD ZOONOSIS
 
PRION 2016 CONFERENCE TOKYO
 
Saturday, April 23, 2016
 
*** SCRAPIE WS-01: Prion diseases in animals and zoonotic potential 2016 ***
 
Prion. 10:S15-S21. 2016 ISSN: 1933-6896 printl 1933-690X
 
 
Transmission of scrapie prions to primate after an extended silent incubation period
 
***Moreover, sporadic disease has never been observed in breeding colonies or primate research laboratories, most notably among hundreds of animals over several decades of study at the National Institutes of Health25, and in nearly twenty older animals continuously housed in our own facility.***
 
 
Wednesday, June 29, 2016
 
CWD, SCRAPIE, ZOONOSIS, it’s for real folks, the risk factors have increased greatly, and science has spoken, cwd and scrapie to humans as sporadic cjd may have already happened.
 
Transmission of scrapie prions to primate after an extended silent incubation period
 
Emmanuel E. Comoy , Jacqueline Mikol , Sophie Luccantoni-Freire , Evelyne Correia , Nathalie Lescoutra-Etchegaray , Valérie Durand , Capucine Dehen , Olivier Andreoletti , Cristina Casalone , Juergen A. Richt , Justin J. Greenlee , Thierry Baron , Sylvie L. Benestad , Paul Brown & Jean-Philippe Deslys
 
Abstract
 
Classical bovine spongiform encephalopathy (c-BSE) is the only animal prion disease reputed to be zoonotic, causing variant Creutzfeldt-Jakob disease (vCJD) in humans and having guided protective measures for animal and human health against animal prion diseases. Recently, partial transmissions to humanized mice showed that the zoonotic potential of scrapie might be similar to c-BSE. We here report the direct transmission of a natural classical scrapie isolate to cynomolgus macaque, a highly relevant model for human prion diseases, after a 10-year silent incubation period, with features similar to those reported for human cases of sporadic CJD. Scrapie is thus actually transmissible to primates with incubation periods compatible with their life expectancy, although fourfold longer than BSE. Long-term experimental transmission studies are necessary to better assess the zoonotic potential of other prion diseases with high prevalence, notably Chronic Wasting Disease of deer and elk and atypical/Nor98 scrapie.
 
snip...
 
In addition to previous studies on scrapie transmission to primate1,8,9 and the recently published study on transgenic humanized mice13, our results constitute new evidence for recommending that the potential risk of scrapie for human health should not be dismissed. Indeed, human PrP transgenic mice and primates are the most relevant models for investigating the human transmission barrier. To what extent such models are informative for measuring the zoonotic potential of an animal TSE under field exposure conditions is unknown. During the past decades, many protective measures have been successfully implemented to protect cattle from the spread of c-BSE, and some of these measures have been extended to sheep and goats to protect from scrapie according to the principle of precaution. Since cases of c-BSE have greatly reduced in number, those protective measures are currently being challenged and relaxed in the absence of other known zoonotic animal prion disease. We recommend that risk managers should be aware of the long term potential risk to human health of at least certain scrapie isolates, notably for lymphotropic strains like the classical scrapie strain used in the current study. Relatively high amounts of infectivity in peripheral lymphoid organs in animals infected with these strains could lead to contamination of food products produced for human consumption. Efforts should also be maintained to further assess the zoonotic potential of other animal prion strains in long-term studies, notably lymphotropic strains with high prevalence like CWD, which is spreading across North America, and atypical/Nor98 scrapie (Nor98)50 that was first detected in the past two decades and now represents approximately half of all reported cases of prion diseases in small ruminants worldwide, including territories previously considered as scrapie free. Even if the prevailing view is that sporadic CJD is due to the spontaneous formation of CJD prions, it remains possible that its apparent sporadic nature may, at least in part, result from our limited capacity to identify an environmental origin.
 
