Avoiding pre-senile dementia: recommendations to hunters
Colorado mule deer and elk CWD: just scrapie from domestic sheep?
53 Cases of CWD in Larimer County, Colorado since 1981
Vet says it's ok to eat tainted deer and elk meat
White-tailed deer have it too
Risk to hunters from tanning with brain?
Did captive deer eat rendered beef?
Do deer get it on public lands from domestic sheep and cattle?
Opinions from Cyberspace
Elk from South Dakota stricken in Canada, captive herd to be destroyed
Eliminate game farms, Montanan says
1400 Dead Moose in Sweden said not to have BSE
Reindeer getting scrapie from sheep?
SCIENTIFIC ABSTRACTS


Common-Sense Recommendations


Chronic Wasting Disease - USA

Date: Mon, 6 May 1996 14:08:39 -0400 (EDT)

I'm not sure about this specific case {elk in Canada with CJD], but before going to vet school, I worked for the Colorado Division of Wildlife in Fort Collins, CO. We had captive bred mule [deer?] and elk that acquired a Chronic wasting syndrome similar to what you describe. Though the animals were fed alfalfa hay, native grass in their pens were also available.

This particular tract of land had once been domestic sheep range and at the time it was speculated that scrapie or something similar to scrapie was responsible for the disease.

Joel Stone, D.V.M., Ph.D
Merck Research Laboratories
Rahway, N.J.



Colorado Big-Game Stricken with Mad Cow-like Ailment

McClatchy Western News Service

DENVER - Deer and elk in parts of norther Colorado have been stricken with an ailment similar to Great Britain's mad cow disease, but it doesn't affect humans who eat the tainted meat. [Use extreme caution - brain and spinal tissue is very likely to infect humans - webmaster]

"While the disease is similar, there never has been a link found between it and any human health problems," said Mike Miller, a Colorado Division of Wildlife veterinarian. [No such studies has ever been conducted - webmaster]

Bovine spongiform encephalopathy recently was linked in Britain to brain disorders, blindness and loss of nerve control in humans, although Miller says he is not convinced one causes the other. The British government may destroy up to 4.5 million dairy cows in an attempt to allay fears about the safety of that nations's beef.

The so-called chronic wasting disease damages portions of the brains of deer and elk. Affected animals experience progressive weight and muscle loss, bahavioral changes, excessive salivation, incrased drinking, urination, and depression. Chronic wasting disease is always fatal.

It's suspected that the disease is transmittted frough feces, urine and shedding. [Thus, possibly from wildlife contact with scrapie-infected sheep herds or BSE-infected cattle -webmaster] The known cases are limited to areas from the Wyoming border south to Lyons and along the South Platte River east to Fort Morgan. When a diseased animal is reported, state wildlife officials capture and destroy it.


53 Cases of CWD in Larimer County, Colorado since 1981

Colorado wildlife officials have found a disease similar to BSE in elk and deer in Larimer County. They said chronic wasting disease is similar to BSE and afflicts mule deer, white-tailed deer and elk.

The first case of the rare chronic wasting disease was documented about 14 years ago in northern Colorado but hasn't been widely documented anywhere else in the world. Since 1981, 53 cases, mostly in the foothills of Larimer County, have been reported.

Wes Shields, chief of the Wildlife Section of the Utah Division of Wildlife Rsources, said there have been no reported incidents of the wasting disease in Utah.

Deseret News Archives> Saturday, March 30, 1996


ListServe item:Chronic Wasting Disease showed up in 1967 in captive Colorado deer. It is unknown whether they were fed bovine or sheep based protein rations.

There is a lot of trouble in northern Colorado this year with both deer and elk. This would be on public land grazed by sheep and cattle. A recent letter to Lancet suggested hay mites could transmit the disease horizontally in sheep. So the question is, is CWD really a disease the deer and elk are acquiring from sick livestock?

Hunters here commonly make sausage out of the brain and sometimes use it to tan hides. So the risk of transmission to humans is not far-fetched. People have supposedly gotten CJD from squirrel and wild goat brain as per the medical liturature.


Listserve items:
A letter from Dr. Elizabeth Williams, University of Wyoming, dated 28 April 1996 in which she states that five cases of chronic wasting disease in white-tailed deer have been seen at her laboratory.

Since publication of the review of CWD in 1992 (Williams and Young, 1992, Spongiform Encephalopathies in Cervidae, Rev sci tech Off int Epiz, 11: 551-567) we have identified CWD in several white-tailed deer (Odocoileus virginianus).

