TEXAS TAHC DEER BREEDER CWD PERMIT RULES EMERGENCY ADOPTION PREAMBLE
DEER BREEDER/CWD PERMIT RULES EMERGENCY ADOPTION PREAMBLE
1. Introduction.
Pursuant to Parks and Wildlife Code, §12.027, and Government Code,
§2001.034, the executive director of the Texas Parks and Wildlife Department
(the department) adopts, on an emergency basis, new §§65.90 - 65.93, concerning
Disease Detection and Response. The new emergency rules will be constituted as
new Division 2 within Chapter 65, Subchapter B, entitled Chronic Wasting Disease
- Movement of Breeder Deer. Under Parks and Wildlife Code, Chapter 43,
Subchapter L, the department regulates the possession of captive-raised deer
within a facility for breeding purposes and the release of such deer into the
wild. To the extent that any provision of the new division conflicts with any
other provision of Chapter 65, the new division will prevail, except as
noted.
For the reasons explained in this preamble, the department’s executive
director has determined that the presence of CWD poses an immediate danger to
white-tailed and mule deer, which are species authorized to be regulated by the
department, and that the adoption of these rules on an emergency basis with
fewer than 30 days’ notice is necessary to address this immediate danger.
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 chronic wasting disease (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 breeders and transferred 835 deer to 147 separate sites (including 96
deer breeding facilities, 46 release sites, and two Deer Management Permit (DMP)
facilities in Texas, as well as two destinations in Mexico). (A DMP is a permit
issued by the department under rules adopted pursuant to Parks and Wildlife
Code, Chapter 43, Subchapters R and R-1, that allows the temporary possession of
free-ranging white-tailed or mule deer for breeding purposes.) The department
estimates that more than 728 locations in Texas (including 384 deer breeders)
either received deer from the index facility or received deer from a deer
breeder who had received deer from the index facility, representing
approximately 30% of the total number of deer breeders in the state.
As provided in the Texas Administrative Code, the emergency rules will
initially be in effect for no longer than 120 days, but may be extended for an
additional 60 days. It is the intent of the department to also publish proposed
rules pursuant to the Administrative Procedure Act’s notice and comment
rulemaking process.
The emergency rules impose CWD testing requirements and movement
restrictions for white-tailed deer and mule deer held under the authority of
deer breeder’s permits issued by the department. The new rules are a result of
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 TSE (transmissible spongiform
encephalopathy), a family of diseases that includes scrapie (found in sheep),
bovine spongiform encephalopathy (BSE, found in cattle and commonly known as
“Mad Cow Disease”), and variant Creutzfeldt-Jakob Disease (vCJD) in humans. 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; however, 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 wild populations correlates with deer population
declines and there is evidence that hunters tend to avoid areas of high CWD
prevalence. The implications of CWD for Texas and its multi-billion dollar
ranching, hunting, and wildlife management economies are expected to be
significant, unless contained and controlled.
The department 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).)
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 measures to be taken to protect
white-tailed and mule deer in Texas. Based on recommendations from the CWD Task
Force, the department 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 check stations
to be tested for CWD.
The department has been concerned for over a decade about the possible
emergence of CWD in wild and captive deer populations in Texas. Since 2002, more
than 28,209 “not detected” CWD test results were obtained from free- ranging
(i.e., not breeder) deer in Texas. Deer breeders have submitted 12,759 “not
detected” test results to the department. The intent of the new emergency rules
is to reduce the probability of CWD being spread from facilities where it might
exist and to increase the probability of detecting CWD if it does exist.
The new emergency rules therefore set forth specific testing requirements
for deer breeders, which would have to be satisfied in order to move deer to
other deer breeders or for purposes of release. The new emergency rules also
impose similar testing requirements on sites where breeder deer are liberated
(release sites). The other significant component of the rules is that they
restrict the release of breeder deer solely to enclosures surrounded by a fence
of at least seven feet in height and that is capable of retaining deer at all
times. Because deer held under deer breeder’s permits are frequently liberated
for stocking and/or hunting purposes (27,684 in 2014), the potential for disease
transmission to free-ranging deer is significant, given that the source of CWD
in the index facility is unknown and the large number of deer that have been
moved to other breeding facilities and/or released to the wild. The emergency
action is necessary to protect the state’s white-tailed and mule deer
populations, as well as the associated hunting and deer breeding industries. To
minimize the severity of biological and economic impacts resulting from CWD, the
rules implement a more rigorous testing protocol within certain deer breeding
facilities and at certain release sites. The new emergency rules allow most
breeder deer to continue to be released because the department believes that the
need to protect free-ranging populations must be balanced with the interests of
the more than 1,300 deer breeders in the state.
The rules are adopted on an emergency basis under Parks and Wildlife Code,
§12.027, which authorizes the department’s executive director to adopt emergency
rules if there is an immediate danger to a species authorized to be regulated by
the department, and under Government Code §2001.034, which authorizes a state
agency to adopt such emergency rules without prior notice or hearing. In
addition, Parks and Wildlife Code, Chapter 43, Subchapter L, authorizes the
department to regulate the possession of white-tailed and mule deer for
scientific, management, and propagation purposes.
§65.90. Definitions. The following words and terms shall have the following
meanings, except in cases where the context clearly indicates otherwise.
(1) Accredited testing facility--A laboratory approved by the United States
Department of Agriculture to test white-tailed deer or mule deer for CWD.
(2) Breeder deer--A white-tailed deer or mule deer possessed under a permit
issued by the department pursuant to Parks and Wildlife Code, Chapter 43,
Subchapter L, and Subchapter T of this chapter.
(3) CWD--chronic wasting disease.
(4) CWD-positive facility--A facility where CWD has been confirmed.
(5) Deer breeder--A person who holds a valid deer breeder’s permit issued
pursuant to Parks and Wildlife Code, Chapter 43, Subchapter L, and Subchapter T
of this chapter.
(6) Deer breeding facility (breeding facility)--A facility permitted to
hold breeder deer under a permit issued by the department pursuant to Parks and
Wildlife Code, Chapter 43, Subchapter L, and Subchapter T of this chapter.
(7) Department (department)--Texas Parks and Wildlife Department
(8) Eligible mortality-- A breeder deer that has died within a deer
breeding facility and:
(A) is 16 months of age or older; or
(B) if the deer breeding facility is enrolled in the TAHC CWD Herd
Certification Program, is 12-months of age or older.
(9) Exposed deer--A white-tailed deer or mule deer that:
(A) is in a CWD-positive facility; or
(B) was in a CWD-positive facility within the five years preceding the
confirmation of CWD in that facility.
(10) Hunter-harvested deer--A deer required to be tagged under the
provisions of Subchapter A of this chapter (relating to Statewide Hunting
Proclamation).
(11) Landowner (owner)--Any person who has an ownership interest in a tract
of land, and includes a landowner’s authorized agent.
(12) Landowner’s authorized agent--A person designated by a landowner to
act on the landowner’s behalf.
(13) NUES tag--An ear tag approved by the United States Department of
Agriculture for use in the National Uniform Eartagging System (NUES).
(14) Originating facility-- A facility that is registered in TWIMS and is
authorized to transfer breeder deer.
(15) Reconciled herd--The deer held in a breeding facility for which the
department has determined that the deer breeder has accurately reported every
birth, mortality, and transfer of deer in the previous reporting year.
(16) Release site--A specific tract of land that has been approved by the
department for the release of breeder deer under this division.
(17) Reporting year--For a deer breeder, the period of time from April 1 of
one calendar year to March 31 of the next calendar year.
(18) RFID tag--A button-type ear tag conforming to the 840 standards of the
United States Department of Agriculture’s Animal Identification Number
system.
(19) Status--The level of testing required by this division for any given
deer breeding facility or release site. For the transfer categories established
in §65.92(b) of this title (relating to Transfer Categories and Requirements),
the highest status is Transfer Category 1 (TC 1) and the lowest status is
Transfer Category 3 (TC3). For the release site classes established in §65.93(b)
of this title (relating to Release Sites - Qualifications and Testing
Requirements), Class I is the highest status and Class III is the lowest.
(20) Tier 1 facility--A deer breeding facility that has:
(A) received an exposed deer within the previous five years; or
(B) transferred deer to a CWD-positive facility within the five-year period
preceding the confirmation of CWD in the CWD-positive facility.
(21) TAHC--Texas Animal Health Commission.
(22) TAHC CWD Herd Certification Program--The disease-testing and herd
management requirements set forth in 4 TAC §40.3 (relating to Herd Status Plans
for Cervidae).
