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Wisconsin's CWD effort
Last Post 25 Oct 2007 12:02 AM by flounder. 12 Replies.
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2Chucks
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20 Aug 2007 03:54 AM  
I am one of 15 people who sit on Wisconsin's newly formed CWD Stakeholders Advisory Group. Following are some of my notes from the first two meetings.

I thought the first meeting went well. I came away with a positive feeling. There were 15 men at the table. Some were at large members and others were there representing various orgs. and concerns. Secretary Hassett was supposed to be attendance but felt his resent resignation would be a disruption so Tom Hauge read a statement on Scott's behalf.

The talks were pleasant and professional. Next month we will be given a presentation by DNR scientists that will be recorded for all to see when it is placed on the DNR website made for this advisory group. On that page you will be able to see the faces, names, bio's and contact information for each member. We reviewed a press release that will put out shortly. This meeting and the August meeting will lay the foundation for the next 5 meeting in which we will formulate recommendations for the DNR.

This is our goal or task question.

How should WI manage CWD to minimize the impact of the Disease on Wisconsin's free ranging deer population, the habitats and biological systems that include deer, the economy, hunter, land owners and others that benifit from a healthy deer herd?

Once the site is up and running, I will post the link. This is an open forum and the public is welcomed to attend and at some point we will find a time for public comments. This meeting saw 1 or 2 members of the public and a reporter from the Cap Times so you will be able to read his views on what happened today. We were there for 7 hours and there was not a dull moment in the whole day. I learned a lot and it would take a great deal of typing to share that. The following two pages were given to us and since everything we do is public knowledge, I will share them.



2Chucks
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20 Aug 2007 03:55 AM  
The DNR has updated it's CWD website to include the Bio's for each board member and it added the CWD handbook we were all given. It also added the meeting minutes from the first and the agenda for the 2nd meeting. you can read it all at

http://dnr.wi.gov/org/land/wildlife...alogue.htm

Below is the piece I wrote for the Wisconsin Bowhunters web site that covers a little about the group and the first meeting.

On Saturday July 21st, the first of 7 planned monthly meetings of the DNR formed "Stakeholder Advisory Group" (SAG) was held at the DNR service Center, Fish Hatchery Road, Fitchburg, WI to discuss the issue of CWD in the state. The goal of this process is to engage a diverse group of people in a dialog to guide the Department in future management of the disease. The group’s charter or mission question was stated as such:

"How should WI manage CWD to minimize the impact of the disease on Wisconsin’s free ranging deer population, the habitats and biological systems that include deer, the economy, hunters, landowners and others that benefit from a healthy deer herd?"

My name is Ron Kulas and I am one of 15 members of the "SAG" I am a WBH member from Delafield. I was contacted by Todd Zeuske and asked to attend these meetings for the WBH and to share with you what this group is doing. This group is made up of two member types, both of which are impacted by CWD. Those groups are

1. Partner organizations with a stake in CWD management. (Representative member)

2. Citizens with an interest in CWD and herd management (At large member)

The partner organizations that were present were:

Business interests (sporting goods) Mills Fleet Farm

Conservation Congress

Farmed Cervid Industry (deer/elk farmers)

Food Pantries

WI Assoc of Meat Producers

WI Bowhunters Assoc.

WI Deer Hunters Assoc.

WI Deer Hunters Coalition

The "At Large" members are made up of:

An out-state hunter (WI hunter not in the CWD zone) A new resident hunter recently returned to WI A non-hunter A HRZ hunter A HRZ Land owner A DEZ hunter A DEZ Land owner

The geographical make up of the members of the group shows members from:

Appleton, Baraboo, Barneveld, Blue Mounds, Delafield, Eagle River, Fitchburg, Jefferson, Lodi, Madison, Platteville and Stanley

This first meeting was primarily organizational but it laid the foundation for a discussion of the issues and impacts as well as the goals for the group. The August meeting will provide members with information from the group’s Technical Advisory team made up of DNR Scientists/biologists, The Dept of Agriculture, Health and family services and law enforcement, to name a few. After that, the remaining 5 meetings will be used by the group to formulate recommendations to the DNR Secretary who will then forward the group’s findings to the Natural resources board and then the legislature with public input and dialog along the way.

The public will have the opportunity to follow the progress of the Advisory Group on the CWD website at http://www.dnr.state.wi.us/org/land...ssues/cwd/

Members of the public are encouraged to observe the group in action. The public may engage members of the SAG during breaks in the working sessions. Members will also be available to the public outside the advisory group sessions as contact information for all the members will be available on the web site.

I will do my best to keep the members of WBH informed of what the group is doing.

Respectfully submitted

Ron Kulas
2Chucks
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20 Aug 2007 03:55 AM  
Saturday (Aug. 18th) was a very informative day. I have to say that it was hard to be in attendance as both my Sons were getting awards today at our Scout Troop’s Court of Honor and I have never missed one of these in my history with the Scouts. Nevertheless, I was out the door this morning at 7:30 and got home tonight around 6:30. Today’s meeting was very well attended by the group. There was only one member who was at the first meeting who was not in attendance today. This was not the meeting to miss if you were looking for information on CWD. We also picked up two members to our board. The room at the Lowell center was huge and had enough seats for the general public to attend (around 50 seats) but only 5 or 6 showed up. The entire day was captured by an audio visual person and the entire 7 ½ hours will be posted on the CWD website.

Today was filled with presentations by UW Madison Scientists. We had much to cover and questions made each presentation run long so we skipped our lunch break and had a working lunch while presenters continued with their talks. even with that we ran out of time so two presenters agreed to come to the Sept. Meeting to give their reports. I am looking forward to both of them as one speakers topic is “what do Wisconsinites think” The presenter is the research sociologist for the DNR and the other is the CWD project leader with the USGS National Wildlife health center. His topic is “What are other states doing about CWD.

Before we started, Each member gave a talk on their outreach activities with the public and how they were spreading the word about the work we are doing. Next we were given two questions to answer after we completed listening to the presenters. The questions were:

“What are the likely long term effects of CWD on WI, it’s citizens, livestock and natural landscape? “

“Is CWD a disease that can be eradicated?, contained to S.W. Wisconsin given the current social and political environment or even if nothing was held sacred and all avenues were explored?

The first speaker of the day was Scott Caven who is a UW Madison Extension Professor, Forest and wildlife ecology. His topic was CWD: why should we care? His concern is that CWD has dropped off most people’s radar and that it is not getting enough attention. He gave an over view of the past 5 years and what we have learned and what some of the successes and failures have been. His job was to remind us about why we were there. His was not a scientific speech but rather a plea to care. When he was done, one member asked him directly if CWD can be stopped/eradicated........ Scott’s answer was “No but it can be managed”

The second speaker was Jim Kazmierczak, Epidemiologist, Division of public health. Jim gave a talk on the human health risks. He said that Creutzfeldt Jakob Disease (CJD) has been around for more than 80 years. A new variant strain was discovered in 1995 In England but there has never been a case of it in the US. Scrappies has been around since the 1600's and has never transferred to humans even with humans consuming all parts of the sheep (including brains) There has never been a cross species transfer. He said that Scrappies can be found in the muscle (meat) of sheep and then he said that CWD has been found in venison. This is the first time I had heard that CWD prions were found in the meat of deer.

He talked about how People have been eating CWD infected meat in WI for years and it is not transferring. He mentioned that when a deer that is tested, shows up positive for CWD. The hunter is contacted and in most cases the hunter tells the DNR that the meat has been consumed. The DNR and the UW are keeping a record of all the people who have eaten known infected deer so that over time they will be able to see if they come down with CJD.

They are also monitoring all death certificates and looking over all the records of people that had human prion disease. He also noted that cases of human CJD are not more common in locations where CWD infected Cervids live and has been monitoring that for decades with data from Colorado. He gave a break down of all tests that have been done on trying to force a deer to human transfer without success. The work they have done over the years is very impressive. They can prove that Bovine to human transfer is possible (Mad cow in England) but not Cervid to human and that included injecting CWD infected brain matter directly into the brains of humanized mice. All of the tests done to prove or disprove a species transfer are done by this method and if the transfer occurs then they test the two subject animals again and this is done by feeding the animal brain matter to see if it can transfer. Most of those tests prove that oral transfer is far less likely but they did not completely rule out the possibility. He did say that in the last 30 years that there has been ample opportunity for human consumption of CWD infected meat and yet no cases of cross species transfer has occurred. He then said that the World health org. and the CDC state that there is no scientific evidence that CWD can cause human illness and that there is a species barrier that can’t be breeched even in test tubes. And that experimental inoculations of humanized mice (mice altered to express the human prion protien) with CWD prions resulted in zero infections. When asked how long CWD has most likely been in WI, the answer was “Decades”. When he was finished, he too was asked the question “Do you think CWD can be stopped/eradicated......... He would not give an answer.

The next speaker was Chad Johnson who is a scientist at the school of veterinary medison for UW Madison. His talk was on the risk of CWD transfers to other species as well as humans. He spoke of tests done to prove a link between deer and cattle and trying to transfer CWD to cows. He stated that a direct species transfer will take place if CWD brain matter in injected into a living cow’s brain. No such transfer has taken place through oral tests of tests of close quarter co habitation. These tests have been going on for decade in Colorado because the beef industry out West is very concerned. The UW is in the 7th year of a ten year study of a field test where CWD infected deer are living with healthy cattle. They keep bringing in sick deer to live with the cows but the cows never get sick. Not all deer are susceptible to CWD. Mule deer are the most susceptible, followed by whitetail and then elk. One moose has been known to get CWD but it is thought to have been a spontaneous or natural occurrence. Similar but still a species away are the Fallow and red deer. They too are not as likely to get CWD. No cases have ever been found in Caribou or antelope.

No deer to avian transfers have ever been found and this was done to disprove a link to scavenger birds such as crows. He was confident in the species barrier with birds. Dogs, skunks and raccoons tested also showed that CWD can’t be transferred to those animals and he felt that this is due to an evolutionary barrier due to these types of scavengers being long known to eat sick and diseased carrion. Some of the animals that showed an ability to contract CWD from deer are mice and voles as well as large cats (cougars) but not domestic house cats. Again, these are tests done by injecting infected brain matter into these animals. It is not as likely to transfer orally. When asked to give an example of how infectious brain matter was, he said it was the most infectious of all the matter compared to lymph or spinal matter. Asked how brain matter compared to saliva, he said that brain matter was around 10,000 times more infectious and when oral doses were given it was in large amounts over at least 5 times to ensure a reasonable amount of the CWD prions were transferred. This presentation was the most interesting of the day.

The next presenter was Richard Bishop, Professor Emeritus, Agriculture and applied economics UW Madison. He spoke on the economic impacts of CWD on the deer herd. He spoke of surveys conducted with resident and non resident hunters and their views on how their hunting habits have changed since CWD was discovered. His findings show that there are 6000 fewer non resident hunters in WI and 20,000 resident hunters due to CWD.

When surveyed, hunters were asked what would they be willing to pay per year over a five year period to ensure CWD was eradicated. That is, what is the max they would pay “extra” if given a guarantee that CWD would be gone in 5 years. The answer was $24 a year. (Big spenders huh?)

The next speaker was Erik Osnas who is an assistant scientist, forest and wildlife ecology UW Madison. He is an ecologist who is studying trends and theoretical models of the spread of CWD. He again agreed that CWD has been here for decades. He was the least impressive speaker in the bunch but that was due to his poor communications abilities. When questioned about his models, even he had little faith in them. We could not nail him down or get him to commit to any predictions of future infection percentages.

The last speaker of the day was Joel Pederson, Associate Professor Soil Science UW Madison. His topic was the role of environmental contamination. Joel is the guy who came out with the report that the soil is 700% more infections that deer to deer contact. He pointed out that it is actually 680%.

He told us of the many studies done both in the US and abroad using deer and scrappie infected sheep which mimic each other very closely. One o the interesting comments he made was that there are deer that are CWD carriers meaning that they never show clinical signs but when tested, the prions are evident. All the stories we have heard about the deer or sheep that were moved out of areas and then allowed back in after as much as 16 years only to have the new animals come down with the disease are from his studies.

He confirms that once it’s in the soil, it is there to stay but he could not say for how long. He would say that it would be at least 16 years based on tests. He has tested a wide range of soils from around the state and some are more likely to allow the infected prions to cling to them than are others. Clay was the most likely to hold the prions. He has even done tests where CWD prion infected clay was injected into the brains of healthy animals and they came down with the disease. He even states that structures/buildings that were cleaned and then healthy animals placed back into them got sick indicating that other surfaces can hold the prions. The discussion went to licking branches and rubs and scrapes made by infected deer and that they would most likely remain infected. When asked how he could test the amount of infected prions in soils and other structures we were told that there is currently no test equipment that will detect the prions and that the tests with live deer have indicated that this is so. Brain matter taken from infected deer was placed in soil and allowed to decompose over many years and then the soil was washed and both the soil and the wash water was injected into the brains of healthy animals which then got sick. When asked if CWD can be stopped/eradicated he said. “No”

A lot of questions were asked of all the presenters and in all, I felt we got a great deal out of the day. I took a lot of notes and what I have typed above is only a brief bit of what each speaker presented. I am sure I have left a lot out. We were told that if we came up with any questions over the next month that we could submit them to the group of presenters and they would respond.
Chuck Manetta
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21 Aug 2007 01:39 PM  
2Chucks,

Thanks for the informative post and your dedication to the sport. 
Chuck Manetta
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2Chucks
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23 Aug 2007 11:20 PM  
In recent weeks I have been doing a lot more research on CWD and its spread. I am learning that there are more unknowns than facts about how it spreads. For nearly every study done, there is another study that can contradict. Is the spread frequency dependent or Density dependent? There are equally valid arguments on both sides. Both are based on assumptions and theories. What does that mean to the Deer hunters in WI? Well, Depending on who you choose to listen to, you could presumably form a different set of beliefs. I have read research data and have heard presentations that will make your head spin. Here are some of my thoughts on the matter.

CWD is the end result of prion infection so it is the prion that I am most interested in. The deer is simply a vehicle. At this point, even without the deer we still have an environmental reservoir.

CWD is NOT always fatal and there is proof that deer can have the infectious prions and never get sick (go clinical). These are "Carriers"

Some deer seem to have an immunity to becoming infected though little is know as to why. Some theorize CWD rates are affected by twinning and triplets where the firstborn gets all the colostrum from the mother. This sets up an irreversible process where the remaining offspring never get the antibodies from the mother, and therefore never generate an immune system hardy enough to stave off chronic wasting from multiple disease venues.

The above two thoughts may have something to do with infection rates from 1% to 6% in the WI herd. No wild herd has ever seen infection rates above 15% (That I know of) Why does the majority of the herd remain uninfected???? Is it a time issue? I was told CWD has been in WI for at least a decade. Is this not enough time????

How does the infected prion spread? How is the infected prion shed? More and more research papers are being written about where the prions are in the deer. At first we were all told that it is contained to the brain, Spleen, Spine, Lymph nodes, eyes and tonsils. Then it was reported to be in the muscles (meat) I was told that it is in the blood, saliva, the organs, all of the digestive tract and In May of this year it was reported that it is in the Skin/hair so arguably it is in every part of the deer. I think that is important.