Beth Williams
Department of Veterinary Sciences
University of Wyoming
Laramie, Wyoming 82070



Canadian Statement on CWD in Elk:

In early 1996, Agriculture and Agri-Food Canada (AAFC) confirmed a case of Chronic Wasting Disease (CWD) in a single elk located on a small game farm facility in southern Saskatchewan. The affected animal was imported as a yearling, in 1989, as part of a small shipment of elk originating from Soout Dakota, U.S.

We don't the feeding history of the elk in question before it was imported to Canada. However, we know that on the game ranch in Saskatchewan, she and her herdmates were fed a diet of high-quality alfalfa hay and other home-grown grains. The only commercial products fed to the herd consisted of vitamins and mineral supplements.

[Rendered livestock protein supplement may have been fed to the elk back in South Dakota; CWD also showed up in 1967 in a captive mule deer herd in Colorado. The odds of 'familial' or sporadic CWD, if it is a prion disease, showing up in a herd of 24 elk is essentially zero. --webmaster]

In 1990, Canada imposed a prohibition on the importation of cervids (such as deer and elk) and camelids (notably, llamas and alpacas) from the U.S. The ban was a reaction to the presence of sporadic outbreaks of tuberculosis among some captive ungulate herds in the U.S. The ban has been extended (by regulation) until December 31, 1997.

The game farm in question is not located near other (alternative or conventional) livestock operations. No animals on this farm have died, nor have any animals moved off the premises, for any reason, since the elk herd was established.

Following the confirmation of CWD, the carcass of the affected elk was incinerated and the following actions took place:

1) AAFC carried out an inventory of all elk on the farm; 2) no 'movement permits' for the elk were issued to the owner; (All captive ungulates in Canada require numbered permits to allow their movement anywhere within the country, including farm-to-farm) 3) all animals that were part of the original shipment from the U.S. were traced and located; and 4) the affected herd was put in isolation. [On 4.30.96, Dr. George Luterbach in Canada stated all 23 elk will be destroyed -- webmaster]

Chronic Wasting Disease is not a "reportable disease", and the Office International des ?pizooties (OIE) (the organization that establishes international animal health guidelines), does not require notification its presence.

Agriculture and Agri-Food Canada has developed a policy for the eradication of CWD in ranched deer and elk, and in the case of a confirmed case of CWD, we will order the destruction of all animals considered to be at risk.

CWD, like BSE of cattle and scrapie of sheep, belongs to the transmissible spongiform encephalopathies disease group. According to the available scientific literature, it affects the mule deer family (including mule deer, black-tailed deer, and mule/white-tailed hybrids) and elk. White-tailed deer have not developed the disease, to date.

The cause of CWD is unknown, there is no treatment, and no test for the disease in live animals. CWD was first seen in Colorado (U.S.), in 1967, in deer belonging to research facilities. Since then, the disease has been diagnosed in captive and wild deer and elk in northern Colorado and southern Wyoming. Steve Sullivan
Senior Communications Advisor
(Animal Health/Welfare Issues)
Agriculture and Agri-Food Canada
Ottawa, Canada


H3>Eliminate game farms, Montanan says Elk and deer farms threaten Montana's wild herds and there is too much at stake to let the industry continue, said state Sen. Terry Klampe, who is sponsoring a game-farm moratorium and phaseout bill. The two main issues are tuberculosis being spread to wild animals and cross-breeding of commercial and wild game. Tuberculosis has been found in elk at six Montana game farms since 1991 and cross breeding of game farm animals with elk in the wild could bring greater susceptibility to disease, said Herb Johnson, chairman of the Montana Wildlife Federation's committee on game farms.

ENN Daily News -- Jan. 18, 1995
Copyright © 1995, Environmental News Network Inc.


ListServe Item: While we can't say with certainty that the chronic wasting disease is passed on to humans from elk velvet, it does seem to be transmitted through contaminated blood and milk, the disease agent is extremely stable to heat and drying, and so no one in their right mind would eat it, since material cannot be tested for the presence of infectious prion protein. The disease first showed up in North America in a captive deer herd in Colorado in 1967. The elk in Canada came from South Dakota in 1989.

Pre-senile dementia is an uncomfortable issue for hunters, who tend to think of themselves as self-reliant and woods-smart. I am not familiar with cultural attitudes towards dementia in Asia. The fourth line above is interview with a living victim -- a 30 year old teacher in England with diagnosed bovine-CJD.

