TEXAS CWD DEER BREEDERS PLEA TO GOVERNOR ABBOTT TO CIRCUMVENT TPWD SOUND SCIENCE TO LET DISEASE SPREAD
TEXAS CWD DEER BREEDERS PLEA TO GOVERNOR ABBOTT TO CIRCUMVENT TPWD SOUND
SCIENCE TO LET DISEASE SPREAD
Letter to
Governor Greg Abbott
Dan Patrick
Dan Friedkin Governor Abbott,
Your reputation as Governor of the State of Texas is being tarnished by the
ILLEGAL actions of the Texas Parks and Wildlife Department and its Executive
Director, Carter Smith.
Under the leadership of Mr. Smith, the TPWD is in clear violation of the
Texas Open Meetings Act; the very same act that you wrote in 2014 when you were
Texas Attorney General.
Beginning in July 2015, Carter Smith and his Agency have violated the Texas
Open Meetings Act on multiple occasions.
As a result of those CLOSED and ILLEGAL meetings, TPWD ordered new rules
that are discriminatory against a class of Texans. These illegal rules have also
resulted in the killing of thousands of perfectly healthy whitetail deer,
lowered rural Texas property values and a loss of jobs in rural Texas.
I respectfully request the following:
1. Immediately FIRE Carter Smith for his illegal and repeated violations of
the Texas Open Meetings Act.
2. Immediately revert to the Texas Deer Breeder rules that were in place
PRIOR to TPWD’s illegal closed-door meetings.
3. Immediately begin the process of Rules evaluation pertaining to Deer
Breeders in a legal and lawful manner following the Texas Open Meetings Act of
2014 (that you wrote).
To not do these things immediately will:
• Cause additional hardship on rural Texans
• Lower property values
• Result in the killing of more perfectly healthy Texas wildlife
• RESULT IN THE LOSS OF SUPPORT FOR YOU AS TEXAS GOVERNOR
With all due respect, please take immediate action and fire Carter Smith.
Sincerely,
Texas CWD Stakeholder Conference Dear Texas Deer Breeder,
In February of 2016 there were numerous deer, wildlife and government
associations called to Austin to craft a CWD testing solution for the impending
future of the deer industry. An official stakeholder group was formed. Every
Association sent their valid representatives to attend with the goal of forming
a consensus on a solution that would represent the entire State of Texas.
Everyone attending and representing these associations on the first day signed a
formal agreement to work on a solution, come to a consensus on a solution and
then support the solution upon completion of the conferences. The entire process
was to be monitored, recorded and managed by a neutral mediator.
On the beginning of day two of the first conference meeting, a CWD testing
plan was created by the TDA and presented by their President and Executive
Director. The entire stakeholder committee then proceeded with the proposed "TDA
Plan" and continued to use it as a foundation and add amendments to cover the
numerous operational variables that could be encountered by land owners, deer
breeders, deer hunting operations and state agencies.
Weeks later a complete consensus was reached on the concepts of the amended
TDA Plan and agreed upon by every association present. All these facts were
recorded during the conference and can be reviewed by anyone as it is a public
document of record by the mediator.
After weeks of negotiations and amending the original TDA Plan, the TDA
then said their Association could not support the proposal.
The TDA Plan that was proposed, amended and agreed to by the entire
stakeholder committee was printed, recorded in the Registry, and then presented
to committee members of Texas Parks and Wildlife.
At the May 6th stakeholder meeting TDA presented a new plan to all members
of the stakeholder committee and to all deer associations. That plan was agreed
upon and signed by TDA, DBC, EWA and NADeFA. We were hopeful that this totally
new plan could replace the plan that was already recorded in the registry and
presented to the committee of Texas Parks and Wildlife.
However, all the other stakeholders quickly replied along with state
agencies rejecting our new proposed plan and made aware to everyone that the
original TDA plan of record in the registry was the only solution that was to
going be considered by Texas Parks and Wildlife.
Problem was, there were a quite a number of items in the TDA Plan that had
been recognized and needed to be amended. Realizing our new proposal was dead
and the plan of record was the only one being considered, the DBC offered
amendments to the original TDA Plan to fill the obvious holes that had been
recognized. We proceeded to work quickly to resolve the mistakes that were
noticed in the previous plan and got significant additional agreements to reduce
the percentages of CWD testing and improving numerous aspects of the original
TDA Plan. These continued efforts were heavily criticized by many, but will be
very much appreciated by all in the near future.
Contrary to many reports, the DBC did not introduce their own plan. We
continued to amend and improve the original TDA Plan of record that is going to
be considered next week by Texas Parks and Wildlife. The new amended TDA Plan is
better.
This is not the end. We agree with everyone that CWD is a political disease
and will work tirelessly with the TDA, NADeFA and EWA to eliminate CWD testing
in the near future. We are not blind and deaf and realize many people were upset
with our efforts. However, everything was done with one motive and that was to
get the best CWD testing plan for everyone. The DBC will not and does not throw
stones and will continue to work with integrity. It is unfortunate about all the
misinformation that was presented to everyone about our efforts and the obvious
heartburn that was created, but promise that we will continue to work for a
stronger deer industry.
>>>This is not the end. We agree with everyone that CWD is a
political disease and will work tirelessly with the TDA, NADeFA and EWA to
eliminate CWD testing in the near future.<<<
frightening. absolutely frightening, that pretty much says it
all...imo.
if the breeders are left to regulate themselves by Governor Abbott, in
place of Texas Parks and Wildlife Department, because of sound testing for CWD,
then there is no hope. but I would not put it past Government Abbott or Dan
Partick. Texas covered up mad cow disease for seven months and almost got away
with it the second time (after getting away with it once before), and that is
well documented. so this will not surprise me cwd. the lack of timely updates by
TAHC about cwd is just more of the same when it comes to TSE Prion disease in
Texas. breeders keep crying over headless dead deer photos due to testing to
stop a deadly disease that is 100% fatal once clinical, yet they breed and raise
these cervid to be slaughtered in shooting pens to have the heads removed to be
mounted on a wall. LOL, your argument is BSe, imo.
These results suggest that cattle experimentally inoculated with CWD may
have some limited amount of prion infectivity outside of the brain and spinal
cord that may represent a previously unrecognized risk for transmission. This
information could have an impact on regulatory officials developing plans to
reduce or eliminate TSEs and farmers with concerns about ranging cattle on areas
where CWD may be present.
Scrapie transmits to white-tailed deer by the oral route and has a
molecular profile similar to chronic wasting disease
(Abstract Only) - (12-Aug-15)
Transmission of chronic wasting disease to sentinel reindeer (Rangifer
tarandus tarandus)
(Abstract Only) - (12-Aug-15) Transmission of scrapie prions to primate
after an extended silent incubation period - (Peer Reviewed Journal) Comoy,
E.E., Mikol, J., Luccantoni-Freire, S., Correia, E., Lescoutra-Etchegaray, N.,
Durand, V., Dehen, C., Andreoletti, O., Casalone, C., Richt, J.A., Greenlee,
J.J., Baron, T., Benestad, S., Brown, P., Deslys, J. 2015.
Transmission of scrapie prions to primate after an extended silent
incubation period. Scientific Reports.
5:11573. Transmission of the agent of sheep scrapie to deer results in
PrPSc with two distinct molecular profiles - (Abstract Only) Greenlee, J.,
Moore, S.J., Smith, J.., West Greenlee, M.H., Kunkle, R. 2015.
Scrapie transmits to white-tailed deer by the oral route and has a
molecular profile similar to chronic wasting disease and distinct from the
scrapie inoculum. Prion 2015. p. S62.
Monday, April 04, 2016
Limited amplification of chronic wasting disease prions in the peripheral
tissues of intracerebrally inoculated cattle
”The occurrence of CWD must be viewed against the contest of the locations
in which it occurred. It was an incidental and unwelcome complication of the
respective wildlife research programmes. Despite it’s subsequent recognition as
a new disease of cervids, therefore justifying direct investigation, no specific
research funding was forthcoming. The USDA veiwed it as a wildlife problem and
consequently not their province!” page 26.
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:
J Vet Diagn Invest 20:698–703 (2008)
Chronic wasting disease in a Wisconsin white-tailed deer farm
Delwyn P. Keane,1 Daniel J. Barr, Philip N. Bochsler, S. Mark Hall, Thomas
Gidlewski, Katherine I. O’Rourke, Terry R. Spraker, Michael D. Samuel
Abstract.
In September 2002, chronic wasting disease (CWD), a prion disorder of
captive and wild cervids, was diagnosed in a white-tailed deer (Odocoileus
virginianus) from a captive farm in Wisconsin. The facility was subsequently
quarantined, and in January 2006 the remaining 76 deer were depopulated. Sixty
animals (79%) were found to be positive by immunohistochemical staining for the
abnormal prion protein (PrPCWD) in at least one tissue; the prevalence of
positive staining was high even in young deer. Although none of the deer
displayed clinical signs suggestive of CWD at depopulation, 49 deer had
considerable accumulation of the abnormal prion in the medulla at the level of
the obex. Extraneural accumulation of the abnormal protein was observed in 59
deer, with accumulation in the retropharyngeal lymph node in 58 of 59 (98%), in
the tonsil in 56 of 59 (95%), and in the rectal mucosal lymphoid tissue in 48 of
58 (83%). The retina was positive in 4 deer, all with marked accumulation of
prion in the obex. One deer was considered positive for PrPCWD in the brain but
not in the extraneural tissue, a novel observation in white-tailed deer. The
infection rate in captive deer was 20- fold higher than in wild deer. Although
weakly related to infection rates in extraneural tissues, prion genotype was
strongly linked to progression of prion accumulation in the obex. Antemortem
testing by biopsy of recto– anal mucosal-associated lymphoid tissue (or other
peripheral lymphoid tissue) may be a useful adjunct to tonsil biopsy for
surveillance in captive herds at risk for CWD infection.
Key words: Cervids; chronic wasting disease; prion; transmissible
spongiform encephalopathy.
State pays farmer $298,000 for infected deer herd
Jan. 16, 2016 8:05 p.m.
The State of Wisconsin paid nearly $300,000 to the Eau Claire County farmer
whose deer herd was depopulated after it was found to be infected with chronic
wasting disease.
Rick Vojtik, owner of Fairchild Whitetails in Fairchild, received an
indemnity payment of $298,770 for 228 white-tailed deer killed on his farm,
according to officials with the Department of Agriculture, Trade and Consumer
Protection.
The money was taken from the agency's general program revenue funded by
Wisconsin taxpayers.
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)
Docket No. FDA-2003-D-0432 (formerly 03D-0186) Use of Material from Deer
and Elk in Animal Feed Singeltary Submission
31 Jan 2015 at 20:14 GMT
*** Ruminant feed ban for cervids in the United States? ***
Singeltary et al
31 Jan 2015 at 20:14 GMT
*** Singeltary reply ; Molecular, Biochemical and Genetic Characteristics
of BSE in Canada Singeltary reply ;
*** It also suggests a similar cause or source for atypical BSE in these
countries. ***
Discussion: The C, L and H type BSE cases in Canada exhibit molecular
characteristics similar to those described for classical and atypical BSE cases
from Europe and Japan.
*** This supports the theory that the importation of BSE contaminated
feedstuff is the source of C-type BSE in Canada.
*** It also suggests a similar cause or source for atypical BSE in these
countries. ***
see page 176 of 201 pages...tss
Docket No. APHIS-2007-0127 Scrapie in Sheep and Goats Terry Singeltary Sr.
Submission
Comment Period Closed Dec 9 2015, at 11:59 PM ET
Comment from Terry Singeltary Sr.
This is a Comment on the Animal and Plant Health Inspection Service (APHIS)
Notice: Agency Information Collection Activities; Proposals, Submissions, and
Approvals: Bovine Spongiform Encephalopathy; Importation of Animals and Animal
Products
Docket No. APHIS-2014-0107 Bovine Spongiform Encephalopathy; Importation of
Animals and Animal Products Singeltary Submission ;
AttachmentsView All (1)
Docket No. APHIS-2014-0107 Bovine Spongiform Encephalopathy; Importation of
Animals and Animal Products Singeltary Submission View Attachment:
2001 FDA CJD TSE Prion Singeltary Submission
Cervid to human prion transmission
Kong, Qingzhong
Case Western Reserve University, Cleveland, OH, United States
Abstract
Prion disease is transmissible and invariably fatal. Chronic wasting
disease (CWD) is the prion disease affecting deer, elk and moose, and it is a
widespread and expanding epidemic affecting 22 US States and 2 Canadian
provinces so far. CWD poses the most serious zoonotic prion transmission risks
in North America because of huge venison consumption (>6 million deer/elk
hunted and consumed annually in the USA alone), significant prion infectivity in
muscles and other tissues/fluids from CWD-affected cervids, and usually high
levels of individual exposure to CWD resulting from consumption of the affected
animal among often just family and friends. However, we still do not know
whether CWD prions can infect humans in the brain or peripheral tissues or
whether clinical/asymptomatic CWD zoonosis has already occurred, and we have no
essays to reliably detect CWD infection in humans. We hypothesize that:
(1) The classic CWD prion strain can infect humans at low levels in the
brain and peripheral lymphoid tissues;
(2) The cervid-to-human transmission barrier is dependent on the cervid
prion strain and influenced by the host (human) prion protein (PrP) primary
sequence;
(3) Reliable essays can be established to detect CWD infection in
humans;and
(4) CWD transmission to humans has already occurred. We will test these
hypotheses in 4 Aims using transgenic (Tg) mouse models and complementary in
vitro approaches.
