The Facts About CWD From One Of The World's Leading ExpertsLately there has been some conflicting information on CWD being reported in the media. This includes statements such as "little is known about CWD" or "we don't know how CWD is spread." The following is a response to a WDHA inquiry about the current state of knowledge on CWD. This was written by Professor Val Geist from the University of Calgary, who is considered one of the world's leading experts on CWD.
March 28, 2002
Dear Mr. Toso,
I shall comment on the CWD issues that concern you, but before I do so you need to be aware of my qualifications and motives. My narrow field of scientific expertise is the behavior, ecology and evolutionary history of cloven-hoofed mammals, the deer and bovid family in particular. I also have some expertise in and have taught and published on wildlife conservation policy and management. I became aware of CWD as a potential conservation problem for free-living cervids very early after its discovery. I have had some time to get to know it. I have followed the European BSE controversy closely, having the advantage of reading and speaking German and thus having access to not only scholarly writings but the excellent investigative reporting of Germany's foremost weekly, DER SPIEGEL, which has displayed a consistent and very informed interest in the mad cow issue. I know the foremost of our American researchers into CWD and have had contacts with them, and have been with them in common court cases. I have published on the matter of CWD in relation to game farming and its policy implications in the second chapter of Geist, V. and I. McTaggart Cowan (eds.1995) Wildlife Conservation Policy. (Detselig, Calgary. You may call Mr. Ted Giles, the publisher, at 403-283-0900 to obtain a copy, unless such is in a university library close by. This book is not unimportant in current context). Precisely because I have an understanding of what free-living deer do and where they do it, I can see and discuss links to CWD research, and come to insights foreclosed to veterinarians who deal with deer in captivity. Moreover, both agricultural and wildlife veterinarians have currently very much at stake, and their pronouncements are - unfortunately - colored by their fears and occasionally by crucial misjudgments. Unless veracity is practiced I am afraid that we as scientists may be branded as scoundrels, as DER SPIEGEL did with those that handled the PR on BSE in England. Let me state from the outset, CWD can be defeated and eradicated. However, whether the cure is palatable to all concerned, is another matter.
Chronic Wasting Disease (CWD) is a Transmissible Spongiform Encephalopathy (TSE) a sister-disease to Bovine Spongiform Encephalopathy (BSE) or mad cow disease. That is, in its known characteristics, it is quite close to BSE - as we shall see below. The statement that CWD is "species specific" is false. I occurs in elk, mule deer and white-tailed deer. Elk not only belong to different species than mule deer or white-tailed deer, but to a different genus and a different subfamily, the Cervinae or Old World deer. These are very different from the New World Deer to which belong mule deer and white-tailed deer, two separate species in their own rights. Our currently best hypothesis is that CWD arose from scrapie, a TSE found in sheep, a stable and for humans apparently not infective form of TSE. From sheep, CWD jumped to mule deer, then to elk, and then to white-tailed deer. The theoretical significance is that with each jump one expects its infectivity to increase. CWD has been experimentally transferred to various species including among other mink, cattle and squirrel monkeys. What is missing to date are in vivo studies on laboratory Old World primates fed oral dosages of CWD infected tissues. Such studies, carried out with BSE, proved to be predictive for BSE infecting humans, a number of years before the first case of new variant Creutzfeld-Jakob Disease (CJD) was found in humans. nvCJD is one of four variants of TSE's in humans. There is also talk of a "species barrier" as if this barrier is absolute. It is not. It is a relative barrier. In vitro (test tube) experiments have shown that deformed or pathologic CWD prions (the infective agent) convert healthy human prions at about the same rate as do pathological BSE prions. In both cases it is about 7 (seven) percent. The rate at which defective human CJD prions convert healthy ones into pathological ones is taken as 100 percent. If we are concerned about BSE we cannot be cavalier with CWD.
A half-truth perpetrated by agencies is that no humans have been found with a CJD that has come from CWD. A half-truth is a technically correct statement that is misleading. Moreover, it is based on a gross misjudgment, confusing detectability with infectivity. For BSE - the standard of comparison - there are good connections to CJD, and uncritical comparisons are made to it discussing the infectivity of CWD. However, that's comparing apples and oranges. the epidemiological factors concerning BSE and CWD are vastly different, making it very unlikely that a CWD caused CJD would be discovered. Let's go through the epidemiological factors one by one. There are at least ten that preclude a ready comparison, however before discussing these one must know tissues of prion concentration. Prions are most highly concentrated in metabolically very active tissues such as brain, neural tissues, bone marrow, the lining of the gut, lymphatic tissues, to a lesser extend in blood and least of all in muscle meat. If the rule holds, that prions are produced massively in highly active tissues than velvet deer antlers are primary candidates for CWD infectivity. Here are the epidemiological factors making detection of CWD unlikely.1. The geographic area with CWD is found in the USA is a tiny fraction of are in Great Britain (UK) contaminated with BSE.
Therefore, the probability of detecting a CWD caused CJD infection is low, but the probability of infection is unknown - and the two must not be confused. However, they are continually confused!
What to do about CWD? Observations on captive herds indicate lateral transmission probably via super-saturation of the facilities with infective prions originating in the faces (gut-lining) or body fluids. The implications for free-living deer is that artificial feeding, watering and salting sites will transmit the disease. At least until the earth surface has been rinsed by rains and melting snow and the diseased prions are dissipated into the soil beyond any reach by deer. A second source, obvious to those who have observed free-living deer or elk is that they chew bones. Even if the bone marrow and brain rot inside bones, a dried tissue residue remains inside well-protected against the elements, particularly within marrow bones. Consequently, the scattered bones of deer dying of CWD are likely to remain infective agents for a very, very long time. Consequently, one must find a way to find and destroy bones of deer deceased in the free state. It could be done by teams of sportsmen with trained dogs - a Herculean task, no doubt, but a feasible one - for sportsmen, not for the DNR or agricultural bureaucracies. An owner of a farm can scour his land most effectively as he or she will know where deer hand out. Such bones must be destroyed with in a high temperature incinerator. Depopulating deer populations without removing the bones of deer that died naturally will not be effective in eliminating CWD.
Personally? Do not eat obviously sick deer. Debone the healthy ones using a knife only and discard bones and internal organs into incineration. Do not saw through bone marrow and back bone, spraying marrow and spinal chord on meat. Use knife only (old style European butchering. Gives a superior cut anyway). Give head away for testing, if negative, eat deer with relish. I case of doubt give it to man's best friend.
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