WYOMING GAME AND FISH DEPARTMENT CHRONIC WASTING DISEASE MANAGEMENT PLAN APRIL 22, 2016
WYOMING GAME AND FISH DEPARTMENT CHRONIC WASTING DISEASE MANAGEMENT PLAN
April 22, 2016
EXECUTIVE SUMMARY
The purpose of this CWD Management Plan (Plan) is to provide flexible and
adaptable direction for spread, prevention and management of chronic wasting
disease (CWD) in cervids — mule deer, (Odocoileus hemionus), white-tailed deer
(Odocoileus virginianus), elk (Cervus elaphus) and moose (Alces alces).
The Plan will be reviewed and updated as warranted.
The Plan consists of four components: Disease Management, Applied Research,
Public Information and Funding.
Based upon current research and known epidemiology of CWD in free—ranging
cervids, eradication is currently not realistic, but eradication is the desired
long—term disease management objective.
The Wyoming Game and Fish Department (WGFD) will coordinate the management
of CWD with other state, federal and tribal agencies.
The WGFD will conduct surveillance to monitor and estimate spatial
distribution and prevalence of CWD, as well as actively cooperate and coordinate
CWD research with other state, federal, tribal agencies and entities of higher
education, universities and other researchers. WGFD will expand its CWD efforts
beyond being the “field control” state.
The WGFD will provide timely, complete and accurate CWD informational and
educational material to the public, via the WGFD website (http://wgfd.wyo.gov), other media and social
media outlets.
The WGFD will continue to work cooperatively with the Wyoming Department of
Health and other human health organizations to monitor current research on CWD
and human health to provide up—to—date-information to the public.
GOALS The following goals will be addressed through the four components
outlined in this Plan.
Manage deer, elk, moose and their habitats in Wyoming to delay the spread
of CWD and reduce the effects of CWD on wildlife health and human enjoyment of
wildlife resources.
Monitor the change in spatial distribution and prevalence of CWD over
time.
Reduce the rate of spread and prevalence of CWD.
Coordinate CWD management and research with other state, federal and tribal
agencies and entities of higher education, universities and other
researchers.
Adapt CWD management in response to surveillance and research
findings.
Provide timely, complete and accurate CWD information to the public.
INTRODUCTION
Chronic wasting disease (CWD) is a transmissible spongiform encephalopathy
(TSE) and is a chronic fatal disease of the central nervous system of deer, elk
and moose. Other wildlife species do not appear to be susceptible to CWD. TSE
disorders are thought to be caused by abnormal proteins called “prions.” Prions
are neither bacteria nor viruses. They are proteins devoid of nucleic acid, thus
they are not living organisms. Prions have similar amino acid sequences as
normal cellular proteins but in a different conformation. The functional
role of the normal cellular proteins is unknown. Prions cause a conformational
change in the normal cellular protein and disease is induced when the normal
cellular protein is converted into the prion protein, which apparently can no
longer serve its normal role. This eventually causes cells of the central
nervous system to die. As more and more cells die, the disease can be observed
to progress, ultimately ending in death.
In early disease, there may be no observable clinical signs of CWD. As the
disease progresses, affected animals may have one or more of the following
signs:
1. Emaciation, poor body condition, rough hair coat.
2. Behavioral changes (hyperactive when constrained; reluctance to move;
ears droop).
3. Excessive salivation (sometimes).
4. Excessive drinking (or staying close to water source).
5. Lethargy (but will react when approached closely).
6. Death
CWD was first observed in captive mule deer in Colorado in 1967 (Williams
and Young, 1980), but was not observed in free—ranging deer and elk in Wyoming
until 1986. The disease was rare and of little interest to wildlife managers or
the public until another TSE, bovine spongiform encephalopathy (BSE), caused
human disease in the United Kingdom (Bruce, 1997). Because BSE is similar to
CWD, people became concerned CWD could also affect human health. Initial
incursion of CWD is thought to be by animal-to—animal contact, with later phases
of transmission driven by animal to environment and vice versa. In this 30-year
interim, CWD became firmly established in deer and elk in southeastern Wyoming
and has spread into the Bighorn Basin, the east side of the Bighorn Mountains,
south-central Wyoming, southern Green River Basin, eastern slope of the Wind
River Mountains and northeastern Wyoming. Deer, elk and moose hunt areas in
Wyoming where CWD has been found can be seen on the WGFD website:
Disease management in wildlife is an important responsibility of the WGFD.
The purpose of this Plan is to provide flexible and adaptable direction for
monitoring and management of CWD in Wyoming. The plan will be reviewed and
updated as warranted. The plan consists of four components:
1. Disease Management
II. Applied Research
III. Public Information
IV. Funding
COMPONENT I. DISEASE MANAGEMENT
Based on current scientific information, eradication of CWD from free
ranging cervids is currently not a realistic disease management objective,
particularly since the disease has become established in multiple states and
Canadian provinces (Government of Alberta, 2008; James, 2008), but eradication
remains the ultimate desired outcome. Early mathematical models predicted CWD
would drive affected cervid populations to extinction (Gross and Miller, 2001).
More recent modeling suggests CWD may have a population level impact in Rocky
Mountain National Park elk (Monello, 2013, 2014), in Wyoming white—tailed deer
(Edmunds, 2013), and in Wyoming mule deer (DeVivo, pers. Comm.). Other research
suggests certain populations may be
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able to survive through disease-driven genetic selection and some level of
hunting season restrictions (Robinson, 2012; Williams, 2014). Nonetheless, it is
anticipated endemic CWD will depress some cervid populations to some unknown
level (Miller, 2008; Edmunds 2013; Monello 2014). Even though eradication is not
feasible at this time, the WGFD will consider management actions to slow the
spread and/or reduce the prevalence of the disease statewide, based on accepted
scientific information and wildlife management practices.
Through adoption of this Plan, the WGFD has chosen an adaptive management
strategy allowing flexibility to alter disease management activities depending on
future research findings, CWD distribution, prevalence, funding, and level of
concern (public, WGFD and other governmental agencies). The Disease Management
component of this plan addresses nine objectives. Most of these objectives were
identified by a panel of 60 wildlife disease experts and categorized relative to
their estimated efficacy in endemic CWD areas (Government of Alberta, 2008). The
WGFD will use the best scientific information available and will take necessary
and reasonable steps to achieve these objectives:
1. Surveillance.
Surveillance allows the WGFD to identify which deer, elk, or moose hunt
areas have one or more of these species testing positive for CWD. These hunt
areas will comprise the “CWD Endemic Area” within Wyoming.
The WGFD will conduct CWD surveillance as funding permits, and will modify
its surveillance based on funding and distribution of CWD within the state. Much
of the WGFD’s surveillance emphasis will remain in the “core endemic area” (Deer
Hunt Areas 59, 64 - 66 and Elk Hunt Areas 7 and 19), around the 22 state elk
feedgrounds and National Elk Refuge (NER), and monitoring along the western
frontier of the CWD endemic area. Surveillance is conducted by collecting
retropharyngeal lymph nodes, tonsil tissue, or the obex from hunter and
vehicle-killed cervids, cervids exhibiting clinical signs consistent with CWD
(i.e., targeted surveillance), cervids found dead from unknown causes or those
killed by predators.
Hunters, who participate in the WGFD’s CWD surveillance program by
providing deer, elk, or moose tissue samples and provide adequate information,
can obtain test results through the WGFD's website at:
If a sample submitted to the WGFD’s CWD surveillance program tests positive
and adequate contact information is provided, the hunter will be notified of the
positive test result.
Other than the WGFD surveillance program, WGFD will not be responsible for
the testing of individual hunter’s deer, elk, or moose. The WGFD will provide
information regarding testing by the Wyoming State Veterinary Laboratory for
hunters who choose to have their deer, elk or moose tested at their own
expense.
The WGFD may donate deer, elk and moose carcasses acquired from the CWD
endemic area to individuals after the animal has been tested with no evidence of
CWD being found. The recipient must also sign an affidavit of informed consent.
While the WGFD may donate meat from cervids testing CWD negative to individuals,
it will not donate
3
meat from animals killed within the CWD endemic area to organizations or
entities whose purpose is to redistribute the meat.
To provide for additional surveillance opportunities, WGFD will provide
training on recognition of CWD clinical signs and collecting CWD samples for
testing to WGFD employees, other state and federal employees, hunters,
outfitters, and the general public as needed or requested.
Carcass Movement Regulatory Restrictions.
Tissues of CWD-infected carcasses can transmit CWD to uninfected cervids
(Miller, 2004). To minimize this potential source of transmission to other areas
within and outside of Wyoming, the WGFC Chapter 2 General Hunting Regulation
directs the transportation and disposal of harvested cervids taken from within
Wyoming. Likewise, the WGFC Chapter 2 General Hunting Regulation controls the
importation of harvested cervids/cervid parts taken from any state, province or
country within areas designated by the appropriate jurisdictional agency known
to have CWD. The Chapter 2 General Hunting Regulation pertaining to CWD is
enforced by WGFD law enforcement personnel on a year-round basis. The Chapter 2
General Hunting Regulation can be found on the WGFD website at:
Translocation of cervids within and outside of Wyoming.
Live free-ranging cervids originating within Wyoming will not be moved to
other locations for any reason within or outside of Wyoming without prior
review, approval, or permitting by the WGFD and/or WGFC.
Remove cervids suspected of being affected by CWD.
Removal of cervids exhibiting signs consistent with CWD may reduce the
spread and persistence of the disease, as well as contribute to statewide
targeted surveillance data and provide research material for WGFD or other
researchers. When possible, WGFD personnel will lethally take, collect
appropriate biological samples (including whole carcasses for complete necropsy)
for disease testing or remove targeted cervids from the field and properly
dispose of the carcass in a manner that will minimize CWD transmission and
environmental contamination. In addition, the WGFD will continue its public
information and education efforts strongly encouraging the public to immediately
report sick cervids on a year round basis to aid in CWD monitoring efforts.
Research has shown that such targeted surveillance and lethal removal is
effective to document presence of CWD as well as removing source of
infection.
Appropriate WGFD personnel will participate in intra- and interdepartmental
and intra- and interstate CWD coordination meetings.
Sharing research and coordination among state, federal, and tribal agencies
is important in the management of CWD. The WGFD will coordinate and collaborate
with state, federal, tribal agencies and entities of higher education,
universities and other researchers on relevant CWD management and research
issues as requested or needed. The WGFD encourages other state, federal, tribal
agencies and entities of higher education,
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universities and other researchers to initiate inter-agency CWD
coordination meetings as well.
Maintain the Wyoming statutory prohibition of cervid ownership, importation
and facilities in Wyoming and the effectiveness of the WGFC’s Chapter 10
regulation.
Wyoming has some of the most stringent laws and regulations pertaining to
the private ownership and importation of live cervids in the United States.
These laws and regulations were developed to protect Wyoming’s wildlife from
disease, genetic, ecological, environmental, and other threats. WGFC Chapter 10
Regulation, “Regulation for Importation, Possession, Confinement, Transportation,
Sale and Disposition of Live Wildlife,” addresses CWD in relation to the only
privately owned elk facility permitted in Wyoming by statute. Any captive cervid
imported into Wyoming must originate from facilities certified to be free of CWD
in accordance with federal regulations (9 CFR, parts 55 and 81) and WGFC Chapter
10 regulation. These WGFC and federal restrictions are intended to prevent
spread of CWD. There are no other captive, privately owned cervids within
Wyoming. Future establishment of captive, commercial native cervid facilities in
Wyoming is prohibited by statute.
Hunter harvest will continue to be the primary tool for monitoring CWD in
cervids.
The flexibility inherent in Wyoming’s hunting regulations allows the WGFC to
modify hunting seasons to meet specific management objectives. This flexibility,
combined with the long and rich hunting heritage in the State of Wyoming, makes
the use of hunter harvest an effective and preferred tool in monitoring CWD in
cervids.
Herd population management.
Large—scale culling in an attempt to reduce animal populations and minimize
animal to animal contact has been attempted in other states and provinces. While
such culling has shown it can reduce or maintain prevalence levels, it has
proven to be expensive, unpopular, requires continued long-term application, and
ultimately is unable to eradicate CWD (State of Wisconsin, 2006; James, 2008;
Holsman, 2010; VerCauteren, Kurt, and Scott E. Hygnstrom, 2011; Wasserberg,
2009, 2014; Manjerovic 2014). The WGFD will consider disease
transmission/prevalence when developing herd population objectives and other
management recommendations. The WGFD will strive to meet herd population
objectives by taking in account all factors and influences. Small scale culling
may be considered in some circumstances to slow disease spread.
Feedgrounds.
Elk have been fed in northwest Wyoming since the early 1900s. Originally,
elk feedgrounds were designed to mitigate loss of winter range, reduce human/elk
conflicts and maintain a traditional population of elk. More recently, elk
feedgrounds have continued to address those issues as well as facilitating
separation of elk and cattle to prevent the potential spread of brucellosis.
Supplemental feeding of elk creates complex biological, social, economic and
political issues. Wildlife disease adds to this complexity. Recent modeling
based on a combination of captive and free-ranging elk data suggested that
feedground elk may survive in the face of CWD at significantly reduced
numbers
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through a combination of genetic selection and elimination of antlerless
elk harvest (Williams, 2014). However, extrapolating data from captive
situations is difficult at best and it is still unknown what impact CWD could
ultimately have on feedground elk populations. Disease transmission can be
related to density of animals in a given area as well as the frequency of
contact between animals. Artificially concentrating elk on feedgrounds may result
in more rapid spread of CWD and contribute to increased persistence of prions in
the soil and uptake by vegetation.
The WGFD will continue to prioritize identification, removal and testing of
cervids exhibiting signs consistent with CWD on and around elk feedgrounds.
Hunter harvest and other CWD surveillance in northwestern Wyoming will be
conducted in coordination with the NER and the National Park Service — Grand
Teton National Park (GTNP).
The WGFD will work with the NER, GTNP, and United States Forest Service
(USFS)- Bridger-Teton National Forest (BTNF) on implementing the Jackson Elk and
Bison Management Plan to manage wintering populations and reduce their reliance
on supplemental feed.
The WGFD will collaborate with stakeholders to acquire critical winter
range habitat and migration corridors for elk in order to protect elk from human
disturbance.
The WGFD will work with federal and state land management agencies and non-
governmental agencies to develop, fund and implement habitat improvement
projects for elk to reduce dependence on feedgrounds.
Based on research that grass plants can bind, retain, uptake and transport
prions (Pritzkow, 2015), the WGFD assess potential CWD transmission risks of hay
harvested from the CWD endemic area that is fed at state elk feedgrounds. Prior
to hay being purchased and transported to elk feedgrounds, the WGFD will look at
the spatial and temporal relationships between the location(s) and prevalence
rate(s) of CWD positive cervids and hay fields from which hay is used for elk
feedgrounds. The WGFD will attempt to only use hay for elk feedgrounds from
outside the CWD endemic area. Additionally, the WGFD will communicate with the
appropriate land management agency(s) as it pertains to elk feedground hay use
and CWD.
Additionally, WGFD will:
Review WGFC supplemental feeding policy to determine if changes are
warranted to address CWD.
Determine if closures of specific feedgrounds can occur where dispersal of
elk will not cause damage/conflict/co-mingling issues with private property,
stored crops and domestic livestock or create a need to drastically reduce
overall elk herd sizes.
The WGFD will consider CWD transmission/prevalence/negative impacts when
developing herd population objectives, feedground quotas, hunting seasons and
other management recommendations. The WGFD will strive to meet herd population
objectives/feedground quotas by taking in account all factors and
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influences; however, if CWD becomes established on a feedground, populations
and hunting opportunity may decrease overtime.
As funding and testing/field capacity allows, expand and increase the WGFD’s
CWD surveillance efforts in the Pinedale and Jackson Regions.
If a single case of CWD is confirmed in a deer, elk or moose in or adjacent
to an elk herd unit with feedgrounds, WGFD will intensify surveillance in a
timely manner, both in the new positive hunt area(s) and within the elk herd
unit with feedgrounds. This will include increased sample collection efforts
through hunter harvest, targeted removal and road-kill of deer, elk and moose.
The data will be reviewed and management actions will be considered to minimize
the spread of CWD for the specific feedground(s) and surrounding areas. WGFD will
communicate, consult and coordinate with GTNP, NER and BTNF pertaining to any
proposed actions to address CWD being confirmed in or adjacent to an elk herd
unit containing feedgrounds.
If CWD is detected in elk inhabiting feedgrounds, WGFD personnel shall
monitor the feedground and surrounding area intensively, lethally remove,
sample, test and properly dispose of any elk exhibiting clinical signs of CWD.
Large scale culling of elk on a feedground and on native winter range is not an
anticipated action to address CWD.
The WGFD will continue, to the extent possible, to: 1) maximize the feeding
area to decrease animal-to-animal contact (low density feeding); 2) decrease
days of feeding to promote the dispersion of elk; 3) take additional actions to
decrease elk concentration provided such actions are consistent with other
necessary wildlife management and feedground practices.
Properly dispose of carcasses from feedgrounds to limit soil contamination
and the spread of CWD; this may include incineration or other acceptable methods
of disposal to minimize CWD transmission and environmental contamination.
As personnel and budget capacity allow, establish a baseline genetic
inventory for individual herds in the Jackson and Pinedale Regions. This will
allow the WGFD to track if genetic shift is occurring over time toward alleles
that have a prolonged incubation period for CWD and increased rates of
survival.
Continue researching and monitoring cervid migration and dispersal routes
in and out of the Jackson and Pinedale Regions and how these migrating animals
may expand CWD.
Monitor predatory animal presence and their impacts on feedground elk,
including the implementation of proper management actions for gray wolves that
are causing unacceptable impacts to elk at any state operated feedground in
accordance with W.S. 23—l—304 and WGFC Chapter 21 Gray Wolf Management
regulation.
Consider the potential role of predators and scavengers to remove CWD
infected animals and carcasses to reduce CWD transmission (Krumm, 2010; Wild,
2011).
COMPONENT II. APPLIED RESEARCH
CWD management, research, and public information activities are expensive.
With federal CWD funding no longer available, the WGFD will continue to request
general funds for CWD surveillance and research as part of the WGFD’s Veterinary
Services program budget. The WGFD is not a primary research agency and does not
contain a research branch which limits its abilities to conduct CWD research.
Therefore, WGFD will focus research on implementing sustainable CWD “on the
ground” management strategies in select areas across the state with the goal of
evaluating long-term efficacy of such management strategies to reduce or maintain
CWD prevalence and expansion. In addition, the WGFD will collaborate with
external entities (multi- state and agency collaboration, institutions of higher
education) on CWD research proposals, projects and funding that will facilitate
continued expansion of knowledge of CWD. The WGFD will expand its CWD research
and management efforts beyond being the “field control” state. The WGFD is
committed to a long-term investment in research and “on the ground” management
strategy work implementation. The WGFD will continue to monitor published
research on CWD and similar diseases to ensure the WGFD has the most current and
comprehensive data and scientific information available to make CWD and cervid
management decisions.