The UW scientists told us that infected brain matter is the most infectious medium followed by blood. Saliva, we were told is also known to contain the infected prions but that brain matter was 10,000 times more infectious/volatile. The Colorado test that showed saliva as a vehicle for transport also showed that prion transmission through a single blood transfusion from two symptomatic and one asymptomatic CWD positive donor is important in at least two contexts: (1) It reinforces that no tissue from CWD-infected deer can be considered free of the prions (2) it poses the possibility of the spread of prions, such as through insects i.e. mosquitoes/ticks. I found that very interesting.

While the CO tests said a single blood exchange was all that was required, the saliva tests were done by placing 50 ml of infected saliva 3 times a day over a 3 day period into the mouths of healthy deer. The UW test did this over a 5 day period to ensure enough of an exposure as they told us that saliva is a poor medium for transfer. Nonetheless, prion transfer was noted.

Infected deer shed infectious prions into the environment (which has been proven to hold these infectious prions for many years) but how? What other means of prion transfers exist? I thought of a few but I am sure there are far more.

Natural browsing and eating of mast crops and gardens as the season allows (12 months of the year)
Social interactions between deer (12 months of the year)
Rutting activity (3 months of the year)
Mosquito/ticks/insect transferring infected blood (6 months of the year)
Car kills allowing infected matter to enter the soil (12 months of the year)
Death by natural causes allowing infected matter to enter the soil (12 months of the year)
Shedding of hair /dander /coat changes (12 months of the year)
Excreta (urine, feces) currently thought to have a low probability of containing prions but certainly the largest single means of shedding (12 months of the year)
Blood trails, next to brains the blood is the best medium of transfer (3 months of the year)
Gut piles, To me this is a HUGE source of transmission and it provides a big steaming pile of prions exposed to the environment as well as a medium for other animals to transfer the matter. All of which get placed directly into the soil. (3 months of the year)
Carcass disposal (after butchering) back into the environment such as skin, blood, meat, bones ect. (3 months of the year)
Carcass transfers of killed deer from infected areas to non infected areas for butchering/consumption (3 months of the year)
The environmental reservoir that already exists due to a decade of infected deer shedding (12 months of the year)
I did not include bait/feeding as the DEZ and the HRZ are in the 6th year of a moratorium on that practice. (0 months of the year)

With all of the above methods of transfer, one would think that an infection rate of 100% should be the norm and yet after all these years it is incredibly low. I find this very puzzling. If it is truly density dependent and we certainly have high deer densities, why the low infection rate????

In my humble opinion, It is wise to reduce the deer herd in the DEZ and HRZ for a variety of reasons including CWD but to what levels and by what means. What about hunter/landowner support? Will a 10 deer per square mile herd have an equal percentage of infected deer as a 16 deer per square mile herd? For the sake of math, a square mile is 640 acres or (16) 40's so a population goal of 16 deer per square mile puts one deer per 40 acre parcel of deer habitat which is 12,000 deer in all of the Western DEZ. For comparison, the density in the CO CWD endemic area is about 6 deer per square mile. Will hunters even bother to hunt in an area with such a low deer population meaning that either an outside extermination force will need to be employed or herd size would be allowed to return to high densities?

At this point, the question needs to be asked. Is the spread of CWD a big problem, a medium sized problem or No problem. Until we can agree on the answer to that question, we can not plan out a strategy.

If it is No problem, the answer is simple. Return to the traditional season framework. Done

If it is a medium sized problem then the actions have to be stepped up a notch from the “No problem” strategy. And that may look similar to what we have now in the DEZ and HRZ .

If it is a big problem, then an appropriate strategy must be implemented. This would be radical and unconventional and would of course have to have the endorsement of the landowners.

Lets say it is a big problem, I conclude that herd reduction is the answer. All that remains is the means to that end. I prefer hunter/landowner driven/endorsed efforts and think that the long term effectiveness depends on this premise. Hunters have proven that they will kill deer if they are assured that the meat will go to good use. The DNR funding of the food pantry is a must. Registration stations need adequate deer drop off facilities and a processing plant(s) would be needed to support deer donations. The deer donation need not stop at the food pantry level but should be expanded so that distribution of meat could be done through additional outlets (i.e. church groups, community action groups etc.) and be made available to every citizen (not just the needy) Testing of all deer would be mandatory. Liberal hunting seasons and unlimited free either sex tags would be needed. This would not be weapon dependant. Relaxing or reducing DEZ hunting regulations should also be considered. I do not fear the over harvest of bucks and in fact think that would lead to a natural population decrease.

Let focus on it being a big problem since the “No problem” and “Medium problem” scenarios require less problem solving. What would be your solutions to solving the “Big Problem”

I remain open minded and willing to learn. Please provide feedback.
2Chucks
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30 Aug 2007 10:33 PM  
Today, I got a big package in the mail from the DNR. It included some research info I was looking for but also all the power point print outs from the last CWD meeting. I poured over it again to make sure I heard what I thought I heard. It made be draw the conclusions below.

P.S. For those that have 6 hours to kill and don't mind watching a 3 inch my 2 inch screen with crappy sound, you can go to the link to see all the data that was presented to our team.

http://www.dnr.state.wi.us/org/land...visory.htm

I think that the reason we see such low infection rates within the herd (1 to 5 percent) is that not all deer are susceptible to infection. I conclude This because of a research study in which healthy deer were fed infected brain matter (which is the most infectious and concentrated material available) and not all host subjects got sick. Deer eating deer brains is of course very unlikely to happen in the real world. but nonetheless, a small percentage of deer are contracting CWD in the wild and it is most likely through shedding via urine, feces, saliva, blood, gut piles, decomposition such as car kills or natural deaths, hair/dander etc.

It is not known at what point in an infected deer's life that it begins to shed into the environment but even when shedding occurs, the remaining deer that are susceptible to the infectious prions must encounter these infectious agents in high concentrations or over a substantial period of time to become infected. Couple that with the data that says oral transmission is not very effective and that infected brain matter is more than 10 thousand times more infectious than saliva and the fact that some of the deer that were given oral applications of infected saliva never got sick and I think you might draw the same conclusions.

I am impressed with the researchers focus on soil and it's importance in the transmissibility of CWD. They recognize that soil is a relevant reservoir for the infectious prions and that these prions bind themselves well with certain types of soil. What they discovered is that the infectious prions remain in the soils for long periods of time (as long as 16 years in Scrapie sheep tests) which increases both the contact and exposure rates to other deer. More important was the discovery that the infectious prions when mixed with Montmorillonite clay and other soils actually increased or enhanced the infectivity. In research where small amounts of infected brain matter was injected into the brains of healthy host animals while other subjects were injected with a mixture of soil and brain matter, the soil/brain mixture was found to be much more infectious or effective at causing the hosts to get CWD.

Since there is no real world application for deer to get a mixture of dirt and brain matter injected into their brains, a second study was conducted in which infected brain matter was fed to a group of host animals and another group was fed a mixture of infected brain matter and soil. A control group was fed uncontaminated soil. The control group showed no infection but both groups that were fed brain matter became infected.

What was surprising was that the animals that were fed the mixture of brain matter and soil had a higher infection rate and a shorter incubation period meaning that more of them got sick and did so in a shorter period of time proving that the prions in the soil are more infectious and efficient at transmitting CWD than is deer to deer contact. effectively 700% more infectious. Research links soils with high organic carbon content to being the most likely to enhance the effectively rate. More studies are under way.

It would appear that deer might be getting CWD directly from other deer through social interactions (which has been indicated through co-habitation studies) but a more likely means of transmission is from prions shed into the environment that are then enhanced by the soil which is consumed by other deer during normal feeding and rutting activity as well as the long list of other reasons deer might encounter dirt.

I invite others thoughts.
2Chucks
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25 Sep 2007 04:34 PM  
Well, meeting number 3 of the CWD Advisory group is behind us. We heard from Jordan Petchenick, the resource biologist for the DNR. His presentation was called "What do Wisconsinites think?" I've already read a lot of Jordan's work and was impressed with the info he has gathered in the last few years. What it boils down to is that what hunters say they will do and what they actually do are two different things. and that there is a real disconnect between hunters attitudes and DNR goals on how to manage not only the disease but also the deer herd. The agency realizes (correctly so) that despite their best ideas and efforts that without support of hunters and landowners, they are powerless.

They admit that hunters have told the DNR that they have little or no fear over CWD effecting their personal health. Surveys have shown that if CWD was proven to be a serious health issue to people or cattle that hunters would feel an obligation to reduce the deer herd to very low levels. Since personal health is a very low incentive to shoot more deer, the monetary incentives were added. I found the incentive program to be one of the most interesting tactics that the DNR has tried in an effort to get hunters to shoot more deer. They learned that paying hunters to shoot deer in an effort to reduce CWD does not work because hunters don't think is a problem that warrants the shooting of more deer to begin with. I think he learned that hunters do not hunt for reasons as simple as cash.

Jordan did not mention this but I suspect one of the reasons the cash incentive program failed was due to the way it was structured. In this case, the odds worked against them. Hunters were paid anywhere from $200 to $400 for every deer that tested positive for CWD.Everyone that submitted a deer was entered into a $20 drawing. Since the odds were so low that a hunter would actually shoot an infected deer, many hunters were paid nothing and the same was true of the random $20 drawing. This was complicated by the suspicion that even if a hunter shot a positive deer that the DNR would tell the hunter that it tested negative in an effort to save money. I don't suggest that was the case but such a rumor would spread fast and kill the program. Jordan thinks that managing the people is far more important than trying to manage the disease. If hunters can be convinced that there is a real need to seriously reduce the herd, that they would and could do just that and everything else will fall into place without agency intervention. It's all about incentives to harvest more deer than one can use. At this point, The DNR has not found any that have worked.

The next speaker was Bryan Richards. Bryan is the CWD project leader, USGS National Wildlife Health Center. His presentation is called: "What are other states learning about CWD". We learned that 14 states and a few Canadian Provinces now have CWD but failed to tell us if it was because the disease is spreading or if they have it only because they are now looking for it. When asked about WI, Bryan agrees that CWD has most likely been in WI for "Decades" I found his presentation and tone to be a bit adversarial and and he seemed to have a real dislike for deer farmers. He made a lot of correlations that were questioned by our panel. He did admit that a state that did not allow deer farming, also had CWD and that even though WI has several hundred deer/elk farms that the vast majority of the farms do not have CWD. In talking with the representative of the captive cervid industry that sits on our board, I was told that the majority of those farms are North of Hwy 29 and have not instances of CWD. His talk turned to Colorado and the steps that state has taken in it's 40 year battle with CWD. In the end, Bryan told us that just because Colorado stopped culling that WI should not follow that tactic. I found his talk to be biased in opinion more so than rooted in facts and science.

The third speaker was supposed to be the DNR's Senior Vet., Julie Landenberg but she fell ill and was not in attendance. After lunch we were introduced to Matt Frank who is the newly appointed DNR Secretary. We were given the chance to ask questions and he spent about a half hour fielding questions. That is another topic altogether. With the speakers and presentations complete, we discussed the need to see or hear any other information or data, prior to beginning our task of making recommendations. A few members brought up that we should have a presentation by Nancy Matthews to learn about her telemetry studies and what she learned over the years about deer travel patterns and ranges. Group member Tom Givnish will give a 20 minute talk about how the UK government ended a foot and mouth outbreak by using an extreme eradication program. It was also discussed that we should hear from Dr. James Kroll. Dr. Kroll is a well known whitetail management expert and we agreed to begin by watching a video from Dr. Kroll and then if needed, we would ask him to address the group. The remainder of our day was spent detailing the process and procedures involved with making our recommendations. I grew tired of a talk about how we plan to go about making recommendations and asked that we get to the meat and potatoes. and start brainstorming ideas. We meet again on the 20th of October.
wisconsincamofem
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30 Sep 2007 11:58 PM  
At least they are not paying tax dollar money for sharpshooters. I know I voted against that at our conservation meeting... good thing the majority of the population agrees.
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15 Oct 2007 02:23 AM  
" The next presenter was Richard Bishop, Professor Emeritus, Agriculture and applied economics UW Madison. He spoke on the economic impacts of CWD on the deer herd. He spoke of surveys conducted with resident and non resident hunters and their views on how their hunting habits have changed since CWD was discovered. His findings show that there are 6000 fewer non resident hunters in WI and 20,000 resident hunters due to CWD.

When surveyed, hunters were asked what would they be willing to pay per year over a five year period to ensure CWD was eradicated. That is, what is the max they would pay “extra” if given a guarantee that CWD would be gone in 5 years. The answer was $24 a year. (Big spenders huh?)


I grew up in Wisconsin and have been hunting on my uncles farm for 15 years but if it gets any more expensive I'm not going to be able hunt there anymore because of the non-resident fees. My friends have already stopped going down to hunt with me because they dont want to pay $160 for what they assume is a diseased deer. I know the state thinks the solution to every problem is higher taxes but in this case what the state needs is more hunters not money. You dont get more hunters by charging more for hunting, you get less. If it weren't for my family expecting to come home for it you'd have one fewer now. Just a thought.

Thanks for all the work your doing on this and I think a lot of the programs will have a positive effect. The bonus and extended seasons as well as the tags. I just think the DEZ and HRZ out of state license fees should be a lot more aggressive and resident fees shouldn't go up at all.
TSS
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--
16 Oct 2007 03:40 AM  
Quantifying the Species Barrier in Chronic Wasting Disease by a Novel in
vitro Conversion Assay


Li, L1; Coulthart, MB2; Balachandran, A3; Chakrabartty, A4; Cashman, NR1
1University of British Columbia, Brain Research Centre, Canada; 2Public
Health Agency
of Canada, National Microbiology Laboratory, Canada; 3Animal Diseases
Research Institute, Canada Food Inspection Agency, National Reference
Laboratory for
Scrapie and CWD, Canada; 4Ontario Cancer Institute and Department of Medical
Biophysics, University of Toronto, Canada


Background: Chronic wasting disease (CWD) is a transmissible spongiform
encephalopathy that can affect North American cervids (deer, elk, and moose).
Although the risk of CWD crossing the species barrier and causing human
disease is still unknown, however, definite bovine spongiform encephalopathy
(BSE) transmission to humans as variant CJD (vCJD), it would seem prudent to limit
the exposure of humans to CWD.


Aim: In view of the fact that BSE can be readily transmitted to non-bovid
species, it is important to establish the species susceptibility range of
CWD.


Methods: In vitro conversion system was performed by incubation of prions
with normal brain homogenates as described before, and protease K (PK)
resistant PrP was determined by immunoblotting with 6H4 monoclonal prion antibody.


Results: Our results demonstrate that PrPC from cervids (including moose)
can be efficiently converted to a protease-resistant form by incubation with
elk CWD prions, presumably due to sequence and structural similarities between
these species. Interestingly, hamster shows a high conversion ratio by PrPCWD.
Moreover, partial denaturation of substrate PrPC can apparently overcome the
structural barriers between more distant species.


