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
By Angus M. Thuermer Jr. | December 15, 2015
Chronic Wasting Disease will cause a Wyoming deer herd to go virtually
extinct in 41 years, a five-year study predicts.
The investigation, which relied on the capture of 143 deer, examined the
dynamics in the Southern Converse County Mule Deer Herd that lives southwest of
Douglas near Laramie Peak. There, a population that once numbered some 14,000 in
the early 2000s dwindled to half that size in about a decade.
The Chronic Wasting Disease study is one of only three that have been
conducted on wild deer, elk or moose herds, none of which have yet seen print.
While wildlife managers have long suspected CWD as a principle agent in the
ravaged Converse herd, the study puts numbers on the problem, calculating a 19
percent decline annually.
University of Wyoming doctoral student Melia DeVivo spent four years of
fieldwork and another year crunching numbers before defending her PhD thesis on
the herd. She calculated the herd would go extinct in 41 years, without taking
into account genetic differences that make some deer more resistant to CWD, or
accounting for deer migration into the area. Even when taking in those factors,
the herd will decline dramatically, she said.
“I estimated that CWD was causing a 19 percent annual reduction in the
population, which is pretty significant,” she said. “Potentially, in 41 years,
it would be locally extinct.”
snip...see full text ;
Melia DeVivo, Ph.D. - Veterinary Sciences
Indiana, Pennsylvania
Project: Epidemiology of chronic wasting disease in a mule deer in the
endemic area of Wyoming
Advisor: Dr. Todd Cornish
Project Summary: The effects of chronic wasting disease (CWD) in mule deer
(Odocoileus hemionus) populations are poorly understood. This study was designed
to investigate the epidemiology of CWD in a free-ranging mule deer population in
the CWD endemic area of Wyoming. Our first hypothesis is that CWD alters the
behavior and activity patterns of free-ranging mule deer, resulting in
differences in landscape use between CWD-positive and CWD-negative deer. Our
second hypothesis is that CWD is negatively impacting mule deer populations by
reducing the average lifespan of CWD-positive deer, and consequently their
lifetime reproductive contribution to the population. Additionally, CWD-positive
deer may produce fewer fawns compared to CWD-negative deer due to their
diminished ability to adequately care for their young. Our study objectives are
to determine disease status, pregnancy rates, and genetic susceptibility of
free-ranging mule deer annually and monitor these deer using radio-telemetry and
global positioning system (GPS) collars throughout their lifespan to determine:
a) survival rates; b) home range size and habitat use; c) dispersal rates; d)
migration patterns; e) daily activity patterns; and f) fawn
productivity/recruitment. We will compare our results between the two
sub-populations (CWD-positive and CWD-negative deer) and attempt to determine
the role of CWD in population decline by calculating a population growth rate
(λ) curve in response to CWD prevalence. Biosketch: Melia’s first wildlife job
was working for the Pennsylvania Game Commission on research regarding elk
calving habitat and survival in north-central PA as an undergrad at Indiana
University of Pennsylvania (IUP). She graduated from IUP in 2007 with her B.S.
in Pre-Medicine and then went on to receive her M.S. in Biology, also from IUP
in 2009. While pursuing her M.S. degree, she became increasingly interested in
wildlife diseases and was fortunate to have the opportunity to enroll at the
University of Wyoming in 2010 to conduct research on chronic wasting disease in
a free-ranging mule deer population. Currently, Melia is wrapping up her third
field season and will be capturing deer in February 2013 for her fourth and
final field year. She plans on graduating in the fall of 2014 and remaining in
the Rocky Mountain West. In her “free time”, Melia enjoys downhill skiing,
hiking, and crocheting while listening to RadioLab and This American Life.
Tuesday, December 08, 2015
Wyoming Game and Fish finds CWD in new elk hunt area in Johnson County
Friday, November 27, 2015
Wyoming Game and Fish finds CWD in new Deer Hunt Area near Sheridan
Wyoming WGF Commission Meeting 11/6/2015 Afternoon Edition Video
CWD starts at minute 58:51 of first hour of meeting discussion of previous
models predicting extinction of deer population and elk population.
please mark hour 1:02 where remarks were made about potential resistant
genes and prolonged survival, however a recent study (I posted directly next
after youtube link) where it states ;
‘’Our study also demonstrates that mice expressing the deer S96-PRNP
allele, previously shown to be resistant to various cervid prions, are
susceptible to H95+ CWD prions. The potential for the generation of novel
strains raises the possibility of an expanded host range for CWD. ‘’
hour minute mark 1:03
captive Elk study
39 femail elk calves captured on National Elk Refuge In Jackson, WY
Transported to WGFD Thorne-Williams Wildlife Research Unit (Sybille,
TWWRU)
Worst-case scenario for prion exposure
Genotypes
-27 M/M132 (69.2%)
-11 M/L132 (28.2%)
-1 L/L132 (2.6%)
38 of 39 elk died over 10-year study
1 remaining elk was L/L132
still alive and remained negative for PrPCWD by rectal biopsy
Appears healthy, weighs 242kg, and bore healthy calf in May, 2012
CWD infection rate in this study ???
