The growth and use of veterinary epidemiology.
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Biomedical subjects
Publications and source records attributed to J W Wilesmith.
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A comprehensive analysis of the bovine spongiform encephalopathy (BSE) epidemic in cattle in Great Britain assesses past, present and future patterns in the incidence of infection and disease, and allows a critical appraisal of different culling policies for eradication of the disease.
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Bovine spongiform encephalopathy (BSE) occurred in cattle in Great Britain after the inclusion of protein derived from infected tissues in their feed, and the incidence of the disease has been reduced by the introduction of legislation to prevent the inclusion of such protein in ruminant feed. This paper describes a case-control study designed to investigate whether there is any evidence for direct transmission of infection to cattle born after the introduction of this legislation. The offspring of animals that were subsequently affected with BSE were not found significantly more often among the cases. There was a statistically significant risk for animals born up to three days after a subsequently affected animal calved, but it may not indicate a causal association. Even after adjusting for an animal's exposure to infected animals that calved but would have been culled from the herd before developing clinical signs of BSE these routes of transmission could not account for the majority of cases born after the introduction of the legislation. A between herd comparison is suggested as a method of investigating alternative sources of infection.
The associations between three major categories of the neurohistological diagnoses and the epidemiological data were examined in unconfirmed cases of clinically suspect bovine spongiform encephalopathy (BSE). The diagnostic categories were focal spongiosis of white matter (37 cases), encephalic listeriosis (13 cases) and no significant lesions (78 cases). An additional control category of 200 confirmed cases of BSE were included for comparison. Epidemiological variables were the frequencies of specific clinical signs, the season of clinical onset, the age, the duration of the clinical signs and the geographical origin of the cases. Discriminant analysis was used to assess the contribution of these variables to the distinction between the diagnostic categories. The analyses characterised the cases of listeriosis by their shortest clinical duration, the greater prevalences of certain clinical signs and their occurrence mainly in winter and spring, consistent with current understanding of the disease. Cases of focal spongiosis, a lesion of unknown significance, but potentially with a metabolic causation, were tentatively separable from cases with no significant lesions by their winter onset. The results also confirmed that among the categories, the cases of BSE had the longest clinical duration. Despite their statistical significance, the findings do not have sufficient predictive power to be of value in making clinical decisions.
The occurrence of Mycobacterium bovis infection in cattle herds during the period 1966-92 in two geographically related areas in South-West England is compared. In one area comprising 104 km2 all badgers were systematically destroyed from 1975-81, after which recolonization was allowed; in the other, comprising 116 km2, small scale, statutory badger removal operations were undertaken from 1975 onwards where specific herds were detected with M. bovis infection. In the area with total clearance, no further incidents with M. bovis isolation occurred from 1982-92. Survival analysis and proportional hazards regression indicated that the risk of herds being identified with infection was less once badgers had been cleared from their neighbourhood, whereas it was greater in herds with 50 or more animals, and once cattle in a herd had responded positively to the tuberculin skin test, even though infection with M. bovis was not confirmed subsequently. The study provides further evidence that badgers represent an important reservoir of M. bovis infection for cattle and that badger control is effective in reducing incidents of cattle infection with M. bovis if action is thorough and recolonization is prevented.
Bovine spongiform encephalopathy (BSE), defined originally from its characteristic neuropathology, retains a place of particular interest in the scrapie-like or prion disease group, presenting uniquely an example of such diseases occurring as a nationwide food-borne epidemic in Great Britain. Comprehensive monitoring of the epidemic, both pathologically and epidemiologically, has facilitated our present understanding of the disease. BSE presents the classical neuropathological features of the transmissible spongiform encephalopathies. Although particularly similar to natural scrapie of sheep, BSE has, unlike scrapie, a stereotypic lesion profile from which it has been concluded that host and agent factors, including probably the strain of agent, which influence the profile, are constant in this disease. Neuronal loss in BSE may make an important but hitherto inapparent contribution to functional deficits. Preliminary ultrastructural studies have confirmed light microscopic features of brain changes in BSE but have as yet not established significant new findings. Immunohistochemical studies of PrP accumulation reveal distinctive forms and distributions of immunolabelling, confirming features reported previously in experimental models of scrapie, including perineuronal and perineuritic "synapse-like" reactivity. The histopathological diagnosis of BSE, validated on a single section of the medulla for the statutory diagnosis of large numbers of cases, is supplemented where necessary by fibril (SAF) examination which performs similarly to the histological diagnosis in the majority of cases. Epidemiological studies of BSE have supported the pathological findings that there is no detectable variation in susceptibility within the cattle population. The detailed monitoring of the epidemic has revealed the expected effects on the incidence as a result of statutory measures intended to prevent food-borne exposure after July 1988. The main effect has been a reduction in the national incidence during 1993 which has been continued into 1994. Analytical studies have not revealed any means of transmission, other than the food-borne source, capable of maintaining the epidemic in Great Britain. An international comparison of risk factors for the occurrence of BSE indicates that an epidemic of similar magnitude outside the British Isles is unlikely.
