Pathogenesis of classical swine fever: Renal haemorrhages and erythrodiapedesis

Thirty pigs were inoculated with a virulent isolate (Quillota strain) of cl assical swine fever (hog cholera) virus to establish the chronological occu rrence of lesions in the kidney and to determine the mechanism responsible for renal haemorrhages. The study included the use of histopathological, ul trastructural, immunohistochemical (detection of viral antigen gp55, MAC387 , lambda chains, CD3 and Clq) and morphometrical techniques (vascular area) . Renal interstitial oedema and haemorrhages were detected from 7 da's post -inoculation (dpi), associated with a slight interstitial mononuclear infil trate and evidence of viral infection in macrophages and fibroblasts, and i n a small proportion of lymphocytes. Viral infection was not detected in ca pillary endothelial cells. An intense mononuclear infiltrate, with B cells, T cells and small numbers of macrophages, was detected from 10 dpi. In the final phase of the experiment (14 dpi, slight proliferation and degranulat ion of mast cells were observed. Increased expression of the Clq component of complement was also detected. A significant increase in vascular area wa s observed from 7 dpi. These results suggest that haemorrhages observed in the kidneys of pigs inoculated with the Quillota strain resulted from eryth rodiapedesis and increased vascular permeability, probably aggravated by ma st cell degranulation in the final stage of the experiment. The results sug gested that mast cell degranulation was linked to activation of the complem ent system. (C) 2000 Harcourt Publishers Ltd.