COMPONENT III. PUBLIC INFORMATION
Chronic wasting disease is of interest to various groups at different
levels locally, nationally and internationally. As the public agency charged
with managing Wyoming’s wildlife populations, the WGFD has an obligation to
provide timely, complete, accurate, and unbiased information about CWD to the
public. The WGFD’s information efforts related to CWD will focus on: where CWD
has been found in Wyoming; public health risk as determined by public health
departments and public health experts; WGFD efforts to monitor the disease;
efforts by WGFD and others to learn more about the disease; potential impacts to
deer, elk or moose populations; laws and regulations related to CWD; and how the
public can minimize the spread of CWD during the hunting season and throughout
the year. The WGFD will provide current CWD information on its website, various
media and social media outlets, and public presentations and contacts.
COMPONENT IV. FUNDING
CWD management, research, and public information activities are expensive,
and the WGFD’s financial status will not allow complete implementation of this
plan without additional funding. The WGFD will continue to request general funds
for CWD work as part of the WGFD’s Veterinary Services program budget and will
pursue additional funding sources (e.g. Wyoming Wildlife/Livestock Disease
Research Partnership, USDA—APHIS, Wyoming Governor’s Big Game License Coalition,
Wyoming Wildlife and Natural Resource Trust, University of Wyoming) to implement
this plan and research projects. Based on available funding, disease management
would be the top priority, followed by public information and education, and
research.
ACKNOWLEDGEMENTS
Many elements of this CWD Plan would not be possible without the
cooperation of sportspersons, landowners, game meat processors, taxidermists,
outfitters and professional guides, scientists, and professional wildlife
managers. We appreciate their interest and assistance.
LITERATURE CITED
Bruce, M. E., Will, R. G., Ironside, J. W., McConnell, 1., Drummond, D.,
Suttie, A., & Cousens, S. (1997). Transmissions to mice indicate that ‘new
variant’CJD is caused by the BSE agent. Nature, 389(6650), 498-501.
Edmunds, David R. (2013) Chronic Wasting Disease Ecology and Epidemiology
of Wliite—tailed Deer in Wyoming (doctoral dissertation). University of Wyoming,
Department of Veterinary Sciences, Laramie, WY.
Government of Alberta, Alberta Sustainable Resource Development. 2008.
Chronic Wasting Disease Workshop. Online citation: http://aep.alberta.ca/fish-wildlife/wildlife-diseases/chronic-wasting-disease/documents/AlbertaChronicWastingDiseaseManagement.pdf
Gross, J. E., & Miller, M. W. (2001). Chronic wasting disease in mule
deer: disease dynamics and control. The Journal of wildlife management,
205-215.
Holsman, R. H., Petchenik, J ., & Cooney, E. E. (2010). CWD after “the
fire”: Six reasons why hunters resisted Wisconsin's eradication effort. Human
Dimensions of Wildlife, 15(3), 180-193.
James, P. C. (2008). Both sides of the fence: A strategic review of chronic
wasting disease management costs and benefits.
Krumm, C. E., Conner, M. M., Hobbs, N. T., Hunter, D. 0., & Miller, M.
W. (2010). Mountain lions prey selectively on prion-infected mule deer. Biology
letters, 6(2), 209-211.
Manjerovic, M. B., Green, M. L., Mateus-Pinilla, N., & Novakofski, J.
(2014). The importance of localized culling in stabilizing chronic wasting
disease prevalence in white-tailed deer populations. Preventive veterinary
medicz'ne,1 1 3 (1), 139-145.
Miller, M. W., Williams, E. S., Hobbs, N. T., & Wolfe, L. L. (2004).
Environmental sources of prion transmission in mule deer. Emerg Infect
Dis,10(6), 1003-1006.
Miller, M. W., Swanson, H. M., Wolfe, L. L., Quartarone, F. G., Huwer, S.
L., Southwick, C. H., & Lukacs, P. M. (2008). Lions and prions and deer
demise. PLoS one, 3(l2), e40l9- e4019.
Monello, R. J., Powers, J. G., Hobbs, N. T., Spraker, T. R., O'Rourke, K.
I., & Wild, M. A. (2013). Efficacy of antemortem rectal biopsies to diagnose
and estimate prevalence of chronic wasting disease in free-ranging cow elk
(Cervus elaphus nelsoni). Journal of wildlife diseases, 49(2), 270-278.
Monello, R. J., Powers, J . G., Hobbs, N. T., Spraker, T. R., Watry, M. K.,
& Wild, M. A. (2014). Survival and population growth of a free-ranging elk
population with a long history of exposure to chronic wasting disease. The
Journal of Wildlife Management, 78(2), 214- 223.
Pritzkow, S., Morales, R., Moda, F., Khan, U., Telling, G. C., Hoover, E.,
& Soto, C. (2015). Grass Plants Bind, Retain, Uptake, and Transport
Infectious Prions. Cell reports, 11(8), 1168-1175.
Robinson, S. J ., Samuel, M. D., Johnson, C. J ., Adams, M., &
McKenzie, D. I. (2012). Emerging prion disease drives host selection in a
wildlife population. Ecological Applications, 22(3), 1050-1059.
State of Wisconsin, Joint Legislative Audit Committee, 2006. An Evaluation.
Chronic Wasting Disease. Department of Natural Reesources. Report 06-13. Online
citation available at:
VerCauteren, K., & Hygnstrom, S. E. (2011). Managing white-tailed deer:
Midwest North America.
Wasserberg, G., Osnas, E. E., Rolley, R. E., & Samuel, M. D. (2009).
Host culling as an adaptive management tool for chronic wasting disease in
white-tailed deer: a modelling study. Journal of Applied Ecology, 46(2),
457-466.
Wild, M. A., Hobbs, N. T., Graham, M. S., & Miller, M. W. (2011). The
role of predation in disease control: a comparison of selective and nonselective
removal on prion disease dynamics in deer. Journal of Wildlife Diseases,-4 7(1),
78-93.
Williams, A. L., Kreeger, T. J ., & Schumaker, B. A. (2014). Chronic
wasting disease model of genetic selection favoring prolonged survival in Rocky
Mountain elk (Cervus elaphus). Ecosphere, 5(5), art60.
Williams, E. S., & Young, S. (1980). CHRONIC WASTING DISEASE OF CAPTIVE
MULE DEER: A SPONGIFORM ENCEPHALOPATHY 1. Journal of wildlife diseases, 16(1),
89-98.
Adopted by the Wyoming Game and Fish Commission on April 22, 2016.
‘X (W . ! Signed: \~ \Q)~l\}*5L .
T. Carrie Little, President
>>>Based on research that grass plants can bind, retain, uptake
and transport prions (Pritzkow, 2015), the WGFD assess potential CWD
transmission risks of hay harvested from the CWD endemic area that is fed at
state elk feedgrounds. Prior to hay being purchased and transported to elk
feedgrounds, the WGFD will look at the spatial and temporal relationships
between the 1ocation(s) and prevalence rate(s) of CWD positive cervids and hay
fields from which hay is used for elk feedgrounds. The WGFD will attempt to only
use hay for elk feedgrounds from outside the CWD endemic area. Additionally, the
WGFD will communicate with the appropriate land management agency(s) as it
pertains to elk feedground hay use and CWD.<<<
PLEASE NOTE MY CONCERN WITH FIRST CASE OF CWD DOCUMENTED IN EUROPE I.E.
NORWAY AND HAY ;
Hay/Straw
Norway does not require any APHIS-Veterinary Services certification for the
import of hay/straw.
Tuesday, April 12, 2016
The first detection of Chronic Wasting Disease (CWD) in Europe
>>>Consider the potential role of predators and scavengers to
remove CWD infected animals and carcasses to reduce CWD transmission (Krumm,
2010; Wild, 2011).<<<
ABSOLUTELY A BAD DECISION, BASED ON THE FACT THAT THE CANINE AND FELINE
SPECIES ARE SUSCEPTIBLE TO THE TSE PRION, AND THE FACT THAT THE TSE PRION
SURVIVES THE Digestive System OF THE American crows (Corvus brachyrhynchos) AND
THE Coyotes (Canis latrans).
ALSO, it was well documented that domestic feline and big cage cats in
zoos contracted the TSE Prion disease.
ALSO, it was well documented that HOUNDS were susceptible to a TSE PRION,
and later science shows the same thing for canines.
THIS CONSIDERATION SHOULD BE TABLED AND NEVER MENTIONED AGAIN FOR THE
FOLLOWING REASONS ;
Saturday, December 05, 2015
CWD Prions Remain Infectious after Passage Through the Digestive System of
Coyotes (Canis latrans)
Wednesday, October 17, 2012
Prion Remains Infectious after Passage through Digestive System of American
Crows (Corvus brachyrhynchos)
Sunday, November 01, 2009
AS THE CROW FLIES, SO DOES CWD
American crows (Corvus brachyrhynchos) and potential spreading of CWD
through feces of digested infectious carcases
Monday, July 13, 2009
Deer Carcass Decomposition and Potential Scavenger Exposure to Chronic
Wasting Disease
Sunday, July 07, 2013
Could avian scavengers translocate infectious prions to disease-free areas
initiating new foci of chronic wasting disease?
Prion. 2013 Jul 3;7(4). [Epub ahead of print]
Monday, February 14, 2011
THE ROLE OF PREDATION IN DISEASE CONTROL: A COMPARISON OF SELECTIVE AND
NONSELECTIVE REMOVAL ON PRION DISEASE DYNAMICS IN DEER
NO, NO, NOT NO, BUT HELL NO !
Journal of Wildlife Diseases, 47(1), 2011, pp. 78-93 © Wildlife Disease
Association 2011
OR-09: Canine spongiform encephalopathy—A new form of animal prion disease
Monique David, Mourad Tayebi UT Health; Houston, TX USA
It was also hypothesized that BSE might have originated from an
unrecognized sporadic or genetic case of bovine prion disease incorporated into
cattle feed or even cattle feed contaminated with prion-infected human remains.1
However, strong support for a genetic origin of BSE has recently been
demonstrated in an H-type BSE case exhibiting the novel mutation E211K.2
Furthermore, a specific prion protein strain causing BSE in cattle is believed
to be the etiological agent responsible for the novel human prion disease,
variant Creutzfeldt-Jakob disease (vCJD).3 Cases of vCJD have been identified in
a number countries, including France, Italy, Ireland, the Netherlands, Canada,
Japan, US and the UK with the largest number of cases. Naturally occurring
feline spongiform encephalopathy of domestic cats4 and spongiform
encephalopathies of a number of zoo animals so-called exotic ungulate
encephalopathies5,6 are also recognized as animal prion diseases, and are
thought to have resulted from the same BSE-contaminated food given to cattle and
humans, although and at least in some of these cases, a sporadic and/or genetic
etiology cannot be ruled out. The canine species seems to display resistance to
prion disease and no single case has so far been reported.7,8 Here, we describe
a case of a 9 week old male Rottweiler puppy presenting neurological deficits;
and histological examination revealed spongiform vacuolation characteristic of
those associated with prion diseases.9 Initial biochemical studies using
anti-PrP antibodies revealed the presence of partially proteinase K-resistant
fragment by western blotting. Furthermore, immunohistochemistry revealed
spongiform degeneration consistent with those found in prion disease and
displayed staining for PrPSc in the cortex.
Of major importance, PrPSc isolated from the Rottweiler was able to cross
the species barrier transmitted to hamster in vitro with PMCA and in vivo (one
hamster out of 5). Futhermore, second in vivo passage to hamsters, led to 100%
attack rate (n = 4) and animals displayed untypical lesional profile and shorter
incubation period.
In this study, we show that the canine species might be sensitive to prion
disease and that PrPSc isolated from a dog can be transmitted to dogs and
hamsters in vitro using PMCA and in vivo to hamsters.
If our preliminary results are confirmed, the proposal will have a major
impact on animal and public health and would certainly lead to implementing new
control measures for ‘canine spongiform encephalopathy’ (CSE).
References 1. Colchester AC, Colchester NT. The origin of bovine spongiform
encephalopathy: the human prion disease hypothesis. Lancet 2005; 366:856-61;
PMID:16139661; http://
dx.doi.org/10.1016/S0140-6736(05)67218-2.
2. Richt JA, Hall SM. BSE case associated with prion protein gene mutation.
PLoS Pathog 2008; 4:e1000156; PMID:18787697; http://dx.doi.org/10.1371/journal.
ppat.1000156.
3. Collinge J. Human prion diseases and bovine spongiform encephalopathy
(BSE). Hum Mol Genet 1997; 6:1699-705; PMID:9300662; http://dx.doi.org/10.1093/
hmg/6.10.1699.
4. Wyatt JM, Pearson GR, Smerdon TN, Gruffydd-Jones TJ, Wells GA, Wilesmith
JW. Naturally occurring scrapie-like spongiform encephalopathy in five domestic
cats. Vet Rec 1991; 129:233-6; PMID:1957458; http://dx.doi.org/10.1136/vr.129.11.233.
5. Jeffrey M, Wells GA. Spongiform encephalopathy in a nyala (Tragelaphus
angasi). Vet Pathol 1988; 25:398-9; PMID:3232315; http://dx.doi.org/10.1177/030098588802500514.
6. Kirkwood JK, Wells GA, Wilesmith JW, Cunningham AA, Jackson SI.
Spongiform encephalopathy in an arabian oryx (Oryx leucoryx) and a greater kudu
(Tragelaphus strepsiceros). Vet Rec 1990; 127:418-20; PMID:2264242.
7. Bartz JC, McKenzie DI, Bessen RA, Marsh RF, Aiken JM. Transmissible mink
encephalopathy species barrier effect between ferret and mink: PrP gene and
protein analysis. J Gen Virol 1994; 75:2947-53; PMID:7964604; http://dx.doi.org/10.1099/0022-1317-
75-11-2947.
8. Lysek DA, Schorn C, Nivon LG, Esteve-Moya V, Christen B, Calzolai L, et
al. Prion protein NMR structures of cats, dogs, pigs, and sheep. Proc Natl Acad
Sci U S A 2005; 102:640-5; PMID:15647367; http://dx.doi.org/10.1073/pnas.0408937102.
9. Budka H. Neuropathology of prion diseases. Br Med Bull 2003; 66:121-30;
PMID:14522854; http://dx.doi.org/10.1093/bmb/66.1.121.
Monday, March 26, 2012
CANINE SPONGIFORM ENCEPHALOPATHY: A NEW FORM OF ANIMAL PRION DISEASE
http://caninespongiformencephalopathy.blogspot.com/2012/03/canine-spongiform-encephalopathy-new.html
Monday, March 8, 2010
Canine Spongiform Encephalopathy aka MAD DOG DISEASE
=======================================
2013
Strain characteristics of the in vitro-adapted rabbit and dog BSE agent
remained invariable with respect to the original cattle BSE prion, suggesting
that the naturally low susceptibility of rabbits and dogs to prion infections
should not alter their zoonotic potential if these animals became infected with
BSE.
=======================================
Neurobiology of Disease
Bovine Spongiform Encephalopathy Induces Misfolding of Alleged
Prion-Resistant Species Cellular Prion Protein without Altering Its
Pathobiological Features
Enric Vidal3, Natalia Fernández-Borges1, Belén Pintado4, Montserrat
Ordóñez3, Mercedes Márquez6, Dolors Fondevila5,6, Juan María Torres7, Martí
Pumarola5,6, and Joaquín Castilla1,2 + Author Affiliations
1CIC bioGUNE, 48160 Derio, Bizkaia, Spain,
2IKERBASQUE, Basque Foundation for Science, 48011 Bilbao, Bizkaia, Spain,
3Centre de Recerca en Sanitat Animal, Campus de la Universitat Autònoma de
Barcelona (UAB)-IRTA, 08193 Bellaterra, Barcelona, Spain,
4Centro Nacional de Biotecnología, Campus de Cantoblanco, 28049
Cantoblanco, Madrid, Spain,
5Department of Animal Medicine and Surgery, Veterinary Faculty, UAB, 08193
Bellaterra (Cerdanyola del Vallès), Barcelona, Spain,
6Murine Pathology Unit, Centre de Biotecnologia Animal i Teràpia Gènica,
UAB, 08193 Bellaterra (Cerdanyola del Vallès), Barcelona, Spain, and
7Centro de Investigación en Sanidad Animal-Instituto Nacional de
Investigación y Tecnología Agraria y Alimentaria, 28130 Valdeolmos, Madrid,
Spain
Author contributions: E.V., N.F.-B., and J.C. designed research; E.V.,
N.F.-B., B.P., M.O., M.M., D.F., and J.C. performed research; E.V., N.F.-B.,
B.P., and J.C. contributed unpublished reagents/analytic tools; E.V., N.F.-B.,
B.P., M.O., M.M., D.F., J.M.T., M.P., and J.C. analyzed data; E.V. and J.C.
wrote the paper.
Abstract
Bovine spongiform encephalopathy (BSE) prions were responsible for an
unforeseen epizootic in cattle which had a vast social, economic, and public
health impact. This was primarily because BSE prions were found to be
transmissible to humans. Other species were also susceptible to BSE either by
natural infection (e.g., felids, caprids) or in experimental settings (e.g.,
sheep, mice). However, certain species closely related to humans, such as canids
and leporids, were apparently resistant to BSE. In vitro prion amplification
techniques (saPMCA) were used to successfully misfold the cellular prion protein
(PrPc) of these allegedly resistant species into a BSE-type prion protein. The
biochemical and biological properties of the new prions generated in vitro after
seeding rabbit and dog brain homogenates with classical BSE were studied.
Pathobiological features of the resultant prion strains were determined after
their inoculation into transgenic mice expressing bovine and human PrPC. Strain
characteristics of the in vitro-adapted rabbit and dog BSE agent remained
invariable with respect to the original cattle BSE prion, suggesting that the
naturally low susceptibility of rabbits and dogs to prion infections should not
alter their zoonotic potential if these animals became infected with BSE. This
study provides a sound basis for risk assessment regarding prion diseases in
purportedly resistant species.
Received January 18, 2013. Revision received March 7, 2013. Accepted March
23, 2013. Copyright © 2013 the authors 0270-6474/13/337778-09$15.00/0
2005
DEFRA Department for Environment, Food & Rural Affairs
Area 307, London, SW1P 4PQ Telephone: 0207 904 6000 Direct line: 0207 904
6287 E-mail: h.mcdonagh.defra.gsi.gov.uk
GTN: FAX:
Mr T S Singeltary P.O. Box 42 Bacliff Texas USA 77518
21 November 2001
Dear Mr Singeltary
TSE IN HOUNDS
Thank you for e-mail regarding the hounds survey. I am sorry for the long
delay in responding.
As you note, the hound survey remains unpublished. However the Spongiform
Encephalopathy Advisory Committee (SEAC), the UK Government's independent
Advisory Committee on all aspects related to BSE-like disease, gave the hound
study detailed consideration at their meeting in January 1994. As a summary of
this meeting published in the BSE inquiry noted, the Committee were clearly
concerned about the work that had been carried out, concluding that there had
clearly been problems with it, particularly the control on the histology, and
that it was more or less inconclusive. However was agreed that there should be a
re-evaluation of the pathological material in the study.
Later, at their meeting in June 95, The Committee re-evaluated the hound
study to see if any useful results could be gained from it. The Chairman
concluded that there were varying opinions within the Committee on further work.
It did not suggest any further transmission studies and thought that the lack of
clinical data was a major weakness.
