Texas Chronic Wasting Disease Response Update and Interim Deer Management Permit Rules Recommended Adoption of Proposed Rules
Work Session Item No. 8 Presenter: Clayton Wolf
Work Session Chronic Wasting Disease Response Update and Interim Deer
Management Permit Rules Recommended Adoption of Proposed Rules January 20, 2016
I. Executive Summary: This item:
provides an update on events related to the discovery of chronic wasting
disease (CWD) in deer breeding facility in Medina County on June 30, 2105;
and
seeks adoption of a proposed new interim 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 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 require all
deer introduced to Level 3 DMP facilities or Class III release sites to be
tagged with an Radio Frequency Identification (RFID) or National Uniform
Eartagging System (NUES) ear tag. II. Discussion: Since the discovery of CWD in
a deer breeding facility in Medina County on June 30, 2015, staff have provided
briefings to apprise the Commission of CWD response efforts. This briefing will
include an update on recent efforts by the Texas Animal Health Commission and
the department related to facility hold orders, a CWD ante-mortem testing
symposium, and CWD hunter-harvest surveillance for the 2015-2016 hunting
season.
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 numerous 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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Work Session Item No. 8 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
SNIP...
Work Session Item No. 19 Staff: Ann Bright
Work Session Chronic Wasting Disease Legal Strategy January 20, 2016
I. Executive Summary: Texas Parks and Wildlife Department (TPWD) attorneys
will discuss with and advise the Texas Parks and Wildlife Commission regarding
legal strategy and legal issues regarding TPWD’s response to chronic wasting
disease.
Tuesday, December 16, 2014
Texas 84th Legislature 2015 H.R. No. 2597 Kuempel Deer Breeding Industry
TAHC TPWD CWD TSE PRION
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
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.
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
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.
‘’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
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
***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
*** Infectious agent of sheep scrapie may persist in the environment for at
least 16 years ***
Gudmundur Georgsson1, Sigurdur Sigurdarson2 and Paul Brown3
*** 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.
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.
see ;
Wednesday, December 16, 2015
Objects in contact with classical scrapie sheep act as a reservoir for
scrapie transmission
Objects in contact with classical scrapie sheep act as a reservoir for
scrapie transmission
Timm Konold1*, Stephen A. C. Hawkins2, Lisa C. Thurston3, Ben C. Maddison4,
Kevin C. Gough5, Anthony Duarte1 and Hugh A. Simmons1
1 Animal Sciences Unit, Animal and Plant Health Agency Weybridge,
Addlestone, UK, 2 Pathology Department, Animal and Plant Health Agency
Weybridge, Addlestone, UK, 3 Surveillance and Laboratory Services, Animal and
Plant Health Agency Penrith, Penrith, UK, 4 ADAS UK, School of Veterinary
Medicine and Science, University of Nottingham, Sutton Bonington, UK, 5 School
of Veterinary Medicine and Science, University of Nottingham, Sutton Bonington,
UK
Classical scrapie is an environmentally transmissible prion disease of
sheep and goats. Prions can persist and remain potentially infectious in the
environment for many years and thus pose a risk of infecting animals after
re-stocking. In vitro studies using serial protein misfolding cyclic
amplification (sPMCA) have suggested that objects on a scrapie affected sheep
farm could contribute to disease transmission. This in vivo study aimed to
determine the role of field furniture (water troughs, feeding troughs, fencing,
and other objects that sheep may rub against) used by a scrapie-infected sheep
flock as a vector for disease transmission to scrapie-free lambs with the prion
protein genotype VRQ/VRQ, which is associated with high susceptibility to
classical scrapie. When the field furniture was placed in clean accommodation,
sheep became infected when exposed to either a water trough (four out of five)
or to objects used for rubbing (four out of seven). This field furniture had
been used by the scrapie-infected flock 8 weeks earlier and had previously been
shown to harbor scrapie prions by sPMCA. Sheep also became infected (20 out of
23) through exposure to contaminated field furniture placed within pasture not
used by scrapie-infected sheep for 40 months, even though swabs from this
furniture tested negative by PMCA. This infection rate decreased (1 out of 12)
on the same paddock after replacement with clean field furniture. Twelve grazing
sheep exposed to field furniture not in contact with scrapie-infected sheep for
18 months remained scrapie free. The findings of this study highlight the role
of field furniture used by scrapie-infected sheep to act as a reservoir for
disease re-introduction although infectivity declines considerably if the field
furniture has not been in contact with scrapie-infected sheep for several
months. PMCA may not be as sensitive as VRQ/VRQ sheep to test for environmental
contamination.
snip...
