Chronic Wasting Disease: 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

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

News Release

Media Contact: Steve Lightfoot, 512-389-4701, steve.lightfoot@tpwd.texas.gov

Jan. 22, 2016

TPW Commission Takes Action on Deer Management Permit; Aerial Wildlife Management Clarified AUSTIN – The Texas Parks and Wildlife Commission at its Thursday public hearing adopted a 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.

Modifications to the DMP are needed for consistency in movement qualification standards developed by the Texas Parks and Wildlife Department and Texas Animal Health Commission. These standards help to increase the probability of detecting CWD if a deer infected with CWD is released from a DMP facility. The new rule establishes classifications for DMP facilities and imposes testing requirements at DMP release sites where deer trapped on Class II Triple T trap sites or breeder deer from TC 2 or TC 3 deer breeding facilities have been released and would require all deer introduced to Level 3 DMP facilities or released on Class III release sites to be tagged with an Radio Frequency Identification Device (RFID) or National Uniform Eartagging System (NUES) ear tag.

In other action, the Commission also approved amendments to rules governing permits for the aerial management of wildlife and exotic species. The changes are designed to remove problematic provisions, streamline the process, clarify regulatory language to enhance compliance and enforcement, and achieve greater administrative efficiencies.

Adopted Commission actions take effect 20 days after they are published in the Texas Register in February.

SL 2016-01-22

http://tpwd.texas.gov/newsmedia/releases/?req=20160122a

http://tpwd.texas.gov/business/feedback/meetings/2016/0121/agenda/index.phtml

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Commission Agenda Item No. 2 Presenter: Clayton Wolf

Action Chronic Wasting Disease Response - Interim Deer Management Permit Rules – Recommended Adoption of Proposed Rules January 21, 2016

I. Executive Summary: This item seeks adoption of a proposed new rule governing Deer Management Permit (DMP) activities as part of the department’s response to the detection of chronic wasting disease (CWD) in captive cervid populations and subsequent efforts to ascertain its prevalence/stop its spread in both farmed and free-ranging populations. The new rule would establish classifications for DMP facilities and impose testing requirements at DMP release sites where deer trapped on Class II Triple T trap sites or breeder deer from TC 2 or TC 3 deer breeding facilities have been released and would require all deer introduced to Level 3 DMP facilities or released on Class III release sites to be tagged with an Radio Frequency Identification (RFID) or National Uniform Eartagging System (NUES) ear tag.

II. Discussion: CWD is a fatal neurodegenerative disorder that affects cervid species such as white-tailed deer, mule deer, elk, and others (susceptible species). It is classified as a transmissible spongiform encephalopathy, a family of diseases that includes scrapie (found in sheep) and bovine spongiform encephalopathy (BSE, found in cattle). The department has been concerned for over a decade about the possible emergence of CWD in wild and captive deer populations in Texas. The department closed the Texas border in 2005 to the entry of out-of-state captive white-tailed and mule deer and increased regulatory requirements regarding disease monitoring and recordkeeping. As of July 1, 2015, the department had tested more than 32,882 free-ranging deer in Texas for CWD, and cervid producers had submitted more than 12,759 test results to the department.

Following the confirmation in June of 2015 that a two-year-old white-tailed deer held in a deer breeding facility in Medina County (“index facility”) had tested positive for CWD, the department engaged in multiple rulemakings intended to identify, isolate, and contain CWD, including an emergency DMP rule adopted on October 5, 2015 (40 TexReg 7305). The proposed DMP rule located at Exhibit A would replace the current emergency rule on an interim basis and be in effect until the August 31, 2016 expiration date for all CWD response-related rules established by the Commission at the November 2015 meeting.

Based on additional information from the ongoing epidemiological investigation, disease surveillance data collected from captive and free ranging deer herds, guidance from the Texas Animal Health Commission, and input from stakeholder groups, the department intends to review the interim rule, if adopted, following the close of the deer season and present the results of that review to the Parks and Wildlife Commission (Commission) in the spring of 2016 for possible modifications.

III. Recommendation: The staff recommends the Texas Parks and Wildlife Commission adopt the following motion:

The Texas Parks and Wildlife Commission adopts new 31 TAC §65.94, concerning Disease Detection and Response, with changes as necessary to the proposed text (located at Exhibit A) as published in the December 18, 2015 issue of the Texas Register (40 TexReg 9086).

Attachments – 1

Exhibit A – Proposed DMP Rules

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Commission Agenda Item No. 2 Exhibit A

DEER MANGEMENT PERMIT CWD RULES

PROPOSAL PREAMBLE

1. Introduction.

The Texas Parks and Wildlife Department proposes new §65.94, concerning Chronic Wasting Disease — Deer Management Permit Provisions. The new rules will be part of Subchapter B, Division 2, Chronic Wasting Disease — Movement of Deer. The department wishes to emphasize that the proposed new rules, if adopted, would be an interim replacement for the current rule, adopted on an emergency basis on October 5, 2015 (40 TexReg 7305), which is necessary to maintain regulatory continuity for the duration of the 2015-16 deer season and the period immediately thereafter. Based on additional information from the ongoing epidemiological investigation, disease surveillance data collected from captive and free ranging deer herds, guidance from the Texas Animal Health Commission, and input from stakeholder groups, the department intends to review the interim rule, along with the interim breeder rules, and Triple T (Permits to Trap, Transport, and Transplant Game Animals and Game Birds) rules following the close of the deer season and present the results of that review to the Parks and Wildlife Commission (Commission) in the spring of 2016 for possible modifications.

The proposed new rule is part of a more comprehensive regulatory response intended to increase the probability of detecting chronic wasting disease (CWD) if a deer infected with CWD is released from a DMP facility. The proposed new rule is also part of a broader cooperation between the department and the Texas Animal Health Commission (TAHC) to protect susceptible species of exotic and native wildlife from CWD. TAHC is the state agency authorized to manage “any disease or agent of transmission for any disease that affects livestock, exotic livestock, domestic fowl, or exotic fowl, regardless of whether the disease is communicable, even if the agent of transmission is an animal species that is not subject to the jurisdiction” of TAHC. Tex. Agric. Code §161.041(b).

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 transmissible spongiform encephalopathy (TSE), a family of diseases that includes scrapie (found in sheep), bovine spongiform encephalopathy (BSE) 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, and is transmitted both directly (through deer-to-deer contact) and indirectly (through environmental contamination). Moreover, a high prevalence of the disease in free-ranging populations has been correlated to deer population declines, and human dimensions research suggests that hunters will avoid areas of high CWD prevalence. The implications of CWD to the multi-billion dollar ranching, hunting, and wildlife management economies in Texas are significant, unless it is contained and controlled.

Under Parks and Wildlife Code, Chapter 43, Subchapters R and R-1, and Deer Management Permit (DMP) regulations for white-tailed deer at 31 TAC Chapter 65, Subchapter D, the department may allow the temporary possession of free-ranging white-tailed or mule deer for breeding purposes within an enclosure on property surrounded by a fence capable of retaining deer. At the current time, there are no rules authorizing DMP activities for mule deer.

In addition to authorizing the temporary possession of free-ranging white-tailed deer for breeding purposes, department regulations authorize the introduction of a buck deer from a deer breeding facility into a DMP facility for breeding purposes. Deer breeders are permitted under Parks and Wildlife Code, Chapter 43, Subchapter L and 31 TAC Chapter 65, Subchapter T. The current rules provide, among other things, that a buck deer introduced to a DMP pen from a deer breeding facility may be liberated from the DMP pen to the surrounding or adjacent high-fenced acreage identified in the deer management plan associated with the DMP facility, returned to the deer breeding facility from which the buck deer was transferred, or transferred to another deer breeding facility. All other deer introduced to a DMP pen, whether by trapping from a free-ranging herd or transfer from a deer breeding facility, must be liberated from the DMP enclosure by a date specified by the department in the DMP permit.

The department has been concerned for over a decade about the possible emergence of CWD in free-ranging and captive deer populations in Texas, and has engaged in several rulemakings over the years to address the threat posed by CWD. In 2005, the department closed the Texas border to the entry of out-of-state captive white-tailed and mule deer and increased regulatory requirements regarding disease monitoring and record keeping. (The closing of the Texas border to entry of out-of-state captive white-tailed and mule deer was updated, effective in January 2010, to address other disease threats to white-tailed and mule deer (35 TexReg 252).) Prior to 2012, CWD had not been known to exist in Texas; however, on July 10, 2012, the department confirmed that two mule deer sampled in the Texas portion of the Hueco Mountains tested positive for CWD. In response, the department and the Texas Animal Health Commission (TAHC) convened the CWD Task Force, comprised of wildlife-health professionals and cervid producers, to advise the department on the appropriate regulatory and policy measures to be taken to protect white-tailed and mule deer in Texas. Based on recommendations from the CWD Task Force, the department subsequently adopted new rules in 2013 (37 TexReg 10231) to implement a CWD containment strategy in far West Texas. The rules among other things require deer harvested in a specific geographical area to be presented at designated check stations to be tested for CWD.

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 (“index facility”) had tested positive for CWD. Subsequent testing confirmed the presence of CWD in additional white-tailed deer at the index facility. The source of the CWD at the index facility is unknown at this time. Within the last five years, the index facility accepted deer from 30 other Texas deer breeding facilities and transferred 835 deer to 147 separate sites (including 96 deer breeding facilities, 46 release sites, and three Deer Management Permit (DMP) facilities in Texas, as well as two destinations in Mexico). The department estimates that in the past five years, more than 728 locations in Texas (including 384 deer breeding facilities) either received deer from the index facility or received deer from a deer breeding facility that had received deer from the index facility. CWD has subsequently been detected in an additional deer breeding facility.

In response, the department engaged in a vigorous effort to involve and solicit input from other regulatory agencies, various stakeholder groups, and the regulated community to develop a regulatory response that both discharged the department’s duty to protect the wildlife resources of the state for the enjoyment of the people and to the greatest extent possible minimized disruption to the regulated community. As a result of that effort, the department on August 18, 2015, adopted emergency rules governing deer breeder permits (40 TexReg 5566). Interim rules governing deer breeder permits were proposed on September 21, 2015 (40 TexReg 6856), and were approved, with changes, by the Parks and Wildlife Commission on November 5, and will be published in a future issue of the Texas Register.

Those rules (§§65.90-65.93 of this subchapter, or “CWD deer breeder rules”) address CWD testing requirements and movement restrictions for white-tailed deer and mule deer held under the authority of deer breeder permits issued by the department. The rules set forth specific CWD testing requirements for deer breeders, which would have to be satisfied in order to transfer deer to other deer breeders, DMP facilities, or for purposes of release. The CWD deer breeder rules also impose CWD testing requirements on sites where certain breeder deer are liberated (release sites). The CWD deer breeder rules create a tiered system of testing requirements for deer breeding facilities and release sites based on the level of risk of transmission of CWD. To facilitate this testing, the CWD deer breeder rules classify breeding facilities and release sites according to degree of CWD testing and level of risk of exposure to CWD.

Epidemiological science dictates that a population receiving individuals from a higher risk population is itself at greater risk. Therefore, the CWD deer breeder rules address transfers from higher risk to lower risk populations by requiring the receiving deer breeding facility or release site to comply with the testing requirements associated with the status of the originating facility, if the status of the originating facility is lower than the status of the receiving facility. Because deer from deer breeding facilities and release sites may be introduced into a DMP facility, and then either released or returned to a breeding facility, it is necessary to identify how DMP activities impact the level of testing required by breeding facilities and release sites that receive deer from DMP facilities. The level of risk is based on the degree of testing and exposure to CWD-positive or CWD-exposed animals.

The department notes for purposes of clarification that the provisions of §§65.90-65.93 of this subchapter would also apply to the proposed new rule. The applicable provisions would include, for example, the definitions in §65.90 of this subchapter and the testing requirements for the categories and classes of breeding facilities and release sites established in §§65.90-65.93 of this subchapter.

As noted previously, the new rule proposed herein, if adopted, would replace the emergency rules adopted on October 5. The proposed new rule differs from the emergency rule as follows:

1. In subsection (a)(1) of the emergency rule, a DMP facility is described as “a property (including the pen in which deer are temporarily detained for breeding purposes and the high-fenced acreage to which the deer are released).” This is technically incorrect. In TWIMS (defined in §65.90 of this title as the “department’s Texas Wildlife Information Management Services (TWIMS) online application”), each DMP property gets one facility identification for the enclosure (pen) in which deer are temporarily detained and one facility identification for surrounding acreage to which the deer are released. To avoid confusion, the proposed new rule would establish that the word “facility” as used in the rule text means the DMP pen.

2. In subsection (b) of the emergency rule, the department set forth the various requirements and restrictions for Level 2 and Level 3 DMP facilities. Level 1 DMP facilities were not addressed because the Level 1 DMP category is a default value, consisting of all DMP facilities that either do not receive breeder deer at all or received breeder solely from TC 1 breeding facilities (and did not receive any deer from a Class II or Class III release site). As a result, the acreage to which deer are released from those facilities are Class 1 release sites and no CWD testing is required under §§65.90-65.93 of this subchapter.

3. Subsection (b)(4) of the emergency rule imposed tagging requirements for deer introduced to a Level 3 DMP facility or released on a Class III release site. The department has determined that because paragraphs (1) – (3), (5) and (6) address the assignment of DMP category designations, paragraph (4) interrupts that process, since it addresses a different topic; therefore, in the proposed new rule the tagging requirements from subsection (b)(4) of the emergency rule are designated as subsection (b)(8).

Proposed new §65.94(a) would set forth two general provisions.

Proposed new §65.94(a)(1) would identify exactly what is meant by “DMP facility.” A DMP facility is an enclosure in which deer are temporarily detained for breeding purposes permitted under the provisions of Parks and Wildlife Code, Subchapter R or R-1 and Subchapter D of this chapter (relating to Deer Management Permit (DMP)). The provision is necessary in order to prevent any ambiguity arising from the use of the term “DMP facility.”

Proposed new §65.94(a)(2) would define “status” as “the level of testing required by this division for any facility registered in TWIMS (deer breeding facility, trap site, release site, or DMP facility).” The definition of “status” is necessary because the status of any given facility determines the testing and movement requirements that apply to the facility and because it is necessary to clarify that the term applies to all types of permits authorizing the possession of live deer. The proposed new rule would also establish that the highest status for DMP facilities is Level 1 and the lowest status is Level 3, which is necessary to prevent potential misinterpretation. The designation of DMP facility status will also provide consistency with the §§65.90-65.93 of this subchapter, regarding Chronic Wasting Disease – Movement of Breeder Deer, which designate a Transfer Category (TC) status (TC 1, TC 2, TC 3) for deer breeding facilities and a status for release sites (Class I, II, III). Under §§65.90-65.93 of this subchapter, the lower number is the higher status. For example, for deer breeding facilities, a TC 1 is the highest status. For release sites, Class I is this highest status.