***Moreover, sporadic disease has never been observed in breeding colonies or primate research laboratories, most notably among hundreds of animals over several decades of study at the National Institutes of Health25, and in nearly twenty older animals continuously housed in our own facility.***
 
 
 
2015
 
O.05: Transmission of prions to primates after extended silent incubation periods: Implications for BSE and scrapie risk assessment in human populations
 
Emmanuel Comoy, Jacqueline Mikol, Valerie Durand, Sophie Luccantoni, Evelyne Correia, Nathalie Lescoutra, Capucine Dehen, and Jean-Philippe Deslys Atomic Energy Commission; Fontenay-aux-Roses, France
 
Prion diseases (PD) are the unique neurodegenerative proteinopathies reputed to be transmissible under field conditions since decades. The transmission of Bovine Spongiform Encephalopathy (BSE) to humans evidenced that an animal PD might be zoonotic under appropriate conditions. Contrarily, in the absence of obvious (epidemiological or experimental) elements supporting a transmission or genetic predispositions, PD, like the other proteinopathies, are reputed to occur spontaneously (atpical animal prion strains, sporadic CJD summing 80% of human prion cases). Non-human primate models provided the first evidences supporting the transmissibiity of human prion strains and the zoonotic potential of BSE. Among them, cynomolgus macaques brought major information for BSE risk assessment for human health (Chen, 2014), according to their phylogenetic proximity to humans and extended lifetime. We used this model to assess the zoonotic potential of other animal PD from bovine, ovine and cervid origins even after very long silent incubation periods.
 
*** We recently observed the direct transmission of a natural classical scrapie isolate to macaque after a 10-year silent incubation period,
 
***with features similar to some reported for human cases of sporadic CJD, albeit requiring fourfold long incubation than BSE. Scrapie, as recently evoked in humanized mice (Cassard, 2014),
 
***is the third potentially zoonotic PD (with BSE and L-type BSE),
 
***thus questioning the origin of human sporadic cases. We will present an updated panorama of our different transmission studies and discuss the implications of such extended incubation periods on risk assessment of animal PD for human health.
 
===============
 
***thus questioning the origin of human sporadic cases***
 
===============
 
***our findings suggest that possible transmission risk of H-type BSE to sheep and human. Bioassay will be required to determine whether the PMCA products are infectious to these animals.
 
==============
 
 
*** Infectious agent of sheep scrapie may persist in the environment for at least 16 years ***
 
Gudmundur Georgsson1, Sigurdur Sigurdarson2 and Paul Brown3
 
 
***Moreover, sporadic disease has never been observed in breeding colonies or primate research laboratories, most notably among hundreds of animals over several decades of study at the National Institutes of Health25, and in nearly twenty older animals continuously housed in our own facility.***
 
 
Thursday, August 18, 2016
 
PROCEEDINGS ONE HUNDRED AND Nineteenth ANNUAL MEETING of the USAHA BSE, CWD, SCRAPIE, PORCINE TSE PRION October 22 28, 2015
 
 
Sunday, July 17, 2016
 
West Virginia Chronic Wasting Disease CWD has been found in 195 white-tailed deer As of June 2016
 
 
Sunday, July 17, 2016
 
Virginia Chronic Wasting Disease CWD As of March 2016 has diagnosed 13 CWD-positive white-tailed deer
 
 
Wednesday, August 10, 2016
 
Arkansas Chronic Wasting Disease CWD TSE Prion Potentially Trucked in from Missouri, what about Florida and ?
 
 
Friday, June 24, 2016
 
Arkansas AGFC passes special regulations to slow disease CWD TSE PRION
 
 
Tuesday, May 03, 2016
 
Arkansas Chronic Wasting Disease CWD TSE Prion and Elk Restoration Project and Hunkering Down in the BSE Situation Room USDA 1998
 
 
Tuesday, April 19, 2016
 
Arkansas First Phase of CWD sampling reveals 23 percent prevalence rate in focal area With 82 Confirmed to Date
 
 
Friday, August 05, 2016
 
MINNESOTA CHRONIC WASTING DISEASE SURVEILLANCE AND TESTING CWD TSE PRION UPDATE
 
 
Thursday, April 14, 2016
 
Louisiana Chronic Wasting Disease CWD TSE Prion Surveillance and Testing Program?
 
