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African swine fever is an acute haemorrhagic disease of pigs which may serve as a model for the study of the pathogenesis of other viral haemorrhagic fevers. This paper describes an ultrastructural study of the sequence of lesions produced in the perisinusoidal functional unit of the liver of pigs inoculated with the Malawi '83 strain of African swine fever virus, which is classified as haemadsorbing and highly virulent. Virus replication was observed in Kupffer cells and monocytes from three days after inoculation, in hepatocytes and fat-storing cells at five and seven days after inoculation, and in sinusoidal endothelial cells at seven days after inoculation. Further observations included intravascular coagulation, which peaked at five days after inoculation, and fibroblast and myofibroblast transformation of fat-storing cells at seven days after inoculation. These results suggest that activated cells of the mononuclear phagocyte system may play a major role in this sequence of lesions and the possible role of the cytokines that may be released by these cells is discussed.

Summary African swine fever is a viral disease of pigs characterized predominantly by haemorrhagic lesions. This paper reports the lesions observed in the renal interstitial capillaries of pigs inoculated with African swine fever virus strains of differing virulence: the Malawi'83 strain (haemadsorbent and highly virulent) and the Dominican Republic'78 strain (haemadsorbent and moderately virulent). In pigs infected with the Malawi'83 strain, petechial haemorrhages and microhaemorrhages were observed 5 days after inoculation and lesions were evident in the renal capillaries. Signs of phagocyte activation were noticeable in endothelial cells, with enlarged fenestrations and even loss of endothelium, leaving the basement membrane of the vessels exposed. Platelet plugs and microthrombi were also observed in these vessels. At 7 days after inoculation these lesions had intensified, and were accompanied by virus replication in the endothelial cells. In pigs infected with the Dominican Republic'78 strain, haemorrhages were more abundant and more extensive, and although no endothelial cell lesions were observed, there was intense vasodilation with diapedesis of erythrocytes.

Recent studies of pulmonary intravascular macrophages have led to the re-examination of the mechanisms giving rise to alveolar oedema. A highly virulent isolate of African swine fever virus was replicated in pulmonary intravascular macrophages, interstitial and alveolar macrophages, fibroblasts and neutrophils. The alveolar oedema — characteristic of acute forms of African swine fever — and the vascular changes observed, which consisted of the formation of fibrin microthrombi in septal capillaries and the vacuolisation of endothelial cells, may have been due, however, to the activation of pulmonary intravascular macrophages, and not to the cytopathic effect subsequent to the replication of the African swine fever virus. Furthermore, it was observed that virus replication in cells not belonging to the mononuclear phagocyte system — such as fibroblasts and neutrophils — occurred earlier than in cells belonging to that system.