Proposed new §65.94(b) would set forth several provisions specific to the acquisition and transfer of deer for DMP purposes.

Proposed new §65.94(b)(1)-(7) would set forth the status (and therefore, the testing requirements) for release sites for deer from DMP facilities based on the status of the source of deer obtained for DMP purposes.

Proposed new subsection (b)(1) would stipulate that a DMP facility that is not a Level 2 or Level 3 DMP facility is a Level 1 DMP facility. Because the status of a deer breeding facility or a release is not impacted by receiving deer from a Level 1 DMP facility, no additional provisions are needed to address the impact of deer being held in a Level 1 DMP facility.

Proposed new subsection (b)(2) would stipulate that a DMP facility that receives deer from a Class II release site or TC 2 breeding facility is a Level 2 DMP facility, unless the DMP facility receives deer from a TC 3 breeding facility or Class III release site.

Proposed new subsection (b)(3) stipulates that a DMP facility receiving deer from a TC 3 breeding facility or Class III release site is a Level 3 DMP facility and that the release site to which the deer are liberated from the DMP pen becomes a Class III release site beginning on the Saturday nearest to September 30 of the following year (the first day of lawful deer hunting).

Proposed new subsection (b)(4) would stipulate that if a breeder deer is transferred from a TC 3 breeding facility to a Level 1 or 2 DMP facility, the DMP facility immediately becomes a Level 3 DMP facility and the release site to which the deer are liberated from the DMP pen becomes a Class III release site beginning on the Saturday nearest to September 30 of the following year.

Proposed new subsection (b)(5) would provide that if a breeder deer is transferred from a TC 2 breeding facility to a Level 1 DMP facility, the DMP facility immediately becomes a Level 2 DMP facility and the release site to which with deer are liberated from the DMP facility becomes a Class II release site beginning on the Saturday nearest to September 30 of the following year (the first day of lawful deer hunting), unless the release site is or becomes a Class III release site pursuant to other provisions of this division.

Proposed new subsection (b)(6) would provide that if a breeder deer is transferred to a deer breeding facility from a DMP facility of lower status, the breeding facility receiving the breeder deer automatically assumes the numeric status of the DMP facility. For example, if a breeder deer is transferred to a TC 2 breeding facility from a Level 3 DMP facility, the deer breeding facility becomes a TC 3 breeding facility. Proposed new subsection (b)(7) would provide that a DMP facility automatically becomes a Level 3 DMP facility if deer are introduced to the DMP facility from a Tier 1 facility. (A Tier 1 facility is a facility that has a direct connection to a CWD-positive facility, and is defined in §65.90(21) of this subchapter).

Proposed new §65.94(b)(8) would prohibit the introduction of a breeder deer into a Level 3 DMP facility unless the deer is tagged, prior to leaving the originating facility, by attaching a button-type RFID or NUES tag approved by the department to one ear. (RFID and NUES ear tags are defined in current §65.91.) Proposed new §65.94(b)(8) would also prohibit the release of a breeder deer onto a Class III release site unless the deer is tagged, prior to leaving the originating facility, by attaching a button-type RFID or NUES tag approved by the department to one ear. A Level 3 DMP facility is a highest risk DMP facility. Similarly, deer within a Class III release site are at a higher risk for CWD. Therefore, the department believes that breeder deer introduced into a Level 3 DMP facility or released onto a Class III site should be readily identifiable for purposes of subsequent CWD testing. Therefore, the proposed new rule would require such deer to be ear-tagged prior to release.

2. Fiscal Note.

Clayton Wolf, Wildlife Division Director, has determined that for each of the first five years that the rule as proposed is in effect there will be no fiscal implications to state and local governments as a result of enforcing or administering the rule as proposed, as department personnel currently allocated to the administration and enforcement of the permit programs affected will continue administer and enforce the rules as part of their current job duties.

3. Public Benefit/Cost Note.

Mr. Wolf also has determined that for each of the first five years the new rule as proposed is in effect:

(A) The public benefit anticipated as a result of enforcing or administering the rule as proposed will be a reduction of the probability of CWD being spread from facilities where it might exist and an increase in the probability of detecting CWD if it does exist, thus ensuring the public of continued enjoyment of the resource and ensuring the continued beneficial economic impacts of hunting in Texas.

(B) There could be adverse economic impact on persons required to comply with the rule as proposed.

As noted previously, a DMP allows the introduction of breeder deer into a DMP facility for purposes of propagation. Except for fawns born in a DMP facility during the permit year, no DMP facility may contain more than 1 buck deer and 20 doe deer. Also, deer may be introduced to DMP facility beginning on September 1 and no later than the breeding chronology for the ecoregion in which the DMP facility is located, which ranges from October 21 (Gulf Prairies and Marshes) to December 14 (South Texas Plains). A person seeking to engage in DMP activities, must obtain a new DMP permit each year. Deer held in a DMP facility must be allowed to leave the DMP facility by no later than 45 days prior to the trapping deadline of the subsequent DMP trapping season for the ecoregion in which the DMP facility is located, which ranges from September 6 (Gulf Prairies and Marshes) to October 30 (South Texas Plains), or a date specified in the permit.

Upon conclusion of DMP activities, a buck introduced into the DMP pen from a deer breeding facility may be returned to the originating deer breeding facility, moved to another deer breeding facility, or released. All other deer held in the DMP facility must be released to the adjoining high-fenced acreage.

The proposed new rule imposes no new testing requirements in addition to those imposed on deer breeding facilities and release sites by §§65.90-65.93 of this subchapter. While there are no testing requirements directly imposed on DMP permittees during the temporary detention of deer pursuant to a DMP permit, the release of breeder deer obtained from a TC 2 or TC 3 deer breeding facility or deer from a Class II release site (via Triple T permit) could result in additional testing requirements for the DMP acreage (the high-fenced acreage in which the DMP facility is located) to which the DMP deer are released. There also could be testing requirements for a deer breeder who acquires or re-acquires a breeder buck from a DMP facility of lower status than the receiving deer breeding facility since the receiving facility assumes the status, if lower, of the originating facility. There would be no additional testing requirements as a result of DMP activities if the DMP facility receives no breeder deer and no deer via Triple T permit from a Class II release site, or if the DMP facility only receives breeder deer and deer via Triple T permit from deer breeding facilities and release sites that have a status that is equal to or higher than the DMP facility. However, if a release site or deer breeding facility receives deer from a DMP facility that has lower status than the receiving deer breeding facility or release site, the deer breeding facility or release site could incur additional costs associated with CWD testing.

With regard to testing, if a release site becomes a Class II release site as a result of the introduction of deer onto the release site following DMP activities, under the provisions of §65.90-65.93 of this subchapter the following number of deer would have to be tested for CWD in the following year: 50 percent of the number of breeder deer released at the site between the last day of lawful deer hunting at the site in the previous year and the last day of lawful deer hunting at the site in the current year, or 50 percent of all hunter-harvested deer, as well as 50 percent of any hunter-harvested deer that were released breeder deer, which may be counted to satisfy the total testing requirement.

If a release site becomes a Class III release site as a result of the introduction of deer onto the release site following DMP activities, under the provisions of §65.90-65.93 of this subchapter the following number of deer would have to be tested for CWD in the following year: 100 percent of all hunter-harvested deer or one hunter-harvested deer per breeder deer released between the last day of lawful deer hunting at the site in the previous year and the last day of lawful deer hunting. The exact number of deer that must be tested at Class II and Class III release sites would depend on the number of hunter-harvested deer and the number of breeder deer released on the property.

The estimated cost for each test and the cost of compliance for deer breeders is as specified in the discussion of the proposed rule’s impact on small and micro-business later in this preamble.

(C) There could be adverse economic impact on small businesses and microbusinesses required to comply with the rule as proposed.

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.

Although many DMP permittees engage in the for-profit sale of the opportunity to hunt deer that have been held under a DMP and subsequently liberated, Parks and Wildlife Code, §62.021, prohibits the sale, offer for sale, purchase, offer to purchase, or possession after purchase of a live game animal, but makes an exception for activities conducted under a deer breeder permit which allows the purchase and sale of deer. Therefore, the department has determined that the since activities pursuant to a DMP permit are statutorily not for profit, the proposed rulemaking does not impose any adverse economic impacts from the perspective of any DMP permittee’s status as a for-profit enterprise, be it a small business or microbusiness or not.

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, deer breeders are authorized to engage in business activities; namely, the purchase and sale of breeder deer.

Since the rule as proposed could impact the ability of a deer breeder to engage in certain activities undertaken to generate a profit, the proposed rule may have an adverse impact on deer breeders. However, those impacts would result from a deer breeder’s receipt of deer from a DMP facility of lower status than the breeder facility. It should be emphasized that it is unlikely that a deer breeder would seek to introduce a deer of lower status into a deer breeding facility.

It should also be noted that the variety of business models utilized by deer breeders makes meaningful estimates of potential adverse economic impacts difficult. Although a deer breeder has the permit 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 property for hunting opportunity. Once a breeder deer is liberated, it cannot be returned to a breeding facility and assumes the same status as all other free ranging deer. Thus, if the 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 does not require deer breeders to report the buying or selling prices of deer. However, publicly available and anecdotal 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.

It should also be noted that some aspects of this analysis are based on anticipated marketplace behavior which cannot be accurately predicted. In addition, to the extent that any marketplace analysis can be conducted, it is difficult, if not impossible, to accurately separate and distinguish marketplace behavior that is the result of the proposed rules from marketplace behavior that is the result of the discovery of CWD. For reasons unrelated to the regulations, it is possible, perhaps even likely, that breeders and release site owners would be reluctant to acquire a breeder deer from a facility with a close relationship (as indicated by the facility’s status) to a facility at which CWD has been detected.

For deer breeders, the department has determined that for TC 1 facilities there will likely be no adverse economic impact on sales as a result of the proposed new rule, so long as the TC 1 facility does not receive a breeder buck deer from a DMP facility of a lower status. Under §§65.90-65.93 of this subchapter, only those breeding facilities that are not Tier I facilities and have obtained a “fifth-year” or “certified” status from TAHC, are considered TC 1 facilities. In order to maintain “fifth year” or “certified” from TAHC, such facilities may receive deer only from other “fifth-year” or “certified” breeding facilities. As a result, transfers of breeder deer from TC 1 facilities are subject to the fewest restrictions under §§65.90-65.93 of this subchapter. Therefore, breeder deer from a TC 1 facility can more easily be sold to other breeders or to landowners for purposes of liberation on a release site. In addition, TC 1 facilities are already subject to monitoring and testing at a higher level. Department records indicate that there are currently 63 TC 1 facilities in the state.

If a TC 1 deer breeding facility becomes a TC 2 facility as a result of receipt of a breeder buck deer from a DMP facility, the adverse economic impact of the proposed new rule would consist of the cost of the additional testing requirements (described in more detail later in this preamble) and possible loss of sales to TC 1 facilities and Class I release sites. The change in status would not prohibit the transfer of breeder deer by an affected facility, but because of the change (lowering) in status resulting from the proposed new rules, it can be assumed that TC 1 facilities will be less likely destinations for breeder deer coming from DMP facilities of lower status.

Department records indicate that there are currently 759 TC 2 facilities in the state, and that in the last year, 528 of them transferred breeder deer to facilities that are now TC 1 or Class I release sites. The most breeder deer transferred from any single breeding facility was 175, but the overwhelming majority of transfers involved 10 or fewer deer. If a TC 1 deer breeding facility’s status is lowered to TC 2 as a result of the receipt of a breeder buck deer from a Level II DMP facility, the impact to the deer breeder could include the loss of sales and any attendant profit from the sale of deer due to the deer breeder’s lower status. However, as noted above, a TC 1 facility is not a likely destination for a deer from a DMP facility of lower status.

For facilities that become TC 3 facilities as a result of acquiring breeder deer from a Level 3 DMP facility, the adverse economic impact of the proposed new rules would consist of the cost of the additional testing requirements and possible loss of sales to TC 1 and TC 2 facilities and Class I and Class II release sites. Because the proposed new rule would cause any deer breeding facility that accepts deer from a DMP facility of lower status to assume the status (and regulatory obligations, such as testing) of that originating facility, it can be assumed that higher status facilities and release sites will be less likely destinations for breeder deer coming from facilities of lower status.

Because the issuance period for DMPs had not concluded as of the submission of the proposed new rule, the department cannot provide a definitive value for the number of DMPs issued for the 2015-16 permit year; however, in the 2014-2015 permit year, 168 DMPs were issued and the final value for the current year is expected to be similar. Of the permits issued thus far for this year, 111 did not involve breeder deer. Four DMP facilities have received breeder deer only from a TC 1 deer breeding facility. Forty-three DMP facilities have received breeder deer from a TC 2 deer breeding facility. One DMP facility has received deer from a TC 3 breeding facility.

With regard to the degree of impact due to possible loss of sales, the department does not require holders of deer breeder permits to disclose the dollar values of sales and purchases of breeder deer; therefore, an exact quantification of the possible impact of the proposed new rule on deer breeding facilities due to lost sales cannot be calculated. However, based on public and anecdotal information, such impact could be from few hundred dollars or less per deer or to thousands of dollars per deer.

Testing Costs

In all cases, the costs to persons required to comply, as well as to any small or microbusiness affected by the proposed new rule, would consist of the cost of CWD testing. The cost of a CWD test administered by the Texas Veterinary Medicine Diagnostic Lab (TVMDL) on a sample collected and submitted by a DMP permittee is a minimum of $46, to which is added a $6 submission fee (which may cover multiple samples submitted at the same time). If a whole head is submitted to TVDML there is an additional $20 sample collection fee, plus a $20 disposal fee. Thus, the fee for submitting an obex or obex/medial retropharyngeal lymph node pair would be $52, plus any veterinary cost (which the department cannot quantify) and the fee for submitting an entire head for testing would be $92. Therefore, the department estimates that the direct economic impact of the proposed new rule on persons required to comply would be between $52 and $92 per deer per year for each permittee. If the sample is collected, fixed, and submitted by a private veterinarian, the cost could be higher. The cost to any person, small business or microbusiness would be the cost of a CWD test multiplied by the number of deer required to be tested.

