Bovine spongiform encephalopathy

Bovine spongiform encephalopathy

R BRADLEY AND D W VERWOERD

Introduction

Bovine spongiform encephalopathy (BSE) is regarded as a new disease with the first confirmed case being identified in the UK in November 1986 and the first comprehensive report on the disease was made in the following year.90 Once the epidemic developed it was possible to investigate epidemiologically and retrospectively the first date of clinical occurrence and this was considered to be April 1985.

In the French literature, singleton suspected cases of scrapie (la tremblante) in cattle have been described, the most notable of which was that reported in 1893 in an eightyear-old Gasconne cow.67 However, this diagnosis was based on the clinical signs alone since the microscopic lesions associated with transmissible spongiform encephalopathy (TSE) were not reported until 1898 when the neuropathology of sheep with natural scrapie was studied.6 The accuracy of the assumed pathological diagnosis (spongiform encephalopathy) in the Gasconne cow must therefore remain doubtful.

Bovine spongiform encephalopathy is now by far the best-known naturally occurring TSE, or prion disease. The media named the malady ‘Mad cow disease’ and it is known to the public by this pseudonym.

Bovine spongiform encephalopathy affects adult cattle, mainly breeding dairy cows since it was largely these that were exposed to infection via concentrate feed when they were calves. The disease is fatal and has all the general clinical and pathological features seen in prion diseases.

The agent that causes BSE so far has been of a consistent, single, biological strain type and, in this regard, the disease differs from scrapie. Other features that distinguish BSE from scrapie are: the pathogenesis/distribution of infectivity in the body of affected animals, absence so far of signifi- cant genetic variation in susceptibility of breeds or individuals, a generally longer mean incubation period (60 months), and older age of clinical onset, typically of four to six years (range 20 months to 19 years).

There is little evidence for horizontal transmission. Evidence for an enhanced risk for the development of BSE in the offspring of BSE-confirmed cases comes largely from the statistical analysis of data from a cohort study,101 but the mechanism of this transmission has so far avoided detection. Unfortunately this study was unavoidably confounded by the exposure of some or all of the two groups of animals to infected feed. Furthermore the results cannot distinguish between a genetic component (for which thereis no biological ormolecular evidence) and truematernal transmission or a combination of both risks. Importantly, those concerned with the study conclude that whatever is the mechanism and risk, it will not unduly prolong the BSE epidemic in the UK or alone prevent eradication of the disease. No case of BSE in an offspring of a case has been reported in the absence of a feed-borne source.

Bovine spongiform encephalopathy has a restricted geographical distribution. Countries with cases in native-born cattle are restricted to Western Europe and Japan. By far the majority have occurred in the UK (178 531 cases to November 2001). There have been a total of 2 132 cases in other countries to November 2001.62 Three countries with no cases reported in native-born cattle to date and as far apart as Canada (one case), the Falkland Islands (one case) and the Sultanate of Oman (two cases) have imported a total of four cattle from the UK in the incubating phase of disease that resulted in clinical disease some time later. These cases have all been identified, confirmed and completely destroyed and so present no possibility for the recycling of infection to other animals or exposure of humans. In addition some other countries with BSE in their native-born cattle including Denmark, Germany, Ireland, Italy, Portugal, (all from the UK), Spain and Germany (from Switzerland) have imported small numbers of cattle in the incubating phase that subsequently developed BSE. The total number so imported is less than 40. These figures date to November 2001. They show that there is a risk of importing BSE-infected animals, but that disregarding possible under-reporting, the risk is apparently small.

As with scrapie there is no prophylaxis or effective treatment. Compulsory slaughter and safe destruction of the carcasses is the only solution.

There are epidemiological and aetiological relationships between BSE and several other recently reported TSE of animals (see Transmissible spongiform encephalopathies related to bovine spongiform encephalopathy in other domestic and captive wild species) and, importantly, a new variant form of Creutzfeldt-Jakob disease (v-CJD) of humans. There have been 113 definite or probable cases of v-CJD in humans in the UK until December 2001 of which ten are still alive. The disease has also been confirmed in four human patients in France, a country with 455 cases of BSE in native-born cattle to December 2001, one patient in the Republic of Ireland (766 cases of BSE) and one patient in Hong Kong (zero cases of BSE). This last-mentioned patient spent some time in the UK during the risk time for exposure.

The biological strain type of the BSE agent and of the agent isolated from three domestic cats, a captive greater kudu (Tragelaphus strepsiceros) and a captive nyala (Tragelaphus angasi

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