NR ARWW
AU Rees-Mogg,W.
TI Let's not all go mad about BSE
QU The Times (London) 1996 March 25
PT Zeitungsartikel
VT
The species barrier may not protect us completely, but this disease may have existed for centuries.
Diseases come and go, and their history is obscure. There is still controversy over the real cause of the Plague of Athens, despite its importance to the history of the ancient world; we know that syphilis was epidemic at the Siege of Naples in the 1490s, but cannot be certain whether it was taken to America by Columbus in 1492, or brought back from there; we do not even know for sure whether, as seems likely, the HIV virus crossed the species barrier from monkey to man. We should, however, make the general assumption that diseases have a long history, and exist for centuries before they are accurately identified. Of course, diseases do transmute and can become much milder, or more dangerous.
The dictionary seems to suggest that BSE itself may always have existed among cattle. Since the 16th century, a disease, or a group of diseases, known as "the staggers" have been recorded. The Oxford English Dictionary defines "staggers" as "a name for various diseases affecting domestic animals, of which a staggering gait is a symptom". The first citation is from 1577, "if he [a bullock] has the staggers, he wyl looke very red about the eyes". The mid-19th-century veterinary writer W.C.C. Martin, in his book Ox, refers to "inflammation of the brain, phrenzy, mad staggers or sough and apoplexy".
"Staggers" appears in Samuel Johnson's great Dictionary of 1755, though he calls it "a kind of horse apoplexy"; he quotes Shakespeare, "his horse starks boiled with the staggers". No doubt the Oxford Dictionary is right that the staggers were symptomatic of various diseases, but nevertheless it seems probable that BSE was one of them, and existed as a rare disease in cattle, as Creutzfeldt-Jakob disease has been in human beings, for a long time. The comparable disease in sheep, scrapie, has of course been much more common, and is more freely trans mitted between sheep. Pasture land can become infected with the scrapie agent, but there is no evidence of cross-infection of this sort by the BSE agent, which passes either by eating infected material or possibly by breeding from infected cattle.
The point is not merely an academic one. No one can prove that the "mad staggers" was the same as "mad cow" disease, but in some cases it probably was. If that is so, human beings have been eating BSE-infected animals for hundreds of years. If the BSE agent easily crossed the species barrier and infected humans, one would expect there to have been many clusters of Creutzfeldt-Jakob, in families and even in whole villages which had consumed the same infected carcass. In pre-20th-century medicine the condition could not have been precisely diagnosed, but the clusters themselves would have been remarked upon it might well have been thought that this was a hereditary disease, concentrated on particular families and communities.
In Somerset it is in any case widely believed that the present epidemic did not start in the mid 1980s, but some years earlier. There is anecdotal evidence of cows suffering from what would now be diagnosed as BSE in the late 1970s, and these cases were not confined to the West Country. No one knows what the latency period of Creutzfeldt-Jakob disease is in human beings. Most infections which have a long latency period, such as syphilis or Aids, have a very variable one the onset of full-blown Aids after the initial HIV infection certainly varies from less than three to more than 20 years. If BSE-infected cattle from the early stages of the present epidemic were being eaten, wholly without precautions, by human beings as long as 20 years ago, then one would expect a human epidemic to be only too evident by now, if human beings were highly susceptible. There were only 40 cases of Creutzfeldt-Jakob in 1995.
The ten cases which have changed the view that BSE is most unlikely to infect human beings are paralleled by a small epidemic in cats, although there does not seem to have been a comparable epidemic in dogs, which must also have eaten their share of BSE-infected meat and offal. The cat epidemic has been a small one fewer than 200 infected cats seem to have been reported and is now rapidly trailing off, with about one case a month. The epidemic in cttle itself is also now past its peak, though the total numbers have been much larger, and the epidemic has persisted longer than was originally expected.
I suspect that the cattle epidemic may eventually prove to be similar to the recorded epidemic of Creutzfeldt-Jakob in New Guinea. That was caused by cannibalism. Until the mid 1980s, cattle were being fed the meat of other cattle in their protein feeds. They were at the same time being fed sheep protein, which in some cases would inevitably have contained the scrapie agent. The rapid spread of the epidemic suggests that it is rather more likely to have been an indigenous cattle disease than a cross-species sheep disease. Cows have historically been able to crop scrapie-infected pastures quite safely, where sheep become infected. The infection of some zoo animals, cats and possibly the ten human beings, does suggest that the BSE agent may be able in some cases to cross the species barrier; nevertheless, the history of the disease, probably existing in sporadic form for centuries, and in epidemic form for 20 years, suggests that the risk to humans is likely to prove low. There were only four suspected cases in 1995, which is at least ten and probably 20 years after the first exposure of substantial human populations to the BSE agent. It seems likely that the species barrier is still a substantial safeguard, even if it proves not to have been a perfect one.
Nevertheless, people will feel safe eating beef only when the whole British herd is BSE-free. These ten cases have raised a doubt, and no one can be sure whether the human epidemic will prove non-existent, tiny, as it has been so far, small, as it has been with cats, or larger. If the cross-species infection reached the same level in human beings as in cats, the deaths from Creutzfeldt-Jakob disease might rise from about the present 50 spontaneous cases to about 200 cases a year, or something on that scale.
The experience of local farms in Somerset seems to support the view that the animal feed was responsible for the epidemic. A small local dairy farm has always bred its own cows and grown its own feed; it has not had a single case of infection. Another somewhat larger farm used to buy in some feed; early in the epidemic it had three cases of BSE, all in cows which had eaten feed from a single delivery. This farm too has decided to rely entirely on home-grown feed, and has had no recurrence of the disease. As I understand it, there have been no cases of BSE on organic farms, except among bought-in cattle. It is safe to say that nobody will ever again try to turn herbivorous cows into cannibal carnivores.
The Government ought now to concentrate on producing a BSE-free national herd as quickly as possible. Only when that has been achieved will other countries be willing to import British beef, or will British consumers feel entirely safe in buying it. The evidence is that much the largest reservoir of BSE infection is among the older dairy cows. A policy of culling them, with full compensation and not necessarily all at once, followed by post-mortem examinations to establish whether they were showing early symptoms of the disease, could speed the ending of the epidemic. That at least ought to be done.
At the same time, disease-free herds should be identified. No doubt there has been evasion and some downright lying otherwise a policy of separating the disease-free from the high-risk herds would be straightforward. Yet the Government's objectives should be those that commonsense suggests. First we need to establish beyond doubt which herds are already clear. Then we need to establish that the epidemic is over, and that Britain is clear of BSE.
SP englisch
PO England