Alternatives Considered

The department considered several alternatives to achieve the goals of the proposed new rule while reducing potential adverse impacts on small and micro-businesses and persons required to comply. The department considered proposing no rule. This alternative was rejected because the presence of CWD in the state is not hypothetical, but has been confirmed and presents an actual, direct threat to free-ranging and farmed cervid populations and the economies that depend upon them. A regulation that clearly sets out prudent and sensible restrictions on the regulated community is more likely to achieve the desired result of stemming the spread of CWD than having no regulations. The department concluded that the need to protect the wildlife resources that sustain the state’s annual multi-billion-dollar hunting industry outweighs the temporary adverse impacts to small and micro-businesses and persons required to comply.

The department also considered, in lieu of a regulatory response, the alternative of prohibiting the transfer of breeder deer to DMP facilities except from TC 1 facilities. This alternative was rejected because it would result in disruption of the bulk of interactions between deer breeders and DMP holders, which, with proper monitoring, would not be unnecessary.

(D) The department has not drafted a local employment impact statement under the Administrative Procedures Act, §2001.022, as the agency has determined that the rules as proposed will not result in direct impacts to local economies.

(E) The department has determined that there will not be a taking of private real property, as defined by Government Code, Chapter 2007, as a result of the proposed new rules. Any impacts resulting from the discovery of CWD in or near private real property would be the result of the discovery of CWD and not the proposed 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.texas.gov); or via the department’s website at www.tpwd.texas.gov.

5. Statutory Authority.

The new rule is proposed under the authority of Parks and Wildlife Code, Chapter 43, 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, and 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 the department has not yet established a 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 new rule affects Parks and Wildlife Code, Chapter 43, Subchapters C, R and R-1, and Chapter 61.

§65.94. Chronic Wasting Disease — Deer Management Permit Provisions.

(a) General Provisions.

(1) A DMP facility is an enclosure in which deer are temporarily detained for breeding purposes permitted under the provisions of Parks and Wildlife Code, Subchapter R or R-1 and Subchapter D of this chapter (relating to Deer Management Permit (DMP)).

(2) For the purposes of this section, “status” means the level of testing required by this division for any facility registered in TWIMS (deer breeding facility, trap site, release site, or DMP facility). For the levels of DMP facilities established in this section, the highest status is Level 1 and the lowest status is Level 3.

(b) Special Provisions.

(1) A DMP facility that is not a Level 2 or Level 3 DMP facility is a Level 1 DMP facility.

(2) A DMP facility that receives deer from a Class II release site or a TC 2 breeding facility is a Level 2 DMP facility unless the DMP facility receives deer from a TC 3 breeding facility or Class III release site.

(3) A DMP facility that receives deer from a Class III release site is a Level 3 DMP facility.

(4) If a breeder deer is transferred from a TC 3 breeding facility to a DMP facility, the DMP facility immediately becomes a Level 3 DMP facility and the release site to which the deer are liberated from the DMP pen becomes a Class III release site beginning on the Saturday nearest to September 30 of the following year.

(5) If a breeder deer is transferred from a TC 2 breeding facility to a Level 1 DMP facility:

(A) the DMP facility immediately becomes a Level 2 DMP facility; and

(B) the release site to which the deer are liberated from the DMP pen becomes a Class II release site beginning on the Saturday nearest to September 30 of the following year, unless the release site is or becomes a Class III release site pursuant to other provisions of this division.

(6) If a breeder deer is transferred to a deer breeding facility from a DMP facility of lower status, the deer breeding facility receiving the breeder deer automatically assumes the numeric status of the DMP facility. For example, if a breeder deer is transferred to a TC 2 breeding facility from a Level 3 DMP facility, the deer breeding facility becomes a TC 3 breeding facility.

(7) A DMP facility automatically becomes a Level 3 DMP facility if deer are introduced to the DMP facility from a Tier 1 facility.

(8) No person may introduce a breeder deer into a Level 3 DMP facility or allow the release of a breeder deer on a Class III release site unless the deer has been tagged, prior to leaving the originating facility, by attaching a button-type RFID or NUES tag approved by the department to one ear.

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

http://tpwd.texas.gov/business/feedback/meetings/2016/0121/agenda/item_02/index.phtml

Tuesday, December 16, 2014

Texas 84th Legislature 2015 H.R. No. 2597 Kuempel Deer Breeding Industry TAHC TPWD CWD TSE PRION

http://chronic-wasting-disease.blogspot.com/2014/12/texas-84th-legislature-2015-hr-no-2597.html

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

http://chronic-wasting-disease.blogspot.com/2014/12/texas-84th-legislature-commencing-this.html

83R30157 BPG-D By: Kuempel H.R. No. 2597

R E S O L U T I O N

WHEREAS, Texas is home to the largest population of white-tailed deer in the nation, and deer breeding and hunting make important contributions to the state's economy; and

WHEREAS, A Texas A&M University study conducted in 2007 found that deer breeding and ranching generated over $650 million annually and supported more than 7,300 jobs; as land ownership becomes increasingly fragmented, deer breeding is particularly well suited to the utilization of smaller tracts, and the industry is now one of the fastest growing in rural America; by 2012, Texas had permitted over 1,200 breeder facilities containing over 100,000 breeder deer in nearly 200 counties; and

WHEREAS, Disease issues that arise in the deer industry are handled by the Texas Animal Health Commission, but most industry activities fall under the purview of the wildlife division of the Texas Parks and Wildlife Department; although TPWD is noted for its vast knowledge of wildlife biology, it is the TAHC that maintains expertise in agriculture, animal husbandry, and related matters of genetics, health, nutrition, breeding, and marketability; moreover, the TAHC manages certain breeds of cervid animals, including red deer and sika deer; and

WHEREAS, Properly managing this growing industry is of long-term importance, and an in-depth consideration of relevant issues would be beneficial to this state; now, therefore, be it

RESOLVED, That the House of Representatives of the 83rd Texas Legislature hereby request the speaker of the house to create a select interim committee to study regulatory oversight of the deer breeding industry in order to ensure that the industry is served by the state agency tasked with promoting and ensuring animal health and productivity; and, be it further

RESOLVED, That the study include recommendations on measures to ensure the vitality of the industry and encompass assurances that the Texas Parks and Wildlife Department will remain involved in the industry through its responsibility for issuing hunting licenses and providing game wardens; and, be it further

RESOLVED, That the committee submit a full report, including findings and recommendations for legislation, to the speaker and the members of the house of the 84th Texas Legislature when it convenes in January 2015.

http://www.legis.state.tx.us/tlodocs/83R/billtext/html/HR02597I.htm

Howdy Texas Hunters, and TPWD et al,

First, many thanks to the TPWD et al, and hunters, for the continued efforts to detected and try and stop Chronic Wasting CWD TSE Prion Disease.

with that said, game farms, breeders, and cervid industry there from, help spread cwd, simple fact. it’s been proven. game farms are not the only risk factor though, however, they are a big part of the problem, history shows this.

the quarantine of cwd tse prion infected game farms must be extended to 16 years now.

the CWD LOTTO ENTITLEMENT of captive game farms where the states pays game farms for CWD MUST BE STOPPED. if the cwd infected farm does not buy insurance for any and all loss from CWD for them and any party that does business with them, and or any loss to the state, and or any products there from, that’s to bad, they should never be allowed to be permitted. in fact, for any state that does allow game farming, urine mills, sperm mills, antler mills, velvet mills, big high fence ranch, little low fence farm, in my opinion, it’s that states responsibility to protect that state, thus, any states that allow these farms and business there from, it should be mandatory before any permit is allowed, that game farm must have enough personal insurance that would cover that farm, any farm that does business with them, and or any products there from, and the state, before such permit is issued. personally, I am sick and tired of all the big ag entitlement programs, and that’s all cwd indemnity is. in fact, the USDA CWD INDEMNITY PROGRAM, should read, THE USDA CWD ENTITLEMENT PROGRAM.

we cannot, and must not, let the industry regulate itself, especially with the junk science they try to use.

if they are not going to be science based, they must be banned.

science has told us for 3 decade or longer, that these are the things that _might_ work, yet thanks to the industry, and government catering to industry, regulations there from have failed, because of catering to the industry, and the cwd tse prion agent has continued to spread during this time. a fine example is Texas.

just follow the money in Indiana ;

Thursday, January 21, 2016

*** INDIANA With end of long legal challenge last year, high-fence hunting operations currently unregulated

http://chronic-wasting-disease.blogspot.com/2016/01/indiana-with-end-of-long-legal.html

CHRONIC WASTING DISEASE CWD TSE PRION AKA MAD COW TYPE DISEASE

Friday, January 01, 2016

Bayesian Modeling of Prion Disease Dynamics in Mule Deer Using Population Monitoring and Capture-Recapture Data

Chris Geremia, Michael W. Miller, Jennifer A. Hoeting, Michael F. Antolin, N. Thompson Hobbs PLOS x Published: October 28, 2015 DOI: 10.1371/journal.pone.0140687

Abstract

Epidemics of chronic wasting disease (CWD) of North American Cervidae have potential to harm ecosystems and economies. We studied a migratory population of mule deer (Odocoileus hemionus) affected by CWD for at least three decades using a Bayesian framework to integrate matrix population and disease models with long-term monitoring data and detailed process-level studies. We hypothesized CWD prevalence would be stable or increase between two observation periods during the late 1990s and after 2010, with higher CWD prevalence making deer population decline more likely. The weight of evidence suggested a reduction in the CWD outbreak over time, perhaps in response to intervening harvest-mediated population reductions. Disease effects on deer population growth under current conditions were subtle with a 72% chance that CWD depressed population growth. With CWD, we forecasted a growth rate near one and largely stable deer population. Disease effects appear to be moderated by timing of infection, prolonged disease course, and locally variable infection. Long-term outcomes will depend heavily on whether current conditions hold and high prevalence remains a localized phenomenon.

Discussion

The protracted time-scale of the CWD outbreak is much longer than the timespan of our research, which limits our ability to identify the true explanation of our findings. Nonetheless, our research suggests that, at least for the foreseeable future (e.g., decades), mule deer populations sharing the overall survival and infection probabilities estimated from our analyses may persist but likely will not thrive where CWD becomes established as an endemic infectious disease.

http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0140687

‘’Nonetheless, our research suggests that, at least for the foreseeable future (e.g., decades), mule deer populations sharing the overall survival and infection probabilities estimated from our analyses may persist but likely will not thrive where CWD becomes established as an endemic infectious disease. ‘’

*** Bayesian Modeling of Prion Disease Dynamics in Mule Deer Using Population Monitoring and Capture-Recapture Data

‘’Mountain lions prey selectively on CWD infected deer [33] and CWD could result in an abundance of vulnerable prey, thereby enhancing mountain lion survival and reproduction [20].’’

please see ;

‘’preliminary results suggesting that bobcats (Lynx rufus) may be susceptible to white-tailed deer (Odocoileus virginianus) chronic wasting disease agent.’’

references on Feline Spongiform Encephalopathy FSE toward the bottom, see ;

Assessing Transmissible Spongiform Encephalopathy Species Barriers with an In Vitro Prion Protein Conversion Assay

Tuesday, December 15, 2015

Chronic Wasting Disease will cause a Wyoming deer herd to go virtually extinct in 41 years, a five-year study predicts

Study: Chronic Wasting Disease kills 19% of deer herd annually

http://chronic-wasting-disease.blogspot.com/2015/12/chronic-wasting-disease-will-cause.html

Research Project: TRANSMISSION, DIFFERENTIATION, AND PATHOBIOLOGY OF TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES

***Title: Transmission of chronic wasting disease to sentinel reindeer (Rangifer tarandus tarandus)

Authors

item Moore, S - item Kunkle, Robert item Nicholson, Eric item Richt, Juergen item Hamir, Amirali item Waters, Wade item Greenlee, Justin

Submitted to: American College of Veterinary Pathologists Meeting Publication Type: Abstract Only Publication Acceptance Date: August 12, 2015 Publication Date: N/A

Technical Abstract:

Chronic wasting disease (CWD) is a naturally-occurring, fatal neurodegenerative disease of North American cervids. Reindeer (Rangifer tarandus tarandus) are susceptible to CWD following oral challenge, but CWD has not been reported in free-ranging caribou (Rangifer tarandus caribou) or farmed reindeer. Potential contact between CWD-affected cervids and Rangifer species that are free-ranging or co-housed on farms presents a potential risk of CWD transmission. The aims of this study were to 1) investigate the transmission of CWD from white-tailed deer (Odocoileus virginianus; CWD-wtd), mule deer (Odocoileus hemionus; CWD-md), or elk (Cervus elaphus nelsoni; CWD-elk) to reindeer via the intracranial route, and 2) to assess for direct and indirect horizontal transmission to non-inoculated sentinels. Three groups of 5 reindeer fawns were challenged intracranially with CWD-wtd, CWD-md, or CWD-elk. Two years after challenge of inoculated reindeer, non-inoculated control reindeer were introduced into the same pen as the CWD-wtd inoculated reindeer (n=4) or into a pen adjacent to the CWD-md inoculated reindeer (n=2). Reindeer were allowed to develop clinical disease. At death/euthanasia a complete necropsy examination was performed, including immunohistochemical testing of tissues for disease-associated CWD prion protein (PrP-CWD). Intracranially challenged reindeer developed clinical disease from 21 months post-inoculation (MPI). PrP-CWD was detected in 5/6 sentinel reindeer although only 2/6 developed clinical disease during the study period (<57 div="" mpi="">

***We have shown that reindeer are susceptible to CWD from various cervid sources and can transmit CWD to naive reindeer both directly and indirectly.

Last Modified: 12/3/2015

http://www.ars.usda.gov/research/publications/publications.htm?SEQ_NO_115=317903

***PrP-CWD was detected in 5/6 sentinel reindeer although only 2/6 developed clinical disease during the study period (<57 div="" mpi="">

***We have shown that reindeer are susceptible to CWD from various cervid sources and can transmit CWD to naive reindeer both directly and indirectly.

