Cardiopathology in acute African Swine Fever

The present study describes the gross, histopathologic lesions of the heart arising in pigs infected with acute African Swine Fever (ASF) and their biochemical profile. Ten pigs were infected by intramuscular injection of ASF virus (Georgia 2007). Selected heart samples were submitted for histopathological examination and Hematoxylin-Basic Fuchsin-Picric Acid (HBFP) staining. Enzymatic abnormalities were evaluated by measurement of main cardiac markers, whose activity increased during the early stage of infection, with histopathological changes occurring later. Minor myocardial haemorrhages were first observed at four days post infection (dpi), and were noted in all pigs by six dpi. Early vascular response to infection was manifested as increased capillary permeability leading to diapedesis and the retention of blood cells in myocardial tissue. The terminal stage of the disease was characterised by massive haemorrhages caused by the rupture of large vessels. Substantial ischemic areas were detected by HBFP staining at the terminal stages of ASF.

Association of hemophagocytic lymphohistiocytosis with kidney lesions in acute African swine fever virus infection

Glomerulonephritis due to African swine fever (ASF) is well documented. However, there is absence of good understanding of mechanisms involved in the development of pathology development. This study examines glomerulonephritis in association with acute infection induced by II genotype (Georgia 2007) of ASF virus. Taken together, the results of urinary analysis and the renal histological analysis led to the diagnosis of diffuse endocapillary proliferative glomerulonephritis with severe tubular injury associated with acute ASF (Georgia 2007). According to the pathogenesis, we have found that the diffuse endocapillary proliferative glomerulonephritis associated with the acute ASF develops with a delay of one to two days compared to development of hemophagocytic lymphohistiocytosis. The diagnosis of endocapillary proliferative glomerulonephritis confirms the characteristic of pathological changes in the composition of urine and urine sediment. The development of acute proliferative glomerulonephritis begins at 3 dpi, and finished at 4­6 dpi with the development of tubular necrosis. Our study demonstrates local macrophage proliferation. Local proliferation may be an important mechanism for amplifying macrophage-mediated renal injury. We have shown that the development of diffuse acute proliferative glomerulonephritis during ASF does not coincide with the presence of the virus in the blood or kidney tissues, but coincides with the developmental of ASFV derived hemophagocytic lymphohistiocytosis. The development of hemophagocytic lymphonocytosis also begins at least at 2­3 dpi and continues up to the terminal stage of the disease.