Wednesday, July 01, 2015

DRAFT Virginia Deer Management Plan 2015-2024 (bans urine scents do to CWD 2015)

DRAFT Virginia Deer Management Plan 2015-2024




Chronic wasting disease (CWD) surveillance began in Virginia in 2002 when the disease was first diagnosed east of the Mississippi River. Virginia and other eastern states initiated CWD planning efforts and established regulations to detect and minimize the spread of the disease. Since 2002, VDGIF has instituted a number of management actions to prevent the introduction of CWD into Virginia. These actions include restricting movement of captive deer (2002); revising CWD surveillance and response plans to address risk factors in adjacent states (2005); restricting import of hunter-killed deer from areas with CWD (2005) or from enclosures intended to confine deer or elk (2013); ***and, prohibiting possession or use of deer scents/lures that contain natural deer urine or other bodily fluids used for the purposes of taking, attempting to take, attracting, or scouting wildlife (2015).


To assess whether CWD was present in Virginia’s wild deer population, VDGIF has maintained a surveillance program since 2002. The CWD surveillance program monitors the wild deer population using three different approaches: (a) random sampling of hunter-killed or road-killed deer, (b) targeted sampling of deer exhibiting disease symptoms, and (c) testing of all captive deer mortalities. In September 2005, CWD was discovered in a free-ranging white-tailed deer in Hampshire County, West Virginia less than 10 miles from Frederick County, Virginia. Following this discovery, VDGIF’s surveillance efforts have focused on western Frederick and northwestern Shenandoah counties. In 2009, Virginia’s first CWD-positive deer was harvested in western Frederick County within one mile of the West Virginia border. Since then, 7 more CWD-positive deer have been killed in this same area of western Frederick County. In 2013, a hunter killed a positive deer in southern Frederick County approximately 10 miles southeast of the original positive deer. A positive road-




killed deer was found in northeastern Shenandoah County near the Frederick County line in 2014. From 2002-2014, over 7,800 Virginia deer were tested for CWD, 10 of which were positive. As of February 2015, 183 CWD-positive deer have been diagnosed in Hampshire and Hardy Counties, West Virginia, several of which have been close to the Virginia state line.


Since becoming a CWD-positive state in 2009, VDGIF has implemented a number of management actions to slow the spread of CWD. A disease Containment Area (CA) was established in Frederick and Shenandoah counties and expanded to Clark and Warren counties in 2015. Feeding of deer was prohibited year-round both in and near the CA. With a few exceptions, the movement of deer carcasses and carcass parts out of the CA was prohibited. Restrictions were placed on the disposal of deer offal from the CA. Rehabilitation of deer in the CA was prohibited, and deer seasons and bag limits on private lands were liberalized in an attempt to reduce the deer population. These actions are in keeping with responses to a Department survey conducted following the discovery of CWD in Frederick County where respondents supported 5 of 7 potential strategies to control CWD in affected areas, including mandatory disease testing of hunter-killed deer, deer feeding prohibitions, deer carcass movement restrictions, restrictions on deer rehabilitation, and reduction of deer populations using hunters. Respondents did not support the use of sharpshooting to reduce localized deer populations (42% opposed, 36% supported, 22% were neutral), but the strongest opposition was for doing nothing to control CWD (79 % opposed vs. 8% supported).


Captive Deer.---- Deer held in zoos or other captive settings are regulated by VDGIF to achieve the following goals:


(1) Protect the wild white-tailed deer resource.


(2) Manage white-tailed deer as a public resource.


(3) Protect health and safety of humans and domestic animals.


(4) Provide educational and recreational viewing opportunities for citizens, advance scientific knowledge (research), conserve globally rare species, and serve other legitimate purposes for the benefit of society or the environment.


Captive deer have been strictly regulated in Virginia since at least 1994, when a moratorium was placed on fallow deer farming permits (the last permitted facility closed in 2012). Since November 2002, a DGIF permit has been required to possess any member of the deer family (Cervidae) in Virginia (§4 VAC 15-30-40). As of June 2015, 16 permitted facilities—primarily those that exhibit deer to the public—held approximately 600 deer in captivity in Virginia. Permit conditions established in 2002 prohibit the importation or movement of any deer species into or within Virginia. Facilities are also required to individually mark all captive deer, keep detailed records, and report deaths and escapes immediately. CWD testing of all captive adult deer mortalities is mandatory. Since 2008, DGIF has allowed limited movements of nonnative captive cervids between compliant, permitted exhibitors on a case-by-case basis.


Private citizens in Virginia are not allowed to keep deer as pets or as part of a private menagerie, and a protocol to address unpermitted captive deer was developed in 2009 and updated in 2012. To educate citizens about the legal, biological, and management issues associated with keeping deer as pets, VDGIF developed a brochure and maintains a webpage entitled, Keeping Deer Wild in Virginia.


