Wyoming Chronic Wasting Disease Found in Deer Hunt Area 97 Near Muddy Gap
Chronic Wasting Disease Found in Deer Hunt Area 97 Near Muddy Gap 8/18/2014
LANDER - Chronic Wasting Disease (CWD), a fatal neurological disease of
deer, elk and moose, has been discovered in deer hunt area 97, near Muddy Gap.
Chronic Wasting Disease has been previously discovered in several areas
bordering hunt area 97.
A mule deer doe from hunt area 97 was confirmed CWD positive by the Wyoming
Game and Fish Department’s wildlife disease laboratory in Laramie on August 3,
2014. The animal was dispatched by wardens after being reported as acting
strangely west of Muddy Gap. Hunt area 97 borders deer CWD endemic areas 87 and
89 to the east. Hunt area 89 became positive in 2002 and 87 in 2007.
After a review of available scientific data, the World Health Organization
in December 1999 stated, “There is currently no evidence that CWD in cervidae
(deer and elk) is transmitted to humans.” In 2004, Dr. Ermias Belay of the
Center for Disease Control said, “The lack of evidence of a link between CWD
transmission and unusual cases of CJD, [Creutzfeldt-Jakob disease, a human prion
disease] despite several epidemiological investigations, suggest that the risk,
if any, of transmission of CWD to humans is low.” Nonetheless to avoid risk,
both organizations say parts or products from any animal that looks sick and/or
tests positive for CWD should not be eaten.
Game and Fish personnel will continue to collect samples through hunter
field checks, and at CWD sampling stations during the 2014 hunting season.
For more information on chronic wasting disease and regulations on
transportation and disposal of carcasses please visit the Game and Fish website
at: wgfd.wyo.gov.
(Contact: Rene Schell (307) 332-2688)
-WGFD-
Chronic Wasting Disease Ecology and Epidemiology of Mule Deer and
White-tailed Deer in Wyoming
Dr. Brant Schumaker of the University of Wyoming reported that the effects
of high chronic wasting disease (CWD) prevalence in free-ranging deer
populations are unknown. In south-central Wyoming, CWD prevalence exceeds 50% in
hunter harvested deer. We hypothesized that 1) vital rates are depressed by CWD
and the finite rate of population growth (λ) is subsequently lowered, 2) CWD
alters normal deer behavior during preclinical and clinical disease, and 3)
genetic differences associated with CWD incubation periods drives natural
selection to favor less susceptible deer. To test these hypotheses, we
radio-collared white-tailed deer (Odocoileus virginianus) and mule deer
(Odocoileus hemionus) and monitored them to determine a) survival probability,
pregnancy rates, and annual recruitment, b) cause of death, c) home range area
and habitat use, d) migration patterns, e) dispersal behavior, and f) genetic
variation in incubation period based on CWD-status. Deer were tested for CWD
using tonsil tissue collected by biopsy at capture and immunohistochemistry.
White-tailed deer positive for CWD were 4.5 times more likely to die annually
compared to CWD-negative deer. High CWD prevalence depressed survival of young
females and resulted in an unsustainable white-tailed deer population (λ <
1.0); however, when female harvest was eliminated, the population became stable
(λ =1.0). Female CWD-positive white-tailed deer maintain locally high CWD
incidence as they migrated less and occupied smaller home ranges compared to
other deer. Male CWD-positive white-tailed deer migrated at the highest
proportion and likely contributed to spread of CWD to disparate populations. In
the last nine years, mule deer genetically associated with prolonged incubation
periods to CWD have increased in frequency in the population. However, it is
still unknown whether or not this change will counteract the negative impacts of
CWD on the population. The white-tailed deer population is adversely affected by
high CWD prevalence; however, implementing management techniques to increase
annual survival of females may maintain deer populations. The impact of CWD on
mule deer populations is currently unknown; however, the present study is in its
final stages with results to be completed in the near future.
*** We conclude that TSE infectivity is likely to survive burial for long
time periods with minimal loss of infectivity and limited movement from the
original burial site. However PMCA results have shown that there is the
potential for rainwater to elute TSE related material from soil which could lead
to the contamination of a wider area. These experiments reinforce the importance
of risk assessment when disposing of TSE risk materials.
*** The results show that even highly diluted PrPSc can bind efficiently to
polypropylene, stainless steel, glass, wood and stone and propagate the
conversion of normal prion protein. For in vivo experiments, hamsters were ic
injected with implants incubated in 1% 263K-infected brain homogenate. Hamsters,
inoculated with 263K-contaminated implants of all groups, developed typical
signs of prion disease, whereas control animals inoculated with non-contaminated
materials did not.
