Iowa DNR TO HOST NOV. 20 MEETING ON CHRONIC WASTING DISEASE FOR DAVIS AND WAPELLO COUNTY LANDOWNERS
Subject: DNR TO HOST NOV. 20 MEETING ON CHRONIC WASTING DISEASE FOR
DAVIS AND WAPELLO COUNTY LANDOWNERS
DNR TO HOST NOV. 20 MEETING ON CHRONIC WASTING DISEASE FOR DAVIS AND
WAPELLO COUNTY LANDOWNERS
MEDIA CONTACT: Kevin Baskins, DNR, at Kevin.Baskins@dnr.iowa.gov or
515-249-2814.
BLOOMFIELD —The Iowa Department of Natural Resources is holding a meeting
for landowners in Davis and Wapello counties to discuss chronic wasting disease
and the DNR’s plan to collect additional samples for testing during the upcoming
deer hunting season.
The meeting is November 20, at 6:30 p.m., at the Davis County Courthouse
Courtroom, 100 Courthouse Square, in Bloomfield. The DNR will give an overview
of chronic wasting disease, present its statewide testing plan for the 2012 deer
hunting season, and discuss proper sampling procedures and protocols.
Chronic wasting disease was confirmed in a Davis County hunting preserve
earlier this summer.
“We hope to have as many Davis and Wapello County landowners attend as
possible as they will be a vital component to our overall CWD containment plan,”
said Dr. Dale Garner, chief of the Iowa DNR’s Wildlife Bureau. “We need to
collect additional samples in the county and in the area surrounding the
facility to ascertain if anything is happening in the wild deer herd,” Garner
said.
The majority of samples are collected during the shotgun deer seasons from
hunters and the lockers where deer are processed.
Iowa has tested 42,557 wild deer and more than 4,000 captive deer and elk
as part of the surveillance program since 2002 when CWD was found in Wisconsin.
-30-
Greetings Iowa Hunters, legislators, et al,
I saw the meeting coming up, and thought I might update you a bit on some
of the CWD science and updates from other states. the recent studies, and
science there from are in the blogs (I don’t advertise as the science for human
and animal TSE prion disease should be free, and I made a promise).
human risk factors and species barrier towards the bottom.
please use as you wish, and good luck. ...
kind regards,
terry
Wednesday, October 17, 2012
Prion Remains Infectious after Passage through Digestive System of American
Crows (Corvus brachyrhynchos)
Game Farms, and risk there from CWD
Friday, October 26, 2012
CHRONIC WASTING DISEASE CWD PENNSYLVANIA GAME FARMS, URINE ATTRACTANT
PRODUCTS, BAITING, AND MINERAL LICKS
Thursday, November 01, 2012
ALABAMA BIG BUCK PROJECT, A CWD TSE PRION ACCIDENT WAITING TO HAPPEN
Saturday, September 01, 2012
Resistance of Soil-Bound Prions to Rumen Digestion
Friday, October 12, 2012
*** Texas Animal Health Commission (TAHC) is Now Accepting Comments on Rule
Proposals for “Chronic Wasting Disease (CWD)” ***
TO: comments@tahc.state.tx.us;
Texas Animal Health Commission (TAHC)
Saturday, July 07, 2012
TEXAS Animal Health Commission Accepting Comments on Chronic Wasting
Disease Rule Proposal
Considering the seemingly high CWD prevalence rate in the Sacramento and
Hueco Mountains of New Mexico, CWD may be well established in the population and
in the environment in Texas at this time.
Tuesday, July 10, 2012
Chronic Wasting Disease Detected in Far West Texas
Friday, June 01, 2012
TEXAS DEER CZAR TO WISCONSIN ASK TO EXPLAIN COMMENTS
Monday, March 26, 2012
Texas Prepares for Chronic Wasting Disease CWD Possibility in Far West
Texas
Thursday, November 01, 2012
PA GAME COMMISSION TO HOLD PUBLIC MEETING TO DISCUSS CWD Release #128-12
Thursday, October 11, 2012
Pennsylvania Confirms First Case CWD Adams County Captive Deer Tests
Positive
Monday, October 15, 2012
PENNSYLVANIA GAME COMMISSION AND AGRICULTURE DEPARTMENT TO HOLD PUBLIC
MEETING TO DISCUSS CWD MONITORING EFFORTS FOR IMMEDIATE RELEASE: October 15,
2012 Release #124-12
Pennsylvania CWD number of deer exposed and farms there from much greater
than first thought
Published: Wednesday, October 17, 2012, 10:44 PM Updated: Wednesday,
October 17, 2012, 11:33 PM
Tuesday, October 23, 2012
PA Captive deer from CWD-positive farm roaming free
Wednesday, October 24, 2012
WYOMING Deer Hunt Area 132 Near Green River Added to CWD List
Monday, October 08, 2012
VDGIF has discovered four positive cases of CWD in Virginia Updated
9/24/2012
Friday, September 28, 2012
Stray elk renews concerns about deer farm security Minnesota
Friday, September 21, 2012
Chronic Wasting Disease CWD raises concerns about deer farms in Iowa
Tuesday, September 11, 2012
Agreement Reached with Owner to De-Populate CWD Deer at Davis County
Hunting Preserve Iowa
Wednesday, September 05, 2012
Additional Facility in Pottawatamie County Iowa Under Quarantine for CWD
after 5 deer test positive
Friday, July 20, 2012
CWD found for first time in Iowa at hunting preserve
Generation of a new form of human PrPSc in vitro by inter-species
transmission from cervids prions
Marcelo A. Barria1, Glenn C. Telling2, Pierluigi Gambetti3, James A.