Deer Hunting Enclosures.----In 2001, the Virginia General Assembly passed §29.1-525.1 to prohibit (a) the erection of a fence with intent to confine deer, and (b) hunting within a fenced area that prevents or impedes the free egress of deer. Exceptions were made to avoid impacts upon areas fenced to ensure human safety (e.g., military installations), permitted captive deer facilities, and 5 existing deer hunting enclosures in existence or under construction at the time the law was passed. The 5 enclosures were required to register with VDGIF and operate under management practices approved by VDGIF. Currently, 4 registered deer hunting enclosures remain in Virginia. In 2006, VDGIF enacted a regulation describing the attributes of an enclosed or fenced area deemed to prevent or impede the free egress of deer in response to landowner questions regarding this issue (4VAC15-90-291).


Deer Research--- The deer program’s primary involvement in research pertains to projects directly related tothe Deer Management Plan. Currently, two research studies are being conducted.




Potential Strategies


a. Discourage supplemental feeding and other activities which unnaturally concentrate deer to reduce risk of disease transmission.


b. Remove and test illegally-held captive deer for CWD, bovine tuberculosis, and other diseases as appropriate.




c. Regulate captive deer, including rehabilitated wild deer, to minimize risk of disease transmission to wild deer.


d. Prevent introduction and spread of infectious diseases using management techniques supported by regulations and policies.


e. Develop and update disease surveillance and response plans as needed.






• 2002 Virginia begins CWD surveillance.


• 2002, implemented captive deer movement restrictions.


• 2005 CWD found in Hampshire County WV.


• 2005, implemented deer carcass importation restrictions.


• 2006, prohibited feeding deer during September 1 through early January.


• 2008, required mandatory testing of hunter-killed deer.


• 2009 CWD found in Frederick County VA.


• 2010, developed CWD Response Management Actions and put them in regulation (2013).


• 2013, prohibited importation of carcasses from an enclosure anywhere.



CWD Snapshot - Updated 6/2015 Due to the detection of a new positive in the northeastern corner of Shenandoah County, it has been decided to expand the Containment Area in 2015 to include all of Frederick, Warren, Clarke, and Shenandoah Counties.


Beginning in 2015, all hunters who harvest deer within the new CA on the first two Saturdays of the general firearms season (November 14th and 21st) must bring their deer to a CWD check station for testing.


Effective July 1, 2015, it will be illegal to possess or use deer scents/lures that contain natural deer urine or other bodily fluids while taking, attempting to take, attracting, or scouting wildlife in Virginia. For more information see the links below.


As of January 2015, Virginia has diagnosed ten CWD-positive white-tailed deer. CWD has been found in 22 states and 2 Canadian provinces.


Check back regularly for updates!


Is CWD dangerous to humans? There currently is no evidence that CWD is transmissible to humans. Data from states with both CWD in deer and large populations of deer hunters show no greater likelihood of humans developing prion diseases. Further, testing of macaques (primates commonly used as human surrogates for research) and genetically-engineered mice provide evidence that there is likely a species barrier that prevents humans from getting CWD or a related disease. However, public health officials recommend that human exposure to the CWD agent be avoided as they continue to evaluate the potential risk, if any.




 >>> Is CWD dangerous to humans? <<<


>>>However, there is no evidence at this time that humans can contract CWD from consuming venison, nor has the disease been shown to transmit to livestock under natural conditions. The susceptibility of exotic species of deer held in captivity (e.g., fallow, axis, muntjac) is currently unknown.<<<








Zoonotic Potential of CWD Prions


Liuting Qing1, Ignazio Cali1,2, Jue Yuan1, Shenghai Huang3, Diane Kofskey1, Pierluigi Gambetti1, Wenquan Zou1, Qingzhong Kong1 1Case Western Reserve University, Cleveland, Ohio, USA, 2Second University of Naples, Naples, Italy, 3Encore Health Resources, Houston, Texas, USA


Chronic wasting disease (CWD) is a widespread and expanding prion disease in free-ranging and captive cervid species in North America. The zoonotic potential of CWD prions is a serious public health concern. Current literature generated with in vitro methods and in vivo animal models (transgenic mice, macaques and squirrel monkeys) reports conflicting results. The susceptibility of human CNS and peripheral organs to CWD prions remains largely unresolved. In our earlier bioassay experiments using several humanized transgenic mouse lines, we detected protease-resistant PrPSc in the spleen of two out of 140 mice that were intracerebrally inoculated with natural CWD isolates, but PrPSc was not detected in the brain of the same mice. Secondary passages with such PrPSc-positive CWD-inoculated humanized mouse spleen tissues led to efficient prion transmission with clear clinical and pathological signs in both humanized and cervidized transgenic mice. Furthermore, a recent bioassay with natural CWD isolates in a new humanized transgenic mouse line led to clinical prion infection in 2 out of 20 mice. ***These results indicate that the CWD prion has the potential to infect human CNS and peripheral lymphoid tissues and that there might be asymptomatic human carriers of CWD infection.