Discussion
Classical scrapie is an environmentally transmissible disease because it
has been reported in naïve, supposedly previously unexposed sheep placed in
pastures formerly occupied by scrapie-infected sheep (4, 19, 20). Although the
vector for disease transmission is not known, soil is likely to be an important
reservoir for prions (2) where – based on studies in rodents – prions can adhere
to minerals as a biologically active form (21) and remain infectious for more
than 2 years (22). Similarly, chronic wasting disease (CWD) has re-occurred in
mule deer housed in paddocks used by infected deer 2 years earlier, which was
assumed to be through foraging and soil consumption (23).
Our study suggested that the risk of acquiring scrapie infection was
greater through exposure to contaminated wooden, plastic, and metal surfaces via
water or food troughs, fencing, and hurdles than through grazing. Drinking from
a water trough used by the scrapie flock was sufficient to cause infection in
sheep in a clean building. Exposure to fences and other objects used for rubbing
also led to infection, which supported the hypothesis that skin may be a vector
for disease transmission (9). The risk of these objects to cause infection was
further demonstrated when 87% of 23 sheep presented with PrPSc in lymphoid
tissue after grazing on one of the paddocks, which contained metal hurdles, a
metal lamb creep and a water trough in contact with the scrapie flock up to 8
weeks earlier, whereas no infection had been demonstrated previously in sheep
grazing on this paddock, when equipped with new fencing and field furniture.
When the contaminated furniture and fencing were removed, the infection rate
dropped significantly to 8% of 12 sheep, with soil of the paddock as the most
likely source of infection caused by shedding of prions from the
scrapie-infected sheep in this paddock up to a week earlier.
This study also indicated that the level of contamination of field
furniture sufficient to cause infection was dependent on two factors: stage of
incubation period and time of last use by scrapie-infected sheep. Drinking from
a water trough that had been used by scrapie sheep in the predominantly
pre-clinical phase did not appear to cause infection, whereas infection was
shown in sheep drinking from the water trough used by scrapie sheep in the later
stage of the disease. It is possible that contamination occurred through
shedding of prions in saliva, which may have contaminated the surface of the
water trough and subsequently the water when it was refilled. Contamination
appeared to be sufficient to cause infection only if the trough was in contact
with sheep that included clinical cases. Indeed, there is an increased risk of
bodily fluid infectivity with disease progression in scrapie (24) and CWD (25)
based on PrPSc detection by sPMCA. Although ultraviolet light and heat under
natural conditions do not inactivate prions (26), furniture in contact with the
scrapie flock, which was assumed to be sufficiently contaminated to cause
infection, did not act as vector for disease if not used for 18 months, which
suggest that the weathering process alone was sufficient to inactivate prions.
PrPSc detection by sPMCA is increasingly used as a surrogate for
infectivity measurements by bioassay in sheep or mice. In this reported study,
however, the levels of PrPSc present in the environment were below the limit of
detection of the sPMCA method, yet were still sufficient to cause infection of
in-contact animals. In the present study, the outdoor objects were removed from
the infected flock 8 weeks prior to sampling and were positive by sPMCA at very
low levels (2 out of 37 reactions). As this sPMCA assay also yielded 2 positive
reactions out of 139 in samples from the scrapie-free farm, the sPMCA assay
could not detect PrPSc on any of the objects above the background of the assay.