BSE has occurred in the U.K. as an extended common source epidemic since 1985/86. The vehicle of infection was concentrated feeds containing meat and bone meal produced by the rendering of ovine, bovine and other animal wastes. The epidemic was probably initiated in 1981/82 when a sudden decline in the use of solvents in rendering allowed a low incidence of scrapie-like infection to occur in cattle. However, the presence in feed of bovine material that, from 1984/85 (or earlier), was increasingly infected with a cattle-adapted strain of agent amplified the epidemic greatly. Nevertheless, the incidence of BSE cases nationally has been low because of the generally low effective exposure of cattle to infection in feed. This, and a combination of risk factors that were probably unique to the U.K. can explain why relatively few cases of BSE have occurred in other countries. The feeding of ruminant-derived protein to all species of ruminants was banned in Great Britain in 1988, and in Northern Ireland in 1989. A more selective approach was subsequently adopted to minimize the risks of BSE infection of other species, including man. This was based on excluding from food a small number of bovine offals whose use and predicted infectivity titers would constitute the greatest potential source of infection. Recent studies of BSE support the basis of the specified bovine offals ban and suggest that more tissues were restricted than may have been necessary.
Bovine spongiform encephalopathy was first recognized in Great Britain in 1986 and was the result of infection with a scrapie-like agent surviving in meat and bone meal used in feedstuffs. This effective exposure commenced in 1981-82 and was associated with a reduction in the use of hydrocarbon solvents in the manufacture of meat and bone meal. The epidemiological features are consistent with sheep scrapie as the original source, but the epidemic was amplified by the recycling of infected cattle tissue resulting in a marked increase in incidence from 1989. The food borne source was eliminated by legislation introduced in July 1988. The first effects of this became apparent during 1991 and these have become more obvious during 1993 with a reduction in the national incidence. Specific studies are still in progress to determine whether other means of transmission can occur, but none capable of maintaining the epidemic have been detected.
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A statistical comparison was made between the results of the statutory neurohistopathological method for the post mortem diagnosis of bovine spongiform encephalopathy (BSE) and the detection of abnormal brain fibrils (SAF). A total of 773 suspect cases was examined by both methods; it comprised 531 animals born before the feeding of ruminant-derived protein to ruminant species was prohibited and 242 born after the ban. The relative sensitivities and specificities of the methods were calculated for the diagnosis of clinically suspected BSE. The agreement between the results of the methods was excellent for 331 of the cases born before the ban and for all the cases born after it. In these cases the samples were not autolysed. For the 200 cases in which autolysis was recorded there was poor agreement between the diagnostic methods and this was attributed to an apparently reduced specificity of the histopathological diagnosis in the autolysed material. Despite the potentially greater specificity of fibril detection in the diagnosis of scrapie-like disease, this study indicates that a reliance on fibril detection alone may result in some false negative diagnoses, probably owing to the inadequate sampling of the tissues.
This review examines the incidence of tuberculosis in badgers, the pathogenesis and diagnosis of the disease in the badger, and the control prospects related to spread of tuberculosis from badgers to cattle.
A small herd of greater kudu, derived from three individuals, has been maintained at the Zoological Society of London since 1970. Spongiform encephalopathy has been diagnosed in five out of eight of the animals born in this herd since 1987. With the possible exception of the first confirmed case, none of these is thought to have been exposed to feeds containing ruminant-derived protein. The pattern of incidence suggests that greater kudu are very susceptible to the disease and that natural lateral transmission may have occurred among them.
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The occurrence of bovine spongiform encephalopathy in Great Britain, first detected in 1986, has necessarily stimulated a large research programme. Encompassed in this are studies of the epidemiology of the disease. These commenced in 1987 and are continuing. The ensuing results have been reported and reviewed during the course of the epidemic. This paper provides a brief overview of the results of the epidemiological studies, but concentrates on the more recent features of the epidemic which are important in assessing the future course of the disease.