***These results indicate that the CWD prion has the potential to infect human CNS and peripheral lymphoid tissues and that there might be asymptomatic human carriers of CWD infection.***




P.105: RT-QuIC models trans-species prion transmission


Kristen Davenport, Davin Henderson, Candace Mathiason, and Edward Hoover Prion Research Center; Colorado State University; Fort Collins, CO USA


The propensity for trans-species prion transmission is related to the structural characteristics of the enciphering and heterologous PrP, but the exact mechanism remains mostly mysterious. Studies of the effects of primary or tertiary prion protein structures on trans-species prion transmission have relied primarily upon animal bioassays, making the influence of prion protein structure vs. host co-factors (e.g. cellular constituents, trafficking, and innate immune interactions) difficult to dissect. As an alternative strategy, we used real-time quakinginduced conversion (RT-QuIC) to investigate trans-species prion conversion.


To assess trans-species conversion in the RT-QuIC system, we compared chronic wasting disease (CWD) and bovine spongiform encephalopathy (BSE) prions, as well as feline CWD (fCWD) and feline spongiform encephalopathy (FSE). Each prion was seeded into each host recombinant PrP (full-length rPrP of white-tailed deer, bovine or feline). We demonstrated that fCWD is a more efficient seed for feline rPrP than for white-tailed deer rPrP, which suggests adaptation to the new host.


Conversely, FSE maintained sufficient BSE characteristics to more efficiently convert bovine rPrP than feline rPrP. Additionally, human rPrP was competent for conversion by CWD and fCWD. ***This insinuates that, at the level of protein:protein interactions, the barrier preventing transmission of CWD to humans is less robust than previously estimated.




***This insinuates that, at the level of protein:protein interactions, the barrier preventing transmission of CWD to humans is less robust than previously estimated.***




Willingham, Erin McNulty, Kelly Anderson, Jeanette Hayes-Klug, Amy Nalls, and Candace Mathiason Colorado State University; Fort Collins, CO USA


Chronic wasting disease (CWD) is the transmissible spongiform encephalopathy (TSE), of free-ranging and captive cervids (deer, elk and moose).


The presence of infectious prions in the tissues, bodily fluids and environments of clinical and preclinical CWD-infected animals is thought to account for its high transmission efficiency. Recently it has been recognized that mother to offspring transmission may contribute to the facile transmission of some TSEs. Although the mechanism behind maternal transmission is not yet known, the extended asymptomatic TSE carrier phase (lasting years to decades) suggests that it may have implications in the spread of prions.


Placental trafficking and/or secretion in milk are 2 means by which maternal prion transmission may occur. In these studies we explore these avenues during early and late infection using a transgenic mouse model expressing cervid prion protein. Na€ıve and CWD-infected dams were bred at both timepoints, and were allowed to bear and raise their offspring. Milk was collected from the dams for prion analysis, and the offspring were observed for TSE disease progression. Terminal tissues harvested from both dams and offspring were analyzed for prions.


We have demonstrated that


(1) CWDinfected TgCerPRP females successfully breed and bear offspring, and


(2) the presence of PrPCWD in reproductive and mammary tissue from CWD-infected dams.


We are currently analyzing terminal tissue harvested from offspring born to CWD-infected dams for the detection of PrPCWD and amplification competent prions. These studies will provide insight into the potential mechanisms and biological significance associated with mother to offspring transmission of TSEs.




P.157: Uptake of prions into plants


Christopher Johnson1, Christina Carlson1, Matthew Keating1,2, Nicole Gibbs1, Haeyoon Chang1, Jamie Wiepz1, and Joel Pedersen1 1USGS National Wildlife Health Center; Madison, WI USA; 2University of Wisconsin - Madison; Madison, WI USA


Soil may preserve chronic wasting disease (CWD) and scrapie infectivity in the environment, making consumption or inhalation of soil particles a plausible mechanism whereby na€ıve animals can be exposed to prions. Plants are known to absorb a variety of substances from soil, including whole proteins, yet the potential for plants to take up abnormal prion protein (PrPTSE) and preserve prion infectivity is not known. In this study, we assessed PrPTSE uptake into roots using laser scanning confocal microscopy with fluorescently tagged PrPTSE and we used serial protein misfolding cyclic amplification (sPMCA) and detect and quantify PrPTSE levels in plant aerial tissues. Fluorescence was identified in the root hairs of the model plant Arabidopsis thaliana, as well as the crop plants alfalfa (Medicago sativa), barley (Hordeum vulgare) and tomato (Solanum lycopersicum) upon exposure to tagged PrPTSE but not a tagged control preparation. Using sPMCA, we found evidence of PrPTSE in aerial tissues of A. thaliana, alfalfa and maize (Zea mays) grown in hydroponic cultures in which only roots were exposed to PrPTSE. Levels of PrPTSE in plant aerial tissues ranged from approximately 4 £ 10 ¡10 to 1 £ 10 ¡9 g PrPTSE g ¡1 plant dry weight or 2 £ 105 to 7 £ 106 intracerebral ID50 units g ¡1 plant dry weight. Both stems and leaves of A. thaliana grown in culture media containing prions are infectious when intracerebrally-injected into mice. ***Our results suggest that prions can be taken up by plants and that contaminated plants may represent a previously unrecognized risk of human, domestic species and wildlife exposure to prions.