Conclusions: Our work correctly predicted the transmission of CWD to a wild
moose. We find a species barrier for prion protein conversion between cervids and
other species, however, this barrier might be overcome if the PrPC substrate
has been partially denatured in a cellular environment. Such an environment
might also promote CWD transmission to non-cervid species, *** including humans.
Acid/GdnHCl-treated brain PrPC was a superior substrate for the in vitro
conversion than PrPC treated at physiological pH. This has implications for
the process by which the prion protein is converted in disease.


http://www.prion2007.com/pdf/Prion%...tracts.pdf" target="_blank" rel="nofollow">http://www.prion2007.com/pdf/Prion%...tracts.pdf" target="_blank" rel="nofollow">http://www.prion2007.com/pdf/Prion%...tracts.pdf" target="_blank" rel="nofollow">http://www.prion2007.com/pdf/Prion%...tracts.pdf


JOURNAL OURNAL OF VIROLOGY IROLOGY, Nov. 2005, p. 13794–13796 Vol. 79, No. 21
0022-538X/05/$08.00 !0 doi:10.1128/JVI.79.21.13794–13796.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.

NOTES

Interspecies Transmission of Chronic Wasting Disease Prions to
Squirrel Monkeys (Saimiri sciureus sciureus)

Richard F. Marsh, 1† Anthony nthony E. Kincaid, 2 Richard A. Bessen, 3 and Jason C. Bartz Bartz4*
Department of Animal Health and Biomedical Sciences, University of Wisconsin, Madison 53706 537061; Department of
Physical Therapy Therapy2 and Department of Medical Microbiology and Immunology, 4 Creighton University, Omaha,
Nebraska 68178; and Department of Veterinary Molecular Biology, Montana
State University, Bozeman, Montana 59718 597183
Received 3 May 2005/Accepted 10 August 2005

Chronic wasting disease (CWD) is an emerging prion disease of deer and elk. The risk of CWD transmission
to humans following exposure to CWD-infected tissues is unknown. To assess the susceptibility of nonhuman
primates to CWD, two squirrel monkeys were inoculated with brain tissue from a CWD-infected mule deer. The
CWD-inoculated squirrel monkeys developed a progressive neurodegenerative disease and were euthanized at
31 and 34 months postinfection. Brain tissue from the CWD-infected squirrel monkeys contained the abnormal
isoform of the prion protein, PrP-res, and displayed spongiform degeneration. This is the first reported
transmission of CWD to primates. ...snip...end



Subject: Clinical Observations of BSE Infection in Red Deer
Date: October 4, 2007 at 9:05 am PST

P04.80

Clinical Observations of BSE Infection in Red Deer

Steele, P1; Martin, S2; Jeffrey, M2; González, L2; Sisó, S2; Finlayson, J1;
Hamilton, S1;
Eaton, Samatha L1; Reid, Hugh W1; Todd, R1; Pang, Y1; Chianini, F1;
Dagleish, MP1
1Moredun Research Institute, UK; 2Veterinary Laboratory Agency, Lasswade, UK


Observation of clinical signs is often the first step in the diagnosis of TSE diseases in
experimental, farmed and wild animals. Clinical presentation of chronic wasting
disease (CWD) infected deer varies widely as disease progresses and many clinical
signs observed can be non-specific to TSE infection, however by terminal
stage the majority of cases involve behavioural changes and loss of body condition.
We present here the first description of clinical disease in deer experimentally infected
with BSE. These data are part of the results of an ongoing project to
investigate the susceptibility of UK red deer (Cervus elaphus elaphus) to BSE infection
either by alimentary or intra-cerebral infection.
Eighteen European red deer calves (mean 64 days old) were challenged intragastrically
with 25g of BSE-infected bovine brain. Six challenged and 2 control deer
were culled at 6 and 12 month post infection. These animals showed no clinical signs
and no disease-specific PrP (PrPd) on immunohistochemistry (IHC) examination of a
wide range of tissues collected at post-mortem. Six BSE-dosed and 4 negative
control deer are still alive at time of writing (1384 dpi).
Subsequently, 6 red deer of the same cohort (mean 341 days old) were challenged with
0.05g of BSE positive bovine brain material and 2 with sterile saline by the intracerebral
route. Currently (1106 dpi), five of the six challenged animals have developed
clinical signs and terminal disease confirmed by IHC and western blot detection of
PrPd. Clinical signs similar to CWD cases have been observed including behavioral change,
wide stance, lowered head, and excessive salivation. All animals had significant weight
loss attributed to inability or unwillingness to feed, with inhalation pneumonia occurring
in the case of one animal which is commonly observed in CWD cases. The first
animal to show clinical signs was markedly different to the four subsequent cases.
This animal had to be culled following several behavioral episodes causing
physical
injury. Our results prove for the first time that UK red deer are
susceptible to intra-cerebral
BSE infection and shows that the clinical presentation of disease shares
many
similarities to that recorded for CWD.


http://www.prion2007.com/pdf/Prion%...tracts.pdf" target="_blank" rel="nofollow">http://www.prion2007.com/pdf/Prion%...tracts.pdf" target="_blank" rel="nofollow">http://www.prion2007.com/pdf/Prion%...tracts.pdf" target="_blank" rel="nofollow">http://www.prion2007.com/pdf/Prion%...tracts.pdf


P04.61

Survival of PrPSc during Simulated Wastewater Treatment Processes

Pedersen, J1; Hinckley, G1; McMahon, K2; McKenzie, D3; Aiken, JM3
1University of Wisconsin, Soil Science/Civil and Environmental Engineering,
USA; 2University of Wisconsin, Civil and Environmental Engineering, USA;
3University of Wisconsin, Comparative Biosciences, USA


Concern has been expressed that prions could enter wastewater treatment
systems
through sewer and/or septic systems (e.g., necropsy laboratories, rural meat
processors, private game dressing) or through leachate from landfills that
have
received TSE-contaminated material. Prions are highly resistant to
degradation and
many disinfection procedures raising concern that they could survive
conventional
wastewater treatment. Here, we report the results of experiments examining
the
partitioning and survival of PrPSc during simulated wastewater treatment
processes
including activated and mesophilic anaerobic sludge digestion. We establish
that PrPSc
can be efficiently extracted from activated and anaerobic digester sludges
with 1%
sodium dodecyl sulfate, 10% sodium undecyl sulfate, and 1% sodium N-lauryl
sarcosinate. Activated sludge digestion does not result in significant
degradation of
PrPSc. The protein partitions strongly to the activated sludge solids and is
expected to enter biosolids treatment processes. A large fraction of PrPSc
survived
simulated mesophilic anaerobic sludge digestion. Our results suggest that if
prions
were to enter municipal waste water treatment systems, most of the agent
would partition to activated sludge solids, survive mesophilic anaerobic
digestion, and
be present in treated biosolids. Land application of biosolids containing
prions could
represent a route for their unintentional introduction into the environment.
Our results
argue for excluding inputs of prions to municipal wastewater treatment
facilities that
would result in unacceptable risk of prion disease transmission via
contaminated
biosolids.


http://www.prion2007.com/pdf/Prion%...tracts.pdf" target="_blank" rel="nofollow">http://www.prion2007.com/pdf/Prion%...tracts.pdf" target="_blank" rel="nofollow">http://www.prion2007.com/pdf/Prion%...tracts.pdf" target="_blank" rel="nofollow">http://www.prion2007.com/pdf/Prion%...tracts.pdf


P04.01

Chronic Wasting Disease in a Captive White-Tailed Deer Farm

Keane, D1; Barr, D1; Bochsler, P1; Hall, M2; Gidlewski, T3; O'Rourke, K4;
Spraker, T5
1University of Wisconsin, USA; 2US Department of Agriculture, USA; 3US
Department
of Agriculture, USA; 4USDA ARS-ADRU, Washington |State University, USA;
5Veterinary Diagnostic Laboratory, Colorado State University, USA


A white-tailed deer farm in Portage, Wisconsin, was depopulated in January
2006,
after chronic wasting disease (CWD) had been initially discovered on the
property in
September 2002. Prior to the depopulation, a total of 22 positive animals
had been
removed from the property: one in 2002, six in 2003, ten in 2004, four in
2005 and one
in 2006. At the time of depopulation a total of 76 animals remained: 47
females and 29
males. Age was assessed by visual examination of teeth at the time of death
and
revealed 26 adult, 8 fawn and 42 yearling animals. The following tissues
were
examined by immunohistochemistry for PrPCWD using Ab99/97.6.1: obex, tonsil,
retropharyngeal, submandibular, parotid, prescapular, axillary, inguinal,
prefemoral and
popliteal lymph nodes, recto-anal mucosal tissue and eye. Seventy-nine
percent of
animals (sixty) were found to be positive in at least one tissue; 49 were
obex positive,
58 retropharyngeal positive, 56 tonsil positive, 48 recto-anal mucosal
associated
lymphoid tissue positive and 4 animals were positive for PrPCWD in the
retina. Prion
genotype was determined for all animals.


http://www.prion2007.com/pdf/Prion%...tracts.pdf" target="_blank" rel="nofollow">http://www.prion2007.com/pdf/Prion%...tracts.pdf" target="_blank" rel="nofollow">http://www.prion2007.com/pdf/Prion%...tracts.pdf" target="_blank" rel="nofollow">http://www.prion2007.com/pdf/Prion%...tracts.pdf


Oral Transmissibility of Prion Disease Is Enhanced by Binding to Soil
Particles

Christopher J. Johnson1,2, Joel A. Pedersen3, Rick J. Chappell4, Debbie
McKenzie2, Judd M. Aiken1,2*

1 Program in Cellular and Molecular Biology, University of
Wisconsin-Madison, Madison, Wisconsin, United States of America, 2
Department of Comparative Biosciences, School of Veterinary Medicine,
University of Wisconsin-Madison, Madison, Wisconsin, United States of
America, 3 Department of Soil Science and Molecular and Environmental
Toxicology Center, University of Wisconsin-Madison, Madison, Wisconsin,
United States of America, 4 Biostatistics and Medical Informatics,
University of Wisconsin Medical School, Madison, Wisconsin, United States of
America

Soil may serve as an environmental reservoir for prion infectivity and
contribute to the horizontal transmission of prion diseases (transmissible
spongiform encephalopathies [TSEs]) of sheep, deer, and elk. TSE infectivity
can persist in soil for years, and we previously demonstrated that the
disease-associated form of the prion protein binds to soil particles and
prions adsorbed to the common soil mineral montmorillonite (Mte) retain
infectivity following intracerebral inoculation. Here, we assess the oral
infectivity of Mte- and soil-bound prions. We establish that prions bound to
Mte are orally bioavailable, and that, unexpectedly, binding to Mte
significantly enhances disease penetrance and reduces the incubation period
relative to unbound agent. Cox proportional hazards modeling revealed that
across the doses of TSE agent tested, Mte increased the effective infectious
titer by a factor of 680 relative to unbound agent. Oral exposure to
Mte-associated prions led to TSE development in experimental animals even at
doses too low to produce clinical symptoms in the absence of the mineral. We
tested the oral infectivity of prions bound to three whole soils differing
in texture, mineralogy, and organic carbon content and found soil- bound
prions to be orally infectious. Two of the three soils increased oral
transmission of disease, and the infectivity of agent bound to the third
organic carbon-rich soil was equivalent to that of unbound agent. Enhanced
transmissibility of soil-bound prions may explain the environmental spread
of some TSEs despite the presumably low levels shed into the environment.
Association of prions with inorganic microparticles represents a novel means
by which their oral transmission is enhanced relative to unbound agent.


snip...


Discussion These experiments address the critical question of whether soil
particle­bound prions are infectious by an environmentally relevant exposure
route, namely, oral ingestion. Oral infectivity of soil particle­bound
prions is a conditio sine qua non for soil to serve as an environmental
reservoir for TSE agent. The maintenance of infectivity and enhanced
transmissibility when TSE agent is bound to the common soil mineral Mte is
remarkable given the avidity of the PrPTSE­Mte interaction [22]. One might
expect the avid interaction of PrPTSE with Mte to result in the mineral
serving as a sink, rather than a reservoir, for TSE infectivity. Our results
demonstrate this may not be the case. Furthermore, sorption of prions to
complex whole soils did not diminish bioavailability, and in two of three
cases promoted disease transmission by the oral route of exposure. While
extrapolation of these results to environmental conditions must be made with
care, prion sorption to soil particles clearly has the potential to increase
disease transmission via the oral route and contribute to the maintenance of
TSE epizootics.

Two of three tested soils potentiated oral prion disease transmission. The
reason for increased oral transmissibility associated with some, but not
all, of the soils remains to be elucidated. One possibility is that
components responsible for enhancing oral transmissibility were present at
higher levels in the Elliot and Bluestem soils than in the Dodge soil. The
major difference between the Dodge soil and the other two soils was the
extremely high natural organic matter content of the former (34%, [22]). The
Dodge and Elliot soils contained similar levels of mixed-layer
illite/smectite, although the contribution of smectite layers was higher in
the Dodge soil (14%­16%, [22]). The organic matter present in the Dodge soil
may have obstructed access of PrPTSE to sorption sites on smectite (or other
mineral) surfaces.

The mechanism by which Mte or other soil components enhances the oral
transmissibility of particle-bound prions remains to be clarified.
Aluminosilicate minerals such as Mte do not provoke inflammation of the
intestinal lining [39]. Although such an effect is conceivable for whole
soils, soil ingestion is common in ruminants and other mammals [25]. Prion
binding to Mte or other soil components may partially protect PrPTSE from
denaturation or proteolysis in the digestive tract [22,40] allowing more
disease agent to be taken up from the gut than would otherwise be the case.
Adsorption of PrPTSE to soil or soil minerals may alter the aggregation
state of the protein, shifting the size distribution toward more infectious
prion protein particles, thereby increasing the specific titer (i.e.,
infectious units per mass of protein) [41]. In the intestine, PrPTSE
complexed with soil particles may be more readily sampled, endocytosed
(e.g., at Peyer's patches), or persorbed than unbound prions.
Aluminosilicate (as well as titanium dioxide, starch, and silica)
microparticles, similar in size to the Mte used in our experiments, readily
undergo endocytotic and persorptive uptake in the small intestine [42­44].
Enhanced translocation of the infectious agent from the gut lumen into the
body may be responsible for the observed increase in transmission
efficiency.

Survival analysis indicated that when bound to Mte, prions from both BH and
purified PrPTSE preparations were more orally infectious than unbound agent.
Mte addition influenced the effective titer of infected BH to a lesser
extent than purified PrPTSE. Several nonmutually exclusive factors may
explain this result: (1) other macromolecules present in BH (e.g., lipids,
nucleic acids, other proteins) compete with PrPTSE for Mte binding sites;
(2) prion protein is more aggregated in the purified PrPTSE preparation than
in BH [45], and sorption to Mte reduces PrPTSE aggregate size, increasing
specific titer [41]; and (3) sorption of macromolecules present in BH to Mte
influences mineral particle uptake in the gut by altering surface charge or
size, whereas the approximately 1,000-fold lower total protein concentration
in purified PrPTSE preparations did not produce this effect.

We previously showed that other inorganic microparticles (kaolinite and
silicon dioxide) also bind PrPTSE [22]. All three types of microparticles
are widely used food additives and are typically listed as bentonite (Mte),
kaolin (kaolinite), and silica (silicon dioxide). Microparticles are
increasingly included in Western diets. Dietary microparticles are typically
inert and considered safe for consumption by themselves, do not cause
inflammatory responses or other pathologies, even with chronic consumption,
and are often sampled in the gut and transferred from the intestinal lumen
to lymphoid tissue [39,46,47]. Our data suggest that the binding of PrPTSE
to dietary microparticles has the potential to enhance oral prion disease
transmission and warrants further investigation.

