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Between October 2001 and December 2006 an estimated total of 6 million cattle in Japan were tested for BSE, with 31 returning a positive result. Exploratory mapping, the space-time scan statistic, and ordinal logistic regression have been used to describe the epidemiology of the 24 cases identified in the prefecture of Hokkaido, and to quantify the risk factors for the disease. Two birth cohort groups were affected: cattle born during a period of seven months in 1996, and cattle born between 1999 and 2001. The descriptive spatial analyses showed that eight of the 10 cases born in 1996 were born in areas with a relatively high density of dairy farms in the east of Hokkaido, but that the 14 later cases were more widely distributed throughout the prefecture, with equal numbers of cases in the east and the west. These findings provide indirect evidence of a single localised contamination of the cattle feed supply in 1996, and recycling of the infection after 1999.

A spatial simulation model of foot-and-mouth disease was used in March and early April 2001 to evaluate alternative control policies for the 2001 epidemic in Great Britain. Control policies were those in operation from March 20, 2001, and comprised a ban on all animal movements from February 23, 2001, and a stamping-out policy. Each simulation commenced with the known population of infected farms on April 10, 2001, and ran for 200 days. For the control policy which best approximated that actually implemented from late March, the model predicted an epidemic of approximately 1800 to 1900 affected farms, and estimated that the epidemic would be eradicated between July and October 2001, with a low probability of continuing beyond October 2001. This policy included the slaughter-out of infected farms within 24 hours, slaughter of about 1.3 of the surrounding farms per infected farm within a further 48 hours, and minimal interfarm movements of susceptible animals. Delays in the slaughter of animals on infected farms beyond 24 hours after diagnosis slightly increased the epidemic size, and failure to achieve pre-emptive slaughter on an adequate number of at-risk farms substantially increased the expected size of the epidemic. Vaccination of up to three of the most outbreak-dense areas carried out in conjunction with the adopted control policy reduced the predicted size of the epidemic by less than 100 farms. Vaccination of buffer zones (designed to apply available vaccine and manpower as effectively as possible) carried out in place of the adopted control policy allowed the disease to spread out of control, producing an epidemic involving over 6000 farms by October 2001, with no prospect of immediate eradication.

A longitudinal observational study of 15 red deer farms was carried out in New Zealand for two years from March 1992. The deer were monitored for performance and health problems, and farm management practices were recorded. Numbers at risk were 4,683 hind-years, 2,459 stag-years and 3,202 weaner-years. The numbers of primiparous and adult hinds at risk of losing their progeny by weaning were 653 and 3,364, respectively. Where possible, postmortem examinations were carried out, and organs were sampled for histological and microbiological investigation. Rates of mortality varied with season with most stag and hind deaths in winter and weaner deaths in autumn and winter. Overall mortality rates were 1.77, 2.60 and 5.87 per 100 deer-years for hinds, stags and weaners, respectively. Malignant catarrhal fever accounted for 0.53 stag and 0.17 hind deaths per 100 deer-years at risk Misadventure, including broken bones, accounted for 15.4 per cent of weaner mortalities, or 0.53 weaner mortalities per 100 weaner-three months in autumn. Yersiniosis was confirmed in 18.6 per cent of weaner deaths, or 1.09 weaners per 100 weaner-years during the first six months after weaning, but was also suspected but unconfirmed in a further 41 per cent of weaner mortalities. Overall, 17 per cent of yearling hinds, and 9.2 per cent of adult hinds lost their progeny between pregnancy diagnosis in June and weaning in March. One outbreak of osteochondrosis was recorded. Mortality rates varied between farms and many mortalities were preventable.

This was a spatial analysis of the epidemic of bovine spongiform encephalopathy (BSE) in Great Britain, based on agricultural census data collected between 1986 and 1996 and BSE case data collected up to June 1997. Kernel smoothing techniques were used to plot the distribution of BSE-positive cattle holdings per 100 holdings per square kilometre and the distribution of confirmed BSE cases per 100 head of cattle per square kilometre. In the early stages of the epidemic reported BSE cases were scattered widely throughout Great Britain, with no clearly identifiable focus. By June 1997, a statistically significant cluster of BSE-positive holdings was identifiable in the eastern part of the South west region of England. During the epidemic the highest densities of confirmed BSE cases per 100 cattle per square kilometre occurred in the greater part of the South west region of England and within Dyfed in the south west of Wales. In Wales, a small number of holdings experienced large numbers of confirmed BSE cases. In the South west region of England a large number of holdings experienced small numbers of confirmed cases. By June 1997, the distribution of BSE-positive holdings across Great Britain was largely determined by factors that influenced the amount of recycled infectious material they were exposed to.