***Our results suggest that prions can be taken up by plants and that contaminated plants may represent a previously unrecognized risk of human, domestic species and wildlife exposure to prions.***




Friday, May 15, 2015


Grass Plants Bind, Retain, Uptake, and Transport Infectious Prions







P.136: Mother to offspring transmission of CWD—Detection in fawn tissues using the QuIC assay


Amy Nalls, Erin McNulty, Clare Hoover, Jeanette Hayes-Klug, Kelly Anderson, Edward Hoover, and Candace Mathiason Colorado State University; Fort Collins, CO USA


To investigate the role mother to offspring transmission plays in chronic wasting disease (CWD), we have employed a small, polyestrous breeding, indoor maintainable cervid model, the Reeves’ muntjac deer. Muntjac doe were inoculated with CWD and tested positive by lymphoid biopsy at 4 months post inoculation. From these CWD-infected doe, we obtained 3 viable fawns. These fawns tested IHC-positive for CWD by lymphoid biopsy as early as 40 d post birth, and all have been euthanized due to clinical disease at 31, 34 and 59 months post birth. The QuIC assay demonstrates sensitivity and specificity in the detection of conversion competent prions in peripheral IHC-positive tissues including tonsil, mandibular, partotid, retropharyngeal, and prescapular lymph nodes, adrenal gland, spleen and liver. In summary, using the muntjac deer model, we have demonstrated CWD clinical disease in offspring born to CWD-infected doe and found that the QuIC assay is an effective tool in the detection of prions in peripheral tissues. ***Our findings demonstrate that transmission of prions from mother to offspring can occur, and may be underestimated for all prion diseases.




***Our findings demonstrate that transmission of prions from mother to offspring can occur, and may be underestimated for all prion diseases.




cwd environmental load factor in the land and surrounding plants and objects.


transportation of cervids and HUMANS from cwd zone should be regarded as a great risk factor, and environmental contamination.




Using in vitro prion replication for high sensitive detection of prions and prionlike proteins and for understanding mechanisms of transmission.


Claudio Soto


Mitchell Center for Alzheimer's diseases and related Brain disorders, Department of Neurology, University of Texas Medical School at Houston.


Prion and prion-like proteins are misfolded protein aggregates with the ability to selfpropagate to spread disease between cells, organs and in some cases across individuals. I n T r a n s m i s s i b l e s p o n g i f o r m encephalopathies (TSEs), prions are mostly composed by a misfolded form of the prion protein (PrPSc), which propagates by transmitting its misfolding to the normal prion protein (PrPC). The availability of a procedure to replicate prions in the laboratory may be important to study the mechanism of prion and prion-like spreading and to develop high sensitive detection of small quantities of misfolded proteins in biological fluids, tissues and environmental samples. Protein Misfolding Cyclic Amplification (PMCA) is a simple, fast and efficient methodology to mimic prion replication in the test tube. PMCA is a platform technology that may enable amplification of any prion-like misfolded protein aggregating through a seeding/nucleation process. In TSEs, PMCA is able to detect the equivalent of one single molecule of infectious PrPSc and propagate prions that maintain high infectivity, strain properties and species specificity. Using PMCA we have been able to detect PrPSc in blood and urine of experimentally infected animals and humans affected by vCJD with high sensitivity and specificity. Recently, we have expanded the principles of PMCA to amplify amyloid-beta (Aβ) and alphasynuclein (α-syn) aggregates implicated in Alzheimer's and Parkinson's diseases, respectively. Experiments are ongoing to study the utility of this technology to detect Aβ and α-syn aggregates in samples of CSF and blood from patients affected by these diseases.


***Recently, we have been using PMCA to study the role of environmental prion contamination on the horizontal spreading of TSEs. These experiments have focused on the study of the interaction of prions with plants and environmentally relevant surfaces. Our results show that plants (both leaves and roots) bind tightly to prions present in brain extracts and excreta (urine and feces) and retain even small quantities of PrPSc for long periods of time. Strikingly, ingestion of prioncontaminated leaves and roots produced disease with a 100% attack rate and an incubation period not substantially longer than feeding animals directly with scrapie brain homogenate. Furthermore, plants can uptake prions from contaminated soil and transport them to different parts of the plant tissue (stem and leaves). Similarly, prions bind tightly to a variety of environmentallyrelevant surfaces, including stones, wood, metals, plastic, glass, cement, etc. Prion contaminated surfaces efficiently transmit prion disease when these materials were directly injected into the brain of animals and strikingly when the contaminated surfaces were just placed in the animal cage. These findings demonstrate that environmental materials can efficiently bind infectious prions and act as carriers of infectivity, suggesting that they may play an important role in the horizontal transmission of the disease.


Since its invention 13 years ago, PMCA has helped to answer fundamental questions of prion propagation and has broad applications in research areas including the food industry, blood bank safety and human and veterinary disease diagnosis.