(23) TAHC Herd Plan--A set of requirements for disease testing and
management developed by TAHC for a specific facility.
(24) TWIMS--The department’s Texas Wildlife Information Management Services (TWIMS) online application.
§65.91. General Provisions.
(a) To the extent that any provision of this division conflicts with any
other provision of this chapter, this division prevails.
(b) Except as provided in this division, no live breeder deer may be
transferred anywhere for any purpose.
(c) Notwithstanding any other provision of this chapter, no person shall
introduce into or remove breeder deer from or allow or authorize breeder deer to
be introduced into or removed from any deer breeding facility for which a CWD
test result of 'detected' has been obtained from an accredited testing facility.
The provisions of this subsection take effect immediately upon the notification
of a CWD 'detected' test result for a deer breeding facility, and continue in
effect until the department expressly authorizes the resumption of permitted
activities at that facility.
(d) No exposed breeder deer may be transferred from a breeding facility
unless expressly authorized in a TAHC herd plan and then only in accordance with
the provisions of this division.
(e) A breeding facility or release site that receives breeder deer from an
originating facility of lower status automatically assumes the status of the
originating facility and becomes subject to the testing and release requirements
of this division at that status.
(f) A CWD test is not valid unless it is performed by an accredited testing
facility on the obex of an eligible mortality, which may be collected by anyone.
A medial retropharyngeal lymph node collected from the eligible mortality by an
accredited veterinarian or other person approved by the department may be
submitted to an accredited testing facility for testing in addition to the obex
of the eligible mortality.
(g) Unless expressly provided otherwise in this division, all applications
and notifications required by this division shall be submitted electronically
via TWIMS or by another method expressly authorized by the department.
(h) A person who is subject to the provisions of this division shall comply
with the provisions of TAHC regulations at 4 TAC Chapter 40 (relating to Chronic
Wasting Disease) that are applicable to white-tailed or mule deer.
(i) The provisions of this division that affect TC 1 facilities take effect
immediately; the remaining provisions of this division take effect upon
notification of deer breeders by the department or at 11:59 p.m. on August 24,
2015, whichever is sooner.
§65.92. Transfer Categories and Requirements.
(a) General.
(1) A breeding facility that is a TC 1, Transfer Category 2 (TC 2), or TC 3
facility may transfer breeder deer under a valid transfer permit that has been
activated and approved by the department as provided in §65.610(e) of this title
(relating to Transfer of Deer) to:
(A) another breeding facility;
(B) an approved release site as provided in §65.93 of this division
(relating to Release Sites - Qualifications and Testing Requirements);
(C) a DMP facility under Chapter 65, Subchapter D of this title (relating
to Deer Management Permits); or
(D) to another person for nursing purposes.
(2) Notwithstanding the provisions of paragraph (1) of this subsection, a
breeding facility is prohibited from transferring breeder deer anywhere for any
purpose if:
(A) such a transfer is not authorized pursuant to a TAHC Herd Plan
associated with a hold order or quarantine;
(B) “not detected” CWD test results have been submitted for less than 20%
of eligible mortalities at the breeding facility since May 23, 2006;
(C) the breeding facility has an unreconciled herd inventory; or
(D) the breeding facility is not in compliance with the provisions of
§65.608 of this title (relating to Annual Reports and Records).
(3) A deer breeder may not transfer a breeder deer to a Class III release
site unless the deer has been tagged by attaching a button-type RFID or NUES tag
approved by the department to one ear.
(4) A deer breeding facility that is permitted on or after the effective
date of this division will assume the lowest status among all originating
facilities from which deer are received; provided, however, a breeding facility
shall not assume TC 1 status unless it meets the criteria established in
subsection (b)(1) of this section.
(b) Types of Facilities.
(1) TC 1. A breeding facility is a TC 1 facility if:
(A) it is not a Tier 1 facility; and
(B) it has “fifth-year” or “certified” status in the TAHC CWD Herd
Certification Program.
(2) TC 2. A breeding facility is a TC 2 facility if:
(A) it is not a Tier 1 facility; and
(B) CWD test results of “not detected” have been returned for one of the
following values, whichever represents the lowest number of tested breeder
deer:
i) 4.5 percent or more of the breeder deer held within the facility during
the immediately preceding two reporting years, based on the average population
of deer in the facility that were at least 16 months of age on March 31 of each
year (including eligible mortalities for those years); or
(ii) 50 percent of all eligible mortalities from the preceding two
reporting years, provided at least one eligible mortality was tested.
(3) TC 3.
(A) A breeding facility is a TC 3 facility if it is neither a TC 1 facility
nor a TC 2 facility.
(B) A breeding facility may increase status from TC 3 to TC 2 if CWD test
results of “not detected” have been obtained for:
(i) each breeder deer received by the breeding facility from any
CWD-positive site;
(ii) each exposed breeder deer that has been transferred by the breeding
facility to another breeding facility or released; and
(iii) 4.5 percent or more of the breeder deer held within the breeding
facility during the immediately preceding two reporting years, based on the
average population of deer in the facility that were at least 16 months of age
on March 31 of each year (including eligible mortalities for those years).
(c) Breeder deer may be temporarily transferred to a veterinarian for
medical care.
§65.93. Release Sites - Qualifications and Testing Requirements.
(a) General.
(1) An approved release site consists solely of the specific tract of land
and acreage designated as a release site in TWIMS.
(2) All release sites must be surrounded by a fence of at least seven feet
in height that is capable of retaining deer at all times. The owner of the
release site is responsible for ensuring that the fence and associated
infrastructure retain the deer under ordinary and reasonable
circumstances.
(3) The owner of a Class II or Class III release site shall maintain a
legible daily harvest log at the release site.
(A) The daily harvest log shall be on a form provided or approved by the
department and shall be maintained until the report required by subparagraph (E)
of this paragraph has been submitted to and acknowledged by the department. (B)
For each deer harvested on the release site and tagged under the provisions of
Subchapter A of this chapter (relating to Statewide Hunting Proclamation), the
landowner must, on the same day that the deer is harvested, legibly enter the
information required by this subparagraph in the daily harvest log.
(C) The daily harvest log shall contain the following information for each
deer harvested on the release site:
(i) the name and hunting license or driver’s license number of the person
who harvested the deer;
(ii) the date the deer was harvested;
(iii) the species (white-tailed or mule deer) and type of deer harvested
(buck or antlerless);
(iv) any alphanumeric identifier tattooed on the deer;
(v) any RFID or NUES tag number of any RFID or NUES tag affixed to the
deer; and
(vi) any other identifier and identifying number on the deer.
(D) The daily harvest log shall be made available upon request to any
department employee acting in the performance of official duties.
(E) By not later than March 15 of each year, the owner of a release site
shall submit the contents of the daily harvest log to the department via TWIMS
or other format authorized by the department.
(4) Release site status cannot be altered by the sale or subdivision of a
property if the purpose of the sale or subdivision is to avoid the requirements
of this division.
(5) The owner of a release site agrees, by consenting to the release of
breeder deer on the release site, to submit all required CWD test results to the
department as soon as possible but not later than May 1, 2016. Failure to comply
with this paragraph will result in the release site being declared ineligible to
be a destination for future releases for a period of five years.
(6) No person may intentionally cause or allow any live deer to leave or
escape from a release site.
(b) Types of Release Sites
(1) Class I.
(A) A release site is a Class I release site if after July 1, 2015,
it:
(i) is not a Tier 1 facility; and
(ii) receives breeder deer only from TC 1 facilities.
(B) There are no testing requirements for a Class I release site.
(2) Class II.
(A) A release site is a Class II release site if, after July 1, 2015,
it:
(i) is not a Tier 1 facility;
(ii) receives any breeder deer from TC 2 facility; and
(iii) receives no deer from a TC 3 facility.
(B) The landowner of a Class II release site must obtain valid CWD test
results for one of the following values, whichever represents the lowest number
of deer tested:
(i) if deer are hunter-harvested, a number of deer equivalent to 50 percent
of the number of breeder deer released at the site between the effective date of
this division and the end of any open season for deer established for the site
under this chapter; or
(ii) 50 percent of all hunter-harvested deer.
(C) If any hunter-harvested deer were breeder deer released between the
effective date of this division and the end of any open season for deer
established for the site under this chapter, 50 percent of those
hunter-harvested deer must be submitted for CWD testing, which may be counted to
satisfy the requirements of subparagraph (B) of this paragraph.
(d) Class III.
(1) A release site is a Class III release site if, after July 1, 2015, it
receives deer from an originating facility that is a TC 3 facility.