False positive reactions with sPMCA at a low frequency associated with de novo
formation of infectious prions have been reported (27, 28). This is in contrast
to our previous study where we demonstrated that outdoor objects that had been
in contact with the scrapie-infected flock up to 20 days prior to sampling
harbored PrPSc that was detectable by sPMCA analysis [4 out of 15 reactions
(12)] and was significantly more positive by the assay compared to analogous
samples from the scrapie-free farm. This discrepancy could be due to the use of
a different sPMCA substrate between the studies that may alter the efficiency of
amplification of the environmental PrPSc. In addition, the present study had a
longer timeframe between the objects being in contact with the infected flock
and sampling, which may affect the levels of extractable PrPSc. Alternatively,
there may be potentially patchy contamination of this furniture with PrPSc,
which may have been missed by swabbing. The failure of sPMCA to detect
CWD-associated PrP in saliva from clinically affected deer despite confirmation
of infectivity in saliva-inoculated transgenic mice was associated with as yet
unidentified inhibitors in saliva (29), and it is possible that the sensitivity
of sPMCA is affected by other substances in the tested material. In addition,
sampling of amplifiable PrPSc and subsequent detection by sPMCA may be more
difficult from furniture exposed to weather, which is supported by the
observation that PrPSc was detected by sPMCA more frequently in indoor than
outdoor furniture (12). A recent experimental study has demonstrated that
repeated cycles of drying and wetting of prion-contaminated soil, equivalent to
what is expected under natural weathering conditions, could reduce PMCA
amplification efficiency and extend the incubation period in hamsters inoculated
with soil samples (30). This seems to apply also to this study even though the
reduction in infectivity was more dramatic in the sPMCA assays than in the sheep
model. Sheep were not kept until clinical end-point, which would have enabled us
to compare incubation periods, but the lack of infection in sheep exposed to
furniture that had not been in contact with scrapie sheep for a longer time
period supports the hypothesis that prion degradation and subsequent loss of
infectivity occurs even under natural conditions.
In conclusion, the results in the current study indicate that removal of
furniture that had been in contact with scrapie-infected animals should be
recommended, particularly since cleaning and decontamination may not effectively
remove scrapie infectivity (31), even though infectivity declines considerably
if the pasture and the field furniture have not been in contact with
scrapie-infected sheep for several months. As sPMCA failed to detect PrPSc in
furniture that was subjected to weathering, even though exposure led to
infection in sheep, this method may not always be reliable in predicting the
risk of scrapie infection through environmental contamination. These results
suggest that the VRQ/VRQ sheep model may be more sensitive than sPMCA for the
detection of environmentally associated scrapie, and suggest that extremely low
levels of scrapie contamination are able to cause infection in susceptible sheep
genotypes.
Keywords: classical scrapie, prion, transmissible spongiform
encephalopathy, sheep, field furniture, reservoir, serial protein misfolding
cyclic amplification
Wednesday, December 16, 2015
*** Objects in contact with classical scrapie sheep act as a reservoir for
scrapie transmission ***
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.
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...
Saturday, January 31, 2015
European red deer (Cervus elaphus elaphus) are susceptible to Bovine
Spongiform Encephalopathy BSE by Oral Alimentary route
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
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.
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 ;
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
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.
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.
2011
*** After a natural route of exposure, 100% of white-tailed deer were
susceptible to scrapie.
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 ;
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.
see ;
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
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
Monday, November 3, 2014
Persistence of ovine scrapie infectivity in a farm environment following
cleaning and decontamination
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.
*** 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.
© 2016, Journal Sentinel Inc. All rights reserved.
About Paul A. Smith Paul A. Smith covers outdoors and conservation
issues.
@mjsps psmith@journalsentinel.com 414-224-2313
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:
$298,770 + $465,000
Friday, December 04, 2015
Wisconsin CWD-positive white-tailed deer found on Oneida County hunting
preserve December 3, 2015
Wednesday, March 04, 2015
*** Disease sampling results provide current snapshot of CWD in Wisconsin
finding 324 positive detections statewide in 2014
Wednesday, December 16, 2015
Wisconsin Chronic wasting disease confirmed in Crawford County buck
harvested on private land
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.
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:
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).
*** see history of this CWD blunder here ;
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.
The overall incidence of clinical CWD in white-tailed deer was 82%
Species (cohort) CWD (cases/total) Incidence (%) Age at CWD death (mo)
”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.
Sunday, January 06, 2013
USDA TO PGC ONCE CAPTIVES ESCAPE
*** "it‘s no longer its business.”
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.
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.
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.
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.
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.
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.
