Pathogenesis of liver lesions caused by experimental infection with Piscirickettsia salmonis in juvenile Atlantic salmon, Salmo salar L

Department of Pathology and Microbiology, Atlantic Veterinary College, Charlottetown, Prince Edward Island, Canada. Piscirickettsia salmonis, the etiologic agent of salmonid rickettsial septicemia (SRS), or piscirickettsiosis, causes substantial economic losses to the salmon industry. The pathogenes...

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Bibliographic Details
Published in:	Journal of veterinary diagnostic investigation Vol. 12; no. 6; pp. 552 - 557
Main Authors:	Almendras, FE, Fuentealba, IC, Frederick Markham, RF, Speare, DJ
Format:	Journal Article
Language:	English
Published:	Los Angeles, CA J Vet Diagn Invest 01-11-2000 SAGE Publications American Association of Veterinary Laboratory Diagnosticians
Subjects:	Animals Biological and medical sciences Fish Diseases - microbiology Fish Diseases - pathology Fish Diseases - physiopathology Fundamental and applied biological sciences. Psychology Liver - microbiology Liver - pathology Microbiology Rickettsiaceae - isolation & purification Rickettsiaceae Infections - pathology Rickettsiaceae Infections - physiopathology Rickettsiaceae Infections - veterinary Salmo salar Time Factors
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Summary:	Department of Pathology and Microbiology, Atlantic Veterinary College, Charlottetown, Prince Edward Island, Canada. Piscirickettsia salmonis, the etiologic agent of salmonid rickettsial septicemia (SRS), or piscirickettsiosis, causes substantial economic losses to the salmon industry. The pathogenesis of the disease has not been fully characterized. The aim of this study is to describe the hepatic lesions associated with experimental P. salmonis infection in Atlantic salmon juveniles. Fish were maintained in fresh water and inoculated intraperitoneally (IP), orally, or on the gill surface with P. salmonis. A group of uninfected fish was kept as control. Liver samples from 5 fish in each inoculated group and 3 controls were collected weekly and processed for histological and immunohistochemical examination. Thickening of the liver capsule by inflammatory cells was a characteristic histologic feature of IP inoculated fish. Three weeks post-IP inoculation, 8 fish had died and 2 fish were sampled. Histological changes at this time consisted of vasculitis, presence of fibrin thrombi, vacuolated hepatocytes and focal areas of necrosis. Leukocytes containing intracytoplasmic basophilic microorganisms were seen within hepatic sinusoids. Vasculitis and intracytoplasmic vacuoles were prominent features in fish inoculated orally and on the gill surface. The presence of P. salmonis within hepatocellular vacuoles, endothelial cells, and leucocytes was confirmed by immunohistochemistry. The intracellular location of P. salmonis and the vascular damage seen in infected fish are characteristic of rickettsial infections. Histological lesions induced by experimental infection with P. salmonis using the oral and gill surface routes were similar to those observed in natural outbreaks of piscirickettsiosis. The tropism of P. salmonis for endothelial cells explains the vascular lesions observed in SRS, whereas hepatic lesions are due to ischemic necrosis and direct injury by intracytoplasmic organisms.
Bibliography:	ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23
ISSN:	1040-6387 1943-4936
DOI:	10.1177/104063870001200610