Some folks are of the opinion that "chronic wasting disease" is not an indigenous ungulate disease at all [like NPS concluded with bison and brucellosis], but simply scrapie or mad cow disease, passed on through hay mites on public lands grazed by sheep or cattle, or via rendered downer cow protein supplements.



A wasting syndrome in moose in Sweden

Since 1985, moose have been found dead or dying of a syndrome in an area of southwestern Sweden, northeast of the city of Gothenburg. The core area for affected animals has been and still is southern Cavsborg county, although a spread is noted to the closest counties and individual cases with the syndrome have been reported from the entire country. At last count, more than 1400 animals are reported to have died in the sickness. Both sexes and all age class animals have been found with the syndrome, although animals more than 4 years are more prone to the syndrome.

The research has shown that the moose population in this area initially was in good condition, with a high reprodutive capability. However, the population has been on the decline during the end of the 1980's due to an increased harvest, and locally due to the disease. From the very beginning there seemed to be no indication of a general overbrowsing in southern =C4lvsborg county, but now there is indications of reduced browse. Moose shot in the areas with a high frequency of sick animals have initially shown better body condition, higher reproductive capability/output, and even a higher density than in control areas, which seems to be indicative of a higher carrying capacity in the affected areas. But now it seems that the body condition is detoriating. Lastly, it is known that the entire =C4lvsborgs county is one of the most acidified areas in all of Sweden, with high amounts of heavy metals in wild-life.

None of the research carried out thus far would indicate that the browse situation in the investigated areas, qualitatively, is or has been such that this could cause a strong reduction in animals' condition and in turn make them more susceptible to infection. The analyses carried out thus far on moose browse in these areas has not revealed any exceptionally low amounts of trace elements. Higher amounts of bark stripping on spruce has been found to occur in spruce stands on the most productive areas. However, bark stripping could not be related to any other particular forest variables investigated thus far. Lastly, analyses of spruce bark as a moose browse have not indicated that such bark has particularly high nutrient contents or contain exeptionally high amounts of any essential minerals. However studies of trace elements and metals in moose organs indicates that moose have low content of certain trace elements, while others have increased.

As the number of animal deaths has increased, so has the interest to discover the origin and spread of the disease, explain the mechanisms underlying the cause, and if possible take measures to reduce or minimize it's spread. Thus, in 1989 a research program was initiated to examine the problem: why were so many dead or dying moose found during a relatively short time interval and to a great extent within the same geographic area? and what was the cause?

A number of factors had been suggested to explain the above phenomenon including environmental changes, lack of browse, abnormal behavior in browsing and different agents in conjunction with the syndrome. The following is a brief summary of the results thus far within the four research areas:

Approximately 200 moose of the 1400 reported cases of the syndrome have been necropsied at the lab. and in the field. Initially, many domestic livestock disesases were checked for, including BVD, herpes virus, and mad cow disease (BSE). All results were negative. A previously unknown retrovirus belonging to the family Retroviridae has been isolated from the sick moose. Additionally antibodies against a pestvirus have also been detected in diseased moose.

Symptoms

Necropsy findings

Rehbinder, C; Gimeno, E; Belak, K; Belak, S; St=E9en, M; Rivera, M; Nikkile, T, 1991: A bovine viral diarrhoea/mucosal disease-like syndrome in moose (Alces alces): investigations on the central nervous system. Sten, M., R. Diaz, and W.E.Faber. 1993. An erosive/ulcerative alimentary disease of undetermined etiology in Swedish moose (Alces alces L.). Rangifer 13(3): 149-156. Merza, M; Larsson, E; Sten, M and Morein, B, 1994: Association of a Retrovirus with a Wasting Condition in the Swedish Moose. Question 1: what test was conducted for BSE? Some variants of this are not going to exhibit spongiform vacuoles. I would be more comfortable with fluorescent antibody raised to avidin-complexed biotinylated bovine or ovine prion peptide. Was this done?

Answer 1. The peroxidas-antiperoxidase technique was applied to nervous tissue sections for the immunodetection of the glial fibrillary acidic protein. (ref; Rehbinder et al. 1991. A bovine viral diarrhoea etc. Vet. rec. 129, 552-554). Today we do not consider this disease/syndrome to have anything to do with BSE.

Question 2: a recent letter in Lancet asserted that hay mites might transmit BSE horizontally. Do the moose share pasture with sheep or cows? Has there been scrapie and BSE in this part of Sweden?