Aim 1 will prove that the classical CWD strain may infect humans in brain
or peripheral lymphoid tissues at low levels by conducting systemic bioassays in
a set of "humanized" Tg mouse lines expressing common human PrP variants using a
number of CWD isolates at varying doses and routes. Experimental "human CWD"
samples will also be generated for Aim 3.
Aim 2 will test the hypothesis that the cervid-to-human prion transmission
barrier is dependent on prion strain and influenced by the host (human) PrP
sequence by examining and comparing the transmission efficiency and phenotypes
of several atypical/unusual CWD isolates/strains as well as a few prion strains
from other species that have adapted to cervid PrP sequence, utilizing the same
panel of humanized Tg mouse lines as in Aim 1.
Aim 3 will establish reliable essays for detection and surveillance of CWD
infection in humans by examining in details the clinical, pathological,
biochemical and in vitro seeding properties of existing and future experimental
"human CWD" samples generated from Aims 1-2 and compare them with those of
common sporadic human Creutzfeldt-Jakob disease (sCJD) prions.
Aim 4 will attempt to detect clinical CWD-affected human cases by examining
a significant number of brain samples from prion-affected human subjects in the
USA and Canada who have consumed venison from CWD-endemic areas utilizing the
criteria and essays established in Aim 3. The findings from this proposal will
greatly advance our understandings on the potential and characteristics of
cervid prion transmission in humans, establish reliable essays for CWD zoonosis
and potentially discover the first case(s) of CWD infection in humans.
Public Health Relevance There are significant and increasing human exposure
to cervid prions because chronic wasting disease (CWD, a widespread and highly
infectious prion disease among deer and elk in North America) continues
spreading and consumption of venison remains popular, but our understanding on
cervid-to-human prion transmission is still very limited, raising public health
concerns. This proposal aims to define the zoonotic risks of cervid prions and
set up and apply essays to detect CWD zoonosis using mouse models and in vitro
methods. The findings will greatly expand our knowledge on the potentials and
characteristics of cervid prion transmission in humans, establish reliable
essays for such infections and may discover the first case(s) of CWD infection
in humans.
Funding Agency Agency National Institute of Health (NIH)
Institute National Institute of Neurological Disorders and Stroke (NINDS)
Type Research Project (R01)
Project # 1R01NS088604-01A1
Application # 9037884
Study Section Cellular and Molecular Biology of Neurodegeneration Study
Section (CMND)
Program Officer Wong, May
Project Start 2015-09-30
Project End 2019-07-31
Budget Start 2015-09-30
Budget End 2016-07-31
Support Year 1
Fiscal Year 2015
Total Cost $337,507
Indirect Cost $118,756
Institution
Name Case Western Reserve University
Department Pathology
Type Schools of Medicine
DUNS # 077758407
City Cleveland
State OH
Country United States
Zip Code 44106
===========================================================
We hypothesize that:
(1) The classic CWD prion strain can infect humans at low levels in the
brain and peripheral lymphoid tissues;
(2) The cervid-to-human transmission barrier is dependent on the cervid
prion strain and influenced by the host (human) prion protein (PrP) primary
sequence;
(3) Reliable essays can be established to detect CWD infection in
humans;and
(4) *** CWD transmission to humans has already occurred. *** We will test
these hypotheses in 4 Aims using transgenic (Tg) mouse models and complementary
in vitro approaches.
============================================================
Key Molecular Mechanisms of TSEs
Zabel, Mark D.
Colorado State University-Fort Collins, Fort Collins, CO, United States
Abstract Prion diseases, or transmissible spongiform encephalopathies (TSEs),
are fatal neurodegenerative diseases affecting humans, cervids, bovids, and
ovids. The absolute requirement of PrPC expression to generate prion diseases
and the lack of instructional nucleic acid define prions as unique infectious
agents. Prions exhibit species-specific tropism, inferring that unique prion
strains exist that preferentially infct certain host species and confront
transmission barriers to heterologous host species. However, transmission
barriers are not absolute. Scientific consensus agrees that the sheep TSE
scrapie probably breached the transmission barrier to cattle causing bovine
spongiform encephalopathy that subsequently breached the human transmission
barrier and likely caused several hundred deaths by a new-variant form of the
human TSE Creutzfeldt-Jakob disease in the UK and Europe. The impact to human
health, emotion and economies can still be felt in areas like farming, blood and
organ donations and the threat of a latent TSE epidemic. This precedent raises
the real possibility of other TSEs, like chronic wasting disease of cervids,
overcoming similar human transmission barriers. A groundbreaking discovery made
last year revealed that mice infected with heterologous prion strains facing
significant transmission barriers replicated prions far more readily in spleens
than brains6. Furthermore, these splenic prions exhibited weakened transmission
barriers and expanded host ranges compared to neurogenic prions. These data
question conventional wisdom of avoiding neural tissue to avoid prion
xenotransmission, when more promiscuous prions may lurk in extraneural tissues.
Data derived from work previously funded by NIH demonstrate that Complement
receptors CD21/35 bind prions and high density PrPC and differentially impact
prion disease depending on the prion isolate or strain used. Recent advances in
live animal and whole organ imaging have led us to generate preliminary data to
support novel, innovative approaches to assessing prion capture and transport.
We plan to test our unifying hypothesis for this proposal that CD21/35 control
the processes of peripheral prion capture, transport, strain selection and
xenotransmission in the following specific aims. 1. Assess the role of CD21/35
in splenic prion strain selection and host range expansion. 2. Determine whether
CD21/35 and C1q differentially bind distinct prion strains 3. Monitor the
effects of CD21/35 on prion trafficking in real time and space 4. Assess the
role of CD21/35 in incunabular prion trafficking
Public Health Relevance Transmissible spongiform encephalopathies, or prion
diseases, are devastating illnesses that greatly impact public health,
agriculture and wildlife in North America and around the world. The impact to
human health, emotion and economies can still be felt in areas like farming,
blood and organ donations and the threat of a latent TSE epidemic. This
precedent raises the real possibility of other TSEs, like chronic wasting
disease (CWD) of cervids, overcoming similar human transmission barriers. Early
this year Canada reported its first case of BSE in over a decade audits first
case of CWD in farmed elk in three years, underscoring the need for continued
vigilance and research. Identifying mechanisms of transmission and zoonoses
remains an extremely important and intense area of research that will benefit
human and other animal populations.
Funding Agency Agency National Institute of Health (NIH)
Institute National Institute of Allergy and Infectious Diseases (NIAID)
Type High Priority, Short Term Project Award (R56)
Project # 1R56AI122273-01A1
Application # 9211114
Study Section Cellular and Molecular Biology of Neurodegeneration Study
Section (CMND)
Program Officer Beisel, Christopher E
Project Start 2016-02-16
Project End 2017-01-31
Budget Start 2016-02-16
Budget End 2017-01-31
Support Year 1
Fiscal Year 2016
Total Cost
Indirect Cost Institution Name Colorado State University-Fort Collins
Department Microbiology/Immun/Virology
Type Schools of Veterinary Medicine
DUNS # 785979618 City Fort Collins
State CO
Country United States
Zip Code 80523
PMCA Detection of CWD Infection in Cervid and Non-Cervid Species
Hoover, Edward Arthur
Colorado State University-Fort Collins, Fort Collins, CO, United States
Abstract Chronic wasting disease (CWD) of deer and elk is an emerging highly
transmissible prion disease now recognized in 18 States, 2 Canadian provinces,
and Korea. We have shown that Infected deer harbor and shed high levels of
infectious prions in saliva, blood, urine, and feces, and in the tissues
generating those body fluids and excreta, thereby leading to facile transmission
by direct contact and environmental contamination. We have also shown that CWD
can infect some non-cervid species, thus the potential risk CWD represents to
domestic animal species and to humans remains unknown. Whether prions borne in
blood, saliva, nasal fluids, milk, or excreta are generated or modified in the
proximate peripheral tissue sites, may differ in subtle ways from those
generated in brain, or may be adapted for mucosal infection remain open
questions. The increasing parallels in the pathogenesis between prion diseases
and human neurodegenerative conditions, such as Alzheimer's and Parkinson's
diseases, add relevance to CWD as a transmissible protein misfolding disease.
The overall goal of this work is to elucidate the process of CWD prion
transmission from mucosal secretory and excretory tissue sites by addressing
these questions: (a) What are the kinetics and magnitude of CWD prion shedding
post-exposure? (b) Are excreted prions biochemically distinct, or not, from
those in the CNS? (c) Are peripheral epithelial or CNS tissues, or both, the
source of excreted prions? and (d) Are excreted prions adapted for horizontal
transmission via natural/trans-mucosal routes? The specific aims of this
proposal are: (1) To determine the onset and consistency of CWD prion shedding
in deer and cervidized mice; (2); To compare the biochemical and biophysical
properties of excretory vs. CNS prions; (3) To determine the capacity of
peripheral tissues to support replication of CWD prions; (4) To determine the
protease- sensitive infectious fraction of excreted vs. CNS prions; and (5) To
compare the mucosal infectivity of excretory vs. CNS prions. Understanding the
mechanisms that enable efficient prion dissemination and shedding will help
elucidate how horizontally transmissible prions evolve and succeed, and is the
basis of this proposal. Understanding how infectious misfolded proteins (prions)
are generated, trafficked, shed, and transmitted will aid in preventing,
treating, and managing the risks associated with these agents and the diseases
they cause.
Public Health Relevance Chronic wasting disease (CWD) of deer and elk is an
emergent highly transmissible prion disease now recognized throughout the USA as
well as in Canada and Korea. We have shown that infected deer harbor and shed
high levels of infectious prions in saliva, blood, urine, and feces thereby
leading to transmission by direct contact and environmental contamination. In
that our studies have also shown that CWD can infect some non-cervid species,
the potential risk CWD may represents to domestic animal species and humans
remains unknown. The increasing parallels in the development of major human
neurodegenerative conditions, such as Alzheimer's and Parkinson's diseases, and
prion diseases add relevance to CWD as a model of a transmissible protein
misfolding disease. Understanding how infectious misfolded proteins (prions) are
generated and transmitted will aid in interrupting, treating, and managing the
risks associated with these agents and the diseases they cause.
Funding Agency Agency National Institute of Health (NIH)
Institute National Institute of Neurological Disorders and Stroke (NINDS)
Type Research Project (R01)
Project # 4R01NS061902-07
Application # 9010980
Study Section Cellular and Molecular Biology of Neurodegeneration Study
Section (CMND)
Program Officer Wong, May Project Start 2009-09-30
Project End 2018-02-28
Budget Start 2016-03-01
Budget End 2017-02-28
Support Year 7
Fiscal Year 2016
Total Cost $409,868
Indirect Cost $134,234 Institution Name Colorado State University-Fort
Collins
Department Microbiology/Immun/Virology
Type Schools of Veterinary Medicine
DUNS # 785979618 City Fort Collins
State CO
Country United States
Zip Code 80523
Zoonotic Potential of CWD Prions: An Update
Ignazio Cali1, Liuting Qing1, Jue Yuan1, Shenghai Huang2, Diane Kofskey1,3,
Nicholas Maurer1, Debbie McKenzie4, Jiri Safar1,3,5, Wenquan Zou1,3,5,6,
Pierluigi Gambetti1, Qingzhong Kong1,5,6
1Department of Pathology, 3National Prion Disease Pathology Surveillance
Center, 5Department of Neurology, 6National Center for Regenerative Medicine,
Case Western Reserve University, Cleveland, OH 44106, USA.
4Department of Biological Sciences and Center for Prions and Protein
Folding Diseases, University of Alberta, Edmonton, Alberta, Canada,
2Encore Health Resources, 1331 Lamar St, Houston, TX 77010
Chronic wasting disease (CWD) is a widespread and highly transmissible
prion disease in free-ranging and captive cervid species in North America. The
zoonotic potential of CWD prions is a serious public health concern, but the
susceptibility of human CNS and peripheral organs to CWD prions remains largely
unresolved. We reported earlier that peripheral and CNS infections were detected
in transgenic mice expressing human PrP129M or PrP129V. Here we will present an
update on this project, including evidence for strain dependence and influence
of cervid PrP polymorphisms on CWD zoonosis as well as the characteristics of
experimental human CWD prions.
PRION 2016 TOKYO
In Conjunction with Asia Pacific Prion Symposium 2016
PRION 2016 Tokyo
Prion 2016
Prion 2016
Purchase options Price * Issue Purchase USD 198.00
Prion. 10:S15-S21. 2016 ISSN: 1933-6896 printl 1933-690X online
Taylor & Francis
Prion 2016 Animal Prion Disease Workshop Abstracts
WS-01: Prion diseases in animals and zoonotic potential
Juan Maria Torres a, Olivier Andreoletti b, J uan-Carlos Espinosa a.
Vincent Beringue c. Patricia Aguilar a,
Natalia Fernandez-Borges a. and Alba Marin-Moreno a
"Centro de Investigacion en Sanidad Animal ( CISA-INIA ). Valdeolmos,
Madrid. Spain; b UMR INRA -ENVT 1225 Interactions Holes Agents Pathogenes. ENVT.
Toulouse. France: "UR892. Virologie lmmunologie MolécuIaires, Jouy-en-Josas.
France
Dietary exposure to bovine spongiform encephalopathy (BSE) contaminated
bovine tissues is considered as the origin of variant Creutzfeldt Jakob (vCJD)
disease in human. To date, BSE agent is the only recognized zoonotic prion.
