Transmissions of bovine spongiform encephalopathy (BSE) from seven unrelated cattle sources have given remarkably uniform disease characteristics in mice, differing from over twenty previous and contemporary transmissions of sheep and goat scrapie. Transmissions to mice of spongiform encephalopathy from six species (including sheep and goats) which have been experimentally or naturally infected with BSE have given similar results to direct BSE transmissions from cattle. Therefore the BSE agent has retained its identity when passaged through a range of species and the 'donor' species has little specific influence on disease characteristics in mice, adding to evidence for an agent-specific informational molecule. On transmission of BSE or scrapie to mice the incubation periods are long compared with subsequent mouse-to-mouse passages (the 'species barrier'). Contributing factors include a low efficiency of infection on interspecies transmission, the apparent failure of intracerebrally injected 'foreign' inoculum to establish infection directly in mouse brain and the selection of variant strains of agent which replicate most readily in the new host species.

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Archive central nervous tissue from 286 cats with neurological disorders was reviewed for histological evidence of feline spongiform encephalopathy (FSE), which may have occurred before it was first recognized in 1990. The following six categories of disease were identified: congenital; degenerative; inflammatory; neoplastic; FSE; lesion-free. The largest category (inflammatory) contained 92 cats, of which 47 were considered to be consistent with infection by feline infectious peritonitis (FIP) virus. Six cats showed evidence of more than one disease process; thus, one cat with FIP also had toxocara infection of the lateral ventricles and five cats with FSE also showed perivascular cuffing suggestive of concurrent viral infection. In only two cases did the diagnosis on review differ significantly from the original interpretation. There was no evidence of FSE before the original case was recognized in April 1990.

Naturally occurring transmissible spongiform encephalopathies have been recognised in sheep, man, mink, captive deer and cattle. Recently a similar disease was reported in a domestic cat. This paper describes the clinical and pathological findings in five cats with similar signs, including further observations on the original case. All the cats had a progressive, neurological disease involving locomotor disturbances, abnormal behaviour and, in most cases, altered sensory responses. Histopathological examination of the central nervous system revealed changes pathognomonic of the scrapie-like encephalopathies, including widespread vacuolation of the grey matter neuropil, vacuolation of neuronal perikarya and an astrocytic reaction.

This report highlights the fact that bacterial cholangitis/cholangiohepatitis with or without concurrent cholecystitis should be considered as a potential differential in dogs presenting with signs referable to biliary tract disease.

Summary Specificity of the oral glucose tolerance test (OGTT) for the diagnosis of small intestinal malabsorption in the horse was assessed by comparing the results of OGTT with the results of a histopathological examination of the small intestine in 42 adult horses affected by chronic weight loss. The horses were assigned to three groups on the basis of the results of the test. Five horses were considered to have a normal OGTT absorption result (Group 1); all the horses had a histologically normal small intestine. Twenty‐five horses had a partial malabsorption result (Group 2) seven of which had normal small intestinal morphology, whereas the remaining 18 had a variety of pathological lesions including lymphosarcoma, villous atrophy, granulomatous enteritis and eosinophilic gastroenteritis. Twelve of the 42 horses had a total malabsorption result (Group 3), and all had a severe infiltrative lesion in the small intestinal wall (either lymphosarcoma or granulomatous enteritis).

Enteric bacteria with a demonstrable or potential ability to form attaching-effacing lesions, so-called attaching-effacing (AE) bacteria, have been found in the intestinal tracts of a wide variety of warm-blooded animal species, including man. In some host species, for example cattle, pigs, rabbits and human beings, attaching-effacing Escherichia coli (AEEC) have an established role as enteropathogens. In other host species, AE bacteria are of less certain significance. With continuing advances in the detection and typing of AE strains, the importance of these bacteria for many hosts is likely to become clearer. The pathogenic effects of AE bacteria result from adhesion to the intestinal mucosa by a variety of mechanisms, culminating in the formation of the characteristic intimate adhesion of the AE lesion. The ability to induce AE lesions is mediated by the co-ordinated expression of some 40 bacterial genes organized within a so-called pathogenicity island, known as the "Locus for Enterocyte Effacement". It is also believed that the production of bacterial toxins, principally Vero toxins, is a significant virulence factor for some AEEC strains. Recent areas of research into AE bacteria include: the use of Citrobacter rodentium to model human AEEC disease; quorum-sensing mechanisms used by AEEC to modulate virulence gene expression; and the potential role of adhesion in the persistent colonization of the intestine by AE bacteria. This review of AE bacteria covers their molecular biology, their occurrence in various animal species, and the diagnosis, pathology and clinical aspects of animal diseases with which they are associated. Reference is made to human pathogens where appropriate. The focus is mainly on natural colonization and disease, but complementary experimental data are also included.

SummaryReasons for performing study: Gastric impaction in the horse is poorly described in the veterinary literature. Objectives: To review the clinical and pathological features of gastric impaction. Methods: The clinical details of horses presenting with colic over a 7-year period and cases in which gastric impaction was considered to determine the outcome were reviewed. Clinical and clinicopathological data were recorded. Results: Twelve cases of gastric impaction were recorded (1.4% of 857 horses hospitalised for colic). Diagnosis was achieved by ultrasonographic examination, gastroscopy, exploratory celiotomy and/or post mortem examination. Five out of 12 horses were successfully treated, 5/12 were subjected to euthanasia (3 at celiotomy and 2 due to recurrence of impaction) and 2/12 died. Three out of 12 horses had spontaneous gastric rupture despite attempted treatment (one was subjected to euthanasia at celiotomy and 2 died). Post mortem examination (7 horses) revealed gross muscular thickening of the stomach wall in 6/7 horses. Histological examination revealed focal fibrosis of the stomach wall in 4/6 and focal myositis in 1/6 horses. Conclusions and practical significance: Gastric impaction is a rare cause of colic and affected horses can present with acute, chronic or recurrent colic in the presence or absence of other gastrointestinal disease. Spontaneous gastric rupture may occur. A proportion of affected horses have gross thickening of the muscular layers of the stomach wall.