In conclusion, our results provide compelling support for the hypothesis
that soil serves as a biologically relevant reservoir of TSE infectivity.
Our data are intriguing in light of reports that naïve animals can contract
TSEs following exposure to presumably low doses of agent in the environment
[5,7­9]. We find that Mte enhances the likelihood of TSE manifestation in
cases that would otherwise remain subclinical (Figure 3B and 3C), and that
prions bound to soil are orally infectious (Figure 5). Our results
demonstrate that adsorption of TSE agent to inorganic microparticles and
certain soils alter transmission efficiency via the oral route of exposure.


snip...full text is here:

http://pathogens.plosjournals.org/p...at.0030093

http://pathogens.plosjournals.org/p...0093-L.pdf

http://pathogens.plosjournals.org/p...0093-S.pdf


--TSS


http://lists.ifas.ufl.edu/cgi-bin/w...742&P=7260


From: "Terry S. Singeltary Sr."
Subject: CWD UPDATE 88 AUGUST 31, 2007

http://lists.ifas.ufl.edu/cgi-bin/w...&T=0&P=450

Date: Wed, 29 Aug 2007 21:13:08 -0500
From: "Terry S. Singeltary Sr."
Subject: CWD NEW MEXICO RECORDS IT'S 19 CASE (near Texas border again)

http://lists.ifas.ufl.edu/cgi-bin/w...=0&P=26079

Monitoring the Potential Transmission of Chronic Wasting Disease to Humans
Using a Hunter Registry Database in Wyoming (405 lines)
From: Terry S. Singeltary Sr.
Date: Thu, 30 Aug 2007 21:23:42 -0500

http://lists.ifas.ufl.edu/cgi-bin/w...S=&P=27654


J Biol Chem. 2007 Aug 20; : 17709374

Cross-sequence transmission of sporadic Creutzfeldt-Jakob disease creates a
new prion strain.



####################################

our results raise the possibility that CJD cases
classified as VV1 may include cases caused by
iatrogenic transmission of sCJD-MM1 prions or
food-borne infection by type 1 prions from animals,
e.g., chronic wasting disease prions in cervid. In fact,
two CJD-VV1 patients who hunted deer or
consumed venison have been reported (40, 41). The
results of the present study emphasize the need for
traceback studies and careful re-examination of the
biochemical properties of sCJD-VV1 prions.

###################################


FULL TEXT ;

http://www.jbc.org/cgi/content/abstract/M704597200v1?maxtoshow=&HITS=10&hits=10&RESULTFORMAT=&fulltext=Cross-sequence+transmission+of+sporadic+Creutzfel
dt-Jakob+disease+creates+a+new+&searchid=1&FIRSTINDEX=0&resourcetype=HWCIT


http://lists.ifas.ufl.edu/cgi-bin/wa.exe?A2=ind0708&L=sanet-mg&T=0&P=21267


Re: Colorado Surveillance Program for Chronic Wasting Disease
Transmission to Humans (TWO SUSPECT CASES)

http://lists.ifas.ufl.edu/cgi-bin/wa.exe?A2=ind0704&L=sanet-mg&T=0&P=1165



ABSTRACTS SPORADIC CJD AND H BASE MAD COW ALABAMA AND TEXAS
SEPTEMBER 2007

Date: Mon, 24 Sep 2007 21:31:55 -0500

I suggest that you all read the data out about h-BASE and sporadic CJD, GSS,
blood, and some of the other abstracts from the PRION2007. ...

http://lists.ifas.ufl.edu/cgi-bin/wa.exe?A2=ind0709&L=sanet-mg&T=0&F=&S=&P=19744


*** PLEASE READ AND UNDERSTAND THE RAMIFICATIONS OF THIS !!!
THE PRICE OF POKER INDEED GOES UP. ...TSS

USA BASE CASE, (ATYPICAL BSE), AND OR TSE (whatever they are calling it
today), please note that both the ALABAMA COW, AND THE TEXAS COW, both were
''H-TYPE'', personal communication Detwiler et al Wednesday, August 22, 2007
11:52 PM. ...TSS

http://lists.ifas.ufl.edu/cgi-bin/wa.exe?A2=ind0708&L=sanet-mg&T=0&P=19779


see full text 143 pages ;

http://www.prion2007.com/pdf/Prion%...tracts.pdf" target="_blank" rel="nofollow">http://www.prion2007.com/pdf/Prion%...tracts.pdf" target="_blank" rel="nofollow">http://www.prion2007.com/pdf/Prion%...tracts.pdf" target="_blank" rel="nofollow">http://www.prion2007.com/pdf/Prion%...tracts.pdf


FC5.5.1
BASE Transmitted to Primates and MV2 sCJD Subtype Share PrP27-30 and PrPSc
C-terminal Truncated Fragments

We here show that the PrPSc pattern obtained in infected primates is
identical to BASE
and sCJD MV-2 subtype. These data strongly support the link, or at least a
common
ancestry, between a sCJD subtype and BASE.

This work was supported by Neuroprion (FOOD-CT-2004-506579)

FC5.5.2
Transmission of Italian BSE and BASE Isolates in Cattle Results into a
Typical BSE Phenotype and a Muscle Wasting Disease

This study further confirms that BASE is caused by a distinct prion isolate
and discloses a novel disease
phenotype in cattle, closely resembling the phenotype previous reported in
scrapie-inoculated
cattle and in some subtypes of inherited and sporadic Creutzfeldt-Jakob
disease.


http://www.prion2007.com/pdf/Prion%...tracts.pdf" target="_blank" rel="nofollow">http://www.prion2007.com/pdf/Prion%...tracts.pdf" target="_blank" rel="nofollow">http://www.prion2007.com/pdf/Prion%...tracts.pdf" target="_blank" rel="nofollow">http://www.prion2007.com/pdf/Prion%...tracts.pdf


ABSTRACTS SPORADIC CJD AND H BASE MAD COW ALABAMA AND TEXAS SEPTEMBER 2007

Date: Mon, 24 Sep 2007 21:31:55 -0500

I suggest that you all read the data out about h-BASE and sporadic CJD, GSS,
blood, and some of the other abstracts from the PRION2007. ...

http://lists.ifas.ufl.edu/cgi-bin/wa.exe?A2=ind0709&L=sanet-mg&T=0&F=&S=&P=19744


*** PLEASE READ AND UNDERSTAND THE RAMIFICATIONS OF THIS !!! THE PRICE OF
POKER INDEED GOES UP. ...TSS

USA BASE CASE, (ATYPICAL BSE), AND OR TSE (whatever they are calling it
today), please note that both the ALABAMA COW, AND THE TEXAS COW, both were
''H-TYPE'', personal communication Detwiler et al Wednesday, August 22, 2007
11:52 PM. ...TSS

http://lists.ifas.ufl.edu/cgi-bin/wa.exe?A2=ind0708&L=sanet-mg&T=0&P=19779


PLEASE NOTE IN USA CJD UPDATE AS AT JUNE 2007, please note steady increase
in ''TYPE UNKNOWN''. ...TSS


1 Acquired in the United Kingdom; 2 Acquired in Saudi Arabia; 3 Includes 17
inconclusive and 9 pending (1 from 2006, 8
from 2007); 4 Includes 17 non-vCJD type unknown (2 from 1996, 2 from 1997, 1
from 2001, 1 from 2003, 4 from 2004, 3
from 2005, 4 from 2006) and 36 type pending (2 from 2005, 8 from 2006, ***
26 from 2007)

http://www.cjdsurveillance.com/pdf/case-table.pdf


Subject: NOR-98 SCRAPIE UPDATE AUGUST 31, 2007 (RISES TO 5 DOCUMENTED CASES
IN USA)
Date: October 9, 2007 at 7:15 am PST

Greetings, seems the NOR-98 atypical scrapie cases are the rise in the USA.
...tss


INFECTED AND SOURCE FLOCKS

AS of August 31, 2007, there were 33 scrapie infected and source flocks with
open statuses (Figure 3). Five new source flocks and one new infected flock
were reported n August (Figure 4) with a total of 64 reported for FY 2007
(Figure 5).


snip...


IN FY 2007 TWO FIELD CASES, ONE VALIDATION CASE, AND TWO RSSS CASES WERE
CONSISTENT WITH NOR-98 SCRAPIE. ...

(BRINGS A TOTAL OF 5 NOR-98 CASES DOCUMENTED IN 2007 IN USA. ...TSS)


http://www.aphis.usda.gov/animal_health/animal_diseases/scrapie/downloads/monthly_scrapie_rpt.pps



NOW, why in the world is no one much speaking about the latest 5 cases of the
NOR-98 case in the USA,
and what are the potential ramifications thereof;



Subject: Aspects of the Cerebellar Neuropathology in Nor98 Date: September
26, 2007 at 4:06 pm PST



P03.141



Aspects of the Cerebellar Neuropathology in Nor98



Gavier-Widén, D1; Benestad, SL2; Ottander, L1; Westergren, E1 1National
Veterinary Insitute, Sweden; 2National Veterinary Institute, Norway



Nor98 is a prion disease of old sheep and goats. This atypical form of
scrapie was first described in Norway in 1998. Several features of Nor98
were shown to be different from classical scrapie including the distribution
of disease associated prion protein (PrPd) accumulation in the brain. The
cerebellum is generally the most affected brain area in Nor98. The study
here presented aimed at adding information on the neuropathology in the
cerebellum of Nor98 naturally affected sheep of various genotypes in Sweden
and Norway. A panel of histochemical and immunohistochemical (IHC) stainings
such as IHC for PrPd, synaptophysin, glial fibrillary acidic protein,
amyloid, and cell markers for phagocytic cells were conducted. The type of
histological lesions and tissue reactions were evaluated. The types of PrPd
deposition were characterized. The cerebellar cortex was regularly affected,
even though there was a variation in the severity of the lesions from case
to case. Neuropil vacuolation was more marked in the molecular layer, but
affected also the granular cell layer. There was a loss of granule cells.
Punctate deposition of PrPd was characteristic. It was morphologically and
in distribution identical with that of synaptophysin, suggesting that PrPd
accumulates in the synaptic structures. PrPd was also observed in the
granule cell layer and in the white matter. *** The pathology features of
Nor98 in the cerebellum of the affected sheep showed similarities with those
of sporadic Creutzfeldt-Jakob disease in humans.


http://www.prion2007.com/pdf/Prion%...tracts.pdf" target="_blank" rel="nofollow">http://www.prion2007.com/pdf/Prion%...tracts.pdf" target="_blank" rel="nofollow">http://www.prion2007.com/pdf/Prion%...tracts.pdf" target="_blank" rel="nofollow">http://www.prion2007.com/pdf/Prion%...tracts.pdf


what does the Nobel Prize Winner Stanely Prusiner say about atypical
scrapie, lets look at that first ;



Published online before print October 20, 2005

Proc. Natl. Acad. Sci. USA, 10.1073/pnas.0502296102
Medical Sciences

A newly identified type of scrapie agent can naturally infect sheep with
resistant PrP genotypes

( sheep prion | transgenic mice )

Annick Le Dur *, Vincent Béringue *, Olivier Andréoletti , Fabienne Reine *,
Thanh Lan Laï *, Thierry Baron , Bjørn Bratberg ¶, Jean-Luc Vilotte ||,
Pierre Sarradin **, Sylvie L. Benestad ¶, and Hubert Laude *
*Virologie Immunologie Moléculaires and ||Génétique Biochimique et
Cytogénétique, Institut National de la Recherche Agronomique, 78350
Jouy-en-Josas, France; Unité Mixte de Recherche, Institut National de la
Recherche Agronomique-Ecole Nationale Vétérinaire de Toulouse, Interactions
Hôte Agent Pathogène, 31066 Toulouse, France; Agence Française de Sécurité
Sanitaire des Aliments, Unité Agents Transmissibles Non Conventionnels,
69364 Lyon, France; **Pathologie Infectieuse et Immunologie, Institut
National de la Recherche Agronomique, 37380 Nouzilly, France; and
¶Department of Pathology, National Veterinary Institute, 0033 Oslo, Norway


Edited by Stanley B. Prusiner, University of California, San Francisco, CA,
and approved September 12, 2005 (received for review March 21, 2005)

Scrapie in small ruminants belongs to transmissible spongiform
encephalopathies (TSEs), or prion diseases, a family of fatal
neurodegenerative disorders that affect humans and animals and can transmit
within and between species by ingestion or inoculation. Conversion of the
host-encoded prion protein (PrP), normal cellular PrP (PrPc), into a
misfolded form, abnormal PrP (PrPSc), plays a key role in TSE transmission
and pathogenesis. The intensified surveillance of scrapie in the European
Union, together with the improvement of PrPSc detection techniques, has led
to the discovery of a growing number of so-called atypical scrapie cases.
These include clinical Nor98 cases first identified in Norwegian sheep on
the basis of unusual pathological and PrPSc molecular features and "cases"
that produced discordant responses in the rapid tests currently applied to
the large-scale random screening of slaughtered or fallen animals.
Worryingly, a substantial proportion of such cases involved sheep with PrP
genotypes known until now to confer natural resistance to conventional
scrapie. Here we report that both Nor98 and discordant cases, including
three sheep homozygous for the resistant PrPARR allele (A136R154R171),
efficiently transmitted the disease to transgenic mice expressing ovine PrP,
and that they shared unique biological and biochemical features upon
propagation in mice. These observations support the view that a truly
infectious TSE agent, unrecognized until recently, infects sheep and goat
flocks and may have important implications in terms of scrapie control and
public health.


----------------------------------------------------------------------------
----

Author contributions: H.L. designed research; A.L.D., V.B., O.A., F.R.,
T.L.L., J.-L.V., and H.L. performed research; T.B., B.B., P.S., and S.L.B.
contributed new reagents/analytic tools; V.B., O.A., and H.L. analyzed data;
and H.L. wrote the paper.

A.L.D. and V.B. contributed equally to this work.

To whom correspondence should be addressed.

Hubert Laude, E-mail: laude@jouy.inra.fr

www.pnas.org/cgi/doi/10.1073/pnas.0502296102


http://www.pnas.org/cgi/content/abstract/0502296102v1


Un document de 1991 indiqué dans la liste BSE-L par Terry S. Singeltary
A CONTRIBUTION TO THE NEUROPATHOLOGY OF THE RED-NECKED OSTRICH (STRUTHIO CAMELUS) - SPONGIFORM ENCEPHALOPATHY

http://www.bseinquiry.gov.uk/files/sc/Seac10/tab06.pdf


In Confidence - Perceptions of unconventional slow virus diseases
of animals in the USA - APRIL-MAY 1989 - G A H Wells



http://www.bseinquiry.gov.uk/files/mb/m11b/tab01.pdf


HOUND STUDY


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

HOUND STUDY

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.

snip...

http://www.bseinquiry.gov.uk/files/yb/1991/01/04004001.pdf

76 pages on hound study;

http://www.bseinquiry.gov.uk/files/sc/seac16/tab04.pdf

> 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
investigation.

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).

http://www.bseinquiry.gov.uk/witness/htm/stat067.htm

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
consumption.

snip...

http://www.bseinquiry.gov.uk/files/ws/s324.pdf


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

======================


TO BE CONTINUED................TSS


TSS
TSS
6 Point
6 Point
Send Private Message
Posts:132

--
16 Oct 2007 04:24 PM  
continued on ;



Oral transmission of kuru, Creutzfeldt-Jakob disease, and scrapie to
nonhuman primates.

