LET'S TALK ABOUT CHRONIC WASTING DISEASE

I have created this thread in light of the recent interesting posts regarding Chronic Wasting Disease (CWD), found on an infamous posting.

The topic is certainly interesting enough to discuss on its own, sans the B.S.

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I'll kick us off...

ETIOLOGY
Etiology is the branch of medical science concerned with the causes and origins of diseases.

The etiology of CWD and other spongiform encephalopathies are being investigated at numerous research institutions worldwide, my medical school being one of them.

DNA & RNA
Bacteria, viruses, fungi, and protozoa all have something in common: NUCLEIC ACIDS (either DNA or RNA).

These "bugs" depend on nucleic acids for their proliferation and survival. Some of the chemicals we refer to as "antibiotics" kill these disease causing organisms (pathogens) by disrupting their ability to use DNA or RNA. Thus, killing the pathogen.

CELL WALLS
Unlike humans, BACTERIA and FUNGUS lack a skeleton, and therefore depend on shell-like structure called a cell wall for their support(much like plants have).

Since humans lack cell walls, many "antibiotics" target the CELL WALL of the pathogen and either break it down or prevent its synthesis. Thus, killing the pathogen.

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Please bear with me, this discussion DOES have a point...
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PRIONS
Prions have been defined as: "Small proteinaceous infectious particles which resist inactivation by procedures that modify nucleic acids."

You say, "huhhh?" Simply stated, prions are proteins that infect a host, and they cannot be deactivated by antibiotics using the same methods mentioned above. VERY SCARY!!

"If it ain't alive, you can't kill it!"

This means, that at present, there is no magical pill that can be swallowed and ingested to kill a prion.

Only the body's own EXTREMELY complex and SELECTIVE immune system is able to recongize and destroy SPECIFIC proteins.
-For example, our immune system is able to reject an organ transplant from another human (eventhough it is primarily the same tissue) based soley on a couple of differences in proteins found on the donor kidney cells.

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ABOUT PRIONS
It was a considerable surprise to the scientific community that a PROTEIN can transmit an infectious disease.

These PRION diseases are called spongiform encephalopathies because of the appearance of large voids found in the brain during an autopsy.

ANIMAL PRION DISEASES
Some specific examples of these diseases in mammalian species other than man are:

- Scrapie : sheep
- TME (transmissible mink encephalopathy): mink
- BSE (bovine spongiform encephalopathy): cows

and of course...
- CWD (chronic wasting disease): deer/elk

HUMAN PRION DISEASES
As mentioned in the other thread, humans are susceptible to prion diseases as well...

- CJD : Creutzfeld-Jacob Disease
- FFI : Fatal familial insomnia
- GSS : Gerstmann-Straussler-Scheinker syndrome
- Kuru
- Alpers Syndrome

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SIDE NOTE :
Kudos to whoever mentioned KURU in New Guinea! (pun intended) In the 1950s it was a disease found among tribes in the Fore highlands who, for religious reasons, were grinding up dead relative�s brains, making a pale gray soup, heating it up, and eating it! MMMmmmmm... Just like mama's cookin'!!

Someone on the other thread mentioned that many animals (specifically, male lions) practice cannibalism and they do not seem to be affected. Great observation!... and one that was also made by the researchers studying KURU in New Guinea.

The researchers noticed that other tribes practicing the same ritual did not develop the disease. It was suspected that KURU developed in a single deceased tribal member and it was spread throughout the tribe (since brain tissue is highly infective). This was explained to them, they stopped the practice for some time, and the incidence rapidly declined.
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CJD
According to the Centers for Disease Control and Prevention, the incidence of sporadic CJD (Cruezfeld-Jacob disease) is about 1 PER million PER year. It is estimated that 1 in 10,000 people are infected with it at the time of death.

There may very well be a link from this to CWD. It is being heavily investigated.

SUMMARY
There is a lot of interesting information regarding the actual mode of transmission and mechanism for absorption of prions into the nervous system, but that is way to deep for this thread. Hell, if you made it this far� I�M IMPRESSED!!

So here�s what I think�

1) ORIGIN = Chronic Wasting Disease (and other spongiform encephalopathies) begin as a spontaneous Mendelian genetic mutation in a single animal (just like the spontaneous cases reported with CJD resulting in one (1) person per million per year).

2) TRANSMISSION = in the case of animals in close captive proximity or animals eating their own flesh (including cannibalistic tribes) the highly infective proteins (PRIONs) are passed to one another.