Overall, it is clear that SEAC had major concerns about the survey as
conducted. As a result it is likely that the authors felt that it would not
stand up to r~eer review and hence it was never published. As noted above, and
in the detailed minutes of the SEAC meeting in June 95, SEAC considered whether
additional work should be performed to examine dogs for evidence of TSE
infection. Although the Committee had mixed views about the merits of conducting
further work, the Chairman noted that when the Southwood Committee made their
recommendation to complete an assessment of possible spongiform disease in dogs,
no TSEs had been identified in other species and hence dogs were perceived as a
high risk population and worthy of study. However subsequent to the original
recommendation, made in 1990, a number of other species had been identified with
TSE ( e.g. cats) so a study in hounds was less
critical. For more details see- http://www.bseinquiry.gov.uk/files/yb/1995/06/21005001.pdf
As this study remains unpublished, my understanding is that the ownership
of the data essentially remains with the original researchers. Thus
unfortunately, I am unable to help with your request to supply information on
the hound survey directly. My only suggestion is that you contact one of the
researchers originally involved in the project, such as Gerald Wells. He can be
contacted at the following address.
Dr Gerald Wells, Veterinary Laboratories Agency, New Haw, Addlestone,
Surrey, KT 15 3NB, UK
You may also wish to be aware that since November 1994 all suspected cases
of spongiform encephalopathy in animals and poultry were made notifiable. Hence
since that date there has been a requirement for vets to report any suspect SE
in dogs for further investigation. To date there has never been positive
identification of a TSE in a dog.
I hope this is helpful
Yours sincerely 4
HUGH MCDONAGH BSE CORRESPONDENCE SECTION
======================================
HOUND SURVEY
I am sorry, but I really could have been a co-signatory of Gerald's
minute.
I do NOT think that we can justify devoting any resources to this study,
especially as larger and more important projects such as the pathogenesis study
will be quite demanding.
If there is a POLITICAL need to continue with the examination of hound
brains then it should be passed entirely to the VI Service.
J W WILESMITH Epidemiology Unit 18 October 1991
Mr. R Bradley
cc: Mr. G A H Wells
3.3. Mr R J Higgins in conjunction with Mr G A Wells and Mr A C Scott would
by the end of the year, indentify the three brains that were from the
''POSITIVE'' end of the lesion spectrum.
TSE in dogs have not been documented simply because OF THE ONLY STUDY,
those brain tissue samples were screwed up too. see my investigation of this
here, and to follow, later follow up, a letter from defra, AND SEE SUSPICIOUS
BRAIN TISSUE SAF's. ...TSS
TSE & HOUNDS
GAH WELLS (very important statement here...TSS)
HOUND STUDY
AS implied in the Inset 25 we must not _ASSUME_ that transmission of BSE to
other species will invariably present pathology typical of a scrapie-like
disease.
snip...
76 pages on hound study;
snip...
The spongiform changes were not pathognomonic (ie. conclusive proof) for
prion disease, as they were atypical, being largely present in white matter
rather than grey matter in the brain and spinal cord. However, Tony Scott, then
head of electron microscopy work on TSEs, had no doubt that these SAFs were
genuine and that these hounds therefore must have had a scrapie-like disease. I
reviewed all the sections myself (original notes appended) and although the
pathology was not typical, I could not exclude the possibility that this was a
scrapie-like disorder, as white matter vacuolation is seen in TSEs and Wallerian
degeneration was also present in the white matter of the hounds, another feature
of scrapie.
38.I reviewed the literature on hound neuropathology, and discovered that
micrographs and descriptive neuropathology from papers on 'hound ataxia'
mirrored those in material from Robert Higgins' hound survey. Dr Tony Palmer
(Cambridge) had done much of this work, and I obtained original sections from
hound ataxia cases from him. This enabled me provisionally to conclude that
Robert Higgins had in all probability detected hound ataxia, but also that hound
ataxia itself was possibly a TSE. Gerald Wells confirmed in 'blind' examination
of single restricted microscopic fields that there was no distinction between
the white matter vacuolation present in BSE and scrapie cases, and that
occurring in hound ataxia and the hound survey cases.
39.Hound ataxia had reportedly been occurring since the 1930's, and a known
risk factor for its development was the feeding to hounds of downer cows, and
particularly bovine offal. Circumstantial evidence suggests that bovine offal
may also be causal in FSE, and TME in mink. Despite the inconclusive nature of
the neuropathology, it was clearly evident that this putative canine spongiform
encephalopathy merited further investigation.
40.The inconclusive results in hounds were never confirmed, nor was the
link with hound ataxia pursued. I telephoned Robert Higgins six years after he
first sent the slides to CVL. I was informed that despite his submitting a
yearly report to the CVO including the suggestion that the hound work be
continued, no further work had been done since 1991. This was surprising, to say
the very least.
41.The hound work could have provided valuable evidence that a scrapie-like
agent may have been present in cattle offal long before the BSE epidemic was
recognised. The MAFF hound survey remains unpublished.
Histopathological support to various other published MAFF experiments
42.These included neuropathological examination of material from
experiments studying the attempted transmission of BSE to chickens and pigs (CVL
1991) and to mice (RVC 1994).
It was thought likely that at least some, and probably all, of the cases in
zoo animals were caused by the BSE agent. Strong support for this hypothesis
came from the findings of Bruce and others (1994) ( Bruce, M.E., Chree, A.,
McConnell, I., Foster, J., Pearson, G. & Fraser, H. (1994) Transmission of
bovine spongiform encephalopathy and scrapie to mice: strain variation and
species barrier. Philosophical Transactions of the Royal Society B 343, 405-411:
J/PTRSL/343/405 ), who demonstrated that the pattern of variation in incubation
period and lesion profile in six strains of mice inoculated with brain
homogenates from an affected kudu and the nyala, was similar to that seen when
this panel of mouse strains was inoculated with brain from cattle with BSE. The
affected zoo bovids were all from herds that were exposed to feeds that were
likely to have contained contaminated ruminant-derived protein and the zoo
felids had been exposed, if only occasionally in some cases, to tissues from
cattle unfit for human consumption.
snip...
NEW URL ;
2016 USA CWD ROUNDUP UPDATE
Monday, April 25, 2016
Arkansas AGFC Phase 2 sampling reveals CWD positive deer in Madison and
Pope counties
Tuesday, April 19, 2016
Arkansas First Phase of CWD sampling reveals 23 percent prevalence rate in
focal area With 82 Confirmed to Date
Friday, April 08, 2016
Arkansas AGFC Chronic Wasting Disease CWD TSE Prion Confirms 23 Additional
Cases Total At 79 To Date
Friday, April 01, 2016
ARKANSAS CHRONIC WASTING DISEASE CWD TSE PRION CASES EXPLODE BY 27 NEW
CASES WITH 50 CASES TOTAL TO DATE
Friday, April 22, 2016
Texas Scrapie Confirmed in a Hartley County Sheep where CWD was detected in
a Mule Deer
Saturday, April 02, 2016
TEXAS TAHC BREAKS IT'S SILENCE WITH TWO MORE CASES CWD CAPTIVE DEER
BRINGING TOTAL TO 10 CAPTIVES REPORTED TO DATE
Friday, February 26, 2016
TEXAS Hartley County Mule Deer Tests Positive for Chronic Wasting Disease
CWD TSE Prion
Friday, April 22, 2016
Texas Scrapie Confirmed in a Hartley County Sheep where CWD was detected in
a Mule Deer
Saturday, April 23, 2016
SCRAPIE WS-01: Prion diseases in animals and zoonotic potential 2016
Prion. 10:S15-S21. 2016 ISSN: 1933-6896 printl 1933-690X online
Friday, February 05, 2016
TEXAS NEW CHRONIC WASTING DISEASE CWD CASE DISCOVERD AT CAPTIVE DEER
RELEASE SITE
Friday, April 22, 2016
Missouri MDC finds seven new cases of ChronicWasting Disease CWD during
past‐season testing
Wednesday, April 20, 2016
UTAH CHRONIC WASTING DISEASE CWD TSE PRION SURVEILLANCE AND TESTING PROGRAM
70 mule deer and two elk have tested positive
WISCONSIN CWD CASES OUT OF CONTROL
Wednesday, March 16, 2016 Wisconsin CWD sample survey 2015 confirms 290
cases of Chronic Wasting Disease TSE Prion
KANSAS CWD CASES ALARMING
Wednesday, March 02, 2016 Kansas Chronic Wasting Disease CWD TSE Prion 52
cases 2015 updated report 'ALARMING'
Tuesday, February 02, 2016
Illinois six out of 19 deer samples tested positive for CWD in the Oswego
zone of Kendall County
Friday, April 22, 2016
*** COLORADO CHRONIC WASTING DISEASE CWD TSE PRION SURVEILLANCE AND TESTING
PROGRAM IS MINIMAL AND LIMITED ***
SEE HIGH INFECTION RATE MAPS!
In Confidence - Perceptions of unconventional slow virus diseases of
animals in the USA - APRIL-MAY 1989 - G A H Wells
22
Visits to Colorado State University, College of Veterinary Medicine and the
Wyoming Game and Fish Department, Sybille Wildlife Research and Conservation
Education Unit.
The main objective here was to obtain some understanding of CWD. A visit
was made to the University of wyoming Game and Fish Department, Sybille wildlife
Research and Conservation Education Unit where most of the cases of CWD have
occurred. The Sybille Wildlife facility is situated some 50 miles northeast of
Laramie, Wyoming through the Laramie Mountains. Here most of the hoofed big game
species of North America; Hule Deer (odocoileus hemionus), Whitetail Deer
(Odocoileus virginianus), Elk (Cervis canadensis) Mountain Goat (Oreamnos
americana), Bighorn Sheep (0vis canadensis} and Pronghorn (Antilocapra
americana) and some other wildlife species are kept in small numbers for
experimental use in the investigation of wildlife diseases.
A colony of the blackfooted ferret (Hustela nigripes) has been established
because of its imminent extinction. At present there are only 35 but it is
proposed to breed up to 200 and then, probably in 1991, re-introduce them into
the wild in a nation wide operation. Blackfooted ferret diet is mainly Prairie
Dog (Cynoms spp.) and it is thought that the elimination of this species from
large areas by poisoning campaigns in the past has been responsible for the
precipitous ferret decline.
The buildings and pens at the facility are entirely of wooden/log
construction with heavy duty wire mesh fences. Pen floors are bare earth. A long
race connecting many different areas within the facility enables movement of
deer and antelope between pens when necessary. There is provision for holding
deer of different sizes in a custom built crush for bleeding and
treatments.
23
The educational role of the unit includes school visits to provide
instruction in the work of the department and to promote conservation. I was
accompanied on this visit by Stuart Young and Beth Williams. on arrival I was
introduced to Hughie Dawson who has managed the facility for some 20
years.
CWD occurred principally in two locations, this one at Sybille and in a
similar facility at Fort Collins, Colorado, some 120 miles southwest. It was
estimated that in total probably 60-10 cases of CWD have occurred.
It was difficult to gain a clear account of incidence and temporal sequence
of events ( - this presumably is data awaiting publication - see below) but
during the period 1981-84, 10-15 cases occurred at the Sybille facility.
Recollections as to the relative total numbers of cases at each facility were
confusing. Beth Williams recalled that more cases had occurred in the Colorado
facility.
The morbidity amongst mule deer in the facilities ie. those of the natural
potentially exposed group has been about 90% with 100% mortality. the age
distribution of affected deer was very similar to that in ESE. The clinical
duration of cases was 6-8 weeks. Mortality in CWD cases was greatest in winter
months which can be very cold.
When the problem was fully appreciated both the Sybille and the Colorado
facilities were depopulated. All cervids were culled but Pronghorn, Bighorn
Sheep and Mountain goat, where present simultaneously in the facility, were
retained. There have been no cases of CWD in these non cervid species.
A few cases continue to occur at Sybille, the last was 4 months ago.
24
An account of the occurrence of CWD at the Colorado facility was obtained
from Terry spraker, Diagnostic Laboratory, CSU College of Veterinary Medicine,
Fort Collins. He examined tissues from cases of CWD at the Colorado facility
some time prior to Beth Williams's involvement and examination of brains which
resulted in the initial diagnosis. The deer holding facilities in Colorado
comprise the Colorado Division of Wildlife Research Pen, established 10 years
ago and some older deer pens at the Foot Hills Campus of CSU, close to Fort
Collins. Originally there were just 1-2 cases CWD/year and a total of 24 over
several years. In contrast to Beth Williams recollection Terry Spraker thought
more cases had‘ occurred at Sybille than in Colorado. The cull at the Colorado
facility involved 20-30 clinically normal deer. Early lesions in dorsal nucleus
of the vagus and olfactory cortex were found in (some) of these deer. At the
time of the cull here Pronghorn was the only other hoofed species present.
Bighorn sheep and Mountain Goat were introduced only one year after the cull and
occupied ground where CWD had occurred. Immediately after depopulation the
ground was ploughed and disinfection was carried out using ?1% NaOH. The
buildings/pens were not changed. There has been no recurrence of disease at the
Colorado facility since the cull.
25
Transmission Studies
Mule deer transmissions of CWD were by intracerebral inoculation and
compared with natural cases (‘’first passage by this route’’ MARKED OUT...TSS)
resulted in a more rapidly progressive clinical disease with repeated episodes
of synocopy ending in coma. one control animal became affected, it is J believed
through contamination of inoculum (?saline). Further CWD transmissions were
carried out by Dick Marsh into ferret, mink and squirrel monkey. Transmission
occurred in all of these species with the shortest incubation period in the
ferret.
Mouse and hamster transmissions were attempted at Wyoming State Diagnostic
Laboratory, Laramie and at CSU Fort Collins but were unsuccessful.
Also at the Wyoming State Diagnostic Laboratory, Laramie, transmission to
goats was attempted. In 1984 three goats were inoculated intracerebrally with a
10% CWD brain suspension. one goat, untreated, was placed in contact with the
CWD inoculated goats and three controls, housed separately, received saline
intracerebrally. To date these animals remain healthy.
Epidemiology of CWD
Descriptive epidemiological data has been collected from the two wildlife
facilities and a publication is in preparation.
The occurrence of CWD must be viewed against the context of the locations
in which it occurred. It was an incidental and unwelcome complication of the
respective wildlife research programmes. Despite its subsequent recognition as a
new disease of cervids, therefore justifying direct investigation, no specific
research funding was forthcoming. The USDA viewed it as a wildlife problem and
consequently not their province! Thus
26
there have been no specific epidemiological studies, other than information
gained from noting the occurrence of cases. Because of the relatively short term
nature of the programmed research at the facilities it has not been possible to
keep Mule Deer under the appropriate experimental circumstances or for
sufficient periods to establish horizontal or maternal transmission. Beth
Williams is of the view that the occurrence of CWD at Sybille is entirely
related to propagative spread by contagion. Investigations have failed to
identify any common source of infection and the incident has presented a
protracted time course with sporadic cases throughout. There is no evidence that
wild born deer were responsible for introduction of the disease to the
facility.
I asked Hughie Dawson about the nutritional aspects of the deer kept at
Sybille. Mule Deer calves are reared on condensed milk and homogenised or
pasteurised domestic cow's milk from birth to 1 month or to 6 months. some would
be given "Lamb milk replacer" which has a higher butter fat content than either
of the former products, but is derived also from domestic cow's milk. It was
thought that at the Colorado facility calves would receive only "evaporated
milk". Calves are weaned on to a pelletted feed containing corn, wheat bran and
linseed meal with no crude mineral suppliment. Salt licks ("sulphur blocks")
which have a specific mineral composition are supplied.
CWD has occurred or is suspected to have occurred in establishments
supplied with Mule Deer from the Colorado facility. In some cases evidence for
this is tenuous. For example, it is understood that Denver zoo state that "they
have not had cases of CWD" and yet they have had cases of Mule Deer succumbing
to a chronic wasting disorder which was not diagnosed. A case of CWD occurred in
a Mule Deer in Toronto zoo in 1976. The animal in
27
question came from Denver zoo but was originally from the Colorado wildlife
facility.
Pathology of CWD
A paper (Williams et al) is in preparation on the distribution of brain
lesions in CWD. Vacuolar changes occur predominantly in the dorsal nucleus of
the vagus nerve (this nucleus is invariably affected), the hypothalamus and the
olfactory cortex with occasional vacuolation of the olfactory tract white
matter.
Cerebellar lesions are sometimes present but there are very few changes in
the spinal cord which probably accounts for the rarity of ataxia clinically. As
in sheep scrapie the hypothalamic lesions correlate with the common clinical
occurrence of polydipsia. Beth Williams is aware of occasional neuronal vacuoles
occurring in the red nucleus of clinically normal deer! Spraker has added that
he has experienced vacuoles in neurons of Gasserian ganglia and at the level of
the obex in normal deer.
It has never been reported but Pat Merz carried out SAF detection on CWD
brain material. Work may be undertaken with NIH on the immunohistological
demonstration of PrP in sections but to date there has been no PrP work.
Does CWD occur in free-living cervids?
There is some, mostly circumstantial, evidence that CWD occurs in
free-living cervids but to what extent, if at all, this represents an
established reservoir of infection in the wild is not known.
At Sybille two Mule Deer orphans (wild caught) and a White—tail Deer
(Odocoileus virginianus) hybrid developed clinical signs when only 2 1/2 years
of age.
28
An Elk (Cervus canadensis) wild caught as an adult, presumed 2 years old,
developed signs when 3-4 years old.
Another group of elk, wild caught 400 miles from the facility, with an age
range 2-8 years, old subsequently developed the disease in the facility (?period
of captivity). The location of capture relative to the facility did not
apparently rule out that they may have at some time had fence-line nose contact
with animals in the facility!
Cases have also occurred in Mule Deer that were obtained from the wild
within one hour of birth but these were never kept completely isolated through
to maturity.
Also at Sybille there has been one case of CWD diagnosed in a free ranging
Elk. It was killed in Sybille Canyon 3 miles from the facility. It could have
had fence-line contact with captive Mule Deer in the facility.
Similar incidents had occurred in Colorado. In 1985 a free-ranging affected
Elk was caught in the Rocky Mountain National Park within a 2 mile radius of the
Colorado Division of Wildlife Research Pen. In 1986 and again in 1987 a single
affected Mule Deer on each occasion was caught within a 5 mile radius of the
Pen. These latter cases occurred within 2 years of the -cervid cull at the Pen
(?1985). Brain tissue from the free—ranging Elk brain was inoculated into mice
but for some reason these were kept for only 6 months and then the experiment
was abandoned.
A specific exercise has been carried out by Beth Williams with the Wyoming
State Diagnostic Laboratory and Fish Department to sample the brains of healthy
wild Mule Deer for histological examination. On two separate occasions the first
in 1985 and again in 1987 a total of 150 Mule Deer
29
brains were collected from areas of, and ajacent to, Sybille Canyon. These
deer would have been shot under a game permit by local hunters. As they were
brought down from the hills to the Game station for the mandatory registration
of the kill the heads were removed and ages estimated. Most were 2-5 year old
with a few 6 year old. For obvious reasons hunters were reluctant to give up
stag heads. Thus, but for 15-20 brains from stags, examinations were on brains
from females. No evidence of CWD lesions was found in any of these brains.
However, it was considered that sporadic cases of CWD, should they occur in the
wild population, would soon become separated from the herd and fall prey to
coyotes (Canis latrans).
The possibility of any reservoir of infection in wild cervids originating
from scrapie in domestic sheep flocks seems remote. Scrapie has been recorded in
only three flocks in Wyoming since 1947 and Beth Williams could recall only one
previous occurrence in 1966. This had involved a Suffolk flock close to the
border with Nebraska. However, there has been one new confirmed and a suspected
affected flock this year in Wyoming. In the latter a ewe bought—in from an
Illinois flock is incriminated.