Gibbs CJ Jr, Amyx HL, Bacote A, Masters CL, Gajdusek DC.

Kuru and Creutzfeldt-Jakob disease of humans and scrapie disease of
sheep and goats were transmitted to squirrel monkeys (Saimiri
sciureus) that were exposed to the infectious agents only by their
nonforced consumption of known infectious tissues. The asymptomatic
incubation period in the one monkey exposed to the virus of kuru was
36 months; that in the two monkeys exposed to the virus of
Creutzfeldt-Jakob disease was 23 and 27 months, respectively; and
that in the two monkeys exposed to the virus of scrapie was 25 and
32 months, respectively. Careful physical examination of the buccal
cavities of all of the monkeys failed to reveal signs or oral
lesions. One additional monkey similarly exposed to kuru has
remained asymptomatic during the 39 months that it has been under
observation.

PMID: 6997404

http://www.ncbi.nlm.nih.gov/entrez/...t=Abstract


PAGE 25

Transmission Studies

Mule deer transmissions of CWD were by intracerebral inoculation and
compared with natural cases resulted in a more rapidly
progressive clinical disease with repeated episodes of synocopy ending
in coma. One control animal became affected, it is believed through
contamination of inoculam (?saline). Further CWD transmissions were
carried out by Dick Marsh into ferret, mink and squirrel monkey.
Transmission occurred in all of these species with the shortest
incubation period in the ferret.

[hmmm, CWD transmission to squirrel monkey. are humans primates?TSS]

snip...

The occurrence of CWD must be viewed against the context of the
locations in which it occurred. It was an incidental and unwelcome
complication of the respective wildlife research programmes. Despite its
subsequent recognition as a new disease of cervids, therefore justifying
direct investigation, no specific research funding was forthcoming.
The USDA viewed it as a wildlife problem and consequently not their
province!

[figures...TSS]

snip...

VISIT TO USA - DR A E WRATHALL - INFO ON BSE AND SCRAPIE

1. Dr Clark lately of the Scrapie Research Unit, Mission Texas has
successfully transmitted ovine and caprine scrapie to cattle. The
experimental results have not been published but there are plans to do
this. This work was initiated in 1978. A summary of it is:-

better cut this short, you can read full text of part 2 here;

snip...

In Reply to: In Confidence - Perceptions of unconventional slow virus
diseases of animals in the USA - APRIL-MAY 1989 - G A H Wells


http://www.bseinquiry.gov.uk/files/.../tab01.pdf




-------- Original Message --------

Subject: DOCKET-- 03D-0186 -- FDA Issues Draft Guidance on Use of
Material >From Deer and Elk in Animal Feed; Availability
Date: Fri, 16 May 2003 11:47:37 -0500
From: "Terry S. Singeltary Sr."
To: fdadockets@oc.fda.gov



Greetings FDA,

i would kindly like to comment on;

Docket 03D-0186

FDA Issues Draft Guidance on Use of Material From Deer and Elk in Animal
Feed; Availability

Several factors on this apparent voluntary proposal disturbs me greatly,
please allow me to point them out;

1. MY first point is the failure of the partial ruminant-to-ruminant feed
ban of 8/4/97. this partial and voluntary feed ban of some ruminant
materials being fed back to cattle is terribly flawed. without the
_total_ and _mandatory_ ban of all ruminant materials being fed
back to ruminants including cattle, sheep, goat, deer, elk and mink,
chickens, fish (all farmed animals for human/animal consumption),
this half ass measure will fail terribly, as in the past decades...

2. WHAT about sub-clinical TSE in deer and elk? with the recent
findings of deer fawns being infected with CWD, how many could
possibly be sub-clinically infected. until we have a rapid TSE test to
assure us that all deer/elk are free of disease (clinical and sub-clinical),
we must ban not only documented CWD infected deer/elk, but healthy
ones as well. it this is not done, they system will fail...

3. WE must ban not only CNS (SRMs specified risk materials),
but ALL tissues. recent new and old findings support infectivity
in the rump or ass muscle. wether it be low or high, accumulation
will play a crucial role in TSEs.

4. THERE are and have been for some time many TSEs in the
USA. TME in mink, Scrapie in Sheep and Goats, and unidentified
TSE in USA cattle. all this has been proven, but the TSE in USA
cattle has been totally ignored for decades. i will document this
data below in my references.

5. UNTIL we ban all ruminant by-products from being fed back
to ALL ruminants, until we rapid TSE test (not only deer/elk) but
cattle in sufficient numbers to find (1 million rapid TSE test in
USA cattle annually for 5 years), any partial measures such as the
ones proposed while ignoring sub-clinical TSEs and not rapid TSE
testing cattle, not closing down feed mills that continue to violate the
FDA's BSE feed regulation (21 CFR 589.2000) and not making
freely available those violations, will only continue to spread these
TSE mad cow agents in the USA. I am curious what we will
call a phenotype in a species that is mixed with who knows
how many strains of scrapie, who knows what strain or how many
strains of TSE in USA cattle, and the CWD in deer and elk (no
telling how many strains there), but all of this has been rendered
for animal feeds in the USA for decades. it will get interesting once
someone starts looking in all species, including humans here in the
USA, but this has yet to happen...

6. IT is paramount that CJD be made reportable in every state
(especially ''sporadic'' cjd), and that a CJD Questionnaire must
be issued to every family of a victim of TSE. only checking death
certificates will not be sufficient. this has been proven as well
(see below HISTORY OF CJD -- CJD QUESTIONNAIRE)

7. WE must learn from our past mistakes, not continue to make
the same mistakes...

REFERENCES

Six white-tailed deer fawns test positive for CWD

MADISON -- Six fawns in the area of south central Wisconsin where
chronic wasting disease has been found in white-tailed deer have tested
positive for the disease, according to Department of Natural Resources
wildlife health officials. These are the youngest wild white-tailed deer
detected with chronic wasting disease (CWD) to date.

Approximately 4,200 fawns, defined as deer under 1 year of age, were
sampled from the eradication zone over the last year. The majority of
fawns sampled were between the ages of 5 to 9 months, though some were
as young as 1 month. Two of the six fawns with CWD detected were 5 to 6
months old. All six of the positive fawns were taken from the core area
of the CWD eradication zone where the highest numbers of positive deer
have been identified.

snip...

http://www.dnr.state.wi.us/org/caer...3.htm#art4

===================================================

Issued: Monday, 28 August 2000
NEW EVIDENCE OF SUB-CLINICAL PRION INFECTION: IMPORTANT RESEARCH
FINDINGS RELEVANT TO CJD AND BSE

A team of researchers led by Professor John Collinge at the Medical
Research Council Prion Unit1 report today in the Proceedings of the
National Academy of Sciences, on new evidence for the existence of a
'sub-clinical' form of BSE in mice which was unknown until now.

The scientists took a closer look at what is known as the 'species
barrier' - the main protective factor which limits the ability of
prions2 to jump from one species to infect another. They found the mice
had a 'sub-clinical' form of disease where they carried high levels of
infectivity but did not develop the clinical disease during their normal
lifespan. The idea that individuals can carry a disease and show no
clinical symptoms is not new. It is commonly seen in conventional
infectious diseases.

Researchers tried to infect laboratory mice with hamster prions3 called
Sc237 and found that the mice showed no apparent signs of disease.
However, on closer inspection they found that the mice had high levels
of mouse prions in their brains. This was surprising because it has
always been assumed that hamster prions could not cause the disease in
mice, even when injected directly into the brain.

In addition the researchers showed that this new sub-clinical infection
could be easily passed on when injected into healthy mice and hamsters.

The height of the species barrier varies widely between different
combinations of animals and also varies with the type or strain of
prions. While some barriers are quite small (for instance BSE easily
infects mice), other combinations of strain and species show a seemingly
impenetrable barrier. Traditionally, the particular barrier studied here
was assumed to be robust.

Professor John Collinge said: "These results have a number of important
implications. They suggest that we should re-think how we measure
species barriers in the laboratory, and that we should not assume that
just because one species appears resistant to a strain of prions they
have been exposed to, that they do not silently carry the infection.
This research raises the possibility, which has been mentioned before,
that apparently healthy cattle could harbour, but never show signs of, BSE.

"This is a timely and unexpected result, increasing what we know about
prion disease. These new findings have important implications for those
researching prion disease, those responsible for preventing infected
material getting into the food chain and for those considering how best
to safeguard health and reduce the risk that theoretically, prion
disease could be contracted through medical and surgical procedures."

ISSUED FRIDAY 25 AUGUST UNDER EMBARGO. PLEASE NOTE THAT THE EMBARGO IS
SET BY THE JOURNAL.

FOR FURTHER INFORMATION CONTACT THE MRC PRESS OFFICE ON 020 7637 6011
(OFFICE HOURS) OR 07818 428297 OR 0385 774357 (OUT-OF-OFFICE-HOURS) OR
PROFESSOR JOHN COLLINGE ON 020 7594 3760. PLEASE NOTE THAT OWING TO
TRAVEL COMMITMENTS PROFESSOR COLLINGE WILL ONLY BE AVAILABLE UNTIL 16.30
ON FRIDAY 25 AUGUST AND CONTACTABLE AGAIN ON MONDAY 28 AUGUST VIA THE
MRC PRESS OFFICE. DR ANDREW HILL (A CO-AUTHOR ON THE PAPER) FROM THE
DEPARTMENT OF PATHOLOGY AT THE UNIVERSITY OF MELBOURNE WILL BE AVAILABLE
ON 00 61 3 8344 3995 (DURING OFFICE HOURS) OR 00 61 3 9443 0009
(OUT-OF-OFFICE HOURS). PLEASE NOTE THAT AUSTRALIA IS TEN HOURS AHEAD OF
UK TIME.

NOTES FOR EDITORS

Professor Collinge is a consultant neurologist and Director of the newly
formed MRC Prion Unit based at The Imperial College School of Medicine
at St Mary's Hospital. He is also a member of the UK Government's
Spongiform Encephalopathy Advisory Committee (SEAC). The MRC prion unit
is was set up in 1999, and its work includes molecular genetic studies
of human prion disease and transgenic modelling of human prion diseases.

Prions are unique infectious agents that cause fatal brain diseases such
as Creutzfeldt-Jakob disease (CJD) in humans and scrapie and BSE (mad
cow disease) in animals. In some circumstances prions from one species
of animals can infect another and it is clear that BSE has done this to
cause the disease variant CJD in the UK and France. It remains unclear
how large an epidemic of variant CJD will occur over the years ahead.

The strain of prion used here to infect the mice is the Sc237 strain
(also known as 263K) which infects hamsters, and until now was assumed
not to infect mice.

This research was funded by the Medical Research Council and Wellcome Trust.

The Medical Research Council (MRC) is a national organisation funded by
the UK tax-payer. Its business is medical research aimed at improving
human health; everyone stands to benefit from the outputs. The research
it supports and the scientists it trains meet the needs of the health
services, the pharmaceutical and other health-related industries and the
academic world. MRC has funded work which has led to some of the most
significant discoveries and achievements in medicine in the UK. About
half of the MRC's expenditure of £345 million is invested in over 50 of
its Institutes and Units, where it employs its own research staff. The
remaining half goes in the form of grant support and training awards to
individuals and teams in universities and medical schools.

The Wellcome Trust is the world's largest medical research charity with
a spend of some £600 million in the current financial year 1999/2000.
The Wellcome Trust supports more than 5,000 researchers, at 400
locations, in 42 different countries to promote and foster research with
the aim of improving human and animal health. As well as funding major
initiatives in the public understanding of science, the Wellcome Trust
is the country's leading supporter of research into the history of medicine.

©2002 Medical Research Council
Data Protection policy | Contact the MRC

http://www.mrc.ac.uk/index/public_i...-43-00.htm

======================================

Oral transmission and early lymphoid tropism of chronic wasting disease
PrPres in mule deer fawns (Odocoileus hemionus )
Christina J. Sigurdson1, Elizabeth S. Williams2, Michael W. Miller3,
Terry R. Spraker1,4, Katherine I. O'Rourke5 and Edward A. Hoover1

Department of Pathology, College of Veterinary Medicine and Biomedical
Sciences, Colorado State University, Fort Collins, CO 80523- 1671, USA1
Department of Veterinary Sciences, University of Wyoming, 1174 Snowy
Range Road, University of Wyoming, Laramie, WY 82070, USA 2
Colorado Division of Wildlife, Wildlife Research Center, 317 West
Prospect Road, Fort Collins, CO 80526-2097, USA3
Colorado State University Veterinary Diagnostic Laboratory, 300 West
Drake Road, Fort Collins, CO 80523-1671, USA4
Animal Disease Research Unit, Agricultural Research Service, US
Department of Agriculture, 337 Bustad Hall, Washington State University,
Pullman, WA 99164-7030, USA5

Author for correspondence: Edward Hoover.Fax +1 970 491 0523. e-mail
ehoover@lamar.colostate.edu

Mule deer fawns (Odocoileus hemionus) were inoculated orally with a
brain homogenate prepared from mule deer with naturally occurring
chronic wasting disease (CWD), a prion-induced transmissible spongiform
encephalopathy. Fawns were necropsied and examined for PrP res, the
abnormal prion protein isoform, at 10, 42, 53, 77, 78 and 80 days
post-inoculation (p.i.) using an immunohistochemistry assay modified to
enhance sensitivity. PrPres was detected in alimentary-tract-associated
lymphoid tissues (one or more of the following: retropharyngeal lymph
node, tonsil, Peyer's patch and ileocaecal lymph node) as early as 42
days p.i. and in all fawns examined thereafter (53 to 80 days p.i.). No
PrPres staining was detected in lymphoid tissue of three control fawns
receiving a control brain inoculum, nor was PrPres detectable in neural
tissue of any fawn. PrPres-specific staining was markedly enhanced by
sequential tissue treatment with formic acid, proteinase K and hydrated
autoclaving prior to immunohistochemical staining with monoclonal
antibody F89/160.1.5. These results indicate that CWD PrP res can be
detected in lymphoid tissues draining the alimentary tract within a few
weeks after oral exposure to infectious prions and may reflect the
initial pathway of CWD infection in deer. The rapid infection of deer
fawns following exposure by the most plausible natural route is
consistent with the efficient horizontal transmission of CWD in nature
and enables accelerated studies of transmission and pathogenesis in the
native species.

snip...

These results indicate that mule deer fawns develop detectable PrP res
after oral exposure to an inoculum containing CWD prions. In the
earliest post-exposure period, CWD PrPres was traced to the lymphoid
tissues draining the oral and intestinal mucosa (i.e. the
retropharyngeal lymph nodes, tonsil, ileal Peyer's patches and
ileocaecal lymph nodes), which probably received the highest initial
exposure to the inoculum. Hadlow et al. (1982) demonstrated scrapie
agent in the tonsil, retropharyngeal and mesenteric lymph nodes, ileum
and spleen in a 10-month-old naturally infected lamb by mouse bioassay.
Eight of nine sheep had infectivity in the retropharyngeal lymph node.
He concluded that the tissue distribution suggested primary infection
via the gastrointestinal tract. The tissue distribution of PrPres in the
early stages of infection in the fawns is strikingly similar to that
seen in naturally infected sheep with scrapie. These findings support
oral exposure as a natural route of CWD infection in deer and support
oral inoculation as a reasonable exposure route for experimental studies
of CWD.

snip...

http://vir.sgmjournals.org/cgi/cont...80/10/2757
===================================

now, just what is in that deer feed? _ANIMAL PROTEIN_

Subject: MAD DEER/ELK DISEASE AND POTENTIAL SOURCES
Date: Sat, 25 May 2002 18:41:46 -0700
From: "Terry S. Singeltary Sr."
Reply-To: BSE-L
To: BSE-L

8420-20.5% Antler Developer
For Deer and Game in the wild
Guaranteed Analysis Ingredients / Products Feeding Directions

snip...

