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Wednesday, October 29, 2014

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

 


 

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

 


 

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

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