Commentary on Houston Chronicle article [below] by Dr. Thomas Pringle

Date: Fri, 10 May 2002 11:03:29 -0800
Subject: nice cwd reporting


My compliments on these superb CWD Houston Chronical articles: not mincing words, they display an excellent -- and most rare -- journalistic understanding of the origin and continuing spread of CWD. (A couple of technical points were not quite on target, see bottom.)

It is really refreshing to see in print the probable origin as sheep scrapie-to-penned cervids in 1967 at Foothills Research Station, after decades of relentless PR out of Colorado DOW seeking to distance itself from responsibility (and liability). Facility workers at Colorado Dept of Wildlife commented on the similarity to scrapie already in 1967 but never autopsied any of their many dead research animals until 1979, discovering immediately an obvious spongiform encephalopathy.

By that time of course, release to the wild and transfer of surplus animals to zoos, game farms, and sister facilities had seeded widespread dissemination of the disease. This was subsequently aggravated by the explosive growth in game farms and intra- and inter-state cervid shipping, which at industry insistence was in essence unregulated (eg regulated by state ag dept boosters). It is not just the shoot-deer-in-a-barrel industry --elk velvet nutriceutical was never tested by anyone for abnormal prions despite its troublesome composition (the market collapsed from live CWD exported to Korea).

DOW itself did nothing to change its practises or control the disease until very recently. Only last year, in the face of published evidence [below] that the disease is expected to transfer to humans at the same low efficency as BSE (129 human deaths to date), did they back off from encouraging human consumption of venison from the endemic area. Nebraska fish and game even offered a deer-neck stew recipe on its web site, even though spinal cord was long known to have high infectious titres.

State fish and game depts are basically unfenced game farms. They have a commercial concession that allows them earn a salary from sale of antler tags. This motivates them to set up winter feeding stations, watering holes, salt blocks, control predators, fight CWD testing, anything and everything that increases numbers and leads to more or continued sales. Unfortunately, practises leading to high cervid concentrations and testing avoidance are highly conducive to the spread of CWD.

States such as Montana require testing of every game farm cervid dead for any reason and an accounting of each animal's provenance and disposition; other states adopt a "don't look, don't find" policy of testing avoidance with no monitoring whatsoever of facilities. Absence of evidence is not evidence of absence when it comes to TSEs. This disease just does not go away on its own, be it kuru in New Guinea or scrapie in the US.

Given the numbers of Texas game farms, massive importation statistics, and the high likelihood of trace-backs to affected facilities, it would be most surprising if CWD were not already entrenched in Texas along the lines of Wisconsin. It really questionable if stonewalling really is in the industry's best interest -- who is going to hunt in a state that fears to test? The longer infectious foci are allowed to operate, the greater the probability of multiple introductions into wild deer. To ban imports (only after everyone has finished importing all they want) just locks the barn door after the horse is long gone.

Half-measures on prion diseases are worse than no measures because they put off the day of reckoning while exacerbating it immensely. Wisconsin's hasty policy of culling 15,000 wild deer, yet business as usual (no testing, no trace-backs, no inspection, no recordkeeping, no culls) at its sacrosanct 535 game farms. will result in CWD in perpetuity. The focus is on temporary abatement for purposes of hunter reassurance. Dr. Charles Southwick is a good source of scientific information on cwd control strategies.

A few technical notes. First, the word mutation is reserved for genetic change affecting DNA. It is not applicable to mere protein conformational changes and fibril formation seen in amyloid diseases such as Alzheimer and CWD. Mutation has been ruled out in CWD amplification. The prion gene of hundreds of CWD and non-CWD animals have been sequenced by Dr. O'Rourke at Pullman. There is no counterpart to the mutations that cause 15% of human CJD, much to the disappointment of DOW.

No TSE has ever been seen in natural populations of any wild animal anywhere in the world, making Colorado's story of a natural pocket (by coincidence located adjacent to Foothills and Sybille research stations) a bit far-fetched. Now by golly another natural pocket has flared up next to a game farm in Wisconsin. How about the supposed natural pocket adjacent to the massively infected game farm in the Black Hills -- despite its import history, the industry PR firm in Ketchum turned this around 180 degrees -- now it's the wild animals infecting innocent game farms!?! There has invariably been a nexus to intensive livestock operations, be that cows fed rendered cows, mink farms fed downer cows or deer quartered in a scrapie research facility.

Second, the "best available scientific evidence" upon which public policy is normally based (more studies are needed, they always are, but something must be used for the interim) is that published by Byron Caughey's group at Rocky Mtn labs (after two years of delay by co-author Mike Miller of DOW who controlled sample access). A proxy test was used since human volunteers cannot be considered. Transmission efficiencies to human were similar to BSE -- low, but hardly reassuring given England's experience.

Third, CWD has already been experimentally transferred to 6-7 species including rodents, primates, and bovids, as published in peer-reviewed scientific journals. The first round of transmission can be inefficient in TSEs; after that, no species barrier. It is really the human-to-human second round (plasma donation, childhood vaccines, cornea transplants) that has cause the greatest consternation in England. A Ft. Collins hunter/blood donor with preclinical cwd-induced CJD would have no idea he is ill.