Answer 2: Scrapie is very rare here in Sweden, as far as we know. It is not reported from this region. Moose are browsers and are more bound to the forests and are seldom seen in the fields.



SCRAPIE and CHRONIC WASTING DISEASE in REINDEER

Europe's largest wild reindeer herd occupies a large (>8000 km2) mountain plateau in central Norway. Much of the area is also grazed by sheep in the summer. Recently, several cases of scrapie have been reported among herds which may have come in contact with reindeer on the summer range. Upon positive diagnosis, infected herds are no longer permitted to be released onto the range. However, due to scrapie's long incubation period, it is impossible to know just how many sheep/herds are infected before symptoms become apparent.

Concern has been raised as to whether scrapie-infected sheep may pose a threat to the reindeer herd. Chronic wasting disease (CWD) in cervids is a prion-disease, as is scrapie (see Prusiner 1995), and since trans-specific infection of prion diseases is, at least in the laboratory, possible, I have asked whether there appears to be any connection between CWD in cervids and scrapie in sheep; i.e. can cervids contract CWD from scrapie-infected sheep in an open range situation?


Date: Wed, 10 Apr 1996 15:37
From: Tom Warren, Biol. Inst., U of Oslo
Subject: Re: Scrapie/reindeer investigation

We have been investigating problems related to sheep grazing on alpine ranges which are used by wild reindeer. So far, the main problem seems to be between sheep owners and reindeer hunters, rather than between the animals themselves. It is important to mention that sheep/livestock grazing is in no way new in the area and summer grazing is abundant; winter habitat is the bottleneck for the reindeer.

Private and public concern over the possible negative effects of sheep and sheep grazing on wild reindeer is not new; there has been competition for access to grazing resources/hunting for years. Since it is difficult on this particular range to argue that sheep "out-graze" reindeer, other possibilities such as disease/parasite transmission (from sheep to reindeer) have been advanced. When reports of scrapie among flocks of sheep which graze sympatrically with reindeer surfaced in 1994, concern for the reindeer was again voiced.

Last year, after a short review of existing literature, we concluded that there "seemed to be" a sufficient species barrier between sheep and reindeer, such that contraction of chronic wasting disease by the latter was unlikely. Inter-species transmission of prion diseases is apparently possible only through ingestion of infected tissue, especially brain/nerve tissue, which would not (likely) occur on the open range. This seems to be the concenses among reseachers working on CWD in the US. There is apparently no corelation between the occurence of CWD and sheep grazing. (Based on work in Colorado and Wyoming)

We found scrapie and the other prion disease so interesting that we wrote a popular account/description of scrapie and prions for the Norwegian Sheep and Goat Association's magazine. This article, written in Norwegian, appeared in February before the latest events in England. Since then, we have been inundated, locally, by requests for more information.

We still maintain that in an open range situation the chances of reindeer contracting CWD due to scrapie-infected sheep are, at best, remote. (Once scrapie is diagnosed, the flock is destroyed and no longer grazes on the open range. Uncertainty arises due to the long incubation times associated with prion diseases.) Our interest was, and remains, in the range management/ecolgy aspects of livestock/reindeer interactions; we are neither pathologists or veterinarians. We are currently following the debate here in Europe on BSE/CJD with great interest, however. Various theories circulate from week to week. Of greatest interest to us (and many others) is the question of the species barrier, and its role/function in extensive grazing situations.

To clarify the situation here in Norway: Since 1994, the number of flocks with (confirmed) scrapie have increased from 0 to a total 12, at last count. All flocks are located in the SW part of the country, and are primarily of 1 breed. The source is likely (an) illegally imported animal(s) from Britain. A few of these infected flocks, and probably other flocks not yet diagnosed or confirmed, graze (very extensively) on summer range that is also used by wild reindeer. Contact between sheep and reindeer on the range is "casual". The range is vast, though flocks of sheep and of reindeer may frequent the same grazing areas during the summer; closest contact likely occurs around saltlicks.

We have no known cases of CWD among the wild reindeer. What possible dangers to reindeer may scrapie-infected sheep represent in the extensive summer grazing situation we have in Norway? I might add that upon confirmation of scrapie, the flock is destroyed, and other flocks which have had direct contact with that which is destroyed are quarantined?

The information I have received so far (new info. welcomed) has indicated possible dangers associated with situations in which animals, either sheep, deer or both, have in some way be confined and/or have grazed in or been fed from areas where infected sheep have been held.

