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

Citation
Fe. Almendras et al., Pathogenesis of liver lesions caused by experimental infection with Piscirickettsia salmonis in juvenile Atlantic salmon, Salmo salar L, J VET D INV, 12(6), 2000, pp. 552-557
Citations number
23
Categorie Soggetti
Veterinary Medicine/Animal Health
Journal title
JOURNAL OF VETERINARY DIAGNOSTIC INVESTIGATION
ISSN journal
10406387 → ACNP
Volume
12
Issue
6
Year of publication
2000
Pages
552 - 557
Database
ISI
SICI code
1040-6387(200011)12:6<552:POLLCB>2.0.ZU;2-2
Abstract
Piscirickettsia salmonis, the etiologic agent of salmonid rickettsial septi cemia (SRS), or piscirickettsiosis, causes substantial economic losses to t he salmon industry. The pathogenesis of the disease has not been fully char acterized. The aim of this study is to describe the hepatic lesions associa ted with experimental P. salmonis infection in Atlantic salmon juveniles. F ish were maintained in fresh water and inoculated intraperitoneally (IP), o rally, 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 immuno histochemical 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. Histolo gical changes at this time consisted of vasculitis, presence of fibrin thro mbi, vacuolated hepatocytes and focal areas of necrosis. Leukocytes contain ing intracytoplasmic basophilic microorganisms were seen within hepatic sin usoids. Vasculitis and intracytoplasmic vacuoles were prominent features in fish inoculated orally and on the gill surface. The presence of P. salmoni s within hepatocellular vacuoles, endothelial cells, and leucocytes was con firmed by immunohistochemistry. The intracellular location of P. salmonis a nd the vascular damage seen in infected fish are characteristic of ricketts ial infections. Histological lesions induced by experimental infection with P. salmonis using the oral and gill surface routes were similar to those o bserved in natural outbreaks of piscirickettsiosis. The tropism of P. salmo nis for endothelial cells explains the vascular lesions observed in SRS, wh ereas hepatic lesions are due to ischemic necrosis and direct injury by int racytoplasmic organisms.