Bovine Spongiform Encephalopathy (BSE) is one of a group of diseases known as the Transmissible Spongiform Encephalopathies (TSEs), so called because they cause a spongy appearance to occur in affected brains. They rarely cross the species barrier. In cattle, the disease occurs in adult animals, typically 4-5 years old. It is a neurological disease and the brain changes produce abnormalities in posture, movement, behaviour and sensation. There is a gradual development of clinical signs over several weeks and the disease is progressive and fatal. Since the disease was first diagnosed in the UK (see history below), a great deal of research has been carried out to determine the cause both in terms of the agent(s) affecting the brain and the method by which it entered the cattle population.

Firstly, the agent. There is still some uncertainty here because the specific infectious agent has never been isolated and there is no detectable immune response. However research strongly suggests that the cause of all TSEs is the presence of a structurally modified form of the Prion Protein which is found in the central nervous system normally.

Secondly, the method. Many studies have been carried out to look at all the factors which might have been responsible for the appearance of the disease or affected its course. The only common feature found in all the herds and cases studied, was the feeding of commercially produced compound feed containing meat and bone meal. This is supported by the fact that the disease has been more prevalent in dairy herds where compound feeds are fed to calves from a very young age. Several hypotheses have been suggested for the source of the contamination. It is possible that the 'Scrapie agent' believed to cause Scrapie in sheep, entered the compound feed, facilitated by the large increase in the UK sheep population in the 1980s. This would mean a jump of the agent across the species barrier. Or possibly BSE was already a rare disease in cattle prior to the 1980s which for some reason was able to enter the food chain. Whatever the cause of the disease's first appearance, the large number of subsequent cases have been caused by affected cattle being fed to other cattle.

The History of Bovine Spongiform Encephalopathy - BSE
BSE was first identified at the Central Veterinary Laboratory in Weybridge in November, 1986, in two unrelated cows from different areas of the country. Initial investigations into the cause of the disease ( as the number of cases increased ) concluded that cattle feed containing contaminated ruminant protein in Meat and Bone Meal was strongly implicated. A ban on the feeding of ruminant protein was made in 1988. At the same time the disease was made legally notifiable and a compulsory slaughter policy introduced. In 1989 the EC banned the export of cattle born before July 1988 - this was followed by other legislation culminating in the complete ban of beef/live cattle/ cattle products by 1990. The effect on the UK beef industry was enormous. As the numbers of affected farms and cattle began to escalate, the government introduced several orders requiring farmers to keep detailed records of cattle identification, marking and breeding, cattle movements, the introduction of individual cattle passports in 1996 and the formation of the Cattle Tracing Service in 1998. By 1993, over 100,000 cases of BSE had been diagnosed - at the height of the epidemic in 1992/1993 this amounted to 1000 cattle per week being slaughtered.

The Current Status of the Disease
As a result of the control measures implemented since the epidemic began, the number of cases diagnosed since 1992 have fallen by 40-50% per year. At this time, approximately 20 cases per week are being slaughtered with fewer subsequently confirmed as positive cases.

BSE and Public Health
The TSEs have been recognised as diseases which are species specific, with few cases where the species barrier has been jumped. Therefore at the beginning of the cattle epidemic of BSE, there were not thought to be any major public health issues. However in 1996 a previously unrecognised pattern of the TSE in humans, Creutzfeldt Jacob Disease (CJD), was reported. This involved young people, with a far quicker onset and development of symptoms than the previously described CJD and was subsequently known as new variant CJD (vCJD). Although there was no clear-cut direct evidence of a link with BSE, it was strongly suspected that the disease had resulted by exposure to contaminated bovine foodstuffs before 1989. Since that time, there have been over 100 cases of 'definite or probable' vCJD, where definite cases have been confirmed at post-mortem, and probable cases have symptoms strongly suggestive of vCJD. However the numbers of cases diagnosed are now decreasing and the earlier fears of a vCJD epidemic have not come to pass.

Any future risk to public health has been reduced to negligible levels by several measures still in place - the banning of all risk materials from the human food chain, the compulsory slaughter and incineration of any animal suspected of having BSE, the veterinary inspection of all adult cattle prior to slaughter and the banning of all cattle over 30 months for human consumption, with controlled exceptions under the Beef Assurance Scheme.

BSE continues to be notifiable in cattle with compulsory slaughter and incineration of all cases. If nothing else was done it is believed the disease would be self limiting. However, this has been added to by a selective cull of any remaining animals which are thought to be at a higher risk of contracting BSE - for example animals which have been traced back to being related to cases, or animals which have been reared as calves with subsequent cases whether they or their offspring have ever shown any symptoms of the disease. As would be expected, the majority of these animals are already dead from other causes and numbers subjected to this selective cull are low and getting lower. Current research is being done into the production of accurate tests for the diagnosis of BSE in carcasses and in the living animals.

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