SPONTANEOUS MUTATION ---then--- CAPTIVITY/CANNIBALISM ---then--- INFECTION

Breading or holding deer/elk in captivity as well as selectively breading larger antlered animals (which may make them less resistant to genetic mutation) fit well into this model.

What do you guys/gals think?

[ 08-14-2002, 06:07: Message edited by: Kenati ]

Not being in the medical industry that went over my head really quick...!



Buell

Kuru as you said was spread by cannibilism of the dead - the tribes in New Guinea called the dead "Long Pig" so if I tell you to "eat me" look out ....BTW this could be a very informative thread. I still think that CWD is Scrapie that crossed a species barrier, but who knows. Another thing, I never thought about the cattle that got the BSE in England after eating recycled nerve tissue from other infected cows. CWD could also be a species-jumping infection from feeding protien supplements made from BSE or other infected animals tissue here in the states. I know that there supposedly there was no BSE infected feeds imported to the US, but again, who knows.... In any case blaming game ranches for CWD is not right. Whatever the source, it is a BIG problem and getting bigger every day. Let's hope that our respective states' game biologists can devise plans to eliminate it, though as underfunded as they generally are, I don't hold out much hope. It will take another "species jump" into cows before the problem is really dealt with.

[ 08-13-2002, 04:03: Message edited by: Long Pig ]

Kenati,

Thanks for the very informative and obviously spooky post. Just one more thing for us hypochondriacs to worry about eh?

JohnTheGreek

Kenati

great background. here is the web site for the Wisconsin DNR CWD site which has good info and links to other sites:

http://www.dnr.state.wi.us/org/land/wildlife/whealth/issues/CWD/index.htm

Out of curiousity, do any of you think that it is possible that CWD may be more prevalent in other states than has been identified and that it is just due to a lack of testing that it has not been identified?

My reasoning is that if it is a genetic defect that affects a certain % of deer it should affect the same % all over. In places like WI which have a very large deer population, the actual observed numbers are higher. (could some of the biologists out there adress this one?)

I agree with your suggestions of how CWD may be transmitted through injestion of contaminated material (antler and bone for the calcium?)

I also agree with you that and that seletive in-breeding in captive herds may actually increase the probability of the disease. I wonder, in areas where Quality Deer management (which is believed to improve a herd's genetics) is practiced, whether or not there is less CWD?

Kenati in your opinion how similar is Creutzfeld-Jacob Disease and CWD. Are they similar but unrelated (ie like scrapie and CWD)?

thereason for my question is that there has been conclusion drawn in newspapers of Wi about some hunters that have contracted Creutzfeld-Jacob Disease, their relatives blame CWD. I don't see the evidence, though there are other communities that in this area (the native Americans) that are heavy consumers of deer and I do not not believe they have any greater incidence of Creutzfeld-Jacob Disease than any other group.

[ 08-13-2002, 06:19: Message edited by: rockhead ]

Kenati,

Very interesting post. I think Long Pig is thinking in the right direction. My uneducated guess on this is look at the feed. Protein-enhanced, -contanimated, or -mutated feed. Hopefully you folks will figure this one out quick.

i, have read they have already destroyed 8000 farm raised elk in manitoba and saskatchewan. also heard if the government don't help these farm raised elk farmer's with the drought they arte going through . they are going to turn them loose to the wild. now that is getting scary. maybe some of my western neibour's can enliten us a little more.

also heard from a hunter , who guide.s out of B.C. that waisting desease origanated in the wild elk . ???????????????

CWD was described in the 1960's and several hunters have died from CJD like signs after eating deer brains. If the disease is spread by consuming nerve tissue how do ruminants get it in the wild? Scares the hell out of me too!

Critrchik

keep the links coming. I believe you have a biology background, maybe you could answer a question.

what about transmission between species? Oviously I am interested in deer-human transmission. But so far there has been no direct link established only anedotal evidence like the Wisconsin cases.

correct me if I'm wrong but Dr. Duk I believe deer do eat antlers and bones of other (dead)deer in their search for calcium and it is possible that is where they get the disease in the wild????

If there were any inter-species transmission why don't we see mad-bear, mad-wolf or mad-eagle (mad-etc.) these animals clearly consume more deer per pound than humans and by their nature atck and kill sick animals including no doubt deer infected by CWD.