O.05: Transmission of prions to primates after extended silent incubation
periods: Implications for BSE and scrapie risk assessment in human populations
Emmanuel Comoy, Jacqueline Mikol, Valerie Durand, Sophie Luccantoni,
Evelyne Correia, Nathalie Lescoutra, Capucine Dehen, and Jean-Philippe Deslys
Atomic Energy Commission; Fontenay-aux-Roses, France
Prion diseases (PD) are the unique neurodegenerative proteinopathies
reputed to be transmissible under field conditions since decades. The
transmission of Bovine Spongiform Encephalopathy (BSE) to humans evidenced that
an animal PD might be zoonotic under appropriate conditions. Contrarily, in the
absence of obvious (epidemiological or experimental) elements supporting a
transmission or genetic predispositions, PD, like the other proteinopathies, are
reputed to occur spontaneously (atpical animal prion strains, sporadic CJD
summing 80% of human prion cases). Non-human primate models provided the first
evidences supporting the transmissibiity of human prion strains and the zoonotic
potential of BSE. Among them, cynomolgus macaques brought major information for
BSE risk assessment for human health (Chen, 2014), according to their
phylogenetic proximity to humans and extended lifetime. We used this model to
assess the zoonotic potential of other animal PD from bovine, ovine and cervid
origins even after very long silent incubation periods.
*** We recently observed the direct transmission of a natural classical
scrapie isolate to macaque after a 10-year silent incubation period,
***with features similar to some reported for human cases of sporadic CJD,
albeit requiring fourfold long incubation than BSE. Scrapie, as recently evoked
in humanized mice (Cassard, 2014),
***is the third potentially zoonotic PD (with BSE and L-type BSE),
***thus questioning the origin of human sporadic cases. We will present an
updated panorama of our different transmission studies and discuss the
implications of such extended incubation periods on risk assessment of animal PD
for human health.
===============
***thus questioning the origin of human sporadic cases***
===============
==========================================
***our findings suggest that possible transmission risk of H-type BSE to
sheep and human. Bioassay will be required to determine whether the PMCA
products are infectious to these animals.
==========================================
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.***
================
*** These results would seem to suggest that CWD does indeed have zoonotic
potential, at least as judged by the compatibility of CWD prions and their human
PrPC target. Furthermore, extrapolation from this simple in vitro assay suggests
that if zoonotic CWD occurred, it would most likely effect those of the PRNP
codon 129-MM genotype and that the PrPres type would be similar to that found in
the most common subtype of sCJD (MM1).***
*** The potential impact of prion diseases on human health was greatly
magnified by the recognition that interspecies transfer of BSE to humans by beef
ingestion resulted in vCJD. While changes in animal feed constituents and
slaughter practices appear to have curtailed vCJD, there is concern that CWD of
free-ranging deer and elk in the U.S. might also cross the species barrier.
Thus, consuming venison could be a source of human prion disease. Whether BSE
and CWD represent interspecies scrapie transfer or are newly arisen prion
diseases is unknown. Therefore, the possibility of transmission of prion disease
through other food animals cannot be ruled out. There is evidence that vCJD can
be transmitted through blood transfusion. There is likely a pool of unknown size
of asymptomatic individuals infected with vCJD, and there may be asymptomatic
individuals infected with the CWD equivalent. These circumstances represent a
potential threat to blood, blood products, and plasma supplies.
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 ;
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.
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 ***
*** 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).***
***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.
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.
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.
Monday, November 16, 2015
*** Docket No. APHIS-2007-0127 Scrapie in Sheep and Goats Terry Singeltary
Sr. Submission ***
Saturday, December 12, 2015
*** CHRONIC WASTING DISEASE CWD TSE PRION REPORT DECEMBER 14, 2015
Friday, May 22, 2015
*** Chronic Wasting Disease and Program Updates - 2014 NEUSAHA Annual
Meeting 12-14 May 2014
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
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
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
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
Friday, January 15, 2016
TEXAS PARKS & WILDLIFE CWD Ante-Mortem Testing Symposium Texas Disposal
Systems Events Pavilion January 12, 2016
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. ***
Saturday, December 12, 2015
*** CHRONIC WASTING DISEASE CWD TSE PRION REPORT DECEMBER 14, 2015
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
Monday, November 16, 2015
*** TEXAS PARKS AND WILDLIFE DEPARTMENT EXECUTIVE DIRECTOR ORDER NO.
015-006
*** Chronic Wasting Disease (CWD) immediate danger to the white-tailed deer
and mule deer resources of Texas
Saturday, November 14, 2015
TEXAS CAPTIVE BREEDER CHRONIC WASTING DISEASE CWD 2 MORE SUSPECTS DECTECTED
BRINGING NUMBER TO 7 DETECTED IN CAPTIVE BREEDER (if/when the last two are
confirmed).
