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From: TSS ()
Subject: CWD INFECTED DEER no problem, throw a party and feed it to the guests MDs 'ongoing case study'
Date: October 22, 2007 at 1:15 pm PST

Completely Edited Version


CWD INFECTED DEER no problem, throw a party and feed it to the guests MDs 'ongoing case study'

page 22 - 36. ...tss


Dr. Terry Spraker: Max asked me to give an overview of CWD and then talk about the research being done at CSU. CWD was first noticed in the Colorado Division of Wildlife pens in Ft. Collins. CWD in the literature was first said to be seen in captive deer pens in 1967. I remember being there and those deer pens weren't even built until 1968, so the early history of CWD is confusing, but CWD was at least seen in the very early 1970’s as far as I can remember.

Beth Williams verified that is was truly a spongiform encephalopathy in the deer. She and Stuart Young described CWD in deer and elk in Colorado and Wyoming. George Bear A big Game Biologist for the Colorado Division of Wildlife found a sick elk in Rocky Mountain National Park in 1981 and I posted it for him and it turned out to be a case of CWD. At that time, there was lots of interchange from the Colorado Division of Wildlife with the animals from Rocky Mountain National Park. They took animals from the deer facilities and released them into the park to study food habits, and brought the deer and elk back.

We found the first case in mule deer in 1984 about half a mile west of the Colorado Division of Wildlife deer pens. In 1985, we found the first case in white-tail deer in Loveland, about 30 miles south of Ft. Collins. There has in the past been a question whether CWD started in the CDOW deer pens or came from the wild. The man who built the deer pens in 1968 did put deer and sheep together. These animals were placed on starvation trials. He obtained the sheep from CSU. This is where this theory has come about that one biologist started CWD in the Colorado Division of Wildlife deer pens. He still has sheep today from the original group, and he's never had a case of scrapie. There is no real evidence that this was the start of CWD.

The other part of the history of CWD was when it was first found in captive elk in 1996. The man who had CWD in Canada has gotten elk from a place in South Dakota that had CWD for probably 10 years, but it was not diagnosed. The year after it was diagnosed in Canada, it was diagnosed on his farm in South Dakota. He claims he received deer from Colorado. So there is a fairly good link from deer and elk originally from Colorado and spreading northward.
The natural host for CWD is only three cervids: mule deer, elk and white-tail deer. Recently, CWD has been found everywhere north of Interstate 70 in Colorado. Now a case has been found south of I-70 and one in central Utah. We just looked at several deer from Mexico and those were negative. CWD has been found in wild populations in Wyoming, Nebraska, Wisconsin, Utah, South Dakota, New Mexico, and Illinois.

Dr. Thornsberry: I have a classmate who deals with the Wisconsin Department of Natural Resources, and he's done a lot of work with them on CWD. How did we get this hot pocket of CWD in Wisconsin? Did they trace that to somebody introducing it, or did it just show up?

Dr. Spraker: No one knows. People bring carcasses back to their homes. I've had calls from so many states and people want to know what to do with the carcass. One guy in Maine called me after he'd already thrown the carcass away. One person has taken six cases of CWD to British Columbia. The last couple he said he fed to the crabs—threw them in the ocean. There is a lot of movement of animals and lots of movement of animal parts. There was a big trade of Wisconsin deer that somehow went to Missouri and then were released in Texas.

Dr. Spraker: The captive herds are primarily in the same areas where there's lots of CWD in the wild. I'm sure there's some evidence that it goes both ways. What are some of the epidemiological observations? There is evidence of transmission of the disease in captive animals to wild and vice versa. In the wild, there's natural expansion.
Clinical signs include emaciation. These clinical signs are not manifested until the terminal aspects of the disease, so an animal might have the disease for two or three years without showing clinical signs. You'll see emaciation and occasionally you'll see hair loss. There are similarities to Scrapie, although you don’t get the weight loss with Scrapie.
The clinical signs are obvious only in the terminal stages. They are depressed and you'll find them lying down. If you approach them, they do not get up.

Dr. Thornsberry: Is the chronic weight loss due to lack of neural functions of the muscles, or is it due to being mentally affected and they just don’t eat?