> During the analysis, 37 of 39 elk died, all of which were positive for
CWD.
*** Our study also demonstrates that mice expressing the deer S96-PRNP
allele, previously shown to be resistant to various cervid prions, are
susceptible to H95+ CWD prions. ***
*** The potential for the generation of novel strains raises the
possibility of an expanded host range for CWD. ***
Deer Prion Proteins Modulate the Emergence and Adaptation of Chronic
Wasting Disease Strains
Camilo Duque Velásqueza,b, Chiye Kima,c, Allen Herbsta,b, Nathalie
Daudea,d, Maria Carmen Garzaa,e, Holger Willea,e, Judd Aikena,b and Debbie
McKenziea,c aCentre for Prions and Protein Folding Diseases, University of
Alberta, Edmonton, Alberta, Canada bDepartment of Agricultural, Food and
Nutritional Science, University of Alberta, Edmonton, Alberta, Canada
cDepartment of Biological Sciences, University of Alberta, Edmonton, Alberta,
Canada dDepartment of Medicine, University of Alberta, Edmonton, Alberta, Canada
eDepartment of Biochemistry, University of Alberta, Edmonton, Alberta, Canada
B. Caughey, Editor
+ Author Affiliations
ABSTRACT
Transmission of chronic wasting disease (CWD) between cervids is influenced
by the primary structure of the host cellular prion protein (PrPC). In
white-tailed deer, PRNP alleles encode the polymorphisms Q95 G96 (wild type
[wt]), Q95 S96 (referred to as the S96 allele), and H95 G96 (referred to as the
H95 allele), which differentially impact CWD progression. We hypothesize that
the transmission of CWD prions between deer expressing different allotypes of
PrPC modifies the contagious agent affecting disease spread. To evaluate the
transmission properties of CWD prions derived experimentally from deer of four
PRNP genotypes (wt/wt, S96/wt, H95/wt, or H95/S96), transgenic (tg) mice
expressing the wt allele (tg33) or S96 allele (tg60) were challenged with these
prion agents. Passage of deer CWD prions into tg33 mice resulted in 100% attack
rates, with the CWD H95/S96 prions having significantly longer incubation
periods. The disease signs and neuropathological and protease-resistant prion
protein (PrP-res) profiles in infected tg33 mice were similar between groups,
indicating that a prion strain (Wisc-1) common to all CWD inocula was amplified.
In contrast, tg60 mice developed prion disease only when inoculated with the
H95/wt and H95/S96 CWD allotypes. Serial passage in tg60 mice resulted in
adaptation of a novel CWD strain (H95+) with distinct biological properties.
Transmission of first-passage tg60CWD-H95+ isolates into tg33 mice, however,
elicited two prion disease presentations consistent with a mixture of strains
associated with different PrP-res glycotypes. Our data indicate that H95-PRNP
heterozygous deer accumulated two CWD strains whose emergence was dictated by
the PrPC primary structure of the recipient host. These findings suggest that
CWD transmission between cervids expressing distinct PrPC molecules results in
the generation of novel CWD strains.
IMPORTANCE CWD prions are contagious among wild and captive cervids in
North America and in South Korea. We present data linking the amino acid variant
Q95H in white-tailed deer cellular prion protein (PrPC) to the emergence of a
novel CWD strain (H95+). We show that, upon infection, deer expressing H95-PrPC
molecules accumulated a mixture of CWD strains that selectively propagated
depending on the PRNP genotype of the host in which they were passaged. Our
study also demonstrates that mice expressing the deer S96-PRNP allele,
previously shown to be resistant to various cervid prions, are susceptible to
H95+ CWD prions. The potential for the generation of novel strains raises the
possibility of an expanded host range for CWD.
*** Our study also demonstrates that mice expressing the deer S96-PRNP
allele, previously shown to be resistant to various cervid prions, are
susceptible to H95+ CWD prions. ***
*** The potential for the generation of novel strains raises the
possibility of an expanded host range for CWD. ***
UPDATE CWD VACCINE ELK minute mark 1:22:00
VACCINE
RECOMBINANT PROTEIN FUSION VACCINE
Hedlin, PD et al ‘’Design and delivery of a cryptic PrP c epitope for
induction of Prp Sc-specific antibody responses.’’ Vaccine 28.4 (2010)
981-988.
PAN-PROVINCIAL VACCINE ENTERPRISES (PREVENT)
Dose: 2ml IM CWD VACCINE UPDATE IS A FAILURE, I REPEAT, A NEGATIVE RESULTS
FOR CWD VACCINE. .tss
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
TSE PRION (MAD COW TYPE) REPORTS DECEMBER 14, 2015
some of the most recent peer review science, some old science, about
chronic wasting disease cwd tse prion.
some of you might want to read this.
this mad cow debacle i.e. BSE TSE Prion goes far beyond the mad cow
hamburger.
