document: The epidemic of bovine spongiform encephalopathy or ` mad cow ' disease - which has killed more than 100,000 animals in the UK - is causing a new wave of public concern . New cases are still running at almost 1,000 a week and last month a second dairy farmer died of Creutzfeld-Jacob Disease , a brain disorder similar to BSE . Richard Lacey , a microbiology professor at Leeds University and the leading critic of government policy on BSE , said the deaths this year of two farmers whose herds had suffered from mad cow disease could not be put down to chance . He believes that BSE can trigger human brain disease . ` Our worst predictions are coming true , ' he said . ' I find it unbelievable that the government and their hand-picked advisers can go on telling the public there is no danger . ' The advisers , led by the government 's chief medical officer Kenneth Calman and chief veterinary officer Keith Meldrum , put out a detailed statement to justify their view that last month 's death of 65-year-old Duncan Templeman - following that of Peter Warhurst , 61 , a year ago - showed ` no features that give cause for undue concern ' . The official view is that the deaths are an unfortunate coincidence , even though it is statistically unlikely that two dairy farmers should contract a disease as rare as CJD . Robert Will of Edinburgh 's Western General Hospital , who has been monitoring CJD in the UK since 1990 on behalf of the health department , calculated that there was only a five per cent probability of even a single case occurring by chance among dairy farmers with BSE-affected herds . One argument put forward by the health department is that CJD has such a long incubation period - typically 10 to 20 years - that clinical symptoms would not yet have appeared , even if BSE had triggered any cases of CJD . ` Since the illness of the cows -LRB- in Templeman 's herd -RRB- and the patient occurred within months of each other , the animals and the patient had presumably incubated disease in parallel for some years , ' the health department said . ` It is most unlikely therefore that there is any direct link between the cases of BSE and the occurrence of disease in the patient . ' Another reassuring argument is that both farmers showed clinical features typical of the ` sporadic form ' of CJD - of unknown cause - that usually occurs in late middle age . The handful of patients known to have developed CJD through infection -LRB- from contaminated human growth hormone -RRB- showed a different pattern of symptoms . The second annual report of Will 's National CJD Surveillance Unit in Edinburgh , published last month , shows what looks at first sight like a disturbing rise in incidence : from 32 UK cases in the year ended April 1991 to 37 in 1991/92 and 46 in 1992/3 . But the report says that this is not statistically significant and is probably due to increasing awareness of CJD -LRB- some cases were previously attributed to Alzheimer 's or other forms of dementia -RRB- . Meanwhile , cattle are succumbing to BSE at a rate of about one per 100 every year . The epidemic continues to defy the ministry of agriculture 's predictions that it is about to wane ; so far this year there have been 26,695 reported cases , compared with 25,898 to the same date last year . The source of infection was protein-rich cattle feed contaminated with scrapie , a related brain disease of sheep . Although sheep-derived feeds were banned from sale in 1988 , farmers apparently continued to use existing stocks for longer than the ministry had expected . The incubation period is also longer than originally expected . Veterinary experts say that almost all of the 102,000 confirmed BSE cases so far can be attributed to scrapie-contaminated feed . According to their investigations , maternal transmission from cow to calf - which would prolong the epidemic - is very rare or non-existent . Scientists trying to understand the epidemic face an unusual problem : BSE , scrapie and CJD are caused by a bizarre , infectious agent , the prion , which does not follow the normal rules of microbiology . Recent research shows that the prion is an abnormal form of a protein that is normally present in the brain -LRB- though its normal function is not yet known -RRB- . Unlike viruses and bacteria , prions contain no genetic material of their own . The prion may arise by a genetic mutation -LRB- spontaneous or inherited -RRB- in the host animal . Or - in the case of BSE - it may arrive from another animal . Once in place in the victim 's brain , it catalyses what John Collinge , a prion researcher at St Mary 's Hospital Medical School , London , called a slow ` chemical chain reaction ' , converting the normal protein into its own abnormal form . The prion molecule is folded in a way that makes it extremely stable and therefore difficult to destroy by conventional sterilisation . Experiments show that BSE can be transmitted between species , for example from cow to monkey , by injecting or eating large amounts of infected tissue . But ` transmission is dose dependent , ' Collinge says . Most independent experts maintain that no human being - dairy farmer or beef eater - is likely to be exposed to BSE in sufficient quantities to develop brain disease .
extractive_keyphrases: mad cow disease bse bovine spongiform encephalopathy public concern human brain disease maternal transmission epidemic
abstractive_keyphrases: scrapie-contaminated feed