Pennsylvania Confirms First Case CWD Adams County Captive Deer Tests Positive
News for Immediate Release
Oct. 11, 2012
First Case of Chronic Wasting Disease Found in Pennsylvania Deer
Adams County Captive Deer Tests Positive;
No Evidence of Effect on Humans Harrisburg – The Pennsylvania Department of
Agriculture today confirmed the first positive case of Chronic Wasting Disease
(CWD) in the state on a deer farm in Adams County.
The disease is fatal in deer, elk and moose, but there is no evidence that
CWD can be transmitted to humans, according to the Centers for Disease Control
and Prevention and The World Health Organization.
The positive sample was taken from a white-tailed deer at 1491 New Chester
Rd., New Oxford, and tested as part of Pennsylvania’s intensive CWD monitoring
efforts. The sample tissue was tested at the Pennsylvania Veterinary Laboratory
in Harrisburg and verified at the National Veterinary Services Laboratory in
Ames, Iowa.
In addition to the Adams County location, the department has quarantined
two farms directly associated with the positive deer at 6464 Jacks Hollow Rd.,
Williamsport, Lycoming County, and 61 Pickett Rd., Dover, York County. The
quarantine prevents movement of animals on and off the premises.
“Pennsylvania has an aggressive Chronic Wasting Disease surveillance
program and a strong response plan,” said Agriculture Secretary George Greig.
“Steps are being taken to prevent further spread of this disease to the state’s
captive and wild deer populations.”
An interagency CWD task force is in place to address the threat of the
disease to Pennsylvania’s captive and wild deer, elk and moose populations. The
task force includes representatives of the departments of Agriculture,
Environmental Protection and Health, the Pennsylvania Game Commission and the
U.S. Department of Agriculture.
The task force will carry out the response plan, which includes education
and outreach with public meetings and minimizing risk factors through continued
surveillance, testing and management.
“To date CWD has not been found in Pennsylvania’s wild deer population,”
said Pennsylvania Game Commission Executive Director Carl G. Roe. ”Concerns over
CWD should not prevent anyone from enjoying deer hunting and consuming meat from
healthy animals.”
Roe said that hunters should shoot only healthy-appearing animals, and take
precautions like wearing rubber gloves when field-dressing their deer and wash
thoroughly when finished.
“Though no human disease has been associated with CWD, the Centers for
Disease Control and Prevention recommends people or other animals do not eat any
part of an animal diagnosed with or showing signs of CWD,” said Acting Health
Secretary Michael Wolf.
CWD attacks the brains of infected deer, elk and moose, producing small
lesions that eventually result in death. It is transmitted by direct
animal-to-animal contact through saliva, feces and urine.
Signs of the disease include weight loss, excessive salivation, increased
drinking and urination, and abnormal behavior like stumbling, trembling and
depression. Infected deer and elk may also allow unusually close approach by
humans or natural predators. The disease is fatal and there is no known
treatment or vaccine. CWD was first discovered in Colorado captive mule deer in
1967, and has since been detected in 22 states and Canadian provinces, including
Pennsylvania’s neighboring states of New York, West Virginia and Maryland.
Pennsylvania is the 23rd state to find CWD in either a captive or wild
population of deer and the 13th state to have it only in a captive deer
herd.
Surveillance for CWD has been ongoing in Pennsylvania since 1998. The
agriculture department coordinates a mandatory CWD monitoring program for more
than 23,000 captive deer on 1,100 breeding farms, hobby farms and shooting
preserves. In addition, the Game Commission collects samples from
hunter-harvested deer and elk and those that appear sick or behave abnormally.
Since 1998, the commission has tested more than 38,000 free-ranging deer and elk
for CWD and all have tested negative.
