Porcine reproductive and respiratory syndrome (PRRS) was first known as blue-eared pig disease in the United Kingdom and the causative agent as 'Lelystad virus'. The disease is characterised by very variable clinical signs, including reproductive failure and respiratory disease. The respiratory syndrome is often associated with severe infection with secondary bacterial agents including Pasteurella multocida, Haemophilus parasuis and Streptococcus suis. However, some seropositive herds show no clinical signs of disease. The secondary infections may be facilitated by the destruction of circulating lymphocytes, by the destruction of the mucociliary clearance system and, most importantly, by a large reduction in the numbers of alveolar macrophages. The clinical syndrome observed in a herd may therefore depend in part upon the other diseases present.

Studies to test the transmissibility of the bovine spongiform encephalopathy (BSE) agent to pigs began in 1989. Parenteral inoculation of the agent by three routes simultaneously (intracranially, intravenously and intraperitoneally) produced disease with an incubation period range of 69-150 weeks. Pre-clinical pathological changes were detected in two pigs killed electively at 105 and 106 weeks post-inoculation. Infectivity was detected by bioassay in inbred mice in the CNS of those pigs that developed spongiform encephalopathy. Infectivity was also found in the stomach, jejunum, distal ileum and pancreas of terminally affected pigs. These findings show that pigs are susceptible to BSE. In contrast, disease failed to occur in pigs retained for 7 years after exposure by feeding BSE-affected brain on three separate days, at 1-2 week intervals. The amounts fed each day were equivalent to the maximum daily intake of meat and bone meal in rations for pigs aged 8 weeks. No infectivity was found in tissues assayed from the pigs exposed orally. This included tissues of the alimentary tract. It is suggested that these pigs did not become infected. The relatively high oral exposure used in these experiments compared with feed-borne exposure in the field may explain the absence of an epidemic of spongiform encephalopathy in domestic pigs concurrent with the BSE epidemic in the UK.

Despite early attempts to control the spread of the disease, porcine reproductive and respiratory syndrome (PRRS) has now become endemic in many countries including Britain. The occurrence of subclinical herd infections, the prolonged circulation of virus within herds and probable aerogenic virus spread all mitigated against the success of control measures. The origin of the disease is unknown but the causative agent has been shown to be an arterivirus with shared features to lactate dehydrogenase virus of mice. There is evidence of extreme genetic and antigenic variability between American and European isolates. PRRS virus has a predilection for alveolar macrophages and does not grow in most cell lines. In infected pigs, viraemia can persist for many weeks in the face of circulating antibodies and little is known about the mechanisms by which immunity to infection develops. A wide spectrum of disease has been reported from the field, accompanied in some cases by heavy economic losses. Reproductive and perinatal losses were most prominent when the disease first appeared. In the endemic phase, PRRS may be more significant as a contributory factor to a post-weaning respiratory syndrome of young pigs of 3-8 weeks. On-farm techniques have been developed to reduce the recycling of PRRS virus from older infected nursery pigs to the younger newly weaned pig. Vaccines are now marketed for the control of PRRS, but are not licensed for use in Britain. Improvements in knowledge of virion composition and antigenic stability and in the nature of the immune response of the pig should result in genetically engineered subunit vaccines becoming available. Diagnosis of PRRS is still difficult as many animals do not show clinical signs and may only be detected by serology and often only when other respiratory diseases are being investigated. Now that the infection is widespread, serological testing must be properly targeted and interpreted to give meaningful results about virus circulation. An increasing arsenal of diagnostic methods are becoming available to detect virus in both fresh and fixed specimens. The pathogenic mechanisms of PRRS remain poorly defined and more work is needed to reveal the nature of the interaction between PRRS virus and other factors in disease.

The clinical and radiographic findings associated with the presence of hemivertebra ("wedge-shaped"vertebra) in small and brachycephalic breeds of dogs are reported together with the results of post mortem examination in the availabel cases. The condition is characterised clinically by progressive hind-leg weakness, spinal pain, abnormalities of the nervous system and evidence of muscle atrophy or other abnormalities of conformation. Confirmation of the clinical diagnosis is by radiography. It is suggested that the condition is congenital in origin. Breed incidences are reported. The occurrence of the disorder in certain families of dogs suggests also that it may be hereditary. Other congenital abnormalities are seen in some dogs affected by hemivertebrae.

Detailed neuropathological findings in 222 cases of naturally occurring scrapie from Great Britain are described. The material consisted of formalin-fixed brain from eight breeds of sheep submitted between 1982 and 1991. Paraffin-embedded histological sections were made from several specified brain areas, including the medulla oblongata, cerebellum, pons, mesencephalon, diencephalon, septal area, basal ganglia and frontal cortex. Sections were examined by conventional and polarised light microscopy and the type and distribution of the lesions were recorded. Histologically, the lesions included vacuolation of neuronal perikarya and grey matter neuropil, neuronal degeneration (especially "dark' neurons) and loss, a reactive glial (predominantly astrocytic) response and amyloidosis. Vacuolar lesions were present in the cerebral cortex of 37 per cent of cases, centred around the superior frontal gyrus. Vacuolar lesions were detected in the neocortex for as long as sections have been taken from the superior frontal gyrus and are thus probably not a new feature of the disease. The distribution of vacuolation in the grey matter neuropil could be classified into seven patterns. Data from individual breeds of sheep showed that in some breeds there were significant differences in the age at which animals with different patterns of vacuolation died from scrapie.