How now mad cow?

Since the BM7's last editorial on the topic' another 40 000 cases of bovine spongiform encephalopathy have been confirmed in cattle. New cases are being confirmed at the rate of 500 a week. Does it matter that between 1986 and 1989 we actually had the offal, which is now proscribed, going into the food chain?2 Several reasons are given for dismissing bovine spongiform encephalopathy as carrying an unimportant risk to humans.' 3-7 Most are based on extrapolation from the natural or experimental spread of scrapie (the equivalent disease in sheep) and from epidemiological studies of the human spongiform encephalopathies, notably Creutzfeldt-Jakob disease. Importantly, no association has been found between the incidences of bovine and human forms of disease. This is probably due to the species barrier, which makes transmission of the diseases between species difficult if not impossible. Neither do the characteristics of Creutzfeldt-Jakob disease point to an infective origin. As we have long been exposed to scrapie these findings suggest that we do not contract spongiform encephalopathy from animals or their products. As further reassurance, experimental dietary transmission of bovine spongiform encephalopathy and scrapie, although it has been achieved, is often unsuccessful even with large amounts of infected offal, and no appreciable infectivity of milk or meat has been shown. Finally, the lack of evidence of spongiform encephalopathy spreading in cows suggests that cows are an end host for the disease, which will die out over the next few years given the precautions already taken. Other considerations, however, imply that the risks of bovine spongiform encephalopathy cannot be ruled out.468 These diseases are transmissible orally, conjunctivally, and iatrogenically-evidence of the causative agent's extreme resistance to inactivation. The prolonged infectivity of soil contaminated with scrapie is further evidence of this.9 Furthermore, the species barrier did not stop foodstuffs infected with scrapie causing bovine spongiform encepha-lopathy'0 and, as passage through a species may alter the pathogen's properties, the lack of risk to humans posed by scrapie might not apply to the agent causing bovine spongi-form encephalopathy. Recent cases of spongiform encephalopathy in species not previously known to be affected (for example, cats) may also be a new occurrence causally related to bovine spongiform encephalopathy rather than just reflecting heightened surveillance .3" Additionally, the long incubation period during which animals can transmit disease means that offal from asymptomatic cows with the disease must have been eaten before the restrictions were imposed in …