For more information from the departments of Agriculture and Health and the
Pennsylvania Game Commission, visit:
· www.agriculture.state.pa.us (click on the “Chronic Wasting Disease
Information” button on the homepage),
· www.pgc.state.pa.us (click on “CWD Info”), and
· www.health.state.pa.us (click on “Diseases and Conditions”)
Media contacts:
Samantha Elliott Krepps, Agriculture, 717-787-5085
Aimee Tysarczyk, Health, 717-787-1783
Jerry Feaser, PGC, 717-705-6541
###
Pennsylvania Game Commission CWD
PENNSYLVANIA CWD RESPONSE PLAN JULY 2011 (BOTTOM OF PAGE)
NEWS RELEASES
WHITE-TAILED DEER http://www.portal.state.pa.us/portal/server.pt/community/deer/11949
FIELD REPORTS
==========================================================
2012 POTENTIAL FOR CWD TO HUMANS
Envt.06:
Zoonotic Potential of CWD: Experimental Transmissions to Non-Human Primates
Emmanuel Comoy,1,† Valérie Durand,1 Evelyne Correia,1 Aru Balachandran,2
Jürgen Richt,3 Vincent Beringue,4 Juan-Maria Torres,5 Paul Brown,1 Bob Hills6
and Jean-Philippe Deslys1
1Atomic Energy Commission; Fontenay-aux-Roses, France; 2Canadian Food
Inspection Agency; Ottawa, ON Canada; 3Kansas State University; Manhattan, KS
USA; 4INRA; Jouy-en-Josas, France; 5INIA; Madrid, Spain; 6Health Canada; Ottawa,
ON Canada
†Presenting author; Email: emmanuel.comoy@cea.fr
The constant increase of chronic wasting disease (CWD) incidence in North
America raises a question about their zoonotic potential. A recent publication
showed their transmissibility to new-world monkeys, but no transmission to
old-world monkeys, which are phylogenetically closer to humans, has so far been
reported. Moreover, several studies have failed to transmit CWD to transgenic
mice overexpressing human PrP. Bovine spongiform encephalopathy (BSE) is the
only animal prion disease for which a zoonotic potential has been proven. We
described the transmission of the atypical BSE-L strain of BSE to cynomolgus
monkeys, suggesting a weak cattle-to-primate species barrier. We observed the
same phenomenon with a cattleadapted strain of TME (Transmissible Mink
Encephalopathy). Since cattle experimentally exposed to CWD strains have also
developed spongiform encephalopathies, we inoculated brain tissue from
CWD-infected cattle to three cynomolgus macaques as well as to transgenic mice
overexpressing bovine or human PrP. Since CWD prion strains are highly
lymphotropic, suggesting an adaptation of these agents after peripheral
exposure, a parallel set of four monkeys was inoculated with CWD-infected cervid
brains using the oral route. Nearly four years post-exposure, monkeys exposed to
CWD-related prion strains remain asymptomatic. In contrast, bovinized and
humanized transgenic mice showed signs of infection, suggesting that CWD-related
prion strains may be capable of crossing the cattle-to-primate species barrier.
Comparisons with transmission results and incubation periods obtained after
exposure to other cattle prion strains (c-BSE, BSE-L, BSE-H and cattle-adapted
TME) will also be presented, in order to evaluate the respective risks of each
strain.
Envt.07:
Pathological Prion Protein (PrPTSE) in Skeletal Muscles of Farmed and Free
Ranging White-Tailed Deer Infected with Chronic Wasting Disease
Martin L. Daus,1,† Johanna Breyer,2 Katjs Wagenfuehr,1 Wiebke Wemheuer,2
Achim Thomzig,1 Walter Schulz-Schaeffer2 and Michael Beekes1 1Robert Koch
Institut; P24 TSE; Berlin, Germany; 2Department of Neuropathology, Prion and
Dementia Research Unit, University Medical Center Göttingen; Göttingen, Germany
†Presenting author; Email: dausm@rki.de
Chronic wasting disease (CWD) is a contagious, rapidly spreading
transmissible spongiform encephalopathy (TSE) occurring in cervids in North
America. Despite efficient horizontal transmission of CWD among cervids natural
transmission of the disease to other species has not yet been observed. Here, we
report a direct biochemical demonstration of pathological prion protein PrPTSE
and of PrPTSE-associated seeding activity in skeletal muscles of CWD-infected
cervids. The presence of PrPTSE was detected by Western- and postfixed frozen
tissue blotting, while the seeding activity of PrPTSE was revealed by protein
misfolding cyclic amplification (PMCA). The concentration of PrPTSE in skeletal
muscles of CWD-infected WTD was estimated to be approximately 2000- to
10000-fold lower than in brain tissue. Tissue-blot-analyses revealed that PrPTSE
was located in muscle- associated nerve fascicles but not, in detectable
amounts, in myocytes. 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.