PRION 2014 CONFERENCE
CHRONIC WASTING DISEASE CWD
A FEW FINDINGS ;
Conclusions. To our knowledge, this is the first established experimental
model of CWD in TgSB3985. We found evidence for co-existence or divergence of
two CWD strains adapted to Tga20 mice and their replication in TgSB3985 mice.
Finally, we observed phenotypic differences between cervid-derived CWD and
CWD/Tg20 strains upon propagation in TgSB3985 mice. Further studies are underway
to characterize these strains.
We conclude that TSE infectivity is likely to survive burial for long time
periods with minimal loss of infectivity and limited movement from the original
burial site. However PMCA results have shown that there is the potential for
rainwater to elute TSE related material from soil which could lead to the
contamination of a wider area. These experiments reinforce the importance of
risk assessment when disposing of TSE risk materials.
The results show that even highly diluted PrPSc can bind efficiently to
polypropylene, stainless steel, glass, wood and stone and propagate the
conversion of normal prion protein. For in vivo experiments, hamsters were ic
injected with implants incubated in 1% 263K-infected brain homogenate. Hamsters,
inoculated with 263K-contaminated implants of all groups, developed typical
signs of prion disease, whereas control animals inoculated with non-contaminated
materials did not.
Our data establish that meadow voles are permissive to CWD via peripheral
exposure route, suggesting they could serve as an environmental reservoir for
CWD. Additionally, our data are consistent with the hypothesis that at least two
strains of CWD circulate in naturally-infected cervid populations and provide
evidence that meadow voles are a useful tool for CWD strain typing.
Conclusion. CWD prions are shed in saliva and urine of infected deer as
early as 3 months post infection and throughout the subsequent >1.5 year
course of infection. In current work we are examining the relationship of
prionemia to excretion and the impact of excreted prion binding to surfaces and
particulates in the environment.
Conclusion. CWD prions (as inferred by prion seeding activity by RT-QuIC)
are shed in urine of infected deer as early as 6 months post inoculation and
throughout the subsequent disease course. Further studies are in progress
refining the real-time urinary prion assay sensitivity and we are examining more
closely the excretion time frame, magnitude, and sample variables in
relationship to inoculation route and prionemia in naturally and experimentally
CWD-infected cervids.
Conclusions. Our results suggested that the odds of infection for CWD is
likely controlled by areas that congregate deer thus increasing direct
transmission (deer-to-deer interactions) or indirect transmission
(deer-to-environment) by sharing or depositing infectious prion proteins in
these preferred habitats. Epidemiology of CWD in the eastern U.S. is likely
controlled by separate factors than found in the Midwestern and endemic areas
for CWD and can assist in performing more efficient surveillance efforts for the
region.
Conclusions. During the pre-symptomatic stage of CWD infection and
throughout the course of disease deer may be shedding multiple LD50 doses per
day in their saliva. CWD prion shedding through saliva and excreta may account
for the unprecedented spread of this prion disease in nature.
see full text and more ;
Monday, June 23, 2014
*** PRION 2014 CONFERENCE CHRONIC WASTING DISEASE CWD
*** Infectious agent of sheep scrapie may persist in the environment for at
least 16 years***
Gudmundur Georgsson1, Sigurdur Sigurdarson2 and Paul Brown3
New studies on the heat resistance of hamster-adapted scrapie agent:
Threshold survival after ashing at 600°C suggests an inorganic template of
replication
Prion Infected Meat-and-Bone Meal Is Still Infectious after Biodiesel
Production
Detection of protease-resistant cervid prion protein in water from a
CWD-endemic area
A Quantitative Assessment of the Amount of Prion Diverted to Category 1
Materials and Wastewater During Processing
Rapid assessment of bovine spongiform encephalopathy prion inactivation by
heat treatment in yellow grease produced in the industrial manufacturing process
of meat and bone meals
PPo4-4:
Survival and Limited Spread of TSE Infectivity after Burial
PPo4-4:
Survival and Limited Spread of TSE Infectivity after Burial
Karen Fernie, Allister Smith and Robert A. Somerville The Roslin Institute
and R(D)SVS; University of Edinburgh; Roslin, Scotland UK
Scrapie and chronic wasting disease probably spread via environmental
routes, and there are also concerns about BSE infection remaining in the
environment after carcass burial or waste 3disposal. In two demonstration
experiments we are determining survival and migration of TSE infectivity when
buried for up to five years, as an uncontained point source or within bovine
heads. Firstly boluses of TSE infected mouse brain were buried in lysimeters
containing either sandy or clay soil. Migration from the boluses is being
assessed from soil cores taken over time. With the exception of a very small
amount of infectivity found 25 cm from the bolus in sandy soil after 12 months,
no other infectivity has been detected up to three years. Secondly, ten bovine
heads were spiked with TSE infected mouse brain and buried in the two soil
types. Pairs of heads have been exhumed annually and assessed for infectivity
within and around them. After one year and after two years, infectivity was
detected in most intracranial samples and in some of the soil samples taken from
immediately surrounding the heads. The infectivity assays for the samples in and
around the heads exhumed at years three and four are underway. These data show
that TSE infectivity can survive burial for long periods but migrates slowly.