(2) The landowner of a Class III release site must obtain valid CWD test
results for one of the following values, whichever represents the greatest
number of deer tested:
(A) 100% of all hunter-harvested deer; or
(B) one hunter-harvested deer per breeder deer released between the
effective date of this division and the end of any open season for deer
established for the site under this chapter.
============
you don’t want a test that will only detect some cwd cases, while missing others.
if I am not mistaken, and since TAHC will not officially confirm on their site the 4th case of captive CWD, or others, evidently we all are not privileged enough to know all the information to date about this Medina Captive Breeder and just how many cases of CWD there really are to date, but at least one of the 4 deer that has tested positive in the index facility had negative biopsies, from what I have read online.
also, it’s very disturbing still, how the TAHC et al are communicating with
the public on this explosive CWD TSE prion disease situation in Texas. of
course, TAHC will say nothing explosive about it, all is well, and no risk from
trace out herd, carry on. and all this downplaying, like the decades of
downplaying before, will only help to spread the disease, by not promptly
educating the public on CWD TSE Prion disease. TAHC, when it comes to mad cow
type disease, they use the old DUMB IT DOWN on communicating to the public. now, communicating with
the industry, that’s a different story, but this is all too typical of the TAHC
et al. ...just saying.
============
Article Citation: (2015)
AGE AND REPEATED BIOPSY INFLUENCE ANTEMORTEM PRPCWD TESTING IN MULE DEER
(ODOCOILEUS HEMIONUS) IN COLORADO, USA.
Journal of Wildlife Diseases In-Press. doi: http://dx.doi.org/10.7589/2014-12-284
Ahead of Print
AGE AND REPEATED BIOPSY INFLUENCE ANTEMORTEM PRPCWD TESTING IN MULE DEER
(ODOCOILEUS HEMIONUS) IN COLORADO, USA
Chris Geremia1,6,7 Jennifer A. Hoeting2, Lisa L. Wolfe3, Nathan L.
Galloway4, Michael F. Antolin4, Terry R. Spraker5, Michael W. Miller3, and N.
Thompson Hobbs1
1 Natural Resource Ecology Laboratory, Graduate Degree Program in Ecology,
Colorado State University, Fort Collins, Colorado, 80523-1499, USA
2 Department of Statistics, Colorado State University, Fort Collins,
Colorado 80523, USA
3 Colorado Division of Parks and Wildlife, Wildlife Health Program, 4330
Laporte Avenue, Fort Collins, Colorado 80521, USA
4 Department of Biology, Colorado State University, Fort Collins, Colorado
80523-1878, USA
5 Colorado State University Diagnostics Laboratory, Colorado State
University, Fort Collins, Colorado 80523, USA
Key words: Bayesian, capture–mark–recapture, chronic wasting disease, mule
deer, prion, test sensitivity
Abstract
Biopsy of rectal-mucosa associated lymphoid tissue provides a useful, but
imperfect, live-animal test for chronic wasting disease (CWD) in mule deer
(Odocoileus hemionus). It is difficult and expensive to complete these tests on
free-ranging animals, and wildlife health managers will benefit from methods
that can accommodate test results of varying quality. To this end, we developed
a hierarchical Bayesian model to estimate the probability that an individual is
infected based on test results. Our model was estimated with the use of data on
210 adult female mule deer repeatedly tested during 2010−2014. The ability to
identify infected individuals correctly declined with age and may have been
influenced by repeated biopsy. Fewer isolated lymphoid follicles (where PrPCWD
accumulates) were obtained in biopsies of older deer and the proportion of
follicles showing PrPCWD was reduced. A deer’s genotype in the prion gene (PRNP)
also influenced detection. At least five follicles were needed in a biopsy to
assure a 95% accurate test in PRNP genotype 225SS deer.
Received: December 15, 2014; Accepted: April 23, 2015
6 Current address: Yellowstone Center for Resources, P.O. Box 168,
Yellowstone National Park, Mammoth Hot Springs, Wyoming 82190, USA
7 Corresponding author (email: chris_geremia@nps.gov)
Longitudinal Detection of Prion Shedding in Saliva and Urine by Chronic Wasting Disease-Infected Deer by Real-Time Quaking-Induced Conversion
Davin M. Henderson, Nathaniel D. Denkers, Clare E. Hoover, Nina Garbino,
Candace K. Mathiason and Edward A. Hoover Prion Research Center, Department of
Microbiology, Immunology, and Pathology, College of Veterinary Medicine and
Biomedical Sciences, Colorado State University, Fort Collins, Colorado, USA
K. L. Beemon, Editor
+ Author Affiliations
ABSTRACT
Chronic wasting disease (CWD) is an emergent, rapidly spreading prion
disease of cervids. Shedding of infectious prions in saliva and urine is thought
to be an important factor in CWD transmission. To help to elucidate this issue,
we applied an in vitro amplification assay to determine the onset, duration, and
magnitude of prion shedding in longitudinally collected saliva and urine samples
from CWD-exposed white-tailed deer. We detected prion shedding as early as 3
months after CWD exposure and sustained shedding throughout the disease course.
We estimated that the 50% lethal dose (LD50) for cervidized transgenic mice
would be contained in 1 ml of infected deer saliva or 10 ml of urine. Given the
average course of infection and daily production of these body fluids, an
infected deer would shed thousands of prion infectious doses over the course of
CWD infection. The direct and indirect environmental impacts of this magnitude
of prion shedding on cervid and noncervid species are surely significant.
IMPORTANCE Chronic wasting disease (CWD) is an emerging and uniformly fatal
prion disease affecting free-ranging deer and elk and is now recognized in 22
U.S. states and 2 Canadian provinces. It is unique among prion diseases in that
it is transmitted naturally through wild populations. A major hypothesis to
explain CWD's florid spread is that prions are shed in excreta and transmitted
via direct or indirect environmental contact. Here we use a rapid in vitro assay
to show that infectious doses of CWD prions are in fact shed throughout the
multiyear disease course in deer. This finding is an important advance in
assessing the risks posed by shed CWD prions to animals as well as humans.
FOOTNOTES Received 14 May 2015. Accepted 23 June 2015. Accepted manuscript
posted online 1 July 2015. Address correspondence to Edward A. Hoover,
edward.hoover@colostate.edu.
D.M.H. and N.D.D. contributed equally to this article.
Citation Henderson DM, Denkers ND, Hoover CE, Garbino N, Mathiason CK,
Hoover EA. 2015. Longitudinal detection of prion shedding in saliva and urine by
chronic wasting disease-infected deer by real-time quaking-induced conversion. J
Virol 89:9338–9347. doi:10.1128/JVI.01118-15.
Insights into Chronic Wasting Disease and Bovine Spongiform Encephalopathy Species Barriers by Use of Real-Time Conversion
Kristen A. Davenport, Davin M. Henderson, Jifeng Bian, Glenn C. Telling,
Candace K. Mathiason and Edward A. Hoover Prion Research Center, Department of
Microbiology, Immunology and Pathology, College of Veterinary Medicine and
Biomedical Sciences, Colorado State University, Fort Collins, Colorado, USA
K. L. Beemon, Editor
+ Author Affiliations
ABSTRACT
The propensity for transspecies prion transmission is related to the
structural characteristics of the enciphering and new host PrP, although the
exact mechanism remains incompletely understood. The effects of variability in
prion protein on cross-species prion transmission have been studied with animal
bioassays, but the influence of prion protein structure versus that of host
cofactors (e.g., cellular constituents, trafficking, and innate immune
interactions) remains difficult to dissect. To isolate the effects of
protein-protein interactions on transspecies conversion, we used recombinant
PrPC and real-time quaking-induced conversion (RT-QuIC) and compared chronic
wasting disease (CWD) and classical bovine spongiform encephalopathy (cBSE)
prions. To assess the impact of transmission to a new species, we studied feline
CWD (fCWD) and feline BSE (i.e., feline spongiform encephalopathy [FSE]). We
cross-seeded fCWD and FSE into each species' full-length, recombinant PrPC and
measured the time required for conversion to the amyloid (PrPRes) form, which we
describe here as the rate of amyloid conversion. These studies revealed the
following: (i) CWD and BSE seeded their homologous species' PrP best; (ii) fCWD
was a more efficient seed for feline rPrP than for white-tailed deer rPrP; (iii)
conversely, FSE more efficiently converted bovine than feline rPrP; (iv) and
CWD, fCWD, BSE, and FSE all converted human rPrP, although not as efficiently as
homologous sCJD prions. These results suggest that (i) at the level of
protein-protein interactions, CWD adapts to a new species more readily than does
BSE and (ii) the barrier preventing transmission of CWD to humans may be less
robust than estimated.