 
Tuesday, July 12, 2016
 
Colorado Chronic Wasting Disease CWD TSE Prion discovered in one deer in Montrose County
 
 
Friday, April 22, 2016
 
COLORADO CHRONIC WASTING DISEASE CWD TSE PRION SURVEILLANCE AND TESTING PROGRAM IS MINIMAL AND LIMITED
 
*** SEE CWD HIGH INFECTION RATE MAPS FOR COLORADO ! ***
 
 
Monday, May 16, 2016
 
Governor Walker Announces Several Initiatives to Combat Chronic Wasting Disease in Wisconsin
 
DAY LATE, DOLLAR SHORT!
 
 
Sunday, May 08, 2016
 
WISCONSIN CHRONIC WASTING DISEASE CWD TSE PRION SPIRALING FURTHER INTO THE ABYSS UPDATE
 
 
Wednesday, March 16, 2016
 
Wisconsin CWD sample survey 2015 confirms 290 cases of Chronic Wasting Disease TSE Prion
 
 
Wednesday, February 10, 2016
 
*** Wisconsin Two deer that escaped farm had chronic wasting disease CWD ***
 
 
Sunday, January 17, 2016
 
*** Wisconsin Captive CWD Lotto Pays Out Again indemnity payment of $298,770 for 228 white-tailed deer killed on farm ***
 
 
Wednesday, March 30, 2016
 
ARIZONA CHRONIC WASTING DISEASE CWD TSE PRION SURVEILLANCE AND TESTING PROGRAM
 
 
Tuesday, March 29, 2016
 
ALABAMA CHRONIC WASTING DISEASE CWD TSE PRION SURVEILLANCE AND TESTING PROGRAM?
 
 
Tuesday, March 29, 2016
 
Maryland Department of Natural Resources Five Deer Test Positive for Chronic Wasting Disease ONE OUTSIDE CWD MANAGEMENT ZONE
 
 
Tuesday, May 03, 2016
 
Wednesday, May 11, 2016
 
PENNSYLVANIA TWELVE MORE CASES OF CWD FOUND: STATE GEARS UP FOR ADDITIONAL CONTROL MEASURES
 
 
Friday, February 26, 2016
 
Pennsylvania Monitoring the Growing Threat of Chronic Wasting Disease CWD TSE Prion
 
 
Friday, April 22, 2016
 
Missouri MDC finds seven new cases of ChronicWasting Disease CWD during past‐season testing
 
 
Sunday, March 06, 2016
 
Missouri 2015-2016 CWD Surveillance Summary to Date, with confirmed cases mounting
 
 
KANSAS CWD CASES ALARMING
 
Wednesday, March 02, 2016 Kansas Chronic Wasting Disease CWD TSE Prion 52 cases 2015 updated report 'ALARMING'
 
 
Tuesday, February 02, 2016
 
Illinois six out of 19 deer samples tested positive for CWD in the Oswego zone of Kendall County
 
 
Wednesday, April 20, 2016
 
UTAH CHRONIC WASTING DISEASE CWD TSE PRION SURVEILLANCE AND TESTING PROGRAM 70 mule deer and two elk have tested positive
 
 
Tuesday, June 07, 2016
 
Wyoming For the first time in several years an ungulate has tested positive for Chronic Wasting Disease (CWD) on the west side of the continental divide
 
 
Wednesday, April 27, 2016
 
WYOMING GAME AND FISH DEPARTMENT CHRONIC WASTING DISEASE MANAGEMENT PLAN APRIL 22, 2016
 
 
Thursday, March 10, 2016
 
WYOMING RIDE EM COWBOY HELICOPTER WRANGLING RAMBO STYLE DEER BULLDOGGING RODEO FOR CWD VIDEO
 
CHRONIC WASTING DISEASE: The Final Epidemic
 
 
Tuesday, March 08, 2016
 
Oklahoma Chronic Wasting Disease CWD of Deer and Elk Surveillance, Testing, and Preparedness ???
 