The objectives of this study were first to determine the cumulative incidence of bovine spongiform encephalopathy (BSE) in the British cattle population from July 1986 to June 1997, secondly, to identify individual animal-associated risk factors that influenced the age of onset of clinical signs in confirmed BSE cases, and, thirdly, to assess the effectiveness of the measures introduced to control BSE during the epidemic. The analyses were based on the population of British cattle at risk, derived from agricultural census data collected between 1986 and 1996, and BSE case data collected up to June 30, 1997. The unit of interest was individual adult cattle recorded on annual agricultural censuses between June 1986 and June 1996. Univariate and multivariate survival analysis techniques were used to characterise the age of onset of clinical signs. In total 167,366 cases of BSE were diagnosed in Great Britain up to June 30, 1997. The cumulative incidence of BSE between July 1986 and June 1997 was 1.10 (95 per cent confidence interval [CI] 1.09 to 1.10) cases per 100 adult cattle at risk. Cattle from the South east, South west and Eastern regions of England had 4.26 to 5.96 (95 per cent CI 4.15 to 6.14) times as great a monthly hazard of being confirmed with BSE as cattle from Scotland. Compared with cattle born before June 1985, those born between July 1987 and June 1988 had 22.5 (95 per cent CI 22.1 to 22.8) times the monthly hazard of being confirmed with BSE, whereas those born in the 12 months after July 1988 had only 7.39 (95 per cent CI 7.24 to 7.54) times the monthly hazard of being confirmed with BSE. This reduction in hazard was directly attributable to the ban on the use of ruminant protein as a feed instituted in July 1988. Successive cohorts from 1989 to 1991 experienced further reductions in the hazard of experiencing BSE. The additional decrease in hazard observed for the 1990 cohort may be attributed to the effect of the Specified Bovine Offal ban instituted in September 1990.

The objectives of this study were first to describe the pattern of the epidemic of bovine spongiform encephalopathy (BSE) in Great Britain in terms of the temporal change in the proportion of all cattle holdings that had experienced at least one confirmed case of BSE to June 30, 1997, and secondly to identify risk factors that influenced the date of onset of a holding's first confirmed BSE case. The analyses were based on the population of British cattle at risk, derived from agricultural census data collected between 1986 and 1996, and the BSE case data collected up to June 30, 1997. The unit of interest was the cattle holding and included all those recorded at least once on annual agricultural censuses conducted between June 30, 1986, and June 30, 1996. The outcome of interest was the date on which clinical signs were recorded in a holding's first confirmed case of BSE, termed the BSE onset date. Univariate and multivariate survival analysis techniques were used to describe the temporal pattern of the epidemic. The BSE epidemic in Great Britain started in November 1986, with the majority of affected holdings having their BSE onset date after February 1992. After adjusting for the effect of the size and type of holding, holdings in the south of England (specifically those in the Eastern, South east and South west regions) had 2.22 to 2.43 (95 per cent confidence interval [CI] 2.07 to 2.58) times as great a monthly hazard of having a BSE index case as holdings in Scotland. After adjusting for the effect of region and type of holding, holdings with more than 53 adult cattle had 5.91 (95 per cent CI 5.62 to 6.21) times as great a monthly hazard of having a BSE index case as holdings with seven to 21 adult cattle. Dairy holdings had 3.06 (95 per cent CI 2.96 to 3.16) times as great a monthly hazard of having a BSE index case as beef suckler holdings. These analyses show that there were different rates of onset in different regions and in holdings of different sizes and types, that the epidemic was propagated most strongly in the south of the country, and that the growth of the epidemic followed essentially the same pattern in each region of the country, with modest temporal lags between them. The control measures imposed in 1988 and 1990 brought the expansion of the epidemic under control, although the rate of progress was slowed by those regions where the effectiveness of the control methods took some time to take full effect.

An interactive computer-based guide (termed RESPITE) was developed to demonstrate to pig producers the expected level of pneumonia in pig herds which follow specified management practices known to influence the severity of pneumonia problems. A program was used to evaluate the combined effect of known risk factors present in the particular herd on the prevalence of lung lesions in slaughter pigs. The expected prevalence was estimated using formulae that were derived from observations and data in the published literature. Eleven risk factors considered are the number of pigs in the same room, all-in/all-out versus continuous flow of pigs, closed versus open herd, temperature fluctuation ratio, width of the buildings, space allotted per pig, the type of partitions separating adjacent pens, the presence or absence of diarrhoea as a clinical problem, liquid versus solid manure disposal, ascarid control efficiency, and the presence or absence of active Aujeszky's disease in the herd. Each of the factors can be assessed in the farrowing, nursery and grow-finish stages of production and the appropriate observations are entered. The computer uses the data to calculate the expected prevalence of pneumonia in animals leaving that stage of production. Of the pneumonia developing in the farrowing, nursery and grow-finish stages, 90 per cent, 75 per cent and 25 per cent respectively is considered to resolve before slaughter inspection at 100 kg. Adjusting for this degree of resolution, the program then estimates the expected final prevalence of pneumonic lesions in slaughter pigs. Comparison of predictions with slaughterhouse data from four herds indicated that the guide was realistic in its estimates.