Biomedical subjects
Publications and source records attributed to R H Sutton.
Bilateral mesothelioma in the tunica vaginalis of an 18-month-old bull is described. Differentiation from adenocarcinoma was based on ultrastructural features, particularly on the morphology of the microvilli and the presence of microfilaments. The aetiology of this neoplasm in the tunica vaginalis is not known.
A young Friesian heifer developed multiple skin nodules. Histologically, the tumours appeared similar to the canine cutaneous histiocytoma. Over the next few weeks, the tumours underwent regression. These findings are considered to be consistent with a case of hitherto unreported bovine cutaneous histiocytoma. The only previously reported cases have been in dogs.
Thirteen cases of lymphoid neoplasia were examined in koalas from New South Wales and Queensland. Haematological and biochemical data were collected from 2 cases while all were subjected to detailed necropsies. Affected koalas were adults of both sexes and the disease had a variable time course. The 2 koalas examined haematologically were leukaemic. On a morphological basis, 5 cases were classified as multicentric, 7 cases as abdominal (but not necessarily with alimentary tract involvement) and one case as solitary. In most cases, the neoplastic cells appeared to be either lymphoblasts or prolymphocytes.
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Dead adult D. immitis were inserted into the pulmonary arteries of 10 healthy pups, five of which were given a crude antigenic extract of D. immitis subcutaneously. Two dogs, one from each group were then killed 1, 3, 5, 7 and 9 days after the insertion of filariae and the associated pulmonary artery pathology examined. Microscopically, haemorrhage was evident at day 1, followed by suppuration and organization at days 5 to 7, with organization, fibrosis and focal pleural retraction evident on days 7 to 9. Within arteries haemorrhage and thrombosis was evident, particularly on days 1, 3 and 5. Histology confirmed the extent of haemorrhage evident grossly and, as no rupture was evident, suggested it to be due to diapedesis. Wall disruption occurred due to the local pressure effects of impacted filariae, but also due to inflammation, which was initially suppurative, later being replaced by plasma cell and lymphocyte involvement. Maximal wall disruption occurred at day 5 followed by organization and fibrosis. After day 5 there was more intense organization in the dogs given antigen, in association with the development of interstitial thickening, a finding previously reported in dogs with similar antigenic exposure.
Pulmonary arterial disease was produced by the placement of flexible polyvinyl chloride threads (similar in size, shape and flexibility to adult female Dirofilaria immitis) in the pulmonary arteries of dogs. Several different types of pathological change were apparent ranging from subendothelial oedema and endothelial loss, mild intimal proliferation and thrombus formation to organised fibrous encasement of the threads in areas where they had become impacted in the lumen of the artery. This range of pathological changes is very similar to that produced by D immitis and suggests that the intima of the canine pulmonary artery may react to different insults in a similar way.
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Livers of dogs which were microfilaremic due to infection with Dirofilaria immitis were studied after the administration of diethylcarbamazine. Most dogs had a severe shock-like clinical reaction. The main hepatic features were congestion and hemorrhage around the central vein and irregularly scattered foci of inflammation. The severity of the vascular reaction was associated with the number of microfilariae in the livers. Mast cells associated with the vascular reaction were not degranulated, suggesting that histamine-mediated anaphylaxis was not the cause of the reaction. The observations suggest that the mediator of the hepatic vascular reaction originates from the microfilariae and is influenced or activated by diethylcarbamazine.
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The necropsy results from a puppy with decompensated heart failure suggested that deformities of the right atrium, consisting of triple chamber development and venous obstruction, were the cause of cardiac failure.
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The laryngeal mucosa of cats which had been treated with a lignocaine aerosol spray prior to endotracheal intubation was examined histologically. A degree of oedema and cell damage was apparent. When one side of the larynx was sprayed before intubation and the other side protected in the same cat, cellular damage was greater on the side which received the lignocaine spray. In no cat were the changes considered severe enough to constitute a post-anaesthetic hazard.
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