PLUS, THE CDC DID NOT PUT THIS WARNING OUT FOR THE WELL BEING OF THE DEER
AND ELK ;
Thursday, May 26, 2011
Travel History, Hunting, and Venison Consumption Related to Prion Disease
Exposure, 2006-2007 FoodNet Population Survey
Journal of the American Dietetic Association Volume 111, Issue 6 , Pages
858-863, June 2011.
NOR IS THE FDA recalling this CWD positive elk meat for the well being of
the dead elk ;
Wednesday, March 18, 2009
Noah's Ark Holding, LLC, Dawson, MN RECALL Elk products contain meat
derived from an elk confirmed to have CWD NV, CA, TX, CO, NY, UT, FL, OK RECALLS
AND FIELD CORRECTIONS: FOODS CLASS II
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 ;
CWD ongoing experiment on humans, long term $$$
Monday, November 14, 2011
WYOMING Creutzfeldt Jakob Disease, CWD, TSE, PRION REPORTING 2011
Wednesday, November 16, 2011
Wisconsin Creutzfeldt Jakob Disease, CWD, TSE, PRION REPORTING 2011
Sunday, November 13, 2011
COLORADO CWD CJD TSE PRION REPORTING 2011
UPDATED CORRESPONDENCE FROM AUTHORS OF THIS STUDY I.E. COLBY, PRUSINER ET
AL, ABOUT MY CONCERNS OF THE DISCREPANCY BETWEEN THEIR FIGURES AND MY FIGURES OF
THE STUDIES ON CWD TRANSMISSION TO CATTLE ;
CWD to cattle figures CORRECTION
Greetings,
I believe the statement and quote below is incorrect ;
"CWD has been transmitted to cattle after intracerebral inoculation,
although the infection rate was low (4 of 13 animals [Hamir et al. 2001]). This
finding raised concerns that CWD prions might be transmitted to cattle grazing
in contaminated pastures."
Please see ;
Within 26 months post inoculation, 12 inoculated animals had lost weight,
revealed abnormal clinical signs, and were euthanatized. Laboratory tests
revealed the presence of a unique pattern of the disease agent in tissues of
these animals. These findings demonstrate that when CWD is directly inoculated
into the brain of cattle, 86% of inoculated cattle develop clinical signs of the
disease.
" although the infection rate was low (4 of 13 animals [Hamir et al.
2001]). "
shouldn't this be corrected, 86% is NOT a low rate. ...
kindest regards,
Terry S. Singeltary Sr. P.O. Box 42 Bacliff, Texas USA 77518
Thank you!
Thanks so much for your updates/comments. We intend to publish as rapidly
as possible all updates/comments that contribute substantially to the topic
under discussion.
re-Prions David W. Colby1,* and Stanley B. Prusiner1,2 + Author
Affiliations
1Institute for Neurodegenerative Diseases, University of California, San
Francisco, San Francisco, California 94143 2Department of Neurology, University
of California, San Francisco, San Francisco, California 94143 Correspondence: stanley@ind.ucsf.edu
Mule deer, white-tailed deer, and elk have been reported to develop CWD. As
the only prion disease identified in free-ranging animals, CWD appears to be far
more communicable than other forms of prion disease. CWD was first described in
1967 and was reported to be a spongiform encephalopathy in 1978 on the basis of
histopathology of the brain. Originally detected in the American West, CWD has
spread across much of North America and has been reported also in South Korea.