Mastrianni4 and Claudio Soto1,* 1Mitchell Center for Alzheimer’s disease and
related Brain disorders, Dept of Neurology, University of Texas Houston Medical
School, Houston, TX 77030, USA 2Dept of Microbiology, Immunology & Molecular
Genetics, and Neurology, Sanders Brown Center on Aging, University of Kentucky
Medical Center, Lexington, KY, USA 3Institute of Pathology, Case Western Reserve
University, Cleveland, OH, USA 4Dept of Neurology, University of Chicago,
Chicago, IL, USA. Running Title: Conversion of human PrPC by cervid PrPSc
Keywords: Prion / transmissible spongiform encephalopathy / infectivity /
misfolded prion protein / prion strains * To whom correspondence should be
addressed. University of Texas Houston Medical School, 6431 Fannin St, Houston,
TX 77030. Tel 713-5007086; Fax 713-5000667; E-mail Claudio.Soto@uth.tmc.edu The
latest version is at http://www.jbc.org/cgi/doi/10.1074/jbc.M110.198465
JBC Papers in Press.
Published on January 4, 2011 as Manuscript M110.198465 Copyright 2011 by
The American Society for Biochemistry and Molecular Biology, Inc. 5, Downloaded
from www.jbc.org by guest, on November 11, 2012 2
Prion diseases are infectious neurodegenerative disorders affecting humans
and animals that result from the conversion of normal prion protein (PrPC) into
the misfolded prion protein (PrPSc). Chronic wasting disease (CWD) is a prion
disorder of increasing prevalence within the United States that affects a large
population of wild and captive deer and elk. Determining the risk of
transmission of CWD to humans is of utmost importance, considering that people
can be infected by animal prions, resulting in new fatal diseases. To study the
possibility that human PrPC can be converted into the misfolded form by CWD
PrPSc we performed experiments using the Protein Misfolding Cyclic Amplification
(PMCA) technique, which mimic in vitro the process of prion replication. Our
results show that cervid PrPSc can induce the conversion of human PrPC, but only
after the CWD prion strain has been stabilized by successive passages in vitro
or in vivo. Interestingly, the newly generated human PrPSc exhibits a distinct
biochemical pattern that differs from any of the currently known forms of human
PrPSc. Our results also have profound implications for understanding the
mechanisms of prion species barrier and indicate that the transmission barrier
is a dynamic process that depend on the strain and moreover the degree of
adaptation of the strain. If our findings are corroborated by infectivity
assays, they will imply that CWD prions have the potential to infect humans, and
that this ability depends on CWD strain adaptation.
Various studies aimed to analyze the transmission of CWD to transgenic mice
expressing human PrP have consistently given negative results (9-11), indicating
a strong species barrier. This conclusion is consistent with our many failed
experiments to attempt converting human PrPC with natural CWD, even after
pushing the PMCA conditions (see figure 1). We found successful conversion only
after adaptation of the CWD prion strain by successive passages in vitro or in
cervid transgenic mice. We are not aware that in any of the transgenic mice
studies the inoculum used was a previously stabilized CWD strain. Although, it
has been shown that strain stabilization in vitro by PMCA (17;26) and in vivo
using experimental rodents (36) has similarities with the strain adaptation
process occurring in natural hosts, we cannot rule out that the type of CWD
strain adaptation that is required to produce strains transmissible to humans
may take much longer time in cervids or not occur at all. An important
experiment will be to study transmissibility to humanized transgenic mice of CWD
passed experimentally in deer several times. Besides the importance of our
results for public health in relation to the putative transmissibility of CWD to
humans, our data also illustrate a very important and novel scientific concept
related to the mechanism of prion transmission across species barriers. Today
the view is that species barrier is mostly controlled by the degree of
similarity on the sequence of the prion protein between the host and the
infectious material (4). In our study we show that the strain and moreover the
stabilization of the strain plays a major role in the inter-species
transmission. In our system there is no change on the protein sequence, but yet
strain adaptation results in a complete change on prion transmissibility with
potentially dramatic consequences. Therefore, our findings lead to a new view of
the species barrier that should not be seen as a static process, but rather a
dynamic biological phenomenon that can change over time when prion strains
mature and evolve. It remains to be investigated if other species barriers also
change upon progressive strain adaptation of other prion forms (e.g. the
sheep/human barrier).
