HUNTING: New protocols for mule deer hunting Texas Parks and Wildlife Department due to CWD
HUNTING: New protocols for mule deer hunting Texas Parks and Wildlife
Department
Posted November 17, 2012 at 11 p.m., updated November 17, 2012 at 11 p.m.
SAN ANGELO, Texas — Wildlife officials are reminding mule deer hunters and
landowners in far West Texas about new protocols developed as part of Texas
Parks & Wildlife Department's Chronic Wasting Disease response plan.
The plan includes mandatory check stations for harvested mule deer taken
inside the CWD Containment Zone, which covers portions of Hudspeth and El Paso
counties. See a map of CWD zones at http://www.tpwd.state.tx.us/cwd.
The response plan is being implemented after tissue samples from two mule
deer in far West Texas this past summer tested positive for CWD. These are the
first cases of CWD detected in Texas deer.
Hunters taking mule deer inside the Containment Zone during the general
season, Friday through Dec. 9, are required to submit their harvest (unfrozen
head) for CWD sampling at mandatory check stations within 24 hours of
harvest.
"We recommend hunters in the Containment Zone and High Risk Zone quarter
deer in the field and leave all but the quarters, backstraps and head at the
site of harvest if it is not possible to bury the inedible carcass parts at
least six feet deep on the ranch or take them to a landfill," said Shawn Gray,
Mule Deer Program Leader for TPWD.
Mandatory check stations will be open from 9 a.m. to 9 p.m. Friday through
Dec. 10. Stations will be located in Cornudas at May's Café (on U.S. Highway 62
and 180) and in Van Horn at Van Horn Convention Center (1801 West
Broadway).
Hunters who harvest deer in the Containment Zone outside the general season
under the authority of Managed Lands Deer Permits will need to call TPWD at
(512) 221-8491 the day the deer is harvested to make arrangements to have the
deer sampled for CWD.
In addition to protocols within the Containment Zone, TPWD has created a
High Risk Zone for voluntary CWD sampling during the hunting season. Biologists
have been collecting voluntary mule deer harvest data in the region since 1980,
and this year CWD sampling will be offered in addition to age and weight
measurements.
Voluntary check stations will be set up at the following locations during
the first three weekends of the general season, Saturday through Monday (this
Saturday to Monday, Dec. 1–3 and Dec. 8–10), from 9 a.m. to 5 p.m. Saturday and
Sunday, and 9 a.m. to 1 p.m. Monday:
Midland at Naturally Fresh (1501 Elwyn)
Bakersfield at Chevron Station (south of Interstate 10, Exit 294)
Sanderson at Slim's Auto Repair (823 West Oak; intersection of U.S. 90 and
285)
Alpine at Hip-O Taxidermy (east side of town on U.S. 90, across from Dairy
Queen)
"All deer brought to the check stations this season will be aged as part of
our CWD surveillance," said Gray. "We also intend to collect other biological
information such as antler measurements and field dressed weights as time
allows."
CWD is a member of the group of diseases called transmissible spongiform
encephalopathies. Other diseases in this group include scrapie in sheep, bovine
spongiform encephalopathy (or mad cow disease) in cattle, and Cruetzfeldt-Jakob
disease in humans.
CWD among cervids is a progressive, fatal disease that commonly results in
altered behavior as a result of microscopic changes made to the brain of
affected animals. An animal may carry the disease for years without outward
indication, but in the latter stages, signs may include listlessness, lowering
of the head, weight loss, repetitive walking in set patterns, and a lack of
responsiveness. CWD is not known to affect humans.
There is no vaccine or cure for CWD, but steps have been taken to minimize
the risk of the disease spreading from beyond the area where it currently
exists. For example, within the CWD Containment Zone, human-induced movements of
wild or captive deer, elk or other susceptible species will be restricted, and
mandatory hunter check stations will be established.
Although wildlife officials cannot say how long the disease has been
present in Texas or if it occurs in other areas of the state, they have had an
active CWD surveillance program for more than a decade.