 
Tuesday, July 05, 2016
 
Michigan DNR announces expansion of Chronic Wasting Disease Core Area and Management Zone
 
 
Friday, March 18, 2016
 
Michigan confirms additional CWD-positive free-ranging, white-tailed deer, bringing the total to seven
 
 
Friday, July 29, 2016
 
IOWA CHRONIC WASTING DISEASE CWD TSE PRION TOTAL TO DATE 304 CASES WILD AND CAPTIVE REPORT UPDATE JULY 2016
 
 
Friday, February 05, 2016
 
IOWA Two Wild Deer Test Positive for Chronic Wasting Disease in Allamakee County
 
 
Friday, January 29, 2016
 
NEBRASKA Three Positives for CWD Found in Recent Testing of Deer
 
 
Friday, November 20, 2015
 
ODNR Takes Action to Monitor Chronic Wasting Disease in Ohio's Deer Herd
 
 
Friday, October 23, 2015
 
Ohio Wildlife Council Passes Rule to Help Monitor CWD
 
 
Wednesday, August 05, 2015
 
Ohio confirms to me Chronic Wasting Disease CWD Spreads 19 confirmed cases to date
 
 
Wednesday, February 11, 2015
 
World Class Whitetails quarantined CWD deer Daniel M. Yoder charged with two counts of tampering with evidence
 
 
Thursday, October 23, 2014
 
*** FIRST CASE OF CHRONIC WASTING DISEASE CONFIRMED IN OHIO ON PRIVATE PRESERVE
 
 
Monday, June 11, 2012
 
*** OHIO Captive deer escapees and non-reporting ***
 
 
Tuesday, August 02, 2016
 
Chronic wasting disease of deer – is the battle to keep Europe free already lost?
 
 
Tuesday, April 12, 2016
 
The first detection of Chronic Wasting Disease (CWD) in Europe free-ranging reindeer from the Nordfjella population in South-Norway.
 
 
Tuesday, June 14, 2016
 
*** Chronic Wasting Disease (CWD) in a moose from Selbu in Sør-Trøndelag Norway ***
 
 
Thursday, July 07, 2016
 
Norway reports a third case Chronic Wasting Disease CWD TSE Prion in 2nd Norwegian moose
 
14/06/2016 - Norway reports a third case
 
 
Saturday, July 16, 2016
 
Chronic wasting Disease in Deer (CWD or Spongiform Encephalopathy) The British Deer Society 07/04/2016
 
Red Deer Ataxia or Chronic Wasting Disease CWD TSE PRION?
 
could this have been cwd in the UK back in 1970’S ???
 
 
 
 
 
SEE FULL TEXT ;
 
 
Sunday, July 17, 2016
 
CHRONIC WASTING DISEASE CWD TSE PRION GLOBAL REPORT UPDATE JULY 17 2016
 
 
Monday, May 02, 2016
 
*** Zoonotic Potential of CWD Prions: An Update Prion 2016 Tokyo ***
 
 
 
 
Saturday, April 23, 2016
 
SCRAPIE WS-01: Prion diseases in animals and zoonotic potential 2016
 
Prion. 10:S15-S21. 2016 ISSN: 1933-6896 printl 1933-690X
 
 
Saturday, April 16, 2016
 
APHIS [Docket No. APHIS-2016-0029] Secretary's Advisory Committee on Animal Health; Meeting May 2, 2016, and June 16, 2016 Singeltary Submission
 
 
Tuesday, August 9, 2016
 
*** Concurrence with OIE Risk Designations for Bovine Spongiform Encephalopathy [Docket No. APHIS-2015-0055]
 
 
Saturday, July 23, 2016
 
*** BOVINE SPONGIFORM ENCEPHALOPATHY BSE TSE PRION SURVEILLANCE, TESTING, AND SRM REMOVAL UNITED STATE OF AMERICA UPDATE JULY 2016
 
 
Tuesday, July 26, 2016
 
*** Atypical Bovine Spongiform Encephalopathy BSE TSE Prion UPDATE JULY 2016
 
 
Saturday, July 16, 2016
 
*** Importation of Sheep, Goats, and Certain Other Ruminants [Docket No. APHIS-2009-0095]RIN 0579-AD10
 
WITH great disgust and concern, I report to you that the OIE, USDA, APHIS, are working to further legalize the trading of Transmissible Spongiform Encephalopathy TSE Pion disease around the globe.
 