Risk assessments should take into account the likely long survival rate when
infected material has been buried.
The authors gratefully acknowledge funding from DEFRA.
Monday, August 18, 2014
CWD TSE PRION Singeltary Submission to Indiana Department of Natural
Resources, four out-of-state wildlife disease experts, and to the 14-member
Agriculture and Natural Resources Interim Study Committee
Tuesday, July 15, 2014
Chronic wasting disease model of genetic selection favoring prolonged
survival in Rocky Mountain elk (Cervus elaphus)
*** on a wing and a prayer, and over 100-year modeled timeframes...
Chronic Wasting Disease closes in on Yellowstone
By Ralph Maughan On May 17, 2013
Friday, November 16, 2012
Yellowstone elk herds feeding grounds, or future killing grounds from CWD
Saturday, May 25, 2013
Wyoming Game and Fish Commission Alkali Creek Feedground #39126 Singeltary
comment submission
Dense concentrations of elk at feedgrounds facilitate the transmission of
diseases and increase their prevalence. Free-ranging elk herds have a CWD
prevalence of approximately 1-3% in the core Colorado-Wyoming area where the
disease is endemic. Captive elk herds, whose densities more closely match those
of feedground elk, have shown rates of CWD prevalence between 17- 59%. Many
states now ban the artificial feeding of deer because scientific evidence
suggests that such feeding elevates the risk of CWD transmission. High
concentrations of animals, close contact between animals, and the contaminated
environments that result from these conditions, all contribute to the increased
transmission of CWD and other diseases.
Wednesday, April 30, 2014
WYOMING Mule Deer Found Dead Near Rawlins Tests Positive for CWD
Wednesday, October 24, 2012
WYOMING Deer Hunt Area 132 Near Green River Added to CWD List
Wednesday, November 16, 2011
Chronic wasting disease found in Big Horn basin deer Wyoming's deer hunt
area 165
Monday, November 14, 2011
WYOMING Creutzfeldt Jakob Disease, CWD, TSE, PRION REPORTING 2011
Thursday, July 08, 2010
CWD Controversy still stalking elk feedgrounds in Wyoming 2010
Greetings,
This is very serious, please notice that one of the CWD clusters is only 45
miles from ELK feeding grounds in Wyoming, the second elk feeding ground is 98
miles from CWD cluster, and the third elk feeding ground is 130 miles from the
CWD cluster. Common sense tells us we need to stop those feeding grounds, if you
want your Elk to survive. There is no politics or plot against the hunters or
elk about it. read the science please. ...TSS
chronic wasting disease proximity to elk feedgrounds in wyoming 2009-2010
Thursday, December 30, 2010
WYOMING MULE DEER BUCK HARVESTED NEAR LYSITE TESTS POSITIVE FOR CWD
December 27, 2010
Monday, December 13, 2010
WYOMING DEER AREA 119 ADDED TO CWD LIST DEER AREA 119 ADDED TO CWD
LIST
11/22/2010
Friday, November 12, 2010
WHITE-TAILED BUCK HARVESTED NEAR MOORCROFT TESTS POSITIVE FOR CWD
WYOMING
Sunday, October 31, 2010
TWO DEER HARVESTED NEAR GREYBULL TEST POSITIVE FOR CWD WYOMING
Wednesday, October 20, 2010
WYOMING ELK NEAR GLENDO TESTS POSITIVE FOR CWD 10/18/2010
Wednesday, November 25, 2009
CHRONIC WASTING DISEASE FOUND IN ELK AREA 35 NEAR BUFFALO
Wednesday, November 11, 2009
CHRONIC WASTING DISEASE DISCOVERED IN DEER HUNT AREA 42 WYOMING
Sunday, November 01, 2009
CWD confirmed in Johnson County Wyoming Sunday, November 1, 2009
Wednesday, October 14, 2009
Deer on western Bighorns has chronic wasting disease Shell Creek drainage
Wyoming
Monday, December 22, 2008
CWD DETECTED IN ELK HUNT AREA 117 SOUTH OF SUNDANCE WYOMING
Saturday, October 18, 2008
WYOMING STAR VALLEY MOOSE TESTS POSITIVE FOR CWD
TSS
posted by Terry S. Singeltary Sr. at
9:39 AM
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