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 about 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. Whether they were scrapie infected sheep or
not is unclear. There were domestic sheep and goats present in the facility also
in the 1960's but there is no evidence that these animals developed scrapie.
During the 60's hybridization studies between the Bighorn and domestic sheep
were carried
30
out, again, without evidence of scrapie. Domestic goats were also kept at
Sybille in the 1960's.
Spraker considers that the nasal route is responsible for transmission of
CWD through nose to nose contact, which may well occur also between captive and
free—living individuals.
In domestic cattle of which about 15-20 adults were necropsied per year at
the Diagnostic Laboratory, CSU., Spraker had not encountered any lesions
suggesting BSE. Polioencephalomalacia (PEM) and Encephalic Listeriosis were the
most common morphologic neuropathological diagnoses. No bovine rabies was
seen.
31
Appendix I
VISIT TO USA - OR A E WRATHALL — INFO ON BSE AND SCRAPIE
Dr Clark lately of the Scrapie Research Unit, Mission Texas has I
successfully transmitted ovine and caprine Scrapie to cattle. The experimental
results have not been published but there are plans to do this. This work was
initiated in 1978. A summary of it is:-
Expt A 6 Her x Jer calves born in 1978 were inoculated as follows with a
2nd Suffolk scrapie passage:- i/c 1ml; i/m, 5ml; s/c 5ml; oral 30ml.
1/6 went down after 48 months with a scrapie/BS2-like disease.
Expt B 6 Her or Jer or HxJ calves were inoculated with angora Goat virus
2/6 went down similarly after 36 months.
Expt C Mice inoculated from brains of calves/cattle in expts A & B were
resistant, only 1/20 going down with scrapie and this was the reason given for
not publishing.
Diagnosis in A, B, C was by histopath. No reports on SAF were given.
2. Dr Warren Foote indicated success so far in eliminating scrapie in
offspring from experimentally— (and naturally) infected sheep by ET. He had
found difficulty in obtaining embryos from naturally infected sheep (cf
SPA).
3. Prof. A Robertson gave a brief accout of BSE. The us approach was
to
32
accord it a very low profile indeed. Dr A Thiermann showed the picture in
the "Independent" with cattle being incinerated and thought this was a fanatical
incident to be avoided in the US at all costs. BSE was not reported in
USA.
4. Scrapie incidents (ie affected flocks) have shown a dramatic increase
since 1978. In 1953 when the National Control scheme was started there were
10-14 incidents, in 1978 - 1 and in 1988 so far 60.
5. Scrapie agent was reported to have been isolated from a solitary fetus.
6. A western blotting diagnostic technique (? on PrP) shows some
promise.
7. Results of a questionnaire sent to 33 states on" the subject of the
national sheep scrapie programme survey indicated
17/33 wished to drop it
6/33 wished to develop it
8/33 had few sheep and were neutral
Information obtained from Dr Wrathall‘s notes of a meeting of the U.S.
Animal Health Association at Little Rock, Arkansas Nov. 1988.
33
snip...see full text ;
In Confidence - Perceptions of unconventional slow virus diseases of
animals in the USA - APRIL-MAY 1989 - G A H Wells
3. Prof. A. Robertson gave a brief account of BSE. The US approach was to
accord it a very low profile indeed. Dr. A Thiermann showed the picture in the
''Independent'' with cattle being incinerated and thought this was a fanatical
incident to be avoided in the US at all costs. ...
***These results suggest that cattle experimentally inoculated with CWD may
have some limited amount of prion infectivity outside of the brain and spinal
cord that may represent a previously unrecognized risk for transmission. This
information could have an impact on regulatory officials developing plans to
reduce or eliminate TSEs and farmers with concerns about ranging cattle on areas
where CWD may be present.***
Research Project: TRANSMISSION, DIFFERENTIATION, AND PATHOBIOLOGY OF
TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES
Title: Limited amplification of chronic wasting disease prions in the
peripheral tissues of intracerebrally inoculated cattle Authors
item Haley, Nicholas - item Siepker, Christopher - item Greenlee, Justin
item Richt, Jürgen -
Submitted to: Journal of General Virology Publication
Type: Peer Reviewed Journal Publication Acceptance
Date: March 30, 2016 Publication Date: N/A Interpretive
Summary: Chronic Wasting Disease (CWD), a fatal neurodegenerative disease
that occurs in farmed and wild cervids (deer and elk) of North America, is a
transmissible spongiform encephalopathy (TSE). TSEs are caused by infectious
proteins called prions that are resistant to various methods of decontamination
and environmental degradation. Cattle could be exposed to chronic wasting
disease (CWD) by contact with infected farmed or free-ranging cervids. The
purpose of this study was to use an in vitro amplification method called real
time quaking induced conversion (RT-QuIC) to assess tissues from cattle
inoculated with CWD for low levels of prions not detected by traditional
diagnostic methods such as western blot and immunohistochemistry. This study
reports that prions were identified by RT-QuIC only in cattle that were
confirmed positive by traditional methods. However, prions were rarely
identified in some peripheral tissues such as mesenteric lymph node, tonsil, or
nasal turbinate that were not considered positive by traditional methods. These
results suggest that cattle experimentally inoculated with CWD may have some
limited amount of prion infectivity outside of the brain and spinal cord that
may represent a previously unrecognized risk for transmission. This information
could have an impact on regulatory officials developing plans to reduce or
eliminate TSEs and farmers with concerns about ranging cattle on areas where CWD
may be present.
Technical Abstract: Chronic wasting disease (CWD) is a fatal
neurodegenerative disease, classified as a prion disease or transmissible
spongiform encephalopathy (TSE) similar to bovine spongiform encephalopathy
(BSE). Cervids affected by CWD accumulate an abnormal protease resistant prion
protein throughout the central nervous system (CNS), as well as in both
lymphatic and excretory tissues – an aspect of prion disease pathogenesis not
observed in cattle with BSE. Using seeded amplification through real time
quaking induced conversion (RT-QuIC), we investigated whether the bovine host or
prion agent was responsible for this aspect of TSE pathogenesis. We blindly
examined numerous central and peripheral tissues from cattle inoculated with CWD
for prion seeding activity. Seeded amplification was readily detected in the
CNS, though rarely observed in peripheral tissues, with a limited distribution
similar to that of BSE prions in cattle. This seems to indicate that prion
peripheralization in cattle is a host-driven characteristic of TSE infection.
These results suggest that cattle experimentally inoculated with CWD may
have some limited amount of prion infectivity outside of the brain and spinal
cord that may represent a previously unrecognized risk for transmission. This
information could have an impact on regulatory officials developing plans to
reduce or eliminate TSEs and farmers with concerns about ranging cattle on areas
where CWD may be present.
Scrapie transmits to white-tailed deer by the oral route and has a
molecular profile similar to chronic wasting disease - (Abstract Only) -
(12-Aug-15) Transmission of chronic wasting disease to sentinel reindeer
(Rangifer tarandus tarandus) - (Abstract Only) - (12-Aug-15) Transmission of
scrapie prions to primate after an extended silent incubation period - (Peer
Reviewed Journal) Comoy, E.E., Mikol, J., Luccantoni-Freire, S., Correia, E.,
Lescoutra-Etchegaray, N., Durand, V., Dehen, C., Andreoletti, O., Casalone, C.,
Richt, J.A., Greenlee, J.J., Baron, T., Benestad, S., Brown, P., Deslys, J.
2015. Transmission of scrapie prions to primate after an extended silent
incubation period. Scientific Reports. 5:11573. Transmission of the agent of
sheep scrapie to deer results in PrPSc with two distinct molecular profiles -
(Abstract Only) Greenlee, J., Moore, S.J., Smith, J.., West Greenlee, M.H.,
Kunkle, R. 2015. Scrapie transmits to white-tailed deer by the oral route and
has a molecular profile similar to chronic wasting disease and distinct from the
scrapie inoculum. Prion 2015. p. S62.
Monday, April 04, 2016
Limited amplification of chronic wasting disease prions in the peripheral
tissues of intracerebrally inoculated cattle
Saturday, April 16, 2016
APHIS [Docket No. APHIS-2016-0029] Secretary's Advisory Committee on Animal
Health; Meeting May 2, 2016, and June 16, 2016 Singeltary Submission
2015 Report of the Committee on Wildlife Diseases Chronic Wasting Disease
CWD TSE Prion
Chair: Colin Gillin, OR
Vice Chair: Peregrine Wolff, NV
Chronic Wasting Disease Research and Updates in Colorado
Michael Miller, Colorado Division of Parks and Wildlife
Dr. Michael Miller, Colorado Division of Parks and Wildlife, led a brief
discussion on the implications of a recent study on chronic wasting disease
(CWD) host range. The Case Western study results, presented at an international
prion conference in May 2015, complement other efforts to assess human
susceptibility to chronic wasting disease that have been ongoing since the
mid-1990s. Findings from a variety of experimental & epidemiological studies
support messaging since the mid-1990s that human illness resulting from CWD
exposure appears unlikely. The new study’s results are consistent with other
previous & contemporary data suggesting a low probability of human prion
disease resulting from CWD exposure. Dr. Miller noted that even though human
illness seems unlikely, minimizing the occurrence of CWD and encouraging other
precautions for minimizing human exposure to CWD may be prudent. Trends observed
in Colorado since 2002 suggest increasing infection rates in affected mule deer
and elk herds, with the exception of one population unit intensively managed
through harvest in the early 2000s. Controlling CWD will likely need to rely on
hunting in order to remain politically, socially, and fiscally sustainable.
Consequently, early intervention -- while infection rates are still low -- may
offer the best opportunity to both suppress epidemics and minimize the
likelihood of hunters harvesting infected animals. Dr. Miller suggested that the
timing and approaches to CWD control may deserve more attention and
reconsideration than given in recent years.
Summary of Recent Chronic Wasting Disease events in Texas Mitch Lockwood,
Texas Parks and Wildlife Department
Bob Ditmar (TPWD), Andy Schwartz, Texas Animal Health Commission
Introduction:
• 3.9 million free-ranging white-tailed deer
• 700K white-tailed deer hunters
• 600K white-tailed deer harvested annually
• $3.6 billion economic output for all hunting
• $2.1 billion for deer hunting
• 1,300 deer breeding facilities
• > 110,000 deer in breeding facilities
• > 2,200 free-ranging deer moved annually through various permits
Texas Parks and Wildlife Department (TPWD) has been conducting CWD
surveillance throughout the state since 2002. Biologists have collected more
than 26,000 samples from hunter-harvested deer, and others have collected more
than 21,000 samples in order to meet TPWD permitting requirements, totaling
almost 48,000 samples. Additionally, Texas Animal Health Commission (TAHC) has
maintained a Voluntary CWD Herd Certification Program since 1995. In 2012, CWD
was discovered in 2 mule deer samples from far West Texas (Hueco Mountains) as a
result of a targeted surveillance effort. This area is directly adjacent to a
region in New Mexico with documented CWD occurrence. To date, five more positive
samples have been obtained from this population through hunter harvested mule
deer, indicating a disease prevalence of 10%.
Mule deer and white-tailed deer are regulated by TPWD, while other
susceptible species (including elk) are regulated by the TAHC. This has
generated the need for enhanced coordination and communication between these two
agencies. The TPWD/TAHC CWD Management Plan was developed by both agencies in
consultation with the state’s CWD Task Force. The Task Force is comprised of
wildlife biologists, deer and elk breeders, veterinarians and other
animal-health experts from TPWD, TAHC, Texas Veterinary Medical Diagnostic
Laboratory, Texas Department of State Health Services, Texas A&M College of
Veterinary Medicine, and USDA. The plan includes mandatory check stations for
susceptible species taken inside the CWD Containment Zone, which covers portions
of Hudspeth, Culberson, and El Paso counties. Artificial movement of deer is
prohibited in the CWD Containment Zone.
On June 30, 2015 a sample from a Medina County (area on border of southern
Edwards Plateau and northern South Texas Plains ecoregions) deer breeding
facility was confirmed positive for CWD. The index breeding facility
participated in TAHC’s voluntary CWD Herd Certification Program, and had tested
62 of 65 mortalities prior to June 2015 (60 not detected, 2 location results)
since permitted in 2006. There were a total of 136 adult deer in the inventory
on June 30, 2015, and the herd was considered to be relatively young.
During the previous 5 years, 107 deer were transferred from 30 deer
breeding facilities into the index facility. During that same period, 835 were
transferred from the index facility to 147 different facilities including 96
deer breeding facilities, 46 release sites, 3 DMP sites, and 2 sites in
Mexico.
TPWD and TAHC immediately placed a temporary moratorium on movements of all
captive deer in the state, and TAHC placed a Hold Order on the 177 “Tier 1”
facilities. Since then, TPWD and TAHC worked with the CWD Task Force and
industry stakeholders to develop a plan to lift the moratorium on deer
transfers, which includes additional CWD testing requirements in deer breeding
facilities or on registered release sites. Additionally, TAHC has removed the
Hold Order for 120 facilities, leaving a total 57 facilities remaining under a
Hold Order as of October 16, 2015. Most deer breeding facilities were authorized
to transfer deer by August 24, 2015. Depopulation at the index facility was
initiated in July 28 and completed on September 30, 2015. CWD was detected in a
total of 4 (out of 136 adults) white-tailed deer in the index facility, all of
which were 2-year-old bucks that were natural additions.
On September 15, 2015, CWD was confirmed in one of the trace-forward
facilities, from which 84 deer had transferred out to 9 different facilities (5
deer breeding facilities, 3 release sites, and 1 nursing facility) since it
received deer from the index herd. This resulted in 7 additional Hold Orders
being issued by TAHC, 4 of which have since been released. The CWD-positive at
the trace-forward facility was also a 2-year-old buck that was born in the index
facility. In summary, CWD has been detected in a total of 5 captive white-tailed
deer in Texas, 4 of which were located in the index facility, and 1 was located
in a trace-forward facility. There are 36 deer from the 2-year-old cohort
originating in the index facility that are reported to be alive in 7 deer
breeding facilities, and possibly as many as 6 deer from that cohort still alive
on release sites. Additionally, there are 33 deer that traced through the index
facility that are still alive in 15 deer breeding facilities, and possibly as
many as 51 trace-through deer are still alive on 24 different release sites, and
2 trace-through deer may still be alive in Mexico.
TPWD has intensified the statewide CWD surveillance efforts, with a goal to
collect samples from more than 8,000 hunter-harvested deer, including 300
samples within a 5-mile radius of the index facility. TAHC will continue to
pursue indemnity on exposed deer located in trace-forward facilities in an
attempt to conduct a more thorough epidemiological investigation. TPWD and TAHC
have committed to reevaluate movement qualification standards that apply to deer
breeding facilities and release sites following the 2015-16 hunting season. Both
agencies are exploring ante-mortem testing protocols, and will continue to seek
guidance from experts in the field.
UPDATE
Friday, February 05, 2016
TEXAS NEW CHRONIC WASTING DISEASE CWD CASE DISCOVERD AT CAPTIVE DEER
RELEASE SITE
Saturday, April 02, 2016
TEXAS TAHC BREAKS IT'S SILENCE WITH TWO MORE CASES CWD CAPTIVE DEER
BRINGING TOTAL TO 10 CAPTIVES REPORTED TO DATE
Epidemiology of Recent CWD Cases in Ohio
Susan Skorupski, Assistant Director, USDA-APHIS-VS
Background
Ohio has had a voluntary Chronic Wasting Disease (CWD) Herd Certification
Program for all cervidae for at least 12 years. Ohio has 331 cervidae herds in
the CWD monitoring program with 256 at Certified level. In October 2012, Ohio
White Tail Deer rule became effective. It includes several categories of white
tail deer operations. Monitored Herds cannot sell or give away animals and
includes hunting preserves. Under this rule, hunting preserves cannot move live
animals from the premises and must annually sample 30 animals or 30% of
harvested deer, based on the number of deer harvested during the previous year.
Herds with Status are herds enrolled in the CWD Certification Program but not
yet at certified level. Certified Status Herds are enrolled in the CWD
monitoring program and have reached certified status. Ohio has 135 Monitored
Herds, including 24 hunting preserves, 75 Herds with Status, and 256 Certified
Status herds. Ohio’s approach to infected animals and associated animals and
herds
Infected herd – herd where a CWD infected animal resided when the test
positive sample was collected. Herd quarantined.
Exposed herd – any herd where an animal that tested CWD positive has
resided within the 5 years before the CWD diagnosis. Whole herd quarantined Herd
that contains an exposed animal – whole herd quarantined unless epidemiology
information suggests the animal is of lower risk of spreading CWD.
Exposed animal – animal that was exposed to the CWD infected animal any
time during the five years prior to when the animal died or was euthanized and
sampled/tested positive for CWD.
Recent CWD history in Ohio
a.Pennsylvania traces
In the spring of 2014, Ohio received information on traces associated with
CWD positive cases in Pennsylvania. Three Ohio herds were designated as Exposed
herds because positive deer from infected herds in PA had been in the Ohio herd
s during the previous 5 years. Fifty Ohio herds received 256 exposed deer from
the 5 PA herds and 3 Ohio exposed herds. 85 of those animals were tested with
Not Detected results in Ohio herds. 66 animals were traced to Out of State
herds. That leaves 101 animals either standing in quarantined herds or not
tested when they died or were harvested. 18 herds/preserves remain under
quarantine.
b. First CWD positive found in Ohio
On October 22, 2014, National Veterinary Services Laboratory (NVSL)
confirmed a CWD positive result for a 2.5 year old buck killed at a hunting
preserve in Holmes County Ohio on October 2, 2014. The hunting preserve had been
under quarantine since April 1, 2014 because of PA traces and was required to do
100% sampling of harvested deer. The positive animal had official identification
tracing the animal to a CWD certified Pennsylvania herd. Records including a
Certificate of Veterinary Inspection indicate the animal moved to Ohio March 13,
2013. Genetic testing was conducted to support the accuracy of the trace to the
Pennsylvania herd. This herd was depopulated without indemnity April 27-29,
2015. 224 animals were depopulated at owner expense and sampled for CWD. All
tests had Not Detected results for CWD. The premises was evaluated as a
minimally contaminated facility. No cervidae have been added to the premises at
this time.
The owner of the hunting preserve business also owns or is associated with
breeding herds at other locations in Holmes County.
c. Second positive premises in Ohio
A white tail deer breeding herd owned by the same person who owned the CWD
positive hunting preserve was designated as a positive herd in the spring of
2015. A CWD positive animal was sampled on 3/12/2015 and reported on March 25,
2015. The animal was a 5 year old whitetail doe purchased from a Wisconsin herd
in February 2013. A second CWD positive animal was reported from this herd on
May 22, 2015. This animal was a 1.5 year old natural addition doe. This herd was
initially established in the fall of 2012 with the purchase of a CWD certified
herd from the estate of a deceased owner. In the spring and fall of 2013,
additional animals were added from at least 9 OH herds , 1 WI herd, 17 PA herds,
and 3 IN herds. This herd had been quarantined since April 1,2014 because of
traces from several CWD exposed or positive herds in Pennsylvania, including the
herd that was the source of the CWD positive deer in the Ohio hunting preserve.
It had received over 120 animals from these herds.
On June 15 and 16, this herd was depopulated with federal indemnity.