THIS is absolutely insane. it’s USDA INC.
 
 
Monday, June 20, 2016
 
*** Specified Risk Materials SRMs BSE TSE Prion Program ***
 
 
Evidence That Transmissible Mink Encephalopathy Results from Feeding Infected Cattle
 
Over the next 8-10 weeks, approximately 40% of all the adult mink on the farm died from TME.
 
snip...
 
The rancher was a ''dead stock'' feeder using mostly (>95%) downer or dead dairy cattle...
 
 
 
 
In Confidence - Perceptions of unconventional slow virus diseases of animals in the USA - APRIL-MAY 1989 - G A H Wells
 
3. Prof. A. Robertson gave a brief account of BSE. The US approach was to accord it a very low profile indeed. Dr. A Thiermann showed the picture in the ''Independent'' with cattle being incinerated and thought this was a fanatical incident to be avoided in the US at all costs. ...
 
 
”The occurrence of CWD must be viewed against the contest of the locations in which it occurred. It was an incidental and unwelcome complication of the respective wildlife research programmes. Despite it’s subsequent recognition as a new disease of cervids, therefore justifying direct investigation, no specific research funding was forthcoming. The USDA veiwed it as a wildlife problem and consequently not their province!” ...page 26.
 
 
Thursday, October 22, 2015
 
*** Former Ag Secretary Ann Veneman talks women in agriculture and we talk mad cow disease USDA and what really happened those mad cows in Texas ***
 
 
USA CJD GETTING YOUNGER AND YOUNGER...WHY?
 
Sunday, August 21, 2016
 
Creutzfeldt-Jakob disease CJD TSE Prion USA getting younger and younger, spontaneous sporadic, zoonosis, or iatrogenic?
 
 
August 16th, 2016 - 11:49 am
 
Inaugural Benefactory Festival in Scranton honors Julie Judge
 
Features
 
Proceeds go to TEDxYouth@Scranton
 
By Matt Mattei - Click for more information on Matt mmattei@timesleader.com - @TLArts - 570-991-6651 More Articles By: Matt Mattei
 
Then Judge fell ill.
 
She became afflicted with Creutzfeldt-Jakob disease, a fatal brain protein disorder known as a prion disease.
 
“It affects the brain and it affects it quickly,” Kenny Hill said. “She was lively at one point, and then things started getting bad and getting bad quick.”
 
 
I spoke with the reporter this AM, Mr. Mattei, and he said Julie Judge was 52 or 53...another young victim of CJD in the USA, in Pennsylvania, where CWD in cervid is well established. what about friendly fire or iatrogenic there from ???
 
Tuesday, May 03, 2016 Wednesday, May 11, 2016
 
PENNSYLVANIA TWELVE MORE CASES OF CWD FOUND: STATE GEARS UP FOR ADDITIONAL CONTROL MEASURES
 
 
A Maine mother of four has died of the rare brain disorder Creutzfeldt-Jakob disease.
 
Sandra Tucker Kennedy, 38, died March 3 of sporadic CJD, a degenerative brain disease that affects only one in 1 million people worldwide per year, and about 300 people per year in the U.S.
 
Kennedy, who lived in Kennebunk and worked as a nurse at Maine Medical Center, leaves behind husband Jake Kennedy and their four children: son Tucker, 9, twin boys Asher and Gunner, 5, and daughter Skyler, 2.
 
 
 
Thursday, April 14, 2016
 
Arizona 22 year old diagnosed with Creutzfeldt Jakob Disease CJD
 
 
Thursday, January 15, 2015
 
41-year-old Navy Commander with sporadic Creutzfeldt–Jakob disease CJD TSE Prion: Case Report
 
 
Saturday, January 17, 2015
 
*** Becky Lockhart 46, Utah’s first female House speaker, dies diagnosed with the extremely rare Creutzfeldt-Jakob disease
 
 
Monday, August 22, 2016
 
CEUTZFELDT JAKOB DISEASE USA 2015 SPORADIC CJD TOTAL FIGURES REACHES HIGHEST ANNUAL COUNT TO DATE AT 239 CONFIRMED CASES
 
 
Terry S. Singeltary Sr.