fibrin and African-Swine-Fever

Acute forms of African swine fever are characterized by hemorrhagic lesions in the lymphoid organs. This paper reports the evolution of lesions in the splenic cords of pigs inoculated with African swine fever (ASF) virus (strain Malawi'83). Ultrastructural examination of the splenic cords of the infected pigs revealed numerous macrophages attached to the muscle cells harboring virus replication center and cytopathic effects at 3 dpi (days post-infection). From 5 dpi, the splenic cords contained a large number of erythrocytes associated with abundant fibrin deposits, mainly arranged around the muscle cells, from which macrophages had disappeared. It is likely that the ASF virus replication, and consequent cytopathic effects, observed in the fixed macrophages of splenic cords, may be responsible for the fibrin deposition.

Topics: African Swine Fever; African Swine Fever Virus; Animals; Cytopathogenic Effect, Viral; Erythrocytes; Female; Fibrin; Macrophages; Male; Muscle, Smooth; Spleen; Splenomegaly; Swine; Virion; Virus Replication

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.

Topics: African Swine Fever; African Swine Fever Virus; Animals; Capillaries; Edema; Female; Fibrin; Fibroblasts; Lung; Macrophages, Alveolar; Male; Neutrophils; Swine; Time Factors; Virus Replication

The activity of several proteins involved in fibrinolysis and the morphological changes in the blood vessel walls of pigs infected with highly virulent (Malawi'83) and moderately virulent (Dominican Republic '78-DR'78) ASF virus isolates were determined. Pigs infected with the Malawi'83 virus developed an increased fibrinolytic activity due to high plasma levels of tissue-plasminogen activator (t-PA) of 71.3 +/- 22.8 IU/ml (mean +/- SD), which correlated well with an increased activation of interstitial capillary endothelial cells and high levels of 1150 +/- 73.6 nM of fibrin monomer in the circulation. Animals infected with DR'78 virus, in contrast, showed an inhibition of fibrinolysis in the late stages of disease with almost a 5-fold increase of plasminogen activator inhibitor (PAI) activity of 196.0 AU/ml. These results suggest that activation of the fibrinolytic system in pigs infected with the Malawi'83 virus is probably due to increased formation and deposition of fibrin in the circulation, contributing to an increased bleeding tendency and higher mortality. On the contrary, animals infected with DR'78 virus developed an inhibition of fibrinolysis and thus a reduction in bleeding.

Topics: Acute Disease; African Swine Fever; African Swine Fever Virus; Animals; Edema; Fibrin; Fibrinolysis; Hemorrhage; Kidney; Liver; Plasminogen Inactivators; Swine; Syndrome; Thrombosis; Tissue Plasminogen Activator; Virulence

Twelve miniature pigs were inoculated with an attenuated African swine fever virus to study glomerular involvement in surviving pigs. In acute phase, kidneys were severely affected and displayed a glomerular capillary thrombosis with fibrin deposition in vascular lumen, detected by immunofluorescence. Fibrin-positive deposits were progressively cleared between one to three months after infection in surviving pigs. The histological picture in kidneys of surviving pigs, up to one post-infection year, showed a focal and segmental glomerulonephritis with hyalinosis, and IgM and C3 deposition was detected by immunofluorescence. Its pathogeny as an evolutive stage of acute glomerular injury is pointed out.

Topics: African Swine Fever; Animals; Antibodies; Antigen-Antibody Complex; Complement C3; Fibrin; Glomerulonephritis; Immunoglobulin M; Immunohistochemistry; Kidney Glomerulus; Swine; Viremia

Chronic pneumonia experimentally produced in 14 pigs with African swine fever (ASF) virus was studied by immunofluorescene (IF) and histopathologic techniques. Frozen sections prepared from pulmonary tissues of the infected pigs were stained with fluorescein-conjugated antiserums against ASF viral antigen, porcine immunoglobulin G (IgG), procine complement (C), and porcine fibrinogen. The viral antigen(s) was mainly seen in macrophages and cell debris in alveolar walls and lumens. This finding indicates that the virus replicated in the cytoplasm of alveolar macrophages that subsequently degenerated and released the viral antigen. Diffuse immunoglobulin (Ig) deposition was found in necrotic cells and debris. Immunoglobulin also was seen bound to intracytoplasmic inclusion bodies in some degenerating alveolar macrophages. This finding indicates that antibody against ASF viral antigen(s) excluded from blood circulation or produced by local immunocytes (or both) reacted with viral antigen at intramacrophage and extramacrophage levels and resulted in the formation of insoluble antigen-antibody (Ag-Ab) complexes. The participation of C in the immune complex was evident in the early stage of the pneumonia, but was less evident in the subsequent extensive, progressive necrotic processes. Fibrin deposits were visible only in the early necrotic area of alveolar walls and lumens. Possible mechanisms inducing extensive necrosis are discussed.

Topics: African Swine Fever; Animals; Antigen-Antibody Complex; Antigens, Viral; Complement System Proteins; DNA Viruses; Fibrin; Fibrinogen; Fluorescent Antibody Technique; Immune Sera; Immunoglobulin G; Lung; Macrophages; Necrosis; Pneumonia, Viral; Pulmonary Alveoli; Rabbits; Swine; Swine Diseases