Government To CWD Marked By
Denial And Delay
Scripps Howard News Service

Shortly after mad cow disease was first detected in the British countryside in 1986, officials stampeded to the microphones to assure the public that there was no risk to human health.
Ten years later, they admitted they had been wrong.
With the emergence of a similar disease in Colorado elk and deer, the official response, based on available science, echoes the early years of mad cow: Chronic wasting disease poses little risk to humans.
As recently as April, Mike Miller, the veterinarian spearheading Colorado's effort to contain the disease, lamented that the public's concern about CWD as a human health threat was "misguided." He said there is no evidence that chronic wasting disease in deer and elk will infect humans.
"It just seems that it is not at all likely" that humans could get the disease, he said.
But new federally sponsored research and two small clusters of a disease rarely seen in young people have other scientists concerned that Miller might be overly optimistic.
Response to mad cow in Great Britain and the United States was flawed. Consider:
- After disease detectives in Great Britain determined that mad cow, or bovine spongiform encephalopathy (BSE), was spread by feeding cattle infected meal, British officials banned the practice - in their own country. But they didn't ban the export of the feed around the globe, spreading BSE and causing economic devastation in continental Europe and Japan.
- It took the United States 10 years to follow Britain's lead and ban the feeding of cattle-derived meat and bone meal (MBM) back to cattle.
- One country that exports over a million cattle a year to the United States - Mexico - is just now adopting the ban on MBM as cattle feed.
No one can say if the record of dealing with chronic wasting disease will prove equally inadequate, but it, too, has been marked by caution and denial:
- A decade ago, Beth Williams, the scientist who discovered CWD, warned that the growing practice of raising elk on private ranches could spread CWD not only within those facilities but into the wild. State regulators paid little heed, allowing elk ranching to expand dramatically.
- Two small clusters in the United States of a rare and related disease have appeared in young people. Federal scientists stress that there is no link to CWD. Others are concerned.
Patrick Bosque, a leading TSE researcher who has worked closely with Nobel laureate Stanley Prusiner, said the most recent cluster "was the strangest thing I've ever seen." He said it was improbable that the two cases do not have a common cause, but not impossible.
The British cases started in August 1983.
Several dairy cows got sick and died. Researchers in veterinarian Ray Williams' group "believed we were dealing with an unusual condition for which we had no real diagnosis," the veterinarian later told an investigating committee.
In late 1986 came an answer. English cows were dying from a disease never seen before in cattle: bovine spongiform encephalopathy.
Soon, the world would know it by another name - mad cow disease.
The fight against BSE focused on one question: How were cows becoming infected?
The man tasked with finding the answer was epidemiologist John William Wilesmith of the British Central Veterinary Laboratory.
Wilesmith did what disease detectives do around the world - he tried to find out what these cows had in common. Within a year, Wilesmith had his theory down pat.
He had detected changes in the late 1970s and early 1980s in the amount of meat and bone meal (MBM) being used as a protein supplement in cattle feed, and in the temperatures used to cook the meal.
English sheep had been afflicted with a TSE called scrapie for more than 200 years. Wilesmith believed that a sheep with scrapie was rendered into meat and bone meal and ingested by a cow that caught the disease.
Sick cattle were rendered into still more meat and bone meal, setting off an explosive chain reaction.
Officials presented the issue as a public-relations problem with no implications for public health. BSE, after all, could never infect humans.
That mantra was repeated again and again by official after official. Those expressing doubt were shrugged off as fringe elements.
Wilesmith's epidemiology had proved that scrapie had crossed the species barrier to become mad cow in cattle. But popular opinion remained that it couldn't again cross a species barrier into humans.
The British government did make one concession to public concern. Any animals that looked sick - that is, showing clinical signs of mad cow - would be put to "slaughter and destruction." This, an official report said, would suffice "to protect (humans) against the remote possibility of transmission."