_animal protein_

http://www.surefed.com/deer.htm

BODE'S GAME FEED SUPPLEMENT #400
A RATION FOR DEER
NET WEIGHT 50 POUNDS
22.6 KG.

snip...

_animal protein_

http://www.bodefeed.com/prod7.htm

Ingredients

Grain Products, Plant Protein Products, Processed Grain By-Products,
Forage Products, Roughage Products 15%, Molasses Products,
__Animal Protein Products__,
Monocalcium Phosphate, Dicalcium Pyosphate, Salt,
Calcium Carbonate, Vitamin A Acetate with D-activated Animal Sterol
(source of Vitamin D3), Vitamin E Supplement, Vitamin B12 Supplement,
Riboflavin Supplement, Niacin Supplement, Calcium Panothenate, Choline
Chloride, Folic Acid, Menadione Soduim Bisulfite Complex, Pyridoxine
Hydorchloride, Thiamine Mononitrate, d-Biotin, Manganous Oxide, Zinc
Oxide, Ferrous Carbonate, Calcium Iodate, Cobalt Carbonate, Dried
Sacchoromyces Berevisiae Fermentation Solubles, Cellulose gum,
Artificial Flavors added.

http://www.bodefeed.com/prod6.htm
===================================

MORE ANIMAL PROTEIN PRODUCTS FOR DEER

Bode's #1 Game Pellets
A RATION FOR DEER
F3153

GUARANTEED ANALYSIS
Crude Protein (Min) 16%
Crude Fat (Min) 2.0%
Crude Fiber (Max) 19%
Calcium (Ca) (Min) 1.25%
Calcium (Ca) (Max) 1.75%
Phosphorus (P) (Min) 1.0%
Salt (Min) .30%
Salt (Max) .70%


Ingredients

Grain Products, Plant Protein Products, Processed Grain By-Products,
Forage Products, Roughage Products, 15% Molasses Products,
__Animal Protein Products__,
Monocalcium Phosphate, Dicalcium Phosphate, Salt,
Calcium Carbonate, Vitamin A Acetate with D-activated Animal Sterol
(source of Vitamin D3) Vitamin E Supplement, Vitamin B12 Supplement,
Roboflavin Supplement, Niacin Supplement, Calcium Pantothenate, Choline
Chloride, Folic Acid, Menadione Sodium Bisulfite Complex, Pyridoxine
Hydrochloride, Thiamine Mononitrate, e - Biotin, Manganous Oxide, Zinc
Oxide, Ferrous Carbonate, Calcium Iodate, Cobalt Carbonate, Dried
Saccharyomyces Cerevisiae Fermentation Solubles, Cellulose gum,
Artificial Flavors added.

FEEDING DIRECTIONS
Feed as Creep Feed with Normal Diet

http://www.bodefeed.com/prod8.htm

INGREDIENTS

Grain Products, Roughage Products (not more than 35%), Processed Grain
By-Products, Plant Protein Products, Forage Products,
__Animal Protein Products__,
L-Lysine, Calcium Carbonate, Salt, Monocalcium/Dicalcium
Phosphate, Yeast Culture, Magnesium Oxide, Cobalt Carbonate, Basic
Copper Chloride, Manganese Sulfate, Manganous Oxide, Sodium Selenite,
Zinc Sulfate, Zinc Oxide, Sodium Selenite, Potassium Iodide,
Ethylenediamine Dihydriodide, Vitamin E Supplement, Vitamin A
Supplement, Vitamin D3 Supplement, Mineral Oil, Mold Inhibitor, Calcium
Lignin Sulfonate, Vitamin B12 Supplement, Menadione Sodium Bisulfite
Complex, Calcium Pantothenate, Riboflavin, Niacin, Biotin, Folic Acid,
Pyridoxine Hydrochloride, Mineral Oil, Chromium Tripicolinate

DIRECTIONS FOR USE

Deer Builder Pellets is designed to be fed to deer under range
conditions or deer that require higher levels of protein. Feed to deer
during gestation, fawning, lactation, antler growth and pre-rut, all
phases which require a higher level of nutrition. Provide adequate
amounts of good quality roughage and fresh water at all times.

http://www.profilenutrition.com/Products/Specialty/deer_builder_pellets.html
===================================================

DEPARTMENT OF HEALTH & HUMAN SERVICES
PUBLIC HEALTH SERVICE
FOOD AND DRUG ADMINISTRATION

April 9, 2001 WARNING LETTER

01-PHI-12
CERTIFIED MAIL
RETURN RECEIPT REQUESTED

Brian J. Raymond, Owner
Sandy Lake Mills
26 Mill Street
P.O. Box 117
Sandy Lake, PA 16145
PHILADELPHIA DISTRICT

Tel: 215-597-4390

Dear Mr. Raymond:

Food and Drug Administration Investigator Gregory E. Beichner conducted
an inspection of your animal feed manufacturing operation, located in
Sandy Lake, Pennsylvania, on March 23,
2001, and determined that your firm manufactures animal feeds including
feeds containing prohibited materials. The inspection found significant
deviations from the requirements set forth in
Title 21, code of Federal Regulations, part 589.2000 - Animal Proteins
Prohibited in Ruminant Feed. The regulation is intended to prevent the
establishment and amplification of Bovine Spongiform Encephalopathy
(BSE) . Such deviations cause products being manufactured at this
facility to be misbranded within the meaning of Section 403(f), of the
Federal Food, Drug, and Cosmetic
Act (the Act).

Our investigation found failure to label your
swine feed with the required cautionary statement "Do Not Feed to cattle
or other Ruminants" The FDA suggests that the statement be
distinguished
by different type-size or color or other means of highlighting the
statement so that it is easily noticed by a purchaser.

In addition, we note that you are using approximately 140 pounds of
cracked corn to flush your mixer used in the manufacture of animal
feeds containing prohibited material. This
flushed material is fed to wild game including deer, a ruminant animal.
Feed material which may potentially contain prohibited material should
not be fed to ruminant animals which may become part of the food chain.

The above is not intended to be an all-inclusive list of deviations from
the regulations. As a manufacturer of materials intended for animal
feed use, you are responsible for assuring that your overall operation
and the products you manufacture and distribute are in compliance with
the law. We have enclosed a copy of FDA's Small Entity Compliance Guide
to assist you with complying with the regulation... blah, blah, blah...

http://www.fda.gov/foi/warning_letters/g1115d.pdf
==================================

snip...

posted here;

http://www.fda.gov/ohrms/dockets/dailys/03/Jun03/060903/060903.htm


2003D-0186
Guidance for Industry: Use of Material From Deer and Elk In Animal Feed


EMC 7
Terry S. Singeltary Sr.
Vol #:
1

2003D-0186
Guidance for Industry: Use of Material From Deer and Elk In Animal Feed


EMC 7
Terry S. Singeltary Sr.
Vol #:
1


http://www.fda.gov/ohrms/dockets/dailys/03/oct03/100203/100203.htm

Chronic Wasting Disease and Potential Transmission to Humans

Ermias D. Belay,*Comments
Ryan A.
Maddox,* Elizabeth S. Williams, Michael W. Miller,! Pierluigi
Gambetti,§ and Lawrence B. Schonberger*
*Centers for Disease Control and Prevention, Atlanta, Georgia, USA;
University of Wyoming, Laramie, Wyoming, USA; !Colorado Division of
Wildlife, Fort Collins, Colorado, USA; and §Case Western Reserve
University, Cleveland, Ohio, USA

Suggested citation for this article: Belay ED, Maddox RA, Williams
ES, Miller MW, Gambetti P, Schonberger LB. Chronic wasting disease
and potential transmission to humans. Emerg Infect Dis [serial on
the Internet]. 2004 Jun [date cited]. Available from:
http://www.cdc.gov/ncidod/EID/vol10no6/03-1082.htm

------------------------------------------------------------------------

Chronic wasting disease (CWD) of deer and elk is endemic in a
tri-corner area of Colorado, Wyoming, and Nebraska, and new foci of
CWD have been detected in other parts of the United States. Although
detection in some areas may be related to increased surveillance,
introduction of CWD due to translocation or natural migration of
animals may account for some new foci of infection. Increasing
spread of CWD has raised concerns about the potential for increasing
human exposure to the CWD agent. The foodborne transmission of
bovine spongiform encephalopathy to humans indicates that the
species barrier may not completely protect humans from animal prion
diseases. Conversion of human prion protein by CWD-associated prions
has been demonstrated in an in vitro cell-free experiment, but
limited investigations have not identified strong evidence for CWD
transmission to humans. More epidemiologic and laboratory studies
are needed to monitor the possibility of such transmissions.

snip...

Transmission to Other Animals

Concerns have been raised about the possible transmission of the CWD
agent to domestic animals, such as cattle and sheep, which may come in
contact with infected deer and elk or CWD-contaminated environments. If
such transmissions were to occur, they would potentially increase the
extent and frequency of human exposure to the CWD agent. In addition,
passage of the agent through a secondary host could alter its infectious
properties, increasing its potential for becoming more pathogenic to
humans. This phenomenon may have occurred with BSE when a strain of
scrapie, a possible original source of the BSE outbreak, changed its
pathogenic properties for humans after infecting cattle. However, the
exact origin of BSE remains unknown.

Although CWD does not appear to occur naturally outside the cervid
family, it has been transmitted experimentally by intracerebral
injection to a number of animals, including laboratory mice, ferrets,
mink, squirrel monkeys, and goats (1
,26
). In an
experimental study, the CWD agent was transmitted to 3 of 13
intracerebrally injected cattle after an incubation period of 22 to 27
months (27 ). The
susceptibility of cattle intracerebrally challenged with the agent of
this disease was substantially less than that observed after
intracerebral scrapie challenge: nine of nine cattle succumbed to
scrapie challenge after intracerebral injection (28
). In ongoing
experimental studies, after >6 years of observation, no prion disease
has developed in 11 cattle orally challenged with the CWD agent or 24
cattle living with infected deer herds (E.S. Williams and M.W. Miller,
unpub. data) (1 ).
In addition, domestic cattle, sheep, and goat residing in research
facilities in close contact with infected cervids did not develop a
prion disease.

[PLEASE NOTE, THIS HAS BEEN UPDATED TO AN ADDITIONAL 2 COWS AND ONE SHEEP,
making the total transmission of CWD to cattle at 5 and one transmission
of CWD to one sheep,
MILLER ET AL BSE-L...TSS]

Conclusions

The lack of evidence of a link between CWD transmission and unusual
cases of CJD, despite several epidemiologic investigations, and the
absence of an increase in CJD incidence in Colorado and Wyoming suggest
that the risk, if any, of transmission of CWD to humans is low. Although
the in vitro studies indicating inefficient conversion of human prion
protein by CWD-associated prions raise the possibility of low-level
transmission of CWD to humans, no human cases of prion disease with
strong evidence of a link with CWD have been identified. However, the
transmission of BSE to humans and the resulting vCJD indicate that,
provided sufficient exposure, the species barrier may not completely
protect humans from animal prion diseases. Because CWD has occurred in a
limited geographic area for decades, an adequate number of people may
not have been exposed to the CWD agent to result in a clinically
recognizable human disease. The level and frequency of human exposure to
the CWD agent may increase with the spread of CWD in the United States.
Because the number of studies seeking evidence for CWD transmission to
humans is limited, more epidemiologic and laboratory studies should be
conducted to monitor the possibility of such transmissions. Studies
involving transgenic mice expressing human and cervid prion protein are
in progress to further assess the potential for the CWD agent to cause
human disease. Epidemiologic studies have also been initiated to
identify human cases of prion disease among persons with an increased
risk for exposure to potentially CWD-infected deer or elk meat (47
). If such cases
are identified, laboratory data showing similarities of the etiologic
agent to that of the CWD agent would strengthen the conclusion for a
causal link. Surveillance for human prion diseases, particularly in
areas where CWD has been detected, remains important to effectively
monitor the possible transmission of CWD to humans. Because of the long
incubation period associated with prion diseases, convincing negative
results from epidemiologic and experimental laboratory studies would
likely require years of follow-up. In the meantime, to minimize the risk
for exposure to the CWD agent, hunters should consult with their state
wildlife agencies to identify areas where CWD occurs and continue to
follow advice provided by public health and wildlife agencies. Hunters
should avoid eating meat from deer and elk that look sick or test
positive for CWD. They should wear gloves when field-dressing carcasses,
bone-out the meat from the animal, and minimize handling of brain and
spinal cord tissues. As a precaution, hunters should avoid eating deer
and elk tissues known to harbor the CWD agent (e.g., brain, spinal cord,
eyes, spleen, tonsils, lymph nodes) from areas where CWD has been
identified.

snip...

see full text ;


http://www.cdc.gov/ncidod/EID/vol10no6/03-1082.htm



https://web01.aphis.usda.gov/regpublic.nsf/168556f5aa7a82ba85256ed00044eb1f/eff9eff1f7c5cf2b87256ecf000df08d



BY far, the biggest risk factor of clinical disease, is not from the oral consumption of cwd tainted deer and or elk, it's probably the least likely route. i would say inoculation i.e. not only from needle, but knife cut will gutting and cleaning. BUT from there, that person is exposed, once infected, even if never clinical, the risk factor from secondary friendly fire in the surgical medical, and or dental arena, is a real and disturbing threat. once a hunter exposted, even if never clilnical, risk exposing hundreds if not thousands via these arenas. ...thank you and good luck///


Terry S. Singeltary Sr.
P.O. Box 42
Baycliff, Texas USA 77518
TSS
6 Point
6 Point
Send Private Message
Posts:132

--
24 Oct 2007 11:56 PM  
Greetings again Wisconsin Hunters,


I finally put some old data together, that i think some of you will find most interesting.

like it or not, it's all related.

It's long, complicated, but as a lay person myself, I think you all need to know the rest of the story.



thank you, 
kindest regards, 

terry


NOW, let us look at another BSE ROUNDTABLE DISCUSSION by USDA et al in the
year 2003, please note the BSE science on IHC testing then, and then compare
to now, and then ponder those other 9,200 cattle of the infamous June 2004
BSE cover-up program, that did not have rapid testing or WB, just IHC, the
lease likely to find BSE/TSE ;


Completely Edited Version

PRION ROUNDTABLE


TME hyper/drowsy, INTER-SPECIES TRANSMISSION CWD and strain properties


page 19 of 62. ...tss


Dr. Detwiler: How would you explain that biochemically?

Dr. Bartz: When PRPC is converted to PRPSC, it's misfolded. There have to be
many different stable energy states for the misfolded protein. I would
hypothesize that mink PRPSC, when it interacts with hamster PRPC, it can
fold into several different stable PRPSC molecules. So initially you get the
mink interacting with hamster, and then you get a strain produced. I think
early on in those first few rounds of replication, whatever strain is
produced is probably going to be the predominant one because it has a jump
start on the rest of them. On this really complicated western blot, we are
mixing hyper and drowsy at known ratios, and basically we can mimic these
effects. So it really is the ratio of hyper/drowsy produced by interspecies
transmission that's causing this sort of effect.