Samples were collected for research purposes. 241 animals including 44 fawns
were euthanized, sampled and tested. Sixteen additional positive were
identified. They originated from 5 Ohio CWD certified herds and 4 Pennsylvania
CWD certified herds. One of the Ohio herds was the herd that was used to
initially establish this herd. One positive animal was over 60 months of age so
that Ohio herd was not designated as an exposed herd. The other three Ohio herds
were quarantined as exposed herds.
Records reviews identified 334 exposed animals associated with Ohio exposed
herds. 42 Ohio herds containing these animals were quarantined. They have
remained under quarantine until the quarantined animal(s) are euthanized and
tested Not Detected for CWD or 60 months have passed since animals entered the
herd. From Ohio Exposed Herd 1, 56 animals moved to 21 Ohio herds and 83 animals
moved out of state. 27 animals were either already dead and tested with CWD Not
Detected results or have since been tested with CWD Not Detected results. From
Ohio Exposed Herd 2, 76 animals moved to 16 Ohio herds and 94 animals moved out
of state. 25 animals were either already dead and tested with CWD Not Detected
results or have since been tested with CWD Not Detected results. From Oho
Exposed Herd 3, 21 animals moved to 5 Ohio herds and 4 animals moved out of
state. 7 animals were either already dead and tested with CWD Not Detected
results or have since been tested with CWD Not Detected results. Ohio received 2
exposed animals from the exposed herd in Pennsylvania associated with this case.
In summary, 334 exposed animals were identified and traced to 40 Ohio herds. 59
of those in Ohio have been tested with Not Detected CWD results. 181 have been
traced out of state and 94 are still standing in 26 quarantined herds/hunting
preserves.
Ohio Exposed Herd 1 has been in the CWD Certification Program since
September 2003 and has an inventory as of 48 head over 1 year old. Ohio Exposed
Herd 2 has been in the CWD Certification Program since October 2003 and has an
inventory of 93 animals. Ohio Exposed Herd 3 has been in the CWD Certification
Program since February 2009 but started with a status date of May, 2001 and has
an inventory of 17 deer.
In addition Ohio received reports of 72 exposed deer form OOS Exposed herds
traced to 18 Ohio herds. 18 of those animals had moved to out of state herds. 30
animals were tested in Ohio with Not Detected results. 12 animals remain in 7
quarantined herds.
The summary of all traces associated with positive cases in Ohio and
Pennsylvania in 2014 – 2015 are:
Total exposed animals traced to Ohio:661
Total tested Not Detected: 176
Total animals traced to Out of State Premises: 265
Total premises initially quarantined 87
Total premises remaining quarantined: 40
Total Hunting Preserves quarantined: 10
USDA Cervid Health Program Updates
Randy Pritchard, USDA, APHIS, Veterinary Services
Voluntary Chronic Wasting Disease (CWD) Herd Certification Program
The APHIS National CWD Herd Certification Program (HCP) was implemented in
2014. It is a voluntary Federal-State-industry cooperative program administered
by APHIS and implemented by participating States. The program provides uniform
national herd certification standards that minimize the risk of spreading CWD in
farmed cervid populations. Participating States and herd owners must comply with
requirements for animal identification, fencing, recordkeeping,
inspections/inventories, as well as animal mortality testing and response to any
CWD-exposed, suspect, and positive herds. APHIS monitors the Approved State HCPs
to ensure consistency with Federal standards through annual reporting by the
States. With each year of successful surveillance, participating herds will
advance in status until reaching five years with no evidence of CWD, at which
time herds are certified as being low-risk for CWD. Only captive cervids from
enrolled herds certified as low risk for CWD may move interstate. Currently, 30
States participate in the voluntary CWD Herd Certification Program; 29 have
Approved HCPs and one has Provisional Approved status. VS is working with the
remaining State to transition it to Approved status. FY2015 marks the second
year that Approved States have submitted their CWD HCP annual reports to APHIS.
APHIS is currently reviewing these reports.
Review of CWD Program Standards
The CWD Program Standards provide clarification and guidance on how to meet
CWD Herd Certification Program and interstate movement requirements. VS
committed to an annual review of the Program Standards by representatives of the
cervid industry and appropriate State and Federal agencies. VS planned to
perform a review in FY2015; however, this did not occur due to the response to
highly pathogenic avian influenza (HPAI). VS expects to conduct a review in
FY2016.
CWD in Farmed and Wild Cervids
Retrospective Epidemiology of CWD in Farmed Cervids: In response to a 2014
USAHA Resolution, VS asked States to include a retrospective summary of the
epidemiology of all positive herds with their annual HCP reports for FY2015.
Unfortunately, the response to HPAI delayed completion of this summary. Five
States reported information to date. A few States indicated that they did not
have the resources to devote to this request. VS will continue to gather this
data and to collect more comprehensive data in the future.
Summary of CWD detections. As of September 30, 2015, CWD has been confirmed
in wild deer and elk in 21 U.S. States, and in farmed cervids in 16 States. In
total, 23 States have identified CWD in wild and/or farmed cervids. CWD has been
reported in 70 farmed cervid herds in the United States. Confirmation of the
disease in 3 free-ranging, wild white-tailed deer in Michigan in 2015 marked the
first report of CWD in the wild cervid population in this State. FY2015 CWD
Detections in Farmed Cervids: In FY2015, CWD was identified in eight farmed
cervid herds: one white-tailed deer breeding herd in Pennsylvania, one elk
breeding herd in Utah (traced back from a hunting facility in Utah), one
white-tailed deer (WTD) breeding herd and one WTD hunting preserve in Ohio
(owned by the same producer), two WTD breeding herds in Wisconsin, one WTD and
elk herd in Texas, and a second WTD herd in Texas (traced from the first
positive herd in Texas). The positive animals in Utah, Ohio, and Texas
represented the first reported cases of CWD in captive cervids in all three of
these States.
White-Tailed Deer Breeding Herd, Pennsylvania: On October 6, 2014, the
National Veterinary Services Laboratories (NVSL) confirmed CWD in a 6-year-old
doe from a captive WTD breeding facility in Reynoldsville, Pennsylvania. The doe
was euthanized and tested because she was classified as a CWD- exposed animal
that had previously resided in two trace back exposed herds. This herd was
assembled in 2013 through the purchase of 16 animals from other HCP-certified
herds in Pennsylvania, and had been under quarantine for receiving exposed
animals from a trace back exposed herd. The remaining herd of eight WTD was
depopulated with Federal indemnity on February 18, 2015, and no additional
positive animals were detected. USDA collected samples for research
purposes.
Elk Breeding Herd, Utah: On December 23, 2014, NVSL confirmed CWD in
3-year-old captive elk. The elk had been at a hunting park located in northern
Utah, where he had resided for approximately 3 weeks prior to being hunter
killed. All hunter-killed animals at the hunt park are required to be tested for
CWD, and this animal was sampled through routine surveillance. The elk was
traced back to its herd of origin, and that facility was quarantined. The herd
was assembled in 1999 with bulls, and later elk cows, that originated from
Colorado. Historical testing records for the herd were unavailable. The
remaining 70 elk were depopulated using Federal indemnity funds on March 3,
2015, and an additional 25 elk were confirmed as CWD-positive. USDA collected
samples for research purposes.
White-Tailed Deer Hunting Preserve, Ohio: On October 22, 2014, NVSL
confirmed CWD in a buck taken from a captive WTD deer hunting preserve in Ohio.
This was the first time that CWD had been detected in Ohio. The preserve was
tested as part of Ohio’s CWD monitoring program. The herd had been under
quarantine since April 2014 because it was a trace-forward herd associated with
a CWD-exposed herd in Pennsylvania. The positive animal was traced to its herd
of origin, a captive WTD breeding herd in Pennsylvania, through DNA identity
testing. On November 26, 2014, the Ohio State Veterinarian issued an Order of
Destruction for animals on the hunting preserve. The State executed this Order
on April 27-30, 2015. The herd of 224 WTD was depopulated and no other positives
were detected. USDA did not provide Federal indemnity.
White-Tailed Deer Breeding Herd, Ohio: On March 31, 2015, NVSL confirmed
CWD infection in a 5-year-old WTD doe from a captive breeding herd in
Holmesville, Ohio. The index animal was received from a Wisconsin WTD farm in
January 2013. The CWD-positive herd was owned by the same individual as the Ohio
hunt preserve that was found to be CWD positive in October 2014. On May 22,
2015, NVSL confirmed a second positive case in the same herd -- a yearling WTD
doe that was a natural addition in the same breeding herd. The herd had been
under quarantine since April 1, 2014 due to epidemiological linkages with two
WTD herds in Pennsylvania – one a positive herd and the other a traceback
exposed herd. USDA provided Federal indemnity and depopulated this herd on June
15 and 16, 2015. USDA collected samples for research purposes. NVSL confirmed
CWD in 16 additional animals in the herd. Of the 16 positives, one was natural
addition and the rest were purchased additions. The positive animals were
purchased from February 26, 2013 through September 24, 2013, except for one
purchased in 2012. Eleven purchased additions traced-back to 3 herds in
Pennsylvania and four purchased additions traced to three other herds in
Ohio.
White-Tailed Deer Breeding Herd, Wisconsin: On October 6, 2014, NVSL
confirmed CWD in a 2-year-old doe born in June of 2012 that died on a Richland
County farm. The facility is within the CWD management zone in Wisconsin. The
remaining 51 deer were euthanized on November 20, 2014, and seven additional
positives (all males born in 2012) were found. Two of these 7 were purchased
additions with the last added to the herd in January 2013. All sales from this
herd were to shooting preserves. This premises was double fenced and had been
compliant in a herd certification program for over 10 years.
White-Tailed Deer Breeding Herd, Wisconsin: On June 19, 2015, NVSL
confirmed CWD in a 7-year-old female WTD from a breeding facility in Eau Claire
County. The doe was a natural addition to this breeding herd. This is the first
positive CWD case, captive or wild, in this county. The doe was found dead and
was showing no clinical signs of CWD at the time of death. Since 2003, this herd
has tested 391 animals for CWD and all had “not detected” results. In addition,
317 animals have tested “not detected” from the associated hunting preserve over
the same time period. A second positive natural addition doe from this herd was
confirmed positive by NVSL on September 10, 2015. Several escape episodes have
occurred from this herd. The herd is currently under quarantine and plans are
underway for depopulation with State indemnity.
White-Tailed Deer and Elk Breeding Herd, Texas: On June 30, 2015, NVSL
confirmed CWD in a 2-year-old WTD buck from a captive WTD and elk breeding herd
in Medina County, Texas, approximately 500 miles from previously reported
positive free-ranging mule deer in far West Texas. This was the first time that
the disease had been detected in farmed cervids in the State. The index buck was
born on the premises and found dead on June 18, 2015. Over 40 high-risk deer
(i.e., pen mates, dam, others) were euthanized and tested after the index case
was found. The NVSL confirmed CWD infection in two of those deer. Interestingly,
all three of the positive deer identified to date on this premises have the same
AI sire. However, the significance of this finding is unclear. In the past 5
years, records indicate that 130 WTD from 33 facilities moved into the positive
herd and 838 WTD moved out of the positive herd to 147 different herds. One
positive WTD was found in one of these trace-out herds (see herd description
below). Additionally, 23 elk were also moved from this herd to another herd in
TX in 2014. All trace-outs have been intrastate except for movements to two
premises in Mexico. Premises that have received deer from the index herd are
under movement restrictions. VS is collaborating with animal health authorities
in Mexico. VS paid indemnity and depopulated this herd on September 30, 2015,
and no additional positive animals were detected. USDA collected samples for
research purposes.
White-Tailed Deer Herd, Texas: On September 14, 2015 NVSL confirmed CWD
from tissues from a WTD in Lavaca County, Texas. This animal was a traceout from
the first CWD positive herd from June 30, 2015. Additional epidemiology is
ongoing.
Poster 26
“Atypical” Chronic Wasting Disease in PRNP Genotype 225FF Mule Deer
Lisa Wolfe, Karen Fox, Michael Miller
Colorado Parks and Wildlife, Fort Collins, CO
Narrative: We compared mule deer (Odocoileus hemionus) of two different
PRNP genotypes (225SS, 225FF) for susceptibility to chronic wasting disease
(CWD) in the face of environmental exposure to infectivity. All three 225SS deer
had immunohistochemistry (IHC)-positive tonsil biopsies by 710 days post
exposure (dpe), developed classical clinical signs 723-1,200 dpe, and showed
postmortem gross and microscopic pathology, enzyme-linked immunosorbent assay
(ELISA) results, and IHC staining typical of prion disease in mule deer. In
contrast, although all three 225FF deer also became infected, the two
individuals surviving >720 dpe were consistently biopsy negative, developed
more subtle clinical signs of chronic wasting disease, and died 924 or 1,783
dpe. 225FF deer were ELISA “suspect” postmortem but showed negative or equivocal
IHC staining of lymphoid tissues; both clinically-affected 225FF deer had
spongiform encephalopathy in the absence of IHC staining in brain tissue. The
experimental cases resembled three cases encountered among five additional
captive 225FF deer that were not part of our experiment but also succumbed to
chronic wasting disease. In all of these cases of CWD in 225FF mule deer,
clinical presentation was atypical, as were the IHC staining properties of the
associated PRPCWD. Our findings suggest that the current gold standard of IHC
testing for diagnosis of CWD is insensitive for detection of disease in 225FF
deer.
Managing CWD in Farmed Cervids ◊
Nicholas J. Haley
Diagnostic Medicine and Pathobiology, Kansas State University, Manhattan,
KS
Narrative: Chronic wasting disease (CWD) is an efficiently transmitted
spongiform encephalopathy of cervids (e.g. deer, elk, and moose), and is the
only known prion disease affecting both free-ranging wildlife and captive
animals. The management of CWD in farmed cervids will require three avenues of
research: 1) the development of a sensitive live animal test, 2) the discovery
and implementation of a safe and effective vaccine strategy, and 3) with or
without a vaccine, the identification and cultivation of CWD-resistant cervids.
The antemortem detection of CWD and other prion diseases has proven difficult,
due in part to difficulties in identifying an appropriate peripheral tissue
specimen and complications with conventional test sensitivity. At present,
biopsies of the recto-anal mucosalassociated lymphoid tissues (RAMALT) have
shown promising sensitivity in various assays and are not impractical to collect
in live animals. Nasal brush collections have likewise proven both sensitive and
practical for identification of prion infections in humans, though in cervids
both rectal biopsy and nasal brush collection sensitivity is critically
dependent on stage of infection and genetic background. A blood test would be
ideal; however rudimentary assays currently in development have yet to be
evaluated blindly on naturally occurring populations or on a large scale.
Vaccine development is currently underway at several institutions, though an
effectively protective strategy has yet to be identified. Ultimately, genetic
resistance to CWD may be a critical corner piece in the management of CWD in
farmed cervids – an approach which has been used effectively to reduce the
incidence of scrapie in sheep worldwide. By exploiting resistant PrP alleles in
currently available white-tail and elk genetic pools, and searching various
isolated populations for evidence of additional resistance mechanisms, a
suitable approach to improving CWD resistance in farmed cervids may be
identified. Our research has specifically sought to develop an antemortem test
for CWD using amplification-based assays on collections from recent CWD
depopulations, while additionally using these assays to model CWD resistance in
cervid populations. Our findings from this research represent the early stages
in the management and ultimately eradication of CWD in farmed deer and elk. ◊
USAHA Paper
LOOKING FOR CWD IN HUMANS AS nvCJD or as an ATYPICAL CJD, LOOKING IN ALL
THE WRONG PLACES $$$
*** 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).***
PRION 2015 CONFERENCE FT. COLLINS CWD RISK FACTORS TO HUMANS
*** LATE-BREAKING ABSTRACTS PRION 2015 CONFERENCE ***
O18
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
*** 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
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.***
================
*** PRICE OF CWD TSE PRION POKER GOES UP 2014 ***
Transmissible Spongiform Encephalopathy TSE PRION update January 2, 2014
*** chronic wasting disease, there was no absolute barrier to conversion of
the human prion protein.
*** Furthermore, the form of human PrPres produced in this in vitro assay
when seeded with CWD, resembles that found in the most common human prion
disease, namely sCJD of the MM1 subtype.
*** 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.
Chronic Wasting Disease and Potential Transmission to Humans
Ermias D. Belay,* Ryan A. Maddox,* Elizabeth S. Williams,† Michael W.
Miller,‡ Pierluigi Gambetti,§ and Lawrence B. Schonberger*
Chronic wasting disease (CWD) of deer and elk is endemic in a tri-corner
area of Colorado, Wyoming, and Nebraska, and new foci of CWD have been detected
in other parts of the United States. Although detection in some areas may be
related to increased surveillance, introduction of CWD due to translocation or
natural migration of animals may account for some new foci of infection.
Increasing spread of CWD has raised concerns about the potential for increasing
human exposure to the CWD agent. The foodborne transmission of bovine spongiform
encephalopathy to humans indicates that the species barrier may not completely
protect humans from animal prion diseases. Conversion of human prion protein by
CWDassociated prions has been demonstrated in an in vitro cellfree experiment,
but limited investigations have not identified strong evidence for CWD
transmission to humans. More epidemiologic and laboratory studies are needed to
monitor the possibility of such transmissions.
Conclusions
The lack of evidence of a link between CWD transmission and unusual cases
of CJD, despite several epidemiologic investigations, and the absence of an
increase in CJD incidence in Colorado and Wyoming suggest that the risk, if any,
of transmission of CWD to humans is low. Although the in vitro studies
indicating inefficient conversion of human prion protein by CWD-associated
prions raise the possibility of low-level transmission of CWD to humans, no
human cases of prion disease with strong evidence of a link with CWD have been
identified. However, the transmission of BSE to humans and the resulting vCJD
indicate that, provided sufficient exposure, the species barrier may not
completely protect humans from animal prion diseases. Because CWD has occurred
in a limited geographic area for decades, an adequate number of people may not
have been exposed to the CWD agent to result in a clinically recognizable human
disease. The level and frequency of human exposure to the CWD agent may increase
with the spread of CWD in the United States. Because the number of studies
seeking evidence for CWD transmission to humans is limited, more epidemiologic
and laboratory studies should be conducted to monitor the possibility of such
transmissions. Studies involving transgenic mice expressing human and cervid
prion protein are in progress to further assess the potential for the CWD agent
to cause human disease. Epidemiologic studies have also been initiated to
identify human cases of prion disease among persons with an increased risk for
exposure to potentially CWD-infected deer or elk meat (47). If such cases are
identified, laboratory data showing similarities of the etiologic agent to that
of the CWD agent would strengthen the conclusion for a causal link. Surveillance
for human prion diseases, particularly in areas where CWD has been detected,
remains important to effectively monitor the possible transmission of CWD to
humans. Because of the long incubation period associated with prion diseases,
convincing negative results from epidemiologic and experimental laboratory
studies would likely require years of follow-up. In the meantime, to minimize
the risk for exposure to the CWD agent, hunters should consult with their state
wildlife agencies to identify areas where CWD occurs and continue to follow
advice provided by public health and wildlife agencies. Hunters should avoid
eating meat from deer and elk that look sick or test positive for CWD. They
should wear gloves when field-dressing carcasses, boneout the meat from the
animal, and minimize handling of brain and spinal cord tissues. As a precaution,
hunters should avoid eating deer and elk tissues known to harbor the CWD agent
(e.g., brain, spinal cord, eyes, spleen, tonsils, lymph nodes) from areas where
CWD has been identified.
now, let’s see what the authors said about this casual link, personal
communications years ago. see where it is stated NO STRONG evidence. so, does
this mean there IS casual evidence ???? “Our conclusion stating that we found no
strong evidence of CWD transmission to humans”
From: TSS (216-119-163-189.ipset45.wt.net)
Subject: CWD aka MAD DEER/ELK TO HUMANS ???