Tuesday, September 29, 2015

*** Transmission of chronic wasting disease to sentinel reindeer (Rangifer tarandus tarandus) can transmit CWD to naive reindeer both directly and indirectly

Research Project: TRANSMISSION, DIFFERENTIATION, AND PATHOBIOLOGY OF TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES

http://chronic-wasting-disease.blogspot.com/2015/09/transmission-of-chronic-wasting-disease.html

*** Infectious agent of sheep scrapie may persist in the environment for at least 16 years ***

Gudmundur Georgsson1, Sigurdur Sigurdarson2 and Paul Brown3

http://jgv.sgmjournals.org/content/87/12/3737.full

*** Spraker suggested an interesting explanation for the occurrence of CWD. The deer pens at the Foot Hills Campus were built some 30-40 years ago by a Dr. Bob Davis. At or abut that time, allegedly, some scrapie work was conducted at this site. When deer were introduced to the pens they occupied ground that had previously been occupied by sheep.

http://collections.europarchive.org/tna/20080102193705/http://www.bseinquiry.gov.uk/files/mb/m11b/tab01.pdf

PL1

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.

https://prion2015.files.wordpress.com/2015/05/programguide1.pdf

see ;

http://www.tandfonline.com/doi/pdf/10.4161/pri.28467

http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0058630

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3567181/pdf/ppat.1003113.pdf

http://www.nature.com/srep/2015/150210/srep08358/full/srep08358.html?WT.ec_id=SREP-639-20150217

http://www.cell.com/cell-reports/pdfExtended/S2211-1247(15)00437-4

Wednesday, December 16, 2015

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

http://journal.frontiersin.org/article/10.3389/fvets.2015.00032/full

Wednesday, December 16, 2015

*** Objects in contact with classical scrapie sheep act as a reservoir for scrapie transmission ***

http://scrapie-usa.blogspot.com/2015/12/objects-in-contact-with-classical.html

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.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4397813/pdf/13567_2015_Article_176.pdf

Friday, December 14, 2012

DEFRA U.K. What is the risk of Chronic Wasting Disease CWD being introduced into Great Britain? A Qualitative Risk Assessment October 2012

snip...

In the USA, under the Food and Drug Administration’s BSE Feed Regulation (21 CFR 589.2000) most material (exceptions include milk, tallow, and gelatin) from deer and elk is prohibited for use in feed for ruminant animals. With regards to feed for non-ruminant animals, under FDA law, CWD positive deer may not be used for any animal feed or feed ingredients. For elk and deer considered at high risk for CWD, the FDA recommends that these animals do not enter the animal feed system. However, this recommendation is guidance and not a requirement by law.

Animals considered at high risk for CWD include:

1) animals from areas declared to be endemic for CWD and/or to be CWD eradication zones and

2) deer and elk that at some time during the 60-month period prior to slaughter were in a captive herd that contained a CWD-positive animal.

Therefore, in the USA, materials from cervids other than CWD positive animals may be used in animal feed and feed ingredients for non-ruminants.

The amount of animal PAP that is of deer and/or elk origin imported from the USA to GB can not be determined, however, as it is not specified in TRACES. It may constitute a small percentage of the 8412 kilos of non-fish origin processed animal proteins that were imported from US into GB in 2011.

Overall, therefore, it is considered there is a __greater than negligible risk___ that (nonruminant) animal feed and pet food containing deer and/or elk protein is imported into GB.

There is uncertainty associated with this estimate given the lack of data on the amount of deer and/or elk protein possibly being imported in these products.

snip...

36% in 2007 (Almberg et al., 2011). In such areas, population declines of deer of up to 30 to 50% have been observed (Almberg et al., 2011). In areas of Colorado, the prevalence can be as high as 30% (EFSA, 2011). The clinical signs of CWD in affected adults are weight loss and behavioural changes that can span weeks or months (Williams, 2005). In addition, signs might include excessive salivation, behavioural alterations including a fixed stare and changes in interaction with other animals in the herd, and an altered stance (Williams, 2005). These signs are indistinguishable from cervids experimentally infected with bovine spongiform encephalopathy (BSE). Given this, if CWD was to be introduced into countries with BSE such as GB, for example, infected deer populations would need to be tested to differentiate if they were infected with CWD or BSE to minimise the risk of BSE entering the human food-chain via affected venison.

snip...

The rate of transmission of CWD has been reported to be as high as 30% and can approach 100% among captive animals in endemic areas (Safar et al., 2008).

snip...

In summary, in endemic areas, there is a medium probability that the soil and surrounding environment is contaminated with CWD prions and in a bioavailable form. In rural areas where CWD has not been reported and deer are present, there is a greater than negligible risk the soil is contaminated with CWD prion.

snip...

In summary, given the volume of tourists, hunters and servicemen moving between GB and North America, the probability of at least one person travelling to/from a CWD affected area and, in doing so, contaminating their clothing, footwear and/or equipment prior to arriving in GB is greater than negligible. For deer hunters, specifically, the risk is likely to be greater given the increased contact with deer and their environment. However, there is significant uncertainty associated with these estimates.

snip...

Therefore, it is considered that farmed and park deer may have a higher probability of exposure to CWD transferred to the environment than wild deer given the restricted habitat range and higher frequency of contact with tourists and returning GB residents.

snip...

http://webarchive.nationalarchives.gov.uk/20130822084033/http://www.defra.gov.uk/animal-diseases/files/qra_chronic-wasting-disease-121029.pdf

Saturday, January 31, 2015

European red deer (Cervus elaphus elaphus) are susceptible to Bovine Spongiform Encephalopathy BSE by Oral Alimentary route

http://transmissiblespongiformencephalopathy.blogspot.com/2015/01/european-red-deer-cervus-elaphus.html

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 soon as possible for the following reasons...

======

In the USA, under the Food and Drug Administrations 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.

======

31 Jan 2015 at 20:14 GMT

*** Ruminant feed ban for cervids in the United States? ***

31 Jan 2015 at 20:14 GMT

http://www.plosone.org/annotation/listThread.action?root=85351

Research Project: TRANSMISSION, DIFFERENTIATION, AND PATHOBIOLOGY OF TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES

Title: Scrapie transmits to white-tailed deer by the oral route and has a molecular profile similar to chronic wasting disease

Authors

item Greenlee, Justin item Moore, S - item Smith, Jodi - item Kunkle, Robert item West Greenlee, M -

Submitted to: American College of Veterinary Pathologists Meeting Publication Type: Abstract Only Publication Acceptance Date: August 12, 2015 Publication Date: N/A Technical Abstract: The purpose of this work was to determine susceptibility of white-tailed deer (WTD) to the agent of sheep scrapie and to compare the resultant PrPSc to that of the original inoculum and chronic wasting disease (CWD). We inoculated WTD by a natural route of exposure (concurrent oral and intranasal (IN); n=5) with a US scrapie isolate. All scrapie-inoculated deer had evidence of PrPSc accumulation. PrPSc was detected in lymphoid tissues at preclinical time points, and deer necropsied after 28 months post-inoculation had clinical signs, spongiform encephalopathy, and widespread distribution of PrPSc in neural and lymphoid tissues. Western blotting (WB) revealed PrPSc with 2 distinct molecular profiles. WB on cerebral cortex had a profile similar to the original scrapie inoculum, whereas WB of brainstem, cerebellum, or lymph nodes revealed PrPSc with a higher profile resembling CWD. Homogenates with the 2 distinct profiles from WTD with clinical scrapie were further passaged to mice expressing cervid prion protein and intranasally to sheep and WTD. In cervidized mice, the two inocula have distinct incubation times. Sheep inoculated intranasally with WTD derived scrapie developed disease, but only after inoculation with the inoculum that had a scrapie-like profile. The WTD study is ongoing, but deer in both inoculation groups are positive for PrPSc by rectal mucosal biopsy. In summary, this work demonstrates that WTD are susceptible to the agent of scrapie, two distinct molecular profiles of PrPSc are present in the tissues of affected deer, and inoculum of either profile readily passes to deer.

http://www.ars.usda.gov/research/publications/publications.htm?SEQ_NO_115=317901

http://www.ars.usda.gov/research/publications/publications.htm?SEQ_NO_115=260467

White-tailed Deer are Susceptible to Scrapie by Natural Route of Infection

Jodi D. Smith, Justin J. Greenlee, and Robert A. Kunkle; Virus and Prion Research Unit, National Animal Disease Center, USDA-ARS

Interspecies transmission studies afford the opportunity to better understand the potential host range and origins of prion diseases. Previous experiments demonstrated that white-tailed deer are susceptible to sheep-derived scrapie by intracranial inoculation. The purpose of this study was to determine susceptibility of white-tailed deer to scrapie after a natural route of exposure. Deer (n=5) were inoculated by concurrent oral (30 ml) and intranasal (1 ml) instillation of a 10% (wt/vol) brain homogenate derived from a sheep clinically affected with scrapie. Non-inoculated deer were maintained as negative controls. All deer were observed daily for clinical signs. Deer were euthanized and necropsied when neurologic disease was evident, and tissues were examined for abnormal prion protein (PrPSc) by immunohistochemistry (IHC) and western blot (WB). One animal was euthanized 15 months post-inoculation (MPI) due to an injury. At that time, examination of obex and lymphoid tissues by IHC was positive, but WB of obex and colliculus were negative. Remaining deer developed clinical signs of wasting and mental depression and were necropsied from 28 to 33 MPI. Tissues from these deer were positive for scrapie by IHC and WB. Tissues with PrPSc immunoreactivity included brain, tonsil, retropharyngeal and mesenteric lymph nodes, hemal node, Peyer’s patches, and spleen. This work demonstrates for the first time that white-tailed deer are susceptible to sheep scrapie by potential natural routes of inoculation. In-depth analysis of tissues will be done to determine similarities between scrapie in deer after intracranial and oral/intranasal inoculation and chronic wasting disease resulting from similar routes of inoculation.

see full text ;

http://www.usaha.org/Portals/6/Reports/2010/report-cwal-2010.pdf

PO-039: A comparison of scrapie and chronic wasting disease in white-tailed deer

Justin Greenlee, Jodi Smith, Eric Nicholson US Dept. Agriculture; Agricultural Research Service, National Animal Disease Center; Ames, IA USA

http://www.landesbioscience.com/journals/prion/03-Prion6-2-Transmission-and-strains.pdf

White-tailed deer are susceptible to the agent of sheep scrapie by intracerebral inoculation

snip...

It is unlikely that CWD will be eradicated from free-ranging cervids, and the disease is likely to continue to spread geographically [10]. However, the potential that white-tailed deer may be susceptible to sheep scrapie by a natural route presents an additional confounding factor to halting the spread of CWD. This leads to the additional speculations that

1) infected deer could serve as a reservoir to infect sheep with scrapie offering challenges to scrapie eradication efforts and

2) CWD spread need not remain geographically confined to current endemic areas, but could occur anywhere that sheep with scrapie and susceptible cervids cohabitate.

This work demonstrates for the first time that white-tailed deer are susceptible to sheep scrapie by intracerebral inoculation with a high attack rate and that the disease that results has similarities to CWD. These experiments will be repeated with a more natural route of inoculation to determine the likelihood of the potential transmission of sheep scrapie to white-tailed deer. If scrapie were to occur in white-tailed deer, results of this study indicate that it would be detected as a TSE, but may be difficult to differentiate from CWD without in-depth biochemical analysis.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3199251/?tool=pubmed

http://chronic-wasting-disease.blogspot.com/2011/10/white-tailed-deer-are-susceptible-to.html

2012

PO-039: A comparison of scrapie and chronic wasting disease in white-tailed deer

Justin Greenlee, Jodi Smith, Eric Nicholson US Dept. Agriculture; Agricultural Research Service, National Animal Disease Center; Ames, IA USA

snip...

The results of this study suggest that there are many similarities in the manifestation of CWD and scrapie in WTD after IC inoculation including early and widespread presence of PrPSc in lymphoid tissues, clinical signs of depression and weight loss progressing to wasting, and an incubation time of 21-23 months. Moreover, western blots (WB) done on brain material from the obex region have a molecular profile similar to CWD and distinct from tissues of the cerebrum or the scrapie inoculum. However, results of microscopic and IHC examination indicate that there are differences between the lesions expected in CWD and those that occur in deer with scrapie: amyloid plaques were not noted in any sections of brain examined from these deer and the pattern of immunoreactivity by IHC was diffuse rather than plaque-like.

*** After a natural route of exposure, 100% of WTD were susceptible to scrapie.

Deer developed clinical signs of wasting and mental depression and were necropsied from 28 to 33 months PI. Tissues from these deer were positive for PrPSc by IHC and WB. Similar to IC inoculated deer, samples from these deer exhibited two different molecular profiles: samples from obex resembled CWD whereas those from cerebrum were similar to the original scrapie inoculum. On further examination by WB using a panel of antibodies, the tissues from deer with scrapie exhibit properties differing from tissues either from sheep with scrapie or WTD with CWD. Samples from WTD with CWD or sheep with scrapie are strongly immunoreactive when probed with mAb P4, however, samples from WTD with scrapie are only weakly immunoreactive. In contrast, when probed with mAb’s 6H4 or SAF 84, samples from sheep with scrapie and WTD with CWD are weakly immunoreactive and samples from WTD with scrapie are strongly positive. This work demonstrates that WTD are highly susceptible to sheep scrapie, but on first passage, scrapie in WTD is differentiable from CWD.

http://www.landesbioscience.com/journals/prion/03-Prion6-2-Transmission-and-strains.pdf

2011

*** After a natural route of exposure, 100% of white-tailed deer were susceptible to scrapie.

http://www.usaha.org/Portals/6/Reports/2011/report-cwal-2011.pdf

White-tailed Deer are Susceptible to Scrapie by Natural Route of Infection

Jodi D. Smith, Justin J. Greenlee, and Robert A. Kunkle; Virus and Prion Research Unit, National Animal Disease Center, USDA-ARS

see full text ;

http://www.usaha.org/Portals/6/Reports/2010/report-cwal-2010.pdf

PL1

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.

=========================

========================

https://prion2015.files.wordpress.com/2015/05/programguide1.pdf

see ;

http://www.tandfonline.com/doi/pdf/10.4161/pri.28467

http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0058630

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3567181/pdf/ppat.1003113.pdf

http://www.nature.com/srep/2015/150210/srep08358/full/srep08358.html?WT.ec_id=SREP-639-20150217

http://www.cell.com/cell-reports/pdfExtended/S2211-1247(15)00437-4

98 | Veterinary Record | January 24, 2015

EDITORIAL

Scrapie: a particularly persistent pathogen

Cristina Acín

Resistant prions in the environment have been the sword of Damocles for scrapie control and eradication. Attempts to establish which physical and chemical agents could be applied to inactivate or moderate scrapie infectivity were initiated in the 1960s and 1970s,with the first study of this type focusing on the effect of heat treatment in reducing prion infectivity (Hunter and Millson 1964). Nowadays, most of the chemical procedures that aim to inactivate the prion protein are based on the method developed by Kimberlin and collaborators (1983). This procedure consists of treatment with 20,000 parts per million free chlorine solution, for a minimum of one hour, of all surfaces that need to be sterilised (in laboratories, lambing pens, slaughterhouses, and so on). Despite this, veterinarians and farmers may still ask a range of questions, such as ‘Is there an official procedure published somewhere?’ and ‘Is there an international organisation which recommends and defines the exact method of scrapie decontamination that must be applied?’