In captive populations, up to 90% of mule deer have been reported to be positive
for prions (Williams and Young 1980). The incidence of CWD in cervids living in
the wild has been estimated to be as high as 15% (Miller et al. 2000). The
development of transgenic (Tg) mice expressing cervid PrP, and thus susceptible
to CWD, has enhanced detection of CWD and the estimation of prion titers
(Browning et al. 2004; Tamgüney et al. 2006). Shedding of prions in the feces,
even in presymptomatic deer, has been identified as a likely source of infection
for these grazing animals (Williams and Miller 2002; Tamgüney et al. 2009b). CWD
has been transmitted to cattle after intracerebral inoculation, although the
infection rate was low (4 of 13 animals [Hamir et al. 2001]). This finding
raised concerns that CWD prions might be transmitted to cattle grazing in
contaminated pastures.
snip...
----- Original Message -----
From: David Colby To: flounder9@verizon.net
Cc: stanley@XXXXXXXX
Sent: Tuesday, March 01, 2011 8:25 AM
Subject: Re: FW: re-Prions David W. Colby1,* and Stanley B. Prusiner1,2 +
Author Affiliations
Dear Terry Singeltary,
Thank you for your correspondence regarding the review article Stanley
Prusiner and I recently wrote for Cold Spring Harbor Perspectives. Dr. Prusiner
asked that I reply to your message due to his busy schedule. We agree that the
transmission of CWD prions to beef livestock would be a troubling development
and assessing that risk is important. In our article, we cite a peer-reviewed
publication reporting confirmed cases of laboratory transmission based on
stringent criteria. The less stringent criteria for transmission described in
the abstract you refer to lead to the discrepancy between your numbers and ours
and thus the interpretation of the transmission rate. We stand by our assessment
of the literature--namely that the transmission rate of CWD to bovines appears
relatively low, but we recognize that even a low transmission rate could have
important implications for public health and we thank you for bringing attention
to this matter. Warm Regards, David Colby -- David Colby, PhDAssistant Professor
Department of Chemical Engineering University of Delaware
===========END...TSS==============
SNIP...SEE FULL TEXT ;
UPDATED DATA ON 2ND CWD STRAIN Wednesday, September 08, 2010 CWD PRION
CONGRESS SEPTEMBER 8-11 2010
Sunday, August 19, 2012
Susceptibility of cattle to the agent of chronic wasting disease from elk
after intracranial inoculation 2012
Research Project: TRANSMISSION, DIFFERENTIATION, AND PATHOBIOLOGY OF
TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES Location: Virus and Prion Research
Unit
PO-081: Chronic wasting disease in the cat— Similarities to feline
spongiform encephalopathy (FSE)
PO-081: Chronic wasting disease in the cat— Similarities to feline
spongiform encephalopathy (FSE)
Thursday, May 31, 2012
CHRONIC WASTING DISEASE CWD PRION2012 Aerosol, Inhalation transmission,
Scrapie, cats, species barrier, burial, and more
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
Justin Greenlee, Jodi Smith, Eric Nicholson US Dept. Agriculture;
Agricultural Research Service, National Animal Disease Center; Ames, IA USA
Interspecies transmission studies afford the opportunity to better
understand the potential host range and origins of prion diseases. The purpose
of these experiments was to determine susceptibility of white-tailed deer (WTD)
to scrapie and to compare the resultant clinical signs, lesions, and molecular
profiles of PrPSc to those of chronic wasting disease (CWD). We inoculated WTD
intracranially (IC; n = 5) and by a natural route of exposure (concurrent oral
and intranasal (IN); n = 5) with a US scrapie isolate.
All deer were inoculated with a 10% (wt/vol) brain homogenate from sheep
with scrapie (1ml IC, 1 ml IN, 30 ml oral). All deer inoculated by the
intracranial route had evidence of PrPSc accumulation. PrPSc was detected in
lymphoid tissues as early as 7 months-post-inoculation (PI) and a single deer
that was necropsied at 15.6 months had widespread distribution of PrPSc
highlighting that PrPSc is widely distributed in the CNS and lymphoid tissues
prior to the onset of clinical signs. IC inoculated deer necropsied after 20
months PI (3/5) had clinical signs, spongiform encephalopathy, and widespread
distribution of PrPSc in neural and lymphoid tissues.