IMPORTANCE We demonstrate that bovine spongiform encephalopathy prions
maintain their transspecies conversion characteristics upon passage to cats but
that chronic wasting disease prions adapt to the cat and are distinguishable
from the original prion. Additionally, we showed that chronic wasting disease
prions are effective at seeding the conversion of normal human prion protein to
an amyloid conformation, perhaps the first step in crossing the species barrier.
FOOTNOTES Received 3 June 2015. Accepted 1 July 2015. Accepted manuscript
posted online 8 July 2015. Address correspondence to Edward A. Hoover,
edward.hoover@colostate.edu.
Citation Davenport KA, Henderson DM, Bian J, Telling GC, Mathiason CK, Hoover EA. 2015. Insights into chronic wasting disease and bovine spongiform encephalopathy species barriers by use of real-time conversion. J Virol 89:9524–9531. doi:10.1128/JVI.01439-15.
================TEXAS CWD TSE PRION UPATE AUGUST 2015================
good ol boy system alive and well in the great state of Texas, protect the
industry at all cost, including human and animal health.
where is the official announcement of this 4th case (or more cases), by
the TAHC and or the TPWD? we’re still waiting.
why is the media having to do the TAHC and or the TPWD job, and reporting
this critical information to the public domain?
of course, it took 7+ months and an act of Congress to finally confirm and
announce to the public that last mad cow in Texas as well. political science as
usual in Texas.
IF the state of Texas does not get serious real fast with CWD, and test
all those deer, that 5 year plan is a ticking time bomb waiting to happen.
all cervid tested after slaughter, and test results must be released to
the public.
the tse prion aka mad cow type disease is not your normal pathogen.
The TSE prion disease survives ashing to 600 degrees celsius, that’s
around 1112 degrees farenheit.
you cannot cook the TSE prion disease out of meat.
you can take the ash and mix it with saline and inject that ash into a
mouse, and the mouse will go down with TSE.
Prion Infected Meat-and-Bone Meal Is Still Infectious after Biodiesel
Production as well.
the TSE prion agent also survives Simulated Wastewater Treatment
Processes.
IN fact, you should also know that the TSE Prion agent will survive in the
environment for years, if not decades.
you can bury it and it will not go away.
The TSE agent is capable of infected your water table i.e. Detection of
protease-resistant cervid prion protein in water from a CWD-endemic area.
it’s not your ordinary pathogen you can just cook it out and be done with.
that’s what’s so worrisome about Iatrogenic mode of transmission, a simple
autoclave will not kill this TSE prion agent.
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.
============================================================================
*** Infectious agent of sheep scrapie may persist in the environment for at
least 16 years ***
Gudmundur Georgsson1, Sigurdur Sigurdarson2 and Paul Brown3
============================================================================
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.
cwd environmental load factor in the land and surrounding plants and
objects.
transportation of cervids and HUMANS from cwd zone should be regarded as a
great risk factor, and environmental contamination.
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 ;
*** Infectious agent of sheep scrapie may persist in the environment for at
least 16 years ***
Gudmundur Georgsson1, Sigurdur Sigurdarson2 and Paul Brown3
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.***
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
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.***
From: Terry S. Singeltary Sr.
Sent: Saturday, November 15, 2014 9:29 PM
To: Terry S. Singeltary Sr.
Subject: THE EPIDEMIOLOGY OF CREUTZFELDT-JAKOB DISEASE R. G. WILL 1984
THE EPIDEMIOLOGY OF CREUTZFELDT-JAKOB DISEASE
R. G. WILL
1984
*** The association between venison eating and risk of CJD shows similar
pattern, with regular venison eating associated with a 9 FOLD INCREASE IN RISK
OF CJD (p = 0.04). (SEE LINK IN REPORT HERE...TSS) PLUS, THE CDC DID NOT PUT
THIS WARNING OUT FOR THE WELL BEING OF THE DEER AND ELK ;
snip...
*** 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.
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, Val erie 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 longe 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...TSS
===============
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
Wednesday, July 01, 2015
*** TEXAS Chronic Wasting Disease Detected in Medina County Captive Deer
Tuesday, July 21, 2015
*** Texas CWD Medina County Herd Investigation Update July 16, 2015 ***
Thursday, August 06, 2015
*** WE HAVE LOST TEXAS TO CWD TASK FORCE CATERING TO INDUSTRY
Friday, August 07, 2015
*** Texas CWD Captive, and then there were 4 ?
TEXAS DEER CZAR SENT TO WISCONSIN TO SOLVE CWD CRISIS, WHILE ROME (TEXAS)
BURNS
Tuesday, August 11, 2015
*** Wisconsin doing what it does best, procrastinating about CWD yet again
thanks to Governor Walker
*** Danger of Canned Hunting Indiana Wildlife ***
a review since the TEXAS 84th Legislature commencing this January, deer
breeders are expected to advocate for bills that will seek to further deregulate
their industry...
Sunday, December 14, 2014
TEXAS 84th Legislature commencing this January, deer breeders are expected
to advocate for bills that will seek to further deregulate their industry
Tuesday, December 16, 2014
Texas 84th Legislature 2015 H.R. No. 2597 Kuempel Deer Breeding Industry
TAHC TPWD CWD TSE PRION
I spoke with MASTER Obi-Wan Kenobi about all this. see Obi’s reply ;
GRASSHOPPER TO MASTER Obi-Wan Kenobi CWD TEXAS CAPTIVE
‘’I see no evidence whatsoever here for a genetic link. The numbers are
statistically insignificant and co-housing in contaminated facilities would
strongly predispose to this outcome.’’
‘’if the father did have a bad amino acid variant allele, it would be
diluted to heterozygozity with a normal gene in the half the four descendants
since the father never would have survived to breeding age with two bad copies.
sort of like met/val at position 129 in humans with greatly lengthened
incubation times if prnp is propagating at all. Mutations such as repeat
expansion leading to positive dominant infection have not been documented in
cervids.’’
On 09 08 15, at 9:09 AM, Terry S. Singeltary Sr.
wrote: ‘’
cwd Texas and then there were 4?
genetic link ?
He said 42 deer have been killed and tested since July 28, and three
additional positives were the result.
***He added that all four deer confirmed to have the disease were males
from the same father, which leads him to believe the problem is genetic.
snip...
HAVE YOU BEEN THUNDERSTRUCK ?
on my mothers grave, when I wrote up the ‘have you been thunderstruck’
about super ovulation, and what if? I had no clue about all this. hell, I had it
in draft for a month. then a week or so later, bam.
it’s been like this all along Obi-Wan Kenobi.
every shooting pen owner in Texas are praying this familial cwd is the
going thing now.
no link to sperm.
no link to super ovulation.
they sell those sperm straws like the meth heads and crack heads sell meth
and crack.
genetic link with four deer in the same herd, same father ?
familial ?
sperm ?
super ovulation ?
what say ye master ?
grasshopper
Friday, August 07, 2015
Texas CWD Captive, and then there were 4 ?
TAHC ADOPTS CWD RULE THAT the amendments remove the requirement for a
specific fence height for captives
Texas Animal Health Commission (TAHC)
ANNOUNCEMENT
October 3, 2013
snip...
Summary Minutes from 387th Commission Meeting – 9/10/2013
18
1) The first change is to the definition of “Physical Herd Inventory” to
remove the requirement that all animals in the herd must be restrained in order
to have the identification validated by the person performing the inventory
verification.
2) The second modification is the fencing requirement found in §40.3(a)
which provides that a herd premises must have perimeter fencing of a minimum of
eight feet in height and adequate to prevent ingress or egress of cervids. That
standard is found in the Uniform Method and Rules for CWD, but under the federal
regulations the standard provides merely that the fencing must be adequate to
prevent ingress or egress of cervids and the commission is modifying agency
requirements to meet that standard by removing the eight foot requirement.
The motion to approve the regulation amendment passed.
> The amendments remove the requirement for a specific fence height...
> but under the federal regulations the standard provides merely that
the fencing must be adequate to prevent ingress or egress of cervids and the
commission is modifying agency requirements to meet that standard by removing
the eight foot requirement.
Wednesday, July 22, 2015
Texas Certified Chronic Wasting Disease CWD Sample Collector, like the Wolf
Guarding the Henhouse
Tuesday, July 21, 2015
*** Texas CWD Medina County Herd Investigation Update July 16, 2015
***
Evidence That Transmissible Mink Encephalopathy Results from Feeding
Infected Cattle
Over the next 8-10 weeks, approximately 40% of all the adult mink on the
farm died from TME.
snip...
