title: Classical Swine Fever: pathology of bone marrow.
abstract: Twenty pigs were inoculated with a virulent isolate (Quillota strain) of classical swine fever (CSF) virus to determine the chronological development of lesions in bone marrow. Histopathologic, ultrastructural and immunohistochemical (detection of viral antigen gp55, myeloid-histiocyte antigen, CD3 antigen, and FVIII-rag), and morphometric techniques were employed. Viral antigen was detected from 2 days postinfection (dpi) in stromal and haematopoitic cells, and severe atrophy related to apoptosis of haematopoitic cells was observed. Megakaryocytes (MKs) did not show significant changes in number, but there were important qualitative changes including 1) increased numbers of cloud-nuclei MKs, microMKs, apoptotic MKs, and atypical nucleated MKs and 2) decreased number of typical nucleated MKs. Morphometric study of these cells showed a decrease in cytoplasmic area. MK infection was detected from 2 dpi, but in a small percentage of cells. Myeloid cells showed quantitative changes, with an increase in granulocyte numbers. Apoptosis of lymphocytes and viral infection of erythroblasts were also observed. The main changes in stroma were depletion of T lymphocytes in the middle phase of the experiment and macrophages. Viral infection was also observed in these cells. MK lesions suggest dysmegakaryocytopoiesis, which would aggravate the thrombocytopenia already present and could be responsible for it. Granulocyte changes would lead to the appearance of circulating immature forms, whereas lymphocyte apoptosis in bone marrow would contribute to lymphopenia.
authors.affiliation: Departamento Anatomía y Anatomía Patológica Comparadas, Edificio de Sanidad Animal, Campus Universitario de Rabanales, Córdoba, Spain. jcgomez@uco.es.
authors.forename: J C
authors.initials: JC
authors.lastname: Gomez-Villamandos
authors.forename: F J
authors.initials: FJ
authors.lastname: Salguero
authors.forename: E
authors.initials: E
authors.lastname: Ruiz-Villamor
authors.forename: P J
authors.initials: PJ
authors.lastname: Sánchez-Cordón
authors.forename: M J
authors.initials: MJ
authors.lastname: Bautista
authors.forename: M A
authors.initials: MA
authors.lastname: Sierra
mesh_terms: D000818:Animals; D000956:Antigens, Viral / Q000378:metabolism; D017209:Apoptosis; D001853:Bone Marrow / Q000473:pathology* / Q000648:ultrastructure / Q000821:virology; D017252:CD3 Complex / Q000378:metabolism; D006691:Classical Swine Fever / Q000473:pathology* / Q000821:virology; D006692:Classical Swine Fever Virus / Q000254:growth & development* / Q000648:ultrastructure; D005260:Female; D006098:Granulocytes / Q000821:virology; D007150:Immunohistochemistry / Q000662:veterinary; D007958:Leukocyte Count / Q000662:veterinary; D008297:Male; D008533:Megakaryocytes / Q000821:virology; D008854:Microscopy, Electron / Q000662:veterinary; D010976:Platelet Count / Q000662:veterinary; D013552:Swine; D014841:von Willebrand Factor / Q000378:metabolism
chemical_list: D000956:Antigens, Viral; D017252:CD3 Complex; D014841:von Willebrand Factor