"We have tested more than 26,500 wild deer in Texas since 2002, and the
captive-deer industry has submitted more than 7,400 CWD test results as well,"
said Mitch Lockwood, Big Game Program Director with TPWD. "But that part of West
Texas is the toughest place to conduct an adequate CWD surveillance program
because so few deer are harvested out there each hunting season. Thanks to the
cooperation and active participation of several landowners, we were able to
begin getting an idea of the prevalence and geographic distribution of the
disease without needing to remove many deer."
More information on CWD can be found on TPWD's website, http://www.tpwd.state.tx.us/cwd or at
the Chronic Wasting Disease Alliance website, http://www.cwd-info.org.
CWD has been waltzing across Texas from New Mexico for 10 years. I tried
telling the TAHC in 2001-2002, exactly where CWD was, and tried to get them to
test there. now, 10 years later, if it would not have been for the state of New
Mexico, and their continued efforts to make Texas finally test, they found CWD.
besides this, game farms are another factor in Texas and CWD there from are
another risk factor. right now there is an investigation into PA exposed CWD
deer all the way down in Louisiana. please see ;
Wednesday, November 14, 2012
PENNSYLVANIA 2012 THE GREAT ESCAPE OF CWD INVESTIGATION MOVES INTO
LOUISIANA
Tuesday, November 13, 2012
PENNSYLVANIA 2012 THE GREAT ESCAPE OF CWD
Friday, October 26, 2012
CHRONIC WASTING DISEASE CWD PENNSYLVANIA GAME FARMS, URINE ATTRACTANT
PRODUCTS, BAITING, AND MINERAL LICKS
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)
>>> • Delegates authority to the Executive Director to issue an
order to declare a CWD high risk area or county based on sound epidemiological
principles for disease detection, control and eradication.
IN my opinion, there has been no ‘sound epidemiological principles for disease detection, control and eradication’ in Texas for CWD, or any other TSE. It’s been just the opposite. NOT even speaking about all the risk factors from the cervid game ranch farms in Texas over the years, and trading, and the lax rules and enforcement of said rules there from, the fact that CWD infected deer have been waltzing across Texas for the past decade, in the exact spot I tried warning TAHC back in 2001-2002, i.e. the Texas, New Mexico border at the WSMR area, the complete state of Texas is at risk for CWD, and has been at risk for CWD for years.
*** I propose that Texas, and the Executive Director, should take that
authority, and declare the complete state of Texas (not just a high risk area,
where the State of New Mexico finally forced Texas to finally test, and finally
embarrassed Texas enough to finally do CWD testing where it should have been
done 10 years ago), but I believe the complete state of Texas should be declared
a high risk area for CWD, until proper testing (in sufficient numbers, in all
geographical regions), and tested 100% of all farmed cervids. ...TSS
2001 – 2002
TEXAS OLD STATISTICS BELOW FOR PAST CWD TESTING;
Subject: CWD testing in Texas
Date: Sun, 25 Aug 2002 19:45:14 –0500
From: Kenneth Waldrup
To: flounder@wt.net
Dear Dr. Singletary,
In Fiscal Year 2001, seven deer from Texas were tested by the National
Veterinary Services Laboratory (NVSL) for CWD (5 fallow deer and 2 white-tailed
deer). In Fiscal Year 2002, seven elk from Texas were tested at NVSL (no deer).
During these two years, an additional six elk and one white-tailed deer were
tested at the Texas Veterinary Medical Diagnostic Laboratory (TVMDL). In Fiscal
Year 2002, four white-tailed deer (free-ranging clinical suspects) and at least
eight other white-tailed deer have been tested at TVMDL. One elk has been tested
at NVSL. All of these animals have been found negative for CWD. Dr. Jerry Cooke
of the Texas Parks and Wildlife Department also has records of 601 clinically
ill white-tailed deer which were necropsied at Texas A&M during the late
1960's and early 1970's, and no spongiform encepalopathies were noted. Thank you
for your consideration.
