Chronic wasting disease now rings Greater Yellowstone in Wyoming
Chronic wasting disease now rings Greater Yellowstone in Wyoming
By Ralph Maughan On October 27, 2014 · 9 Comments · In Deer, Disease, Elk,
Moose, Wildlife, Wolves, Wolves and Prey, Wyoming, Wyoming Wolves How much
longer before the feedlots are hit?
Nightmare “mad elk” or “mad deer” disease, the always lethal malady spread
by prions (infectious proteins), keeps creeping ever closer the the Greater
Yellowstone ecosystem in Wyoming and to the massive elk winter feedlots. In
these, it is expected to spread like wildfire in cheatgrass.
According to Wyoming Game and Fish, CWD presence has now been confirmed in
the lab and visually in the field in all the hunting units adjacent to the core
of the Greater Yellowstone in NW Wyoming. The new, bad news is detailed in the
Jackson Hole News and Guide, CWD keeps creeping closer to feedgrounds.
For years critics have wanted to close down the elk feedgrounds to prevent
infection. Now it seems obvious the state game department will never do this. It
is hypothesized that wolves are as close to an ideal way of taking out infected
deer and elk just beginning to show symptoms as any natural method possible.
Wolves, disproportionately target sick ungulate prey. The hypothesis has not
been tested, however, and it is doubtful that it will, given Wyoming’s hostility
to a natural density for the now restored predator.
As hunters wait for the axe to fall, they can have their moose, elk, or
deer tested at Wyoming State Veterinary Lab at 307-766-9925.
CWD does not occur in Montana or Idaho. These states contain the rest of
the Greater Yellowstone.
How much longer before the feedlots are hit?
YOU CANNOT FIX STUPID, WITH MORE STUPID. ...TSS
Terry S. Singeltary Sr. says:
October 29, 2014 at 6:18 am
>>> It is hypothesized that wolves are as close to an ideal way of
taking out infected deer and elk just beginning to show symptoms as any natural
method possible. Wolves, disproportionately target sick ungulate prey. The
hypothesis has not been tested, however, and it is doubtful that it will, given
Wyoming’s hostility to a natural density for the now restored predator.
<<<
PLEASE be careful what you ask for.
recently, canine spongiform encephalopathy has been confirmed.
I proved this in 2005, with a letter from MAFF/DEFRA et al confirming my
suspicions of the ‘hound study’ way back. this was covered up. see documents
below.
also, recently, cwd to the domestic cat is a great concern.
even though to date, as far as I am aware of, the cwd study on the mountain
lion has not produced any confirmation yet, we already know that the feline
species is highly succeptible to the TSE prion. domestic cats and the exotic zoo
big cats.
so in my honest opinion, any program that would use wild animals to prey on
other wild animals, as a tool to help curb CWD TSE prion disease, would only
help enhance the spread of disease, and it would only help spread the disease to
other species. …TSS
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 snip…end…tss
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
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.
SEE FULL TEXT ;
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
Monday, March 8, 2010
Canine Spongiform Encephalopathy aka MAD DOG DISEASE
Saturday, October 18, 2014
Chronic wasting disease threatens Canadian agriculture, Alberta MLA
says
Thursday, October 23, 2014
FIRST CASE OF CHRONIC WASTING DISEASE CONFIRMED IN OHIO ON PRIVATE PRESERVE
Tuesday, October 21, 2014
Pennsylvania Department of Agriculture Tenth Pennsylvania Captive Deer
Tests Positive for Chronic Wasting Disease CWD TSE PRION DISEASE
Tuesday, October 07, 2014
Wisconsin white-tailed deer tested positive for CWD on a Richland County
breeding farm, and a case of CWD has been discovered on a Marathon County
hunting preserve
Thursday, October 02, 2014
IOWA TEST RESULTS FROM CAPTIVE DEER HERD WITH CHRONIC WASTING DISEASE
RELEASED 79.8 percent of the deer tested positive for the disease
Thursday, July 03, 2014
*** How Chronic Wasting Disease is affecting deer population and what’s the
risk to humans and pets?
Tuesday, July 01, 2014
*** CHRONIC WASTING DISEASE CWD TSE PRION DISEASE, GAME FARMS, AND
POTENTIAL RISK FACTORS THERE FROM
Saturday, October 25, 2014
118th USAHA Annual Meeting CWD and Captive Cerivds
Saturday, October 25, 2014
Wyoming Chronic Wasting Disease Found in Two More Deer Hunt Areas
SEE CWD VACCINE UPDATE ;
Friday, November 16, 2012
Yellowstone elk herds feeding grounds, or future killing grounds from CWD
TSS
posted by Terry S. Singeltary Sr. at
7:28 AM
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