Our results have far-reaching implications for human health, since they
indicate that cervid PrPSc can trigger the conversion of human PrPC into PrPSc,
suggesting that CWD might be infectious to humans. Interestingly our findings
suggest that unstable strains from CWD affected animals might not be a problem
for humans, but upon strain stabilization by successive passages in the wild,
this disease might become progressively more transmissible to man.
Generation of a New Form of Human PrPScin Vitro by Interspecies
Transmission from Cervid Prions*
Marcelo A. Barria‡, Glenn C. Telling§, Pierluigi Gambetti¶, James A.
Mastrianni‖ and Claudio Soto‡,1 + Author Affiliations
From the ‡Mitchell Center for Alzheimer's Disease and Related Brain
Disorders, Department of Neurology, University of Texas Medical School at
Houston, Houston, Texas 77030, the §Departments of Microbiology, Immunology, and
Molecular Genetics and Neurology, Sanders Brown Center on Aging, University
of Kentucky Medical Center, Lexington, Kentucky 40506, the ¶Institute of
Pathology, Case Western Reserve University, Cleveland, Ohio 44106, and the
‖Department of Neurology, The University of Chicago, Chicago, Illinois 60637 1
To whom correspondence should be addressed: University of Texas Medical School
at Houston, 6431 Fannin St., Houston, TX 77030. Tel.: 713-500-7086; Fax:
713-500-0667; E-mail: claudio.soto@uth.tmc.edu.
Abstract
Prion diseases are infectious neurodegenerative disorders that affect
humans and animals and that result from the conversion of normal prion protein
(PrPC) into the misfolded prion protein (PrPSc). Chronic wasting disease (CWD)
is a prion disorder of increasing prevalence within the United States that
affects a large population of wild and captive deer and elk. Determining the
risk of transmission of CWD to humans is of utmost importance, considering that
people can be infected by animal prions, resulting in new fatal diseases. To
study the possibility that human PrPC can be converted into the misfolded form
by CWD PrPSc, we performed experiments using the protein misfolding cyclic
amplification technique, which mimics in vitro the process of prion replication.
Our results show that cervid PrPSc can induce the conversion of human PrPC but
only after the CWD prion strain has been stabilized by successive passages in
vitro or in vivo. Interestingly, the newly generated human PrPSc exhibits a
distinct biochemical pattern that differs from that of any of the currently
known forms of human PrPSc. Our results also have profound implications for
understanding the mechanisms of the prion species barrier and indicate that the
transmission barrier is a dynamic process that depends on the strain and
moreover the degree of adaptation of the strain. If our findings are
corroborated by infectivity assays, they will imply that CWD prions have the
potential to infect humans and that this ability progressively increases with
CWD spreading.
UPDATED DATA ON 2ND CWD STRAIN
Wednesday, September 08, 2010 CWD PRION CONGRESS SEPTEMBER 8-11 2010
Tuesday, June 05, 2012
Captive Deer Breeding Legislation Overwhelmingly Defeated During 2012
Legislative Session
Friday, August 31, 2012
COMMITTEE ON CAPTIVE WILDLIFE AND ALTERNATIVE LIVESTOCK and CWD 2009-2012 a
review
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
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
*** 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)
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 ;
CHRONIC WASTING DISEASE CWD RISK FACTORS FOR TRANSMISSION 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.
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...
Saturday, October 6, 2012
TRANSMISSION, DIFFERENTIATION, AND PATHOBIOLOGY OF TRANSMISSIBLE SPONGIFORM
ENCEPHALOPATHIES 2011 Annual Report
Friday, November 09, 2012
Chronic Wasting Disease CWD in cervidae and transmission to other species
Sunday, November 11, 2012
Susceptibilities of Nonhuman Primates to Chronic Wasting Disease November
2012
with kindest regards,
terry
layperson
Terry S. Singeltary Sr.
P.O. Box 42
Bacliff, Texas USA 77518
posted by Terry S. Singeltary Sr. at
11:07 PM
0 Comments:
Post a Comment
Subscribe to Post Comments [Atom]
<< Home