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.
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.
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 ;
*** Spraker suggested an interesting explanation for the occurrence of CWD.
The deer pens at the Foot Hills Campus were built some 30-40 years ago by a Dr.
Bob Davis. At or abut that time, allegedly, some scrapie work was conducted at
this site. When deer were introduced to the pens they occupied ground that had
previously been occupied by sheep.
(PLEASE NOTE SOME OF THESE OLD UK GOVERNMENT FILE URLS ARE SLOW TO OPEN,
AND SOMETIMES YOU MAY HAVE TO CLICK ON MULTIPLE TIMES, PLEASE BE PATIENT, ANY
PROBLEMS PLEASE WRITE ME PRIVATELY, AND I WILL TRY AND FIX OR SEND YOU OLD PDF
FILE...TSS)
Wednesday, February 16, 2011
IN CONFIDENCE
SCRAPIE TRANSMISSION TO CHIMPANZEES
IN CONFIDENCE
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 ;
Volume 18, Number 3—March 2012
Samuel E. Saunders1, Shannon L. Bartelt-Hunt, and Jason C. Bartz
Author affiliations: University of Nebraska-Lincoln, Omaha, Nebraska, USA
(S.E. Saunders, S.L. Bartelt-Hunt); Creighton University, Omaha (J.C. Bartz)
Synopsis
Occurrence, Transmission, and Zoonotic Potential of Chronic Wasting Disease
snip...
Most epidemiologic studies and experimental work have suggested that the
potential for CWD transmission to humans is low, and such transmission has not
been documented through ongoing surveillance (2,3). In vitro prion replication
assays report a relatively low efficiency of CWD PrPSc-directed conversion of
human PrPc to PrPSc (30), and transgenic mice overexpressing human PrPc are
resistant to CWD infection (31); these findings indicate low zoonotic potential.
However, squirrel monkeys are susceptible to CWD by intracerebral and oral
inoculation (32). Cynomolgus macaques, which are evolutionarily closer to humans
than squirrel monkeys, are resistant to CWD infection (32). Regardless, the
finding that a primate is orally susceptible to CWD is of concern...
snip...
Reasons for Caution There are several reasons for caution with respect to
zoonotic and interspecies CWD transmission. First, there is strong evidence that
distinct CWD strains exist (36). Prion strains are distinguished by varied
incubation periods, clinical symptoms, PrPSc conformations, and CNS PrPSc
depositions (3,32). Strains have been identified in other natural prion
diseases, including scrapie, BSE, and CJD (3). Intraspecies and interspecies
transmission of prions from CWD-positive deer and elk isolates resulted in
identification of >2 strains of CWD in rodent models (36), indicating that
CWD strains likely exist in cervids. However, nothing is currently known about
natural distribution and prevalence of CWD strains. Currently, host range and
pathogenicity vary with prion strain (28,37). Therefore, zoonotic potential of
CWD may also vary with CWD strain. In addition, diversity in host (cervid) and
target (e.g., human) genotypes further complicates definitive findings of
zoonotic and interspecies transmission potentials of CWD.
Intraspecies and interspecies passage of the CWD agent may also increase
the risk for zoonotic CWD transmission. The CWD prion agent is undergoing serial
passage naturally as the disease continues to emerge. In vitro and in vivo
intraspecies transmission of the CWD agent yields PrPSc with an increased
capacity to convert human PrPc to PrPSc (30). Interspecies prion transmission
can alter CWD host range (38) and yield multiple novel prion strains (3,28). The
potential for interspecies CWD transmission (by cohabitating mammals) will only
increase as the disease spreads and CWD prions continue to be shed into the
environment. This environmental passage itself may alter CWD prions or exert
selective pressures on CWD strain mixtures by interactions with soil, which are
known to vary with prion strain (25), or exposure to environmental or gut
degradation.