Despite the variety of Transmissible Spongiform Encephalopathy (TSE) agents that
have been circulating for centuries in farmed ruminants there is no apparent
epidemiological link between exposure to ruminant products and the occurrence of
other form of TSE in human like sporadic Creutzfeldt Jakob Disease (sCJD).
However, the zoonotic potential of the diversity of circulating TSE agents has
never been systematically assessed. The major issue in experimental assessment
of TSEs zoonotic potential lies in the modeling of the ‘species barrier‘, the
biological phenomenon that limits TSE agents’ propagation from a species to
another. In the last decade, mice genetically engineered to express normal forms
of the human prion protein has proved essential in studying human prions
pathogenesis and modeling the capacity of TSEs to cross the human species
barrier.
To assess the zoonotic potential of prions circulating in farmed ruminants,
we study their transmission ability in transgenic mice expressing human PrPC
(HuPrP-Tg). Two lines of mice expressing different forms of the human PrPC
(129Met or 129Val) are used to determine the role of the Met129Val dimorphism in
susceptibility/resistance to the different agents.
These transmission experiments confirm the ability of BSE prions to
propagate in 129M- HuPrP-Tg mice and demonstrate that Met129 homozygotes may be
susceptible to BSE in sheep or goat to a greater degree than the BSE agent in
cattle and that these agents can convey molecular properties and
neuropathological indistinguishable from vCJD. However homozygous 129V mice are
resistant to all tested BSE derived prions independently of the originating
species suggesting a higher transmission barrier for 129V-PrP variant.
Transmission data also revealed that several scrapie prions propagate in
HuPrP-Tg mice with efficiency comparable to that of cattle BSE. While the
efficiency of transmission at primary passage was low, subsequent passages
resulted in a highly virulent prion disease in both Met129 and Val129 mice.
Transmission of the different scrapie isolates in these mice leads to the
emergence of prion strain phenotypes that showed similar characteristics to
those displayed by MM1 or VV2 sCJD prion. These results demonstrate that scrapie
prions have a zoonotic potential and raise new questions about the possible link
between animal and human prions.
Saturday, April 23, 2016
SCRAPIE WS-01: Prion diseases in animals and zoonotic potential 2016
Prion. 10:S15-S21. 2016 ISSN: 1933-6896 printl 1933-690X online
LOOKING FOR CWD IN HUMANS AS nvCJD or as an ATYPICAL CJD, LOOKING IN ALL
THE WRONG PLACES $$$
*** These results would seem to suggest that CWD does indeed have zoonotic
potential, at least as judged by the compatibility of CWD prions and their human
PrPC target. Furthermore, extrapolation from this simple in vitro assay suggests
that if zoonotic CWD occurred, it would most likely effect those of the PRNP
codon 129-MM genotype and that the PrPres type would be similar to that found in
the most common subtype of sCJD (MM1).***
PRION 2015 CONFERENCE FT. COLLINS CWD RISK FACTORS TO HUMANS
*** LATE-BREAKING ABSTRACTS PRION 2015 CONFERENCE ***
O18
Zoonotic Potential of CWD Prions
Liuting Qing1, Ignazio Cali1,2, Jue Yuan1, Shenghai Huang3, Diane Kofskey1,
Pierluigi Gambetti1, Wenquan Zou1, Qingzhong Kong1 1Case Western Reserve
University, Cleveland, Ohio, USA, 2Second University of Naples, Naples, Italy,
3Encore Health Resources, Houston, Texas, USA
*** These results indicate that the CWD prion has the potential to infect
human CNS and peripheral lymphoid tissues and that there might be asymptomatic
human carriers of CWD infection.
==================
***These results indicate that the CWD prion has the potential to infect
human CNS and peripheral lymphoid tissues and that there might be asymptomatic
human carriers of CWD infection.***
==================
P.105: RT-QuIC models trans-species prion transmission
Kristen Davenport, Davin Henderson, Candace Mathiason, and Edward Hoover
Prion Research Center; Colorado State University; Fort Collins, CO USA
Conversely, FSE maintained sufficient BSE characteristics to more
efficiently convert bovine rPrP than feline rPrP. Additionally, human rPrP was
competent for conversion by CWD and fCWD.
***This insinuates that, at the level of protein:protein interactions, the
barrier preventing transmission of CWD to humans is less robust than previously
estimated.
================
***This insinuates that, at the level of protein:protein interactions, the
barrier preventing transmission of CWD to humans is less robust than previously
estimated.***
================
*** PRICE OF CWD TSE PRION POKER GOES UP 2014 ***
Transmissible Spongiform Encephalopathy TSE PRION update January 2, 2014
*** chronic wasting disease, there was no absolute barrier to conversion of
the human prion protein.
*** Furthermore, the form of human PrPres produced in this in vitro assay
when seeded with CWD, resembles that found in the most common human prion
disease, namely sCJD of the MM1 subtype.
*** These results would seem to suggest that CWD does indeed have zoonotic
potential, at least as judged by the compatibility of CWD prions and their human
PrPC target. Furthermore, extrapolation from this simple in vitro assay suggests
that if zoonotic CWD occurred, it would most likely effect those of the PRNP
codon 129-MM genotype and that the PrPres type would be similar to that found in
the most common subtype of sCJD (MM1).***
*** The potential impact of prion diseases on human health was greatly
magnified by the recognition that interspecies transfer of BSE to humans by beef
ingestion resulted in vCJD. While changes in animal feed constituents and
slaughter practices appear to have curtailed vCJD, there is concern that CWD of
free-ranging deer and elk in the U.S. might also cross the species barrier.
Thus, consuming venison could be a source of human prion disease. Whether BSE
and CWD represent interspecies scrapie transfer or are newly arisen prion
diseases is unknown. Therefore, the possibility of transmission of prion disease
through other food animals cannot be ruled out. There is evidence that vCJD can
be transmitted through blood transfusion. There is likely a pool of unknown size
of asymptomatic individuals infected with vCJD, and there may be asymptomatic
individuals infected with the CWD equivalent. These circumstances represent a
potential threat to blood, blood products, and plasma supplies.
Chronic Wasting Disease and Potential Transmission to Humans
Ermias D. Belay,* Ryan A. Maddox,* Elizabeth S. Williams,† Michael W.
Miller,‡ Pierluigi Gambetti,§ and Lawrence B. Schonberger*
Chronic wasting disease (CWD) of deer and elk is endemic in a tri-corner
area of Colorado, Wyoming, and Nebraska, and new foci of CWD have been detected
in other parts of the United States. Although detection in some areas may be
related to increased surveillance, introduction of CWD due to translocation or
natural migration of animals may account for some new foci of infection.
Increasing spread of CWD has raised concerns about the potential for increasing
human exposure to the CWD agent. The foodborne transmission of bovine spongiform
encephalopathy to humans indicates that the species barrier may not completely
protect humans from animal prion diseases. Conversion of human prion protein by
CWDassociated prions has been demonstrated in an in vitro cellfree experiment,
but limited investigations have not identified strong evidence for CWD
transmission to humans. More epidemiologic and laboratory studies are needed to
monitor the possibility of such transmissions.
Conclusions
The lack of evidence of a link between CWD transmission and unusual cases
of CJD, despite several epidemiologic investigations, and the absence of an
increase in CJD incidence in Colorado and Wyoming suggest that the risk, if any,
of transmission of CWD to humans is low. Although the in vitro studies
indicating inefficient conversion of human prion protein by CWD-associated
prions raise the possibility of low-level transmission of CWD to humans, no
human cases of prion disease with strong evidence of a link with CWD have been
identified. However, the transmission of BSE to humans and the resulting vCJD
indicate that, provided sufficient exposure, the species barrier may not
completely protect humans from animal prion diseases. Because CWD has occurred
in a limited geographic area for decades, an adequate number of people may not
have been exposed to the CWD agent to result in a clinically recognizable human
disease. The level and frequency of human exposure to the CWD agent may increase
with the spread of CWD in the United States. Because the number of studies
seeking evidence for CWD transmission to humans is limited, more epidemiologic
and laboratory studies should be conducted to monitor the possibility of such
transmissions. Studies involving transgenic mice expressing human and cervid
prion protein are in progress to further assess the potential for the CWD agent
to cause human disease. Epidemiologic studies have also been initiated to
identify human cases of prion disease among persons with an increased risk for
exposure to potentially CWD-infected deer or elk meat (47). If such cases are
identified, laboratory data showing similarities of the etiologic agent to that
of the CWD agent would strengthen the conclusion for a causal link. Surveillance
for human prion diseases, particularly in areas where CWD has been detected,
remains important to effectively monitor the possible transmission of CWD to
humans. Because of the long incubation period associated with prion diseases,
convincing negative results from epidemiologic and experimental laboratory
studies would likely require years of follow-up. In the meantime, to minimize
the risk for exposure to the CWD agent, hunters should consult with their state
wildlife agencies to identify areas where CWD occurs and continue to follow
advice provided by public health and wildlife agencies. Hunters should avoid
eating meat from deer and elk that look sick or test positive for CWD. They
should wear gloves when field-dressing carcasses, boneout the meat from the
animal, and minimize handling of brain and spinal cord tissues. As a precaution,
hunters should avoid eating deer and elk tissues known to harbor the CWD agent
(e.g., brain, spinal cord, eyes, spleen, tonsils, lymph nodes) from areas where
CWD has been identified.
now, let’s see what the authors said about this casual link, personal
communications years ago. see where it is stated NO STRONG evidence. so, does
this mean there IS casual evidence ???? “Our conclusion stating that we found no
strong evidence of CWD transmission to humans”
From: TSS (216-119-163-189.ipset45.wt.net)
Subject: CWD aka MAD DEER/ELK TO HUMANS ???
Date: September 30, 2002 at 7:06 am PST
From: "Belay, Ermias"
To: Cc: "Race, Richard (NIH)" ; ; "Belay, Ermias"
Sent: Monday, September 30, 2002 9:22 AM
Subject: RE: TO CDC AND NIH - PUB MED- 3 MORE DEATHS - CWD - YOUNG HUNTERS
Dear Sir/Madam,
In the Archives of Neurology you quoted (the abstract of which was attached
to your email), we did not say CWD in humans will present like variant CJD. That
assumption would be wrong. I encourage you to read the whole article and call me
if you have questions or need more clarification (phone: 404-639-3091). Also, we
do not claim that "no-one has ever been infected with prion disease from eating
venison." Our conclusion stating that we found no strong evidence of CWD
transmission to humans in the article you quoted or in any other forum is
limited to the patients we investigated.
Ermias Belay, M.D. Centers for Disease Control and Prevention
-----Original Message-----
From: Sent: Sunday, September 29, 2002 10:15 AM
To: rr26k@nih.gov; rrace@niaid.nih.gov; ebb8@CDC.GOV
Subject: TO CDC AND NIH - PUB MED- 3 MORE DEATHS - CWD - YOUNG HUNTERS
Sunday, November 10, 2002 6:26 PM ......snip........end..............TSS
Thursday, April 03, 2008
A prion disease of cervids: Chronic wasting disease 2008 1: Vet Res. 2008
Apr 3;39(4):41 A prion disease of cervids: Chronic wasting disease Sigurdson CJ.
snip...
*** twenty-seven CJD patients who regularly consumed venison were reported
to the Surveillance Center***,
snip... full text ;
CJD is so rare in people under age 30, one case in a billion (leaving out
medical mishaps), that four cases under 30 is "very high," says Colorado
neurologist Bosque. "Then, if you add these other two from Wisconsin [cases in
the newspaper], six cases of CJD in people associated with venison is very, very
high." Only now, with Mary Riley, there are at least seven, and possibly eight,
with Steve, her dining companion. "It's not critical mass that matters,"
however, Belay says. "One case would do it for me." The chance that two people
who know each other would both contact CJD, like the two Wisconsin sportsmen, is
so unlikely, experts say, it would happen only once in 140 years.
Given the incubation period for TSEs in humans, it may require another
generation to write the final chapter on CWD in Wisconsin. "Does chronic wasting
disease pass into humans? We'll be able to answer that in 2022," says Race.
Meanwhile, the state has become part of an immense experiment.
I urge everyone to watch this video closely...terry
*** you can see video here and interview with Jeff's Mom, and scientist
telling you to test everything and potential risk factors for humans ***
Envt.07:
Pathological Prion Protein (PrPTSE) in Skeletal Muscles of Farmed and Free
Ranging White-Tailed Deer Infected with Chronic Wasting Disease
***The presence and seeding activity of PrPTSE in skeletal muscle from
CWD-infected cervids suggests prevention of such tissue in the human diet as a
precautionary measure for food safety, pending on further clarification of
whether CWD may be transmissible to humans.
Prions in Skeletal Muscles of Deer with Chronic Wasting Disease Rachel C.
Angers1,*, Shawn R. Browning1,*,†, Tanya S. Seward2, Christina J. Sigurdson4,‡,
Michael W. Miller5, Edward A. Hoover4, Glenn C. Telling1,2,3,§ snip...
Abstract The emergence of chronic wasting disease (CWD) in deer and elk in
an increasingly wide geographic area, as well as the interspecies transmission
of bovine spongiform encephalopathy to humans in the form of variant Creutzfeldt
Jakob disease, have raised concerns about the zoonotic potential of CWD. Because
meat consumption is the most likely means of exposure, it is important to
determine whether skeletal muscle of diseased cervids contains prion
infectivity. Here bioassays in transgenic mice expressing cervid prion protein
revealed the presence of infectious prions in skeletal muscles of CWD-infected
deer, demonstrating that humans consuming or handling meat from CWD-infected
deer are at risk to prion exposure.