To summarize inter-species transmission, we have PRPSC interacting with the
new host PRPC molecule to change it into PRPSC. We think that, in certain
instances, multiple strains can be produced. Intra-species transmission
results in competition between these strains and eventual emergence of a
predominant strain. We think the initial ratio of strains is important and
affects this whole passage history. Probably the replication properties of
strains is important. We think that drowsy is the predominant strain
produced, but hyper replicates so much faster, it has an advantage.

One really important thing I want to point out here is that strain
properties can change upon inter-species transmission. Chronic wasting
disease doesn't cause disease when you passage it in a hamster, but if you
passage CWD into ferrets, and then take that ferret passage tissue, it can
cause disease in hamsters. So inter-species transmission can expand the host
range. Also, with the hyper and drowsy, the more hamster passages you do, if
you back-passage the inoculum into mink, hyper loses pathogenicity for mink
quite quickly, where drowsy retains pathogenicity for mink.
The important point I want to make is that, when you're assessing
inter-species transmission and you do a transmission study and it's
negative, you have to be careful in saying it's negative for the strains you
looked at. With this example, it's clear you could take hyper TME, inoculate
mink, and they don't come down with the disease, so you might assume hamster
prions don't cause disease in mink. That strain doesn't. You have to be
careful assessing negative transmission results based on what's known about
the strain properties.

The last thing I want to talk about is persistence. This would be the case
where PRPSC interacts with the host PRPC and you get really slow
replication. The replication agent is so slow that the animal dies of old
age before clinical signs can occur.

This study is from Rick Race at NIH, transmitting hamster PRPSC into mice.
He collected animals post-infection out to 782 days. None of these animals
had clinical signs of prion disease, which is consistent with everything we
knew about this species barrier. But when he went back and looked for PRP
residue in these animals, he couldn't detect hamster PRP residue, but in a
few of these animals with very long times post-infection, he could detect
mouse PRP residue.

When he did the second passage, into either hamsters or mice, clinical signs
appeared in the second passage. The point is that first inter-species
transmission may not cause clinical signs, but you still can get replication
to agent that subsequently, when you passage it into the same host species,
results in clinical signs of the disease.

In the cell-free conversion studies, hamster PRPSC could not convert mouse
PRPSC. Every sort of assay has limitations. The cell-free conversion said it
couldn’t replicate. It could, but it was so slow and so long that the assay
could not detect them.

I think persistence is very important. If you have inter-species
transmission occurring and it doesn't cause clinical disease, and if you
take the tissue and keep feeding it to that same host species, you’re going
to get amplification and potentially emergence of the disease.

Is PRPSC shed in the environment? I have no idea. Terry can talk about that.
Does PRPSC survive in the environment? The studies on deer PRPSC have not
been done, but if deer PRPSC behaves like any other PRPSC, yes it can
survive in the environment. Can PRPSC reach a new host species? I don't
know. If they share common pastures, it's a possibility. Can PRPSC get to
the central nervous system? Clearly, cattle are susceptible to oral
infection, so that's yes. Can deer PRPSC convert cattle PRPC to the host
PRPSC? Self-reconversion experiments would say yes, but very inefficiently.
But really, the gold standard is the transmission studies, and there are two
of these ongoing right now. One is at the USDA at Ames, and this is
intra-cerebral inoculation. They are susceptible to IC infections. This
means that once the agent reaches the brain, it can cause disease, but
obviously in the field, that's not the natural route. Beth Williams is doing
some oral infection studies, but I'm not sure of the status of those.

Dr. Thornsberry: So what you’re saying is that, inter-cerebrally, we can get
CWD/PRPSC conversion, but that has not occurred, to anyone's knowledge, in
the natural route.

Dr. Bartz: Right. IC inoculation is used because it has a short incubation
period. It only tells us that replication can occur once the agent reaches
the brain.

Dr. Thornsberry: Let's hypothesize that I had some cattle on the eastern
slope and they were in the same pasture with elk with CWD. If a cow had been
exposed to the PRP Scrapie and it did develop disease four years later,
would that look like BSE? Would there be a way to determine if it came from
CWD?

Dr. Bartz: The IC studies in cattle indicate it does not look like BSE. The
clinical signs of the IC/CWD cattle are more like downer cattle, and not
aggressive. As far as finding the source of a bovine TSE, the gold standard
is the lesion profile study where you take cattle tissue and inoculate it
into mice with appropriate controls, wait until the mice come down, and do
the lesion profiling.

Dr. Thornsberry: There were two cases in Japan, but they indicated that
tissue was not classical BSE as seen in Europe. Have you heard anything
about that?

Dr. Bartz: This is based on differences on migration and the glycoform ratio
of PrPSc.

Dr. Detwiler: Canada based that question because the herd that that animal
came from was in Saskatchewan, in an area with CWD. That was one of the
questions they faced right off the bat: is this BSE or is this some kind of
transmission from CWD-infected elk in the area? Not only the histological
lesions were classic BSE lesions, but clinically it's very difficult because
if you miss the other behavioral changes, which this owner did. It was
someone who had been a catfish farmer. He missed the early signs. The animal
presented to slaughter as a down animal, non-responsive. Clinically it
looked like just a down cow, but they did send that on to the United Kingdom
and they did do some comparison glycoform patterns. Those haven’t been
validated, but at least on preliminary work, it looked like classical BSE.

The Japanese case was a 23-month-old which was born in October. Their
scientists say the western blot pattern looked different. The most recent
case, which was a 21-month-old, looked more like classic BSE. The Italian
cases were older animals, 15 and 16 years of age. But is it methodology? Is
it really standard? That has to be sorted out before too much can be said.

Dr. Bartz: Glycoform ratio is dependent on very technical matters, what
antibodies you use, what detection system you use. Those have to be
standardized before you can start comparing from one lab to another.

Dr. Detwiler: The Japanese used a western blot they'd developed in their
lab. It can't be compared across laboratories.

Dr. Bartz: That's problematic.


snip...


snip...page 5 of 62


Dr. Prusiner made some comments about Parkinson's disease. He said a protein
being improperly handled in the substantia nigra cells is what causes
Parkinson's disease because it causes a decrease in dopamine production. His
theory is that Parkinson’s disease is a prion-related problem, that
Parkinson's disease is the direct result of those cells being killed because
of prion accumulation that he believes is a familial transfer.


"Can it be transmitted by blood transfusions?" His answer is that We don't
know.


We believe that ALS, or Lou Gehrig's disease, is a prion-related disease.


The last question that was asked of Dr. Prusiner was a simple question. The
person said, "Dr. Prusiner, do you eat meat?" He answered immediately "Not
in Europe." He was asked to elaborate, and he said these prion-related
diseases are all over Europe. He said wherever you go, if you eat meat, you
have the potential of picking them up. He believes the prions are in the
muscle tissue. He does not believe they're just in the spinal column.


My son is an M.D. and they are getting a lot of information on these
prion-related diseases and most of it is coming from Dr. Prusiner. The
medical community has an understanding about prion-related diseases that's
much different from that of the veterinary community, from what I can
determine. ...


snip...



USDA 2003

We have to be careful that we don't get so set in the way we do things that
we forget to look for different emerging variations of disease. We've gotten
away from collecting the whole brain in our systems. We're using the brain
stem and we're looking in only one area. In Norway, they were doing a
project and looking at cases of Scrapie, and they found this where they did
not find lesions or PRP in the area of the obex. They found it in the
cerebellum and the cerebrum. It's a good lesson for us. Ames had to go
back and change the procedure for looking at Scrapie samples. In the USDA,
we had routinely looked at all the sections of the brain, and then we got
away from it. They've recently gone back.
Dr. Keller: Tissues are routinely tested, based on which tissue provides an
'official' test result as recognized by APHIS
.

Dr. Detwiler: That's on the slaughter. But on the clinical cases, aren't
they still asking for the brain? But even on the slaughter, they're looking
only at the brainstem. We may be missing certain things if we confine
ourselves to one area.


snip.............


Dr. Detwiler: It seems a good idea, but I'm not aware of it.
Another important thing to get across to the public is that the negatives
do not guarantee absence of infectivity. The animal could be early in the
disease and the incubation period. Even sample collection is so important.
If you're not collecting the right area of the brain in sheep, or if
collecting lymphoreticular tissue, and you don't get a good biopsy, you
could miss the area with the PRP in it and come up with a negative test.
There's a new, unusual form of Scrapie that's been detected in Norway. We
have to be careful that we don't get so set in the way we do things that we
forget to look for different emerging variations of disease. We've gotten
away from collecting the whole brain in our systems. We're using the brain
stem and we're looking in only one area. In Norway, they were doing a
project and looking at cases of Scrapie, and they found this where they did
not find lesions or PRP in the area of the obex. They found it in the
cerebellum and the cerebrum. It's a good lesson for us. Ames had to go
back and change the procedure for looking at Scrapie samples. In the USDA,
we had routinely looked at all the sections of the brain, and then we got
away from it. They've recently gone back.

Dr. Keller: Tissues are routinely tested, based on which tissue provides an
'official' test result as recognized by APHIS
.

Dr. Detwiler: That's on the slaughter. But on the clinical cases, aren't
they still asking for the brain? But even on the slaughter, they're looking
only at the brainstem. We may be missing certain things if we confine
ourselves to one area.


snip...



Environmental Contamination
 We're finding out on a smaller scale with CWD and Scrapie that
environmental contamination is becoming a big concern.  It's something we’ve
never had to deal with.  Even with anthrax, we never had as much interest
like we’re seeing with prions.  If potential environmental contamination is
a problem, then how do you safely dispose of suspect animals?  It takes a
lot of time and  communication with the health department and the landfill
owners in trying to get everybody to a comfort level.  Legal concerns do
need to be addressed.
 It is a ripple effect.  You may have feedlot contamination, and then you
have all the water that ran off.  In many of these large feedlots, they're
using that water run-off to irrigate fields nearby.
Unfortunately, perception often wins over science in these situations,
whether it is a real risk or not!
 Here's an example of  a situation we dealt with in our state.  A wild deer
was shot in a state that has areas endemic with CWD.  This animal was
harvested just outside of that area.  We received a call that this animal
had tested positive.  The brain had been pulled in that state, but the
carcass was allowed to leave with the hunter before the results were
reported.  By that time, the hunter had taken the meat to a ND processor for
final processing and packaging.    Then we had to tell the processing plant
that they'd had a CWD-positive animal go through their facility and we gave
them advice on a recommended cleaning process.

Dr. Bartz:  What is the recommended cleaning process?

Dr. Keller:  There is no ‘officially approved’ disinfectant for surface
cleaning, but strong chlorine solutions, sodium hydroxide or Environ LPH
have been recommended.

Dr. Thornsberry:  Steam cleaning is part of the process.

Dr. Keller:  There has been discussion about the potential approval of
Environ LPH for surface cleaning.

Dr. Detwiler:  Rick Race has a publication coming out on the different
versions of the LPh.  The company's supposed to come back out with the old
formulation.  It's not as corrosive.

Dr. Spraker:  When you use it, hold your breath.

Dr. Keller:  Another concern I have that's been talked about today already
is ‘what is the infectious dose’ and how does that affect the incubation
period?  We have been focusing on animals, but I know that human health
concerns usually supercede animal health concerns in our state.
 What's at stake?  Supposedly an estimate came out of Canada saying they
were still losing $10 million per day.  Extrapolating that to the number of
cattle in our country, you could be looking at up to $50 million a day.  I
think that's a very conservative estimate.
 Price of human life:  should we be talking money when we're talking about a
disease with so many unknowns yet about its pathogenicity and infectivity?
It appears we can’t talk about zero tolerance anymore, because prions are
here in many forms (normal and abnormal). And we will not ever make all
prion diseases just ‘go away’, but we do need to put all the effective
mitigating factors in place that we can to decrease the introduction and
amplification of prion diseases.  We need to look at what we can do to
‘prevent’ and then also be ready to deal with the disease if needed.

Dr. Detwiler:  I went through one of the biggest cull cow plants up in
Canada.  They have to do the full SRM—the vertebral column and everything.
I asked what it cost to implement that and it's about two cents per pound.
That's really not much when you consider the ramifications.

Dr. Keller:  If there are going to be costs, they usually trickle down in
the cattle business to the producer.  But there's probably not a producer
who wouldn't spend a few cents to save his industry and assure his customer
about the safety of the final product.  From the estimates I’ve read, I don’
t think cost is as big an issue as some would like us to believe.

Dr. Thornsberry:  If the USDA decides to open the border the first of March
with no restrictions, does North Dakota have the authority to turn away
Canadian cattle?

Dr. Keller:  We cannot stop animals coming through our state, but we could
prevent them from unloading in North Dakota.

Dr. Thornsberry:  So some state along the border could put a stop to cattle
coming into the state to stay.  The interesting thing about Missouri, where
I live, is that Canada will not allow us to export any cattle.  We are a
southern state with endemic Anaplasmosis and we have potential blue tongue
virus infection in our cattle herd.  They have all these restrictions based
on those two disease control programs, but yet the government is going to
force us to take cattle from Canada.  Our state veterinarian is under the
impression that, if they open the border, there's no way we can restrict
them coming in.  In Missouri, it's a federal rule.  My understanding was
that the state veterinarian could make a ruling that because of disease
control, nothing could come in to Missouri.

Dr. Keller:  I'm really not the person to answer this from a legal
perspective, but we've always been counseled that state laws could be more
restrictive than federal laws.

Dr. Detwiler:  If you recall some of the conference calls where the states
had more restrictive rules, the federal government said they would challenge
those in court.

Dr. Thornsberry:  California has always been able to do that for years, and
everybody seems to abide by it.

Dr. Detwiler:  Our attorney says that's wrong; they can't.  I've heard it
both ways.  I've heard it from the federal side that yes, you can be
restrictive on some diseases, and then they say no on others.

Dr. Thornsberry:  I'd like Dr. Detwiler and Dr. Keller to comment on the
Harvard risk assessment.  The USDA is kind of using that as a carte blanche
for opening up the border to Canada, and I think they've already made their
mind up.  Yet the Harvard risk assessment, if you get into the depth of it a
little bit, says that yes, there is an inherent risk of bringing
prion-related diseases into this country if the border is opened.  Nobody
can say that risk is not there.  What we’re saying is if it does come in, we
have enough safe-guards in place to contain it.  That one case in Japan
created the loss of 40% of their demand for beef products overnight, and it
lasted for several months until they instituted the program to test every
animal.  I'm not sure we'd have that much of a ramification.  However, just
saying we can identify the case is not sufficient.  Our government should be
more oriented toward preventing a case from ever coming rather than letting
us figure out how to deal with it once it gets here.
 I have a meat plant in Missouri and I have a zero tolerance for Listeria
spp., for E. coli O157:H7, and Salmonella, which are sometimes fatal to
children and older people.  Everyone else survives.  If they find that in my
plant, I'm shut down until I can prove to USDA that it's not there.  And yet
we're going to open up our borders and allow a disease to come through
that's 100% fatal if a human being should contract the disease.  There's an
inconsistency in the regulations concerning these animal diseases.  One of
the comments we're probably going to make to the USDA as a veterinary group,
is that the Harvard risk assessment is fine, but once one case is here and
identified, we now have potentially seeded large areas with prions.  And we
know they exist forever.  How should the livestock industry view the Harvard
risk assessment?