[ 08-13-2002, 06:37: Message edited by: rockhead ]

Richard wayne-The extreme drought in saskatchewan and manitoba has been very hard on all farmers including game ranchers.The fact is that game farming is a business and in the farming business drought is a risk you face.It is too bad for the families ranching these elk but they can't expect the government to come running to bail them out.If they were to turn these animals loose as they are threatening to do, they better leave the country very quickly as the results will not go well for the game ranchers.The first person who hits one with a vehicle will sue as a farmer is responsible for his stock in saskatchewan.That is mild compared to what will happen if these elk get into another farmers precious supply of feed that he badly needs to get his cattle through the winter.The same applies to these released elk getting into and damaging crops in their search for food.This threat may be the tool the ranchers are using to blackmail the government but it would certainly not bode well for the game ranchers to follow through on this threat.I was born and raised in rural saskatchewan and remember how farmers were not pleased to see game ranching in the first place so I am in a pretty good position to predict how they would react if this threat was to be followed through on.

[ 08-13-2002, 06:54: Message edited by: stubblejumper ]

Critrchik:

I think the squirrel brain hypothesis has been discredited(very hard to prove any of these theories because of the time frames involved) upon further research, but don't have a link.

One of the scarier details about prion transmission is that the original detection site, the Co. DOW research facility was heavily decontaminated 3 times as I recall, new animals introduced, not fed any contaminated products, and they still developed CWD. Prions are very hard to get rid of, and, as far as I know, no one is certain of their longevity(if that is the correct term for what is more or less a chemical)in the wild.

Unless there is a major breakthrough in our understanding of this disease, cervid hunting as we know it, anywhere but on game ranches which may, due to their fenced nature prevent the introduction of the disease, may be a doomed activity. Possibly where you have poor habitat or mass dieoffs the lesser population density might allow a breeding population to survive without coming into contact with the transmitting agents(presumably prions). One reason the disease has spread relatively slowly out west, where the habitat does not allow large numbers of animals per sq. mile. It will almost certainly spread faster in more concentrated populations. It will be interesting and enlightening to see if the Wisconsin controls are effective. I hope so, but have serious doubts.

Critrchik

Have you come across any research in areas, which examined groups that subsist heavily on Deer and campared their % Creuzfeldt-Jacob with other populations that don't consume much (or any) deer?

here is another link:

http://www.mad-cow.org/~tom/prion_evol.html#Nature

[ 08-13-2002, 07:49: Message edited by: rockhead ]

I believe prions are nearly impossible to kill. I have seen on TV where they took the one that causes Jacobs D. and they subjected it to 10,000 Degree heat, and it did not die.

I believe this is capable of eventually killing every deer/elk in the US if its not stopped soon.

Gordo,
I think a distinction needs to be made between game farms and the hunting ranch operations in Texas. The game farms are exactly that, farms. They are primarily elk and red deer ranching operations for the products they produce. Velvet elk antler is about $ 70 a pound and it has been traditionally sold into Asian medicine. But the market for it in this country and Europe is growing. I see it in a powdered form in the health food/herbal stores. Farm raised game meats have large markets as well.
Public fear regarding CWD/CJD can easily erode those markets and without markets game ranching as a business is in trouble. I would imagine that the sale of trophy animals is reativley small. I'd love to see figures on that.
I looked at the Texas style hunting ranches a while back as a result of my curiousity on private lands management programs. Particularly in relation to endangered species conservation efforts. Texas has more ESA candidate species than any state if I remember correctly and the hunting ranches provided a substantial amount of habitat that benefitted those species, mostly birds (my buddies!).
I see that as a positive and the hunting ranches as a low impact land use. I can't fault anything which has the net effect of conserving biological diversity.
In addition, what is the functional difference between those and privately owned/managed/created wetlands that economically exist because of waterfowl hunters. They too have a positive net effect on the conservation of biological diversity.
The timber plantations of the Southeast that are also managed for wildlife, ie. bobwhite quail are another example.
In the minds of the public and policy makers how do we differentiate between these various operations. All of them are essentially raising species or creating a productive refugia that attracts them. But the bottom line is that those animals are harvested and the economics of that is what primarily or partially pays the bills for the landowner.
Who decides the ethics in this ?

I have just returned today from destroying 220 elk from 2 farms. Game farming in Sask/Man Alta is in serious trouble even if it is not responsible for CWD spread. There is a very small market for the meat at this time and farmers in drought areas cannot move animals to areas with feed. Most of what is said by Kenati is thought to true by the federal vets here. At this time there is no credible evidence that CWD crosses up with CJD,at least not here. Some wild deer and farm elk have tested positive in recent weeks and more are expected. What we have found is a possible link between infected herds and their origin. The seed stock for the infected tame elk came from Wyo/Colo many years ago. While true that this could be coincidence it is suspicious.Mark

Buell,
This will explain what a prion is,

Prions: Infectious Proteins

Rockhead,
I have not seen a comparison related to venison consumption/CJD occurence. But I'll bet it's underway or has been done and I've not run across it yet.