Date: September 30, 2002 at 7:06 am PST
From: "Belay, Ermias"
To: Cc: "Race, Richard (NIH)" ; ; "Belay, Ermias"
Sent: Monday, September 30, 2002 9:22 AM
Subject: RE: TO CDC AND NIH - PUB MED- 3 MORE DEATHS - CWD - YOUNG HUNTERS
Dear Sir/Madam,
In the Archives of Neurology you quoted (the abstract of which was attached
to your email), we did not say CWD in humans will present like variant CJD. That
assumption would be wrong. I encourage you to read the whole article and call me
if you have questions or need more clarification (phone: 404-639-3091). Also, we
do not claim that "no-one has ever been infected with prion disease from eating
venison." Our conclusion stating that we found no strong evidence of CWD
transmission to humans in the article you quoted or in any other forum is
limited to the patients we investigated.
Ermias Belay, M.D. Centers for Disease Control and Prevention
-----Original Message-----
From: Sent: Sunday, September 29, 2002 10:15 AM
To: rr26k@nih.gov; rrace@niaid.nih.gov; 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.
snip...
*** twenty-seven CJD patients who regularly consumed venison were reported
to the Surveillance Center***,
snip... full text ;
CJD is so rare in people under age 30, one case in a billion (leaving out
medical mishaps), that four cases under 30 is "very high," says Colorado
neurologist Bosque. "Then, if you add these other two from Wisconsin [cases in
the newspaper], six cases of CJD in people associated with venison is very, very
high." Only now, with Mary Riley, there are at least seven, and possibly eight,
with Steve, her dining companion. "It's not critical mass that matters,"
however, Belay says. "One case would do it for me." The chance that two people
who know each other would both contact CJD, like the two Wisconsin sportsmen, is
so unlikely, experts say, it would happen only once in 140 years.
Given the incubation period for TSEs in humans, it may require another
generation to write the final chapter on CWD in Wisconsin. "Does chronic wasting
disease pass into humans? We'll be able to answer that in 2022," says Race.
Meanwhile, the state has become part of an immense experiment.
I urge everyone to watch this video closely...terry
*** you can see video here and interview with Jeff's Mom, and scientist
telling you to test everything and potential risk factors for humans ***
Envt.07:
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).
snip...
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).
snip...
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. ...
snip...
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 ;
CJD9/10022
October 1994
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
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.
http://web.archive.org/web/20030511010117/http://www.bseinquiry.gov.uk/files/yb/1994/10/00003001.pdf
*** 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).***
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, Valerie 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 long 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***
===============
***our findings suggest that possible transmission risk of H-type BSE to
sheep and human. Bioassay will be required to determine whether the PMCA
products are infectious to these animals.
==============
Research Project: TRANSMISSION, DIFFERENTIATION, AND PATHOBIOLOGY OF
TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES
Title: Transmission of scrapie prions to primate after an extended silent
incubation period
Authors
item Comoy, Emmanuel - item Mikol, Jacqueline - item Luccantoni-Freire,
Sophie - item Correia, Evelyne - item Lescoutra-Etchegaray, Nathalie - item
Durand, Valérie - item Dehen, Capucine - item Andreoletti, Olivier - item
Casalone, Cristina - item Richt, Juergen item Greenlee, Justin item Baron,
Thierry - item Benestad, Sylvie - item Hills, Bob - item Brown, Paul - item
Deslys, Jean-Philippe -
Submitted to: Scientific Reports Publication Type: Peer Reviewed Journal
Publication Acceptance Date: May 28, 2015 Publication Date: June 30, 2015
Citation: Comoy, E.E., Mikol, J., Luccantoni-Freire, S., Correia, E.,
Lescoutra-Etchegaray, N., Durand, V., Dehen, C., Andreoletti, O., Casalone, C.,
Richt, J.A., Greenlee, J.J., Baron, T., Benestad, S., Brown, P., Deslys, J.
2015. Transmission of scrapie prions to primate after an extended silent
incubation period. Scientific Reports. 5:11573.
Interpretive Summary: The transmissible spongiform encephalopathies (also
called prion diseases) are fatal neurodegenerative diseases that affect animals
and humans. The agent of prion diseases is a misfolded form of the prion protein
that is resistant to breakdown by the host cells. Since all mammals express
prion protein on the surface of various cells such as neurons, all mammals are,
in theory, capable of replicating prion diseases. One example of a prion
disease, bovine spongiform encephalopathy (BSE; also called mad cow disease),
has been shown to infect cattle, sheep, exotic undulates, cats, non-human
primates, and humans when the new host is exposed to feeds or foods contaminated
with the disease agent. The purpose of this study was to test whether non-human
primates (cynomologous macaque) are susceptible to the agent of sheep scrapie.
After an incubation period of approximately 10 years a macaque developed
progressive clinical signs suggestive of neurologic disease. Upon postmortem
examination and microscopic examination of tissues, there was a widespread
distribution of lesions consistent with a transmissible spongiform
encephalopathy. This information will have a scientific impact since it is the
first study that demonstrates the transmission of scrapie to a non-human primate
with a close genetic relationship to humans. This information is especially
useful to regulatory officials and those involved with risk assessment of the
potential transmission of animal prion diseases to humans. Technical Abstract:
Classical bovine spongiform encephalopathy (c-BSE) is an animal prion disease
that also causes variant Creutzfeldt-Jakob disease in humans. Over the past
decades, c-BSE's zoonotic potential has been the driving force in establishing
extensive protective measures for animal and human health.
*** In complement to the recent demonstration that humanized mice are
susceptible to scrapie, we report here the first observation of direct
transmission of a natural classical scrapie isolate to a macaque after a 10-year
incubation period. Neuropathologic examination revealed all of the features of a
prion disease: spongiform change, neuronal loss, and accumulation of PrPres
throughout the CNS.
*** This observation strengthens the questioning of the harmlessness of
scrapie to humans, at a time when protective measures for human and animal
health are being dismantled and reduced as c-BSE is considered controlled and
being eradicated.
*** Our results underscore the importance of precautionary and protective
measures and the necessity for long-term experimental transmission studies to
assess the zoonotic potential of other animal prion strains.
why do we not want to do TSE transmission studies on chimpanzees $
5. A positive result from a chimpanzee challenged severly would likely
create alarm in some circles even if the result could not be interpreted for
man. I have a view that all these agents could be transmitted provided a large
enough dose by appropriate routes was given and the animals kept long enough.
Until the mechanisms of the species barrier are more clearly understood it might
be best to retain that hypothesis.
snip...
R. BRADLEY
”The occurrence of CWD must be viewed against the contest of the locations
in which it occurred. It was an incidental and unwelcome complication of the
respective wildlife research programmes. Despite it’s subsequent recognition as
a new disease of cervids, therefore justifying direct investigation, no specific
research funding was forthcoming. The USDA veiwed it as a wildlife problem and
consequently not their province!” page 26.
In Confidence - Perceptions of unconventional slow virus diseases of
animals in the USA - APRIL-MAY 1989 - G A H Wells
3. Prof. A. Robertson gave a brief account of BSE. The US approach was to
accord it a very low profile indeed. Dr. A Thiermann showed the picture in the
''Independent'' with cattle being incinerated and thought this was a fanatical
incident to be avoided in the US at all costs. ...
Evidence That Transmissible Mink Encephalopathy Results from Feeding
Infected Cattle Over the next 8-10 weeks, approximately 40% of all the adult
mink on the farm died from TME.
snip...
The rancher was a ''dead stock'' feeder using mostly (>95%) downer
or dead dairy cattle...
LOOKING FOR CWD IN HUMANS AS nvCJD or as an ATYPICAL CJD, LOOKING IN ALL
THE WRONG PLACES $$$
*** 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).***
Research Project: TRANSMISSION, DIFFERENTIATION, AND PATHOBIOLOGY OF
TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES
Title: Scrapie transmits to white-tailed deer by the oral route and has a
molecular profile similar to chronic wasting disease
Authors
item Greenlee, Justin item Moore, S - item Smith, Jodi - item Kunkle,
Robert item West Greenlee, M -
Submitted to: American College of Veterinary Pathologists Meeting
Publication Type: Abstract Only Publication Acceptance Date: August 12, 2015
Publication Date: N/A Technical Abstract: The purpose of this work was to
determine susceptibility of white-tailed deer (WTD) to the agent of sheep
scrapie and to compare the resultant PrPSc to that of the original inoculum and
chronic wasting disease (CWD). We inoculated WTD by a natural route of exposure
(concurrent oral and intranasal (IN); n=5) with a US scrapie isolate. All
scrapie-inoculated deer had evidence of PrPSc accumulation. PrPSc was detected
in lymphoid tissues at preclinical time points, and deer necropsied after 28
months post-inoculation had clinical signs, spongiform encephalopathy, and
widespread distribution of PrPSc in neural and lymphoid tissues. Western
blotting (WB) revealed PrPSc with 2 distinct molecular profiles. WB on cerebral
cortex had a profile similar to the original scrapie inoculum, whereas WB of
brainstem, cerebellum, or lymph nodes revealed PrPSc with a higher profile
resembling CWD. Homogenates with the 2 distinct profiles from WTD with clinical
scrapie were further passaged to mice expressing cervid prion protein and
intranasally to sheep and WTD. In cervidized mice, the two inocula have distinct
incubation times. Sheep inoculated intranasally with WTD derived scrapie
developed disease, but only after inoculation with the inoculum that had a
scrapie-like profile. The WTD study is ongoing, but deer in both inoculation
groups are positive for PrPSc by rectal mucosal biopsy. In summary, this work
demonstrates that WTD are susceptible to the agent of scrapie, two distinct
molecular profiles of PrPSc are present in the tissues of affected deer, and
inoculum of either profile readily passes to deer.
White-tailed Deer are Susceptible to Scrapie by Natural Route of Infection
Jodi D. Smith, Justin J. Greenlee, and Robert A. Kunkle; Virus and Prion
Research Unit, National Animal Disease Center, USDA-ARS
Interspecies transmission studies afford the opportunity to better
understand the potential host range and origins of prion diseases. Previous
experiments demonstrated that white-tailed deer are susceptible to sheep-derived
scrapie by intracranial inoculation. The purpose of this study was to determine
susceptibility of white-tailed deer to scrapie after a natural route of
exposure. Deer (n=5) were inoculated by concurrent oral (30 ml) and intranasal
(1 ml) instillation of a 10% (wt/vol) brain homogenate derived from a sheep
clinically affected with scrapie. Non-inoculated deer were maintained as
negative controls. All deer were observed daily for clinical signs. Deer were
euthanized and necropsied when neurologic disease was evident, and tissues were
examined for abnormal prion protein (PrPSc) by immunohistochemistry (IHC) and
western blot (WB). One animal was euthanized 15 months post-inoculation (MPI)
due to an injury. At that time, examination of obex and lymphoid tissues by IHC
was positive, but WB of obex and colliculus were negative. Remaining deer
developed clinical signs of wasting and mental depression and were necropsied
from 28 to 33 MPI. Tissues from these deer were positive for scrapie by IHC and
WB. Tissues with PrPSc immunoreactivity included brain, tonsil, retropharyngeal
and mesenteric lymph nodes, hemal node, Peyer’s patches, and spleen. This work
demonstrates for the first time that white-tailed deer are susceptible to sheep
scrapie by potential natural routes of inoculation. In-depth analysis of tissues
will be done to determine similarities between scrapie in deer after
intracranial and oral/intranasal inoculation and chronic wasting disease
resulting from similar routes of inoculation.
see full text ;
PO-039: A comparison of scrapie and chronic wasting disease in white-tailed
deer
Justin Greenlee, Jodi Smith, Eric Nicholson US Dept. Agriculture;
Agricultural Research Service, National Animal Disease Center; Ames, IA USA
White-tailed deer are susceptible to the agent of sheep scrapie by
intracerebral inoculation
snip...
It is unlikely that CWD will be eradicated from free-ranging cervids, and
the disease is likely to continue to spread geographically [10]. However, the
potential that white-tailed deer may be susceptible to sheep scrapie by a
natural route presents an additional confounding factor to halting the spread of
CWD. This leads to the additional speculations that
1) infected deer could serve as a reservoir to infect sheep with scrapie
offering challenges to scrapie eradication efforts and
2) CWD spread need not remain geographically confined to current endemic
areas, but could occur anywhere that sheep with scrapie and susceptible cervids
cohabitate.
This work demonstrates for the first time that white-tailed deer are
susceptible to sheep scrapie by intracerebral inoculation with a high attack
rate and that the disease that results has similarities to CWD. These
experiments will be repeated with a more natural route of inoculation to
determine the likelihood of the potential transmission of sheep scrapie to
white-tailed deer. If scrapie were to occur in white-tailed deer, results of
this study indicate that it would be detected as a TSE, but may be difficult to
differentiate from CWD without in-depth biochemical analysis.
2012
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
snip...
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.
2011
*** After a natural route of exposure, 100% of white-tailed deer were
susceptible to scrapie.
White-tailed Deer are Susceptible to Scrapie by Natural Route of Infection
Jodi D. Smith, Justin J. Greenlee, and Robert A. Kunkle; Virus and Prion
Research Unit, National Animal Disease Center, USDA-ARS
Interspecies transmission studies afford the opportunity to better
understand the potential host range and origins of prion diseases. Previous
experiments demonstrated that white-tailed deer are susceptible to sheep-derived
scrapie by intracranial inoculation. The purpose of this study was to determine
susceptibility of white-tailed deer to scrapie after a natural route of
exposure. Deer (n=5) were inoculated by concurrent oral (30 ml) and intranasal
(1 ml) instillation of a 10% (wt/vol) brain homogenate derived from a sheep
clinically affected with scrapie. Non-inoculated deer were maintained as
negative controls. All deer were observed daily for clinical signs. Deer were
euthanized and necropsied when neurologic disease was evident, and tissues were
examined for abnormal prion protein (PrPSc) by immunohistochemistry (IHC) and
western blot (WB). One animal was euthanized 15 months post-inoculation (MPI)
due to an injury. At that time, examination of obex and lymphoid tissues by IHC
was positive, but WB of obex and colliculus were negative. Remaining deer
developed clinical signs of wasting and mental depression and were necropsied
from 28 to 33 MPI. Tissues from these deer were positive for scrapie by IHC and
WB. Tissues with PrPSc immunoreactivity included brain, tonsil, retropharyngeal
and mesenteric lymph nodes, hemal node, Peyer’s patches, and spleen. This work
demonstrates for the first time that white-tailed deer are susceptible to sheep
scrapie by potential natural routes of inoculation. In-depth analysis of tissues
will be done to determine similarities between scrapie in deer after
intracranial and oral/intranasal inoculation and chronic wasting disease
resulting from similar routes of inoculation.
see full text ;
Monday, November 3, 2014
Persistence of ovine scrapie infectivity in a farm environment following
cleaning and decontamination
PL1
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 environmentally relevant 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.
see ;
Potential role of soil properties in the spread of CWD in western
Canada
Alsu Kuznetsova, Debbie McKenzie, Pamela Banser, Tariq Siddique & Judd
M. Aiken
Estimating Prion Adsorption Capacity of Soil by BioAssay of Subtracted
Infectivity from Complex Solutions (BASICS)
Estimating Prion Adsorption Capacity of Soil by BioAssay of Subtracted
Infectivity from Complex Solutions (BASICS) A. Christy Wyckoff, Krista L.
Lockwood, Crystal Meyerett-Reid, Brady A. Michel, Heather Bender, Kurt C.
VerCauteren, Mark D. Zabel PLOS x Published: March 4, 2013 http://dx.doi.org/10.1371/journal.pone.0058630
Behavior of Prions in the Environment: Implications for Prion Biology
Shannon L. Bartelt-Hunt1*, Jason C. Bartz2*
Prion Amplification and Hierarchical Bayesian Modeling Refine Detection of
Prion Infection
A. Christy Wyckoff1, 2 n1 , Nathan Galloway3 n1 , Crystal Meyerett-Reid1 ,
Jenny Powers4 , Terry Spraker1 , Ryan J. Monello4 , Bruce Pulford1 , Margaret
Wild4 , Michael Antolin3 , Kurt VerCauteren2 […] & Mark Zabel1 - Show fewer
authors Scientific Reports 5, Article number: 8358 (2015) doi:10.1038/srep08358
Download Citation
Molecular ecology Proteins Statistics Received: 27 June 2014
CELL REPORTS
Report
Grass Plants Bind, Retain, Uptake, and Transport Infectious Prions
PRION UPDATE VIA VEGETABLE PLANTS FROM THE SOIL
56. Members considered that there is no evidence that crops grown on the
land which received composted excreta from BSE-challenged animals pose a TSE
risk to humans or animals. One member suggested that, as some of these animals
are orally challenged with high doses of BSE-infected materials, and the
distribution of infectivity in the digestive system is not completely
understood, it might be premature to conclude that there is no infective agent
in the manure.
Furthermore, an unpublished study had indicated low level absorption of PrP
from soil by tomato plants although it should be noted that this study had not
been repeated. Details of this work would be sent to the SEAC Secretary. Dr
Matthews explained that most of the manure from animals challenged with high
doses of BSE had already been composted and used for coppicing. Members agreed
that the risks from disposal of residual manure from experimental animals would
be much less than historic risks of on farm contamination from naturally
infected animals at the height of the BSE epidemic. ...SNIP...END
SRM are certain cattle tissues capable of transmitting BSE. There is no
human health risk assessment to indicate the absence of human health concerns
associated with use of composted SRM domestically. To date, scientific evidence
has not been able to demonstrate that composting destroys prions. Although
domestic use would pose a negligible risk to livestock, there is a potential
risk to humans via direct ingestion of the compost or of compost particles
adhered to skin or plant material (e.g. carrots). Another potential route of
exposure is by ingestion of prions that have been taken up by plants. It has
been proven that bacteria are readily taken up by some plants (e.g. E. coli in
lettuce) thus the uptake of prions by plants cannot be precluded or dismissed at
this time. As a science-based regulator, the CFIA cannot change the policy on
this issue without a risk assessment demonstrating that the use of composted SRM
poses an acceptable risk to humans.
The BSE Inquiry / Statement No 19B (supplementary) Dr Alan Colchester
Issued 06/08/1999 (not scheduled to give oral evidence) SECOND STATEMENT TO THE
BSE INQUIRY Dr A Colchester BA BM BCh PhD FRCP Reader in Neurosciences &
Computing, University of Kent at Canterbury; Consultant Neurologist, Guy’s
Hospital London and William Harvey Hospital Ashford April 1999
snip...