Given that prion disease in humans can be difficult to diagnose and the
asymptomatic incubation period can last decades, continued research,
epidemiologic surveillance, and caution in handling risky material remain
prudent as CWD continues to spread and the opportunity for interspecies
transmission increases. Otherwise, similar to what occurred in the United
Kingdom after detection of variant CJD and its subsequent link to BSE, years of
prevention could be lost if zoonotic transmission of CWD is subsequently
identified,...
snip...
Sunday, January 22, 2012
Chronic Wasting Disease CWD cervids interspecies transmission
Saturday, September 01, 2012
Resistance of Soil-Bound Prions to Rumen Digestion
Friday, July 20, 2012
CWD found for first time in Iowa at hunting preserve
Wednesday, September 05, 2012
Additional Facility in Pottawatamie County Iowa Under Quarantine for CWD
after 5 deer test positive
meanwhile, Texas is still floundering after two recent CWD confirmations,
and a decade of CWD waltzing across it’s borders. what’s another decade, right
$$$
Friday, September 07, 2012
Texas Wildlife Officials Considering New Deer Movement Rules in Response to
CWD
Wednesday, October 03, 2012
TAHC Chronic Wasting Disease Rule What you need to know
Monday, September 17, 2012
Rapid Transepithelial Transport of Prions Following Inhalation
Friday, September 21, 2012
Chronic Wasting Disease CWD raises concerns about deer farms in Iowa
Friday, September 28, 2012
Stray elk renews concerns about deer farm security Minnesota
Friday, August 24, 2012
Diagnostic accuracy of rectal mucosa biopsy testing for chronic wasting
disease within white-tailed deer (Odocoileus virginianus) herds in North America
Friday, August 31, 2012
COMMITTEE ON CAPTIVE WILDLIFE AND ALTERNATIVE LIVESTOCK and CWD 2009-2012 a
review
Wednesday, June 01, 2011
Management of CWD in Canada: Past Practices, Current Conditions, Current
Science, Future Risks and Options
Thursday, June 09, 2011
Detection of CWD prions in salivary, urinary, and intestinal tissues of
deer: potential mechanisms of prion shedding and transmission
Thursday, February 17, 2011
Environmental Sources of Scrapie Prions
CWD, GAME FARMS, BAITING, AND POLITICS
Saturday, October 6, 2012
TRANSMISSION, DIFFERENTIATION, AND PATHOBIOLOGY OF TRANSMISSIBLE SPONGIFORM
ENCEPHALOPATHIES 2011 Annual Report
2005 huntingpa http://www.huntingpa.com/
BANS/CENSORS Terry Singeltary for speaking about Chronic Wasting Disease CWD.
...
Original Message -----
From: Terry S. Singeltary Sr.
To: xxxxxxxxxxx
Cc: xxxxxxxxxxxx
Sent: Tuesday, December 20, 2005 1:37 PM
Subject: CWD PA BOARDS TSS BAN ???
hello samuel,
i see you deleted my postings as being bogus about cwd? odd, the news i
first posted was from your own agency. most are glad to get the data, and
welcome my postings. you are the only state to do this in my 8 years of
investigating this nightmare. please advise.....
since i was not suppose to post about cwd on the
Pennsylvania Game Commission board re ;
Welcome Terry S. Singeltary Sr.. [Logout] My Home · Main Index · Search ·
Active Topics
Who's Online · FAQ · User List · Calendar
CWD Postings.
From: Samuel
Terry,
I have to request that you discontinue from posting information on CWD. I
have received concerns from individuals on the validity of your information.
Since I am not educated on the subject, I cannot validate that the information
is correct and or factual. As time moves on, this subject will become quite a
"touchy subject" and any information, factual or not, will be scrutinized. From
now on, we will have to rely on the PGC to educate the residents here in PA on
the subject.
Thank you for your concern in this matter and keeping a close vigil on the
topic.
