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From: TSS ()
Subject: Throw CWD disease to the wolves? HOUND ATAXIA OR TSE?
Date: August 8, 2005 at 10:22 am PST

Throw disease to the wolves?

Park eyes predators to control chronic wasting in elk

Article Launched: 08/07/2005 03:42:37 AM

By Theo Stein
Denver Post Staff Writer

Predation by wolves may be an effective way to stop a deadly brain disease of deer and elk in Colorado, according to a recent study.

A modeling study based on conditions at Rocky Mountain National Park shows wolves could have "potent effects" on the rate of chronic wasting disease in the park's overabundant elk herds, according to three Colorado researchers.

Existing control efforts, which focus on intensive culling to reduce herd numbers, have been expensive and, so far, ineffective.

"We need to think outside the box," said National Park Service wildlife veterinarian Margaret Wild. "We've got to come up with some different tools."

Chronic wasting disease is a transmissible spongiform encephalopathy like mad cow disease. Unlike mad cow, it is contagious and persists in the environment for years.

There is no evidence that CWD has ever sickened a human, but health experts warn hunters not to eat the meat of an infected animal.

Since it was identified in Colorado in 1977, CWD has hopscotched to Wyoming, Utah, Nebraska, Illinois, Wisconsin, New York and Saskatchewan.

Studies have shown that wolves prey on the weak or sick. That behavior could help remove contagious animals from the population and reduce infection rates, according to Wild. Wolves also could help scatter herds of deer and elk, further reducing the risk of transmission, she said.

Field research will be needed to show what effect, if any, wolves have on CWD, she said.

Some prominent wolf biologists have offered cautious support.

"I need to see the data," said L. David Mech, a University of Minnesota professor. "If the claim is valid, there may be some value in terms of controlling CWD. But it needs some pretty good documentation before it will be accepted."

Rocky Mountain National Park is evaluating whether wolves could help cull and redistribute elk herds that have overbrowsed aspen and willow.

The only promising CWD control technique is now in a third year of study in Estes Park. The Colorado Division of Wildlife has biopsied the tonsils of tranquilized mule deer, fitted the animals with radio collars and removed those found to be infected.

CWD rates do appear to be declining in the project area, division veterinarian Mike Miller said. But at about $660 an animal, the cost makes the technique unsuitable for backcountry applications.

The research does not involve elk because no live test for elk has been developed.

The strategy of testing and culling is essentially what wolves do, Miller said.

"They'd be paid by the pound, not by the hour," he said. "Wolves would always be on the clock."

Staff writer Theo Stein can be reached at 303-820-1657 or

THIS is not a good idea!
YOU are just asking for trouble...

GAH WELLS (very important statement here...TSS)


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.


76 pages on hound study;

> I thought that in Britain dogs had contracted BSE, but perhaps not.

not so fast here;

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

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


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