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-
DRAFT 2015-2024 VIRGINIA DEER MANAGEMENT PLAN 22
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
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
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
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.
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.
85 DRAFT 2015-2024 VIRGINIA DEER MANAGEMENT PLAN
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
• 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
• 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
• 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
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
>>> 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
*** LATE-BREAKING ABSTRACTS PRION 2015 CONFERENCE ***
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
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
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
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
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
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
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
***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
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
***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
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.
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
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
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 : email@example.com
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
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,
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
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
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
PRION 2015 ORAL AND POSTER CONGRESSIONAL ABSTRACTS
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
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
***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***********
CREUTZFELDT JAKOB DISEASE SURVEILLANCE IN THE UNITED KINGDOM THIRD ANNUAL
REPORT AUGUST 1994
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
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 ;
Mr R.N. Elmhirst Chairman British Deer Farmers Association Holly Lodge
Spencers Lane BerksWell Coventry CV7 7BZ
Dear Mr Elmhirst,
CREUTZFELDT-JAKOB DISEASE (CJD) SURVEILLANCE UNIT REPORT
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
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
Sent: Sunday, September 29, 2002 10:15 AM
To: firstname.lastname@example.org; email@example.com; 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
*** 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
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
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,
Subject: MAD DEER/ELK DISEASE AND POTENTIAL SOURCES
Date: Sat, 20 Jul 2002 09:43:10 -0700
From: "Terry S. Singeltary Sr."
Subject: MAD DEER/ELK DISEASE AND POTENTIAL SOURCES
Date: Sat, 25 May 2002 18:41:46 -0700
From: "Terry S. Singeltary Sr."
Reply-To: Bovine Spongiform Encephalopathy To: BSE-L@uni-karlsruhe.de
######## Bovine Spongiform Encephalopathy #########
MAD DEER/ELK DISEASE AND POTENTIAL SOURCES
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.
ELK SCENT/SPRAY BOTTLE
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?
[PDF] A URINE TEST FOR THE IN-VIVO DIAGNOSIS OF PRION DISEASES
Terry S. Singeltary Sr.
Thank You For Your Comments
Thank you for submitting your comments on the
Draft Deer Management Plan.