Failure to transmit bovine spongiform encephalopathy to mice by feeding them with extraneural tissues of affected cattle.

Single tissue pools of brain and five extraneural tissues were prepared from four clinical cases of bovine spongiform encephalopathy (BSE) and fed to C57B1 and/or CRH mice. The disease was transmitted only to C57B1 mice fed brain. Intracerebral passages at 12 and 18 months of spleen and spinal cord homogenates from this group of mice to C57B1 mice resulted in reduced incubation periods. Similar blind passages from all other groups failed to produce evidence of infection in a cumulative incubation period of 42 months. The results suggest that the probability of human infection occurring as a result of the consumption of non-neural bovine tissues is remote.

Effects of concurrent oral administration of monensin on the toxicity of increasing doses of selenium in lambs.

The effects of concurrent administration of monensin sodium on the toxicity of progressively increasing oral doses of selenium (0.2 to 2.4 mg per kg body weight), given as sodium selenite twice weekly, have been examined in growing lambs. To link the chemically determined selenium concentration in tissues with observable pathological changes, the histochemical method of Danscher, which visualizes selenium bonds within tissues, was utilized. Findings included damage to conduction and contractile myofibres in the heart, segmental sarcoplasmal necrosis with lysis and atrophic change in skeletal musculature and selective accumulation of Danscher reaction-product in damaged areas of the liver, kidney and secondary lymphoid tissue. Concurrent administration of monensin sodium at a constant safe dosage enhanced the toxicity of selenium as demonstrated by increased severity of the signs of intoxication, fatalities, tissue selenium concentrations and intensified gross, histopathological and histochemical changes.

Experimental acute selenium intoxication in lambs.

The toxic effects of 5 mg per kg body weight of selenium given as sodium selenite orally or parenterally to growing lambs were examined. There was considerable individual variation in both susceptibility to intoxication and the degree of pathological change displayed. The results affirm the previously reported deleterious effects on the cardiovascular, respiratory and urinary systems and highlight damage to secondary lymphoid tissue in various organs. The use of a histochemical method for detecting selenium bonds demonstrated correlation between the density of reaction-product and histopathological changes within tissues, and showed the distribution of selenium in other tissues in which the gross and histopathological findings were non-specific or minimal.

Observations on the pathogenesis of Chlamydia psittaci infection of pregnant sheep.

Susceptible pregnant sheep were infected with Chlamydia psittaci at different stages of early and mid-gestation. Placentas and foetuses were examined by microbiological, serological, histopathological and immunochemical methods at various intervals thereafter. While ewes were susceptible to infection from early gestation onwards and infections of placentas and foetuses occurred from about 60 days gestation (dg), pathological changes were not detected until after 90 dg. These changes consisted of initial rapid replication of C. psittaci in the trophoblast at the limbus of the placentomal hilus, leading to local necrosis and contiguous spread of infection to involve the cotyledonary and intercotyledonary placenta and apposing endometrium. Foetal pathology consisted of focal necrosis in liver and other organs suggestive of embolic dissemination of infection from the placenta. An early foetal immune response was detected including the demonstration of IgM and IgG antibody to C. psittaci and quantitative evidence of a B cell response to infection. Pathogenetic mechanisms are discussed.

Clinical, biochemical and pathological study of perinatal lambs in a commercial flock.

The birth and fate of 818 lambs born to 571 ewes on a low-ground farm in the Scottish Borders with a history of substantial perinatal mortality were monitored with a range of physiological, biochemical and pathological measurements. In lambs which survived, the rectal temperature, birthweight and plasma concentrations of fructose, insulin, thyroxine and the third component of complement at birth, and the weight at four months of age, decreased with litter size. One hundred and thirty-seven lambs were stillborn or died within four days and seven others died later. The mothers of 77 per cent of these lambs had low condition scores, but the lamb deaths did not correlate significantly with the condition scores. From data relating to birthweight, temperature, packed cell volume and plasma composition it was deduced that placental insufficiency was involved in 24 per cent of these deaths; acute hypoxaemia at birth accounted for 35 per cent, inadequate thermogenesis for 12 per cent and starvation for 13 per cent. The remaining 16 per cent of dead lambs could not be assigned to any of these categories. Using only clinicopathological criteria, 37 per cent of the lamb deaths were attributed to antenatal influences which included immaturity, developmental anomalies, and degenerative or inflammatory changes. Thirty-three per cent of the deaths were due to post natal factors which included, in declining order of frequency, starvation, enteritis, misadventure, pneumonia, navel infections and septicaemia. No conclusions could be drawn from the pathological examinations alone in the remaining 30 per cent, although almost half of these had low rectal temperatures after birth, death being attributed to hypothermia.(ABSTRACT TRUNCATED AT 250 WORDS)

Border disease without nervous signs or fleece changes.