From a European perspective, it is difficult to find a treatment that could be applied, especially in relation to the disinfection of surfaces in lambing pens of affected flocks. A 999/2001 EU regulation on controlling spongiform encephalopathies (European Parliament and Council 2001) did not specify a particular decontamination measure to be used when an outbreak of scrapie is diagnosed. There is only a brief recommendation in Annex VII concerning the control and eradication of transmissible spongiform encephalopathies (TSE s).

Chapter B of the regulation explains the measures that must be applied if new caprine animals are to be introduced to a holding where a scrapie outbreak has previously been diagnosed. In that case, the statement indicates that caprine animals can be introduced ‘provided that a cleaning and disinfection of all animal housing on the premises has been carried out following destocking’.

Issues around cleaning and disinfection are common in prion prevention recommendations, but relevant authorities, veterinarians and farmers may have difficulties in finding the specific protocol which applies. The European Food and Safety Authority (EFSA ) published a detailed report about the efficacy of certain biocides, such as sodium hydroxide, sodium hypochlorite, guanidine and even a formulation of copper or iron metal ions in combination with hydrogen peroxide, against prions (EFSA 2009). The report was based on scientific evidence (Fichet and others 2004, Lemmer and others 2004, Gao and others 2006, Solassol and others 2006) but unfortunately the decontamination measures were not assessed under outbreak conditions.

The EFSA Panel on Biological Hazards recently published its conclusions on the scrapie situation in the EU after 10 years of monitoring and control of the disease in sheep and goats (EFSA 2014), and one of the most interesting findings was the Icelandic experience regarding the effect of disinfection in scrapie control. The Icelandic plan consisted of: culling scrapie-affected sheep or the whole flock in newly diagnosed outbreaks; deep cleaning and disinfection of stables, sheds, barns and equipment with high pressure washing followed by cleaning with 500 parts per million of hypochlorite; drying and treatment with 300 ppm of iodophor; and restocking was not permitted for at least two years. Even when all of these measures were implemented, scrapie recurred on several farms, indicating that the infectious agent survived for years in the environment, even as many as 16 years after restocking (Georgsson and others 2006).

In the rest of the countries considered in the EFSA (2014) report, recommendations for disinfection measures were not specifically defined at the government level. In the report, the only recommendation that is made for sheep is repopulation with sheep with scrapie-resistant genotypes. This reduces the risk of scrapie recurrence but it is difficult to know its effect on the infection.

Until the EFSA was established (in May 2003), scientific opinions about TSE s were provided by the Scientific Steering Committee (SSC) of the EC, whose advice regarding inactivation procedures focused on treating animal waste at high temperatures (150°C for three hours) and high pressure alkaline hydrolysis (SSC 2003). At the same time, the TSE Risk Management Subgroup of the Advisory Committee on Dangerous Pathogens (ACDP) in the UK published guidance on safe working and the prevention of TSE infection. Annex C of the ACDP report established that sodium hypochlorite was considered to be effective, but only if 20,000 ppm of available chlorine was present for at least one hour, which has practical limitations such as the release of chlorine gas, corrosion, incompatibility with formaldehyde, alcohols and acids, rapid inactivation of its active chemicals and the stability of dilutions (ACDP 2009).

In an international context, the World Organisation for Animal Health (OIE) does not recommend a specific disinfection protocol for prion agents in its Terrestrial Code or Manual. Chapter 4.13 of the Terrestrial Code, General recommendations on disinfection and disinsection (OIE 2014), focuses on foot-and-mouth disease virus, mycobacteria and Bacillus anthracis, but not on prion disinfection. Nevertheless, the last update published by the OIE on bovine spongiform encephalopathy (OIE 2012) indicates that few effective decontamination techniques are available to inactivate the agent on surfaces, and recommends the removal of all organic material and the use of sodium hydroxide, or a sodium hypochlorite solution containing 2 per cent available chlorine, for more than one hour at 20ºC.

The World Health Organization outlines guidelines for the control of TSE s, and also emphasises the importance of mechanically cleaning surfaces before disinfection with sodium hydroxide or sodium hypochlorite for one hour (WHO 1999).

Finally, the relevant agencies in both Canada and the USA suggest that the best treatments for surfaces potentially contaminated with prions are sodium hydroxide or sodium hypochlorite at 20,000 ppm. This is a 2 per cent solution, while most commercial household bleaches contain 5.25 per cent sodium hypochlorite. It is therefore recommended to dilute one part 5.25 per cent bleach with 1.5 parts water (CDC 2009, Canadian Food Inspection Agency 2013).

So what should we do about disinfection against prions? First, it is suggested that a single protocol be created by international authorities to homogenise inactivation procedures and enable their application in all scrapie-affected countries. Sodium hypochlorite with 20,000 ppm of available chlorine seems to be the procedure used in most countries, as noted in a paper summarised on p 99 of this issue of Veterinary Record (Hawkins and others 2015). But are we totally sure of its effectiveness as a preventive measure in a scrapie outbreak? Would an in-depth study of the recurrence of scrapie disease be needed?

What we can conclude is that, if we want to fight prion diseases, and specifically classical scrapie, we must focus on the accuracy of diagnosis, monitoring and surveillance; appropriate animal identification and control of movements; and, in the end, have homogeneous and suitable protocols to decontaminate and disinfect lambing barns, sheds and equipment available to veterinarians and farmers. Finally, further investigations into the resistance of prion proteins in the diversity of environmental surfaces are required.

References

snip...

98 | Veterinary Record | January 24, 2015

http://veterinaryrecord.bmj.com/content/176/4/97.extract

Persistence of ovine scrapie infectivity in a farm environment following cleaning and decontamination

Steve A. C. Hawkins, MIBiol, Pathology Department1, Hugh A. Simmons, BVSc MRCVS, MBA, MA Animal Services Unit1, Kevin C. Gough, BSc, PhD2 and Ben C. Maddison, BSc, PhD3 + Author Affiliations

1Animal and Plant Health Agency, Woodham Lane, New Haw, Addlestone, Surrey KT15 3NB, UK 2School of Veterinary Medicine and Science, The University of Nottingham, Sutton Bonington, Loughborough, Leicestershire LE12 5RD, UK 3ADAS UK, School of Veterinary Medicine and Science, The University of Nottingham, Sutton Bonington, Loughborough, Leicestershire LE12 5RD, UK E-mail for correspondence: ben.maddison@adas.co.uk Abstract Scrapie of sheep/goats and chronic wasting disease of deer/elk are contagious prion diseases where environmental reservoirs are directly implicated in the transmission of disease. In this study, the effectiveness of recommended scrapie farm decontamination regimens was evaluated by a sheep bioassay using buildings naturally contaminated with scrapie. Pens within a farm building were treated with either 20,000 parts per million free chorine solution for one hour or were treated with the same but were followed by painting and full re-galvanisation or replacement of metalwork within the pen. Scrapie susceptible lambs of the PRNP genotype VRQ/VRQ were reared within these pens and their scrapie status was monitored by recto-anal mucosa-associated lymphoid tissue. All animals became infected over an 18-month period, even in the pen that had been subject to the most stringent decontamination process. These data suggest that recommended current guidelines for the decontamination of farm buildings following outbreaks of scrapie do little to reduce the titre of infectious scrapie material and that environmental recontamination could also be an issue associated with these premises.

SNIP...

Discussion

Thorough pressure washing of a pen had no effect on the amount of bioavailable scrapie infectivity (pen B). The routine removal of prions from surfaces within a laboratory setting is treatment for a minimum of one hour with 20,000 ppm free chlorine, a method originally based on the use of brain macerates from infected rodents to evaluate the effectiveness of decontamination (Kimberlin and others 1983). Further studies have also investigated the effectiveness of hypochlorite disinfection of metal surfaces to simulate the decontamination of surgical devices within a hospital setting. Such treatments with hypochlorite solution were able to reduce infectivity by 5.5 logs to lower than the sensitivity of the bioassay used (Lemmer and others 2004). Analogous treatment of the pen surfaces did not effectively remove the levels of scrapie infectivity over that of the control pens, indicating that this method of decontamination is not effective within a farm setting. This may be due to the high level of biological matrix that is present upon surfaces within the farm environment, which may reduce the amount of free chlorine available to inactivate any infectious prion. Remarkably 1/5 sheep introduced into pen D had also became scrapie positive within nine months, with all animals in this pen being RAMALT positive by 18 months of age. Pen D was no further away from the control pen (pen A) than any of the other pens within this barn. Localised hot spots of infectivity may be present within scrapie-contaminated environments, but it is unlikely that pen D area had an amount of scrapie contamination that was significantly different than the other areas within this building. Similarly, there were no differences in how the biosecurity of pen D was maintained, or how this pen was ventilated compared with the other pens. This observation, perhaps, indicates the slower kinetics of disease uptake within this pen and is consistent with a more thorough prion removal and recontamination. These observations may also account for the presence of inadvertent scrapie cases within other studies, where despite stringent biosecurity, control animals have become scrapie positive during challenge studies using barns that also housed scrapie-affected animals (Ryder and others 2009). The bioassay data indicate that the exposure of the sheep to a farm environment after decontamination efforts thought to be effective in removing scrapie is sufficient for the animals to become infected with scrapie. The main exposure routes within this scenario are likely to be via the oral route, during feeding and drinking, and respiratory and conjunctival routes. It has been demonstrated that scrapie infectivity can be efficiently transmitted via the nasal route in sheep (Hamir and others 2008), as is the case for CWD in both murine models and in white-tailed deer (Denkers and others 2010, 2013). Recently, it has also been demonstrated that CWD prions presented as dust when bound to the soil mineral montmorillonite can be infectious via the nasal route (Nichols and others 2013). When considering pens C and D, the actual source of the infectious agent in the pens is not known, it is possible that biologically relevant levels of prion survive on surfaces during the decontamination regimen (pen C). With the use of galvanising and painting (pen D) covering and sealing the surface of the pen, it is possible that scrapie material recontaminated the pens by the movement of infectious prions contained within dusts originating from other parts of the barn that were not decontaminated or from other areas of the farm.

Given that scrapie prions are widespread on the surfaces of affected farms (Maddison and others 2010a), irrespective of the source of the infectious prions in the pens, this study clearly highlights the difficulties that are faced with the effective removal of environmentally associated scrapie infectivity. This is likely to be paralleled in CWD which shows strong similarities to scrapie in terms of both the dissemination of prions into the environment and the facile mode of disease transmission. These data further contribute to the understanding that prion diseases can be highly transmissible between susceptible individuals not just by direct contact but through highly stable environmental reservoirs that are refractory to decontamination.

The presence of these environmentally associated prions in farm buildings make the control of these diseases a considerable challenge, especially in animal species such as goats where there is lack of genetic resistance to scrapie and, therefore, no scope to re-stock farms with animals that are resistant to scrapie.

Scrapie Sheep Goats Transmissible spongiform encephalopathies (TSE) Accepted October 12, 2014. Published Online First 31 October 2014

http://veterinaryrecord.bmj.com/content/early/2014/10/31/vr.102743.abstract

Monday, November 3, 2014

Persistence of ovine scrapie infectivity in a farm environment following cleaning and decontamination

http://transmissiblespongiformencephalopathy.blogspot.com/2014/11/persistence-of-ovine-scrapie.html

PPo3-22:

Detection of Environmentally Associated PrPSc on a Farm with Endemic Scrapie

Ben C. Maddison,1 Claire A. Baker,1 Helen C. Rees,1 Linda A. Terry,2 Leigh Thorne,2 Susan J. Belworthy2 and Kevin C. Gough3 1ADAS-UK LTD; Department of Biology; University of Leicester; Leicester, UK; 2Veterinary Laboratories Agency; Surry, KT UK; 3Department of Veterinary Medicine and Science; University of Nottingham; Sutton Bonington, Loughborough UK

Key words: scrapie, evironmental persistence, sPMCA

Ovine scrapie shows considerable horizontal transmission, yet the routes of transmission and specifically the role of fomites in transmission remain poorly defined. Here we present biochemical data demonstrating that on a scrapie-affected sheep farm, scrapie prion contamination is widespread. It was anticipated at the outset that if prions contaminate the environment that they would be there at extremely low levels, as such the most sensitive method available for the detection of PrPSc, serial Protein Misfolding Cyclic Amplification (sPMCA), was used in this study. We investigated the distribution of environmental scrapie prions by applying ovine sPMCA to samples taken from a range of surfaces that were accessible to animals and could be collected by use of a wetted foam swab. Prion was amplified by sPMCA from a number of these environmental swab samples including those taken from metal, plastic and wooden surfaces, both in the indoor and outdoor environment. At the time of sampling there had been no sheep contact with these areas for at least 20 days prior to sampling indicating that prions persist for at least this duration in the environment. These data implicate inanimate objects as environmental reservoirs of prion infectivity which are likely to contribute to disease transmission.

http://www.prion2010.org/bilder/prion_2010_program_latest_w_posters_4_.pdf?139&PHPSESSID=a30a38202cfec579000b77af81be3099

*** WISCONSIN CWD CAPTIVE LOTTO PAYS OUT AGAIN ***

*** This time State pays farmer $298,000 for infected deer herd

By Paul A. Smith of the Journal Sentinel

Jan. 16, 2016 8:05 p.m.

The State of Wisconsin paid nearly $300,000 to the Eau Claire County farmer whose deer herd was depopulated after it was found to be infected with chronic wasting disease.

Rick Vojtik, owner of Fairchild Whitetails in Fairchild, received an indemnity payment of $298,770 for 228 white-tailed deer killed on his farm, according to officials with the Department of Agriculture, Trade and Consumer Protection.

The money was taken from the agency's general program revenue funded by Wisconsin taxpayers.

The state has a maximum payment of $1,500 per animal in such cases; Vojtik received $1,310 each.

The adult deer killed at Fairchild Whitetails were tested for disease. Including those tested before depopulation, 33 deer at the facility were CWD-positive, according to the DATCP.

The CWD-positive deer on Vojtik's farm were the first and only detected to date in Eau Claire County and triggered a deer baiting and feeding ban in Eau Claire, Clark and Jackson counties.

More than a dozen deer escaped the facility last year but all were captured or killed, according to Rick Rosen, regional warden supervisor for the Department of Natural Resources.

In Wisconsin, the DATCP has authority over deer and elk farms while the DNR has authority over the fences at such facilities and deer and elk outside them.