Dr. Spraker: I don’t know. The rumens are always full, so they are eating right up to the end. Because of the olfactory system that's heavily hit in these animals, I think that, at least in the wild, they lose their sense of smell. Deer are very dependent on smell for which forages to eat. Prion is present in the retina, so their eyes are affected also.

Dr. Detwiler: In Ohio, we did see a wasting condition associated with sheep. I don't think anyone's ever done a study, but there also seems to be an association, at least in flocks, with the abomasal emptying disorder.

Dr. Spraker: We have looked at a few cases of this abomasal emptying syndrome in sheep. We check them for prion disease, because it looks like a classical manifestation of an unusual manifestation of scrapie. We've never been able to show anything. We see abomasal ulcers in deer, but never in elk. With captive deer, you see a slowing of the emptying of the rumen and the animals will drink a lot of water. A clinical sign in captive deer is the sloshing of the rumen when the animal would run.
One clinical sign deer will manifest is excessive salivation. We saw this early in animals in Estes Park. We see animals eating out of food bins, salivating into them, and then other deer would come and eat out of that same feeder. One possible transmission is through the saliva. But when you find the prion in the lymphoid tissue of the gut, it could easily go out the feces also. Excessive salivation is a common clinical sign in terminal cases.

This is a gross necropsy of a deer, fairly typical. You'll see there's no fat at all in this animal. This anterior ventral aspect of the apical lobe is pneumonic. This is typical of aspiration pneumonia and you see this in both elk and deer. It's most likely associated with innervation of swallowing. The animals have trouble swallowing and they'll aspirate food into the lung. Actually, one of the first cases of CWD in captive elk in the US was seen in 1995, a year before the cases found in Canada, and these pathologists in South Dakota missed three or four cases of CWD in elk because they saw the pneumonia and stopped there. This went to court. The elk rancher felt it cost him money because the pathologist missed it. The court ruled in favoroft the pathologist because it had not been diagnosed. The bottom line is that CWD has been missed because people have found pneumonia and have stopped the necropsy. When we see pneumonia in deer or elk, the first thing we think of is CWD.

The clinical signs and gross lesions in the elk are identical to the deer and white tail deer. The histological lesions are similar in all of these TSEs, at least in the ruminants where you have the vacuolization of neuropil cytoplasm, vacuolization of gray matter and the neurons, vacuolization within the neurons, and neural degeneration. You see plaques in a lot of these diseases. They’re not as florid as you see in humans. They are areas of accumulation of prion.
In the literature, you see absence of inflammation. I don't believe this anymore because of the proliferation of the glial cells. The early lesions you see with CWD are the vacuolization within the neuropil. The neurons look good and there's no evidence of neuronal degeneration.
The immunohistochemical stain has been helpful with CWD. At first we were using H&E to diagnose CWD and it was very difficult. With the advent of the antibodies made for scrapie, we showed that the CWD agent also stained with the scrapie agent.

Dr. Thornsberry: If it doesn't stimulate an immune response, how do you get an antibody to it?

Dr. Spraker: The antibody is made in a different animal like a mouse or rabbit, but most of these antibodies are made in cell cultures. The animals do make antibodies or the proteins from other hosts.

Dr. Thornsberry: So the statement that there's no immune response to it is not true.

Dr. Spraker: Deer do not make antibody to their own PRP, but if you put in one that's not recognized as self, it will make antibody. There are hundreds of antibodies made to PRP.

Dr. Thornsberry: So you get a hamster immunized against a deer prion. You're developing a hamster antibody to a deer prion. But you can’t develop a deer antibody to a deer prion.

Dr. Spraker: That's right. People take small segments of the prion and make a specific antibody for that amino acid sequence. This antibody is made for a six-amino-acid sequence. It's made in cell cultures. This antibody has worked very well.

Another boon was that, early on, we found lymphoid tissue being positive in deer and elk. This was an important finding. It was confusing at first. People have ingested deer that had positive lymphoid tissue and the brain being negative. At that time the positive lymphoid testing was quested by some agencies and it was considered not a valid test. Hundreds of people have ingested deer that had positive lymphoid tissues.
Katherine O'Rourke developed a third eyelid test in domestic sheep where they stained for the lymphoid tissue in the third eyelid. They can find positive follicles in the third eyelids of sheep and we've shown you can do this with the tonsils of deer. An article by Margaret Wild has shown you can diagnose CWD a couple of years before the animals come down with clinical signs by doing a tonsilar biopsy.