Thursday, November 05, 2015
*** TPW Commission Adopts Interim Deer Breeder Movement Rules
Friday, October 09, 2015
Texas TWA Chronic Wasting Disease TSE Prion Webinars and Meeting October
2015
Saturday, October 03, 2015
TEXAS CHRONIC WASTING DISEASE CWD TSE PRION GOD MUST NOT BE A TEXAN 2002 TO
2015
Thursday, September 24, 2015
TEXAS Hunters Asked to Submit Samples for Chronic Wasting Disease CWD TSE
Prion Testing
*** I cannot stress enough to all of you, for the sake of your family and
mine, before putting anything in the freezer, have those deer tested for CWD.
...terry
***raw and uncut
Sunday, August 23, 2015
TAHC Chronic Wasting Disease CWD TSE Prion and how to put lipstick on a pig
and take her to the dance in Texas
Friday, August 07, 2015
*** Texas CWD Captive, and then there were 4 ?
Thursday, August 06, 2015
*** WE HAVE LOST TEXAS TO CWD TASK FORCE CATERING TO INDUSTRY
Tuesday, July 21, 2015
*** Texas CWD Medina County Herd Investigation Update July 16, 2015 ***
Thursday, July 09, 2015
TEXAS Chronic Wasting Disease (CWD) Herd Plan for Trace-Forward Exposed
Herd with Testing of Exposed Animals
Wednesday, July 01, 2015
TEXAS Chronic Wasting Disease Detected in Medina County Captive Deer
Wednesday, March 18, 2015
Chronic Wasting Disease CWD Confirmed Texas Trans Pecos March 18,
2015
Wednesday, March 25, 2015
Chronic Wasting Disease CWD Cases Confirmed In New Mexico 2013 and 2014
UPDATE 2015
Thursday, May 02, 2013
*** Chronic Wasting Disease (CWD) Texas Important Update on OBEX ONLY
TEXTING
Monday, February 11, 2013
TEXAS CHRONIC WASTING DISEASE CWD Four New Positives Found in Trans Pecos
Tuesday, July 10, 2012
Chronic Wasting Disease Detected in Far West Texas
Monday, March 26, 2012
Texas Prepares for Chronic Wasting Disease CWD Possibility in Far West
Texas
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."
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.
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.
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
NOW, the MAP of the Exoregion where the samples were taken to test for CWD;
CWD SURVEILLANCE SAMPLE SUBMISSIONS TEXAS
Ecoregions of TEXAS
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 ;
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 ???
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 ;
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.
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
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...
CWD SURVEILLANCE TEXAS
SNIP...SEE FULL TEXT ;
2011 – 2012
Friday, October 28, 2011
CWD Herd Monitoring Program to be Enforced Jan. 2012 TEXAS
Greetings TAHC et al,
A kind greetings from Bacliff, Texas.
In reply to ;
Texas Animal Health Commission (TAHC) Announcement October 27, 2011
I kindly submit the following ;
***for anyone interested, here is some history of CWD along the Texas, New
Mexico border, and my attempt to keep up with it...terry
snip...
see history CWD Texas, New Mexico Border ;
Monday, March 26, 2012
3 CASES OF CWD FOUND NEW MEXICO MULE DEER SEVERAL MILES FROM TEXAS BORDER
Sunday, October 04, 2009
CWD NEW MEXICO SPREADING SOUTH TO TEXAS 2009 2009 Summary of Chronic
Wasting Disease in New Mexico New Mexico Department of Game and Fish
Saturday, January 23, 2016
Texas new interim rule governing Deer Management Permit (DMP) activities as
part of the state’s response to the detection of chronic wasting disease (CWD)
in captive deer populations
Terry S. Singeltary Sr.
posted by Terry S. Singeltary Sr. at
12:04 PM
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