Ken Waldrup, DVM, PhD Texas Animal Health Commission
========================
TEXAS CWD STATUS
Captive Cervids There have been no reported CWD infections of captive elk
or deer in Texas. There is currently no mandatory surveillance program for
susceptible cervids kept on game farms, although, there has been voluntary
surveillance since 1999, which requires owners of participating herds to
maintain an annual herd inventory and submit samples for all mortalities of
animals over 16 months of age.
snip...
SO, i thought i would just see where these Ecoregions were, and just how
the CWD testing was distributed. YOU would think that with the cluster of CWD
bordering TEXAS at the WPMR in NM, you would have thought this would be where
the major CWD testing samples were to have been taken? wrong! let's have a look
at the sample testing. here is map of CWD in NM WPMR bordering TEXAS;
NEW MEXICO 7 POSITIVE CWD WHITE SANDS MISSILE RANGE MAP
NEXT, let's have a look at the overall distribution of CWD in Free-Ranging
Cervids and see where the CWD cluster in NM WSMR borders TEXAS; Current
Distribution of Chronic Wasting Disease in Free-Ranging Cervids
NOW, the MAP of the Exoregion where the samples were taken to test for CWD;
CWD SURVEILLANCE SAMPLE SUBMISSIONS TEXAS
Ecoregions of TEXAS
IF you look at the area around the NM WSMR where the CWD cluster was and
where it borders TEXAS, that ecoregion is called Trans Pecos region. Seems if my
Geography and my Ciphering is correct ;-) that region only tested 55% of it's
goal. THE most important area on the MAP and they only test some 96 samples,
this in an area that has found some 7 positive animals? NOW if we look at the
only other border where these deer from NM could cross the border into TEXAS,
this area is called the High Plains ecoregion, and again, we find that the
sampling for CWD was pathetic. HERE we find that only 9% of it's goal of CWD
sampling was met, only 16 samples were tested from some 175 that were suppose to
be sampled.
AS i said before;
> SADLY, they have not tested enough from the total population to
> know if CWD is in Texas or not.
BUT now, I will go one step further and state categorically that they are
not trying to find it. just the opposite it seems, they are waiting for CWD to
find them, as with BSE/TSE in cattle, and it will eventually...
snip...see full text ;
Wednesday, October 03, 2012
TAHC Chronic Wasting Disease Rule What you need to know
Thursday, September 27, 2012
TAHC Proposes Modifications to Chronic Wasting Disease (CWD) Rules
September 27, 2012 NEWS RELEASE Texas Animal Health Commission
Wednesday, September 26, 2012
TPWD Gearing Up for CWD Response during Deer Season
Monday, September 17, 2012
New Mexico DGF EXPANDS CHRONIC WASTING DISEASE CONTROL AREAS, while Texas
flounders
Friday, September 07, 2012
Texas Wildlife Officials Considering New Deer Movement Rules in Response to
CWD
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
Monday, March 26, 2012
Texas Prepares for Chronic Wasting Disease CWD Possibility in Far West
Texas
Monday, March 26, 2012
3 CASES OF CWD FOUND NEW MEXICO MULE DEER SEVERAL MILS FROM TEXAS BORDER
Saturday, June 09, 2012
USDA Establishes a Herd Certification Program for Chronic Wasting Disease
in the United States
Wednesday, June 13, 2012
TAHC Modifies Entry Requirements Effective Immediately for Cervids DUE TO
CWD FOR IMMEDIATE RELEASE
***Tuesday, July 10, 2012
Chronic Wasting Disease Detected in Far West Texas
key word here is _considering_. so consider this, CWD still spreading in
Texas. ...TSS
Friday, September 07, 2012
Texas Wildlife Officials Considering New Deer Movement Rules in Response to
CWD
TAHC CWD PAGE
Friday, August 31, 2012
COMMITTEE ON CAPTIVE WILDLIFE AND ALTERNATIVE LIVESTOCK and CWD 2009-2012 a
review
Friday, June 01, 2012
TEXAS DEER CZAR TO WISCONSIN ASK TO EXPLAIN COMMENTS
how many states have $465,000., and can quarantine and purchase there from,
each cwd said infected farm, but how many states can afford this for all the cwd
infected cervid game ranch type farms ???