Saturday, December 12, 2015
CHRONIC WASTING DISEASE CWD TSE PRION REPORT DECEMBER 14, 2015
Saturday, December 12, 2015
BOVINE SPONGIFORM ENCEPHALOPATHY BSE TSE PRION REPORT DECEMBER 14, 2015
Saturday, December 12, 2015
NOTICE: Environmental Impact Statement on Large Livestock Carcasses TSE
Prion REPORT December 14, 2015
Saturday, December 12, 2015
CREUTZFELDT JAKOB DISEASE CJD TSE PRION REPORT DECEMBER 14, 2015
Evidence for human transmission of amyloid-β pathology and cerebral amyloid
angiopathy
07 02:27 AM
Terry S. Singeltary Sr. said:
re-Evidence for human transmission of amyloid-? pathology and cerebral
amyloid angiopathy
Nature 525, 247?250 (10 September 2015) doi:10.1038/nature15369 Received 26
April 2015 Accepted 14 August 2015 Published online 09 September 2015 Updated
online 11 September 2015 Erratum (October, 2015)
I would kindly like to comment on the Nature Paper, the Lancet reply, and
the newspaper articles.
snip...see full text ;
Subject: 1992 IN CONFIDENCE TRANSMISSION OF ALZHEIMER TYPE PLAQUES TO
PRIMATES POSSIBILITY ON A TRANSMISSIBLE PRION REMAINS OPEN
BSE101/1 0136
IN CONFIDENCE
CMO
From: . Dr J S Metiers DCMO
4 November 1992
TRANSMISSION OF ALZHEIMER TYPE PLAQUES TO PRIMATES
1. Thank you for showing me Diana Dunstan's letter. I am glad that MRC have
recognised the public sensitivity of these findings and intend to report them in
their proper context. 'This hopefully will avoid misunderstanding and possible
distortion by the media to portray the results as having more greater
significance than the findings so far justify.
2. Using a highly unusual route of transmission (intra-cerebral injection)
the researchers have demonstrated the transmission of a pathological process
from two cases one of severe Alzheimer's disease the other of
Gerstmann-Straussler disease to marmosets. However they have not demonstrated
the transmission of either clinical condition as the "animals were behaving
normally when killed". As the report emphasises the unanswered question is
whether the disease condition would have revealed itself if the marmosets had
lived longer. They are planning further research to see if the conditions, as
opposed to the partial pathological process, is transmissible.
what are the implications for public health?
3. The route 'of transmission is very specific and in the natural state of
things highly unusual. However it could be argued that the results reveal a
potential risk, in that brain tissue from these two patients has been shown to
transmit a pathological process. Should therefore brain tissue from such cases
be regarded as potentially infective? Pathologists, morticians, neuro surgeons
and those assisting at neuro surgical procedures and others coming into contact
with "raw" human brain tissue could in theory be at risk. However, on a priori
grounds given the highly specific route of transmission in these experiments
that risk must be negligible if the usual precautions for handling brain tissue
are observed.
1
92/11.4/1.1
BSE101/1 0137
4. The other dimension to consider is the public reaction. To some extent
the GSS case demonstrates little more than the transmission of BSE to a pig by
intra-cerebral injection. If other prion diseases can be transmitted in this way
it is little surprise that some pathological findings observed in GSS were also
transmissible to a marmoset. But the transmission of features of Alzheimer's
pathology is a different matter, given the much greater frequency of this
disease and raises the unanswered question whether some cases are the result of
a transmissible prion. The only tenable public line will be that "more research
is required’’ before that hypothesis could be evaluated. The possibility on a
transmissible prion remains open. In the meantime MRC needs carefully to
consider the range and sequence of studies needed to follow through from the
preliminary observations in these two cases. Not a particularly comfortable
message, but until we know more about the causation of Alzheimer's disease the
total reassurance is not practical.
J S METTERS Room 509 Richmond House Pager No: 081-884 3344 Callsign: DOH
832 llllYc!eS 2 92/11.4/1.2
>>> The only tenable public line will be that "more research is
required’’ <<<
>>> possibility on a transmissible prion remains
open<<<
O.K., so it’s about 23 years later, so somebody please tell me, when is
"more research is required’’ enough time for evaluation ?
Self-Propagative Replication of Ab Oligomers Suggests Potential
Transmissibility in Alzheimer Disease
Received July 24, 2014; Accepted September 16, 2014; Published November 3,
2014
*** Singeltary comment PLoS ***
Alzheimer’s disease and Transmissible Spongiform Encephalopathy prion
disease, Iatrogenic, what if ?
Posted by flounder on 05 Nov 2014 at 21:27 GMT
Wednesday, September 2, 2015
Clinically Unsuspected Prion Disease Among Patients With Dementia Diagnoses
in an Alzheimer’s Disease Database
Terry S. Singeltary Sr.
posted by Terry S. Singeltary Sr. at
7:58 AM
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