***********CJD REPORT 1994 increased risk for consumption of veal and
venison and lamb***********
CREUTZFELDT JAKOB DISEASE SURVEILLANCE IN THE UNITED KINGDOM THIRD ANNUAL
REPORT AUGUST 1994
Consumption of venison and veal was much less widespread among both cases
and controls. For both of these meats there was evidence of a trend with
increasing frequency of consumption being associated with increasing risk of
CJD. (not nvCJD, but sporadic CJD...tss)
These associations were largely unchanged when attention was restricted to
pairs with data obtained from relatives. ...
Table 9 presents the results of an analysis of these data.
There is STRONG evidence of an association between ‘’regular’’ veal eating
and risk of CJD (p = .0.01).
Individuals reported to eat veal on average at least once a year appear to
be at 13 TIMES THE RISK of individuals who have never eaten veal.
There is, however, a very wide confidence interval around this estimate.
There is no strong evidence that eating veal less than once per year is
associated with increased risk of CJD (p = 0.51).
The association between venison eating and risk of CJD shows similar
pattern, with regular venison eating associated with a 9 FOLD INCREASE IN RISK
OF CJD (p = 0.04).
There is some evidence that risk of CJD INCREASES WITH INCREASING FREQUENCY
OF LAMB EATING (p = 0.02).
The evidence for such an association between beef eating and CJD is weaker
(p = 0.14). When only controls for whom a relative was interviewed are included,
this evidence becomes a little STRONGER (p = 0.08).
snip...
It was found that when veal was included in the model with another
exposure, the association between veal and CJD remained statistically
significant (p = < 0.05 for all exposures), while the other exposures
ceased to be statistically significant (p = > 0.05).
snip...
In conclusion, an analysis of dietary histories revealed statistical
associations between various meats/animal products and INCREASED RISK OF CJD.
When some account was taken of possible confounding, the association between
VEAL EATING AND RISK OF CJD EMERGED AS THE STRONGEST OF THESE ASSOCIATIONS
STATISTICALLY. ...
snip...
In the study in the USA, a range of foodstuffs were associated with an
increased risk of CJD, including liver consumption which was associated with an
apparent SIX-FOLD INCREASE IN THE RISK OF CJD. By comparing the data from 3
studies in relation to this particular dietary factor, the risk of liver
consumption became non-significant with an odds ratio of 1.2 (PERSONAL
COMMUNICATION, PROFESSOR A. HOFMAN. ERASMUS UNIVERSITY, ROTTERDAM). (???...TSS)
snip...see full report ;
CJD9/10022
October 1994
Mr R.N. Elmhirst Chairman British Deer Farmers Association Holly Lodge
Spencers Lane BerksWell Coventry CV7 7BZ
Dear Mr Elmhirst,
CREUTZFELDT-JAKOB DISEASE (CJD) SURVEILLANCE UNIT REPORT
Thank you for your recent letter concerning the publication of the third
annual report from the CJD Surveillance Unit. I am sorry that you are
dissatisfied with the way in which this report was published.
The Surveillance Unit is a completely independant outside body and the
Department of Health is committed to publishing their reports as soon as they
become available. In the circumstances it is not the practice to circulate the
report for comment since the findings of the report would not be amended. In
future we can ensure that the British Deer Farmers Association receives a copy
of the report in advance of publication.
The Chief Medical Officer has undertaken to keep the public fully informed
of the results of any research in respect of CJD. This report was entirely the
work of the unit and was produced completely independantly of the the
Department.
The statistical results reqarding the consumption of venison was put into
perspective in the body of the report and was not mentioned at all in the press
release. Media attention regarding this report was low key but gave a realistic
presentation of the statistical findings of the Unit. This approach to
publication was successful in that consumption of venison was highlighted only
once by the media ie. in the News at one television proqramme.
I believe that a further statement about the report, or indeed statistical
links between CJD and consumption of venison, would increase, and quite possibly
give damaging credence, to the whole issue. From the low key media reports of
which I am aware it seems unlikely that venison consumption will suffer
adversely, if at all.
http://web.archive.org/web/20030511010117/http://www.bseinquiry.gov.uk/files/yb/1994/10/00003001.pdf
*** These results would seem to suggest that CWD does indeed have zoonotic
potential, at least as judged by the compatibility of CWD prions and their human
PrPC target. Furthermore, extrapolation from this simple in vitro assay suggests
that if zoonotic CWD occurred, it would most likely effect those of the PRNP
codon 129-MM genotype and that the PrPres type would be similar to that found in
the most common subtype of sCJD (MM1).***
O.05: Transmission of prions to primates after extended silent incubation
periods: Implications for BSE and scrapie risk assessment in human populations
Emmanuel Comoy, Jacqueline Mikol, Valerie Durand, Sophie Luccantoni,
Evelyne Correia, Nathalie Lescoutra, Capucine Dehen, and Jean-Philippe Deslys
Atomic Energy Commission; Fontenay-aux-Roses, France
Prion diseases (PD) are the unique neurodegenerative proteinopathies
reputed to be transmissible under field conditions since decades. The
transmission of Bovine Spongiform Encephalopathy (BSE) to humans evidenced that
an animal PD might be zoonotic under appropriate conditions. Contrarily, in the
absence of obvious (epidemiological or experimental) elements supporting a
transmission or genetic predispositions, PD, like the other proteinopathies, are
reputed to occur spontaneously (atpical animal prion strains, sporadic CJD
summing 80% of human prion cases). Non-human primate models provided the first
evidences supporting the transmissibiity of human prion strains and the zoonotic
potential of BSE. Among them, cynomolgus macaques brought major information for
BSE risk assessment for human health (Chen, 2014), according to their
phylogenetic proximity to humans and extended lifetime. We used this model to
assess the zoonotic potential of other animal PD from bovine, ovine and cervid
origins even after very long silent incubation periods.
*** We recently observed the direct transmission of a natural classical
scrapie isolate to macaque after a 10-year silent incubation period,
***with features similar to some reported for human cases of sporadic CJD,
albeit requiring fourfold long incubation than BSE. Scrapie, as recently evoked
in humanized mice (Cassard, 2014),
***is the third potentially zoonotic PD (with BSE and L-type BSE),
***thus questioning the origin of human sporadic cases. We will present an
updated panorama of our different transmission studies and discuss the
implications of such extended incubation periods on risk assessment of animal PD
for human health.
===============
***thus questioning the origin of human sporadic cases***
===============
***our findings suggest that possible transmission risk of H-type BSE to
sheep and human. Bioassay will be required to determine whether the PMCA
products are infectious to these animals.
==============
Research Project: TRANSMISSION, DIFFERENTIATION, AND PATHOBIOLOGY OF
TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES
Title: Transmission of scrapie prions to primate after an extended silent
incubation period
Authors
item Comoy, Emmanuel - item Mikol, Jacqueline - item Luccantoni-Freire,
Sophie - item Correia, Evelyne - item Lescoutra-Etchegaray, Nathalie - item
Durand, Valérie - item Dehen, Capucine - item Andreoletti, Olivier - item
Casalone, Cristina - item Richt, Juergen item Greenlee, Justin item Baron,
Thierry - item Benestad, Sylvie - item Hills, Bob - item Brown, Paul - item
Deslys, Jean-Philippe -
Submitted to: Scientific Reports Publication Type: Peer Reviewed Journal
Publication Acceptance Date: May 28, 2015 Publication Date: June 30, 2015
Citation: Comoy, E.E., Mikol, J., Luccantoni-Freire, S., Correia, E.,
Lescoutra-Etchegaray, N., Durand, V., Dehen, C., Andreoletti, O., Casalone, C.,
Richt, J.A., Greenlee, J.J., Baron, T., Benestad, S., Brown, P., Deslys, J.
2015. Transmission of scrapie prions to primate after an extended silent
incubation period. Scientific Reports. 5:11573.
Interpretive Summary: The transmissible spongiform encephalopathies (also
called prion diseases) are fatal neurodegenerative diseases that affect animals
and humans. The agent of prion diseases is a misfolded form of the prion protein
that is resistant to breakdown by the host cells. Since all mammals express
prion protein on the surface of various cells such as neurons, all mammals are,
in theory, capable of replicating prion diseases. One example of a prion
disease, bovine spongiform encephalopathy (BSE; also called mad cow disease),
has been shown to infect cattle, sheep, exotic undulates, cats, non-human
primates, and humans when the new host is exposed to feeds or foods contaminated
with the disease agent. The purpose of this study was to test whether non-human
primates (cynomologous macaque) are susceptible to the agent of sheep scrapie.
After an incubation period of approximately 10 years a macaque developed
progressive clinical signs suggestive of neurologic disease. Upon postmortem
examination and microscopic examination of tissues, there was a widespread
distribution of lesions consistent with a transmissible spongiform
encephalopathy. This information will have a scientific impact since it is the
first study that demonstrates the transmission of scrapie to a non-human primate
with a close genetic relationship to humans. This information is especially
useful to regulatory officials and those involved with risk assessment of the
potential transmission of animal prion diseases to humans. Technical Abstract:
Classical bovine spongiform encephalopathy (c-BSE) is an animal prion disease
that also causes variant Creutzfeldt-Jakob disease in humans. Over the past
decades, c-BSE's zoonotic potential has been the driving force in establishing
extensive protective measures for animal and human health.
*** In complement to the recent demonstration that humanized mice are
susceptible to scrapie, we report here the first observation of direct
transmission of a natural classical scrapie isolate to a macaque after a 10-year
incubation period. Neuropathologic examination revealed all of the features of a
prion disease: spongiform change, neuronal loss, and accumulation of PrPres
throughout the CNS.
*** This observation strengthens the questioning of the harmlessness of
scrapie to humans, at a time when protective measures for human and animal
health are being dismantled and reduced as c-BSE is considered controlled and
being eradicated.
*** Our results underscore the importance of precautionary and protective
measures and the necessity for long-term experimental transmission studies to
assess the zoonotic potential of other animal prion strains.
why do we not want to do TSE transmission studies on chimpanzees $
5. A positive result from a chimpanzee challenged severly would likely
create alarm in some circles even if the result could not be interpreted for
man. I have a view that all these agents could be transmitted provided a large
enough dose by appropriate routes was given and the animals kept long enough.
Until the mechanisms of the species barrier are more clearly understood it might
be best to retain that hypothesis.
snip...
R. BRADLEY
”The occurrence of CWD must be viewed against the contest of the locations
in which it occurred. It was an incidental and unwelcome complication of the
respective wildlife research programmes. Despite it’s subsequent recognition as
a new disease of cervids, therefore justifying direct investigation, no specific
research funding was forthcoming. The USDA veiwed it as a wildlife problem and
consequently not their province!” page 26.
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. ...
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...
LOOKING FOR CWD IN HUMANS AS nvCJD or as an ATYPICAL CJD, LOOKING IN ALL
THE WRONG PLACES $$$
*** These results would seem to suggest that CWD does indeed have zoonotic
potential, at least as judged by the compatibility of CWD prions and their human
PrPC target. Furthermore, extrapolation from this simple in vitro assay suggests
that if zoonotic CWD occurred, it would most likely effect those of the PRNP
codon 129-MM genotype and that the PrPres type would be similar to that found in
the most common subtype of sCJD (MM1).***
Saturday, May 30, 2015
PRION 2015 ORAL AND POSTER CONGRESSIONAL ABSTRACTS
Wednesday, June 10, 2015
Zoonotic Potential of CWD Prions LATE-BREAKING ABSTRACTS
PL1
Using in vitro prion replication for high sensitive detection of prions and
prionlike proteins and for understanding mechanisms of transmission.
Claudio Soto
Mitchell Center for Alzheimer's diseases and related Brain disorders,
Department of Neurology, University of Texas Medical School at Houston.
Prion and prion-like proteins are misfolded protein aggregates with the
ability to selfpropagate to spread disease between cells, organs and in some
cases across individuals. I n T r a n s m i s s i b l e s p o n g i f o r m
encephalopathies (TSEs), prions are mostly composed by a misfolded form of the
prion protein (PrPSc), which propagates by transmitting its misfolding to the
normal prion protein (PrPC). The availability of a procedure to replicate prions
in the laboratory may be important to study the mechanism of prion and
prion-like spreading and to develop high sensitive detection of small quantities
of misfolded proteins in biological fluids, tissues and environmental samples.
Protein Misfolding Cyclic Amplification (PMCA) is a simple, fast and efficient
methodology to mimic prion replication in the test tube. PMCA is a platform
technology that may enable amplification of any prion-like misfolded protein
aggregating through a seeding/nucleation process. In TSEs, PMCA is able to
detect the equivalent of one single molecule of infectious PrPSc and propagate
prions that maintain high infectivity, strain properties and species
specificity. Using PMCA we have been able to detect PrPSc in blood and urine of
experimentally infected animals and humans affected by vCJD with high
sensitivity and specificity. Recently, we have expanded the principles of PMCA
to amplify amyloid-beta (Aβ) and alphasynuclein (α-syn) aggregates implicated in
Alzheimer's and Parkinson's diseases, respectively. Experiments are ongoing to
study the utility of this technology to detect Aβ and α-syn aggregates in
samples of CSF and blood from patients affected by these diseases.
=========================
***Recently, we have been using PMCA to study the role of environmental
prion contamination on the horizontal spreading of TSEs. These experiments have
focused on the study of the interaction of prions with plants and
environmentally relevant surfaces. Our results show that plants (both leaves and
roots) bind tightly to prions present in brain extracts and excreta (urine and
feces) and retain even small quantities of PrPSc for long periods of time.
