IT WAS profoundly disappointing to watch Ann Veneman, the US Agriculture Secretary, announce the first case of BSE in the United States at Christmas, not simply because another country was blighted by this degenerative brain disease, but because the presentation was all too familiar. That an Agriculture rather than Health Secretary sought to reassure about risk to human health, and that she said she would be feeding her own children beef, was as reminiscent of the early stages of the outbreak in Britain as it is scientifically inane. There are many lessons the Americans could learn from the British experience, and the following months will prove crucial.

The first, and most important, is that infection with the human form of so-called “mad cow” disease may be more widespread than commonly assumed. Around 140 people have died of vCJD (the human form of BSE). While each case is a tragedy, this relatively small number in public health terms has been interpreted to mean that the human cost will be small. The largest number of reported cases was in 2000, leading to assumptions that vCJD has peaked and will now decline with a death toll of a couple of hundred. I must point out some uncomfortable facts that challenge such optimism.

We are used to infectious disease epidemics, such as influenza or foot-and-mouth disease, that arise and decline over weeks and months. However, we know from the disease kuru, transmitted among the Fore people in Papua New Guinea during cannibalistic feasts with devastating effects, that human prion disease epidemics can span decades with incubation periods that can exceed 40 years, with an average of around 12 years.

We also need to think about the effect of the so-called “species barrier”. When prions from one species infect another species, the incubation periods seen are typically very much longer. Average incubation periods of BSE prions in human beings of 30 years or more would not be surprising based on such comparisons.

By definition, those who have already got vCJD are those with the shortest incubation periods. These people do not seem to have been exposed to more BSE in their lives, suggesting that they may be particularly vulnerable as a result of their genes, or the presence of unknown environmental factors. We know that our genes have a major bearing on incubation, but until we understand more about this, we cannot know if the current vCJD patients represent a first wave, with other peaks, perhaps much larger, to follow.

In short, while it would be marvellous if it were true, the science suggests much caution in concluding that the human BSE problem is receding at what is, in the timescale of human prion diseases, this early stage.

So has America taken this problem seriously enough? Ann Veneman’s later statement announced some sound measures to protect the public — notably bans of high-risk cattle tissues in human food, on air-injection stunning of cattle and the use of mechanically recovered meat.

However, some of her comments resonated in the British ear: “I will stress again that our food supply and the public health remain safe” and “our goal is to see trade resume as quickly as possible”. But one piece of scientific advice given repeatedly to the British Government on the risks of BSE is that “absence of evidence is not evidence of absence” and no doubt our US scientific colleagues will advise likewise.

WHAT would reassure is proper surveillance of animals, using tests at abattoirs and of fallen stock. It will be interesting to see if Veneman’s scientific advisers agree that testing 20,000 cattle per year in the US (out of a total of more than 35 million slaughtered annually) is the “very aggressive surveillance programme” that she described. If their BSE case is due to contaminated feed, it is hard to imagine that there will not be others in other herds.

While agriculture ministers the world over will quite properly defend their important beef industries, it is to be hoped that they learn the UK lesson. Openness about the uncertainties from the beginning is in the end less damaging to commerce than denial and misleading statements on risk that cannot be scientifically substantiated and that, if proved wrong, severely damage public confidence in government (and science). In these post-9/11 times, restoring and maintaining public confidence in governments’ management of risk on both sides of the Atlantic should be paramount.

The author is director of the Prion Unit at the Medical Research Council

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