My question remains: Are wild reindeer at risk in areas where they share an extensive open range with scrapie-infected sheep? The pathology, genetics and epidemiology of scrapie and the other prion diseases are fascinating, though our concern is more from a range management/conservation standpoint.


ListServe Response:

Thanks for a helpful note on recent history of scrapie and grazing practises in Norway. I would say get rid of the saltblocks immediately as a precaution. CWD is showing up mainly in captive animal / animals confined on sheep range situations. Of course, it could easily pass unnoticed in wild populations. The zoos are getting it too in elands, oryx, kudu, etc., from something they ate, I would guess.

We _do_ have it now in populations of wild deer and elk. I have no information as to whether captive animals were ever released into this area. You can be sure that all of northern Colorado and southern Wyoming are sheep and cattle range.

For me, it sounds like a replay of brucellosis. The disease is brought to wild animals by domestic livestock, gets established, and later there is a big hue and cry to exterminate the wildlife as a subsidy to an economically bogus livestock industry. Native subsistence people who depend on the wildlife get screwed as usual. It makes more sense to exterminate the livestock [which are an economic frivolity for oil-rich Norway or US], or at least keep them out of the wildlands. Is it worth taking the chance that your wild reindeer will get the disease? Do Laplanders tradiltionally eat brain and spinal tissue from reindeer? Have you seen the note from Joel Stone before? It seems to conflict with a Norwegian claim about a US consensus -- the informal consensus seems the other way around even. Note CWD cannot reasonably be 'familial' or 'sporadic' in these captive herds because prion alleles are lethal autosomal dominants of rare frequency, and the herds in Colorado and Canada were tiny.

Also, a new letter to Lancet says hay mites may be capable of transmitting the disease horizontally. It has not helped here with scrapie in Oregon or England to eradicate a sheep flock and then wait a couple of years before reintroduction. The agent has been shown to survive in soil for 2-3 years by Gujdushek.

I predict if you sequence the open reading frame from your sick reindeer, that the animals will all be homozygous wild type in their prion gene. And yet, fluorescent antibody to prion plaque will be positive.

I further predict that although this is cheap and easy to do [$5,000 by outside contract?], the Norwegian gov't will have no interest whatsoever in funding this study, despite many millions for reindeer studies.

The situation in Norway is just like the US or Britain -- whenever there is a conflict between public land ranchers and wildlife or public health, the government errs [or lies] on the side of the economic interest. We have a flat-out cover-up going on over here on CWD, BSE, and CJD as far as I can see.



More Listserve Opinion: ... 5.4.96
While we can't say with certainty that the chronic wasting disease is passed on to humans from elk velvet, it does seem to be transmitted through contaminated blood and milk, the disease agent is extremely stable to heat and drying, and so no one in their right mind would eat it, since material cannot be tested for the presence of infectious prion protein. The disease first showed up in North America in a captive deer herd in Colorado in 1967. The elk in Canada came from South Dakota in 1989.

I am of the opinion that "chronic wasting disease" is not an indigenous ungulate disease at all [like NPS concluded with bison and brucellosis], but simply scrapie or mad cow disease, passed on through hay mites on public lands grazed by sheep or cattle, or via rendered downer cow protein supplements.

Pre-senile dementia is an uncomfortable issue for hunters, who tend to think of themselves as rugged, independent, and self-reliant. I am not familiar with cultural attitudes towards dementia in Asia. That interview with a living victim is appalling -- the 30 year old teacher in England with diagnosed bovine-CJD.



SCIENTIFIC ABSTRACTS


* Guiroy, D. C.; Williams, E. S.; Yanagihara, R.; Gajdusek, D. C. Topographic distribution of scrapie amyloid-immunoreactive plaques in chronic wasting disease in captive mule deer (Odocoileus hemionus hemionus). Acta Neuropathologica 1991 81 5 475-478

Chronic wasting disease (CWD), a progressive neurological disorder of captive mule deer, black-tailed deer, hybrids of mule deer and white-tailed deer and Rocky Mountain elk, is characterized by widespread spongiform change of the neuropil, intracytoplasmic vacuolation in neuronal perikarya and astrocytic hypertrophy and hyperplasia. The topographic distribution of amyloid plaques reactive to antibodies prepared against scrapie amyloid in CWD-affected captive mule deer is described. Scrapie amyloid-immunoreactive plaques were found in the cerebral gray and white matter, in deep subcortical nuclei, in isolation or in clusters in areas of vacuolation, and perivascularly, in subpial and subependymal regions. In the cerebellum, immunoreactive amyloid plaques were observed in the molecular, pyramidal and granular layers. Scrapie amyloid-immunoreactive deposits were also seen in neuronal perikarya. Furthermore, amyloid plaques in CWD-affected captive mule deer were alcianophilic at 0.3 M magnesium chloride indicating the presence of weakly to moderately sulphated glycosaminoglycans. These results confirm that CWD in captive mule deer belongs to the subacute virus spongiform encephalopathies.