Strikingly, ingestion of prioncontaminated leaves and roots produced disease
with a 100% attack rate and an incubation period not substantially longer than
feeding animals directly with scrapie brain homogenate. Furthermore, plants can
uptake prions from contaminated soil and transport them to different parts of
the plant tissue (stem and leaves). Similarly, prions bind tightly to a variety
of environmentally relevant surfaces, including stones, wood, metals, plastic,
glass, cement, etc. Prion contaminated surfaces efficiently transmit prion
disease when these materials were directly injected into the brain of animals
and strikingly when the contaminated surfaces were just placed in the animal
cage. These findings demonstrate that environmental materials can efficiently
bind infectious prions and act as carriers of infectivity, suggesting that they
may play an important role in the horizontal transmission of the disease.
========================
Since its invention 13 years ago, PMCA has helped to answer fundamental
questions of prion propagation and has broad applications in research areas
including the food industry, blood bank safety and human and veterinary disease
diagnosis.
see ;
Wednesday, December 16, 2015
Objects in contact with classical scrapie sheep act as a reservoir for
scrapie transmission
Objects in contact with classical scrapie sheep act as a reservoir for
scrapie transmission
Timm Konold1*, Stephen A. C. Hawkins2, Lisa C. Thurston3, Ben C. Maddison4,
Kevin C. Gough5, Anthony Duarte1 and Hugh A. Simmons1
1 Animal Sciences Unit, Animal and Plant Health Agency Weybridge,
Addlestone, UK, 2 Pathology Department, Animal and Plant Health Agency
Weybridge, Addlestone, UK, 3 Surveillance and Laboratory Services, Animal and
Plant Health Agency Penrith, Penrith, UK, 4 ADAS UK, School of Veterinary
Medicine and Science, University of Nottingham, Sutton Bonington, UK, 5 School
of Veterinary Medicine and Science, University of Nottingham, Sutton Bonington,
UK
Classical scrapie is an environmentally transmissible prion disease of
sheep and goats. Prions can persist and remain potentially infectious in the
environment for many years and thus pose a risk of infecting animals after
re-stocking. In vitro studies using serial protein misfolding cyclic
amplification (sPMCA) have suggested that objects on a scrapie affected sheep
farm could contribute to disease transmission. This in vivo study aimed to
determine the role of field furniture (water troughs, feeding troughs, fencing,
and other objects that sheep may rub against) used by a scrapie-infected sheep
flock as a vector for disease transmission to scrapie-free lambs with the prion
protein genotype VRQ/VRQ, which is associated with high susceptibility to
classical scrapie. When the field furniture was placed in clean accommodation,
sheep became infected when exposed to either a water trough (four out of five)
or to objects used for rubbing (four out of seven). This field furniture had
been used by the scrapie-infected flock 8 weeks earlier and had previously been
shown to harbor scrapie prions by sPMCA. Sheep also became infected (20 out of
23) through exposure to contaminated field furniture placed within pasture not
used by scrapie-infected sheep for 40 months, even though swabs from this
furniture tested negative by PMCA. This infection rate decreased (1 out of 12)
on the same paddock after replacement with clean field furniture. Twelve grazing
sheep exposed to field furniture not in contact with scrapie-infected sheep for
18 months remained scrapie free. The findings of this study highlight the role
of field furniture used by scrapie-infected sheep to act as a reservoir for
disease re-introduction although infectivity declines considerably if the field
furniture has not been in contact with scrapie-infected sheep for several
months. PMCA may not be as sensitive as VRQ/VRQ sheep to test for environmental
contamination.
snip...
Discussion
Classical scrapie is an environmentally transmissible disease because it
has been reported in naïve, supposedly previously unexposed sheep placed in
pastures formerly occupied by scrapie-infected sheep (4, 19, 20). Although the
vector for disease transmission is not known, soil is likely to be an important
reservoir for prions (2) where – based on studies in rodents – prions can adhere
to minerals as a biologically active form (21) and remain infectious for more
than 2 years (22). Similarly, chronic wasting disease (CWD) has re-occurred in
mule deer housed in paddocks used by infected deer 2 years earlier, which was
assumed to be through foraging and soil consumption (23).
Our study suggested that the risk of acquiring scrapie infection was
greater through exposure to contaminated wooden, plastic, and metal surfaces via
water or food troughs, fencing, and hurdles than through grazing. Drinking from
a water trough used by the scrapie flock was sufficient to cause infection in
sheep in a clean building. Exposure to fences and other objects used for rubbing
also led to infection, which supported the hypothesis that skin may be a vector
for disease transmission (9). The risk of these objects to cause infection was
further demonstrated when 87% of 23 sheep presented with PrPSc in lymphoid
tissue after grazing on one of the paddocks, which contained metal hurdles, a
metal lamb creep and a water trough in contact with the scrapie flock up to 8
weeks earlier, whereas no infection had been demonstrated previously in sheep
grazing on this paddock, when equipped with new fencing and field furniture.
When the contaminated furniture and fencing were removed, the infection rate
dropped significantly to 8% of 12 sheep, with soil of the paddock as the most
likely source of infection caused by shedding of prions from the
scrapie-infected sheep in this paddock up to a week earlier.
This study also indicated that the level of contamination of field
furniture sufficient to cause infection was dependent on two factors: stage of
incubation period and time of last use by scrapie-infected sheep. Drinking from
a water trough that had been used by scrapie sheep in the predominantly
pre-clinical phase did not appear to cause infection, whereas infection was
shown in sheep drinking from the water trough used by scrapie sheep in the later
stage of the disease. It is possible that contamination occurred through
shedding of prions in saliva, which may have contaminated the surface of the
water trough and subsequently the water when it was refilled. Contamination
appeared to be sufficient to cause infection only if the trough was in contact
with sheep that included clinical cases. Indeed, there is an increased risk of
bodily fluid infectivity with disease progression in scrapie (24) and CWD (25)
based on PrPSc detection by sPMCA. Although ultraviolet light and heat under
natural conditions do not inactivate prions (26), furniture in contact with the
scrapie flock, which was assumed to be sufficiently contaminated to cause
infection, did not act as vector for disease if not used for 18 months, which
suggest that the weathering process alone was sufficient to inactivate prions.
PrPSc detection by sPMCA is increasingly used as a surrogate for
infectivity measurements by bioassay in sheep or mice. In this reported study,
however, the levels of PrPSc present in the environment were below the limit of
detection of the sPMCA method, yet were still sufficient to cause infection of
in-contact animals. In the present study, the outdoor objects were removed from
the infected flock 8 weeks prior to sampling and were positive by sPMCA at very
low levels (2 out of 37 reactions). As this sPMCA assay also yielded 2 positive
reactions out of 139 in samples from the scrapie-free farm, the sPMCA assay
could not detect PrPSc on any of the objects above the background of the assay.
False positive reactions with sPMCA at a low frequency associated with de novo
formation of infectious prions have been reported (27, 28). This is in contrast
to our previous study where we demonstrated that outdoor objects that had been
in contact with the scrapie-infected flock up to 20 days prior to sampling
harbored PrPSc that was detectable by sPMCA analysis [4 out of 15 reactions
(12)] and was significantly more positive by the assay compared to analogous
samples from the scrapie-free farm. This discrepancy could be due to the use of
a different sPMCA substrate between the studies that may alter the efficiency of
amplification of the environmental PrPSc. In addition, the present study had a
longer timeframe between the objects being in contact with the infected flock
and sampling, which may affect the levels of extractable PrPSc. Alternatively,
there may be potentially patchy contamination of this furniture with PrPSc,
which may have been missed by swabbing. The failure of sPMCA to detect
CWD-associated PrP in saliva from clinically affected deer despite confirmation
of infectivity in saliva-inoculated transgenic mice was associated with as yet
unidentified inhibitors in saliva (29), and it is possible that the sensitivity
of sPMCA is affected by other substances in the tested material. In addition,
sampling of amplifiable PrPSc and subsequent detection by sPMCA may be more
difficult from furniture exposed to weather, which is supported by the
observation that PrPSc was detected by sPMCA more frequently in indoor than
outdoor furniture (12). A recent experimental study has demonstrated that
repeated cycles of drying and wetting of prion-contaminated soil, equivalent to
what is expected under natural weathering conditions, could reduce PMCA
amplification efficiency and extend the incubation period in hamsters inoculated
with soil samples (30). This seems to apply also to this study even though the
reduction in infectivity was more dramatic in the sPMCA assays than in the sheep
model. Sheep were not kept until clinical end-point, which would have enabled us
to compare incubation periods, but the lack of infection in sheep exposed to
furniture that had not been in contact with scrapie sheep for a longer time
period supports the hypothesis that prion degradation and subsequent loss of
infectivity occurs even under natural conditions.
In conclusion, the results in the current study indicate that removal of
furniture that had been in contact with scrapie-infected animals should be
recommended, particularly since cleaning and decontamination may not effectively
remove scrapie infectivity (31), even though infectivity declines considerably
if the pasture and the field furniture have not been in contact with
scrapie-infected sheep for several months. As sPMCA failed to detect PrPSc in
furniture that was subjected to weathering, even though exposure led to
infection in sheep, this method may not always be reliable in predicting the
risk of scrapie infection through environmental contamination. These results
suggest that the VRQ/VRQ sheep model may be more sensitive than sPMCA for the
detection of environmentally associated scrapie, and suggest that extremely low
levels of scrapie contamination are able to cause infection in susceptible sheep
genotypes.
Keywords: classical scrapie, prion, transmissible spongiform
encephalopathy, sheep, field furniture, reservoir, serial protein misfolding
cyclic amplification
Wednesday, December 16, 2015
*** Objects in contact with classical scrapie sheep act as a reservoir for
scrapie transmission ***
Circulation of prions within dust on a scrapie affected farm
Kevin C Gough1, Claire A Baker2, Hugh A Simmons3, Steve A Hawkins3 and Ben
C Maddison2*
Abstract
Prion diseases are fatal neurological disorders that affect humans and
animals. Scrapie of sheep/goats and Chronic Wasting Disease (CWD) of deer/elk
are contagious prion diseases where environmental reservoirs have a direct link
to the transmission of disease. Using protein misfolding cyclic amplification we
demonstrate that scrapie PrPSc can be detected within circulating dusts that are
present on a farm that is naturally contaminated with sheep scrapie. The
presence of infectious scrapie within airborne dusts may represent a possible
route of infection and illustrates the difficulties that may be associated with
the effective decontamination of such scrapie affected premises.
snip...
Discussion
We present biochemical data illustrating the airborne movement of scrapie
containing material within a contaminated farm environment. We were able to
detect scrapie PrPSc within extracts from dusts collected over a 70 day period,
in the absence of any sheep activity. We were also able to detect scrapie PrPSc
within dusts collected within pasture at 30 m but not at 60 m distance away from
the scrapie contaminated buildings, suggesting that the chance of contamination
of pasture by scrapie contaminated dusts decreases with distance from
contaminated farm buildings. PrPSc amplification by sPMCA has been shown to
correlate with infectivity and amplified products have been shown to be
infectious [14,15]. These experiments illustrate the potential for low dose
scrapie infectivity to be present within such samples. We estimate low ng levels
of scrapie positive brain equivalent were deposited per m2 over 70 days, in a
barn previously occupied by sheep affected with scrapie. This movement of dusts
and the accumulation of low levels of scrapie infectivity within this
environment may in part explain previous observations where despite stringent
pen decontamination regimens healthy lambs still became scrapie infected after
apparent exposure from their environment alone [16]. The presence of sPMCA
seeding activity and by inference, infectious prions within dusts, and their
potential for airborne dissemination is highly novel and may have implications
for the spread of scrapie within infected premises. The low level circulation
and accumulation of scrapie prion containing dust material within the farm
environment will likely impede the efficient decontamination of such scrapie
contaminated buildings unless all possible reservoirs of dust are removed.
Scrapie containing dusts could possibly infect animals during feeding and
drinking, and respiratory and conjunctival routes may also be involved. It has
been demonstrated that scrapie can be efficiently transmitted via the nasal
route in sheep [17], as is also the case for CWD in both murine models and in
white tailed deer [18-20].
The sources of dust borne prions are unknown but it seems reasonable to
assume that faecal, urine, skin, parturient material and saliva-derived prions
may contribute to this mobile environmental reservoir of infectivity. This work
highlights a possible transmission route for scrapie within the farm
environment, and this is likely to be paralleled in CWD which shows strong
similarities with scrapie in terms of prion dissemination and disease
transmission. The data indicate that the presence of scrapie prions in dust is
likely to make the control of these diseases a considerable challenge.