What I did see was a comparison of TSE's from other species,

Here's a simple link, look at the commonalities in the feeds. Really makes me wonder about the feed supplements, mineral blocks, etc. used by livestock operators that deer may exploit.

TSE's of Other Species

Is this the same "stuff" that causes wiriling disease in Trout?

No it is not, that is caused by a parasitic infection.

WHAT IS WHIRLING DISEASE?

Whirling Disease is the common name for an affliction that infects certain fish via a microscopic parasite (Myxobolus cerebralis) with a two-host life cycle -- fish and worms. This parasite has a free-swimming stage that enters young trout, attacking the cartilage.



In severe infections, inflammation around the damaged cartilage places pressure on the nervous system, causing the fish to "whirl" when startled. Seriously infected fish have a reduced ability to feed or escape from predators and mortality is high.

Spores formed by the parasite while inside the fish are released upon death. These spores are then ingested by T. tubifex, a common aquatic worm. After a few months inside the worm, the parasite changes into the free swimming infective stage and is released into the water where it infects a fish host to complete its life cycle. Whirling disease has no known human health effects.

You guys wanna see my parasite links ? Really cool pics of parasitic worms bursting out of people.

What origin? If you look at where the majority of elk in the lower 48 came from during the reintroduction periods of the 1900-1920's,you'll find they were captured in the yellowstone and Jackson hole area. These elk found their way into Montana,Idaho,Colorado,Utah,New Mexico and other regions within Wyoming. Canadian elk were also supplied to the U.S in the early 1900's,for reintroduction. There isn't a private elk herd around,that can't trace its blood lines back to wild herds at one point in time. Some of these farm elk can be recently traced back to the wild,since they were illegally obtained through operations like the Chama land and cattle company,which was investigated for selling live wild elk.

CWD is just like a number of diseases found in animals. The disease has always been present and I'm sure numbers of animals have died over the years and the cause may very well have been CWD,but it was never diagnosed,or it was blamed on something else.

Every animal population goes through cycles. The current wild elk herds are at all time population highs,with the peak occuring in 1999. Any time you have a large population within restricted areas,the potential for spreading a disease through that population is increased.


Take all time highs in elk population,then combine mild winters beginning five years ago,which cut winter kill drastically and hunter harvest also. Now you have an elk population that is larger then ever and hasn't been properly managed either naturally or through human intervention. Which means plenty of weak animals that should have died during winter are still alive and most likely carrying disease like CWD. Now add a drought that is probably one of the worst in the mountain states since the dust bowl era and you end up with animals that are starved even during the summer months and because these animals are so stressed,they are more suceptible to disease. Add to this,the fact that elk are a social animal which interact and are in contact with each other through out the year and especially during the winter and early spring when most are cramed into refuges. It's little wonder that CWD has spread through both wild and private elk herds,the conditions have been ideal.

No I don't have a Ph.D in biology,nor do I claim to be an expert in the area.The above post,is based on information I recieved directly from a biologist employed by the Wyoming Game and Fish. According to this biologist,the underlying cause of this disease can be blamed on poor management techniques and taking a reactive stance in elk management rather then a proactive stance. This same biologist also pointed to the failures that were disease related in the black footed ferret program which wyoming was involved in.

Coming back to Whirling disease, it is also different from CWD in that in a modern hatchery it is darn near impossible to complete the life cycle of Whirling. In other words, fish farms (professional, modern ones) can't get Whirling. Also, there is no chance of lateral (fish to fish) transmission. Wish it was so in CWD.......

As an aside, Ann provided the link in one of her posts, but there is a good site put up by, IIRC, the RMEF, Boone and Crocket, and the Mule deer foundation: http://www.CWD-info.org.

Though I am as alarmed as most about CWD, and maybe more, perhaps it is worth offering some perspective. Even after eating BSE infected beef, head-cheese, sausage and such for several years, there are only about 200 cases of NV-CJD in Europe so far. That is, despite direct consumption of products containing brains and nervous system tissue. Considering an exposed population of over 100 million, those are pretty long odds. FWIW, Dutch.

Kenati, thanks for the post. CritrChik, excellant info. I learned more here in five minutes then I have from the local news agencies in five years. Thanks again (of course now I'll have nightmares, but what the hell) - Dan

RMK,

Your post is spot on! Management, population, game ranches, game tansportation, nutrition, and climatic factors are facilitating a disease that might otherwise go undetected.