The rancher was a ''dead stock'' feeder using mostly (>95%) downer or
dead dairy cattle...
In Confidence - Perceptions of unconventional slow virus diseases of
animals in the USA - APRIL-MAY 1989 - G A H Wells
3. Prof. A. Robertson gave a brief account of BSE. The US approach was to
accord it a very low profile indeed. Dr. A Thiermann showed the picture in the
''Independent'' with cattle being incinerated and thought this was a fanatical
incident to be avoided in the US at all costs. ...
human cwd will NOT look like nvCJD. in fact, see ;
*** 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).***
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)
*** 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.
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.
SEE OLD HISTORY OF DIFFERENT STATES TRYING TO STOP THE SPREADING OF CWD VIA
DEER CAPTIVE BREEDER, HUNTING FARMS ;
Friday, January 30, 2015
*** Scrapie: a particularly persistent pathogen ***
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...
==================================
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.
=================================
Draft Guidance on Use of Material From Deer and Elk in Animal Feed; CVM
Updates on Deer and Elk Withdrawn FDA Veterinarian Newsletter July/August 2003
Volume XVIII, No 4
snip...
II. Background
CWD is a neurological (brain) disease of farmed and wild deer and elk that
belong in the animal family cervidae (cervids). Only deer and elk are known to
be susceptible to CWD by natural transmission. The disease has been found in
farmed and wild mule deer,
1 This guidance has been prepared by the Division of Animal Feeds in the
Center for Veterinary Medicine (CVM) at the Food and Drug Administration.
snip...
III.
Use in animal feed of material from CWD-positive deer and elk
Material from CWD-positive animals may not be used in any animal feed or
feed ingredients. Pursuant to Sec. 402(a)(5) of the Federal Food, Drug, and
Cosmetic Act, animal feed and feed ingredients containing material from a
CWD-positive animal would be considered adulterated. FDA recommends that any
such adulterated feed or feed ingredients be recalled or otherwise removed from
the marketplace.
IV.
Use in animal feed of material from deer and elk considered at high risk
for CWD
Deer and elk considered at high risk for CWD include: (1) animals from
areas declared by State officials 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 immediately before the time of slaughter were in a captive herd that
contained a CWD-positive animal.
FDA recommends that materials from deer and elk considered at high risk
for CWD no longer be entered into the animal feed system. Under present
circumstances, FDA is not recommending that feed made from deer and elk from a
non-endemic area be recalled if a State later declares the area endemic for CWD
or a CWD eradication zone. In addition, at this time, FDA is not recommending
that feed made from deer and elk believed to be from a captive herd that
contained no CWD-positive animals be recalled if that herd is subsequently found
to contain a CWD-positive animal. V. Use in animal feed of material from deer
and elk NOT considered at high risk for CWD
FDA continues to consider materials from deer and elk NOT considered at
high risk for CWD to be acceptable for use in NON-RUMINANT animal feeds in
accordance with current agency regulations, 21 CFR 589.2000. Deer and elk not
considered at high risk include: (1) deer and elk from areas not declared by
State officials to be endemic for CWD and/or to be CWD eradication zones; and
(2) deer and elk that were not at some time during the 60-month period
immediately before the time of slaughter in a captive herd that contained a
CWD-positive animal.
*** Singeltary reply ;
ruminant feed ban for cervids in the United States ?
31 Jan 2015 at 20:14 GMT
*** Singeltary reply ; Molecular, Biochemical and Genetic Characteristics
of BSE in Canada Singeltary reply ;
10,000,000+ LBS. of PROHIBITED BANNED MAD COW FEED I.E. BLOOD LACED MBM IN
COMMERCE USA 2007
Date: March 21, 2007 at 2:27 pm PST
RECALLS AND FIELD CORRECTIONS: VETERINARY MEDICINES -- CLASS II
PRODUCT
Bulk cattle feed made with recalled Darling's 85% Blood Meal, Flash Dried,
Recall # V-024-2007
CODE
Cattle feed delivered between 01/12/2007 and 01/26/2007
RECALLING FIRM/MANUFACTURER
Pfeiffer, Arno, Inc, Greenbush, WI. by conversation on February 5, 2007.
Firm initiated recall is ongoing.
REASON
Blood meal used to make cattle feed was recalled because it was cross-
contaminated with prohibited bovine meat and bone meal that had been
manufactured on common equipment and labeling did not bear cautionary BSE
statement.
VOLUME OF PRODUCT IN COMMERCE
42,090 lbs.
DISTRIBUTION
WI
___________________________________
PRODUCT
Custom dairy premix products: MNM ALL PURPOSE Pellet, HILLSIDE/CDL Prot-
Buffer Meal, LEE, M.-CLOSE UP PX Pellet, HIGH DESERT/ GHC LACT Meal, TATARKA, M
CUST PROT Meal, SUNRIDGE/CDL PROTEIN Blend, LOURENZO, K PVM DAIRY Meal, DOUBLE B
DAIRY/GHC LAC Mineral, WEST PIONT/GHC CLOSEUP Mineral, WEST POINT/GHC LACT Meal,
JENKS, J/COMPASS PROTEIN Meal, COPPINI - 8# SPECIAL DAIRY Mix, GULICK, L-LACT
Meal (Bulk), TRIPLE J - PROTEIN/LACTATION, ROCK CREEK/GHC MILK Mineral,
BETTENCOURT/GHC S.SIDE MK-MN, BETTENCOURT #1/GHC MILK MINR, V&C DAIRY/GHC
LACT Meal, VEENSTRA, F/GHC LACT Meal, SMUTNY, A- BYPASS ML W/SMARTA, Recall #
V-025-2007
CODE
The firm does not utilize a code - only shipping documentation with
commodity and weights identified.
RECALLING FIRM/MANUFACTURER
Rangen, Inc, Buhl, ID, by letters on February 13 and 14, 2007. Firm
initiated recall is complete.
REASON
Products manufactured from bulk feed containing blood meal that was cross
contaminated with prohibited meat and bone meal and the labeling did not bear
cautionary BSE statement.
VOLUME OF PRODUCT IN COMMERCE
9,997,976 lbs.
DISTRIBUTION
ID and NV
END OF ENFORCEMENT REPORT FOR MARCH 21, 2007
*** spontaneous TSE prion, that's wishful thinking. on the other hand, if
spontaneous did ever happen (never once documented in the field), it would be
our worst nightmare, due to feed. just saying.
*** We describe the transmission of spongiform encephalopathy in a
non-human primate inoculated 10 years earlier with a strain of sheep c-scrapie.
Because of this extended incubation period in a facility in which other prion
diseases are under study, we are obliged to consider two alternative
possibilities that might explain its occurrence. We first considered the
possibility of a sporadic origin (like CJD in humans). Such an event is
extremely improbable because the inoculated animal was 14 years old when the
clinical signs appeared, i.e. about 40% through the expected natural lifetime of
this species, compared to a peak age incidence of 60–65 years in human sporadic
CJD, or about 80% through their expected lifetimes. ***Moreover, sporadic
disease has never been observed in breeding colonies or primate research
laboratories, most notably among hundreds of animals over several decades of
study at the National Institutes of Health25, and in nearly twenty older animals
continuously housed in our own facility.***
>>> Moreover, sporadic disease has never been observed in
breeding colonies or primate research laboratories, most notably among hundreds
of animals over several decades of study at the National Institutes of Health25,
and in nearly twenty older animals continuously housed in our own facility.
