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A well-established rabbit model of enteropathogenic E. coli (EPEC) disease was used to examine whether vitamin E (VE) nutritional supplementation had an effect on the pathological changes induced in the bowel by EPEC. Quantitative methods were used to evaluate the influence of VE on bacterial colonization, intestinal mucosal architecture and inflammation, and intestinal epithelial proliferation and apoptosis. VE did not affect EPEC colonization and did not give significant protection against EPEC-induced changes and diarrhoea. Although VE had no effect on the EPEC-related increase of enterocyte apoptosis, it clearly contributed to an acceleration of epithelial cell proliferation in the ileal crypts. This finding may explain why ileal morphometry undertaken in this study showed that VE ameliorated somewhat the effects of EPEC on intestinal mucosal architecture. Quantitative studies on inflammatory cells in the intestinal mucosa revealed that VE nutritional supplementation resulted in an increased neutrophilic and mononuclear inflammatory cell response to EPEC infection, which did not contribute, however, to the clearance of infection.

Two cases of canine papillary meningioma are reported. The first animal, an 11-year-old male Boxer, presented with vestibular ataxia and the tumour was located in the left pontomedullary region. The second animal, a 15-year-old female cross-bred Miniature Poodle, presented with dementia, truncal ataxia and hypermetria, and the tumour was located in the right semilunar ganglion of Gasser. In the first case, histopathological examination showed that the papillary pattern merged with a typical syncytial meningioma, with extensive areas of necrosis. In the second case, the multilobular tumour had lobules with a purely syncytial, fibrous or transitional histological pattern, and lobules with intermingling papillary and secretory histological patterns. Both tumours exhibited histological features of malignancy, but evidence of remote metastasis was not found.

An unusual papillary meningioma in a cat with progressive cerebellar ataxia is described. Computed tomography revealed the presence of a primary tumour. Microscopically, the tumour was seen to arise from the cerebellar pia mater, forming perivascular structures composed of a single layer of cuboidal to columnar epithelial cells. By immunolabelling, the neoplastic cells appeared positive for cytokeratin, vimentin and S-100 protein. Ultrastructural examination, together with the immunocytochemical findings, indicated the mesenchymal and epithelial nature of the tumour.

Primary gastric choriocarcinoma (PGC) is a rare neoplasm to date only reported in humans. This report describes a canine gastric tumour with microscopical, histochemical and immunohistochemical features of PGC. The tumour diffusely infiltrated the submucosa and muscularis propria of the pylorus and anterior duodenum, and metastasized to the gastric lymph node. Immunohistochemically, the neoplastic cells displayed aberrant expression of beta-catenin and E-cadherin, but normal expression of the adenomatous polyposis coli (APC) protein. Expression of the oncogenes c-myc and Ras was also increased. These observations suggest that this canine PGC had synchronous activation of both the Wnt/beta-catenin and Ras signalling pathways of carcinogenesis.

The dematiaceous fungus Cladosporium cladosporioides is a widely distributed saprophyte that is reported to occasionally infect the lung, skin, eye and brain of humans. This report describes a German shepherd dog with granulomatous encephalitis and nephritis due to C. cladosporioides infection. Although the fungal organisms appeared non-pigmented in haematoxylin and eosin stained sections, they were readily identified with histochemical stains. Semi-nested polymerase chain reaction using universal fungal primers amplified fungal DNA from fixed tissue that had identity to that of C. cladosporioides on sequencing.

Maedi-visna virus (MVV) in sheep, which infects mainly cells of the monocyte/macrophage lineage, produces changes in the lung, mammary gland, brain and joints. In this study, however, the liver and heart of six naturally infected sheep were examined for the presence of the virus. MVV proviral DNA was demonstrated by polymerase chain reaction (PCR) analysis, and immunohistochemical examination revealed viral antigens in the cytoplasm of hepatocytes and cardiac myocytes. Although histopathological examination showed mild to moderate, chronic lymphocytic cholangiohepatitis and myocarditis and the presence of small lymphoid aggregates, the typical maedi lymphoproliferative lesions (lymphoid follicle-like structures of considerable size with germinal centres) were not seen in the liver and heart. These novel findings suggest that, although the macrophage is the main cell for productive viral replication, the liver and heart represent additional MVV targets.