Infected moose in SW of Jackson, plus Forest Service renewal of elk feedgrounds and doubledealing stoke the issue-
Wildlife disease debate heats up. By Chris Merrill. Casper Star-Tribune environment reporter.
I have this feeling that the Forest Service and Wyoming Game and Fish are about as trusty as sub-prime mortgage investments.
Update. Oct. 22, 2008. Groups call for disease action. CWD found in moose in Star Valley a ‘wake-up call’ to Game and Fish, conservation groups say. By Cory Hatch. Jackson Hole News and Guide.
Comments
The Wyoming Game and Fish is a joke, the only thing they care about is keeping wildlife alive for people to hunt so they can make some money, and of course let’s not forget they care very much about keeping the livestock growers happy. Managing wildlife the correct way is the last thing on their minds.
“The general belief among most conservation groups and many wildlife biologists is that if the disease were to spread to feedground elk, the disease would rip through the populations at much higher rates than it does in normal, “free-ranging” herds, because the animals are artificially concentrated on feedlines in the winter.”
–This is not a “general belief” it is simply common sense.
“Currently, there is neither empirical evidence nor data anywhere in North America suggesting that chronic wasting disease is a (devastating) epidemic.”
–Huh? Contrast this with what agencies are saying about Brucellocis. Brucellocis causes cattle to abort some fetuses, in contrast, CWD is always fatal. Seems like they’re talking out both sides of their mouths.
I agree that feedlots and CWD are bad, but we have had CWD in the midwest for years and it has not hit epidemic proportions. If anything deer populations have continued to grow (they walk through subdivisions, they are everywhere…..as are coyotes) , so there is time to prevent it from becoming a huge problem out west. I do think that everything possible should be done to prevent its spread.
Okay, I have been reading, and asking doctors and biologists some questions. There has been discussion about prions. There is little definitive research or in depth understanding of prions and their part in deseases, CWD or others. So we can’t really say what they have to do with CWD-I prefer to leave out what cannot be supported, I don’t want certain folks that post calling us dishonest or speculative.
But there are some basics. CWD is spread among animals. We know thatt he largest spread occurs in areas where herds intersect and have higher populations.
So it becomes simple math. If you increase the number of animals in one place, then you increase probability of spreading the desease among them. The more you expose, the more you spread, the faster it multiplies in infected animals.
It is like saying “You may get struck by lightening”, which is like saying you may spread the desease. But the feedlot changes that to “If you stand out in the middle of a field holding a steel rod during an electrical storm, you may get struck by lightening.” It obviously magnifies the probability of exposure.
The feedlots host a population of ungulates that migrate for some distance. In that migration, they come into contact with other animals that migrate…it is a ripple effect.
Yes, we may have some time to TRY to contain the spread. But how? Closing the feedlots is a start. But it isn’t any closer to done than a year ago…farther from it in fact. Even if we close feedlots, you still have infected animals and they will move throughout the ecosystem. There is no way, at present, to determine if an animal is infected until the desease is well under way…by then animals may have laready exposed many other animals.
The best chance, that I know of, rests squarely in the nostrils of large predators. Let the predators do what nature had intended…seek out animals that are deseased.
We don’t have an enormous amount of info or scientific data on how the CWD spreads, though it is highly speculated and thought that it is through blood and bodily fluid transmission.
Research should be done to see if the CWD is transfered to predators that prey on the infected animals. No one can smell or detect desease any faster than the predators could.
Vicki, first of all the prion protein has everything to do with TSE’s such as CWD and Mad Cow and the rest. A Nobel prize was awarded for making that definitive linkage. If you want, I can bury you in PDF’s on this subject.
There has not been any evidence (that I know of) that CWD can be transmitted from host to predator, even human predators. It would be more likely to occur to four legged predators since they would gobble up the brain and spinal cord whereas most two legged predators leave that in the gut pile.
I also don’t know at what stage of the disease the infected deer/elk/moose are infectious to others. It may likely be before they actually have the symptoms. The Colo State people should know this since they do real animal to animal transmission studies. So if the deer, etc are infectious before they can be marked and removed as “sick” by a predator, then concerted predation might not solve the problem. But you are basically right: concentrating animals (like first graders in a closed school room in January) only serves to accelerate disease transmission.
John Weis,
Prions may have everything to do with it, but there is no definitive explaination, or cause, for how it occurs. It is unknown how, or why prions have this effect. Basically, knowing that prions are part of the problem is just that, knowing they are part of the problem.
Doctors have been trying to understand CVD for decades-it is basically the human counter part to CWD and Mad Cow Desease. It is the same scenario, a lot of links to this or that, a lot of specualtion, but no real progress, answers or signifigant advances.
We may guage progress differently, but it doesn’t change where the progress lies….thanks for offering the PDF info, but I spent six hours reading about this yesterday. I now have CWD over load! My brain may melt if I read much more in the near future!
I can give you a quote from one of the doctors I asked about it….”If anyone really understood prion association to desease we would have to know more about protein degeneration, we would have found or treatments for numerous degenerative deseases in humans. They wouldn’t spend millions on animals if there were answers, they would spend the money to advance human health.”
To me, that says we have a very long road ahead.
I don’t claim to know much about the subject, but from what I have read the incubation period is a minimum of 17 months.
Since the developement of the desease takes that long, and the infected animals would not show evidence of the desease until several months had passed, I am left to assume that other ungulate would be unaware of the state of desease and would more likely congregate with the sick animals. It would seem that the desease would be able to be spread early on. (Especially since they are unable to detect the desease until it has invaded the lymphatic system and the brain tissue.) At what point does it become infectious? I have no idea. But it is existent in the animals for many months before it takes a toll and attacks the brain, etc. Many deseases are infectious well before the sick become symptomatic. Given nature’s ability to handle these things, I would assume that the healthy animals would instinctively isolate from others that are ill.
At any rate, we know that the desease is spread by contact with other animals or their fluids-which would require animals to be in close proximity to one another. And since we know that the wolf can detect deseases far before they are physically evident to humans….they have a leg up here.