It scares many of us-- including myself-- to see the potential for a decline or broad demise of deer and elk populations. Even so, what RMK touched on and I think we all need to accept, is that it will likely get much worse before it gets better. And accordingly we need to change our realities of what Wildlife Management is. Proactive -vs- Reactive.

Wildlife is like many other things in life (ie the economy, stock market, weather, etc) it goes in cycles. Hence there are going to be population highs and lows, and a "management" goal of maintaing a stable wild population (or a maximum population/density for a given biota) is not realistic. And in the wake of CWD, it may be detrimental.

I don't have a solution and I don't have the arrogance/ignorance to point a finger and play the blame game. But whether we all like it or not good old natural selection for the genetically superior/resistant-- over time-- may be the ultimate solution. Maybe the most we can do or *should do* is to remove/minimize the human factors which facilitate this disease. Then just wait for it to fix itself....

Another thought to throw into the mix the spread of West Nile virus: It's infectious to horses and humans, but what about wildlife like deer?

Also, why can't someone bring a virus overhere that's infectious to something like mosquitos?

Kenati... excellent thread. You did a great job simplifying the subject for a layman like myself.

CrtrChic... excellent info.

From a quick read of this thread it sems that a link is trying to be made between CJD and CWD. Is CJD the human manifestation of CWD, or has that link NOT been established?

The question still begs (I don't have time to read all the links):

How is (if it is) CWD transmittied to human's?

Forgive me if these question's have been covered, I honestly haven't paid much attention to this issue. I should, however, as I contracted Rock Mountain Tick Fever three years ago. I'd never worried much about ticks and it's my understanding that only approx 1:100,000 ticks carry RMTF... won the infectious lottery... makes one think...

BA

Brad, CJD is the "one in a million" human TSE disease. It "always" occurs in older people. In other words, it seems to have a very long incubation time. We do not know the source of the infection.

BSE transferred to humans is referred to as New Variant - CJD. This variant is much faster acting, seems to have an incubation period measured more like 3 to ??? (10?) years, and thus occurs also in young people.

Cases of CJD do not get anyone excited, even in the US. CJD happens about 200 times a year. What gets the docs excited is YOUNG PEOPLE getting CJD, because that very rarely happens.

Now, remember that there are some TSE's that are common, and some that are not. We have know about Scrapie (the sheep version) for over three centuries. Only recently have we documented that there are actually nine DIFFERENT versions, different prions that cause scrapie. At this time, none of them are thought to be transmissable to humans. Thought to be.

At this time, CWD shows in the lab to be "not transmissable" to humans, but using the same tests, BSE is "not transmissable" as well.

As far as eating game; the prions are concentrated in the Central Nervous System, and the lymph system. Lymph nodes usually are associated with fat on the carcass, CNS is of course brains and spinal cord. Blood and meat are thought to have little to no prions in them. Of course, the FDA still won't let me donate blood because I lived in Europe during the BSE period.....

My personal approach is this:

I cut my elk in the field, without quartering. I do not cut through any bones, and I cut the antlers off last. I now cut and wrap my own meat, to prevent cross contamination at the processing plant. I trim all the fat: to remove the strong flavors, and to remove the lymph nodes, best I can.

For the rest, I don't worry about it. FWIW, Dutch.

Interesting thread!

CritrChik, good information!

I did a fairly extensive report on prion disease a year or two back and I think I can add a few things. I apologize for repeated information. I'll begin at the beginning...

Proteins are made up of long chains of amino acids which fold into three dimensional conformations that are more stable than the linear chain of amino acids. Prions are believed to affect a single critical protein by changing the conformation of this protein to a physiologically non-functional form. The reason that a single protein is targetted is that often the prion protein has the exact same amino acid sequence as the protein that it is renderring non-functional. However, the prion protein is folded into a different, and MORE STABILE, conformation. This added stability is the reason for the relative indestructability of these prions. Because they are so stable they can't be destroyed by heat, changes in pH, or proteases. All of which will destroy a normally folded protein, and many of which our own immune system uses to destroy bacterial and viral proteins. In layman's terms, the prion protien effectively "teaches" the normal protein how to fold into this highly stabile, but non-functional, form. And once the normal protein has refolded to the prion conformation, it can act as a prion and help the refolding of other proteins with the same amino acid sequence. All this leads to an exponential growth in the number of prion proteins, and the demise of the infected animal. The demise of the animal is due to a lack of the functional critical protein. For reasons that are not clear it is typically neurological proteins that are effected. SCARY STUFF!!!

