title: Pathogenesis of classical swine fever: renal haemorrhages and erythrodiapedesis.
abstract: Thirty pigs were inoculated with a virulent isolate (Quillota strain) of classical swine fever (hog cholera) virus to establish the chronological occurrence of lesions in the kidney and to determine the mechanism responsible for renal haemorrhages. The study included the use of histopathological, ultrastructural, immunohistochemical (detection of viral antigen gp55, MAC387, lambda chains, CD3 and C1q) and morphometrical techniques (vascular area). Renal interstitial oedema and haemorrhages were detected from 7 days post-inoculation (dpi), associated with a slight interstitial mononuclear infiltrate and evidence of viral infection in macrophages and fibroblasts, and in a small proportion of lymphocytes. Viral infection was not detected in capillary 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 degranulation of mast cells were observed. Increased expression of the C1q component of complement was also detected. A significant increase in vascular area was observed from 7 dpi. These results suggest that haemorrhages observed in the kidneys of pigs inoculated with the Quillota strain resulted from erythrodiapedesis and increased vascular permeability, probably aggravated by mast cell degranulation in the final stage of the experiment. The results suggested that mast cell degranulation was linked to activation of the complement system.
authors.affiliation: Departamento de Anatomía Patológica, Universidad de Córdoba, Campus Universitario de Rabanales, Carretera de Madrid, 14014 Córdoba, Spain.
authors.forename: J C
authors.initials: JC
authors.lastname: Gómez-Villamandos
authors.forename: E
authors.initials: E
authors.lastname: Ruiz-Villamor
authors.forename: M J
authors.initials: MJ
authors.lastname: Bautista
authors.forename: M
authors.initials: M
authors.lastname: Quezada
authors.forename: C P
authors.initials: CP
authors.lastname: Sánchez
authors.forename: F J
authors.initials: FJ
authors.lastname: Salguero
authors.forename: M A
authors.initials: MA
authors.lastname: Sierra
mesh_terms: D000818:Animals; D000956:Antigens, Viral / Q000032:analysis; D015415:Biomarkers / Q000032:analysis; D002196:Capillaries / Q000378:metabolism / Q000648:ultrastructure / Q000821:virology; D002198:Capillary Fragility / Q000502:physiology; D002199:Capillary Permeability / Q000502:physiology; D015550:Cell Degranulation / Q000502:physiology; D002465:Cell Movement / Q000502:physiology*; D006691:Classical Swine Fever / Q000209:etiology* / Q000276:immunology / Q000473:pathology; D006692:Classical Swine Fever Virus / Q000276:immunology; D022162:Cytoplasmic Vesicles / Q000502:physiology / Q000648:ultrastructure; D004487:Edema / Q000209:etiology / Q000473:pathology; D004730:Endothelium, Vascular / Q000378:metabolism / Q000648:ultrastructure / Q000821:virology; D004912:Erythrocytes / Q000166:cytology / Q000502:physiology*; D005260:Female; D006470:Hemorrhage / Q000209:etiology* / Q000473:pathology; D007674:Kidney Diseases / Q000209:etiology* / Q000473:pathology; D008297:Male; D008407:Mast Cells / Q000502:physiology / Q000648:ultrastructure; D013552:Swine
chemical_list: D000956:Antigens, Viral; D015415:Biomarkers