Volume 1: Findings and Conclusions
3. The early years, 1986-88
Identification of a new disease in cattle

166 The epidemic of BSE may have started with a single diseased cow. Why should that cow have developed BSE? It is possible that the disease developed spontaneously as a consequence of a genetic mutation. It is possible (though we believe less likely) that a mutant strain of the scrapie agent transmitted to one or more cows. There are other possibilities. No one will ever know.

167 When was the first case? The epidemiologists, with their skills in back calculation, suggest in the 1970s. Where was it? Again no one can say, though epidemiologists would point to the early concentration of cases in the West Country as suggesting that BSE may well have come from there.

168 Did the first case get ill on the farm and end up in the knacker's yard, or was it sent to be slaughtered for human food - perhaps before the signs of the disease were even showing? We cannot know. What we can deduce is that, by one route or another, the animal's head, together with other unwanted offal, was sent to the renderers. The parts carrying the BSE infection contaminated the batch of meat and bone meal (MBM) produced from the rendering. That MBM was sold to a food compounder and mixed into cattle feed, contaminating that feed. That feed may have infected many cows and some of these, by a similar series of events, infected many more. Thus, like a chain letter, the spread of the disease was almost exponential.

169 The disease spread wide, and it spread at first unnoticed. It spread wide because MBM may travel long distances from renderers to the feedmill and the cattle feed produced by the mill may be widely distributed. The calves which eat the feed may end their lives far from the farms on which they were born.

170 It spread at first unnoticed because most infected cattle were slaughtered before showing clinical signs of the disease. When clinical signs did appear, they were similar to those of some other diseases of cattle. Only histopathology of the brain could reveal the existence of the new disease. Before that could happen the carcass had to be sent by a vet to one of the regional State Veterinary Investigation Centres (VICs), and from there the brain had to be sent to the Pathology Department of MAFF's Central Veterinary Laboratory (CVL) at Weybridge. Most cattle infected with BSE went for slaughter before the clinical signs developed ('subclinical cases'). Where a single cow fell ill, the farmer was unlikely to want a post-mortem examination and, for some reason, not yet clear, BSE tended to strike down single cows in a herd.

171 The first brain from a cow with what we now know as BSE reached the CVL in September 1985. It came from a herd in Pitsham Farm in Sussex where unusually a number of cattle had been struck down with symptoms that we now recognise as typical of BSE. The CVL pathologist identified the condition of the brain as spongiform encephalopathy, but concluded that this, and a kidney condition from which the animal had also suffered, was probably caused by toxicity of some description. ¹

172 At the end of 1986 pathologists at the CVL identified the possibility that cattle had developed a spongiform encephalopathy that was transmissible in the same way as scrapie was in sheep. This followed the submission of brain samples from a herd in Kent and another from near Bristol. Mr Raymond Bradley, head of the Pathology Department, remarked in a note to colleagues:

If the disease turned out to be bovine scrapie it would have severe repercussions to the export trade and possibly also for humans.

173 One witness described meeting Mr William Rees, the Chief Veterinary Officer (CVO), who had just heard the news, with 'steam coming out of his ears'. ²

174 The CVL pathologists identified the emergence of a new disease, which they considered might be a bovine form of scrapie, as soon as could reasonably have been expected. They are to be congratulated - particularly Mr Gerald Wells and Dr Martin Jeffrey, who carried out the initial histopathology.