Dr. Detwiler: I think it's important to note the test could be negative or there could be lack of lymphoid tissue in the third eyelid. You see that especially in sheep. As they get older, it atrophies. So a negative is not definitive. But the positive is very significant. We shouldn’t undersell the fact that the third eyelid had added a new tool for us in the field and in the production side as well as the regulatory side so we can detect the disease in a live animal in the pre-clinical stage. We can get into flocks earlier and start to eliminate animals. It's very good for flock-screening and it's helped us identify flocks in an earlier timeframe. It's added diagnostic capability for us.

Dr. Spraker: Yes, that's very important. A negative test doesn't tell you anything, but a positive test tells you a lot.

Dr. Spraker: So far, we've found a couple of false positives with elk, but that's when we were playing with different techniques and not using PK. With the standard tests that have been published and used now, to my knowledge there have been no false positives. If you do not destroy all the PrP-cellular, you're going to get positive staining. These antibodies are made for the PrP-cellular, but part of the testing is that you are supposed to destroy all the PrP-cellular. There are several different ways of destroying the PrP-cellular.

Here's a suggested pathogenesis for CWD in the deer. I think we're just at the tip of the iceberg with pathogenesis. It appears, at least with deer and elk, there could be an ingestion of the prion. The prion does enter the Peyer's patches and some of this was shown by Christina Sirgudsen. I personally think there is an adaptive phase in the lymphoid tissue. It takes awhile to adapt, and then it goes, I think, up the vagal nerve. It enters the vagus nucleus and then there's an adaptation in the brain and then, after it adapts in the brain, it spreads throughout the brain fairly rapidly. Because of high prevalence of stainable PrP in the lymphoid tissue of the small intestines and colon, I wouldn’t be surprised if it does not go out through the feces and through the saliva because of the tonsil being so heavily infected. There is so much lymphoid involvement so close to the outside of the body. At least that's one way the prion may go out of the body.

The Research

I know only a little bit about what's happening with the Department of Wildlife. It's fairly well known that they're doing susceptibility trials with cattle. Beth Williams and Mike Miller are the two primary investigators on this. They have put 10 or 15 cattle in deer pens that have very high infections of CWD. With this, they're studying environmental contamination. I think Mike is putting some dead deer in certain areas and letting them rot and then later they'll put in other deer to see if they can feed in that area and come down with CWD. The problem with this is that we have so much CWD all around Fort Collins, it would be hard to determine the source. They're also doing a project feeding CWD material to mountain lions. This work is being done in Wyoming and Colorado.
At Ames, they've injected 13 cattle with CWD brain tissue. Five have died. The first three had some vague clinical signs. Prion was found in those cattle, but they had very little spongiform change. The author is Ahamir Hamir.

Dr. Lynn Creekmore is doing a project in Ft. Collins. She's with the National Center for Animal Health. She has purchased 20 fallow deer and has put them in one of the pens where there's a degree of CWD. They're being monitored. At the two-year mark, they show no evidence of CWD. It's a five-year study.

At CSU, there are three groups working. Ed Hoover is doing quite a bit of work on some of the pathogenesis. Barb Powers and I are doing some work with CWD and Mo Solomon in the Department of Environmental Health has done investigation into some of these ELISA tests.

Ed Hoover's graduate students showed that that oral transmission of CWD worked, and they found PRP in intestinal and cranial lymph nodes 42 days after ingestion. These were fawns that received five grams of the brain tissue. They've also done some work with dendritic follicular cells and they've shown that the B cells and the dendritic follicular cells play a part with recognition of prion. They’re also looking at normal location of cellular PRPC throughout the whole body of a deer.

They have a group of white-tail deer and they're going to look at transmission of saliva, feces and repeating the brain experiments, specifically seeing if saliva and feces and be used for transmission of CWD. They're using mule deer material going into white tail deer. I don't know how much of a species jump that's going to be. For all practical purposes, it doesn't look like there should be. Katherine O'Rourke has shown there's quite a bit of difference in the genetics of the PrP gene within white-tail deer and within mule deer.