<<<
FRANCE HAVE AN EPIDEMIC OF SPONTANEOUS ATYPICAL BSE ‘’LOL’’
spontaneous atypical BSE ???
if that's the case, then France is having one hell of an epidemic of
atypical BSE, probably why they stopped testing for BSE, problem solved $$$
As of December 2011, around 60 atypical BSE cases have currently been
reported in 13 countries, *** with over one third in France.
so 20 cases of atypical BSE in France, compared to the remaining 40 cases
in the remaining 12 Countries, divided by the remaining 12 Countries, about 3+
cases per country, besides Frances 20 cases. you cannot explain this away with
any spontaneous BSe. ...TSS
Sunday, October 5, 2014
France stops BSE testing for Mad Cow Disease
2013
Sunday, December 15, 2013
FDA PART 589 -- SUBSTANCES PROHIBITED FROM USE IN ANIMAL FOOD OR FEED
VIOLATIONS OFFICIAL ACTION INDICATED OIA UPDATE DECEMBER 2013 UPDATE
Tuesday, December 23, 2014
FDA PART 589 -- SUBSTANCES PROHIBITED FROM USE IN ANIMAL FOOD OR FEED
VIOLATIONS OFFICIAL ACTION INDICATED OAI UPDATE DECEMBER 2014 BSE TSE PRION
Friday, November 22, 2013
Wasting disease is threat to the entire UK deer population CWD TSE PRION
disease in cervids
***SINGELTARY SUBMISSION
The Scottish Parliament’s Rural Affairs, Climate Change and Environment
Committee has been looking into deer management, as you can see from the
following press release,
***and your email has been forwarded to the committee for information:
Friday, November 22, 2013
Wasting disease is threat to the entire UK deer population
Sunday, July 21, 2013
Welsh Government and Food Standards Agency Wales Joint Public Consultation
on the Proposed Transmissible Spongiform Encephalopathies (Wales) Regulations
2013
*** Singeltary Submission WG18417
*** IBNC Tauopathy or TSE Prion disease, it appears, no one is sure ***
Posted by flounder on 03 Jul 2015 at 16:53 GMT
Friday, August 14, 2015
Susceptibility of cattle to the agent of chronic wasting disease from elk
after intracranial inoculation
Thursday, July 24, 2014
*** Protocol for further laboratory investigations into the distribution
of infectivity of Atypical BSE SCIENTIFIC REPORT OF EFSA New protocol for
Atypical BSE investigations
Wednesday, July 15, 2015
*** Additional BSE TSE prion testing detects pathologic lesion in unusual
brain location and PrPsc by PMCA only, how many cases have we missed?
Wednesday, July 29, 2015
Further characterisation of transmissible spongiform encephalopathy
phenotypes after inoculation of cattle with two temporally separated sources of
sheep scrapie from Great Britain
Wednesday, July 29, 2015
Porcine Prion Protein Amyloid or mad pig disease PSE
Monday, August 10, 2015
Detection and Quantification of beta-Amyloid, Pyroglutamyl A beta, and Tau
in Aged Canines
http://caninespongiformencephalopathy.blogspot.com/2015/08/detection-and-quantification-of-beta.html
Friday, August 7, 2015
Transgenic Mouse Bioassay: Evidence That Rabbits Are Susceptible to a
Variety of Prion Isolates
Friday, August 14, 2015
*** Carcass Management During a Mass Animal Health Emergency Draft
Programmatic Environmental Impact Statement—August 2015
Thursday, August 13, 2015
Iatrogenic CJD due to pituitary-derived growth hormone with genetically
determined incubation times of up to 40 years
Thursday, January 15, 2015
41-year-old Navy Commander with sporadic Creutzfeldt–Jakob disease CJD TSE
Prion: Case Report
Subject: *** Becky Lockhart 46, Utah’s first female House speaker, dies
diagnosed with the extremely rare Creutzfeldt-Jakob disease aka mad cow type
disease
what is CJD ? just ask USDA inc., and the OIE, they are still feeding the
public and the media industry fed junk science that is 30 years old.
why doesn’t some of you try reading the facts, instead of rubber stamping
everything the USDA inc says.
sporadic CJD has now been linked to BSE aka mad cow disease, Scrapie, and
there is much concern now for CWD and risk factor for humans.
My sincere condolences to the family and friends of the House Speaker
Becky Lockhart. I am deeply saddened hear this.
with that said, with great respect, I must ask each and every one of you
Politicians that are so deeply saddened to hear of this needless death of the
Honorable House Speaker Becky Lockhart, really, cry me a friggen river. I am
seriously going to ask you all this...I have been diplomatic for about 17 years
and it has got no where. people are still dying. so, are you all stupid or
what??? how many more need to die ??? how much is global trade of beef and other
meat products that are not tested for the TSE prion disease, how much and how
many bodies is this market worth?
Saturday, January 17, 2015
*** Becky Lockhart 46, Utah’s first female House speaker, dies diagnosed
with the extremely rare Creutzfeldt-Jakob disease
*** ALERT new variant Creutzfeldt Jakob Disease nvCJD or vCJD, sporadic
CJD strains, TSE prion aka Mad Cow Disease United States of America Update
December 14, 2014 Report ***
*** Creutzfeldt-Jakob Disease Public Health Crisis VIDEO
Alzheimer’s, iatrogenic, what if ?
Friday, January 10, 2014
vpspr, sgss, sffi, TSE, an iatrogenic by-product of gss, ffi, familial
type prion disease, what it ???
Tuesday, August 4, 2015
FDA U.S. Measures to Protect Against BSE
Monday, August 17, 2015
FDA Says Endoscope Makers Failed to Report Superbug Problems OLYMPUS
I told Olympus 15 years ago about these risk factors from endoscopy
equipment, disinfection, even spoke with the Doctor at Olympus, this was back in
1999. I tried to tell them that they were exposing patients to dangerous
pathogens such as the CJD TSE prion, because they could not properly clean them.
even presented my concern to a peer review journal GUT, that was going to
publish, but then it was pulled by Professor Michael Farthing et al... see ;
consumption there from, TSE prion disease at a hospital near you ???
Thursday, August 13, 2015
Iatrogenic CJD due to pituitary-derived growth hormone with genetically
determined incubation times of up to 40 years
still kidding ourselves in Texas...it’s still not funny to me.
Singeltary trying to warn where cwd is at in Trans Pecos region 2001-2002 -
2012
TEXAS OLD STATISTICS BELOW FOR PAST CWD TESTING;
Subject: CWD testing in Texas
Date: Sun, 25 Aug 2002 19:45:14 –0500
From: Kenneth Waldrup
To: flounder@wt.net
CC: mcoats@tahc.state.tx.us
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.
Ken Waldrup, DVM, PhD Texas Animal Health Commission
========================
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
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2006
----- Original Message -----
From: "Terry S. Singeltary Sr." flounder9@VERIZON.NET
To: BSE-L@aegee.org
Sent: Saturday, December 23, 2006 1:47 PM
Subject: CWD in New Mexico 35 MILES FROM TEXAS BORDER and low testing
sampling figures -- what gives TAHC ???
Date: December 23, 2006 at 11:25 am PST
Greetings BSE-L members,
i never know if i am going crazy or just more of the same BSe. several
years ago i brought up the fact to the TAHC that CWD was literally at the Texas
borders and that the sample size for cwd testing was no where near enough in the
location of that zone bordering NM. well, i just wrote them another letter
questioning this again on Dec. 14, 2006 (see below) and showed them two
different pdf maps, one referencing this url, which both worked just fine then.
since then, i have NOT received a letter from them answering my question, and
the url for the map i used as reference is no longer working? i had reference
this map several times from the hunter-kill cwd sampling as of 31 August 2005
pdf which NO longer works now??? but here are those figures for that zone
bordering NM, for those that were questioning the url. the testing samples
elsewhere across Texas where much much more than that figure in the zone
bordering NM where CWD has been documented bordering TEXAS, near the White Sands
Missile Range. SO, why was the Texas hunter-kill cwd sampling as of 31 August
2005 document removed from the internet??? you know, this reminds me of the
infamous TEXAS MAD COW that i documented some 7 or 8 months before USDA et al
documented it, when the TAHC accidentally started ramping up for the
announcement on there web site, then removed it (see history at bottom). i am
not screaming conspiracy here, but confusious is confused again on the ciphering
there using for geographical distribution of cwd tissue sample size survey, IF
they are serious about finding CWD in TEXAS. common sense would tell you if cwd
is 35 miles from the border, you would not run across state and have your larger
samples there, and least samples 35 miles from where is what
found..........daaa..........TSS
THEN NOTICE CWD sample along that border in TEXAS, Three Year Summary of
Hunter-Kill CWD sampling as of 31 August 2005 of only 191 samples, then compare
to the other sample locations ;
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 ;
TEXAS CWD STATUS
Captive Cervids
There have been no reported CWD infections of captive elk or deer in Texas.
There is currently no mandatory surveillance program for susceptible cervids
kept on game farms, although, there has been voluntary surveillance since 1999,
which requires owners of participating herds to maintain an annual herd
inventory and submit samples for all mortalities of animals over 16 months of
age.
Free-Ranging (Wild) Cervids
There have been no reported CWD infections of free-ranging susceptible
cervids in Texas. Currently targeted surveillance of free-ranging cervids having
clinical symptoms is ongoing in Texas with no positives identified.
Additionally, sampling of hunter-killed animals was initiated statewide during
the 2002-2003 deer hunting season and sampling will be continued for the next
three to five years.
Historic Status
snip...
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
CJD WATCH
-------- 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
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-------- Original Message --------
Subject: CWD SURVEILLANCE SAMPLE SUBMISSIONS TEXAS ?