I believe that the current hypothesis for the species jumps that have been seen has to do with the homology of proteins in related species. Homology is the term given to the similarity in amino acid sequence of similarly functioning proteins between species. For instance, for years pig insulin was used by human diabetics. While the amino acid sequence of the two insulins is not exactly the same, it is close enough that pig insulin functions well in humans. Therefore, if a cow's neurological protein that has been effected by prion disease has a 99% homology with a human neurological protein, then there is a chance that the cow's neurological prion could "teach" its human counterpart protien how to fold into a prion form of its own, and the process that I described above begins.

Disease without the presence of a bacteria, virus or fungus is a very interesting and very scary topic. Especially if we can't even figure out how to destroy these things in a petri dish!

Bob

Great "homepage" you have there, CritrChik. I have seen it before. Kind of brings into question my sister's comment while denying the Freudian (?) nonsense of penis envy - she always says, "They do seem kind of handy for picnics, though."

Dutch, thank's for the excellent info... I can't ever give blood after a bout of Hep-A contracted in India.

JohnTheGreek,

Wow, small world. I assume you�re referring to Nicky Mihalopoulos. If so, she�s a WONDERFUL person. I�ll be sure and tell her hello.

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Rockhead,

It has been shown that a �species jump� of the infectious proteins can occur, albeit it is a difficult jump to make. Studies have been performed where HAMSTER where �challenged� with MICE infected by a particular prion. The hamsters took 100 times longer to become infected with a higher than normal �dose� of mouse prion. It was found that once a specific gene was �introduced� into the HAMSTER genome, the hamsters became more susceptible to infection by the prion.

So what does all this mean in relation to Creutzfeld-Jacob Disease (CJD) and chronic wasting disease? Simply put, in the wild the jump from CWD to CJD in humans would be a difficult one to make. It might also indicate that because a gene affecting susceptibility may be involved, some people may become infected from eating deer, while others may not.

CritrChik might be on to something with the squirrel brains/CJD report. Infected brains may very well be the abnormally high concentration of prion that is required to make the �species jump,� as seen in the mice/hamster experiment.

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CritrChik,

Very good find!

�The host range of chronic wasting disease is altered on passage in ferrets.

Bartz JC, Marsh RF, McKenzie DI, Aiken JM.�

This study mirrors the HAMSTER/MICE transmission study. I did not mention it above, but�

After the first �species jump� leading to primary infection, subsequent infections within the SAME species are much easier. This easier transmission is thought to be caused by a material called PrP-res. As further evidence of this, this EXACT material was found in the study you posted:

�Western blot analysis of ferret-passaged CWD demonstrated the presence of PrP-res.�

The evidence is definitely pointing in the same direction.

LAYMEN�S TERMS: Once the PRION overcomes the biggest challenge, which is jumping ship from deer to say human, the battle for the prion is all downhill from there.

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358Mark,

That breaks my heart. I wish I could dedicate more energy to this matter. Too many irons in the fire as it is. Hell, it�s tough just trying to post on here! Keep up the good work.

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RMK,

I agree with you observations. I agree that Mother Nature runs in cycles. I would like, and hope, that it will just go away with time. But if the elk/deer herds were decimated, I would hate to learn that humankind played a major role in the event. For now, I think we should press on for understanding.

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Bob,

Great technical and laymen information discussing the protein structures of prions. As you might know, there are several species of bacteria and fungus that undergo similar �indestructible� morphologies, known as spores. They too can endure intense heat, desiccation, pH extremes, and forgo long periods of time without activation (some over 150 years!!)

The PRIONS seem like wannabe bugs� but the damn things still aren�t �alive� and can�t be �killed.� (sorta like a virus, but without DNA/RNA)

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You guys and gals keep up the good work. Knowledge is power. Considering all of our tax dollars that are wasted on government handouts, I would definitely be in favor of the CWD research funded by the National Institutes of Health, Centers for Disease Control and Prevention, U.S. Fish and Wildlife Service, et cetera

Press on.

Kenati

Kenati,

Yes, Nicky is a year or two younger than I but our parents were good friends back in the day. I still see her brother with a degree of regularity.

Back to the CWD discussion and relating to CritrChik's point about interspecies transmission. Correct me if I am wrong, but what we are saying is that once the first species jump has been made from say a hamster to a ferret, it becomes more likely that the prion will be transmitted across other species barriers as well as within the original species (either a ferret or a hamster)? This would, I suppose, explain why Scrapie was never a problem for people over the last couple hundred years (that we know of) but once it jumped to cattle, new, distinctly different, forms of CJD became apparent in humans.