? game farms in a state X $465,000., do all these game farms have insurance
to pay for this risk of infected the wild cervid herds, in each state ???
Tuesday, December 20, 2011
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.
Form 1100-001
(R 2/11)
NATURAL RESOURCES BOARD AGENDA ITEM
SUBJECT: Information Item: Almond Deer Farm Update
FOR: DECEMBER 2011 BOARD MEETING
TUESDAY
TO BE PRESENTED BY TITLE: Tami Ryan, Wildlife Health Section Chief
SUMMARY:
*** 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.
2011
*** After a natural route of exposure, 100% of white-tailed deer were
susceptible to scrapie.
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
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
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
Thursday, May 31, 2012
CHRONIC WASTING DISEASE CWD PRION2012 Aerosol, Inhalation transmission,
Scrapie, cats, species barrier, burial, and more
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
Envt.11: Swine Are Susceptible to Chronic Wasting Disease by Intracerebral
Inoculation
Justin Greenlee,† Robert Kunkle and Jodi Smith National Animal Disease
Center, ARS, USDA; Ames, IA USA †Presenting author; Email:
justin.greenlee@ars.usda.gov
Transmissible spongiform encephalopathies (TSEs, prion diseases) are
chronic neurodegenerative diseases that occur in humans, cattle, sheep, goats,
cervids and a number of laboratory animal models. There is no evidence of the
natural occurrence of any form of TSE in the pig, but pigs have been shown to be
susceptible to Bovine Spongiform Encephalopathy (BSE) infection by
multiple-route parenteral challenge. However, pigs orally exposed at eight weeks
of age to large amounts of brain from cattle clinically affected with BSE did
not support infection after seven years of observation. In the US, feeding of
ruminant by-products to ruminants is prohibited, but feeding of ruminant
materials to swine, mink and poultry still occurs. Although unlikely, the
potential for swine to have access to TSE-contaminated feedstuffs exists. The
potential for swine to serve as a host for the agent of chronic wasting disease
(CWD) is unknown. The purpose of this study was to perform intracerebral
inoculation of the CWD agent to determine the potential of swine as a host for
the CWD agent and their clinical susceptibility. This study utilized 26 swine
randomly divided into controls (n = 6) and intracranial inoculates (n = 20). CWD
inoculum was a pooled 10% (w/v) homogenate derived from three white-tailed deer
clinically ill with CWD from three different sources (elk, white-tailed deer,
mule deer) and was given by a single intracranial injection of 0.75 ml.
Necropsies were done on ten animals at six months post inoculation (PI), at
approximately the time the pigs were expected to reach market weight. Additional
pigs have been necropsied due to intercurrent disease (primarily lameness) over
the course of the study (29–64 months). Samples collected at necropsy were
examined for spongiform change after routine staining (hematoxylin and eosin)
and for immunoreactivity to prion protein (PrPSc) by immunohistochemistry.
Further, brain samples from at least two regions were tested by western blot. No
results suggestive of spongiform encephalopathy were obtained from animals
necropsied at six months PI, but positive results after an incubation period of
only six months would be uncharacteristic. A single animal was positive for CWD
by IHC and WB at 64 months PI. Two inoculated pigs and one control pig remain
alive, so it is not possible to determine the attack rate of CWD in swine at
this time. However, lack of positive results in pigs necropsied at 29–56 months
PI and the long incubation of the single positive case suggest that swine are
unlikely to be affected by CWD if inoculated by a natural route.
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 ;
Title: Transmission of chronic wasting disease of mule deer to Suffolk
sheep following intracerebral inoculation
Authors
Hamir, Amirali Kunkle, Robert Cutlip, Randall - ARS RETIRED Miller, Janice
- ARS RETIRED Williams, Elizabeth - UNIV OF WYOMING, LARAMIE Richt, Juergen
Submitted to: Journal of Veterinary Diagnostic Investigation Publication
Type: Peer Reviewed Journal Publication Acceptance Date: June 20, 2006
Publication Date: November 1, 2006 Citation: Hamir, A.N., Kunkle, R.A., Cutlip,
R.C., Miller, J.M., Williams, E.S., Richt, J.A. 2006. Transmission of chronic
wasting disease of mule deer to Suffolk sheep following intracerebral
inoculation. Journal of Veterinary Diagnostic Investigation. 18(6):558-565.