Barb Powers is working with the Bio-Rad ELISA test. They did a tremendous amount of work last year in validating this test for elk and mule deer in Colorado. It was a political nightmare. Mo Solomon actually started it, doing comparison of Bio-Rad and Prionics. They took the tests that were used for BSE and tried to modify them to work with CWD. The people who produced Prionics and Bio-Rad sent their primary scientists to try to make the tests work. Bio-Rad was the better test of the two, so it was chosen for the extensive surveillance that happened last year that resulted in the validation of this test for CWD in the US for white tail, mule deer and elk. But it's only in the lymphoid tissue.

Dr. Detwiler: Since then, there have been two additional tests.

Dr. Spraker: The tests now are Idexx, validated for white tail deer, and VMRD, validated for white tail and mule deer. It's still only lymphoid tissue.
We found some of the first early cases and we showed that the captive animals and the wild animals had the same disease. That was a big question at first. We found you could not tell the difference between captive and wild mule deer when you looked at the lesions in the brain and at the patterns of lymphoid staining throughout the body.

We developed the IHC test with Katherine O'Rourke that's currently used throughout the US and Canada, and we mapped the prion in mule deer. These were all hunter-killed animals so the time of exposure for CWD was not determined. But we saw definite patterns of prion distribution. We had only the heads. When you do staining only in the tonsil and when you do serial sections of the brain, there's no evidence of prion in the brain.

Then we had an animal with a positive tonsil and a group that had prion only in the vagas nucleus. Then it would spread to the solitarius. What was odd was that the next area where the prion appeared was the hypothalamic region. We're starting to do this same mapping now in elk and the picture looks the same so far. The thing to notice here is that the cerebellum is not affected until the very end. I don't know how it is in sheep, but this is a characteristic we've seen in the deer.
When you're doing any kind of surveillance, if you used brain tissue, you have to get this vagas nucleus. If you don’t, you can miss a lot of the early cases.
We had a chance to work with the state and federal people when they were trying to eliminate CWD from the US and Canada. Between the US and Canada, 12,000 to 14,000 ranch elk were killed. We looked at a lot of the animals. We wanted to look for patterns and also compare the stainability of the lymphoid tissue, because in deer, it seems consistent that the lymphoid tissue was affected with the brain and you would have early cases where you'd have lymphoid staining and no brain staining. In mule deer, we found one case where there was staining in the brain and not staining in the lymph nodes. I think they've also found that in sheep, and we've found a little more of that in elk.

For all this testing we've used IHC. Two different machines are used —the Nexus and the Benchmark. We've used the antibody produced by Katherine O'Rourke. I know this antibody is being produced by VMRD and it's sold, but we have not had very good luck with this commercial antibody.
These are some of the different stages in the elk. We're starting the map the whole brain, so you may be able to look at one section to obex and predict where the prion is in the rest of the brain. A grade one is a negative animal and a grade two is an animal that had negative staining in the brain but positive lymphoid tissue. Grade three is where you may or may not have lymphoid staining, but you have what we call a one-plus staining in the obex. The first area you see affected is the lateral aspect of the middle third of the vagas. In cattle, one of the first areas to be affected is the solitarius nucleus. Another very important difference between BSE and CWD is that we would miss probably 30 to 40% of the cases if we did not use IHC. From what I'm told, with BSE, the immunostaining is not as good in cattle as it is in deer and elk. You can do very well with good H&E sections.

With elk, you see very little intra-nuclear staining, whereas with cattle, you see much more intra-nuclear staining of the prion.
A grade four means that the vagas nucleus is mostly affected. A brain plus three means it's filling the nucleus and the solitarius and it's beginning to spill out into some of the other nuclei. At this stage, the rest of the brain will begin to have prion in it.

We've found that the redex is the vagas is affected later than the nucleus, so the prion accumulates in the nucleus before you can see it in the redex of the vagas. The redex of the vagas is the conduit of nerves coming in and out.

With this grading of elk, we have a variance of CWD staining in the lymphoid tissue. It's not as neat as it is in deer. Even in the more terminal stages, we found a couple of elk that did not have staining. Some of this may be due to not cutting enough lymphoid tissue, but we've really looked at some of these animals and we have not been able to verify immunostaining in these lymphoid tissues. It's not as clean as it is in white tail deer.