Prion2015 Program Guide 7 invited speakers




Early Trafficking and Dissemination of CWD Prions in Deer


Edward A. Hoover1*, Clare E. Hoover1, Davin M. Henderson1, Nathaniel D. Denkers1, Kristin A. Davenport1, Shannon Bartelt-Hunt2, Alan M. Elder1, Anthony E. Kincaid3, 4, Jason C. Bartz3, Mark D. Zabel1, Candace K. Mathiason1


1Prion Research Center, Department of Microbiology, Immunology, and Pathology, Colorado State University, Fort Collins, Colorado, USA 2Department of Civil Engineering, University of Nebraska-Lincoln,


Prion2015 Program Guide 10 invited speakers


PRION 2015


Omaha, Nebraska, USA, 3Department of Medical Microbiology and immunology Creighton University, Omaha, Nebraska, USA 4Department of Pharmacy Science, Creighton University, Omaha, Nebraska, USA * P r e s e n t i n g a u t h o r ’ s e - m a i l :


Efficient horizontal infection is a hallmark of chronic wasting disease (CWD) in freeranging cervids. The mechanisms and pathways that enable this remarkable process, however, remain incompletely understood--in particular the facile transmucosal entry, exit, and environmental persistence of CWD prions. We have focused on trans-mucosal CWD infection in white-tailed deer, specifically on early prion tissue tropism and later stage prion shedding and association with environmental constituents using modifications of real-time quaking-induced conversion combined with amplified immunohistochemistry. We have documented very early trans-mucosal prion passage (within hours), followed by uptake and amplification in upper digestive tract lymphoid t i s s u e s ( 4 w e e k s ) , and dissemination to more distant lymphoid and non-lymphoid tissue sites (8-12 weeks). We have used quantitative approaches to realtime conversion to estimate the relatively low (i.e. vs. tissues) prion concentrations in body fluids and excreta; i.e. >100 (cervidized mouse) LD50 are shed daily in the urine of one CWD infected deer. Using similar methods, we have also demonstrated and quantified the impressive affinity of CWD prions for both silty clay loam (a major environmental soil constituent) and metal surfaces. Mucosal uptake, excretion, and environmental interactions are central to this most transmissible of prion diseases.




Chronic wasting disease prions detected during early stages of infection by mbPMCA in tissues from white-tailed deer o r a l l y inoculated with f r e e and microparticle-bound prions


Alexandra Chesney1, Chad Johnson1, Tracy Nichols2, Hannah Kornely1, Dania Shoukfeh1, Joel Pedersen1


1University of Wisconsin, Madison, WI, USA, 2United States Department of Agriculture (USDA), Animal and Plant Health Inspection Service (APHIS), Wildlife Services (WS), National Wildlife Research Center (NWRC), Fort Collins, CO, USA


Enhanced oral transmission of rodenta d a p t e d p r i o n d i s e a s e has been demonstrated with the disease agent bound to several types of mineral microparticles; however, the generalizability of this finding to ruminants has not been established. Contaminated soil is believed to represent a reservoir for environmental prions and may contribute to horizontal transmission of chronic wasting disease (CWD) in captive and wild cervid populations. Here, we examined the impact of CWD agent association with microparticles o f montmorillonite, an aluminosilicate clay


Prion2015 Program Guide 35


mineral that showed the largest disease transmission enhancement in rodent bioassays, on early disease in orally inoculated white-tailed deer. Amplification of prions by PMCA has been achieved from various contaminated organs and excretions at late stages in disease. Using microplatebased PMCA (mbPMCA), we detected different accumulation patterns in white-tailed deer tissues 42 days after oral inoculation with CWD prions bound to montmorillonite. We expected mbPMCA to be more sensitive than immunohistochemistry (IHC) to determine prion accumulations in tissues. Through evaluation of mb-PMCA positive tissues, we found that mbPMCA is more sensitive than IHC by at least a factor of 106.3, and detected CWD prions in multiple tissue types that were negative by IHC. These findings suggest that microparticles can enhance the transmission of CWD in white-tailed deer and also demonstrates the consistency and high-throughput utility of the mbPMCA assay. Furthermore, our results indicate that enhanced transmission of microparticle-bound CWD agent warrants consideration in evaluating the relative importance o f d i r e c t and i n d i r e c t (environmental) transmission of CWD in natural populations and in disease management.