Date: Mon, 16 Aug 2004 15:09:58 –0500
From: "Terry S. Singeltary Sr."
To: Bovine Spongiform Encephalopathy
Greetings List members,
as i stated in my previous email;
> >> CWD has not been detected in Texas, SADLY, they have not
tested enough from the total population to know if CWD is in Texas or not. time
will tell though. IF they get serious about finding and documenting CWD in
sufficient numbers here in TEXAS, sadly, i am afraid they will find it. ITs
already at NM, Texas border, TSEs knows no borders. HOWEVER, with the recent
finding of a CNS cow with high potential for BSE/TSE in TEXAS, with one high
official over ruling another official that wanted it tested, with the high
official winning out and the damn thing going to render without being tested,
head spinal cord and all. THIS weighs heavy on the credibility of any
surveillance for any TSE in TEXAS, and speaks a great deal for the over all
surveillance of TSE in the USA...TSS
SO, i thought i would just see where these Ecoregions were, and just how
the CWD testing was distributed. YOU would think that with the cluster of CWD
bordering TEXAS at the WPMR in NM, you would have thought this would be where
the major CWD testing samples were to have been taken? wrong! let's have a look
at the sample testing. here is map of CWD in NM WPMR bordering TEXAS;
NEW MEXICO 7 POSITIVE CWD WHITE SANDS MISSILE RANGE MAP
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...
TSS
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 #########
Singeltary trying to warn TAHC that they were covering up mad cow disease
and correspondence with OIG
BUT FIRST, THE FIRST STUMBLING AND STAGGERING MAD COW THAT GOT AWAY FROM
SINGELTARY, 2004, highly suspect stumbling and staggering mad cow reported,
however, NO TESTING DONE, ON ORDERS FROM AUSTIN $
May 4, 2004
Statement on Texas Cow With Central Nervous System Symptoms
On Friday, April 30th, the Food and Drug Administration learned that a cow
with central nervous system symptoms had been killed and shipped to a processor
for rendering into animal protein for use in animal feed.
FDA, which is responsible for the safety of animal feed, immediately began
an investigation. On Friday and throughout the weekend, FDA investigators
inspected the slaughterhouse, the rendering facility, the farm where the animal
came from, and the processor that initially received the cow from the
slaughterhouse.
FDA's investigation showed that the animal in question had already been
rendered into "meat and bone meal" (a type of protein animal feed). Over the
weekend FDA was able to track down all the implicated material. That material is
being held by the firm, which is cooperating fully with FDA.
Cattle with central nervous system symptoms are of particular interest
because cattle with bovine spongiform encephalopathy or BSE, also known as "mad
cow disease," can exhibit such symptoms. In this case, there is no way now to
test for BSE. But even if the cow had BSE, FDA's animal feed rule would prohibit
the feeding of its rendered protein to other ruminant animals (e.g., cows,
goats, sheep, bison)...
USDA regulations, any cow that exhibits signs of central nervous system
(CNS)
According to a 1997 Animal and Plant Health Inspection Service (NHIS)
Memorandum, brain samples all of such animals should be sent for BSE testing.2
The memorandum notes that "it is essential that brain specimens be collected
from adult cattle condemned for CNS signs as part of our national surveillance
of BSE."
The cow slaughtered at the Lone Star Beef slaughterhouse last week
staggered and fell, and was condemned ante mortem by FSIS personnel.4 Despite a
request from APHIS personnel at the plant to conduct BSE testing, however, an
APHIS supervisor in Austin reportedly refused the test and instructed the plant
to send the carcass for rendering.5
May 13,2004
Page 2
snip...
The cow slaughtered at the Lone Star Beef slaughterhouse last week
staggered and fell, and was condemned ante mortem by FSIS personnel.4 Despite a
request from APHIS personnel at the plant to conduct BSE testing, however, an
APHIS supervisor in Austin reportedly refused the test and instructed the plant
to send the carcass for rendering.5
This sequence of events is troubling, and it raises the question of
whether this is an isolated incident. In 1997, USDA noted a major gap between
the number of cattle condemned for CNS symptoms and the number of these cows
actually tested for mad cow disease. The Department found:
-------- Original Message --------
Subject: re-USDA's surveillance plan for BSE aka mad cow disease
Date: Mon, 02 May 2005 16:59:07 -0500
From: "Terry S. Singeltary Sr."
To: paffairs@oig.hhs.gov, HHSTips@oig.hhs.gov, contactOIG@hhsc.state.tx.us
Greetings Honorable Paul Feeney, Keith Arnold, and William Busbyet al at
OIG, ...............
snip...
There will be several more emails of my research to follow. I respectfully
request a full inquiry into the cover-up of TSEs in the United States of America
over the past 30 years. I would be happy to testify...
Thank you, I am sincerely, Terry S. Singeltary Sr. P.O. Box 42 Bacliff,
Texas USA 77518 xxx xxx xxxx
Date: June 14, 2005 at 1:46 pm PST In
Reply to: Re: Transcript Ag. Secretary Mike Johanns and Dr. John Clifford,
Regarding further analysis of BSE Inconclusive Test Results posted by TSS on
June 13, 2005 at 7:33 pm:
Secretary of Agriculture Ann M. Veneman resigns Nov 15 2004, three days
later inclusive Mad Cow is announced. June 7th 2005 Bill Hawks Under Secretary
for Marketing and Regulatory Programs resigns. Three days later same mad cow
found in November turns out to be positive. Both resignation are unexpected.
just pondering... TSS
MAD COW IN TEXAS NOVEMBER 2004 SINGELTARY’S MAD COW THAT DID NOT GET AWAY,
JUST DELAYED FOR POLITICAL PURPOSES...TRADE $$$
-------- Original Message --------
Director, Public Information Carla Everett ceverett@tahc.state.tx.us
Subject: Re: BSE 'INCONCLUSIVE' COW from TEXAS ???
Date: Mon, 22 Nov 2004 17:12:15 –0600
From: "Terry S. Singeltary Sr."
To: Carla Everett References: <[log in to unmask]> <[log in to
unmask] us>
Greetings Carla,still hear a rumor;
Texas single beef cow not born in Canada no beef entered the food chain?
and i see the TEXAS department of animal health is ramping up
forsomething, but they forgot a url for update?I HAVE NO ACTUAL CONFIRMATION
YET...can you confirm???
terry
-------- Original Message --------
Subject: Re: BSE 'INCONCLUSIVE' COW from TEXAS ???
Date: Fri, 19 Nov 2004 11:38:21 –0600
From: Carla Everett
To: "Terry S. Singeltary Sr." References: <[log in to unmask]>
The USDA has made a statement, and we are referring all callers to the
USDA web site. We have no information about the animal being in Texas. Carla At
09:44 AM 11/19/2004, you wrote:>Greetings Carla,>>i am getting
unsubstantiated claims of this BSE 'inconclusive' cow is from>TEXAS. can you
comment on this either way please?>>thank you,>Terry S. Singeltary
Sr.>>
-------- Original Message --------
Subject: Re: BSE 'INCONCLUSIVE' COW from TEXAS ???
Date: Mon, 22 Nov 2004 18:33:20 -0600 From: Carla Everett
To: "Terry S. Singeltary Sr."
References: ...sniptss
our computer department was working on a place holder we could post USDA's
announcement of any results. There are no results to be announced tonight by
NVSL, so we are back in a waiting mode and will post the USDA announcement when
we hear something. At 06:05 PM 11/22/2004,
you wrote:
>why was the announcement on your TAHC site removed?
>>Bovine Spongiform Encephalopathy:
>November 22: Press Release title here
>>star image More BSE information
>>>>terry
>>Carla Everett wrote:
>>>no confirmation on the U.S.' inconclusive test...
>>no confirmation on location of animal.>>>>>>
==========================
-------- Original Message --------
Director, Public Information Carla Everett ceverett@tahc.state.tx.us
Subject: Re: BSE 'INCONCLUSIVE' COW from TEXAS ???
Date: Mon, 22 Nov 2004 17:12:15 –0600
From: "Terry S. Singeltary Sr."
To: Carla Everett References: <[log in to unmask]> <[log in to
unmask] us>
Greetings Carla,still hear a rumor;
Texas single beef cow not born in Canada no beef entered the food chain?
and i see the TEXAS department of animal health is ramping up
forsomething, but they forgot a url for update?I HAVE NO ACTUAL CONFIRMATION
YET...can you confirm???
terry
=====7 MONTHS LATER, SINGELTARY’S MAD COW WAS CONFIRMED=====
HOW TEXAS DOES TRACE OUTS...