It is currently impossible to test humans for cwd-induced CJD because there is no known signature. Rises in baseline CJD cannot be monitored, contrary to CDC, because of very large numbers of missed diagnoses, swings in ascertainment effort, and diagnostic changes.

Best wishes and keep up the good work!

Dr. Thomas Pringle
Sperling Biomedical Foundation
3295 Kincaid St.
Eugene, OR 97405

CWD archives

Wisconsin latest to be hit by deer brain disease

May 10, 2002 The Houston Chronicle by Shannon Tompkins
Wisconsin drew the black bean in the continent's expanding war with chronic wasting disease, and that simple twist of fate promises to be expensive and painful for the state's deer and human populations.

It also serves as a sobering study for Texas in what can happen when the poorly understood but invariably fatal brain disease shows up in a state's wild deer herd.

Just three months after CWD was documented in a handful of white-tailed deer taken by hunters in southwestern Wisconsin, the state is preparing to kill thousands of deer; Gov. Scott McCallum is calling for a special session of the state Legislature to address the issue; politicians are asking for millions of dollars to fight CWD spread; and the hunting-based economies of the region are preparing to take a stunning blow.

Add to that the uncertainty many of Wisconsin's 700,000 deer hunters are expressing about the safety of eating venison, and you have the future of that state's deer and deer hunting hanging in the balance. CWD is a recently discovered transmissible spongiform encephalopathy that affects deer and elk. It is similar to the TSE that causes "mad cow disease" in livestock, and which in Europe "jumped" from infected livestock to humans as a variation of the TSE Creutzfeldt-Jakob disease in humans.

The disease manifests itself via prions, or mutant proteins, which cause deterioration of brain cells. The effects include loss of weight and muscle control, blindness and dementia. There is no treatment and the disease is fatal.

CWD has been proved transmissible between deer and elk, but it has not been shown to be transmittable to humans. But neither has it been proved non-transmittable. The possibility, however minuscule, exists that a human could contract the fatal disease.

Since it was discovered in 1967 in wild deer in the northeast corner of Colorado, CWD has been a mystery. How it came to exist remains a question, but the most accepted theory is that it is a mutation of a TSE called "scrapie" found in sheep. A Colorado research facility that housed sheep, deer and elk in close contact is assumed to have been the genesis of CWD.

The disease for most of the past three decades seems to have remained localized in a small area of Colorado.

Interstate trade in "farmed" live elk and deer, some of which were infected with CWD, is assumed to have begun the diseases' spread to other states.

CWD has been identified in a half-dozen states and a couple of Canadian provinces, almost always associated with penned elk or deer.

The discovery of CWD in three wild deer in Wisconsin during a routine sampling of hunter-taken animals stunned most wildlife scientists and managers.

The disease never had been documented east of the Mississippi River, and never in an area where deer densities are as high as they are in Wisconsin.

The closest CWD cases were more than 900 miles from Wisconsin.

The discovery triggered a rush of states closing their borders to importation of deer and elk.

Texas, which has for years been one of the major players in live deer and elk traffic, shut its borders to all importation of deer and elk within a couple of weeks of the Wisconsin discovery.

Wisconsin officials began addressing the issue by killing and testing 516 deer in the area that produced CWD-infected animals. (There is no certified live-animal test for CWD; animals must be killed and brain or brain stem tissue analyzed to document infection.)

When 11 of those 516 deer proved infected with CWD, the state's Department of Natural Resources and politicians knew they had a severe problem.

In an effort to prevent the spread of CWD, Wisconsin wildlife officials are proposing to kill every deer in a 287-square-mile (about 184,000 acres) area where the infected deer have been found.

That will involve killing 14,000-15,000 deer, officials estimate.

Just how that will be accomplished remains a question. But the slaughter almost certainly will begin next month.

CWD has become a white-hot political issue in the state, where fingers are being pointed at agriculture officials who disregarded warnings about the possibility of CWD-infected deer being brought into the state.

McCallum said this week he will call a special session of the state's Legislature to address CWD-related issues such as regulation of feeding wild deer, a practice that crowds deer together and is suspected of making it easier for CWD to spread.

The Wisconsin Legislature has approved spending $ 4.4 million this year to fight CWD. Officials say they need at least $ 22.5 million over the next three years to contain CWD.

McCallum is asking the federal government for $ 18.5 million.

At least Wisconsin knows it has a CWD problem, and is addressing it. Other states, including Texas, probably have CWD-infected deer within their borders.

But because they do no testing for the disease, they have no evidence of its presence.

Other states are beginning to fashion CWD testing programs, though.

Iowa, which abuts the southwest corner of Wisconsin where the CWD-infected deer have been found, this week announced it will begin collecting brain tissue samples from road-killed deer and submitting them for CWD testing.

Iowa officials said they hope to collect 100-200 road-killed deer for sampling each month.

Texas has no CWD testing program.

But the Texas Deer Association, a trade group representing many of the state's 400-plus state-permitted deer and elk ranches, this past month promised to put together a voluntary CWD monitoring program in cooperation with the Texas Parks and Wildlife Department and Texas Animal Health Commission.

If the voluntary program is not accepted by TPWD and TAHC, the agencies could issue regulations for mandatory CWD testing.

The issue will be discussed at May 29-30 TPW Commission meetings in Austin.

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