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Fourteen 4- to 18-month-old vaccinated Greyhounds (10 males, 4 females) from three kennels in southern Ireland presented over a 2-year period with acute or insidious onset neurological signs. Head tilting, ataxia, recumbency, circling, and blindness were commonly observed, and animals were dull, dehydrated, and had lost weight. Hematologic and biochemical parameters reflected dehydration but were otherwise unremarkable. Microscopic examination revealed severe diffuse and focal gliosis and gemistocytosis accompanied by mononuclear cell perivascular cuffing in caudate nucleus and cortical gray matter of the cerebrum and in the periventricular gray matter of the anterior brainstem. Milder lesions were noted in the caudal brainstem, cranial spinal cord, and in the molecular layer of the cerebellum. This was accompanied by a lymphocyte and plasma cell infiltration of the cerebral and cerebellar meninges. Demyelination, neuropil necrosis, neuronophagia, and vasculitis were not observed. No inclusion bodies, fungi, or protozoal cysts were seen. Additional serologic and molecular pathology tests also failed to determine a cause, suggesting that these cases may represent a previously undiagnosed condition in the dog.

A 9-year-old horse had numerous firm, painless nodules of the skin and subcutis. Moderately vascular granulation tissue with numerous uni- or multinuclear reticuloendothelial cells was in the nodules and the regional lymph nodes but not in the viscera. By using special stains and electron microscopy, widespread amyloid deposits, mainly in the cytoplasm of reticuloendothelial cells, were identified. Amyloid was probably produced within the reticuloendothelial cells, then expelled from the dying cell and deposited in the intercellular space.

Three seronegative sheep persistently infected with Border disease virus and six seropositive, non-viraemic sheep were examined for the cellular distribution of the agent. These animals originated from a closed flock which had been kept in an isolation facility for 5 years. They were killed and immediately necropsied. There were no gross abnormalities other than reduced body weight of the persistently infected sheep. Two samples of each major organ were collected. The first sample was fixed by immersion in formalin and processed for histological examination, which showed no lesions unequivocally attributable to the viral infection. The second sample was snapfrozen for immunohistochemical examination. This revealed viral antigen in all organs of the persistently infected, but in none of the seropositive animals. The infected cells included smooth muscle cells of hollow organs and blood vessels, epithelial cells of the alimentary tract and urogenital organs, lymphocytes in lymphoid organs, endocrine cells neurons and glial cell.

Summary An artificial defect of the umbilical area in ten calves was covered by a pericard graft whose new preparation method has been proved in bovine vessel grafts. Between 2 and 6 months postoperatively (p.o.) two animals at a time were euthanized to sample the graft and its surrounding tissue for histological investigations. On the one hand, there was an inflammatory foreign body type granulomatous reaction, but on the other hand this did not lead to rejection. Within the 6-month observation time the graft fibers were immigrated by the own young collagen fibers. We interpret this as a guide function of the graft fibers. Tiny focal calcifications appeared to be the effect of an intensive tissue irritation which may be caused by an incomplete edulcoration of the chemical substances used during preparation. We recommend a longer edulcoration time to prevent these reactions.

Congenital hepatic fibrosis with autosomal recessive or dominant inheritance has been described in humans, cats, piglets, and dogs. In horses, only two cases of congenital hepatic fibrosis have been previously reported. This retrospective study of records from the Institute for Animal Pathology, University of Berne, identified 30 foals with liver lesions compatible with congenital hepatic fibrosis. Anamnestic data revealed clinical signs of severe liver injury in most affected animals. Pathologic examination showed severely enlarged, firm livers with thin-walled cysts. Histologically, the livers showed diffuse porto-portal bridging fibrosis with many small, irregularly formed and sometimes cystic bile ducts. All foals belonged to the Swiss Freiberger breed. Pedigree analysis revealed that the diseased animals could be traced back to one stallion. These results strongly suggest that congenital hepatic fibrosis in Swiss Freiberger horses is a recessively inherited autosomal genetic defect.