Influence of habitat and demographic components on exposure to chronic wasting disease in white-tailed deer in the eastern United States


W. David Walter1, Tyler Evans2 1U.S. Geological Survey, University Park, Pennsylvania, USA, 2Pennsylvania Cooperative Fish and Wildlife Research Unit, University Park, Pennsylvania, USA


Chronic wasting disease (CWD) is a transmissible spongiform encephalopathy that was first detected in the northeastern United States in 2005 in New York and West Virginia, and has since been found in Maryland, Virginia, and Pennsylvania. We examined demographic and environmental factors in the central Appalachian region to assess the spatial distribution of CWD in white-tailed deer (Odocoileus virginianus). The objectives of our study were to (1) apply Bayesian hierarchical modeling to harvest location data of white-tailed deer tested for CWD in the region since 2005, (2) identify model(s) that best described the spatial distribution of CWD, and (3) map probability of CWD infection across the Northeast. For each deer, environmental covariates were extracted within 6 km2 grid cells as this size reflected our estimate of the 99% size of home range for white-tailed deer in the region. The model with the most support did not include sex and age but contained random spatial effects and percent habitat and accounted for 94.4% of the overall weight for the candidate set of models. Percent forest cover appeared to have the strongest correlation with the distribution of CWD in the region, with increased risk of CWD occurring in areas that had lower amounts of forest cover. Our results also suggest that the use of age and sex data collected from harvested animals, commonly used in CWD modeling, should be further evaluated considering most are adult males, however, <2 are="" commonly="" cwd="" deer="" diagnosed="" div="" in="" old="" region.="" the="" with="" year="">


Wednesday, June 10, 2015


Zoonotic Potential of CWD Prions





Friday, January 30, 2015


*** Scrapie: a particularly persistent pathogen ***



Tuesday, December 16, 2014 Scrapie from sheep could infect humans with 'mad cow disease', study finds


Evidence for zoonotic potential of ovine scrapie prions


Hervé Cassard,1, n1 Juan-Maria Torres,2, n1 Caroline Lacroux,1, Jean-Yves Douet,1, Sylvie L. Benestad,3, Frédéric Lantier,4, Séverine Lugan,1, Isabelle Lantier,4, Pierrette Costes,1, Naima Aron,1, Fabienne Reine,5, Laetitia Herzog,5, Juan-Carlos Espinosa,2, Vincent Beringue5, & Olivier Andréoletti1, Affiliations Contributions Corresponding author Journal name: Nature Communications Volume: 5, Article number: 5821 DOI: doi:10.1038/ncomms6821 Received 07 August 2014 Accepted 10 November 2014 Published 16 December 2014 Article tools Citation Reprints Rights & permissions Article metrics




Although Bovine Spongiform Encephalopathy (BSE) is the cause of variant Creutzfeldt Jakob disease (vCJD) in humans, the zoonotic potential of scrapie prions remains unknown. Mice genetically engineered to overexpress the human ​prion protein (tgHu) have emerged as highly relevant models for gauging the capacity of prions to transmit to humans. These models can propagate human prions without any apparent transmission barrier and have been used used to confirm the zoonotic ability of BSE. Here we show that a panel of sheep scrapie prions transmit to several tgHu mice models with an efficiency comparable to that of cattle BSE. The serial transmission of different scrapie isolates in these mice led to the propagation of prions that are phenotypically identical to those causing sporadic CJD (sCJD) in humans. These results demonstrate that scrapie prions have a zoonotic potential and raise new questions about the possible link between animal and human prions.


Subject terms: Biological sciences• Medical research At a glance



see more here ;



O.05: Transmission of prions to primates after extended silent incubation periods: Implications for BSE and scrapie risk assessment in human populations


Emmanuel Comoy, Jacqueline Mikol, Val erie Durand, Sophie Luccantoni, Evelyne Correia, Nathalie Lescoutra, Capucine Dehen, and Jean-Philippe Deslys Atomic Energy Commission; Fontenay-aux-Roses, France


Prion diseases (PD) are the unique neurodegenerative proteinopathies reputed to be transmissible under field conditions since decades. The transmission of Bovine Spongiform Encephalopathy (BSE) to humans evidenced that an animal PD might be zoonotic under appropriate conditions. Contrarily, in the absence of obvious (epidemiological or experimental) elements supporting a transmission or genetic predispositions, PD, like the other proteinopathies, are reputed to occur spontaneously (atpical animal prion strains, sporadic CJD summing 80% of human prion cases). Non-human primate models provided the first evidences supporting the transmissibiity of human prion strains and the zoonotic potential of BSE. Among them, cynomolgus macaques brought major information for BSE risk assessment for human health (Chen, 2014), according to their phylogenetic proximity to humans and extended lifetime. We used this model to assess the zoonotic potential of other animal PD from bovine, ovine and cervid origins even after very long silent incubation periods. *** We recently observed the direct transmission of a natural classical scrapie isolate to macaque after a 10-year silent incubation period, ***with features similar to some reported for human cases of sporadic CJD, albeit requiring fourfold longe incubation than BSE. Scrapie, as recently evoked in humanized mice (Cassard, 2014), ***is the third potentially zoonotic PD (with BSE and L-type BSE), ***thus questioning the origin of human sporadic cases. We will present an updated panorama of our different transmission studies and discuss the implications of such extended incubation periods on risk assessment of animal PD for human health.




***thus questioning the origin of human sporadic cases...TSS





Saturday, May 30, 2015





 I strenuously once again urge the FDA and its industry constituents, to make it MANDATORY that all ruminant feed be banned to all ruminants, and this should include all cervids as soon as possible for the following reasons...




