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)” ***
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
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.
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.
NATURAL RESOURCES BOARD AGENDA ITEM
SUBJECT: Information Item: Almond Deer Farm Update
FOR: DECEMBER 2011 BOARD MEETING
TO BE PRESENTED BY TITLE: Tami Ryan, Wildlife Health Section Chief
*** 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.
*** 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
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. ...
Terry S. Singeltary Sr. P.O. Box 42 Bacliff, Texas USA 77518
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: firstname.lastname@example.org
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.
----- Original Message -----
From: David Colby To: email@example.com
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
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: firstname.lastname@example.org.
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: email@example.com
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: firstname.lastname@example.org
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.
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Title: Transmission of chronic wasting disease of mule deer to Suffolk sheep following intracerebral inoculation
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.
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.
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”.
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)
Occurrence, Transmission, and Zoonotic Potential of Chronic Wasting Disease
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.
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,...
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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