Under an agreement with state officials, Vojtik will maintain the farm's fences for five years and not put deer or other cervids in the area. Agents with the DATCP will disinfect the property, said Paul McGraw, DATCP veterinarian.

The 228 deer had been held in an enclosure of about 10 acres.

Chronic wasting disease has been found at 13 captive cervid facilities in Wisconsin, according to DATCP records.

Second CWD finding in Oneida County: A second CWD-positive deer has been reported at an Oneida County shooting preserve, according to the DATCP.

The 5-year-old buck was shot at Three Lakes Trophy Ranch LLC in Three Lakes. The agency received the CWD-positive report on the animal Dec. 29.

A 3-year-old buck at the facility also tested positive for the disease in November, initiating a baiting and feeding ban in Oneida, Forest and Vilas counties.

Officials with the DATCP said Friday there was no plan to depopulate the facility. According to records from December, Three Lakes Trophy Ranch had about 425 deer on 570 acres.

The captive animals are the only deer to test positive for CWD in that portion of the Northwoods, including the Upper Peninsula of Michigan.

Last year, Michigan officials unveiled a campaign called "Keep the U.P. CWD Free!" It is illegal to bring whole deer carcasses from Wisconsin into Michigan.

Chronic wasting disease was identified in Colorado in 1967. The disease, among a family of transmissible spongiform encephalopathies including Mad Cow Disease and Creutzfeldt-Jakob, is fatal to deer, elk and moose. The disease was first detected in Wisconsin in 2002 near Mount Horeb. As of this month, 41 of the state's 72 counties are considered "CWD-affected" by the DNR.

Meat from a CWD-positive animal should not be eaten, according to health officials.

DNR hiring for creel survey: The DNR is accepting applications for three fisheries technicians to conduct creel surveys on Lake Michigan.

The limited-term employee positions will run from about March 7 to Oct. 31; the jobs will be based in Mishicot, Plymouth and Sturtevant.

According to the job description, candidates must be able to accurately identify common Lake Michigan fish; have good oral and written communication skills; be able to work independently with limited supervision; be able to approach anglers on piers and breakwaters, rocky shorelines, open sand, cobble beaches and along streams and rivers over uneven terrain; and be willing to work in inclement weather.

The jobs will pay $11.50 to $12.50 per hour depending on experience and training. Work is required on weekends and holidays.

For application materials and more information, visit dnr.wi.gov/employment. The application deadline is Feb. 2.

Interviews are planned the week of Feb. 8 at the DNR's Plymouth Service Center.

About Paul A. Smith Paul A. Smith covers outdoors and conservation issues.

@mjsps psmith@journalsentinel.com 414-224-2313

http://www.jsonline.com/sports/outdoors/state-pays-farmer-298000-for-infected-deer-herd-b99651670z1-365554851.html

CHRONIC WASTING DISEASE CWD WISCONSIN Almond Deer (Buckhorn Flats) Farm Update DECEMBER 2011

The CWD infection rate was nearly 80%, the highest ever in a North American captive herd.

RECOMMENDATION: That the Board approve the purchase of 80 acres of land for $465,000 for the Statewide Wildlife Habitat Program in Portage County and approve the restrictions on public use of the site.

SUMMARY:

http://dnr.wi.gov/about/nrb/2011/december/12-11-2b2.pdf

$298,770 + $465,000

Friday, December 04, 2015

Wisconsin CWD-positive white-tailed deer found on Oneida County hunting preserve December 3, 2015

http://chronic-wasting-disease.blogspot.com/2015/12/wisconsin-cwd-positive-white-tailed.html

Wednesday, March 04, 2015

*** Disease sampling results provide current snapshot of CWD in Wisconsin finding 324 positive detections statewide in 2014

http://chronic-wasting-disease.blogspot.com/2015/03/disease-sampling-results-provide.html

Wednesday, December 16, 2015

Wisconsin Chronic wasting disease confirmed in Crawford County buck harvested on private land

http://chronic-wasting-disease.blogspot.com/2015/12/wisconsin-chronic-wasting-disease.html

HIGHEST INFECTION RATE ON SEVERAL CWD CONFIRMED CAPTIVES

CHRONIC WASTING DISEASE CWD WISCONSIN Almond Deer (Buckhorn Flats) Farm Update DECEMBER 2011

The CWD infection rate was nearly 80%, the highest ever in a North American captive herd.

SUMMARY:

http://dnr.wi.gov/about/nrb/2011/december/12-11-2b2.pdf

For Immediate Release Thursday, October 2, 2014

Dustin Vande Hoef 515/281-3375 or 515/326-1616 (cell) or Dustin.VandeHoef@IowaAgriculture.gov

*** TEST RESULTS FROM CAPTIVE DEER HERD WITH CHRONIC WASTING DISEASE RELEASED 79.8 percent of the deer tested positive for the disease

DES MOINES – The Iowa Department of Agriculture and Land Stewardship today announced that the test results from the depopulation of a quarantined captive deer herd in north-central Iowa showed that 284 of the 356 deer, or 79.8% of the herd, tested positive for Chronic Wasting Disease (CWD).

http://www.iowaagriculture.gov/press/2014press/press10022014.asp

*** see history of this CWD blunder here ;

http://www.iowadnr.gov/Portals/idnr/uploads/Hunting/070313_consent_order.pdf

On June 5, 2013, DNR conducted a fence inspection, after gaining approval from surrounding landowners, and confirmed that the fenced had been cut or removed in at least four separate locations; that the fence had degraded and was failing to maintain the enclosure around the Quarantined Premises in at least one area; that at least three gates had been opened;and that deer tracks were visible in and around one of the open areas in the sand on both sides of the fence, evidencing movement of deer into the Quarantined Premises.

http://www.iowadnr.gov/Portals/idnr/uploads/Hunting/060613_consent_order.pdf

The overall incidence of clinical CWD in white-tailed deer was 82%

Species (cohort) CWD (cases/total) Incidence (%) Age at CWD death (mo)

https://cpw.state.co.us/Documents/Hunting/BigGame/CWD/PDF/ResearchArticles/JWDEpiCWD.pdf

”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.

http://collections.europarchive.org/tna/20080102193705/http://www.bseinquiry.gov.uk/files/mb/m11b/tab01.pdf

Sunday, January 06, 2013

USDA TO PGC ONCE CAPTIVES ESCAPE

*** "it‘s no longer its business.”

http://chronic-wasting-disease.blogspot.com/2013/01/usda-to-pgc-once-captives-escape-its-no.html

CWD, spreading it around...

for the game farm industry, and their constituents, to continue to believe that they are _NOT_, and or insinuate that they have _NEVER_ been part of the problem, will only continue to help spread cwd. the game farming industry, from the shooting pens, to the urine mills, the antler mills, the sperm mills, velvet mills, shooting pens, to large ranches, are not the only problem, but it is painfully obvious that they have been part of the problem for decades and decades, just spreading it around, as with transportation and or exportation and or importation of cervids from game farming industry, and have been proven to spread cwd. no one need to look any further than South Korea blunder ;

===========================================

spreading cwd around...

Between 1996 and 2002, chronic wasting disease was diagnosed in 39 herds of farmed elk in Saskatchewan in a single epidemic. All of these herds were depopulated as part of the Canadian Food Inspection Agency’s (CFIA) disease eradication program. Animals, primarily over 12 mo of age, were tested for the presence CWD prions following euthanasia. Twenty-one of the herds were linked through movements of live animals with latent CWD from a single infected source herd in Saskatchewan, 17 through movements of animals from 7 of the secondarily infected herds.

***The source herd is believed to have become infected via importation of animals from a game farm in South Dakota where CWD was subsequently diagnosed (7,4). A wide range in herd prevalence of CWD at the time of herd depopulation of these herds was observed. Within-herd transmission was observed on some farms, while the disease remained confined to the introduced animals on other farms.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2081988/

spreading cwd around...

Friday, May 13, 2011

Chronic Wasting Disease (CWD) outbreaks and surveillance program in the Republic of Korea

Hyun-Joo Sohn, Yoon-Hee Lee, Min-jeong Kim, Eun-Im Yun, Hyo-Jin Kim, Won-Yong Lee, Dong-Seob Tark, In- Soo Cho, Foreign Animal Disease Research Division, National Veterinary Research and Quarantine Service, Republic of Korea

Chronic wasting disease (CWD) has been recognized as an important prion disease in native North America deer and Rocky mountain elks. The disease is a unique member of the transmissible spongiform encephalopathies (TSEs), which naturally affects only a few species. CWD had been limited to USA and Canada until 2000.

On 28 December 2000, information from the Canadian government showed that a total of 95 elk had been exported from farms with CWD to Korea. These consisted of 23 elk in 1994 originating from the so-called “source farm” in Canada, and 72 elk in 1997, which had been held in pre export quarantine at the “source farm”.Based on export information of CWD suspected elk from Canada to Korea, CWD surveillance program was initiated by the Ministry of Agriculture and Forestry (MAF) in 2001.

All elks imported in 1997 were traced back, however elks imported in 1994 were impossible to identify. CWD control measures included stamping out of all animals in the affected farm, and thorough cleaning and disinfection of the premises. In addition, nationwide clinical surveillance of Korean native cervids, and improved measures to ensure reporting of CWD suspect cases were implemented.

Total of 9 elks were found to be affected. CWD was designated as a notifiable disease under the Act for Prevention of Livestock Epidemics in 2002.

Additional CWD cases - 12 elks and 2 elks - were diagnosed in 2004 and 2005.

Since February of 2005, when slaughtered elks were found to be positive, all slaughtered cervid for human consumption at abattoirs were designated as target of the CWD surveillance program. Currently, CWD laboratory testing is only conducted by National Reference Laboratory on CWD, which is the Foreign Animal Disease Division (FADD) of National Veterinary Research and Quarantine Service (NVRQS).

In July 2010, one out of 3 elks from Farm 1 which were slaughtered for the human consumption was confirmed as positive. Consequently, all cervid – 54 elks, 41 Sika deer and 5 Albino deer – were culled and one elk was found to be positive. Epidemiological investigations were conducted by Veterinary Epidemiology Division (VED) of NVRQS in collaboration with provincial veterinary services.

Epidemiologically related farms were found as 3 farms and all cervid at these farms were culled and subjected to CWD diagnosis. Three elks and 5 crossbreeds (Red deer and Sika deer) were confirmed as positive at farm 2.

All cervids at Farm 3 and Farm 4 – 15 elks and 47 elks – were culled and confirmed as negative.

Further epidemiological investigations showed that these CWD outbreaks were linked to the importation of elks from Canada in 1994 based on circumstantial evidences.

In December 2010, one elk was confirmed as positive at Farm 5. Consequently, all cervid – 3 elks, 11 Manchurian Sika deer and 20 Sika deer – were culled and one Manchurian Sika deer and seven Sika deer were found to be positive. This is the first report of CWD in these sub-species of deer. Epidemiological investigations found that the owner of the Farm 2 in CWD outbreaks in July 2010 had co-owned the Farm 5.

In addition, it was newly revealed that one positive elk was introduced from Farm 6 of Jinju-si Gyeongsang Namdo. All cervid – 19 elks, 15 crossbreed (species unknown) and 64 Sika deer – of Farm 6 were culled, but all confirmed as negative.

http://www.prion2011.ca/files/2011TSEBookletV6Final.pdf

http://www.prion2011.ca/files/PRION_2011_-_Posters_(May_5-11).pdf

http://www.cwd-info.org/index.php/fuseaction/news.detail/ID/c792d0e56e0cb3ee3a6517e754729cac

http://chronic-wasting-disease.blogspot.com/2011/05/chronic-wasting-disease-cwd-outbreaks.html

New studies on the heat resistance of hamster-adapted scrapie agent: Threshold survival after ashing at 600°C suggests an inorganic template of replication

The infectious agents responsible for transmissible spongiform encephalopathy (TSE) are notoriously resistant to most physical and chemical methods used for inactivating pathogens, including heat. It has long been recognized, for example, that boiling is ineffective and that higher temperatures are most efficient when combined with steam under pressure (i.e., autoclaving). As a means of decontamination, dry heat is used only at the extremely high temperatures achieved during incineration, usually in excess of 600°C. It has been assumed, without proof, that incineration totally inactivates the agents of TSE, whether of human or animal origin.

http://www.pnas.org/content/97/7/3418.full

Prion Infected Meat-and-Bone Meal Is Still Infectious after Biodiesel Production

Histochemical analysis of hamster brains inoculated with the solid residue showed typical spongiform degeneration and vacuolation. Re-inoculation of these brains into a new cohort of hamsters led to onset of clinical scrapie symptoms within 75 days, suggesting that the specific infectivity of the prion protein was not changed during the biodiesel process. The biodiesel reaction cannot be considered a viable prion decontamination method for MBM, although we observed increased survival time of hamsters and reduced infectivity greater than 6 log orders in the solid MBM residue. Furthermore, results from our study compare for the first time prion detection by Western Blot versus an infectivity bioassay for analysis of biodiesel reaction products. We could show that biochemical analysis alone is insufficient for detection of prion infectivity after a biodiesel process.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2493038/

Detection of protease-resistant cervid prion protein in water from a CWD-endemic area

The data presented here demonstrate that sPMCA can detect low levels of PrPCWD in the environment, corroborate previous biological and experimental data suggesting long term persistence of prions in the environment2,3 and imply that PrPCWD accumulation over time may contribute to transmission of CWD in areas where it has been endemic for decades. This work demonstrates the utility of sPMCA to evaluate other environmental water sources for PrPCWD, including smaller bodies of water such as vernal pools and wallows, where large numbers of cervids congregate and into which prions from infected animals may be shed and concentrated to infectious levels.

http://www.landesbioscience.com/journals/prion/NicholsPRION3-3.pdf

A Quantitative Assessment of the Amount of Prion Diverted to Category 1 Materials and Wastewater During Processing

Keywords:Abattoir;bovine spongiform encephalopathy;QRA;scrapie;TSE

In this article the development and parameterization of a quantitative assessment is described that estimates the amount of TSE infectivity that is present in a whole animal carcass (bovine spongiform encephalopathy [BSE] for cattle and classical/atypical scrapie for sheep and lambs) and the amounts that subsequently fall to the floor during processing at facilities that handle specified risk material (SRM). BSE in cattle was found to contain the most oral doses, with a mean of 9864 BO ID50s (310, 38840) in a whole carcass compared to a mean of 1851 OO ID50s (600, 4070) and 614 OO ID50s (155, 1509) for a sheep infected with classical and atypical scrapie, respectively. Lambs contained the least infectivity with a mean of 251 OO ID50s (83, 548) for classical scrapie and 1 OO ID50s (0.2, 2) for atypical scrapie. The highest amounts of infectivity falling to the floor and entering the drains from slaughtering a whole carcass at SRM facilities were found to be from cattle infected with BSE at rendering and large incineration facilities with 7.4 BO ID50s (0.1, 29), intermediate plants and small incinerators with a mean of 4.5 BO ID50s (0.1, 18), and collection centers, 3.6 BO ID50s (0.1, 14). The lowest amounts entering drains are from lambs infected with classical and atypical scrapie at intermediate plants and atypical scrapie at collection centers with a mean of 3 × 10−7 OO ID50s (2 × 10−8, 1 × 10−6) per carcass. The results of this model provide key inputs for the model in the companion paper published here.

http://onlinelibrary.wiley.com/doi/10.1111/j.1539-6924.2012.01922.x/abstract

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***

===============

https://prion2015.files.wordpress.com/2015/05/prion2015abstracts.pdf

==========================================

***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.

==========================================

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.***

================

https://prion2015.files.wordpress.com/2015/05/programguide1.pdf

*** 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).***

https://www.landesbioscience.com/journals/prion/article/28124/?nocache=112223249

*** 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.

http://cdmrp.army.mil/prevfunded/nprp/NPRP_Summit_Final_Report.pdf

now, let’s see what the authors said about this casual link, personal communications years ago. 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 ;

http://chronic-wasting-disease.blogspot.com/2008/04/prion-disease-of-cervids-chronic.html

CJD is so rare in people under age 30, one case in a billion (leaving out medical mishaps), that four cases under 30 is "very high," says Colorado neurologist Bosque. "Then, if you add these other two from Wisconsin [cases in the newspaper], six cases of CJD in people associated with venison is very, very high." Only now, with Mary Riley, there are at least seven, and possibly eight, with Steve, her dining companion. "It's not critical mass that matters," however, Belay says. "One case would do it for me." The chance that two people who know each other would both contact CJD, like the two Wisconsin sportsmen, is so unlikely, experts say, it would happen only once in 140 years.