All the feel-good rhetoric came to a sudden end on March 20, 1996, when British officials said they had been wrong. At least 10 young people were dead or dying of new variant Creutzfeldt-Jakob disease, or vCJD, which is the name given the disease that mad cow causes in humans.
American reaction to BSE was marked by some quick action coupled with official blind spots.
In 1989, the United States banned live cattle and most cattle products from countries that had active BSE - but not from countries that had imported British cattle and MBM.
And because of that latter omission, the United States cannot be certain it has remained BSE-free, according to the General Accounting Office, a congressional unit that audits federal programs.
The United States also allowed the continued feeding of meat and bone meal to American cattle even after Wilesmith's warnings that MBM was inherently dangerous.
Dr. Stephen Sundlof, director of the Center for Veterinary Medicine at the U.S. Food and Drug Administration, said the FDA proposed banning the rendering of sheep to be fed to cattle in 1994, but backed down after objections from sheep and rendering interests.
However, "everything changed" when it was announced in March 1996 that BSE had been transmitted to humans. "It was not only an animal disease anymore," Sundlof said.
It took almost another year and a half for the FDA to put its slippered foot down, banning the feeding of most mammalian protein back to cattle and other ruminants.
The GAO revisited the issue this year and was highly critical of the FDA. The GAO said the FDA had failed to enforce the feed ban, issuing warning letters to a small percentage of firms not in compliance and shutting no one down.
A spokesman for the USDA and officials with the National Renderers Association say that foreign trade in U.S. MBM is not a problem because there have been no cases of mad cow disease in this country.
Some countries importing MBM have had few if any rules concerning its use as cattle feed.
Mexico, for example, implemented labeling rules only this year, according to Alberto Celis, the National Renderers Association regional director for Latin America.
That was news to many agricultural business people attending an animal-feed trade show in Guadalajara in March. Representatives from three animal feedbag manufacturers said they had heard of no such regulations and that their bags remain warning-free.
Mexico exports over a million live cattle a year to the United States. Mexican cattlemen said these "feeder" cows are not typically fed animal protein, though there is little evidence that the government has an adequate inspection program to make certain.
Richard Patton, a nutritionist and independent consultant to the American dairy industry, said U.S. MBM in Mexico should be watched as carefully as "you would watch a hand grenade with the pin pulled."
Patton, who was at the Guadalajara animal feed expo, said that while most large operations were likely aware of the dangers of MBM, he doubted smaller ones would be. "Let's be realistic," he said.
MBM isn't the only hole that mad cow disease could slip through. Vaccines using bovine blood serum, cosmetics and even food supplements have all worried scientists. Vaccines are of particular concern because they are given to the most vulnerable - children.
The FDA asked manufacturers of vaccines to stop using bovine blood serum and other materials from British cattle in their products. But this was not an order, simply a recommendation.
Some drug companies ignored the recommendation for seven years, complains Peter Lurie, a doctor and deputy director of the consumer organization, Public Citizen's Health Research Group.
"My main beef about vaccines was the failure of the FDA to regulate the industry and the consequent thumbing of the nose by the industry to the FDA," Lurie said.
The story of CWD disease in U.S. deer and elk has eerie echoes from the early days of BSE in England.
One of Colorado's chief goals has been to dampen any panic and preserve the hunting industry, while reporting what is known about the disease.
What seems clear from the record is that officials and members of the media have not been overly concerned about CWD until quite recently.
The first mention of the disease in Colorado media was in 1995, 18 years after scientists knew there was a TSE spreading in elk and deer.
Reports said officials considered CWD "a minor problem in localized populations of deer and elk."
That same year, big-game managers actually tried to increase deer herds by restricting hunting permits - a policy that could only spread the disease, and one that has since been reversed. State wildlife officials, however, advised hunters not to eat obviously sick animals - a step once taken as an adequate measure for protecting humans in Great Britain.
The problem with this otherwise sound advice is that a deer can last for two to three years having infectious CWD prions without showing outward signs of the disease, according to CWD researchers.
By 1998, officials had extended their advice to include a recommendation that hunters should not eat brain and spinal cord materials from any deer or elk.