A natural infection with border disease virus occurred in a flock on low ground in Argyll in the spring of 1984. The outbreak was unusual in that the typical clinical signs of border disease, ie, tremor and, or, fleece changes were not present; manifestations of disease were restricted to abortion and the birth of small weak lambs. The disease was shown to have been introduced to the flock by four healthy ewes persistently infected with border disease virus among a group of 39 purchased in October 1983. Further investigations in late August 1984 detected viraemia in six of seven ill-thriven lambs and four of 24 apparently healthy lambs. Attempted 'natural vaccination' of susceptible sheep by mixing them at grass for three months with groups of ewes and lambs known to contain virus excretors was largely unsuccessful as only four of 22 'sentinel' sheep seroconverted. In October 1984 the persistently infected purchased animals and all that year's lamb crop were removed from the farm. No disease occurred in 1985 when the lambing percentage was 129 per cent compared with 100 per cent in 1984. Two of the four persistently infected purchased ewes were mated at Moredun Research Institute in December 1984 and both produced healthy but persistently infected lambs.

Persistent bovine virus diarrhoea virus infection in a bull.

Investigation of a sight defect in a pedigree bull, born as a result of artificial insemination and ovum transplantation, led to the finding that the animal was persistently infected with bovine virus diarrhoea virus. Virus was cultured from blood and from nasal and ocular swabs and was present in semen in high titre. At necropsy, virus was cultured from a wide range of tissues. The pathological findings are described and discussed as are the potential hazards of such infections.

Prolonged gestation in sheep in western Scotland associated with diffuse neuronal necrosis of the fetal central nervous system.

A specific disorder of sheep resulting in gestation periods extending up to eight months is reported for the first time. The condition, which is of low prevalence, occurs on hill farms in coastal regions of western Scotland and affected ewes usually die unless relieved of their fetuses by surgery. The fetuses may weigh up to 12 kg and have long hairy coats, skeletal deformities, precocious gonadal development and extensive liquefaction of central nervous system tissue. The aetiology has not been determined but some mechanisms which may be involved in the pathogenesis are discussed.

Ovine listerial encephalitis: analysis, hypothesis and synthesis.

Analysis of field data suggested that listerial encephalitis in sheep was most common in winter and early spring in the age groups of sheep which would be cutting, changing and possibly losing teeth. It was hypothesised that under these conditions ingested Listeria monocytogenes could reach the fine dental terminals of the trigeminal nerve causing an ascending neuritis and encephalitis. Experimental inoculation of organisms into the dental pulp demonstrated the feasibility of this route of infection. Histological encephalitis was evident six days after inoculation but the incubation period to clinical neurological disease was at least three weeks.

Ataxia/paresis syndrome of sheep in West Africa associated with bilateral multifocal cerebrospinal poliomalacia.

Between 1976 and 1981 a specific neurological disorder of sheep was observed in Ghana. It was encountered on eight properties on some of which it was responsible for losses of up to 72 per cent of the sheep stock in some years. The condition affected mainly adult ewes, and was characterised clinically by a brief period of ataxia, followed by paresis prostration and death in four to five days. Morphological examination of nine affected animals revealed significant lesions only in the central nervous system. These consisted of oedema of the intracellular glial compartment and bilateral, sometimes symmetrical, foci of spongy transformation, malacia and haemorrhage in the grey matter of the brain stem, cerebellum and spinal cord. The aetiology of ataxia/paresis syndrome was not determined but some possibilities are discussed in the context of other naturally occurring and experimental focal malacic disorders in animals.

The pathology of a spontaneous and experimental mucosal disease-like syndrome in sheep recovered from clinical border disease.

The pathological changes which accompanied a severe clinical syndrome characterized by intractable diarrhoea and/or respiratory distress in sheep recovered from clinical Border disease consisted of inflammatory lymphoproliferative lesions in several organs, notably the CNS and intestinal tract. The syndrome has been reproduced experimentally by "super-infection" with homologous Border disease virus. The differential diagnosis is discussed and attention drawn to the similarity between the enteric lesions and those of bovine mucosal disease.

Virology and immunology of a spontaneous and experimental mucosal disease-like syndrome in sheep recovered from clinical border disease.

A disease similar to mucosal disease (MD) of cattle has occurred spontaneously in sheep clinically recovered from Border disease (BD). Evidence is presented to suggest that, in such animals, a specific and dynamic equilibrium exists between an attenuated form of the virus and the immunotolerant host. Upset of this equilibrium either by injection of BD virus of the same strain or by some unknown spontaneous event appears to lead to the reassertion of viral pathogenicity with fatal consequences.