We're trying to map the rest of the elk brain and do the same thing with white tail deer, and them compare them to what a single section of the obex would be. Also, we have a project looking at some of the micronutrients —copper, manganese, molybdenum, selenium and zinc—and seeing if that correlates with CWD. We're also looking at lymphoid tissue in really early cases of CWD.

Fear Factor

Another problem that has come up because of the rampant fear factor in the US and in Europe is disposal of carcasses, tissues, and reagents that have come in contact with TSE. In some places, you can't even think about using landfills to dispose of carcasses if they have CWD or Scrapie. At CSU, we have a sodium hydroxide digester that brings the temperature up to 300˚F with 60 pounds of pressure, and you cook this material for six to right hours. This digester cost about a half a million dollars and we've sunk more money into it. Disposal is a big problem. Some communities have hampered the building of incineration facilities with the claim you can get CWD by breathing the air. These thoughts are being propagated and causing us a tremendous amount of trouble.

Dr. Detwiler: Even when you do non, do you still get an odor from the digester?

Dr. Spraker: Yes, especially when you dump it. If you put it into the sewer, it's okay. But our city charges for BOD (biologic oxygen demand). So it costs us $3000 to $4000 a month to dump it in the sewer, and they just came up with a half a million dollar surcharge for having the privilege to dump it. We can't afford it, so we've tried to make a dehydrator. The fragrance of the high ammonia escapes.

The rendering companies in Ft. Collins are going out of business. We were forced to go somewhere and incineration was very difficult, so we went to this system.

Dr. Bartz: Is the operating cost high?

Dr. Spraker: No, it's really not. But you have to take into account all the other problems.

This is the big question. This is the hypocrisy of this disease. We've had to reconvert all these buildings to make them where all the water goes into the digester because we couldn’t let it go down the sewer any more.

Dr. Detwiler: Was this EPA's idea?

Dr. Spraker: That's where it first started, yes.

Dr. Bartz: The digester is just for CWD-infected tissue?

Dr. Spraker: It's for TSE, Scrapie and CWD.

Dr. Bartz: What about rodents?

Dr. Spraker: If it's a TSE, it has to go in here, yes. This is the only way we dispose of animals now, but it's mandatory if it's a TSE—even gloves.
This is data we have to date. People ask Can humans get CWD? You never say never, but this is what we've seen so far: humans have been heavily exposed by handling and consuming CWD-positive deer and elk for the minimum of 35 years. I don't even want to think about how many deer we consumed from the deer pens when I was a graduate student.

This is very important: Prusiner says it and others have, too—that CWD can go to human and there's just not been enough exposure yet. This is my opinion: in Britain, when a cow had BSE it was ground up and diluted and spread. When a hunter kills a deer or elk with CWD, the immediate family eats the deer. They're exposed for a year. Most people take a year and a half to eat an elk. So if CWD is going to go to people, those people would have a high exposure rather than a diluted exposure. Exposure to brain is there, as some of these people do brain tanning. To date, there have been no unusual neuro-degenerative diseases found in people, and they have looked.

The fear factor is unreal. I had a man come to the office in a panic, and he was sincere. He said he'd gotten some drops of blood on his pickup from a deer that came from the CWD area. He thought the back of his pickup was contaminated. He asked if he should sell his pickup

Another man came in with a deer to dispose of it, and he knew it was positive, but when he looked at it, he decided to take it home.

I had a case where a hunter had shot an elk or deer and Game and Fish called and got his wife and told her the deer had CWD. The next day they had a party and fed the deer to their guests. A nasty divorce was going on, and after the party, the wife told her husband about the CWD. This was a group of MDs. As of now, all of them are fine.

Dr. Detwiler: If someone calls you and says he has a known positive animal and wants to know if he should eat it or not, what would you tell him?

Dr. Spraker: I'd tell him "no." I've thrown away a deer and an elk and I hated to do it, but I would not knowingly eat it. I'm not afraid to go and hunt in that area and test, but the test will miss early cases.

Dr. Bartz: Do you have an estimate of the numbers of people you think have been exposed?

Dr. Spraker: No, but I can tell you this year they found 200 positive deer and elk. On a smaller scale, just in Colorado, we’d average 100 to 125 positive cases of CWD. But no testing was done in these other states. A lot of people have eaten these deer for a long time, and they have gone throughout the United States. There have been claimed cases of hunters having CWD, but they were all other conditions.