88. Natural decay: Infectivity persists for a long time in the environment.
A study by Palsson in 1979 showed how scrapie was contracted by healthy sheep,
after they had grazed on land which had previously been grazed by
scrapie-infected sheep, even though the land had lain fallow for three years
before the healthy sheep were introduced. Brown also quoted an early experiment
of his own (1991), where he had buried scrapie-infected hamster brain and found
that he could still detect substantial infectivity three years later near where
the material had been placed. 89. Potential environmental routes of infection:
Brown discusses the various possible scenarios, including surface or subsurface
deposits of TSE-contaminated material, which would lead to a build-up of
long-lasting infectivity. Birds feeding on animal remains (such as gulls
visiting landfill sites) could disperse infectivity. Other animals could become
vectors if they later grazed on contaminated land. "A further question concerns
the risk of contamination of the surrounding water table or even surface water
channels, by effluents and discarded solid wastes from treatment plants. A
reasonable conclusion is that there is a potential for human infection to result
from environmental contamination by BSE-infected tissue residues. The potential
cannot be quantified because of the huge numbers of uncertainties and
assumptions that attend each stage of the disposal process". These comments,
from a long established authority on TSEs, closely echo my own statements which
were based on a recent examination of all the evidence. 90. Susceptibility: It
is likely that transmissibility of the disease to humans in vivo is probably
low, because sheep that die from scrapie and cattle that die from BSE are
probably a small fraction of the exposed population. However, no definitive data
are available.
91. Recommendations for disposal procedures: Brown recommends that material
which is actually or potentially contaminated by BSE should be: 1) exposed to
caustic soda; 2) thoroughly incinerated under carefully inspected conditions;
and 3) that any residue should be buried in landfill, to a depth which would
minimise any subsequent animal or human exposure, in areas that would not
intersect with any potable water-table source.
92. This review and recommendations from Brown have particular importance.
Brown is one of the world's foremost authorities on TSEs and is a senior
researcher in the US National Institutes of Health (NIH). It is notable that
such a respected authority is forthright in acknowledging the existence of
potential risks, and in identifying the appropriate measures necessary to
safeguard public health. Paper by SM Cousens, L Linsell, PG Smith, Dr M
Chandrakumar, JW Wilesmith, RSG Knight, M Zeidler, G Stewart, RG Will,
"Geographical distribution of variant CJD in the UK (excluding Northern
Ireland)". Lancet 353:18-21, 2 nd January 1999 93. The above paper {Appendix 41
(02/01/99)} (J/L/353/18) examined the possibility that patients with vCJD
(variant CJD) might live closer to rendering factories than would be expected by
chance. All 26 cases of vCJD in the UK with onset up to 31 st August 1998 were
studied. The incubation period of vCJD is not known but by analogy with other
human TSEs could lie within the range 5-25 years. If vCJD had arisen by exposure
to rendering products, such exposure might plausibly have occurred 8-10 years
before the onset of symptoms. The authors were able to obtain the addresses of
all rendering plants in the UK which were in production in 1988. For each case
of vCJD, the distance from the place of residence on 1st January 1998 to the
nearest rendering plant was calculated
snip...
Friday, February 08, 2013
*** Behavior of Prions in the Environment: Implications for Prion Biology
Wednesday, December 16, 2015
Objects in contact with classical scrapie sheep act as a reservoir for
scrapie transmission
Objects in contact with classical scrapie sheep act as a reservoir for
scrapie transmission
Timm Konold1*, Stephen A. C. Hawkins2, Lisa C. Thurston3, Ben C. Maddison4,
Kevin C. Gough5, Anthony Duarte1 and Hugh A. Simmons1
1 Animal Sciences Unit, Animal and Plant Health Agency Weybridge,
Addlestone, UK, 2 Pathology Department, Animal and Plant Health Agency
Weybridge, Addlestone, UK, 3 Surveillance and Laboratory Services, Animal and
Plant Health Agency Penrith, Penrith, UK, 4 ADAS UK, School of Veterinary
Medicine and Science, University of Nottingham, Sutton Bonington, UK, 5 School
of Veterinary Medicine and Science, University of Nottingham, Sutton Bonington,
UK
Classical scrapie is an environmentally transmissible prion disease of
sheep and goats. Prions can persist and remain potentially infectious in the
environment for many years and thus pose a risk of infecting animals after
re-stocking. In vitro studies using serial protein misfolding cyclic
amplification (sPMCA) have suggested that objects on a scrapie affected sheep
farm could contribute to disease transmission. This in vivo study aimed to
determine the role of field furniture (water troughs, feeding troughs, fencing,
and other objects that sheep may rub against) used by a scrapie-infected sheep
flock as a vector for disease transmission to scrapie-free lambs with the prion
protein genotype VRQ/VRQ, which is associated with high susceptibility to
classical scrapie. When the field furniture was placed in clean accommodation,
sheep became infected when exposed to either a water trough (four out of five)
or to objects used for rubbing (four out of seven). This field furniture had
been used by the scrapie-infected flock 8 weeks earlier and had previously been
shown to harbor scrapie prions by sPMCA. Sheep also became infected (20 out of
23) through exposure to contaminated field furniture placed within pasture not
used by scrapie-infected sheep for 40 months, even though swabs from this
furniture tested negative by PMCA. This infection rate decreased (1 out of 12)
on the same paddock after replacement with clean field furniture. Twelve grazing
sheep exposed to field furniture not in contact with scrapie-infected sheep for
18 months remained scrapie free. The findings of this study highlight the role
of field furniture used by scrapie-infected sheep to act as a reservoir for
disease re-introduction although infectivity declines considerably if the field
furniture has not been in contact with scrapie-infected sheep for several
months. PMCA may not be as sensitive as VRQ/VRQ sheep to test for environmental
contamination.
snip...
Discussion
Classical scrapie is an environmentally transmissible disease because it
has been reported in naïve, supposedly previously unexposed sheep placed in
pastures formerly occupied by scrapie-infected sheep (4, 19, 20). Although the
vector for disease transmission is not known, soil is likely to be an important
reservoir for prions (2) where – based on studies in rodents – prions can adhere
to minerals as a biologically active form (21) and remain infectious for more
than 2 years (22). Similarly, chronic wasting disease (CWD) has re-occurred in
mule deer housed in paddocks used by infected deer 2 years earlier, which was
assumed to be through foraging and soil consumption (23).
Our study suggested that the risk of acquiring scrapie infection was
greater through exposure to contaminated wooden, plastic, and metal surfaces via
water or food troughs, fencing, and hurdles than through grazing. Drinking from
a water trough used by the scrapie flock was sufficient to cause infection in
sheep in a clean building. Exposure to fences and other objects used for rubbing
also led to infection, which supported the hypothesis that skin may be a vector
for disease transmission (9). The risk of these objects to cause infection was
further demonstrated when 87% of 23 sheep presented with PrPSc in lymphoid
tissue after grazing on one of the paddocks, which contained metal hurdles, a
metal lamb creep and a water trough in contact with the scrapie flock up to 8
weeks earlier, whereas no infection had been demonstrated previously in sheep
grazing on this paddock, when equipped with new fencing and field furniture.
When the contaminated furniture and fencing were removed, the infection rate
dropped significantly to 8% of 12 sheep, with soil of the paddock as the most
likely source of infection caused by shedding of prions from the
scrapie-infected sheep in this paddock up to a week earlier.
This study also indicated that the level of contamination of field
furniture sufficient to cause infection was dependent on two factors: stage of
incubation period and time of last use by scrapie-infected sheep. Drinking from
a water trough that had been used by scrapie sheep in the predominantly
pre-clinical phase did not appear to cause infection, whereas infection was
shown in sheep drinking from the water trough used by scrapie sheep in the later
stage of the disease. It is possible that contamination occurred through
shedding of prions in saliva, which may have contaminated the surface of the
water trough and subsequently the water when it was refilled. Contamination
appeared to be sufficient to cause infection only if the trough was in contact
with sheep that included clinical cases. Indeed, there is an increased risk of
bodily fluid infectivity with disease progression in scrapie (24) and CWD (25)
based on PrPSc detection by sPMCA. Although ultraviolet light and heat under
natural conditions do not inactivate prions (26), furniture in contact with the
scrapie flock, which was assumed to be sufficiently contaminated to cause
infection, did not act as vector for disease if not used for 18 months, which
suggest that the weathering process alone was sufficient to inactivate prions.
PrPSc detection by sPMCA is increasingly used as a surrogate for
infectivity measurements by bioassay in sheep or mice. In this reported study,
however, the levels of PrPSc present in the environment were below the limit of
detection of the sPMCA method, yet were still sufficient to cause infection of
in-contact animals. In the present study, the outdoor objects were removed from
the infected flock 8 weeks prior to sampling and were positive by sPMCA at very
low levels (2 out of 37 reactions). As this sPMCA assay also yielded 2 positive
reactions out of 139 in samples from the scrapie-free farm, the sPMCA assay
could not detect PrPSc on any of the objects above the background of the assay.
False positive reactions with sPMCA at a low frequency associated with de novo
formation of infectious prions have been reported (27, 28). This is in contrast
to our previous study where we demonstrated that outdoor objects that had been
in contact with the scrapie-infected flock up to 20 days prior to sampling
harbored PrPSc that was detectable by sPMCA analysis [4 out of 15 reactions
(12)] and was significantly more positive by the assay compared to analogous
samples from the scrapie-free farm. This discrepancy could be due to the use of
a different sPMCA substrate between the studies that may alter the efficiency of
amplification of the environmental PrPSc. In addition, the present study had a
longer timeframe between the objects being in contact with the infected flock
and sampling, which may affect the levels of extractable PrPSc. Alternatively,
there may be potentially patchy contamination of this furniture with PrPSc,
which may have been missed by swabbing. The failure of sPMCA to detect
CWD-associated PrP in saliva from clinically affected deer despite confirmation
of infectivity in saliva-inoculated transgenic mice was associated with as yet
unidentified inhibitors in saliva (29), and it is possible that the sensitivity
of sPMCA is affected by other substances in the tested material. In addition,
sampling of amplifiable PrPSc and subsequent detection by sPMCA may be more
difficult from furniture exposed to weather, which is supported by the
observation that PrPSc was detected by sPMCA more frequently in indoor than
outdoor furniture (12). A recent experimental study has demonstrated that
repeated cycles of drying and wetting of prion-contaminated soil, equivalent to
what is expected under natural weathering conditions, could reduce PMCA
amplification efficiency and extend the incubation period in hamsters inoculated
with soil samples (30). This seems to apply also to this study even though the
reduction in infectivity was more dramatic in the sPMCA assays than in the sheep
model. Sheep were not kept until clinical end-point, which would have enabled us
to compare incubation periods, but the lack of infection in sheep exposed to
furniture that had not been in contact with scrapie sheep for a longer time
period supports the hypothesis that prion degradation and subsequent loss of
infectivity occurs even under natural conditions.
In conclusion, the results in the current study indicate that removal of
furniture that had been in contact with scrapie-infected animals should be
recommended, particularly since cleaning and decontamination may not effectively
remove scrapie infectivity (31), even though infectivity declines considerably
if the pasture and the field furniture have not been in contact with
scrapie-infected sheep for several months. As sPMCA failed to detect PrPSc in
furniture that was subjected to weathering, even though exposure led to
infection in sheep, this method may not always be reliable in predicting the
risk of scrapie infection through environmental contamination. These results
suggest that the VRQ/VRQ sheep model may be more sensitive than sPMCA for the
detection of environmentally associated scrapie, and suggest that extremely low
levels of scrapie contamination are able to cause infection in susceptible sheep
genotypes.
Keywords: classical scrapie, prion, transmissible spongiform
encephalopathy, sheep, field furniture, reservoir, serial protein misfolding
cyclic amplification
Wednesday, December 16, 2015
*** Objects in contact with classical scrapie sheep act as a reservoir for
scrapie transmission ***
Circulation of prions within dust on a scrapie affected farm
Kevin C Gough1, Claire A Baker2, Hugh A Simmons3, Steve A Hawkins3 and Ben
C Maddison2*
Abstract
Prion diseases are fatal neurological disorders that affect humans and
animals. Scrapie of sheep/goats and Chronic Wasting Disease (CWD) of deer/elk
are contagious prion diseases where environmental reservoirs have a direct link
to the transmission of disease. Using protein misfolding cyclic amplification we
demonstrate that scrapie PrPSc can be detected within circulating dusts that are
present on a farm that is naturally contaminated with sheep scrapie. The
presence of infectious scrapie within airborne dusts may represent a possible
route of infection and illustrates the difficulties that may be associated with
the effective decontamination of such scrapie affected premises.
snip...
Discussion
We present biochemical data illustrating the airborne movement of scrapie
containing material within a contaminated farm environment. We were able to
detect scrapie PrPSc within extracts from dusts collected over a 70 day period,
in the absence of any sheep activity. We were also able to detect scrapie PrPSc
within dusts collected within pasture at 30 m but not at 60 m distance away from
the scrapie contaminated buildings, suggesting that the chance of contamination
of pasture by scrapie contaminated dusts decreases with distance from
contaminated farm buildings. PrPSc amplification by sPMCA has been shown to
correlate with infectivity and amplified products have been shown to be
infectious [14,15]. These experiments illustrate the potential for low dose
scrapie infectivity to be present within such samples. We estimate low ng levels
of scrapie positive brain equivalent were deposited per m2 over 70 days, in a
barn previously occupied by sheep affected with scrapie. This movement of dusts
and the accumulation of low levels of scrapie infectivity within this
environment may in part explain previous observations where despite stringent
pen decontamination regimens healthy lambs still became scrapie infected after
apparent exposure from their environment alone [16]. The presence of sPMCA
seeding activity and by inference, infectious prions within dusts, and their
potential for airborne dissemination is highly novel and may have implications
for the spread of scrapie within infected premises. The low level circulation
and accumulation of scrapie prion containing dust material within the farm
environment will likely impede the efficient decontamination of such scrapie
contaminated buildings unless all possible reservoirs of dust are removed.
Scrapie containing dusts could possibly infect animals during feeding and
drinking, and respiratory and conjunctival routes may also be involved. It has
been demonstrated that scrapie can be efficiently transmitted via the nasal
route in sheep [17], as is also the case for CWD in both murine models and in
white tailed deer [18-20].
The sources of dust borne prions are unknown but it seems reasonable to
assume that faecal, urine, skin, parturient material and saliva-derived prions
may contribute to this mobile environmental reservoir of infectivity. This work
highlights a possible transmission route for scrapie within the farm
environment, and this is likely to be paralleled in CWD which shows strong
similarities with scrapie in terms of prion dissemination and disease
transmission. The data indicate that the presence of scrapie prions in dust is
likely to make the control of these diseases a considerable challenge.
Thursday, April 07, 2016
What is the risk of chronic wasting disease being introduced into Great
Britain? An updated Qualitative Risk Assessment March 2016
Sheep and cattle may be exposed to CWD via common grazing areas with
affected deer but so far, appear to be poorly susceptible to mule deer CWD
(Sigurdson, 2008).
***In contrast, cattle are highly susceptible to white-tailed deer CWD and
mule deer CWD in experimental conditions but no natural CWD infections in cattle
have been reported (Sigurdson, 2008; Hamir et al., 2006). It is not known how
susceptible humans are to CWD but given that the prion can be present in muscle,
it is likely that humans have been exposed to the agent via consumption of
venison (Sigurdson, 2008). Initial experimental research, however, suggests that
human susceptibility to CWD is low and there may be a robust species barrier for
CWD transmission to humans (Sigurdson, 2008). It is apparent, though, that CWD
is affecting wild and farmed cervid populations in endemic areas with some deer
populations decreasing as a result.
snip...
For the purpose of the qualitative risk assessment developed here it is
necessary to estimate the probability that a 30-ml bottle of lure contains urine
from an infected deer. This requires an estimate of the proportion of deer herds
in the USA which are infected with CWD together with the within herd
prevalence.
The distribution map of CWD in US shows it is present mainly in central
states (Figure 1). However, Virginia in the east of the country has recorded
seven recent cases of CWD (Anon 2015a). Some US manufacturers claim to take
steps to prevent urine being taken from infected animals eg by sourcing from
farms where the deer are randomly tested for CWD (Anon 2015a). However, if
disease is already present and testing is not carried out regularly, captive
populations are not necessarily disease free (Strausser 2014). Urine-based deer
lures have been known to be collected from domestic white-tailed deer herds and
therefore there is a recognised risk. This is reflected by 6 US States which
have
14
banned the use of natural deer urine for lures, as the deer urine may be
sourced from CWD-endemic areas in the USA as well as from areas free of CWD. For
example, the US State of Virginia is banning the use of urine-based deer lures
on July 2015 and Vermont from 2016 due to the risk of spread of CWD. Alaska
banned their use in 2012 (Anon 2015a). Pennsylvania Game Commission has banned
urine-based deer lures and acknowledged that there is no way to detect their use
(Strausser 2014). On the basis of unpublished data (J. Manson, Pers. Comm.) it
appears that up to 50% of deer herds can be infected with 80-90% of animals
infected within some herds.
*** It is therefore assumed that probability that a 30-ml bottle of deer
urine lure imported from the USA is sources from an infected deer is
medium.
SNIP...
In the USA, under the Food and Drug Administration’s 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.
***Animals considered at high risk for CWD include:
***1) animals from areas declared to be endemic for CWD and/or to be CWD
eradication zones and
***2) deer and elk that at some time during the 60-month period prior to
slaughter were in a captive herd that contained a CWD-positive animal.
***Therefore, in the USA, materials from cervids other than CWD positive
animals may be used in animal feed and feed ingredients for non-ruminants. The
amount of animal PAP that is of deer and/or elk origin imported from the USA to
GB cannot be determined, however, as it is not specified in TRACES. It may
constitute a small percentage of the very low tonnage of non-fish origin
processed animal proteins that were imported from US into GB.
*** Overall, therefore, it is considered there is a greater than negligible
risk that (non-ruminant) animal feed and pet food containing deer and/or elk
protein is imported into GB. There is uncertainty associated with this estimate
given the lack of data on the amount of deer and/or elk protein possibly being
imported in these products.
SNIP...
Summary and MORE HERE ;
What is the risk of chronic wasting disease being introduced into Great
Britain? An updated Qualitative Risk Assessment March 2016
Saturday, January 31, 2015
European red deer (Cervus elaphus elaphus) are susceptible to Bovine
Spongiform Encephalopathy BSE by Oral Alimentary route
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
see Singeltary comment ;
Monday, March 28, 2016
National Scrapie Eradication Program February 2016 Monthly Report
Docket No. FDA-2003-D-0432 (formerly 03D-0186) Use of Material from Deer
and Elk in Animal Feed Singeltary Submission
Greetings again FDA and Mr. Pritchett et al,
I would kindly like to comment on ;
Docket No. FDA-2003-D-0432 (formerly 03D-0186) Use of Material from Deer
and Elk in Animal Feed Singeltary Submission
#158
Guidance for Industry
Use of Material from Deer and Elk in Animal Feed
This version of the guidance replaces the version made available
September15, 2003.
This document has been revised to update the docket number, contact
information, and standard disclosures. Submit comments on this guidance at any
time.
Submit electronic comments to http://www.regulations.gov. Submit written
comments to the Division of Dockets Management (HFA-305), Food and Drug
Administration, 5630 Fishers Lane, Rm. 1061, Rockville, MD 20852. All comments
should be identified with the Docket No. FDA-2003-D-0432 (formerly 03D-0186).
For further information regarding this guidance, contact Burt Pritchett,
Center for Veterinary Medicine (HFV-222), Food and Drug Administration, 7519
Standish Place, Rockville, MD 20855, 240-402-6276, E-mail:
burt.pritchett@fda.hhs.gov.