Dr. Keller:  I think we need to look at the big picture.  There are bits and
pieces that people quote from the HRA, but even if you look at the executive
summary of the update, there are significant things it says.  It's true that
the United States is robust and resistant.  If the disease is introduced, it
will go away because of the system.  Other countries have demonstrated that
by feed bans.  But it also says we're not totally resistant to the
introduction, and that if you look at the possible scenarios, it could
potentially be a 20-year decline of the agent.  It won’t be like it's here
today and gone tomorrow.  That's one thing that's very significant—to say
that you have to expect a 20-year period to eliminate the agent.
 The other thing is that there are weaknesses in the system, and it's so
important that we don't have high risk SRMs being introduced into our food
supply, because if the agent is in the United States, however small there's
the perception of a potential public health risk.  And, the HRA indicated
that there is definitely a potential for  further transmission to animals if
there are leaks in the feed ban.
 The most significant item is that, in the worst-case scenario, if the agent
comes from Canada, it's below the level of detection of the USDA's current
surveillance system.

Dr. Thornsberry:  That's very significant.  From an epidemiological
standpoint, it blares out.  It asks, “Why would you make this decision with
the current level of surveillance that we have in this country?”

Dr. Detwiler:  To me, the concern is to look at what minimum risk is.
Unless it's further defined, how do you look at all the other countries?
Some have never been evaluated.  Where do they fall in the scheme of things?
Those are concerns I have.  We also really need to be aware that the risk
set a precedent for the US.

Dr. Keller:  We know we're at risk for having our own case of BSE here in
the US, but I don't think two wrongs make a right.  We need to be proactive
in getting something done to identify animals as they come in, if they do
come in.  We need to be able to track animals that are considered minimal
risk.  We need to hold all countries, including ourselves, to a standard to
determine prevalency of all diseases, including prion diseases.  I don’t see
why we would accept animals from other countries until that is done!  It's
easy to say you're free of something if you're not adequately testing for
it.  We've seen that happen with other diseases.

Dr. Detwiler:  I'll play devil's advocate.  If the US found a case tomorrow,
what would we ask of the world?  I think that's valid to ask.  It's valid to
turn the mirror back on yourself.

Dr. Thornsberry:  I guarantee you that we would immediately have individual
animal ID and it wouldn’t be two years later.

Dr. Keller:  And it probably would not be ID that's initially acceptable to
the industry.  Producers need to realize that if they don’t get involved, it
will become mandatory and then they will no longer have the opportunity for
producer input.

Dr. Thornsberry:  It's almost in the process of being mandated now.  I sat
on that task force.  We're just months away.  July 1, 2004, we're supposed
to issue premise IDs to every farm in the nation.  By the first of January,
2005, we're supposed to have some sort of mandatory identification in place,
probably electronic.  Right now they have no funds to do that, nor have they
been given permission, but they say that, because of disease control, they
have the right to mandate this program now.
 The other issue that comes up is the concept of country-of-origin labeling.
At the time the Canadian BSE cow was identified, I did some investigation at
Sterling, Colorado, and a few other packing plants that were taking in
Canadian beef.  There were over 500,000 pounds of Canadian-bred meat out of
two or three different plants in the Colorado area that were in the food
chain and could not be identified.  Once the animal was brought into the
plant and slaughtered, that carcass just went right down the chain with all
the others.  There was no way to identify where that meat went.  If the
government at that time had wanted to put a retention on Canadian meat,
they'd have had to retain a whole bunch of our meat at the same time. That's
been one of the strong arguments for country-of-origin labeling, at least to
maintain some ability to track that carcass past the point that it's
slaughtered.  Right now we don’t have that capability.  Once it receives
that USDA stamp, it's over.  That's an issue that will have to come into
play for disease control concerns.
 We already have, as of the first of July, a country-of-origin labeling
program for Japan and South Korea to guarantee to them that no Canadian meat
will make it into their country through our system.  But our consumers don’t
have the same choice.  I think that's a travesty in our industry that we can
’t offer American consumers a choice.  If we can offer it to Japan's
consumers and South Korea's consumers, it seems only logical we should be
able to offer it to US consumers, but we do not.

Dr. Spraker:  Does the US import a lot of meat from Argentina and South
America?

Dr. Thornsberry:  They don’t right now.  They do import a lot of cooked
product.  They have so much foot and mouth disease.  I've been in a lot of
those countries and I don't see that they'll ever have that problem under
control.

Dr. Keller:  We've had many foreign exchange students at out ranch, and
several from South America. They have insinuated that there is a great deal
of unrestricted movement between South American  countries.

Dr. Thornsberry:  I spent time in Venezuela on a ranch with 50,000 mother
cows and they couldn’t tell you where those cows were at any one time,
period.  They have computers and they keep track of things, but the level of
technology is much more primitive.

Dr. Keller:  Communication indicated that political pressure kept Argentina
animal health officials from reporting the FMD case.  It was actually
producers who encouraged reporting their own FMD case.  I am beginning to
wonder if in this country, too, it's going to take industry and producers to
encourage our officials to do the right thing for US animal health and US
agriculture.

Dr. Thornsberry:  One group of people we haven't discussed today is the
consumers in this country.  Over 90% of the meat in the United States is
purchased by women.  I don't know if the USDA has allowed any input from
consumer groups on this subject.

Dr. Keller:  We should not needlessly scare the public, but there is a
responsibility to take additional precautions in processing if needed.  When
the education and research information does catch up with the buying  and
consuming public, they're going to want to know what’s been done to address
concerns regarding SRMs and AMR meat.

Dr. Spraker:  With CWD, so many men will turn a head in and say they can't
bring the meat in the house because the wife wants it tested first.

Dr. Detwiler:  We get asked all the time why does the public react so
volatily to this? and the only thing that I can figure is that you can't
cook it away, you can't detect it with certainty in the live animal, you can
’t test the product for it.  So the consumer relies on the industry and the
government.  It's an issue where the consumer lacks control.  With E. coli,
they know: if you cook it right and feed it to your kids, it's going to be
okay.  They have some control.

Dr. Bartz:  With many infectious diseases, in two weeks, you’re over it and
you get on with your life.  But if you consume BSE-potentially-tainted beef,
you're going to be worried for the rest of your life.

Dr. Thornsberry:  In 1994, I spent a month in Spain, Portugal and France,
and I know I ate beef when I was there..

Dr. Detwiler:  You ate mutton.

Dr. Thornsberry:  I ate mutton, I ate pork, I ate pig ears.  I ate a lot of
traditional Spanish and Portuguese meat, and I ate beef.  And Portugal and
France have had numerous cases of BSE.  So have I been exposed to BSE?  My
son went with me.

Dr. Spraker:  We know how many deaths occur from alcohol and we know how
many people die from chewing tobacco.  But we're not afraid of those.  Why
not?

Dr. Keller:  It's likely because the use is intentional with alcohol and
tobacco.

Dr. Detwiler:  The risk communicators will tell you that if you make the
choice and take the risk, there's a different kind of perception.

Dr. Thornsberry:  This has been an excellent round-table.  I know I've
learned a lot…

[tape change]

  …There does not seem to be very much risk of CWD being transferred to
other species except cervids.  It hasn't been seen and the chances are not
great, although with any prion disease, the risk is possible.

Dr. Detwiler:  If we let it go unchecked, we increase the biological load.
I think it's prudent for the government to keep the biological load down.

Dr. Spraker:  Because we don’t know if, 10 years from now, there will be an
emergence of a new strain of CWD with a totally different host range.

Dr. Thornsberry:  These prions are infective.  That's the one thing that
we've come to a common knowledge of here today, that's not being released by
some of our cattle organizations.  They are pushing the idea that a prion
disease is an end-stage disease: an animal gets it, he dies, and that's the
end of it.  Being that these prions survive in the environment basically
forever and there's no way to disinfect them, no way to destroy them, no way
to get rid of them, the potential for BSE to be infective to any variety of
animals does exist.  We know that certain risk factors are much more
inherent than others, but it is an infectious disease.
I have a small feed mill and there's no telling how many people have asked
me if they can feed dog food to their show steers to increase the fat in
their diet, not understanding that most dog food has some level of meat and
bone meal in it.

Dr. Spraker:  And people eat dog food and cat food.

Dr. Thornsberry:  The association of dog food manufacturers has fought
against a meat and bone meal ban and they don't even want to list it in
their contents.  They believe if it's listed, people will quit buying it.
You have to fill out paperwork to buy fish food with meat and bone meal, but
I could buy a whole truck load of dog food with meat and bone meal in it and
feed it to my cattle.  It is illegal.
 There are some SRMs that are out there in this industry. Blood meal is one
of my favorite concerns. We have a lot of big corporations that are using
beef tallow in diets to increase the fat content in dairy rations.  They're
doing it as much as a pound per cow per day.

Dr. Detwiler:  The thing that worries me is that those SRM’s are also in
calf rations.  The calves could have more susceptibility.  I worry about the
increased amount of blood going into calf rations.

Dr. Thornsberry:  The concept of the prions making it through the system is
very significant.  Another issue we haven't discussed is the people taking
the cleanings out of poultry barns and scattering them on their pastures for
fertilizer.  The prions don't ever go away, and the cattle eat the pasture
down to the ground.  How many prions are they being exposed to?  There are a
whole lot of issues there to deal with.  Poultry manure can be composted and
used as fuel and other things.  It has alternative uses.
 The swine industry has made better strides in telling people not to feed
hog food to cattle, although I know it still goes on in my area.
Fortunately, most of the swine finishing diets don't have any bone meal.
 There are some things we need to do in our country to do a better job of
surveillance.  The veterinary industry needs to be proactive.  I hope some
of those SRMs are identified and the livestock producers are made aware of
them and we get the information out:  Don’t be feeding what's left over from
your hog feed bin to your cattle.

Dr. Keller:  Is there an economic analysis being done on the current
situation in Canada, that could be used as an educational tool to encourage
immediate consideration of other ways to utilize high risk product?

Dr. Detwiler:  They are doing something on economic alternatives and what
the costs would be.

Dr. Thornsberry:  And there are a number of them.  Any fat-soluble product
has a number of possibilities and we've identified several of them today.
 So here's the plan.  These proceedings will be made available to the
American Association of Bovine Practitioners, the Academy of Veterinary
Consultants, to veterinary schools and whoever would like to have them.  I
will also try to translate and summarize the material into some sort of
publication we can give to the livestock industry.  They obviously don't
want to know all about PRPC and all those things, but there is information
in these presentations that they need to know.
 You may want to add something that you didn’t say that you think might be
pertinent.  A lot of discussions like this have taken place, but nothing has
been made available to the livestock industry—nothing on a practical level
that a livestock producer can understand about the potential for CWD
spreading, etc.  They do not understand what BSE is.  I hope, from this, we
can give our producers a firm grasp of what the disease is and also let them
know how they can participate in the process.  And if we do that, we will
have accomplished what I wanted to do with this program today.


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





FULL TEXT;


Completely Edited Version
PRION ROUNDTABLE


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


2005


National Veterinary Services Laboratory (NVSL) Immunohistochemistry (IHC)
Testing Summary

The BSE enhanced surveillance program involves the use of a rapid screening
test, followed by confirmatory testing for any samples that come back
"inconclusive." The weekly summary below captures all rapid tests conducted
as part of the enhanced surveillance effort. It should be noted that since
the enhanced surveillance program began, USDA has also conducted
approximately 9,200 routine IHC tests on samples that did not first undergo
rapid testing.


http://www.aphis.usda.gov/lpa/issue...sults.html



The roundtable presentations and discussions
were recorded. A transcript will be made available
to the Academy of Veterinary Consultants, the
American Association of Bovine Practitioners, and
the Colleges of Veterinary Medicine throughout the
United States and Canada. A condensed version
translated for the livestock industry will be made
available to educate livestock producers about
prion related diseases.


http://www.r-calfusa.com/Newsletter...anuary.pdf



BSE BASE MAD COW TESTING TEXAS, USA, AND CANADA,  A REVIEW
OF SORTS
 
 
 
 
MADCOW USDA the untold story
 
 
 
 
MADCOW USDA the untold story continued
 
https://www.blogger.com/comment.g?blogID=6472149427883113751&postID=4829467681293855400
 
 
 
ABSTRACTS SPORADIC CJD AND H BASE MAD COW ALABAMA AND TEXAS
SEPTEMBER 2007
 
Date: Mon, 24 Sep 2007 21:31:55 -0500
 
 
 
I suggest that you all read the data out about h-BASE and
sporadic CJD, GSS,
blood, and some of the other abstracts from the
PRION2007. ...
 
 
 
 
 
 
 
 *** PLEASE READ AND UNDERSTAND THE RAMIFICATIONS OF
THIS !!! THE PRICE OF
POKER INDEED GOES UP. ...TSS
 
USA BASE CASE, (ATYPICAL BSE), AND OR TSE (whatever they
are calling it
today), please note that both the ALABAMA COW, AND THE
TEXAS COW, both were
''H-TYPE'', personal communication Detwiler et al
Wednesday, August 22, 2007
11:52 PM. ...TSS
 
 
 
 
 
 
NOR-98 ATYPICAL SCRAPIE USA UPDATE AS AT OCT 2007
 
Tuesday, October 9, 2007
NOR-98 SCRAPIE UPDATE AUGUST 31, 2007 RISES TO 5 DOCUMENTED
CASES
 
 

Transmissible Mink Encephalopathy TME
 
http://transmissible-mink-encephalopathy.blogspot.com/
 
 
 
TME hyper/drowsy, INTER-SPECIES TRANSMISSION CWD and strain
properties
 
 
 
https://www.blogger.com/comment.g?blogID=37955408&postID=116577315153980667
 
 

PLEASE NOTE IN USA CJD UPDATE AS AT JUNE 2007, please note
steady increase
in  ''TYPE UNKNOWN''. ...TSS
 

1 Acquired in the United Kingdom; 2 Acquired in Saudi
Arabia; 3 Includes 17
inconclusive and 9 pending (1 from 2006, 8
from 2007); 4 Includes 17 non-vCJD type unknown (2 from
1996, 2 from 1997, 1
from 2001, 1 from 2003, 4 from 2004, 3
from 2005, 4 from 2006) and 36 type pending (2 from 2005, 8
from 2006,   ***
26 from 2007)
 
 
 
http://www.cjdsurveillance.com/pdf/case-table.pdf
 
 
 
Terry S. Singeltary Sr.
P.O. Box 42
Bacliff, Texas USA 77518

TSS
6 Point
6 Point
Send Private Message
Posts:132

--
25 Oct 2007 12:02 AM  
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

PRION ROUNDTABLE


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


page 22 - 36. ...tss


CHRONIC WASTING DISEASE

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.

snip...


FULL TEXT;


Completely Edited Version
PRION ROUNDTABLE


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



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

The roundtable presentations and discussions
were recorded. A transcript will be made available
to the Academy of Veterinary Consultants, the
American Association of Bovine Practitioners, and
the Colleges of Veterinary Medicine throughout the
United States and Canada. A condensed version
translated for the livestock industry will be made
available to educate livestock producers about
prion related diseases.


http://www.r-calfusa.com/Newsletter...anuary.pdf


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