Research Project: TRANSMISSION, DIFFERENTIATION, AND PATHOBIOLOGY OF
TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES
Title: Scrapie transmits to white-tailed deer by the oral route and has a
molecular profile similar to chronic wasting disease
Authors
item Greenlee, Justin item Moore, S - item Smith, Jodi - item Kunkle,
Robert item West Greenlee, M -
Submitted to: American College of Veterinary Pathologists Meeting
Publication Type: Abstract Only Publication Acceptance Date: August 12, 2015
Publication Date: N/A Technical Abstract: The purpose of this work was to
determine susceptibility of white-tailed deer (WTD) to the agent of sheep
scrapie and to compare the resultant PrPSc to that of the original inoculum and
chronic wasting disease (CWD). We inoculated WTD by a natural route of exposure
(concurrent oral and intranasal (IN); n=5) with a US scrapie isolate. All
scrapie-inoculated deer had evidence of PrPSc accumulation. PrPSc was detected
in lymphoid tissues at preclinical time points, and deer necropsied after 28
months post-inoculation had clinical signs, spongiform encephalopathy, and
widespread distribution of PrPSc in neural and lymphoid tissues. Western
blotting (WB) revealed PrPSc with 2 distinct molecular profiles. WB on cerebral
cortex had a profile similar to the original scrapie inoculum, whereas WB of
brainstem, cerebellum, or lymph nodes revealed PrPSc with a higher profile
resembling CWD. Homogenates with the 2 distinct profiles from WTD with clinical
scrapie were further passaged to mice expressing cervid prion protein and
intranasally to sheep and WTD. In cervidized mice, the two inocula have distinct
incubation times. Sheep inoculated intranasally with WTD derived scrapie
developed disease, but only after inoculation with the inoculum that had a
scrapie-like profile. The WTD study is ongoing, but deer in both inoculation
groups are positive for PrPSc by rectal mucosal biopsy. In summary, this work
demonstrates that WTD are susceptible to the agent of scrapie, two distinct
molecular profiles of PrPSc are present in the tissues of affected deer, and
inoculum of either profile readily passes to deer.
White-tailed Deer are Susceptible to Scrapie by Natural Route of Infection
Jodi D. Smith, Justin J. Greenlee, and Robert A. Kunkle; Virus and Prion
Research Unit, National Animal Disease Center, USDA-ARS
Interspecies transmission studies afford the opportunity to better
understand the potential host range and origins of prion diseases. Previous
experiments demonstrated that white-tailed deer are susceptible to sheep-derived
scrapie by intracranial inoculation. The purpose of this study was to determine
susceptibility of white-tailed deer to scrapie after a natural route of
exposure. Deer (n=5) were inoculated by concurrent oral (30 ml) and intranasal
(1 ml) instillation of a 10% (wt/vol) brain homogenate derived from a sheep
clinically affected with scrapie. Non-inoculated deer were maintained as
negative controls. All deer were observed daily for clinical signs. Deer were
euthanized and necropsied when neurologic disease was evident, and tissues were
examined for abnormal prion protein (PrPSc) by immunohistochemistry (IHC) and
western blot (WB). One animal was euthanized 15 months post-inoculation (MPI)
due to an injury. At that time, examination of obex and lymphoid tissues by IHC
was positive, but WB of obex and colliculus were negative. Remaining deer
developed clinical signs of wasting and mental depression and were necropsied
from 28 to 33 MPI. Tissues from these deer were positive for scrapie by IHC and
WB. Tissues with PrPSc immunoreactivity included brain, tonsil, retropharyngeal
and mesenteric lymph nodes, hemal node, Peyer’s patches, and spleen. This work
demonstrates for the first time that white-tailed deer are susceptible to sheep
scrapie by potential natural routes of inoculation. In-depth analysis of tissues
will be done to determine similarities between scrapie in deer after
intracranial and oral/intranasal inoculation and chronic wasting disease
resulting from similar routes of inoculation.
see full text ;
PO-039: A comparison of scrapie and chronic wasting disease in white-tailed
deer
Justin Greenlee, Jodi Smith, Eric Nicholson US Dept. Agriculture;
Agricultural Research Service, National Animal Disease Center; Ames, IA USA
White-tailed deer are susceptible to the agent of sheep scrapie by
intracerebral inoculation
snip...
It is unlikely that CWD will be eradicated from free-ranging cervids, and
the disease is likely to continue to spread geographically [10]. However, the
potential that white-tailed deer may be susceptible to sheep scrapie by a
natural route presents an additional confounding factor to halting the spread of
CWD. This leads to the additional speculations that
1) infected deer could serve as a reservoir to infect sheep with scrapie
offering challenges to scrapie eradication efforts and
2) CWD spread need not remain geographically confined to current endemic
areas, but could occur anywhere that sheep with scrapie and susceptible cervids
cohabitate.
This work demonstrates for the first time that white-tailed deer are
susceptible to sheep scrapie by intracerebral inoculation with a high attack
rate and that the disease that results has similarities to CWD. These
experiments will be repeated with a more natural route of inoculation to
determine the likelihood of the potential transmission of sheep scrapie to
white-tailed deer. If scrapie were to occur in white-tailed deer, results of
this study indicate that it would be detected as a TSE, but may be difficult to
differentiate from CWD without in-depth biochemical analysis.
2012
PO-039: A comparison of scrapie and chronic wasting disease in white-tailed
deer
Justin Greenlee, Jodi Smith, Eric Nicholson US Dept. Agriculture;
Agricultural Research Service, National Animal Disease Center; Ames, IA USA
snip...
The results of this study suggest that there are many similarities in the
manifestation of CWD and scrapie in WTD after IC inoculation including early and
widespread presence of PrPSc in lymphoid tissues, clinical signs of depression
and weight loss progressing to wasting, and an incubation time of 21-23 months.
Moreover, western blots (WB) done on brain material from the obex region have a
molecular profile similar to CWD and distinct from tissues of the cerebrum or
the scrapie inoculum. However, results of microscopic and IHC examination
indicate that there are differences between the lesions expected in CWD and
those that occur in deer with scrapie: amyloid plaques were not noted in any
sections of brain examined from these deer and the pattern of immunoreactivity
by IHC was diffuse rather than plaque-like.
*** After a natural route of exposure, 100% of WTD were susceptible to
scrapie.
Deer developed clinical signs of wasting and mental depression and were
necropsied from 28 to 33 months PI. Tissues from these deer were positive for
PrPSc by IHC and WB. Similar to IC inoculated deer, samples from these deer
exhibited two different molecular profiles: samples from obex resembled CWD
whereas those from cerebrum were similar to the original scrapie inoculum. On
further examination by WB using a panel of antibodies, the tissues from deer
with scrapie exhibit properties differing from tissues either from sheep with
scrapie or WTD with CWD. Samples from WTD with CWD or sheep with scrapie are
strongly immunoreactive when probed with mAb P4, however, samples from WTD with
scrapie are only weakly immunoreactive. In contrast, when probed with mAb’s 6H4
or SAF 84, samples from sheep with scrapie and WTD with CWD are weakly
immunoreactive and samples from WTD with scrapie are strongly positive. This
work demonstrates that WTD are highly susceptible to sheep scrapie, but on first
passage, scrapie in WTD is differentiable from CWD.
2011
*** After a natural route of exposure, 100% of white-tailed deer were
susceptible to scrapie.
White-tailed Deer are Susceptible to Scrapie by Natural Route of Infection
Jodi D. Smith, Justin J. Greenlee, and Robert A. Kunkle; Virus and Prion
Research Unit, National Animal Disease Center, USDA-ARS
Interspecies transmission studies afford the opportunity to better
understand the potential host range and origins of prion diseases. Previous
experiments demonstrated that white-tailed deer are susceptible to sheep-derived
scrapie by intracranial inoculation. The purpose of this study was to determine
susceptibility of white-tailed deer to scrapie after a natural route of
exposure. Deer (n=5) were inoculated by concurrent oral (30 ml) and intranasal
(1 ml) instillation of a 10% (wt/vol) brain homogenate derived from a sheep
clinically affected with scrapie. Non-inoculated deer were maintained as
negative controls. All deer were observed daily for clinical signs. Deer were
euthanized and necropsied when neurologic disease was evident, and tissues were
examined for abnormal prion protein (PrPSc) by immunohistochemistry (IHC) and
western blot (WB). One animal was euthanized 15 months post-inoculation (MPI)
due to an injury. At that time, examination of obex and lymphoid tissues by IHC
was positive, but WB of obex and colliculus were negative. Remaining deer
developed clinical signs of wasting and mental depression and were necropsied
from 28 to 33 MPI. Tissues from these deer were positive for scrapie by IHC and
WB. Tissues with PrPSc immunoreactivity included brain, tonsil, retropharyngeal
and mesenteric lymph nodes, hemal node, Peyer’s patches, and spleen. This work
demonstrates for the first time that white-tailed deer are susceptible to sheep
scrapie by potential natural routes of inoculation. In-depth analysis of tissues
will be done to determine similarities between scrapie in deer after
intracranial and oral/intranasal inoculation and chronic wasting disease
resulting from similar routes of inoculation.
see full text ;
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.
Veterinary Pathology Onlinevet.sagepub.com Published online before print
February 27, 2014, doi: 10.1177/0300985814524798 Veterinary Pathology February
27, 2014 0300985814524798
Lesion Profiling and Subcellular Prion Localization of Cervid Chronic
Wasting Disease in Domestic Cats
D. M. Seelig1⇑ A. V. Nalls1 M. Flasik2 V. Frank1 S. Eaton2 C. K. Mathiason1
E. A. Hoover1 1Department of Microbiology, Immunology, and Pathology, Colorado
State University, Fort Collins, CO, USA 2Department of Biomedical Sciences,
Colorado State University, Fort Collins, CO, USA D. M. Seelig, University of
Minnesota, Department of Veterinary Clinical Sciences, Room 339 VetMedCtrS,
6192A (Campus Delivery Code), 1352 Boyd Ave, St Paul, MN 55108, USA. Email
address: dseelig@umn.edu
Abstract
Chronic wasting disease (CWD) is an efficiently transmitted, fatal, and
progressive prion disease of cervids with an as yet to be fully clarified host
range. While outbred domestic cats (Felis catus) have recently been shown to be
susceptible to experimental CWD infection, the neuropathologic features of the
infection are lacking. Such information is vital to provide diagnostic power in
the event of natural interspecies transmission and insights into host and strain
interactions in interspecies prion infection. Using light microscopy and
immunohistochemistry, we detail the topographic pattern of neural spongiosis
(the “lesion profile”) and the distribution of misfolded prion protein in the
primary and secondary passage of feline CWD (FelCWD). We also evaluated cellular
and subcellular associations between misfolded prion protein (PrPD) and central
nervous system neurons and glial cell populations. From these studies, we (1)
describe the novel neuropathologic profile of FelCWD, which is distinct from
either cervid CWD or feline spongiform encephalopathy (FSE), and (2) provide
evidence of serial passage-associated interspecies prion adaptation. In
addition, we demonstrate through confocal analysis the successful
co-localization of PrPD with neurons, astrocytes, microglia, lysosomes, and
synaptophysin, which, in part, implicates each of these in the neuropathology of
FelCWD. In conclusion, this work illustrates the simultaneous role of both host
and strain in the development of a unique FelCWD neuropathologic profile and
that such a profile can be used to discriminate between FelCWD and FSE.
prion chronic wasting disease immunohistochemistry interspecies cat feline
spongiform encephalopathy transmissible spongiform encephalopathy adaptation
species barrier
Monday, August 8, 2011 Susceptibility of Domestic Cats to CWD Infection
Oral.29: Susceptibility of Domestic Cats to CWD Infection
Amy Nalls, Nicholas J. Haley, Jeanette Hayes-Klug, Kelly Anderson, Davis M.
Seelig, Dan S. Bucy, Susan L. Kraft, Edward A. Hoover and Candace K.
Mathiason†
Colorado State University; Fort Collins, CO USA†Presenting author; Email:
ckm@lamar.colostate.edu
Domestic and non-domestic cats have been shown to be susceptible to one
prion disease, feline spongiform encephalopathy (FSE), thought to be transmitted
through consumption of bovine spongiform encephalopathy (BSE) contaminated meat.
Because domestic and free ranging felids scavenge cervid carcasses, including
those in CWD affected areas, we evaluated the susceptibility of domestic cats to
CWD infection experimentally. Groups of n = 5 cats each were inoculated either
intracerebrally (IC) or orally (PO) with CWD deer brain homogenate. Between
40–43 months following IC inoculation, two cats developed mild but progressive
symptoms including weight loss, anorexia, polydipsia, patterned motor behaviors
and ataxia—ultimately mandating euthanasia. Magnetic resonance imaging (MRI) on
the brain of one of these animals (vs. two age-matched controls) performed just
before euthanasia revealed increased ventricular system volume, more prominent
sulci, and T2 hyperintensity deep in the white matter of the frontal hemisphere
and in cortical grey distributed through the brain, likely representing
inflammation or gliosis. PrPRES and widely distributed peri-neuronal vacuoles
were demonstrated in the brains of both animals by immunodetection assays. No
clinical signs of TSE have been detected in the remaining primary passage cats
after 80 months pi. Feline-adapted CWD was sub-passaged into groups (n=4 or 5)
of cats by IC, PO, and IP/SQ routes. Currently, at 22 months pi, all five IC
inoculated cats are demonstrating abnormal behavior including increasing
aggressiveness, pacing, and hyper responsiveness.
*** Two of these cats have developed rear limb ataxia. Although the limited
data from this ongoing study must be considered preliminary, they raise the
potential for cervid-to-feline transmission in nature.