Given the incubation period for TSEs in humans, it may require another generation to write the final chapter on CWD in Wisconsin. "Does chronic wasting disease pass into humans? We'll be able to answer that in 2022," says Race. Meanwhile, the state has become part of an immense experiment.

https://www.organicconsumers.org/old_articles/madcow/killer123103.php

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 ***

http://zoomify.uzh.ch:8080/zoomify/videos/video-004/video-004.html

https://www.landesbioscience.com/journals/prion/article/28124/?nocache=112223249

***This information will have a scientific impact since it is the first study that demonstrates the transmission of scrapie to a non-human primate with a close genetic relationship to humans. This information is especially useful to regulatory officials and those involved with risk assessment of the potential transmission of animal prion diseases to humans.

***This observation strengthens the questioning of the harmlessness of scrapie to humans, at a time when protective measures for human and animal health are being dismantled and reduced as c-BSE is considered controlled and being eradicated. Our results underscore the importance of precautionary and protective measures and the necessity for long-term experimental transmission studies to assess the zoonotic potential of other animal prion strains.

http://www.ars.usda.gov/research/publications/publications.htm?SEQ_NO_115=313160

Research Project: TRANSMISSION, DIFFERENTIATION, AND PATHOBIOLOGY OF TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES

Title: Evaluation of the zoonotic potential of transmissible mink encephalopathy

Authors

item Comoy, Emmanuel - item Mikol, Jacqueline - item Ruchoux, Marie-Madeleine - item Durand, Valerie - item Luccantoni-Freire, Sophie - item Dehen, Capucine - item Correia, Evelyne - item Casalone, Cristina - item Richt, Juergen item Greenlee, Justin item Torres, Juan Maria - item Brown, Paul - item Deslys, Jean-Philippe -

Submitted to: Pathogens Publication Type: Peer Reviewed Journal Publication Acceptance Date: July 30, 2013 Publication Date: July 30, 2013 Citation: Comoy, E.E., Mikol, J., Ruchoux, M., Durand, V., Luccantoni-Freire, S., Dehen, C., Correia, E., Casalone, C., Richt, J.A., Greenlee, J.J., Torres, J.M., Brown, P., Deslys, J. 2013. Evaluation of the zoonotic potential of transmissible mink encephalopathy. Pathogens. 2:(3)520-532.

Interpretive Summary: Cases of bovine spongiform encephalopathy (BSE) or mad cow disease can be subclassified into at least 3 distinct disease forms with the predominate form known as classical BSE and the others collectively referred to as atypical BSE. Atypical BSE can be further subdivided into H-type and L-type cases that are distinct from classical BSE and from each other. Both of the atypical BSE subtypes are believed to occur spontaneously, whereas classical BSE is spread through feeding contaminated meat and bone meal to cattle. Transmissible mink encephalopathy (TME) is another prion disease that transmits to cattle and show similarities to L-type BSE when subjected to laboratory testing. The purpose of this study was to use non-human primates (cynomologous macaque) and transgenic mice expressing the human prion protein to determine if TME could represent a potential risk to human health. TME from two sources (cattle and raccoons) was able to infect non-human primates and transgenic mice after exposure by the intracranial route. This result suggest that humans may be able to replicate TME prions after an exposure that allows infectious material access to brain tissue. At this time, it is unknown whether non-human primates or transgenic mice would be susceptible to TME prions after oral exposure. The results obtained in these animal models were similar to those obtained for L-type BSE. Although rare, the existence of TME and that it transmits to cattle, non-human primates, and transgenic mice suggest that feed bans preventing the feeding of mammalian tissues to cattle should stay in place and that regular prion surveillance during the slaughter should remain in place. Parties with interest in the cattle and beef industries and regulatory officials responsible for safe feeding practices of cattle will be interested in this work. Technical Abstract: Successful transmission of Transmissible Mink Encephalopathy (TME) to cattle supports the bovine hypothesis to the still controversial origin of TME outbreaks. Human and primate susceptibility to classical Bovine Spongiform Encephalopathy (c-BSE) and the transmissibility of L-type BSE to macaques assume a low cattle-to-primate species barrier: we therefore evaluated the zoonotic potential of cattle-adapted TME. In less than two years, this strain induced in cynomolgus macaques a neurological disease similar to L-BSE and distinct from c-BSE. TME derived from another donor species (raccoon) induced a similar disease with shorter incubation periods.

*** L-BSE and cattle-adapted TME were also transmissible to transgenic mice expressing human PrP. Interestingly, secondary transmissions to transgenic mice expressing bovine PrP showed the maintenance of prion strain features for the three tested bovine prion strains (cattle TME, c-BSE and L-BSE) regardless of intermediate host.

*** Thus, TME is the third animal prion strain transmissible to both macaques and humanized transgenic mice, suggesting zoonotic potentials that should be considered in the risk analysis of animal prion diseases for human health.

*** Moreover, the similarities between TME and L-BSE are highly suggestive of a link between those strains, and of the presence of L-BSE decades prior to its identification in USA and Europe.

http://www.ars.usda.gov/research/publications/publications.htm?seq_no_115=293985

Research Project: TRANSMISSION, DIFFERENTIATION, AND PATHOBIOLOGY OF TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES

Title: Scrapie transmits to white-tailed deer by the oral route and has a molecular profile similar to chronic wasting disease

Authors

item Greenlee, Justin item Moore, S - item Smith, Jodi - item Kunkle, Robert item West Greenlee, M -

http://www.ars.usda.gov/research/publications/publications.htm?SEQ_NO_115=317901

http://www.ars.usda.gov/research/publications/publications.htm?SEQ_NO_115=260467

Monday, November 16, 2015

*** Docket No. APHIS-2007-0127 Scrapie in Sheep and Goats Terry Singeltary Sr. Submission ***

http://www.regulations.gov/#!documentDetail;D=APHIS-2007-0127-0032

http://scrapie-usa.blogspot.com/2015/11/docket-no-aphis-2007-0127-scrapie-in.html

Saturday, December 12, 2015

*** CHRONIC WASTING DISEASE CWD TSE PRION REPORT DECEMBER 14, 2015

http://chronic-wasting-disease.blogspot.com/2015/12/chronic-wasting-disease-cwd-tse-prion.html

Friday, May 22, 2015

*** Chronic Wasting Disease and Program Updates - 2014 NEUSAHA Annual Meeting 12-14 May 2014

http://chronic-wasting-disease.blogspot.com/2015/05/chronic-wasting-disease-and-program.html

TEXAS CHRONIC WASTING DISEASE CWD TSE PRION

Friday, January 01, 2016

*** Bayesian Modeling of Prion Disease Dynamics in Mule Deer Using Population Monitoring and Capture-Recapture Data

http://chronic-wasting-disease.blogspot.com/2016/01/bayesian-modeling-of-prion-disease.html

Tuesday, December 15, 2015

Chronic Wasting Disease will cause a Wyoming deer herd to go virtually extinct in 41 years, a five-year study predicts

Study: Chronic Wasting Disease kills 19% of deer herd annually

http://chronic-wasting-disease.blogspot.com/2015/12/chronic-wasting-disease-will-cause.html

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

http://chronic-wasting-disease.blogspot.com/2016/01/texas-10000-deer-in-texas-tested-for.html

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

http://chronic-wasting-disease.blogspot.com/2016/01/texas-media-reporting-bit-of-good-news.html

Friday, January 15, 2016

TEXAS PARKS & WILDLIFE CWD Ante-Mortem Testing Symposium Texas Disposal Systems Events Pavilion January 12, 2016

http://chronic-wasting-disease.blogspot.com/2016/01/texas-parks-wildlife-cwd-ante-mortem.html

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. ***

http://chronic-wasting-disease.blogspot.com/2015/12/texas-monthly-chronic-wasting-disease.html

Saturday, December 12, 2015

*** CHRONIC WASTING DISEASE CWD TSE PRION REPORT DECEMBER 14, 2015

http://chronic-wasting-disease.blogspot.com/2015/12/chronic-wasting-disease-cwd-tse-prion.html

actually, if these two new captive suspect CWD cases are confirmed, that would be a total of 7 cases of CWD in Captive in Texas, PLUS the 8 other confirmed cases of CWD up in the Texas Trans Pecos region to date in the mule deer. So the total would be 15 cases of the CWD TSE Prion aka mad cow type disease in Cervid in Texas, to date. just to put everything in perspective. BUT, that would only be IF and WHEN, the TAHC or the TPWD ever confirm these two new recent suspect CWD cases.

I am only reminded of another great article Shannon Tompkins wrote years ago, when the CWD TSE Prion shoe was on the other foot...

March 14, 2002

"Ten years ago, elk and deer (imported into Texas) were not regulated at all," said Dr. Ken Waldrup, an epidemiologist with the Texas Animal Health Commission and one of the agency's point men on CWD. "If Texas doesn't already have CWD, then I say that proves that God is a Texan. "For everyone's sake, I sure hope He is."

========================

*** Tompkins: There are a lot of reasons to be concerned about CWD

Houston Chronicle Published 5:30 a.m., Thursday, March 14, 2002

where are any statements from the TAHC or TPWD either confirming this, or refuting this???

Saturday, November 14, 2015 TEXAS CAPTIVE BREEDER CHRONIC WASTING DISEASE CWD 2 MORE SUSPECTS DECTECTED

http://chronic-wasting-disease.blogspot.com/2015/11/texas-captive-breeder-chronic-wasting.html

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

http://chronic-wasting-disease.blogspot.com/2015/11/texas-parks-and-wildlife-department.html

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).

http://chronic-wasting-disease.blogspot.com/2015/11/texas-captive-breeder-chronic-wasting.html

Thursday, November 05, 2015

*** TPW Commission Adopts Interim Deer Breeder Movement Rules

http://chronic-wasting-disease.blogspot.com/2015/11/tpw-commission-adopts-interim-deer.html

Friday, October 09, 2015

Texas TWA Chronic Wasting Disease TSE Prion Webinars and Meeting October 2015

http://chronic-wasting-disease.blogspot.com/2015/10/texas-twa-chronic-wasting-disease-tse.html

Saturday, October 03, 2015

TEXAS CHRONIC WASTING DISEASE CWD TSE PRION GOD MUST NOT BE A TEXAN 2002 TO 2015

http://chronic-wasting-disease.blogspot.com/2015/10/texas-chronic-wasting-disease-cwd-tse.html

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

http://chronic-wasting-disease.blogspot.com/2015/09/texas-hunters-asked-to-submit-samples.html

***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

http://chronic-wasting-disease.blogspot.com/2015/08/tahc-chronic-wasting-disease-cwd-tse.html

Friday, August 07, 2015

*** Texas CWD Captive, and then there were 4 ?

http://chronic-wasting-disease.blogspot.com/2015/08/texas-cwd-captive-and-then-there-were-4.html

Thursday, August 06, 2015

*** WE HAVE LOST TEXAS TO CWD TASK FORCE CATERING TO INDUSTRY

http://chronic-wasting-disease.blogspot.com/2015/08/we-have-lost-texas-to-cwd-task-force.html

Tuesday, July 21, 2015

*** Texas CWD Medina County Herd Investigation Update July 16, 2015 ***

http://chronic-wasting-disease.blogspot.com/2015/07/texas-cwd-medina-county-herd.html

Thursday, July 09, 2015

TEXAS Chronic Wasting Disease (CWD) Herd Plan for Trace-Forward Exposed Herd with Testing of Exposed Animals

http://chronic-wasting-disease.blogspot.com/2015/07/texas-chronic-wasting-disease-cwd-herd.html

Wednesday, July 01, 2015

TEXAS Chronic Wasting Disease Detected in Medina County Captive Deer

http://chronic-wasting-disease.blogspot.com/2015/07/texas-chronic-wasting-disease-detected.html

Wednesday, March 18, 2015

Chronic Wasting Disease CWD Confirmed Texas Trans Pecos March 18, 2015

http://chronic-wasting-disease.blogspot.com/2015/03/chronic-wasting-disease-cwd-confirmed.html

Wednesday, March 25, 2015

Chronic Wasting Disease CWD Cases Confirmed In New Mexico 2013 and 2014 UPDATE 2015

http://chronic-wasting-disease.blogspot.com/2015/03/chronic-wasting-disease-cwd-cases.html

Thursday, May 02, 2013

*** Chronic Wasting Disease (CWD) Texas Important Update on OBEX ONLY TEXTING

http://chronic-wasting-disease.blogspot.com/2013/05/chronic-wasting-disease-cwd-texas.html

Monday, February 11, 2013

TEXAS CHRONIC WASTING DISEASE CWD Four New Positives Found in Trans Pecos

http://chronic-wasting-disease.blogspot.com/2013/02/texas-chronic-wasting-disease-cwd-four.html

Tuesday, July 10, 2012

Chronic Wasting Disease Detected in Far West Texas

http://chronic-wasting-disease.blogspot.com/2012/07/chronic-wasting-disease-detected-in-far.html

Monday, March 26, 2012

Texas Prepares for Chronic Wasting Disease CWD Possibility in Far West Texas

http://chronic-wasting-disease.blogspot.com/2012/03/texas-prepares-for-chronic-wasting.html

CWD TEXAS TAHC OLD FILE HISTORY

updated from some of my old files. ...

