Pathology of ovine pulmonary adenocarcinoma.
Clinical, gross pathology, histopathology and electron microscopy of the ovine pulmonary adenocarcinoma (OPA, jaagsiekte) either natural or experimentally induced in sheep, goat and moufflon are described. OPA is caused by an oncogenic betaretrovirus,jaagsiekte sheep retrovirus (JSRV). Most natural cases of OPA appear in animals 1-4 years old. There is no evidence of sex or breed susceptibility. Sheep affected by OPA show an afebrile respiratory illness associated with loss of weight. A very characteristic clinical sign is moist rales caused by the accumulation of fluid in the respiratory airways which is discharged from the nostrils when the head is lowered. Gross lesions are confined to the lungs but occasionally thoracic or extrathoracic structures are also affected. Two pathologic forms of OPA are currently recognized, classical and atypical. In classical forms the neoplastic lesions occurs particularly in the cranioventral parts of all lung lobes. They are diffuse or nodular, light grey or light purple in colour. On the cut surface the tumour is moist, and frothy fluid may pour from the airways on slight pressure. Atypical forms tend to be more nodular in both early and advanced tumours. They are pearly white in colour, very hard in consistency, very well demarcated from the surrounding parenchyma and their surface is dry. Histology of the lung sections reveals the presence of several foci of epithelial cell neoplastic proliferation in both alveolar or bronchiolar regions. The tumours, derived from type II pneumocytes and Clara cells, proliferate into mostly papillary but also acinar or occasionally solid growths. The tumour generally shows a benign histological pattern but intra- and extrathoracic metastases have been detected in some cases. Several considerations suggest that the tumour should be classified as an adenocarcinoma of the lung. The histology of atypical OPA is similar to that of the classical disease, with an increase in the stromal reaction accompanying the epithelial proliferations. Pathological features of OPA induced experimentally in sheep, or of OPA in goats and moufflon are similar to those described in sheep. Detailed electron microscopy of tumour material confirms that type II pneumocytes and Clara bronchiolar epithelial cells are the origin of the neoplasia. Also included in this chapter is a description of the morphology of the viral particles associated with OPA.
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