JohnTheGreek

[ 08-14-2002, 06:57: Message edited by: JohnTheGreek ]

Great thread!!

I haven't had the time to read through all the links but do appreciate the info. This is a hairy situation but there is always fear of the unknown. I hope we lern more quickly. Nature has a way of solving these things that we as people don't find very acceptable. As this disease spreads it will cause smaller herds and thin out the densities. As this happens the passing should lessen. Kind of makes me think about how small a part we really are in this world. A disease like this in humans would thin our population quickly and our role would be as helpless observers if there truly is no way to stop it!

JohntheGreek,

That is an interesting assumption that COULD be made, but not exactly what the research indicated in the study I mentioned.

What I meant to say (and did a poor job of doing above), is that a PRION must first make the difficult jump from a mouse to a specific hamster. That infected hamster has an easier time infecting ANOTHER group of hamsters. Once the second group of hamsters is infected, they can more easily infect a THIRD group of hamsters. And perhaps this goes on and on. The study I read only carried this experiment out to the third generation using serial dilutions (decreasing concentrations) of the infectious prions with each generation. Again, a very scary scenario.

Rockhead,

Unfortunately, that very well could be the case. (Don�t you just love all the �could� �maybe� �might� �perhaps� in science?)

Basically though, I wanted to suggest that some people could be more susceptible to CJD and CWD based on weather or not they have a particular gene. I�ll get more specifics and get back to you (I don�t know when though!!)

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P.S. Just in case you might be interested� A former professor of mine is speaking about the West Nile Virus Epidemic on National Public Radio (NPR) today from (I believe) 4-6pm. DEET is my new best friend!!

Here's the CDC site on West Nile Virus on the species it effects or has been detected in thus far,

West Nile Virus- Vertebrate Ecology

Kenati,
This will annoy you,

Rocky Mountain News

drmn/state/article/0,1299,DRMN_21_1324394,00.html
Bush kills $18 million CWD fund

Money earmarked to control disease nixed with airport security, law enforcement

By M.E. Sprengelmeyer, Rocky Mountain News
August 14, 2002

WASHINGTON - President Bush has nixed $18 million in emergency funding for the fight against chronic wasting disease as part of a larger rift with Congress over "spending restraint."

Saying uncontrolled spending would increase deficits and hurt the economy, Bush announced Tuesday that he will not spend $5.1 billion that Congress tacked on to his supplemental spending request for the war on terrorism.

Congress included the money within the $28.9 billion appropriations bill but added a provision requiring Bush to spend all or none of the additional funds.

Bush said some of the additions were for "truly pressing needs," like AIDS prevention and money for the Middle East.

"However, we're not going to spend $4 billion we don't need in order to unlock $1 billion we do," Bush said.

Caught in the dispute is about $18 million meant to help curb the spread of chronic wasting disease, which has ravaged deer and elk populations in Colorado, and now has spread as far as Wisconsin.

The decision eliminates $15 million for the Animal and Plant Health Inspection Service to monitor and manage the spread of the disease, $2 million for the Agricultural Research Service's study of new tests to detect the disease in deer and elk and $1 million for the Centers for Disease Control to study diseases like CWD and their potential effects on humans.

"The chronic wasting disease situation in Colorado is a perfect candidate for this kind of emergency spending," said Lawrence Pacheco, spokesman for Rep. Mark Udall, D-Boulder. "All one has to do is look at how CWD has devastated the deer and elk populations in Colorado to understand why we need this funding."

Republican Sen. Wayne Allard of Loveland said he was disappointed but would push for increased funding in the budget for fiscal year 2003, which begins Oct. 1.

"I'm just upset it got caught up in this battle of wasteful spending, with what I thought was a very important program," Allard said. "I'm sure (Bush) did what he thought was best."

Bush singled out spending for a new facility to store the government's collection of bugs and worms, but his action is far-reaching. The $5.1 billion also included $480 million for airport security, $235 for million nuclear security and $151 million for local and state law enforcement.

New York lawmakers blasted the elimination of $90 million for health monitoring at the World Trade Center site.

Pacheco said some of the cuts could affect Colorado. Bush eliminated $50 million for restoring damage from floods or damage to watersheds caused by wildfires, $33 million for a cyber-security initiative led by Boulder-based National Institute for Standards and Technology and $400 million for states to upgrade their voting equipment.