In the USA, under the Food and Drug Administrations BSE Feed Regulation (21 CFR 589.2000) most material (exceptions include milk, tallow, and gelatin) from deer and elk is prohibited for use in feed for ruminant animals. With regards to feed for non-ruminant animals, under FDA law, CWD positive deer may not be used for any animal feed or feed ingredients. For elk and deer considered at high risk for CWD, the FDA recommends that these animals do not enter the animal feed system.


***However, this recommendation is guidance and not a requirement by law.




31 Jan 2015 at 20:14 GMT


*** Ruminant feed ban for cervids in the United States? ***


31 Jan 2015 at 20:14 GMT





Pathological Prion Protein (PrPTSE) in Skeletal Muscles of Farmed and Free Ranging White-Tailed Deer Infected with Chronic Wasting Disease


***The presence and seeding activity of PrPTSE in skeletal muscle from CWD-infected cervids suggests prevention of such tissue in the human diet as a precautionary measure for food safety, pending on further clarification of whether CWD may be transmissible to humans.



Prions in Skeletal Muscles of Deer with Chronic Wasting Disease Rachel C. Angers1,*, Shawn R. Browning1,*,†, Tanya S. Seward2, Christina J. Sigurdson4,‡, Michael W. Miller5, Edward A. Hoover4, Glenn C. Telling1,2,3,§ snip...


Abstract The emergence of chronic wasting disease (CWD) in deer and elk in an increasingly wide geographic area, as well as the interspecies transmission of bovine spongiform encephalopathy to humans in the form of variant Creutzfeldt Jakob disease, have raised concerns about the zoonotic potential of CWD. Because meat consumption is the most likely means of exposure, it is important to determine whether skeletal muscle of diseased cervids contains prion infectivity. Here bioassays in transgenic mice expressing cervid prion protein revealed the presence of infectious prions in skeletal muscles of CWD-infected deer, demonstrating that humans consuming or handling meat from CWD-infected deer are at risk to prion exposure.



***********CJD REPORT 1994 increased risk for consumption of veal and venison and lamb***********




Consumption of venison and veal was much less widespread among both cases and controls. For both of these meats there was evidence of a trend with increasing frequency of consumption being associated with increasing risk of CJD. (not nvCJD, but sporadic CJD...tss)


These associations were largely unchanged when attention was restricted to pairs with data obtained from relatives. ...


Table 9 presents the results of an analysis of these data.


There is STRONG evidence of an association between ‘’regular’’ veal eating and risk of CJD (p = .0.01).


Individuals reported to eat veal on average at least once a year appear to be at 13 TIMES THE RISK of individuals who have never eaten veal.


There is, however, a very wide confidence interval around this estimate. There is no strong evidence that eating veal less than once per year is associated with increased risk of CJD (p = 0.51).


The association between venison eating and risk of CJD shows similar pattern, with regular venison eating associated with a 9 FOLD INCREASE IN RISK OF CJD (p = 0.04).


There is some evidence that risk of CJD INCREASES WITH INCREASING FREQUENCY OF LAMB EATING (p = 0.02).


The evidence for such an association between beef eating and CJD is weaker (p = 0.14). When only controls for whom a relative was interviewed are included, this evidence becomes a little STRONGER (p = 0.08).




It was found that when veal was included in the model with another exposure, the association between veal and CJD remained statistically significant (p = < 0.05 for all exposures), while the other exposures ceased to be statistically significant (p = > 0.05).




In conclusion, an analysis of dietary histories revealed statistical associations between various meats/animal products and INCREASED RISK OF CJD. When some account was taken of possible confounding, the association between VEAL EATING AND RISK OF CJD EMERGED AS THE STRONGEST OF THESE ASSOCIATIONS STATISTICALLY. ...




In the study in the USA, a range of foodstuffs were associated with an increased risk of CJD, including liver consumption which was associated with an apparent SIX-FOLD INCREASE IN THE RISK OF CJD. By comparing the data from 3 studies in relation to this particular dietary factor, the risk of liver consumption became non-significant with an odds ratio of 1.2 (PERSONAL COMMUNICATION, PROFESSOR A. HOFMAN. ERASMUS UNIVERSITY, ROTTERDAM). (???...TSS)


snip...see full report ;





October 1994


Mr R.N. Elmhirst Chairman British Deer Farmers Association Holly Lodge Spencers Lane BerksWell Coventry CV7 7BZ


Dear Mr Elmhirst,




Thank you for your recent letter concerning the publication of the third annual report from the CJD Surveillance Unit. I am sorry that you are dissatisfied with the way in which this report was published.


The Surveillance Unit is a completely independant outside body and the Department of Health is committed to publishing their reports as soon as they become available. In the circumstances it is not the practice to circulate the report for comment since the findings of the report would not be amended. In future we can ensure that the British Deer Farmers Association receives a copy of the report in advance of publication.


The Chief Medical Officer has undertaken to keep the public fully informed of the results of any research in respect of CJD. This report was entirely the work of the unit and was produced completely independantly of the the Department.


