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J W Wilesmith

Publications and source records attributed to J W Wilesmith.

At least 19 recordsLinked to original sources

Analysis of dam-calf pairs of BSE cases: confirmation of a maternal risk enhancement.

We investigate whether a calf born to a dam that develops bovine spongiform encephalopathy (BSE) (prior or subsequent to the birth) is itself at an enhanced risk of developing BSE. Analyses utilize the main database on reported BSE cases in the British cattle herd maintained by the Central Veterinary Laboratory in Weybridge to trace the dams of BSE-affected animals born following the ruminant feed ban in July 1988. The data reveal a significantly enhanced risk of disease in calves born to BSE-affected dams, with the risk being greatest when birth occurs after the onset of clinical signs of disease in the dam. The dependence of the maternally enhanced risk on the maternal incubation stage at birth argues for a significant component of direct maternal transmission of the aetiological agent of BSE, and offers little support for the hypothesis of genetic predisposition. Using a statistical likelihood model, we obtain estimates of the rate of direct maternal transmission by maternal incubation stage; however, biases in the available data make these values minimum estimates.

Animals

Comparison of histology with maternal and fetal serology for the diagnosis of abortion due to bovine neosporosis.

An indirect fluorescent antibody test was applied to sera from normally calving and aborting cows and to samples of pleural fluid from their aborted calves, and the antibody titres were compared with histology and immunocytochemistry for the diagnosis of Neospora-associated abortion. Two groups of aborting cows and a third group of cows which had calved normally were used; group A consisted of 36 cows which aborted calves showing characteristic non-suppurative inflammatory lesions in which Neospora was demonstrated by immunocytochemistry, group B consisted of 100 cows which aborted calves without histological evidence of neosporosis, and group C consisted of 128 normally calved cows which were sampled within one month of calving. Serology on the maternal sera and fetal fluids was highly specific and sensitive for Neospora infection although 5 per cent of the cows which aborted Neospora-negative calves and 4.7 per cent of the normally calved cows were also seropositive. Anti-Neospora antibodies were also detected in 7 per cent of the samples of fetal fluid from Neospora-negative abortions.

Abortion, Veterinary

A cohort study to examine maternally-associated risk factors for bovine spongiform encephalopathy.

This long-term cohort study, initiated in July 1989, was designed to examine maternally-associated risk factors for bovine spongiform encephalopathy (BSE), forming part of the epidemiological research programme to assess the risks of non-feedborne transmission of BSE. In this study, the incidence of BSE in offspring of cows which developed clinical signs of BSE is compared with that in offspring, born in the same calving season and herd, of cows which had reached at least six years of age and had not developed BSE. All offspring were allowed to live to seven years of age. The results indicate a statistically significant risk difference between the two cohorts of 9.7 per cent and a relative risk of 3.2 for offspring of cows which developed clinical BSE. However, there is some evidence that this enhanced risk for offspring of BSE cases declined the later the offspring was born, but was increased the later the offspring was born in relation to the stage of the incubation period of the dam. The results presented cannot distinguish between a genetic component and true maternal transmission or a combination of both risks, but they do not indicate either that the BSE epidemic will be unduly prolonged or that the future incidence of BSE in Great Britain will increase significantly.

Animals

Risk of BSE from the import of cattle from the United Kingdom into countries of the European Union.

This study assesses quantitatively the risk that other countries, in particular those within the European Union, have incurred by importing cattle from the United Kingdom during the period before or shortly after the ban on the import of live breeding stock was introduced in 1989. It does this by assessing the probability that animals imported from the UK in a certain year would have become a detected BSE case, had they not been exported. Using the annual incidence rates available for separate birth cohorts and a given culling rate, a cumulative incidence for each birth cohort was calculated. These figures were then combined with the numbers of live breeding cattle imported from the UK into the other countries of the EU, to give an import-related risk index for each country, assuming that their culling rates were similar to that in Great Britain. The countries could thus be categorised in terms of the number of cases of BSE they might have expected.

Animals

Sporadic Creutzfeldt-Jakob disease in the United Kingdom: analysis of epidemiological surveillance data for 1970-96.

OBJECTIVE: To identify changes in the occurrence of Creutzfeldt-Jakob disease that might be related to the epidemic of bovine spongiform encephalopathy. DESIGN: Epidemiological surveillance of the United Kingdom population for Creutzfeldt-Jakob disease based on (a) referral of suspected cases by neurologists, neuropathologists, and neurophysiologists and (b) death certificates. SETTING: England and Wales during 1970-84, and whole of the United Kingdom during 1985-96. SUBJECTS: All 662 patients identified as sporadic cases of Creutzfeldt-Jakob disease. MAIN OUTCOME MEASURES: Age distribution of patients, age specific time trends of disease, occupational exposure to cattle, potential exposure to causative agent of bovine spongiform encephalopathy. RESULTS: During 1970-96 there was an increase in the number of sporadic cases of Creutzfeldt-Jakob disease recorded yearly in England and Wales. The greatest increase was among people aged over 70. There was a statistically significant excess of cases among dairy farm workers and their spouses and among people at increased risk of contact with live cattle infected with bovine spongiform encephalopathy. During 1994-6 there were six deaths from sporadic Creutzfeldt-Jakob disease in the United Kingdom in patients aged under 30. CONCLUSIONS: The increase in the incidence of sporadic Creutzfeldt-Jakob disease and the high incidence in dairy farmers in the United Kingdom may be unrelated to bovine spongiform encephalopathy. The most striking change in the pattern of Creutzfeldt-Jakob disease in the United Kingdom after the epidemic of bovine spongiform encephalopathy is provided by the incidence in a group of exceptionally young patients with a consistent and unusual neuropathological profile. The outcome of mouse transmission studies and the future incidence of the disease in the United Kingdom and elsewhere, will be important in judging whether the agent causing bovine spongiform encephalopathy has infected humans.

Adolescent

Transmission dynamics and epidemiology of BSE in British cattle.

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.

Age Factors

An investigation of risk factors for cases of bovine spongiform encephalopathy born after the introduction of the 'feed ban'.

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.

Animal Feed

Clinical and epidemiological correlates of the neurohistology of cases of histologically unconfirmed, clinically suspect bovine spongiform encephalopathy.

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.

Age Distribution

The occurrence of Mycobacterium bovis infection in cattle in and around an area subject to extensive badger (Meles meles) control.

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.

Animals

The neuropathology and epidemiology of bovine spongiform encephalopathy.

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.

Animals

Bovine spongiform encephalopathy. Epidemiology, low dose exposure and risks.

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.

Animals

An epidemiologist's view of bovine spongiform encephalopathy.

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.

Animals