Voice your concerns to the powers that be,

mailto:president@whitehouse.gov

mailto:vice.president@whitehouse.gov

National Prion Research Program

[ 08-15-2002, 06:07: Message edited by: CritrChik ]

FABULOUS!

We're in a recession and this joker is worrying about deficits ?!?!?!
OK, does anyone in class know when deficit spending is appropraite? ANYONE? ANYONE?? BUELLER? BUELLER? During a . . . ANYONE? OK . . starts with "R" . . . rhymes with "ECESSION"! Right! "DURING A RECESSION"!
I have some reading assignments for Mr Bush. That's a hell of a way to make things worse and not get elected, ask Herbert Hoover (well OK he's long dead but you get my point).

CritrChik,

OH GREAT now the West Nile virus is "infecting" this thread? My hypochondria is running into overdrive because of you medical/bio types

Regards,

JohnTheGreek

Wasting disease changes states' wildlife policies
Conference examines challenges of containing migratory threat
By Theo Stein
Denver Post Environment Writer

Thursday, August 08, 2002 - Chronic wasting disease is changing the way wildlife is managed in North America, as biologists who once promoted big herds for bumper harvests now plan to kill thousands of deer to halt the spread of the fatal brain disease.

Extended hunting seasons, unlimited bag limits, major culling operations and demands for expensive testing labs are becoming a fixture of wildlife management agencies across the heartland as states grapple to deal with the emerging wildlife threat.

"We must be prepared to take the drastic action that's needed, no matter how distasteful it may be," said Bruce Morrison, the assistant director of the Nebraska Game and Parks Department.

Morrison's comments came at the end of a two-day conference in Denver on chronic wasting disease, which is threatening the continent's abundant herds of mule deer, white-tailed deer and elk.

Once CWD was thought to be confined to a 16,000-square-mile area of Colorado, Wyoming and Nebraska, but in the last two years, wild deer as far away as Saskatchewan, New Mexico and Wisconsin have been found to be sick.

Since most state wildlife programs depend on hunters to regulate deer numbers, success will depend on hunters' willingness to sacrifice guaranteed kills for the knowledge that they're helping to keep their deer herds healthy, according to Lloyd Fox, a deer biologist with the Kansas Department of Parks and Wildlife.

"This is a complete paradigm shift," Fox said.

Five states and one Canadian province are following the Colorado Division of Wildlife's lead by aggressively seeking out herds that could be infected with the disease and eliminating them wherever they're found.

Even border states such as Kansas are planning to slash deer numbers in a pre-emptive strike against the malady, which makes its victims grow thin and die as it eats holes in their brains. Dense accumulations of deer are thought to be a factor in the spread of CWD.

That's why Colorado wildlife biologists want to cut deer numbers in half in the northeast part of the state, where CWD has existed for decades. But the agency's goals have been hard to achieve as some private landowners resist having their healthy deer targeted because there may be sick animals among them.

The arrival of the mysterious ailment, which is believed to be caused by an abnormal form of a common brain protein, can stagger even well-funded agencies like Wisconsin's, said Tom Hauge, that state's natural resource director.

Wisconsin's lush farmlands can hold more than a hundred white-tails per square mile, many times the carrying capacity of Colorado's arid prairie. America's Dairyland is also home to some of the nation's most fanatical deer hunters, Hauge said at the first-ever national CWD conference.

"We've got more hunters than Wyoming has people," Hauge said.

Hauge's biologists already had a full plate of research projects before Feb. 28, when the first of 18 CWD-positive deer were found in south-central Wisconsin.

Dealing with the disease has exacted a heavy toll on biologists who spent their careers growing big herds and trophy bucks. Now they have to put in 70-hour weeks trying to figure out how to kill 25,000 deer in a 360-square mile eradication zone around the outbreak, assure hunters that it's safe to go into the woods this fall and prepare a new $900,000 testing facility.

"It's like trying to change a tire while you're driving down the road at 60 miles per hour," he said. "But we think we've got a shot at eradicating it, at putting the genie back in the bottle."

A couple of things that I have not seen mentioned here.

The USDA 'pen' that CWD was first noticed in had contained sheep with scabbies immediately prior to the introduction of the elk that were seen to be infected.

Cattle have been put into pens with infected deer and have not been able to catch CWD despite being fed infected brains. The only way it has been transmitted to cattle has been through a direct inoculation into the brain. (ouch) Even then only 2 of 43 contracted CWD.

The first place that seems to show signs of CWD prions is in the tonsils. This is long before it is identified in the brain. This is the hope for a future test, on captive animals at least. Whether or not this means the CWD prions are ingested is open to debate.