The statistical results reqarding the consumption of venison was put into perspective in the body of the report and was not mentioned at all in the press release. Media attention regarding this report was low key but gave a realistic presentation of the statistical findings of the Unit. This approach to publication was successful in that consumption of venison was highlighted only once by the media ie. in the News at one television proqramme.


I believe that a further statement about the report, or indeed statistical links between CJD and consumption of venison, would increase, and quite possibly give damaging credence, to the whole issue. From the low key media reports of which I am aware it seems unlikely that venison consumption will suffer adversely, if at all.



Wednesday, March 18, 2009


Noah’s Ark Holding, LLC, Dawson, MN RECALL Elk products contain meat derived from an elk confirmed to have CWD NV, CA, TX, CO, NY, UT, FL, OK RECALLS AND FIELD CORRECTIONS: FOODS CLASS II



-----Original Message-----




Sent: Sunday, September 29, 2002 10:15 AM


To:;; ebb8@CDC.GOV


Subject: TO CDC AND NIH - PUB MED- 3 MORE DEATHS - CWD - YOUNG HUNTERS Sunday, November 10, 2002 6:26 PM ......snip........end..............TSS


Thursday, April 03, 2008


A prion disease of cervids: Chronic wasting disease


2008 1: Vet Res. 2008 Apr 3;39(4):41 A prion disease of cervids: Chronic wasting disease Sigurdson CJ.




*** twenty-seven CJD patients who regularly consumed venison were reported to the Surveillance Center***,


snip... full text ;



*** These results would seem to suggest that CWD does indeed have zoonotic potential, at least as judged by the compatibility of CWD prions and their human PrPC target.


*** Furthermore, extrapolation from this simple in vitro assay suggests that if zoonotic CWD occurred, it would most likely effect those of the PRNP codon 129-MM genotype and that the PrPres type would be similar to that found in the most common subtype of sCJD (MM1).***



*** The potential impact of prion diseases on human health was greatly magnified by the recognition that interspecies transfer of BSE to humans by beef ingestion resulted in vCJD. While changes in animal feed constituents and slaughter practices appear to have curtailed vCJD, there is concern that CWD of free-ranging deer and elk in the U.S. might also cross the species barrier. Thus, consuming venison could be a source of human prion disease. Whether BSE and CWD represent interspecies scrapie transfer or are newly arisen prion diseases is unknown. Therefore, the possibility of transmission of prion disease through other food animals cannot be ruled out. There is evidence that vCJD can be transmitted through blood transfusion. There is likely a pool of unknown size of asymptomatic individuals infected with vCJD, and there may be asymptomatic individuals infected with the CWD equivalent. These circumstances represent a potential threat to blood, blood products, and plasma supplies.



Friday, May 22, 2015


*** Chronic Wasting Disease and Program Updates - 2014 NEUSAHA Annual Meeting 12-14 May 2014 ***



 Wednesday, February 12, 2014


VIRGINIA VDGIF Reports Two New CWD Positives in Frederick County



Monday, October 08, 2012


VDGIF has discovered four positive cases of CWD in Virginia Updated 9/24/2012



Thursday, March 15, 2012 CWD VIRGINIA TWO NEW CASES



Friday, December 17, 2010


CWD positive in western Frederick County VA VDGIF December 16, 2010



Thursday, January 21, 2010


Chronic Wasting Disease Found in White-tailed Deer in Virginia



Thursday, June 09, 2011


Detection of CWD prions in salivary, urinary, and intestinal tissues of deer: potential mechanisms of prion shedding and transmission



Wednesday, March 18, 2009


Detection of CWD Prions in Urine and Saliva of Deer by Transgenic Mouse Bioassay



doi:10.1016/j.febslet.2008.08.003 Copyright © 2008 Published by Elsevier B.V. Detection of infectious prions in urine Dennisse Gonzalez-Romeroa, Marcelo A. Barriaa, Patricia Leona, Rodrigo Moralesa and Claudio Soto, a,





Date: Sat, 20 Jul 2002 09:43:10 -0700


From: "Terry S. Singeltary Sr."




Date: Sat, 25 May 2002 18:41:46 -0700


From: "Terry S. Singeltary Sr."


Reply-To: Bovine Spongiform Encephalopathy To:


######## Bovine Spongiform Encephalopathy #########






 now, what about those 'deer scents' of 100% urine', and the prion that is found in urine, why not just pass the prion with the urine to other deer...


 Mrs. Doe Pee Doe in Estrus Model FDE1 Mrs. Doe Pee's Doe in Estrus is made from Estrus urine collected at the peak of the rut, blended with Fresh Doe Urine for an extremely effective buck enticer. Use pre-rut before the does come into heat. Use during full rut when bucks are most active. Use during post-rut when bucks are still actively looking for does. 1 oz.







Works anytime of the year *


100 % Cow Elk-in-Heat urine (2oz.) *


Economical - mix with water in spray mist bottle *


Use wind to your advantage


Product Code WP-ESB $9.95



prions in urine?







Terry S. Singeltary Sr.



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