Good News About Mad Cow Disease

This article for The New Republic was written by D.T. Max.

Most experts in America who aren't in the pocket of the meat industry believe we will sooner or later get a case of mad cow through a domestic infection, and that we've almost certainly already had one. The only reason we haven't noticed, they claim, is that we do such a lousy job looking for it, testing only one out of every ten thousand animals going to slaughter. "The way we tested we did not want to find" out, says one.

Still, neither do most experts believe we're in the midst of a mad cow epidemic: Even if we wouldn't have detected it in cows, we would certainly have detected it in humans by now. Yet while Europe has had roughly 200 cases of the human version of mad cow disease, called variant Creutzfeldt-Jakob disease, caused by some hundreds of thousands of infected cows, we've had none. Are we doing something right or is this just dumb luck?

As it happens, maybe a little of both. A cow can get BSE two ways: through feed infected with the prion -- or irregular protein -- that causes mad cow, or through spontaneous disease. In the first instance, we benefited from the fact that our response to English mad cow was swift and severe. Scientists established a link between feed and disease soon after mad cow made its appearance in England. And, soon after that, the USDA tracked down the roughly 17 tons of bone feed and the 500 or so British cattle that had entered the country, all of which were destroyed or contained. (British cattle are believed to have contracted the disease by eating sheep infected with scrapie, another prion-borne disease. The British made a practice of using sheep as cattle feed up until the late 1980s.)

But luck also intervened: It was easy to root out the contaminated food because the quantities were so small. "Our escape to date has a very simple explanation," Paul Brown, an NIH scientist who wrote the Brussels-based International Life Sciences Institute's report on mad cow and related diseases, told me in November. "[T]he reason we didn't [import more cattle feed] is that we didn't need it. If we didn't have any infectious material coming in, we weren't going to get infected."

Canada, by contrast, was not so fortunate. The Canadians have similar feed laws to ours: Ruminants -- sheep and cattle -- cannot be fed other ruminants in their feed. And cattle that collapse on the range (breezily called "downer cattle") are selectively tested. But Canada never tracked down the English cattle and bone feed it imported during the mid '80s and into the '90s, when the incidence of mad cow was at epidemic levels in England. One important reason is that there was so much of it to track. That feed may be the original source of the infection that still haunts the Canadians, producing two known mad cows in the past year.

Theoretically, a single domestic cow could also come down spontaneously with the disease and then enter the food chain. The end-of-year scare has led the administration to try to tighten the rules to prevent this from happening by prohibiting downer cattle, the most likely culprits, from entering the food supply. But there's nothing in the proposed rules that would prevent those cows from being turned into feed for non-ruminants, like pigs and chickens. This leaves us exposed to the same problem that puts peanut traces in unrelated foods: Machine workers aren't surgeons; they don't sterilize. Traces of the last occupant of the conveyer belt often remain. And that's assuming their bosses don't cheat and throw feed meant for pigs into the cow feed trough. This muddled process caused the sickness of an estimated 30,000 cows in England after an initial ban on ruminant feed was put in place in 1988.

Will this be our problem? Unlikely -- thanks again to a mixture of luck and foresight. It's true that we have many stupidities in our mad cow policy. The USDA will never be willing to gore America's ox (to mix my ruminants). England and most European countries test all cows 30 months or older that are to be eaten. We don't. Japan tests every cow destined for the dinner plate. On the other hand, we also denature the animal proteins meant for feed at a higher temperature and with harsher chemicals than the English did (though with this, as with every fact related to mad cow, there are disagreements over the significance).

There will be more cases of mad cow here sooner or later -- more from Canada, some homegrown (though given the interconnectedness of the North American economy, the distinction may be meaningless). And it's always possible that the unthinkable happens -- maybe chronic wasting disease, which afflicts deer, will somehow cross into domestic cattle (that was the rumored route of infection for Canada's spring 2003 mad cow); maybe some very clever terrorist will figure out a way to spike our feed (the military has just awarded research grants of more than $40 million in part to consider the possibility). It's worth remembering that everyone was wrong once before -- when mad cow did what it theoretically couldn't and crossed over to humans in the mid '90s.

But the reason most experts don't foresee huge increases in mad cow down the road is that we don't start from the same level of infectivity as other countries. Epidemics obey the rules of positive feedback loops: Trouble begets trouble. If luck has more or less worked for us thus far, it's a good bet it'll keep working in the future.

D.T. Max is at work on a book about mad cow and other prion diseases.

By D.T. Max
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