AD.63:
Susceptibility of domestic cats to chronic wasting disease
Amy V.Nalls,1 Candace Mathiason,1 Davis Seelig,2 Susan Kraft,1 Kevin
Carnes,1 Kelly Anderson,1 Jeanette Hayes-Klug1 and Edward A. Hoover1 1Colorado
State University; Fort Collins, CO USA; 2University of Minnesota; Saint Paul, MN
USA
Domestic and nondomestic cats have been shown to be susceptible to feline
spongiform encephalopathy (FSE), almost certainly caused by consumption of
bovine spongiform encephalopathy (BSE)-contaminated meat. Because domestic and
free-ranging nondomestic felids scavenge cervid carcasses, including those in
areas affected by chronic wasting disease (CWD), we evaluated the susceptibility
of the domestic cat (Felis catus) to CWD infection experimentally. Cohorts of 5
cats each were inoculated either intracerebrally (IC) or orally (PO) with
CWD-infected deer brain. At 40 and 42 mo post-inoculation, two IC-inoculated
cats developed signs consistent with prion disease, including a stilted gait,
weight loss, anorexia, polydipsia, patterned motor behaviors, head and tail
tremors, and ataxia, and progressed to terminal disease within 5 mo. Brains from
these two cats were pooled and inoculated into cohorts of cats by IC, PO, and
intraperitoneal and subcutaneous (IP/SC) routes. Upon subpassage, feline-adapted
CWD (FelCWD) was transmitted to all IC-inoculated cats with a decreased
incubation period of 23 to 27 mo. FelCWD was detected in the brains of all the
symptomatic cats by western blotting and immunohistochemistry and abnormalities
were seen in magnetic resonance imaging, including multifocal T2 fluid
attenuated inversion recovery (FLAIR) signal hyper-intensities, ventricular size
increases, prominent sulci, and white matter tract cavitation. Currently, 3 of 4
IP/SQ and 2 of 4 PO inoculared cats have developed abnormal behavior patterns
consistent with the early stage of feline CWD.
*** These results demonstrate that CWD can be transmitted and adapted to
the domestic cat, thus raising the issue of potential cervid-to- feline
transmission in nature.
www.landesbioscience.com
PO-081: Chronic wasting disease in the cat— Similarities to feline
spongiform encephalopathy (FSE)
FELINE SPONGIFORM ENCEPHALOPATHY FSE
Wednesday, October 17, 2012
Prion Remains Infectious after Passage through Digestive System of American
Crows (Corvus brachyrhynchos)
Chronic Wasting Disease Susceptibility of Four North American Rodents
Chad J. Johnson1*, Jay R. Schneider2, Christopher J. Johnson2, Natalie A.
Mickelsen2, Julia A. Langenberg3, Philip N. Bochsler4, Delwyn P. Keane4, Daniel
J. Barr4, and Dennis M. Heisey2 1University of Wisconsin School of Veterinary
Medicine, Department of Comparative Biosciences, 1656 Linden Drive, Madison WI
53706, USA 2US Geological Survey, National Wildlife Health Center, 6006
Schroeder Road, Madison WI 53711, USA 3Wisconsin Department of Natural
Resources, 101 South Webster Street, Madison WI 53703, USA 4Wisconsin Veterinary
Diagnostic Lab, 445 Easterday Lane, Madison WI 53706, USA *Corresponding author
email: cjohnson@svm.vetmed.wisc.edu
We intracerebrally challenged four species of native North American rodents
that inhabit locations undergoing cervid chronic wasting disease (CWD)
epidemics. The species were: deer mice (Peromyscus maniculatus), white-footed
mice (P. leucopus), meadow voles (Microtus pennsylvanicus), and red-backed voles
(Myodes gapperi). The inocula were prepared from the brains of hunter-harvested
white-tailed deer from Wisconsin that tested positive for CWD. Meadow voles
proved to be most susceptible, with a median incubation period of 272 days.
Immunoblotting and immunohistochemistry confirmed the presence of PrPd in the
brains of all challenged meadow voles. Subsequent passages in meadow voles lead
to a significant reduction in incubation period. The disease progression in
red-backed voles, which are very closely related to the European bank vole (M.
glareolus) which have been demonstrated to be sensitive to a number of TSEs, was
slower than in meadow voles with a median incubation period of 351 days. We
sequenced the meadow vole and red-backed vole Prnp genes and found three amino
acid (AA) differences outside of the signal and GPI anchor sequences. Of these
differences (T56-, G90S, S170N; read-backed vole:meadow vole), S170N is
particularly intriguing due its postulated involvement in "rigid loop" structure
and CWD susceptibility. Deer mice did not exhibit disease signs until nearly 1.5
years post-inoculation, but appear to be exhibiting a high degree of disease
penetrance. White-footed mice have an even longer incubation period but are also
showing high penetrance. Second passage experiments show significant shortening
of incubation periods. Meadow voles in particular appear to be interesting lab
models for CWD. These rodents scavenge carrion, and are an important food source
for many predator species. Furthermore, these rodents enter human and domestic
livestock food chains by accidental inclusion in grain and forage. Further
investigation of these species as potential hosts, bridge species, and
reservoirs of CWD is required.
please see ;
”The occurrence of CWD must be viewed against the contest of the locations
in which it occurred. It was an incidental and unwelcome complication of the
respective wildlife research programmes. Despite it’s subsequent recognition as
a new disease of cervids, therefore justifying direct investigation, no specific
research funding was forthcoming. The USDA veiwed it as a wildlife problem and
consequently not their province!” page 26.
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. ...
Friday, February 05, 2016
Report of the Committee on Wildlife Diseases FY2015 CWD TSE PRION
Detections in Farmed Cervids and Wild
Saturday, February 6, 2016
Secretary's Advisory Committee on Animal Health; Meeting [Docket No.
APHIS-2016-0007] Singeltary Submission
Wednesday, February 10, 2016
*** Wisconsin Two deer that escaped farm had chronic wasting disease CWD
***
Sunday, January 17, 2016
*** Wisconsin Captive CWD Lotto Pays Out Again indemnity payment of
$298,770 for 228 white-tailed deer killed on farm ***
http://chronic-wasting-disease.blogspot.com/2016/01/wisconsin-captive-cwd-lotto-pays-out.html
Sunday, May 08, 2016
WISCONSIN CHRONIC WASTING DISEASE CWD TSE PRION SPIRALING FURTHER INTO THE
ABYSS UPDATE
http://chronic-wasting-disease.blogspot.com/2016/05/wisconsin-chronic-wasting-disease-cwd.html
Tuesday, May 03, 2016
Arkansas Chronic Wasting Disease CWD TSE Prion and Elk Restoration Project
and Hunkering Down in the BSE Situation Room USDA 1998
Monday, April 25, 2016
Arkansas AGFC Phase 2 sampling reveals CWD positive deer in Madison and
Pope counties
Tuesday, April 19, 2016
Arkansas First Phase of CWD sampling reveals 23 percent prevalence rate in
focal area With 82 Confirmed to Date
http://chronic-wasting-disease.blogspot.com/2016/04/arkansas-first-phase-of-cwd-sampling.html
Wednesday, May 11, 2016
PENNSYLVANIA TWELVE MORE CASES OF CWD FOUND: STATE GEARS UP FOR ADDITIONAL
CONTROL MEASURES
Friday, April 22, 2016
Missouri MDC finds seven new cases of ChronicWasting Disease CWD during
past‐season testing
Friday, April 22, 2016
COLORADO CHRONIC WASTING DISEASE CWD TSE PRION SURVEILLANCE AND TESTING
PROGRAM IS MINIMAL AND LIMITED
KANSAS CWD CASES ALARMING
Wednesday, March 02, 2016 Kansas Chronic Wasting Disease CWD TSE Prion 52
cases 2015 updated report 'ALARMING'
Tuesday, February 02, 2016
Illinois six out of 19 deer samples tested positive for CWD in the Oswego
zone of Kendall County
Sunday, May 22, 2016
Arkansas Commission approves hunting regulations, hears new proposals for
CWD management
Friday, April 22, 2016
Texas Scrapie Confirmed in a Hartley County Sheep where CWD was detected in
a Mule Deer
Saturday, April 02, 2016
TEXAS TAHC BREAKS IT'S SILENCE WITH TWO MORE CASES CWD CAPTIVE DEER
BRINGING TOTAL TO 10 CAPTIVES REPORTED TO DATE
Friday, February 26, 2016
TEXAS Hartley County Mule Deer Tests Positive for Chronic Wasting Disease
CWD TSE Prion
Friday, February 05, 2016
TEXAS NEW CHRONIC WASTING DISEASE CWD CASE DISCOVERD AT CAPTIVE DEER
RELEASE SITE
Sunday, January 17, 2016
Texas 10,000 deer in Texas tested for deadly disease CWD TSE, but not
tested much in the most logical place, the five-mile radius around the Medina
County captive-deer facility where it was discovered
Friday, January 15, 2016
TEXAS PARKS & WILDLIFE CWD Ante-Mortem Testing Symposium Texas Disposal
Systems Events Pavilion January 12, 2016
Tuesday, December 29, 2015
TEXAS MONTHLY CHRONIC WASTING DISEASE CWD JANUARY 2016 DEER BREEDERS STILL
DON'T GET IT $
Chronic Wasting Unease
The emergence of a deadly disease has wildlife officials and deer breeders
eyeing each other suspiciously.
Monday, November 16, 2015
TEXAS PARKS AND WILDLIFE DEPARTMENT EXECUTIVE DIRECTOR ORDER NO. 015-006
Chronic Wasting Disease (CWD) immediate danger to the white-tailed deer and mule
deer resources of Texas
Saturday, November 14, 2015
TEXAS CAPTIVE BREEDER CHRONIC WASTING DISEASE CWD 2 MORE SUSPECTS DECTECTED
BRINGING NUMBER TO 7 DETECTED IN CAPTIVE BREEDER (if/when the last two are
confirmed).
Thursday, November 05, 2015
*** TPW Commission Adopts Interim Deer Breeder Movement Rules
Thursday, September 24, 2015
TEXAS Hunters Asked to Submit Samples for Chronic Wasting Disease CWD TSE
Prion Testing
*** I cannot stress enough to all of you, for the sake of your family and
mine, before putting anything in the freezer, have those deer tested for CWD.
...terry
Sunday, September 13, 2015
TEXAS DETECTS MORE DEER POSITIVE FOR CHRONIC WASTING DISEASE CWD tested at
a Tier 1 facility (a facility that either sold to or purchased directly from the
index facility)
Friday, October 09, 2015
Texas TWA Chronic Wasting Disease TSE Prion Webinars and Meeting October
2015
Tuesday, October 06, 2015
TAHC 393rd Commission Meeting Chronic Wasting Disease CWD TSE Prion October
6, 2015
Saturday, October 03, 2015
TEXAS CHRONIC WASTING DISEASE CWD TSE PRION GOD MUST NOT BE A TEXAN 2002 TO
2015
Wednesday, March 25, 2015
*** Chronic Wasting Disease CWD Cases Confirmed In New Mexico 2013 and 2014
UPDATE 2015
Wednesday, March 18, 2015
Chronic Wasting Disease CWD Confirmed Texas Trans Pecos March 18,
2015
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
TEXAS DEER CZAR SENT TO WISCONSIN TO SOLVE CWD CRISIS, WHILE ROME (TEXAS)
BURNS
Wednesday, March 04, 2015
*** Disease sampling results provide current snapshot of CWD in Wisconsin
finding 324 positive detections statewide in 2014
Friday, June 01, 2012
*** TEXAS DEER CZAR TO WISCONSIN ASK TO EXPLAIN COMMENTS
RAW, UNCUT, AND UNCENSORED
Sunday, August 23, 2015
TAHC Chronic Wasting Disease CWD TSE Prion and how to put lipstick on a pig
and take her to the dance in Texas
Friday, August 07, 2015
*** Texas CWD Captive, and then there were 4 ?
Thursday, August 06, 2015
*** WE HAVE LOST TEXAS TO CWD TASK FORCE CATERING TO INDUSTRY
http://chronic-wasting-disease.blogspot.com/2015/08/we-have-lost-texas-to-cwd-task-force.html
Tuesday, July 21, 2015
*** Texas CWD Medina County Herd Investigation Update July 16, 2015 ***
Thursday, July 09, 2015
TEXAS Chronic Wasting Disease (CWD) Herd Plan for Trace-Forward Exposed
Herd with Testing of Exposed Animals
Wednesday, July 01, 2015
*** TEXAS Chronic Wasting Disease Detected in Medina County Captive Deer
Tuesday, December 16, 2014
Texas 84th Legislature 2015 H.R. No. 2597 Kuempel Deer Breeding Industry
TAHC TPWD CWD TSE PRION
Thursday, May 02, 2013
*** Chronic Wasting Disease (CWD) Texas Important Update on OBEX ONLY
TEXTING
Monday, February 11, 2013
TEXAS CHRONIC WASTING DISEASE CWD Four New Positives Found in Trans Pecos
Tuesday, July 10, 2012
Chronic Wasting Disease Detected in Far West Texas
Monday, March 26, 2012
Texas Prepares for Chronic Wasting Disease CWD Possibility in Far West
Texas
***for anyone interested, here is some history of CWD along the Texas, New
Mexico border, and my attempt to keep up with it...terry
***CWD TEXAS TAHC OLD FILE HISTORY
updated from some of my old files. ...
Subject: CWD SURVEILLANCE STATISTICS TEXAS (total testing figures less than
50 in two years)
Date: Sun, 25 Aug 2002 21:06:49 –0700
From: "Terry S. Singeltary Sr."
Reply-To: Bovine Spongiform Encephalopathy
To: BSE-L@uni-karlsruhe.de
######## Bovine Spongiform Encephalopathy #########
greetings list members,
here are some figures on CWD testing in TEXAS...TSS
Dear Dr. Singletary,
In Fiscal Year 2001, seven deer from Texas were tested by the National
Veterinary Services Laboratory (NVSL) for CWD (5 fallow deer and 2 white-tailed
deer). In Fiscal Year 2002, seven elk from Texas were tested at NVSL (no deer).