Samuel
=============
i decided to go to the
General Hunting Forum
when i posted there, my postings went to the PA Game Comm board??? am i not
allowed to post there? it is a public forum is it not? i am not posting any
abusing postings, cursing, just facts. i am confused sir? could someone please
explain?
thank you,
kind regards, terry
=========================================
2012
From: Terry S. Singeltary Sr. Sent:
Wednesday, January 11, 2012 4:37 PM
To: admin@huntingpa.com Cc: info@pfsc.org ; editor@pfsc.org ;
editor@pfsc.org ; ben@pfsc.org ; brody243@optonline.net ;
lowell.graybill@binkleyhurst.com ; lejlmarsh@msn.com ; tonufrak@uplink.net ;
operations@huntingpa.com ; admin@huntingpa.com ; pgccomments@pa.gov ; calvin.dubrock@pa.gov
Subject: Pennsylvania HUNTINGPA PERMANENT BAN TSS FOR SPEAKING ABOUT CWD
2005 UPDATE 2012
Greetings HUNTINGPA et al,
I thought since you banned me from speaking about Chronic Wasting Disease
way back in 2005, for no reason at all, and the fact CWD is nipping at your
borders now, if not there already, NOT to mention the fact that Pennsylvania is
one of the latest states to document a case of ATYPICAL NOR-98 SCRAPIE. I was
wondering how you plan on handling CWD, and the ramifications from not letting
anyone speak about it, what do you plan on doing about it once you document it,
IF you test enough ???
yep, Pennsylvania is now the only state in the USA that has me banned from
speaking about CWD. congratulations! a permanent ban at that, just for trying to
warn you years ago.
I don’t expect an answer, but I thought I should update you (especially
Samuel), since he thought I did not know what I was talking about. but some
friendly advice, secrecy, cover-ups, lies, and deceit, will get you no where.
what it will get you is a backyard full of prions. let the hunters and others
speak about it. or not, and Good luck with that. ...
yep, I am still disgusted,
terry
Original Message -----
From: Terry S. Singeltary Sr.
To: xxxxxxxxxxx
Cc: xxxxxxxxxxxx
Sent: Tuesday, December 20, 2005 1:37 PM
Subject: CWD PA BOARDS TSS BAN ???
hello samuel,
i see you deleted my postings as being bogus about cwd? odd, the news i
first posted was from your own agency. most are glad to get the data, and
welcome my postings. you are the only state to do this in my 8 years of
investigating this nightmare. please advise.....
since i was not suppose to post about cwd on the
Pennsylvania Game Commission board re ;
Welcome Terry S. Singeltary Sr.. [Logout] My Home · Main Index · Search ·
Active Topics
Who's Online · FAQ · User List · Calendar
CWD Postings.
From: Samuel
Terry,
I have to request that you discontinue from posting information on CWD. I
have received concerns from individuals on the validity of your information.
Since I am not educated on the subject, I cannot validate that the information
is correct and or factual. As time moves on, this subject will become quite a
"touchy subject" and any information, factual or not, will be scrutinized. From
now on, we will have to rely on the PGC to educate the residents here in PA on
the subject.
Thank you for your concern in this matter and keeping a close vigil on the
topic.
Samuel
=============
i decided to go to the
General Hunting Forum
when i posted there, my postings went to the PA Game Comm board??? am i not
allowed to post there? it is a public forum is it not? i am not posting any
abusing postings, cursing, just facts. i am confused sir? could someone please
explain?
thank you,
kind regards, terry
=========================================
Pennsylvania HUNTINGPA PERMANENT BAN TSS FOR SPEAKING ABOUT CWD 2005 UPDATE
2012
Pennsylvania Game Commission CWD
PENNSYLVANIA CWD RESPONSE PLAN JULY 2011 (BOTTOM OF PAGE)
NEWS RELEASES
WHITE-TAILED DEER
ELK
FIELD REPORTS
==========================================================
2011-2012 CWD TSE PRION UDATE USA
Thursday, June 2, 2011
USDA scrapie report for April 2011 NEW ATYPICAL NOR-98 SCRAPIE CASES
Pennsylvania AND California
posted by Terry S. Singeltary Sr. at
2:35 PM
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