Ultrastructural changes related to the lymph node haemorrhages in acute African swine fever

• Published in: Research in veterinary science 1997-05, Vol.62 (3), p.199-204
• Main Authors: Carrasco, L, Chacón-m de Lara, F, Martín de las Mulas, J, Gómez-Villamandos, J.C, Sierra, M.A, Villeda, C.J, Wilkinson, P.J
• Format: Article
• Language: English
• Subjects: African Swine Fever - complications; African Swine Fever - pathology; African Swine Fever - physiopathology; African Swine Fever Virus - isolation & purification; African Swine Fever Virus - physiology; Animals; Disseminated Intravascular Coagulation - pathology; Disseminated Intravascular Coagulation - veterinary; Endothelium, Vascular - pathology; Endothelium, Vascular - ultrastructure; Female; Fibroblasts - pathology; Fibroblasts - ultrastructure; Hemorrhage - etiology; Hemorrhage - pathology; Hemorrhage - veterinary; Lymph Nodes - pathology; Lymph Nodes - ultrastructure; Lymphatic Diseases - etiology; Lymphatic Diseases - pathology; Lymphatic Diseases - veterinary; Macrophages - pathology; Macrophages - ultrastructure; Macrophages - virology; Male; Microscopy, Electron - methods; Microscopy, Electron - veterinary; Monocytes - pathology; Monocytes - ultrastructure; Monocytes - virology; Muscle, Smooth, Vascular - pathology; Muscle, Smooth, Vascular - ultrastructure; Swine; Swine Diseases - etiology; Swine Diseases - pathology; Virus Replication
• ISSN: 0034-5288; 1532-2661
• DOI: 10.1016/S0034-5288(97)90190-9

In order to determine the pathogenic mechanisms involved in lymph node haemorrhages in acute African swine fever ( ASF), eight pigs were inoculated with ASF virus, strain Malawi'83. Lymph node haemorrhages were observed from three days post infection (dpi) onwards, coinciding with ASF virus replication in monocytes and macrophages adjacent to stimulated endothelial cells, phagocytic stimulation of capillary and small-vessel endothelial cells, increase in the number of fenestrations of endothelial cells, and endothelial cell loss, as well as clusters of blood cells and necrotic material beneath the endothelium. Vascular lumina were blocked by platelet plugs and fibrin microthrombi. These phenomena became more marked as the disease progressed. At five dpi, virus replication was also found in circulating neutrophils. At seven dpi, lesions were more intense and were accompanied by virus replication in sinus and capillary endothelial cells, and in other cell populations including pericytes, fibroblasts, smooth muscle fibres and reticular cells. The results obtained in this study suggest that lymph node haemorrhages are related to endothelial stimulation and the onset of disseminated intravascular coagulation. Virus replication in vessel wall cells occurs only in the final stages of the disease and plays a secondary role.