* Williams, E. S.; Young, S. Neuropathology of chronic wasting disease of mule deer (Odocoileus hemionus) and elk (Cervus elaphus nelsoni). Veterinary Pathology 1993 30 1 36-45 USA\Wyoming

The pathology of the central nervous system of 9 mule deer and 6 elk with chronic wasting disease, a spongiform encephalopathy of mule deer and elk, was studied by light microscopy. Lesions were similar in both species and were characterized by spongiform transformation of gray matter, intracytoplasmic vacuolation of neurons, neuronal degeneration and loss, astrocytic hypertrophy and hyperplasia, occurrence of amyloid plaques, and absence of inflammatory response. Distribution and severity of lesions were evaluated at 57 locations; there were only minor differences between deer and elk. Consistent, severe lesions occurred in olfactory tubercule and cortex, hypothalamus, and the parasympathetic vagal nucleus of deer, and sections examined from these regions would be sufficient to establish a diagnosis of chronic wasting disease. Lesions were milder in these locations in elk but were sufficiently apparent to be diagnostic. Other differences included increased severity of lesions in some thalamic nuclei in elk in contrast to deer, the occurrence of amyloid plaques detected by haematoxylin and eosin and histochemical stains in deer in contrast to elk, and the presence of milk white matter lesions in elk but not in deer. Lesions of chronic wasting disease were qualitatively comparable to those of scrapie, bovine spongiform encephalopathy, transmissible mink encephalopathy, and the human spongiform encephalopathies. Topographical distribution and lesion severity of chronic wasting disease were most similar to those of scrapie and bovine spongiform encephalopathy. Duration of clinical disease did not affect lesion distribution or severity in either species.


* Guiroy, D. C.; Williams, E. S.; Liberski, P. P.; Wakayama, I.; Gajdusek, D. C. Ultrastructural neuropathology of chronic wasting disease in captive mule deer. Acta Neuropathologica 1993 85 4 437-444 USA

Chronic wasting disease (CWD), a progressive uniformly fatal neurological disorder, is characterized neuropathologically by intraneuronal vacuolation, spongiform change of the neuropil and astrocytic hyperplasia and hypertrophy. Ultrastructural neuropathological findings consist of extensive vacuolation in neuronal processes, within myelin sheaths, formed by splitting at the major dense lines or within axons; dystrophic neurites (dendrites, axonal preterminals and myelinated axons containing degenerating mitochondria and pleomorphic, electron-dense inclusion bodies); prominent astrocytic gliosis; amyloid plaques; and giant neuronal autophagic vacuoles. Other findings include activated macrophages and occasional spheroidal structures containing densely packed fibrillar material of unknown origin, abundant structures suggestive of degenerating microtubules entrapped in filamentous masses, vacuoles and myelin figures. Similar findings have been previously observed in scrapie-infected hamsters and Creutzfeldt-Jakob disease (CJD)-infected mice, bovine spongiform encephalopathy, and CJD indicating that CWD in captive mule deer (Odocoileus hemionus hemionus) belongs to the subacute spongiform encephalopathies (transmissible brain amyloidoses)


* Guiroy, D. C.; Williams, E. S.; Song, K. J.; Yanagihara, R.; Gajdusek, D. C. Fibrils in brains of Rocky Mountain elk with chronic wasting disease contain scrapie amyloid. Acta Neuropathologica 1993 86 1 77-80 USA

Recently, scrapie amyloid-immunoreactive plaques have been detected in brain tissues of chronic wasting disease (CWD) affected captive mule deer. Rocky Mountain elk and hybrids of captive mule deer and white-tailed deer. Abnormal fibrils were isolated from brain tissues of Rocky Mountain elk using negative-stain electron microscopy. These fibrils resemble those found in scrapie-infected hamster brain. Protein bands with relative molecular masses of 26 to 30 kilodaltons were shown to be immunoreactive to antibodies raised against scrapie amyloid by Western immunoblotting. Immuno-dot blot showed similar reactivity. These results support the clinical and pathological diagnosis of the disease and provide further evidence that CWD belongs to the subacute spongiform encephalopathies.