Additional copies of this guidance document may be requested from the
Policy and Regulations Staff (HFV-6), Center for Veterinary Medicine, Food and
Drug Administration, 7519 Standish Place, Rockville, MD 20855, and may be viewed
on the Internet at either http://www.fda.gov/AnimalVeterinary/default.htm
or http://www.regulations.gov.
U.S. Department of Health and Human Services Food and Drug Administration
Center for Veterinary Medicine March 2016
Contains Nonbinding Recommendations
2
Guidance for Industry Use of Material from Deer and Elk in Animal Feed
This guidance represents the current thinking of the Food and Drug
Administration (FDA or Agency) on this topic. It does not establish any rights
for any person and is not binding on FDA or the public. You can use an
alternative approach if it satisfies the requirements of the applicable statutes
and regulations. To discuss an alternative approach, contact the FDA office
responsible for this guidance as listed on the title page.
I. Introduction
Under FDA’s BSE feed regulation (21 CFR 589.2000) most material from deer
and elk is prohibited for use in feed for ruminant animals. This guidance
document describes FDA’s recommendations regarding the use in all animal feed of
all material from deer and elk that are positive for Chronic Wasting Disease
(CWD) or are considered at high risk for CWD. The potential risks from CWD to
humans or non-cervid animals such as poultry and swine are not well understood.
However, because of recent recognition that CWD is spreading rapidly in
white-tailed deer, and because CWD’s route of transmission is poorly understood,
FDA is making recommendations regarding the use in animal feed of rendered
materials from deer and elk that are CWD-positive or that are at high risk for
CWD.
In general, FDA’s guidance documents do not establish legally enforceable
responsibilities. Instead, guidances describe the Agency’s current thinking on a
topic and should be viewed only as recommendations, unless specific regulatory
or statutory requirements are cited. The use of the word should in Agency
guidances means that something is suggested or recommended, but not required.
II. Background
CWD is a neurological (brain) disease of farmed and wild deer and elk that
belong in the animal family cervidae (cervids). Only deer and elk are known to
be susceptible to CWD by natural transmission. The disease has been found in
farmed and wild mule deer, white-tailed deer, North American elk, and in farmed
black-tailed deer. CWD belongs to a family of animal and human diseases called
transmissible spongiform encephalopathies (TSEs). These include bovine
spongiform encephalopathy (BSE or “mad cow” disease) in cattle; scrapie in sheep
and goats; and classical and variant Creutzfeldt-Jakob diseases (CJD and vCJD)
in humans. There is no known treatment for these diseases, and there is no
vaccine to prevent them. In addition, although validated postmortem diagnostic
tests are available, there are no validated diagnostic tests for CWD that can be
used to test for the disease in live animals.
Contains Nonbinding Recommendations
III. Use in animal feed of material from CWD-positive deer and elk
Material from CWD-positive animals may not be used in any animal feed or
feed ingredients. Pursuant to Sec. 402(a)(5) of the Federal Food, Drug, and
Cosmetic Act, animal feed and feed ingredients containing material from a
CWD-positive animal would be considered adulterated. FDA recommends that any
such adulterated feed or feed ingredients be recalled or otherwise removed from
the marketplace.
IV. Use in animal feed of material from deer and elk considered at high
risk for CWD Deer and elk considered at high risk for CWD include: (1) animals
from areas declared by State officials to be endemic for CWD and/or to be CWD
eradication zones; and (2) deer and elk that at some time during the 60-month
period immediately before the time of slaughter were in a captive herd that
contained a CWD-positive animal.
FDA recommends that materials from deer and elk considered at high risk for
CWD no longer be entered into the animal feed system. Under present
circumstances, FDA is not recommending that feed made from deer and elk from a
non-endemic area be recalled if a State later declares the area endemic for CWD
or a CWD eradication zone. In addition, at this time, FDA is not recommending
that feed made from deer and elk believed to be from a captive herd that
contained no CWD-positive animals be recalled if that herd is subsequently found
to contain a CWD-positive animal.
V. Use in animal feed of material from deer and elk NOT considered at high
risk for CWD FDA continues to consider materials from deer and elk NOT
considered at high risk for CWD to be acceptable for use in NON-RUMINANT animal
feeds in accordance with current agency regulations, 21 CFR 589.2000. Deer and
elk not considered at high risk include: (1) deer and elk from areas not
declared by State officials to be endemic for CWD and/or to be CWD eradication
zones; and (2) deer and elk that were not at some time during the 60-month
period immediately before the time of slaughter in a captive herd that contained
a CWD-positive animal.
3
Docket No. FDA-2003-D-0432 (formerly 03D-0186) Use of Material from Deer
and Elk in Animal Feed Singeltary Submission
Greetings again FDA and Mr. Pritchett et al,
MY comments and source reference of sound science on this very important
issue are as follows ;
Docket No. FDA-2003-D-0432 (formerly 03D-0186) Use of Material from Deer
and Elk in Animal Feed Singeltary Submission
I kindly wish to once again submit to Docket No. FDA-2003-D-0432 (formerly
03D-0186) Use of Material from Deer and Elk in Animal Feed.
Thank you kindly for allowing me to comment again, ...and again...and
again, on a topic so important, why it is ‘NON-BINDING’ is beyond me.
this should have been finalized and made ‘BINDING’ or MANDATORY OVER A
DECADE AGO.
but here lay the problem, once made ‘BINDING’ or ‘MANDATORY’, it is still
nothing but ink on paper.
we have had a mad cow feed ban in place since August 1997, and since then,
literally 100s of millions of pounds BANNED MAD COW FEED has been sent out to
commerce and fed out (see reference materials).
ENFORCEMENT OF SAID BINDING REGULATIONS HAS FAILED US TOO MANY TIMES.
so, in my opinion, any non-binding or voluntary regulations will not work,
and to state further, ‘BINDING’ or MANDATORY regulations will not work unless
enforced.
with that said, we know that Chronic Wasting Disease CWD TSE Prion easily
transmits to other cervid through the oral route.
the old transmission studies of BSE TSE floored scientist once they figured
out what they had, and please don’t forget about those mink that were fed 95%+
dead stock downer cow, that all came down with TME. please see ;
It is clear that the designing scientists must also have shared Mr Bradleys
surprise at the results because all the dose levels right down to 1 gram
triggered infection.
it is clear that the designing scientists must have also shared Mr Bradleys
surprise at the results because all the dose levels right down to 1 gram
triggered infection.
Evidence That Transmissible Mink Encephalopathy Results from Feeding
Infected Cattle
Over the next 8-10 weeks, approximately 40% of all the adult mink on the
farm died from TME.
snip...
The rancher was a ''dead stock'' feeder using mostly (>95%) downer or
dead dairy cattle...
*** PLEASE SEE THIS URGENT UPDATE ON CWD AND FEED ANIMAL PROTEIN ***
Sunday, March 20, 2016
Docket No. FDA-2003-D-0432 (formerly 03D-0186) Use of Material from Deer
and Elk in Animal Feed ***UPDATED MARCH 2016*** Singeltary Submission
Saturday, April 16, 2016
APHIS [Docket No. APHIS-2016-0029] Secretary's Advisory Committee on Animal
Health; Meeting May 2, 2016, and June 16, 2016 Singeltary Submission
Comment from Terry S. Singeltary Sr. Return to Docket Folder Summary This
is a Comment on the Food and Drug Administration (FDA) Notice: Risk Assessment
of Foodborne Illness Associated With Pathogens From Produce Grown in Fields
Amended With Untreated Biological Soil Amendments of Animal Origin; Request for
Scientific Data, Information, and Comments
For related information, Open Docket Folder Docket folder icon
--------------------------------------------------------------------------------
Show agency attachment(s) AttachmentsView All (0)
--------------------------------------------------------------------------------
Comment View document:Greetings FDA et al, I kindly would like to make
comment submission to ;
Docket No. FDA-2016-N-0321 Risk Assessment of Foodborne Illness Associated
with Pathogens from Produce Grown in Fields Amended with Untreated Biological
Soil Amendments of Animal Origin; Request for Comments, Scientific Data, and
Information
A Notice by the Food and Drug Administration on 03/04/2016
MY comment as follows,
There has been proven documented risk for Untreated Biological Soil
Amendments of Animal Origin and risk of transmitting Transmissible Spongiform
Encephalopathy TSE Prion disease aka mad cow type disease such as the typical
and atypical Bovine Spongiform Encephalopathy strains, typical and atypical
Scrapie strains, typical and atypical Chronic Wasting Disease CWD strains, and
even the Transmissible Mink Encephalopathy TME Prion disease.
Science has shown that infected deer harbor and shed high levels of
infectious prions in saliva, blood, urine, and feces thereby leading to
transmission by direct contact and environmental contamination.
Ingestion of prion contaminated 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.
Plants can uptake prions from contaminated soil and transport them to
different parts of the plant tissue (stem and leaves) [please see data from Soto
et al Prion2015 Conference below in Science reference data].
Also, Detection of protease-resistant cervid prion protein in water from a
CWD-endemic area is very concerning.
Science has shown that soil plays a role in the spreading and transmission
of the CWD and Scrapie TSE prion agent.
For these reason and more (see reference materials) I urge the FDA to stop
this practice of Untreated Biological Soil Amendments of Animal Origin,
including blood, for use on our produce grown in fields, for the following
reasons,
please see attachments and updated TSE Prion science on these very
important matters here (I do not advertise or make money the science is there
for educational use for Transmissible Spongiform Encephalopathy TSE Prion
disease.
just made a promise to mom dod 12/14/97 confirmed Heidenhain Variant
Creutzfeldt Jakob Disease, hvCJD. ... AttachmentsView All (1) Comment from Terry
S Singeltary Sr View Attachment:
Tuesday, March 15, 2016
Docket No. FDA-2016-N-0321 Risk Assessment of Foodborne Illness Associated
with Pathogens from Produce Grown in Fields Amended with Untreated Biological
Soil Amendments of Animal Origin; Request for Comments, Scientific Data, and
Information Singeltary Submission
Friday, April 22, 2016
*** Texas Scrapie Confirmed in a Hartley County Sheep where CWD was
detected in a Mule Deer ***
Saturday, April 23, 2016
*** SCRAPIE WS-01: Prion diseases in animals and zoonotic potential 2016
***
Prion. 10:S15-S21. 2016 ISSN: 1933-6896 printl 1933-690X online
Monday, April 25, 2016
TEXAS Nilgai Exotic Antelope Let Loose for Trophy Hunts Blamed for
Spreading Cattle Tick Fever, and what about CWD TSE Prion Disease ?
Tuesday, April 12, 2016
The first detection of Chronic Wasting Disease (CWD) in Europe
Thursday, March 31, 2016
*** Chronic Wasting Disease CWD TSE Prion Roundup USA 2016 ***
APRIL 22, 2015
WYOMING GAME AND FISH DEPARTMENT CHRONIC WASTING DISEASE MANAGEMENT PLAN
APRIL 22, 2015
Tuesday, December 01, 2015
DRAFT for Public Review and Comment – November 30, 2015 WYOMING GAME AND
FISH DEPARTMENT CHRONIC WASTING DISEASE MANAGEMENT PLAN Singeltary Submission
Wednesday, October 29, 2014
Chronic wasting disease now rings Greater Yellowstone in Wyoming
Saturday, May 25, 2013
Wyoming Game and Fish Commission Alkali Creek Feedground #39126 Singeltary
comment submission
Friday, November 16, 2012
Yellowstone elk herds feeding grounds, or future killing grounds from CWD
Thursday, March 10, 2016
WYOMING RIDE EM COWBOY HELICOPTER WRANGLING RAMBO STYLE DEER BULLDOGGING
RODEO FOR CWD VIDEO
CHRONIC WASTING DISEASE: The Final Epidemic
Monday, March 07, 2016
Wyoming Game and Fish Department confirmed chronic wasting disease (CWD) in
a buck mule deer that was found dead southeast of Lander
Wednesday, December 16, 2015
Wyoming Game and Fish finds CWD in new elk hunt area in southeast
Tuesday, December 15, 2015
Chronic Wasting Disease will cause a Wyoming deer herd to go virtually
extinct in 41 years, a five-year study predicts
Study: Chronic Wasting Disease kills 19% of deer herd annually
Thursday, December 10, 2015
Wyoming Game and Fish seeks public comment on draft of updated CWD plan
Tuesday, December 08, 2015
Wyoming Game and Fish finds CWD in new elk hunt area in Johnson County
FOR IMMEDIATE RELEASE CONTACTS: Mary Cernicek (307) 739-5564
DATE: December 2, 2015
The Forest Service Approves Continued Use of Alkali Creek Elk
Feedground
Jackson, Wyo. – The Jackson Ranger District of the Bridger-Teton National
Forest announces that Forest Supervisor Tricia O’Connor signed a Record of
Decision approving the authorization of continued use of Alkali Creek Elk
Feedground by the Wyoming Game and Fish Commission (the Commission).
Alkali Creek Elk Feedground is located within the Gros Ventre drainage
northeast of Jackson, Wyoming along with two other State feedgrounds at Patrol
Cabin and Fish Creek. The Commission uses feedgrounds as tools to reduce damage
to haystack yards and winter pastures on private lands and reduce potential for
transmission of diseases from elk to livestock. Elk feeding sites have been
strategically placed on National Forest System lands with the intent of
preventing elk migration through private lands that are located in historic big
game winter ranges.
Alkali Creek Feedground is situated such that it is critical for holding
elk in the Gros Ventre drainage that otherwise would end up overwintering on
adjoining private agricultural lands or on the National Elk Refuge. The U.S.
Department of the Interior’s 2007 Bison and Elk Management Plan for Grand Teton
National Park and the National Elk Refuge sets an objective for having about
5,000 elk on feed on the National Elk Refuge in the winter. At current herd
populations, this objective cannot be met if substantial numbers of elk leave
the Gros Ventre drainage.
At the feedground, the Wyoming Game and Fish Department (WGFD) will
maintain and operate one elk tagging corral, one horse corral, one tack shed,
one haystack yard containing two hay sheds, and spring and trough developments
including protective fencing and piping as part of their ongoing winter elk
management program. In the winter, elk feeders typically follow a daily routine
of distributing hay on the feedground using a horse drawn sleigh. WGFD personnel
monitor the elk for signs of disease and also count numbers of branch-antlered
bulls, spikes, cows, calves and the total number of elk on the feedground. This
information is used to determine quotas for future hunting seasons.
Forest Supervisor O’Connor intends to amend an existing special use permit
issued to the Commission in 2008 for use at five other feedgrounds to add
authorization for use at Alkali Creek. However, this amendment will not occur
until the WGFD Chronic Wasting Disease Plan update is completed and it
adequately addresses risks and management options for feedgrounds on National
Forest System lands. WGFD recently released a draft of the Chronic Wasting
Disease plan for public comment. If this plan update is not completed and
accepted by the Forest Service prior to initiation of feeding for the winter of
2015-16, a one year temporary permit will be issued for use at Alkali
Creek.
This decision was informed by analysis
Thursday, December 03, 2015
The Forest Service Approves Continued Use of Alkali Creek Elk Feedground,
and risks introducing CWD TSE Prion
Friday, November 27, 2015
Wyoming Game and Fish finds CWD in new Deer Hunt Area near Sheridan
Monday, November 16, 2015
Wyoming Latest round of testing CWD surveillance program has found the
disease in three new hunt areas
Saturday, November 14, 2015
Wyoming Chronic Wasting Disease CWD Surveillance Results 2014 reported in
2015
Wednesday, October 28, 2015 Wyoming Game and Fish Department’s chronic
wasting disease (CWD) surveillance program has found the disease in a new elk
hunt area 21 The Wyoming Game and Fish Department’s chronic wasting disease
(CWD) surveillance program has found the disease in a new elk hunt area.
10/26/2015 3:04:42 PM Green River - CWD is a fatal neurological disease of deer,
elk and moose. Staff at the Game and Fish Department’s wildlife disease
laboratory in Laramie confirmed the presence of CWD in a bull elk harvested on
Oct. 7 near Deep Creek, in elk hunt area 21, which lies about 15 miles northeast
of Baggs. Elk hunt area 21 overlaps with deer hunt area 82 where Game and Fish
documented CWD in 2002. ...
Wednesday, October 14, 2015
Wyoming Game and Fish Finds CWD In New Deer Hunt Area buck mule deer
harvested on Oct. 2 near Flat Top Mountain hunt area 100
WYOMING CWD 1998...
Harry Harju, assistant wildlife chief with Wyoming Fish and Game, reported
that elk or game farming is now prohibited in Wyoming. Only one game ranch
exists in Wyoming, which was operating before the passage of the law. The state
of Wyoming was sued by several game breeders associations for not allowing elk
farming. The game breeders lost their suit in the United States Court of
Appeals, Tenth Circuit. The court maintained that the state had authority to
regulate commerce and protect wildlife. Wyoming has had problems with big game
farming originating in surrounding states. Wyoming has documented the harvest of
red deer and their hybrids during elk hunts on the Snowy Mountain range that
borders Colorado. Wyoming speculates that the red deer were escapees from
Colorado game farms. Hybridization is viewed as threat to the genetic integrity
of Wyoming's wild elk population. In a public hearing, the public voted against
game farms in the state of Wyoming. Wyoming's Cattlemen's Association and
Department of Agriculture opposed elk and big game farms, as well, particularly
due to disease risks. Brucellosis is a major problem for wildlife and livestock
in the Yellowstone Basin.
CWD in Wyoming
Here is information and reports regarding Chronic Wasting Disease in Wyoming's Wildlife.CWD Management Plan
WGFD Chronic Wasting Disease Management Plan2015 CWD Surveillance Maps
Positive-Negative-All-Species
Positive by Species
CWD Endemic Deer Areas
CWD Endemic Elk Areas
2014 CWD Surveillance Maps
2013 CWD Surveillance Maps
CWD Surveillance Positive Deer
Positive Deer by Hunt
Area
(2015)Positive
Deer by Hunt Area
(2012-2014)Positive
Deer by Hunt Area
(2012-2013)Positive
Deer by Hunt Area
(2009-2011)Positive
Deer by Hunt Area
(2006-2008)Positive
Deer by Hunt Area
(2003-2005)
CWD Surveillance Positive Elk
Positive Elk by Hunt Area (2015)Positive Elk by Hunt Area (2012-2014)
Positive
Elk by Hunt Area
(2012-2013)Positive
Elk by Hunt Area
(2009-2011)Positive
Elk by Hunt Area
(2006-2008)Positive
Elk by Hunt Area
(2003-2005)
CWD Surveillance Positive Moose
Positive Moose by Hunt Area (2006-2008)
CWD Surveillance Reports
WGFD Chronic Wasting Disease Surveillance Report (2015)WGFD Chronic Wasting Disease Surveillance Report (2014)WGFD Chronic Wasting Disease Summary Report (2013)WGFD Chronic Wasting Disease Summary Report (2012)Article on CWD - by Chris Madson
Notes
Surveillance and Monitoring of White-Tailed Deer for Chronic Wasting
Disease in the Northeastern United States
Tyler S. Evans,* Krysten L. Schuler, W. David Walter
A Growing Threat
HOW DEER BREEDING COULD PUT PUBLIC TRUST PUBLIC TRUST WILDLIFE AT
RISK
Terry S. Singeltary Sr.
posted by Terry S. Singeltary Sr. at
11:05 AM
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