Interpretive Summary: Chronic wasting disease (CWD) has been identified in
captive and free ranging deer and elk since 1967. To determine the
transmissibility of CWD to sheep and to provide information about the disease
and tests for detection of CWD in sheep, 8 lambs were inoculated with brain
suspension from mule deer naturally affected with CWD. Two other lambs were kept
as controls. Only 1 sheep developed clinical disease at 35 months after
inoculation. The study was terminated at 72 months after the inoculation. At
that time one other sheep was found to be positive for the disease. It is
proposed that the host's genetic makeup may play a role in transmission of the
disease to domestic sheep. Impact. This is the first study which shows that it
is possible to transmit CWD to a small number of sheep. Technical Abstract:
Chronic wasting disease (CWD) has been identified in captive and free-ranging
cervids since 1967. To determine the transmissibility of CWD to sheep and to
provide information about clinical course, lesions, and suitability of currently
used diagnostic procedures for detection of CWD in sheep, 8 Suffolk lambs (4 QQ
and 4 QR at codon 171 of prion protein (PRNP) gene) were inoculated
intracerebrally with brain suspension from mule deer naturally affected with CWD
(CWD**md). Two other lambs (1 QQ and 1 QR at codon 171 of PRNP gene) were kept
as non-inoculated controls. Within 36 months post inoculation (MPI), 2 animals
became recumbent and were euthanized. However, only 1 sheep (euthanized at 35
MPI) had shown clinical signs that were consistent with those of scrapie.
Microscopic lesions of spongiform encephalopathy (SE) were seen in this sheep
and its tissues were positive for the abnormal prion protein (PrPres) by
immunohistochemistry and Western blot. Retrospective examination of the PRNP
genotype of this animal revealed that it was heterozygous (AV) at codon 136. In
the next 24 months, 3 other sheep were euthanized because of conditions
unrelated to TSE. The remaining 3 sheep remained non-clinical at the termination
of the study (72 MPI) and were euthanized at that time. One of these 3 revealed
SE and its tissues were positive for PrPres. These findings demonstrate that it
is possible to transmit CWD**md agent to sheep via the intracerebral route.
However, the host genotype may play a significant part in successful
transmission and incubation period of this agent.
Chronic wasting disease: Fingerprinting the culprit in risk assessments
Volume 6, Issue 1 January/February/March 2012 Pages 17 - 22 http://dx.doi.org/10.4161/pri.6.1.17776
Keywords: Fourier transform-infrared (FT-IR) spectroscopy, chronic wasting
disease (CWD), prion, prion protein (PrP), prion typing, protein misfolding
cyclic amplification (PMCA), risk assessment, seeding activity, strains,
transmissible spongiform encephalopathies (TSE)
Authors: Martin L. Daus and Michael Beekes View affiliations Hide
affiliations Martin L. Daus
P24 -Transmissible Spongiform Encephalopathies; Robert Koch-Institut;
Berlin, Germany Michael Beekes Corresponding author: BeekesM@rki.de P24
-Transmissible Spongiform Encephalopathies; Robert Koch-Institut; Berlin,
Germany
Abstract: Transmissible spongiform encephalopathies (prion diseases) in
animals may be associated with a zoonotic risk potential for humans as shown by
the occurrence of variant Creutzfeldt-Jakob disease in the wake of the bovine
spongiform encephalopathy epidemic. Thus, the increasing exposure of humans in
North America to cervid prions of chronic wasting disease (CWD) in elk and deer
has prompted comprehensive risk assessments. The susceptibility of humans to CWD
infections is currently under investigation in different studies using macaques
as primate models. The necessity for such studies was recently reinforced when
disease-associated prion protein and its seeding activity were detected in
muscles of clinically inconspicuous CWD-infected white-tailed deer (WTD).