Dr. Keller: The cause of death is not always known when people die of neuro-degenerative disease.

Dr. Spraker: Yes, but right now they are really paying close attention to that.

Dr. Detwiler: After being hammered by the public health community that we don’t test nearly enough cattle, they still ask how many full brains really get done. The human community does not do a systematic look at brains of neuro-degenerative diseases.

Dr. Keller: Animal health agencies are being encouraged to determine prevalence of CWD in cervid populations.

Dr. Spraker: But if we had this much CWD in this small of an area and this many people consumed it, I think they would have picked up something. Something would have spiked up. So far there's been no unusual incidence of any kind of clinical neuro-degenerative condition.

Dr. Thornsberry: Dr. Bartz, hearing that from Dr. Spraker, what is an explanation? You've probably done the studies to show that these prions are in the muscle tissue as well.

Dr. Bartz: Prions or PrPSc have been detected in muscle homogenates from prion-infected mink (Marsh et al., 1969), hamsters (Bartz et al., 2002, Thormzig et al., 2003) and humans (Glatzel et al., 2003). Additionally, immunohistochemical data has shown PrPSc to be associated with myocytes in humans with CJD (Kovacs et al., 2004) and in prion-infected hamsters (Mulcahy et al. from the lab of Dr. Richard Bessen, Journal of Virology in Press). It is still unclear if prions replicate in muscle cells, but the presences of PrPSc in muscle cells suggests that prion infectivity and PrPSc that is detected in muscle homogenates is not entirely from innervation of the muscle tissue.

Dr. Thornsberry: What would be an explanation to having that kind of exposure to prions and not developing into a Scrapie-type prion that we call disease?

Dr. Spraker: I don’t know, but I know people have consumed it.

Dr. Thornsberry: Fox news reported on a military man stationed in the Middle East who consumed the traditional breakfast in those Moslem countries—sheep brains scrambled with eggs. He's not be diagnosed with Creutzfeldt-Jakob type disease. They're trying to get military pay for him because of hazard of duty. They think he picked this prion up from Scrapie-infected sheep or goats, not cattle. Yet we know that the ability of that to go to humans is supposed to be minimal. Why are there not outbreaks all through the Middle East of Creutzfeldt-Jakob disease?

Dr. Spraker: We ship a lot of sheep brains over there. It's a complex situation. I think CWD is a unique spongiform encephalopathy. Whether it came from sheep or a spontaneous mutation, I don’t know. At the time, there's no evidence it can be naturally transmitted to any of these animals. If CWD is found to be naturally transmitted to cattle or sheep, there's going to be a lot of change.

Dr. Thornsberry: We do know you can give an intra-cranial injection of this prion and cause lesions? They've documented that. But what about intense natural exposure like the eating of elk placenta or the licking of an elk carcass?

Dr. Spraker: When you have captive animals, you see a lot higher incidence of CWD than in any wild population. A man in Nebraska fenced in some white tail deer, and they ended up killing them and 52% had CWD. When you concentrate them, whatever way they transmit it, you're going to have a lot higher incidence. This is one of the reasons they're killing so many deer, thinking they're going to reduce the number of animals and thus reduce the incidence of the disease. They'll never take it away.

Dr. Thornsberry: Is there a high prevalence of prions in placental tissues?

Dr. Spraker: We've had several elk and several deer that died of terminal CWD that were pregnant. We've not been able to demonstrate PRP in the placenta or any of the fetal tissues with IHC or with Bio-Rad. We can demonstrate IHC in the placentones of domestic sheep. A man out of Katherine O'Rourke's lab has a nice article on demonstrating PRP in the placenta, and Race has an article about finding PRP in the placenta and showing how the PRP of the placenta has different glycoforms than the PRP of the brain. In sheep, they've definitely shown that. For a long time, they said that Scrapies transmitted from the ewe to the lamb during lambing, but it does not go trans-placentally. But this does not seem to occur in elk and deer.

Dr. Detwiler: the important thing with sheep is not only PRP, but they've actually correlated the PRP detection of infectivity with detection of PRPSC, which added on to Patterson's work back in the sixties. In sheep they actually fed placenta to goats and caused the disease by oral ingestion of the placenta from Scrapie-infected animals.