During these two years, an additional six elk and one white-tailed deer were
tested at the Texas Veterinary Medical Diagnostic Laboratory (TVMDL). In Fiscal
Year 2002, four white-tailed deer (free-ranging clinical suspects) and at least
eight other white-tailed deer have been tested at TVMDL. One elk has been tested
at NVSL. All of these animals have been found negative for CWD. Dr. Jerry Cooke
of the Texas Parks and Wildlife Department also has records of 601 clinically
ill white-tailed deer which were necropsied at Texas A&M during the late
1960's and early 1970's, and no spongiform encepalopathies were noted. Thank you
for your consideration.
xxxxxxx
Texas Animal Health Commission
(personal communication...TSS)
Austin 8 news
snip...
"There's about 4 million deer in the state of Texas, and as a resource I
think we need to be doing as much as we can to look for these diseases," said
Doug Humphreys with Texas Parks and Wildlife. "Right now Texas is clear. We
haven't found any, but that doesn't mean we don't look."
With approximately 4 million animals, Texas has the largest population of
white-tailed deer in the nation. In addition, about 19,000 white-tailed deer and
17,000 elk are being held in private facilities. To know if CWD is present in
captive herds, TPWD and Texas Animal Health Commission are working with breeders
to monitor their herds.
How is it spread?
It is not known exactly how CWD is spread. It is believed that the agent
responsible for the disease may be spread both directly (animal to animal
contact) and indirectly (soil or other surface to animal). It is thought that
the most common mode of transmission from an infected animal is via saliva,
feces, and urine.
some surveillance?
beyond the _potential_ methods of transmissions above, why, not a single
word of SRM of various TSE species in feed as a source?
it's a known fact they have been feeding the deer/elk the same stuff as
cows here in USA.
and the oral route has been documented of CWD to mule deer fawns in lab
studies.
not to say that other _potential_ transmission mechanisms are possible, but
why over look the obvious?
TSS
########### http://mailhost.rz.uni-karlsruhe.de/warc/bse-l.html
############
From: Ken Waldrup, DVM, PhD (host25-207.tahc.state.tx.us)
Subject: Re: CWD SAMPLING TEXAS (but NOT in the obvious place, the NM,
TEXAS border)
Date: December 15, 2003 at 3:43 pm PST
In Reply to: CWD SAMPLING TEXAS (but NOT in the obvious place, the NM,
TEXAS border) posted by TSS on December 12, 2003 at 2:15 pm:
Dear sirs:
With regard to your comment about Texas NOT looking for CWD along the New
Mexico border, it is painfully obvious that you do not know or understand the
natural distribution of mule deer out there or the rights of the land owners in
this state. As of 15 December 2003, a total of 42 deer had been sampled from
what we call "Trans-Pecos", beyond the Pecos River. Mule deer are very widely
dispersed through this area, sometimes at densities of one animal per 6 square
miles. The Texas Parks and Wildlife Department does not have the legal authority
to trepass on private property to collect deer. Some landowners are cooperative.
Some are not. Franklin State Park is at the very tip of Texas, and deer from the
park have been tested (all negative). One of the single largest land owners
along the border is the National Park Service. Deer and elk from the Guadalupe
Peak National Park cannot be collected with federal permission. The sampling
throughout the state is based on the deer populations by eco-region and is
dictated by the availability of funds. I am concerned about your insinuation
that CWD is a human health risk. We are at a stand-off - you have no proof that
it is and I have no definitive proof that it isn't. However I would say that the
inferred evidence from Colorado, Wyoming and Wisconsin suggests that CWD is not
a human health concern (i.e. no evidence of an increased incidence of human
brain disorders within the CWD "endemic" areas of these states). From my
professional interactions with the Texas Parks and Wildlife Department, I can
definitely say that they want to do a thorough and sound survey throughout the
state, not willy-nilly "look here, look there". There are limitations of
manpower, finances and, in some places, deer populations. I would congratulate
TPWD for doing the best job with the limitations at hand rather than trying to
browbeat them when you obviously do not understand the ecology of West Texas.
Thank you for your consideration.
======================
From: TSS (216-119-139-126.ipset19.wt.net)
Subject: Re: CWD SAMPLING TEXAS (but NOT in the obvious place, the NM,
TEXAS border)
Date: December 16, 2003 at 11:03 am PST
In Reply to: Re: CWD SAMPLING TEXAS (but NOT in the obvious place, the NM,
TEXAS border) posted by Ken Waldrup, DVM, PhD on December 15, 2003 at 3:43 pm:
HEllo Dr. Waldrup,
thank you for your comments and time to come to this board.
Ken Waldrup, DVM, PhD states;
> it is painfully obvious that you do not know or understand the natural
distribution of mule deer out there or the rights of the land owners in this
state...
TSS states;
I am concerned about all deer/elk not just mule deer, and the rights of
land owners (in the case with human/animal TSEs) well i am not sure of the
correct terminology, but when the States deer/elk/cattle/sheep/humans are at
risk, there should be no rights for land owners in this case. the state should
have the right to test those animals. there are too many folks out there that
are just plain ignorant about this agent. with an agent such as this, you cannot
let landowners (and i am one) dictate human/animal health, especially when you
cannot regulate the movement of such animals...
Ken Waldrup, DVM, PhD states;
> Deer and elk from the Guadalupe Peak National Park cannot be collected
with federal permission.
TSS states;
I do not understand this? so there is no recourse of action even if every
deer/elk was contaminated with CWD in this area (hypothetical)?
Ken Waldrup, DVM, PhD states;
> I am concerned about your insinuation that CWD is a human health risk.
We are at a stand-off - you have no proof that it is and I have no definitive
proof that it isn't. However I would say that the inferred evidence from
Colorado, Wyoming and Wisconsin suggests that CWD is not a human health concern
(i.e. no evidence of an increased incidence of human brain disorders within the
CWD "endemic" areas of these states)...
TSS states;
NEXT, let's have a look at the overall distribution of CWD in Free-Ranging
Cervids and see where the CWD cluster in NM WSMR borders TEXAS;
Current Distribution of Chronic Wasting Disease in Free-Ranging Cervids
NOW, the MAP of the Exoregion where the samples were taken to test for CWD;
CWD SURVEILLANCE SAMPLE SUBMISSIONS TEXAS
Ecoregions of TEXAS
IF you look at the area around the NM WSMR where the CWD cluster was and
where it borders TEXAS, that ecoregion is called Trans Pecos region. Seems if my
Geography and my Ciphering is correct ;-) that region only tested 55% of it's
goal. THE most important area on the MAP and they only test some 96 samples,
this in an area that has found some 7 positive animals? NOW if we look at the
only other border where these deer from NM could cross the border into TEXAS,
this area is called the High Plains ecoregion, and again, we find that the
sampling for CWD was pathetic. HERE we find that only 9% of it's goal of CWD
sampling was met, only 16 samples were tested from some 175 that were suppose to
be sampled.
AS i said before;
> SADLY, they have not tested enough from the total population to
> know if CWD is in Texas or not.
BUT now, I will go one step further and state categorically that they are
not trying to find it. just the opposite it seems, they are waiting for CWD to
find them, as with BSE/TSE in cattle, and it will eventually...
snip...end...TSS
===============================
2005
SEE MAP OF CWD ON THE BORDER OF NEW MEXICO VERY CLOSE TO TEXAS ;
NO update on CWD testing in Texas, New Mexico that i could find. I have
inquired about it though, no reply yet...
-------- Original Message --------
Subject: CWD testing to date TEXAS ?
Date: Mon, 09 May 2005 12:26:20 –0500
From: "Terry S. Singeltary Sr."
To: kristen.everett@tpwd.state.tx.us
Hello Mrs. Everett,
I am most curious about the current status on CWD testing in Texas. could
you please tell me what the current and past testing figures are to date and
what geographical locations these tests have been in. good bust on the illegal
deer trapping case. keep up the good work there.........
thank you, with kindest regards,
Terry S. Singeltary Sr. P.O. Box 42 Bacliff, Texas USA 77518
-------- Original Message --------
Subject: CWD testing in New Mexico
Date: Mon, 09 May 2005 14:39:18 –0500
From: "Terry S. Singeltary Sr."
To: ispa@state.nm.us
Greetings,
I am most curious of the current and past CWD testing in New Mexico, and
there geographical locations...
thank you,
Terry S. Singeltary SR. CJD Watch
#################### https://lists.aegee.org/bse-l.html
####################
2006
----- Original Message -----
From: "Terry S. Singeltary Sr." flounder9@VERIZON.NET
To: BSE-L@aegee.org
Sent: Saturday, December 23, 2006 1:47 PM
Subject: CWD in New Mexico 35 MILES FROM TEXAS BORDER and low testing
sampling figures -- what gives TAHC ???
Subject: CWD in New Mexico 35 MILES FROM TEXAS BORDER and low testing
sampling figures -- what gives TAHC ???
Date: December 23, 2006 at 11:25 am PST
Greetings BSE-L members,
i never know if i am going crazy or just more of the same BSe. several
years ago i brought up the fact to the TAHC that CWD was literally at the Texas
borders and that the sample size for cwd testing was no where near enough in the
location of that zone bordering NM. well, i just wrote them another letter
questioning this again on Dec. 14, 2006 (see below) and showed them two
different pdf maps, one referencing this url, which both worked just fine then.
since then, i have NOT received a letter from them answering my question, and
the url for the map i used as reference is no longer working? i had reference
this map several times from the hunter-kill cwd sampling as of 31 August 2005
pdf which NO longer works now??? but here are those figures for that zone
bordering NM, for those that were questioning the url. the testing samples
elsewhere across Texas where much much more than that figure in the zone
bordering NM where CWD has been documented bordering TEXAS, near the White Sands
Missile Range. SO, why was the Texas hunter-kill cwd sampling as of 31 August
2005 document removed from the internet??? you know, this reminds me of the
infamous TEXAS MAD COW that i documented some 7 or 8 months before USDA et al
documented it, when the TAHC accidentally started ramping up for the
announcement on there web site, then removed it (see history at bottom). i am
not screaming conspiracy here, but confusious is confused again on the ciphering
there using for geographical distribution of cwd tissue sample size survey, IF
they are serious about finding CWD in TEXAS. common sense would tell you if cwd
is 35 miles from the border, you would not run across state and have your larger
samples there, and least samples 35 miles from where is what
found..........daaa..........TSS
THEN NOTICE CWD sample along that border in TEXAS, Three Year Summary of
Hunter-Kill CWD sampling as of 31 August 2005 of only 191 samples, then compare
to the other sample locations ;
TPWD has been conducting surveys of hunter-kill animals since 2002 and has
collected more than 7300 samples (as of 31 August 2005). In total, there have
been over 9400 samples, both hunter-kill and private samples, tested in Texas to
date, and no positives have been found.
SO, out of a total of 9,400 samples taken for CWD surveillance in TEXAS
since 2002 of both hunter-kill and private kill, ONLY 191 samples have been
taken in the most likely place one would find CWD i.e. the border where CWD has
been documented at TEXAS and New Mexico
latest map NM cwd old data
CWD in New Mexico ;
What is the Department doing to prevent the spread of CWD?
Chronic wasting disease (CWD) was recently detected in a mule deer from
Unit 34. Until 2005, CWD had only been found in Unit 19. With this discovery,
the Department will increase its surveillance of deer and elk harvested in Units
29, 30 and 34.
Lymph nodes and/or brain stems from every harvested deer and brain stems
from all elk taken in Unit 34 will be sampled.
snip...
CWD SURVEILLANCE TEXAS
SNIP...SEE FULL TEXT ;
2011 – 2012
Friday, October 28, 2011
CWD Herd Monitoring Program to be Enforced Jan. 2012 TEXAS
Greetings TAHC et al,
A kind greetings from Bacliff, Texas.
In reply to ;
Texas Animal Health Commission (TAHC) Announcement October 27, 2011
I kindly submit the following ;
***for anyone interested, here is some history of CWD along the Texas, New
Mexico border, and my attempt to keep up with it...terry
snip...
see history CWD Texas, New Mexico Border ;
Monday, March 26, 2012
3 CASES OF CWD FOUND NEW MEXICO MULE DEER SEVERAL MILES FROM TEXAS BORDER
Sunday, October 04, 2009
CWD NEW MEXICO SPREADING SOUTH TO TEXAS 2009 2009 Summary of Chronic
Wasting Disease in New Mexico New Mexico Department of Game and Fish
*****2015-2016***
Tuesday, April 19, 2016
Texas Deer-breeder drops suit against state over Chronic Wasting Disease
CWD disease tactics
Wednesday, April 20, 2016
TVMDL hosts legislative representatives, discusses CWD
I could go on, for more see ;
Thursday, March 31, 2016
*** Chronic Wasting Disease CWD TSE Prion Roundup USA 2016 ***
Saturday, April 9, 2016
The Norwegian Veterinary Institute (NVI, 2016) has reported a case of prion
disease Cervid Spongiform Encephalopathy detected in free ranging wild reindeer
(Rangifer tarandus tarandus)
Department for Environment, Food and Rural Affairs
Monday, May 09, 2016
A comparison of classical and H-type bovine spongiform encephalopathy
associated with E211K prion protein polymorphism in wild type and EK211 cattle
following intracranial inoculation
Thursday, October 22, 2015
*** Former Ag Secretary Ann Veneman talks women in agriculture and we talk
mad cow disease USDA and what really happened ***
Terry S. Singeltary Sr.
posted by Terry S. Singeltary Sr. at
10:07 PM
0 Comments:
Post a Comment
Subscribe to Post Comments [Atom]
<< Home