Increasing evidence points to the existence of different CWD strains, and CWD
prions may also change or newly emerge over time. Therefore, CWD isolates
examined in macaques should be characterized as precisely as possible for their
molecular identity. On this basis other CWD field samples collected in the past,
present or future could be systematically compared with macaque-tested inocula
in order to assess whether they are covered by the ongoing risk assessments in
primates. CWD typing by Fourier transform-infrared spectroscopy of pathological
prion protein may provide a method of choice for this purpose.
snip...
Exposure of humans to CWD prions
Chronic wasting disease is a TSE in white-tailed deer, mule deer, Rocky
Mountain elk and moose. Over the past years this disease has shown a sustained
spread in captive as well as free-ranging cervids in North America.6,7 The
increasingly frequent and widespread 5 occurrence of affected animals is likely
to augment the exposure of humans to the CWD agent. Prion infectivity or
TSE-associated prion protein have been detected in the central and peripheral
nervous system, in a variety of lymphoid tissues as well as in heart muscle,
blood, saliva, feces and urine of CWD-infected cervids7. Also, infectious CWD
agent was found in antler velvet of elk and in skeletal muscles of mule deer
with chronic wasting disease.8,9 Thus, particularly persons processing cervid
carcasses, users of medicinal products made from antler velvet and consumers of
venison may be exposed to an elevated risk for contamination with CWD prions.
Recently, PrPTSE and its proteinaceous seeding activity could be directly
demonstrated, for the first time, in skeletal muscles of CWD-infected cervids.10
The animals examined in this study were farmed and free-ranging WTD for which no
clinical signs of CWD had been recognized. However, they had been officially
confirmed positive for CWD based on the detection of PrPTSE in brain tissue or
lymph nodes and were thus apparently in a state of pre or subclinical infection.
Muscles from such clinically inconspicuous carrier animals appear more likely to
enter the human food chain than meat from cervids that show symptoms of CWD.
Whether this may provide a relevant mode for the inadvertent foodborne
transmission of CWD prions is still unclear. Yet, the presence and seeding
activity of PrPTSE in skeletal muscles of pre- or subclinically infected WTD
reinforced the need to comprehensively assess whether humans are susceptible to
zoonotic CWD infections.
snip...
Transmissibility to humans
The current state of epidemiological research suggests a rather robust
barrier for the transmission of CWD to humans. Particularly, the surveillance of
human prion diseases in areas with a long history of endemic CWD such as
Colorado and Wyoming did not reveal evidence for zoonotic transmissions of the
disease to cervid hunters or consumers of meat from elk and deer.6,11 However,
as discussed by Belay et al.,6 the intensity of human exposure to CWD prions may
increase due to a further spread and rising prevalence of the disease in
cervids. Therefore, and with the generally long latency periods of human prion
diseases in mind, previous epidemiological findings cannot be readily
extrapolated. Until recently, experimental studies that pursued biochemical
approaches or used transgenic mice to ascertain the susceptibility of humans to
CWD infections consistently seemed to corroborate current epidemiological
findings: CWD-infected cervid brain tissue did not seed the conversion of PrPC
133 into PrPres in PMCA assays using brain homogenate from macaques or
transgenic mice expressing human PrPC as test substrate12 , and transgenic mice
overexpressing human PrPC were resistant to infection after intracerebral
challenge with CWD prions from mule deer.13 However, a study published by Barria
et al.14 in March 2011 found that cervid PrPTSE can seed the conversion of human
PrPC into PrPres by PMCA when the CWD agent has been previously passaged in
vitro or in vivo. Specifically, this was demonstrated for CWD prions from
naturally affected mule deer either passaged by serial PMCA using deer PrPC as
conversion substrate or in transgenic mice expressing cervid PrPC. The authors
of this study pointed out that CWD prions may undergo a gradual process of
change and adaptation via successive passages in the cervid population. They
concluded that the reported findings, if corroborated by infectivity assays, may
imply “that CWD prions have the potential to infect humans and that this ability
progressively increases with CWD spreading”.
snip...
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...
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...
full text ;
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
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
TSS
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