DATE=3/09/01

TYPE=AGRICULTURE TODAY #2147

NUMBER=7-34604

TITLE=Origins of Mad Cow Disease (CORRECTED)

BYLINE=ROB SIVAK

TELEPHONE=202-619-2023

DATELINE=WASHINGTON

EDITOR=SMART

[RE-RUNNING W/DAVID BROWN'S CORRECT UNIVERSITY ID, P4]

CONTENT=

INTRO:While European health officials wrestle with an expanding outbreak of Foot and Mouth Disease among the region's livestock herds, they continue efforts to control another, slower-moving, but more deadly livestock epidemic of Mad Cow Disease, or B-S-E. VOA's Rob Sivak reports that despite decades of research, scientists still can't agree on the origins of this strange and devastating illness:

TEXT:B-S-E is one of a family of fatal brain-destroying diseases that can infect not only cattle but sheep, mink, wild elk and deer, and, rarely, humans. Research suggests the disease can jump species lines. B-S-E-infected beef, for example, is widely believed to be the source of a new human form of the disease - variant C-J-D - that has so far killed 90 people, most of them in Britain, where B-S-E was first diagnosed in cattle nearly 20 years ago.

Many scientists support the theory - first advanced by American researcher and 1997 Nobel laureate Stanley Prusiner - that B-S-E and the other brain-wasting diseases are the work not of viruses or bacteria but mysterious, mutant forms of nerve-cell proteins called prions.

But how and why did B-S-E suddenly appear in British cattle? The prevailing theory endorsed last year in the British government's formal inquiry into the disease is that the first B-S-E prions might have simply mutated naturally into being, sometime in the 1970s, in a single British cow. Ermias Belay (buh-LYE), an epidemiologist at the U-S Centers for Disease Control and Prevention in Georgia, says B-S-E probably spread to other cattle through unwitting human actions:

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"The original BSE has not been conclusively identified. But the subsequent transmission of B-S-E among the cattle population in the United Kingdom and other European countries has clearly been shown to be associated with consumption of the contaminated meat and bone meal meat and bone meal that was sourced from cattle that had already died of B-S-E."

TEXT:Convinced that this was true, the British government banned the use of meat and bone meal in cattle feed in 1988. Eventually all uses of cattle-derived meat and bone meal were banned. But new cases of B-S-E continue to appear, even in cattle born after the ban.

That doesn't surprise British farmer Mark Purdey, who raises organic beef and feed grains on his Somerset County farm. He believes the B-S-E epidemic has nothing to do with meat and bone-meal. The real trigger, Mr. Purdey argues, was the British government's livestock pest control program in the mid-1980s, in which farmers were ordered to treat the heads and backs of their cattle with organophosphates, a powerful class of chemical pesticides. When B-S-E broke out a few years later, Mark Purdey felt certain there was a connection:

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"Initially, like most things in science, it was an intuitive flash, a sort of hunch I had about this. I mean, I knew that organophosphates were toxic to the nerves, and that they exerted their toxic effect by actually deforming the molecular shape of proteins in the central nervous system. And as I became acquainted with Stanley Prusiner's work in California, I noticed that this disease seemed to be hallmarked by the presence of a particular protein, the prion protein, whose molecular conformation was deformed. So I sort of put two and two together and I thought, well this seems to be, could be, something to do with the origins of the disease."

TEXT:Mark Purdey has been investigating that possibility for the past 16 years, discussing his ideas with biochemists and epidemiologists, and traveling to countries around the world to study isolated outbreaks of similar brain-wasting diseases among sheep, wild animals and humans. What he and other independent researchers have found is that in many victims of the disease, copper molecules that normally are attached to nerve-cell proteins have been replaced with manganese a molecule found, among other places, in organophosphate pesticide.

Mark Purdey presented this evidence to Britain's official B-S-E inquiry board in 1997, but its members were not convinced. In a summary report, the board said it would need to see more evidence to justify government support of research in this area. Mr. Purdey says he believes fear of damage suits arising from the 1980s pest control program could be a factor in the British government's response. Biochemist David Brown of Cambridge University, who has documented how manganese creates deadly prions, believes the pesticide connection is one of several important clues to the origins of B-S-E that Britain and other nations at risk should be studying more closely:

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"Certainly there is reason to investigate as many possibilities as can be imagined as to what is causing these diseases. And the main thing I try to get across to people is not that this is the answer, but simply that we don't have the answer. And if we just say well, 'B-S-E was caused by the offal and variant C-J-D is caused by eating B-S-E,' when we have no real concrete evidence for this, then we are putting ourselves in a dangerous position."

TEXT:Other experts say the organophosphate theory of brain-wasting disease has been studied fairly extensively, though not conclusively. And many involved in B-S-E research point out that Stanley Prusiner's popular prion theory is itself not yet proved. Robert Rohwer (pron. ROAR), a neurovirologist at the Veterans Affairs Medical Center in Maryland, points out that no mutant prions have ever developed in any of America's 100 million cattle a much larger herd than Britain's even though the odds would seem to favor an outbreak. Mr. Rowher says many of his colleagues suspect B-S-E is actually caused by a virus, probably of wild animal, or zoonotic origin, that has so far eluded detection:

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"There's a much better model for what went on in the BSE epidemic, in virology. And in fact it is a recurring model, and that is the phenomenon of newly emerging diseases, diseases which exist in one species and through some event make a jump to a new species, and suddenly expand in that species. AIDS is a perfect example, one of the most recent examples of that. My guess is that BSE originated from some zoonotic source, and we just haven't identified it yet. My guess is we will eventually identify it. Because once we have the chemical re-agents (markers) to look for these things, we'll find them."

TEXT:Mr. Rowher says the biggest challenge to those studying the origins of B-S-E is securing scarce research money. Ermias Belay, with the U-S Centers for Disease Control and Prevention, says governments naturally favor research that can immediately reduce public health risks:

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"Anything is possible, and every lead has to be investigated and ruled out. But...for public health measures to be put in place, you can't wait until you identify what the disease agent is."

TEXT:Yet experts warn that until the cause of B-S-E and similar brain-wasting illnesses is positively identified, public health officials will never be sure how to prevent its spread or how to develop a cure. (SIGNED)

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