>From 1996 through 1998, the Colorado Division of Wildlife made it mandatory for hunters in about a dozen hunting units in the endemic area to bring in the heads of their animals for testing.
In February 1999, wildlife officials said CWD was not spreading, and reiterated that there was no risk to humans, something they repeated almost every time the disease was mentioned.
Even after the disease was detected in elk ranches, no real alarm went off. "We don't think the problem is a big deal," veterinarian Miller said in October 2000.
In November 2000, though, the state began examining plans to try to control the disease by lowering the population of deer in the endemic area.
The disease was spreading faster and wider than anything officials had anticipated.
And the stakes are high.
At least in penned deer and to a lesser extent in the wild, CWD is highly contagious. And there is no proof, but some evidence, that humans are susceptible to the disease.
In test tubes, CWD prions can convert human prion protein into the deadly form, albeit inefficiently. They do this at nearly the identical rate that BSE prions convert human prions to mutants, according to research at the Montana labs.
No one can be certain what CWD might look like if it should pass to humans. And no primate research is currently being conducted to try to answer that question, something the FDA says should change.
There are no proven cases of humans being infected, but there is a statistical anomaly that has caught scientists' eyes.
After mad cow disease had migrated to humans in 1996, researchers began looking for any increase in TSE-like disease in young people, which is almost unheard of. In a 17-year period ending in 1996, there were only four sporadic CJD cases among those 30 or younger in the United States. Then, in short order, there were four more cases.
Researchers found that the four new cases, appearing from 1996 to May 31, 2000, had no known risk factors for CJD, such as taking human growth hormones or travel to Europe.
But they were concerned that three of the four were venison eaters. The U.S. Centers for Disease Control and Prevention in Atlanta launched an investigation to determine if their cases were connected to CWD.
The CDC found that none was known to have hunted in the endemic areas of Colorado or Wyoming, though two did eat meat from animals killed in non-endemic areas in Wyoming and the third had his meat processed at a plant that also butchered Colorado elk.
In microscopic examinations of brain tissue after three died, the disease looked more like traditional CJD than it did tissue from British vCJD victims.
This led scientists to conclude that there was "no strong evidence for a causal link" between CWD and the three young venison eaters.
Ermias Belay, the CDC scientist who wrote those words, said: "I can't say I'm absolutely convinced" that the venison eaters didn't contract their disease from eating venison.
"All I can say is that all the evidence we have to date does not indicate that chronic wasting disease has caused illness in the three patients. I have to be cautious because we can only go by what we have."
Asked if it was possible for CWD to infect humans, he said: "That's possible. Definitely possible. But do we have evidence of it? No."
Bosque, the Colorado prion scientist, said the cases of the three venison eaters constitute "a bit of evidence that the disease might be transmissible to humans."
"I think that if humans were very susceptible to CWD, we would know by now, since hunters have probably been consuming infected deer for some time," he said.
"But if CWD is transmitted at a low rate - say 1 in 1,000 or one in 10,000 - we might not be able to easily see this."
Wildlife veterinarian Miller is less equivocal. "CDC made of it that there's no connection to chronic wasting disease. I would make of it that there's no connection. There simply is or is not a relationship and in this case there's not."
As long ago as 1986, a research paper by Nobel Prize-winner Carleton Gajdusek found a significant statistical link between CJD and human exposure to deer and animal organs.
Denver mathematician George Bardwell called the data - which looked at 26 CJD cases against 40 controls - "highly significant."
Tracie McEwen, the widow of the first young venison eater whose case was investigated by the CDC, has a theory.
"I'm not a scientist, but I don't understand why that's so hard for people to make that leap, when you had them in Britain saying, 'Oh, the beef is safe, the beef is safe.' "
None of this is convincing to Miller.
As far as CWD's connection to CJD, he said, "There's no connection in any way, shape or form." To suggest otherwise, he said, would involve "inference and innuendo.
"There is no evidence that CWD is infective to humans."
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