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Experimental pathogenicity of reovirus 13p 2 for juvenile American oysters Crassostrea virginica (Gmelin) and bluegill fingerlings Lepomis macrochirus (Rafinesque)
Author(s) -
MEYERS T. R.
Publication year - 1980
Publication title -
journal of fish diseases
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.819
H-Index - 85
eISSN - 1365-2761
pISSN - 0140-7775
DOI - 10.1111/j.1365-2761.1980.tb00443.x
Subject(s) - crassostrea , biology , virus , virology , oyster , juvenile , inoculation , microbiology and biotechnology , pathogen , veterinary medicine , fishery , ecology , immunology , medicine
. A viral agent (13p 2 ), isolated from clinically normal juvenile American oysters ( Crassostrea virginica ) and characterized as a new serotype of reovirus, was tested to determine if it could replicate and produce disease in experimental juvenile oysters. Because the virus replicated well in the bluegill fry (BF‐2) fish cell line, fingerling bluegills Lepomis macrochirus were included in the pathogenicity experiments. Exposure of oysters to the 13p 2 virus in ambient seawater resulted in no significant mortality and no increased virus titres or histological lesions. Virus particles were not observed in tissues of exposed oysters when examined with transmission electron microscopy (TEM). Intraperitoneal inoculation of the 13p 2 virus into bluegills resulted in 44% mortality associated with a focal necrotic hepatitis. Evidence of virus replication, when evaluated histological or by virus titration, was observed in 94% of 32 inoculated fish. Samples of infected livers examined with TEM revealed typical cytoplasmic arrays of 13p 2 virus particles in affected hepatocytes. Rising virus titres and hepatic lesions also occurred in bluegills exposed to water containing the 13p 2 virus. These results indicated the natural host of the 13p 2 virus was not the American oyster, but that it was a significant pathogen for at least one fish species.