Executive Summary In June 2005, an inconclusive bovine spongiform
encephalopathy (BSE) sample from November 2004, that had originally been
classified as negative on the immunohistochemistry test, was confirmed positive
on SAF immunoblot (Western blot). The U.S. Department of Agriculture (USDA)
identified the herd of origin for the index cow in Texas; that identification
was confirmed by DNA analysis. USDA, in close cooperation with the Texas Animal
Health Commission (TAHC), established an incident command post (ICP) and began
response activities according to USDA’s BSE Response Plan of September 2004.
Response personnel removed at-risk cattle and cattle of interest (COI) from the
index herd, euthanized them, and tested them for BSE; all were negative. USDA
and the State extensively traced all at-risk cattle and COI that left the index
herd. ***The majority of these animals entered rendering and/or slaughter
channels well before the investigation began. USDA’s response to the Texas
finding was thorough and effective.
snip...
Trace Herd 3 The owner of Trace Herd 3 was identified as possibly having
received an animal of interest. The herd was placed under hold order on 7/27/05.
The herd inventory was conducted on 7/28/05. The animal of interest was not
present within the herd, and the hold order was released on 7/28/05. The person
who thought he sold the animal to the owner of Trace Herd 3 had no records and
could not remember who else he might have sold the cow to. Additionally, a
search of GDB for all cattle sold through the markets by that individual did not
result in a match to the animal of interest. The animal of interest traced to
this herd was classified as ***untraceable because all leads were exhausted.
Trace Herd 4 The owner of Trace Herd 4 was identified as having received
one of the COI through an order buyer. Trace Herd 4 was placed under hold order
on 7/29/05. A complete herd inventory was conducted on 8/22/05 and 8/23/05.
There were 233 head of cattle that were examined individually by both State and
Federal personnel for all man-made identification and brands. ***The animal of
interest was not present within the herd. Several animals were reported to have
died in the herd sometime after they arrived on the premises in April 2005. ***A
final search of GDB records yielded no further results on the eartag of interest
at either subsequent market sale or slaughter. ***With all leads having been
exhausted, this animal of interest has been classified as untraceable. The hold
order on Trace Herd 4 was released on 8/23/05.
Trace Herd 5 The owner of Trace Herd 5 was identified as having received
two COI and was placed under hold order on 8/1/05. Trace Herd 5 is made up of 67
head of cattle in multiple pastures. During the course of the herd inventory,
the owner located records that indicated that one of the COI, a known birth
cohort, had been sold to Trace Herd 8 where she was subsequently found alive.
***Upon completion of the herd inventory, the other animal of interest was not
found within the herd. ***A GDB search of all recorded herd tests conducted on
Trace Herd 5 and all market sales by the owner failed to locate the
identification tag of the animal of interest and she was subsequently classified
as ***untraceable due to all leads having been exhausted. The hold order on
Trace Herd 5 was released on 8/8/05.
Trace Herd 6 The owner of Trace Herd 6 was identified as possibly having
received an animal of interest and was placed under hold order on 8/1/05. This
herd is made up of 58 head of cattle on two pastures. A herd inventory was
conducted and the animal of interest was not present within the herd. ***The
owner of Trace Herd 6 had very limited records and was unable to provide further
information on where the cow might have gone after he purchased her from the
livestock market. A search of GDB for all cattle sold through the markets by
that individual did not result in a match to the animal of interest.
Additionally, many of the animals presented for sale by the owner of the herd
had been re-tagged at the market effectually losing the traceability of the
history of that animal prior to re-tagging. ***The animal of interest traced to
this herd was classified as ***untraceable due to all leads having been
exhausted. The hold order on Trace Herd 6 was released on 8/3/05.
Trace Herd 7 The owner of Trace Herd 7 was identified as having received
an animal of interest and was placed under hold order on 8/1/05. Trace Herd 7
contains 487 head of cattle on multiple pastures in multiple parts of the State,
including a unit kept on an island. The island location is a particularly rough
place to keep cattle and the owner claimed to have lost 22 head on the island in
2004 due to liver flukes. Upon completion of the herd inventory, the animal of
interest was not found present within Trace Herd 7. ***A GDB search of all
recorded herd tests conducted on Trace Herd 7 and all market sales by the owner
failed to locate the identification tag of the animal of interest. ***The cow
was subsequently classified as untraceable. It is quite possible though that she
may have died within the herd, especially if she belonged to the island unit.
The hold order on Trace Herd 7 was released on 8/8/05.
USDA did not test possible mad cows
By Steve Mitchell
United Press International
Published 6/8/2004 9:30 PM
WASHINGTON, June 8 (UPI) -- The U.S. Department of Agriculture claims
ittested 500 cows with signs of a brain disorder for mad cow disease last year,
but agency documents obtained by United Press International show the agency
tested only half that number.
""These 9,200 cases were different because brain tissue samples were
preserved with formalin, which makes them suitable for only one type of
test--immunohistochemistry, or IHC."
THIS WAS DONE FOR A REASON!
THE IHC test has been proven to be the LEAST LIKELY to detect BSE/TSE in
the bovine, and these were probably from the most high risk cattle pool, the
ones the USDA et al, SHOULD have been testing. ...TSS
TEXAS 2ND MAD COW THAT WAS COVERED UP, AFTER AN ACT OF CONGRESS, AND CALLS
FROM TSE PRION SCIENTIST AROUND THE GLOBE, THIS 2ND MAD COW IN TEXAS WAS
CONFIRMED
THE USDA MAD COW FOLLIES POSITIVE TEST COVER UP
JOHANNS SECRET POSTIVE MAD COW TEST THAT WERE IGNORED
OIG AND THE HONORABLE FONG CONFIRMS TEXAS MAD AFTER AN ACT OF CONGRESS 7
MONTHS LATER
TEXAS MAD COW
THEY DID FINALLY TEST AFTER SITTING 7+ MONTHS ON A SHELF WHILE GW BORE THE
BSE MRR POLICY, i.e. legal trading of all strains of TSE. now understand, i
confirmed this case 7 months earlier to the TAHC, and then, only after i
contacted the Honorable Phyllis Fong and after an act of Congress, this animal
was finally confirmed ;
During the course of the investigation, USDA removed and tested a total of
67 animals of interest from the farm where the index animal's herd originated.
All of these animals tested negative for BSE. 200 adult animals of interest were
determined to have left the index farm. Of these 200, APHIS officials determined
that 143 had gone to slaughter, two were found alive (one was determined not to
be of interest because of its age and the other tested negative), 34 are
presumed dead, one is known dead and 20 have been classified as untraceable. In
addition to the adult animals, APHIS was looking for two calves born to the
index animal. Due to record keeping and identification issues, APHIS had to
trace 213 calves. Of these 213 calves, 208 entered feeding and slaughter
channels, four are presumed to have entered feeding and slaughter channels and
one calf was untraceable.
Comments on technical aspects of the risk assessment were then submitted to
FSIS.
Comments were received from Food and Water Watch, Food Animal Concerns
Trust (FACT), Farm Sanctuary, R-CALF USA, Linda A Detwiler, and Terry S.
Singeltary.
This document provides itemized replies to the public comments received on
the 2005 updated Harvard BSE risk assessment. Please bear the following points
in mind:
Owens, Julie
From: Terry S. Singeltary Sr. [flounder9@verizon.net]
Sent: Monday, July 24, 2006 1:09 PM
To: FSIS RegulationsComments
Subject: [Docket No. FSIS-2006-0011] FSIS Harvard Risk Assessment of
Bovine Spongiform Encephalopathy (BSE)
Page 1 of 98
*** FSIS, USDA, REPLY TO SINGELTARY ***
Wednesday, July 15, 2015
Additional BSE TSE prion testing detects pathologic lesion in unusual
brain location and PrPsc by PMCA only, how many cases have we missed?
SEE OUR GOVERNMENT COVER UP OF MAD COW DISEASE IN THE USA ;
Tuesday, August 4, 2015
*** FDA U.S. Measures to Protect Against BSE ***
Thursday, August 20, 2015
TEXAS TAHC DEER BREEDER CWD PERMIT RULES EMERGENCY ADOPTION PREAMBLE
TEXAS CAPTIVE Deer Industry, Pens, Breeding, Big Business, Invites Crooks
and CWD
lost my mom to hvCJD 12/14/97 confirmed, and just made a promise to mom,
never forget, and never let them forget...
Terry S. Singeltary Sr. P.O. Box 42 Bacliff, Texas USA 77518
flounder9@verizon.net
posted by Terry S. Singeltary Sr. at
11:38 AM
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