Dr. Spraker: I'm trying to get some money to do that with deer because I have some sheep placentas.

Dr. Thornsberry: So to summarize, you do not believe, in the data you've examined and your experience in pathology, that there is much risk of transfer of CWD from a cervid to a bovine.

Dr. Spraker: There's been no evidence, but I haven't done any of that work.

Dr. Thornsberry: They're saying,”Is the prion going to be there forever?”

Dr. Spraker: That's the concern that some people are voicing about this. It's been a hot topic.

Dr. Spraker: There's been a project started by Jim Voss and Dan Guald. They talked a group of ranchers living within the enzootic area for CWD into turning in all the heads of their cull cows. The cattle came from enzootic areas for CWD. They had about 270 culled cows that had been in contact with deer from six to 12 years. They did histopath and IHC on these cattle and all were negative for any evidence of a TSE.

Dr. Thornsberry: With that knowledge, where in the world are these BSE cases coming from? Is this spontaneous generation theory going to hold up? If that's possible, then you should be able to get BSE anywhere in the world.

Dr. Spraker: They say that 85% of the CJD cases fall into the sporadic category. That means they cannot find any evidence of a source of the disease. Agussi is beginning to think that sporadic CJD is from sheep, but he doesn't have evidence. If that's the case, why don’t Australia and New Zealand have sporadic CJD? As far as I understand, with the sporadic cases, there's a deterioration or a degeneration of the prion that weakens some of the links and it turns or it changes its configuration.

Dr. Thornsberry: We were shown data that brain tissue heated to 600˚C was still infectious.

Dr. Spraker: To me it's easier to think maybe it's associated with a metal and it comes alongside and causes the normal prion to change.

Dr. Thornsberry: We've established pretty well that CWD probably is not infecting cattle. It's probably not infecting humans. But we have established that it's very infective with deer and elk, and it’s a problem. Whatever transmission is taking place, it is infective. It is a dangerously infective prion within the species that it's established in. And yet we keep hearing this information, as veterinarians, that BSE is not infective. It's a terminal disease. The animal gets it and dies. We know that's not the case with many of these prion diseases.

Dr. Spraker: You also hear that CWD is always fatal. I don’t believe that. I see too many cases of animals that are big and fat and healthy-looking, killed by a hunter, and they have so much prion in the brain it's unbelievable. Even in later cases, there are a lot of them that do not show clinical signs. The degree of spongiform degeneration is not nearly as high in some animals as in others. We're slowing pushing in that direction to see what the difference is.

Dr. Bartz: One of the hallmarks of inter-species transmission, at least in rodents, is that the spongiform degeneration is way out of proportion in the first transmission to what you see in subsequent transmission. If you just look at brain sections, you can always pick out the animal that's the first passage because the spongiform lesions are so much more intense.

Dr. Spraker: And the amount of accumulated prion is less, right?

Dr. Bartz: It can be less. That hasn't been looked at thoroughly enough.

Dr. Spraker: We see animals that have had this disease for three years and we see hardly any spongiform change, but yet you see lots of accumulation of PRP. But when they tell you that every animal that gets CWD dies, how do you prove that?

Dr. Thornsberry: If that animal doesn’t die and he's a plus three or plus four, he's shedding prions all over creation. So you have an infectious disease with an infectious agent in the environment.

Dr. Spraker: The state vets don't like to hear that. No one can prove it. But just with casual observation over the years, I don't believe that statement anymore. It might take a lifetime to prove it, but I think that not even thinking about it is more dangerous than trying it and not being able to prove it. That might help to explain all these mysterious crop-ups of CWD. If it does come from sheep, that would help, but it's not a simple thing. There are two or three cogs that have to go and prions are just one of them. You can make it work with one in the lab, but natural, it's going to take two or three.

Dr. Keller: Do you remember what the requirements are in Canada after finding a positive case of CWD on a cervid premises? I believe they do not let ruminants back into the same facility for three years or five years?

Dr. Spraker: It varies, but I think it’s around five. South Dakota is five.

Dr. Detwiler: They're changing again. They just recently discussed it.



Completely Edited Version

Accomplished this day, Wednesday, December 11, 2003, Denver, Colorado

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