Subject: CWD SURVEILLANCE STATISTICS TEXAS (total testing figures less than 50 in two years)

Date: Sun, 25 Aug 2002 21:06:49 –0700

From: "Terry S. Singeltary Sr."

Reply-To: Bovine Spongiform Encephalopathy

To: BSE-L@uni-karlsruhe.de

######## Bovine Spongiform Encephalopathy #########

greetings list members,

here are some figures on CWD testing in TEXAS...TSS

Dear Dr. Singletary,

In Fiscal Year 2001, seven deer from Texas were tested by the National Veterinary Services Laboratory (NVSL) for CWD (5 fallow deer and 2 white-tailed deer). In Fiscal Year 2002, seven elk from Texas were tested at NVSL (no deer). During these two years, an additional six elk and one white-tailed deer were tested at the Texas Veterinary Medical Diagnostic Laboratory (TVMDL). In Fiscal Year 2002, four white-tailed deer (free-ranging clinical suspects) and at least eight other white-tailed deer have been tested at TVMDL. One elk has been tested at NVSL. All of these animals have been found negative for CWD. Dr. Jerry Cooke of the Texas Parks and Wildlife Department also has records of 601 clinically ill white-tailed deer which were necropsied at Texas A&M during the late 1960's and early 1970's, and no spongiform encepalopathies were noted. Thank you for your consideration.

xxxxxxx

Texas Animal Health Commission

(personal communication...TSS)

Austin 8 news

snip...

"There's about 4 million deer in the state of Texas, and as a resource I think we need to be doing as much as we can to look for these diseases," said Doug Humphreys with Texas Parks and Wildlife. "Right now Texas is clear. We haven't found any, but that doesn't mean we don't look."

http://news8austin.com/content/living/8_outdoors/?ArID=43069

With approximately 4 million animals, Texas has the largest population of white-tailed deer in the nation. In addition, about 19,000 white-tailed deer and 17,000 elk are being held in private facilities. To know if CWD is present in captive herds, TPWD and Texas Animal Health Commission are working with breeders to monitor their herds.

http://www.tahc.state.tx.us/

How is it spread?

It is not known exactly how CWD is spread. It is believed that the agent responsible for the disease may be spread both directly (animal to animal contact) and indirectly (soil or other surface to animal). It is thought that the most common mode of transmission from an infected animal is via saliva, feces, and urine.

http://www.tpwd.state.tx.us/hunt/

some surveillance?

beyond the _potential_ methods of transmissions above, why, not a single word of SRM of various TSE species in feed as a source?

it's a known fact they have been feeding the deer/elk the same stuff as cows here in USA.

and the oral route has been documented of CWD to mule deer fawns in lab studies.

not to say that other _potential_ transmission mechanisms are possible, but why over look the obvious?

TSS

########### http://mailhost.rz.uni-karlsruhe.de/warc/bse-l.html ############

From: Ken Waldrup, DVM, PhD (host25-207.tahc.state.tx.us)

Subject: Re: CWD SAMPLING TEXAS (but NOT in the obvious place, the NM, TEXAS border)

Date: December 15, 2003 at 3:43 pm PST

In Reply to: CWD SAMPLING TEXAS (but NOT in the obvious place, the NM, TEXAS border) posted by TSS on December 12, 2003 at 2:15 pm:

Dear sirs:

With regard to your comment about Texas NOT looking for CWD along the New Mexico border, it is painfully obvious that you do not know or understand the natural distribution of mule deer out there or the rights of the land owners in this state. As of 15 December 2003, a total of 42 deer had been sampled from what we call "Trans-Pecos", beyond the Pecos River. Mule deer are very widely dispersed through this area, sometimes at densities of one animal per 6 square miles. The Texas Parks and Wildlife Department does not have the legal authority to trepass on private property to collect deer. Some landowners are cooperative. Some are not. Franklin State Park is at the very tip of Texas, and deer from the park have been tested (all negative). One of the single largest land owners along the border is the National Park Service. Deer and elk from the Guadalupe Peak National Park cannot be collected with federal permission. The sampling throughout the state is based on the deer populations by eco-region and is dictated by the availability of funds. I am concerned about your insinuation that CWD is a human health risk. We are at a stand-off - you have no proof that it is and I have no definitive proof that it isn't. However I would say that the inferred evidence from Colorado, Wyoming and Wisconsin suggests that CWD is not a human health concern (i.e. no evidence of an increased incidence of human brain disorders within the CWD "endemic" areas of these states). From my professional interactions with the Texas Parks and Wildlife Department, I can definitely say that they want to do a thorough and sound survey throughout the state, not willy-nilly "look here, look there". There are limitations of manpower, finances and, in some places, deer populations. I would congratulate TPWD for doing the best job with the limitations at hand rather than trying to browbeat them when you obviously do not understand the ecology of West Texas. Thank you for your consideration.

======================

From: TSS (216-119-139-126.ipset19.wt.net)

Subject: Re: CWD SAMPLING TEXAS (but NOT in the obvious place, the NM, TEXAS border)

Date: December 16, 2003 at 11:03 am PST

In Reply to: Re: CWD SAMPLING TEXAS (but NOT in the obvious place, the NM, TEXAS border) posted by Ken Waldrup, DVM, PhD on December 15, 2003 at 3:43 pm:

HEllo Dr. Waldrup,

thank you for your comments and time to come to this board.

Ken Waldrup, DVM, PhD states;

> it is painfully obvious that you do not know or understand the natural distribution of mule deer out there or the rights of the land owners in this state...

TSS states;

I am concerned about all deer/elk not just mule deer, and the rights of land owners (in the case with human/animal TSEs) well i am not sure of the correct terminology, but when the States deer/elk/cattle/sheep/humans are at risk, there should be no rights for land owners in this case. the state should have the right to test those animals. there are too many folks out there that are just plain ignorant about this agent. with an agent such as this, you cannot let landowners (and i am one) dictate human/animal health, especially when you cannot regulate the movement of such animals...

Ken Waldrup, DVM, PhD states;

> Deer and elk from the Guadalupe Peak National Park cannot be collected with federal permission.

TSS states;

I do not understand this? so there is no recourse of action even if every deer/elk was contaminated with CWD in this area (hypothetical)?

Ken Waldrup, DVM, PhD states;

> I am concerned about your insinuation that CWD is a human health risk. We are at a stand-off - you have no proof that it is and I have no definitive proof that it isn't. However I would say that the inferred evidence from Colorado, Wyoming and Wisconsin suggests that CWD is not a human health concern (i.e. no evidence of an increased incidence of human brain disorders within the CWD "endemic" areas of these states)...

TSS states;

NEXT, let's have a look at the overall distribution of CWD in Free-Ranging Cervids and see where the CWD cluster in NM WSMR borders TEXAS;

Current Distribution of Chronic Wasting Disease in Free-Ranging Cervids

http://www.aphis.usda.gov/vs/nahps/cwd/cwd-distribution.html

NOW, the MAP of the Exoregion where the samples were taken to test for CWD;

CWD SURVEILLANCE SAMPLE SUBMISSIONS TEXAS

http://www.tahc.state.tx.us/animal_health/diseases/cwd/CWD2003.gif

Ecoregions of TEXAS

http://www.tpwd.state.tx.us/images/tx-eco95.gif

IF you look at the area around the NM WSMR where the CWD cluster was and where it borders TEXAS, that ecoregion is called Trans Pecos region. Seems if my Geography and my Ciphering is correct ;-) that region only tested 55% of it's goal. THE most important area on the MAP and they only test some 96 samples, this in an area that has found some 7 positive animals? NOW if we look at the only other border where these deer from NM could cross the border into TEXAS, this area is called the High Plains ecoregion, and again, we find that the sampling for CWD was pathetic. HERE we find that only 9% of it's goal of CWD sampling was met, only 16 samples were tested from some 175 that were suppose to be sampled.

AS i said before;

> SADLY, they have not tested enough from the total population to

> know if CWD is in Texas or not.

BUT now, I will go one step further and state categorically that they are not trying to find it. just the opposite it seems, they are waiting for CWD to find them, as with BSE/TSE in cattle, and it will eventually...

snip...end...TSS

===============================

2005

SEE MAP OF CWD ON THE BORDER OF NEW MEXICO VERY CLOSE TO TEXAS ;

http://www.wildlife.state.nm.us/conservation/disease/cwd/documents/cwdmap.pdf

http://www.wildlife.state.nm.us/conservation/disease/cwd/documents/cwd_flyer.pdf

NO update on CWD testing in Texas, New Mexico that i could find. I have inquired about it though, no reply yet...

-------- Original Message --------

Subject: CWD testing to date TEXAS ?

Date: Mon, 09 May 2005 12:26:20 –0500

From: "Terry S. Singeltary Sr."

To: kristen.everett@tpwd.state.tx.us

Hello Mrs. Everett,

I am most curious about the current status on CWD testing in Texas. could you please tell me what the current and past testing figures are to date and what geographical locations these tests have been in. good bust on the illegal deer trapping case. keep up the good work there.........

thank you, with kindest regards,

Terry S. Singeltary Sr. P.O. Box 42 Bacliff, Texas USA 77518

-------- Original Message --------

Subject: CWD testing in New Mexico

Date: Mon, 09 May 2005 14:39:18 –0500

From: "Terry S. Singeltary Sr."

To: ispa@state.nm.us

Greetings,

I am most curious of the current and past CWD testing in New Mexico, and there geographical locations...

thank you,

Terry S. Singeltary SR. CJD Watch

#################### https://lists.aegee.org/bse-l.html ####################

2006

----- Original Message -----

From: "Terry S. Singeltary Sr." flounder9@VERIZON.NET

To: BSE-L@aegee.org

Sent: Saturday, December 23, 2006 1:47 PM

Subject: CWD in New Mexico 35 MILES FROM TEXAS BORDER and low testing sampling figures -- what gives TAHC ???

Date: December 23, 2006 at 11:25 am PST

Greetings BSE-L members,

i never know if i am going crazy or just more of the same BSe. several years ago i brought up the fact to the TAHC that CWD was literally at the Texas borders and that the sample size for cwd testing was no where near enough in the location of that zone bordering NM. well, i just wrote them another letter questioning this again on Dec. 14, 2006 (see below) and showed them two different pdf maps, one referencing this url, which both worked just fine then. since then, i have NOT received a letter from them answering my question, and the url for the map i used as reference is no longer working? i had reference this map several times from the hunter-kill cwd sampling as of 31 August 2005 pdf which NO longer works now??? but here are those figures for that zone bordering NM, for those that were questioning the url. the testing samples elsewhere across Texas where much much more than that figure in the zone bordering NM where CWD has been documented bordering TEXAS, near the White Sands Missile Range. SO, why was the Texas hunter-kill cwd sampling as of 31 August 2005 document removed from the internet??? you know, this reminds me of the infamous TEXAS MAD COW that i documented some 7 or 8 months before USDA et al documented it, when the TAHC accidentally started ramping up for the announcement on there web site, then removed it (see history at bottom). i am not screaming conspiracy here, but confusious is confused again on the ciphering there using for geographical distribution of cwd tissue sample size survey, IF they are serious about finding CWD in TEXAS. common sense would tell you if cwd is 35 miles from the border, you would not run across state and have your larger samples there, and least samples 35 miles from where is what found..........daaa..........TSS

THEN NOTICE CWD sample along that border in TEXAS, Three Year Summary of Hunter-Kill CWD sampling as of 31 August 2005 of only 191 samples, then compare to the other sample locations ;

http://www.tahc.state.tx.us/animal_health/diseases/cwd/CWD_Sampling_Aug2005.pdf

http://209.85.165.104/search?q=cache:rH-1sQfZqtQJ:www.ngpc.state.ne.us/cgi-bin/ultimatebb.cgi%3Fubb%3Dget_topic%3Bf%3D12%3Bt%3D000492+Texas+hunter+kill+sample+for+CWD+to+Aug+31,+2005&hl=en&gl=us&ct=clnk&cd=3

TPWD has been conducting surveys of hunter-kill animals since 2002 and has collected more than 7300 samples (as of 31 August 2005). In total, there have been over 9400 samples, both hunter-kill and private samples, tested in Texas to date, and no positives have been found.

http://www.tpwd.state.tx.us/huntwild/wild/diseases/cwd/

SO, out of a total of 9,400 samples taken for CWD surveillance in TEXAS since 2002 of both hunter-kill and private kill, ONLY 191 samples have been taken in the most likely place one would find CWD i.e. the border where CWD has been documented at TEXAS and New Mexico

latest map NM cwd old data

http://www.wildlife.state.nm.us/conservation/disease/cwd/where_is_it.htm

http://www.wildlife.state.nm.us/conservation/disease/cwd/cwd_map.htm

CWD in New Mexico ;

What is the Department doing to prevent the spread of CWD?

Chronic wasting disease (CWD) was recently detected in a mule deer from Unit 34. Until 2005, CWD had only been found in Unit 19. With this discovery, the Department will increase its surveillance of deer and elk harvested in Units 29, 30 and 34.

Lymph nodes and/or brain stems from every harvested deer and brain stems from all elk taken in Unit 34 will be sampled.

snip...

http://www.wildlife.state.nm.us/conservation/disease/cwd/documents/cwd_flyer.pdf

http://www.wildlife.state.nm.us/conservation/disease/cwd/documents/cwdmap.pdf

http://www.wildlife.state.nm.us/documents/cwdcontrolmap.pdf

http://list.uvm.edu/cgi-bin/wa?A2=ind0512b&L=safety&P=11092

http://www.aphis.usda.gov/vs/nahps/cwd/cwd-distribution.html

http://www.wildlife.state.nm.us/documents/CWD_QandA.pdf

CWD SURVEILLANCE TEXAS

http://www.tpwd.state.tx.us//huntwild/wild/diseases/cwd/management_plan/status/

SNIP...SEE FULL TEXT ;

2011 – 2012