Pathogenesis of Liver Lesions Caused by Experimental Infection with Piscirickettsia Salmonis in Juvenile Atlantic Salmon, Salmo Salar L

Abstract

Abstract. 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.

Patterns of Piscirickettsia salmonis load in susceptible and resistant families of Salmo salar

“…Wang et al [18] showed that catfish susceptible to Edwardsiella ictaluri presented increased acute phase responses, but the disease itself, could not be controlled. Macrophages, monocyte-like cells and the endothelium are important for explaining the body dynamics and containment of Piscirickettsia salmonis [19,20]. Our results show that the monocytemacrophage system associated gene LysC was up regulated in resistant fish, which is consistent with previous findings.…”

Comparative evaluation of experimental challenge by intraperitoneal injection and cohabitation of Atlantic salmon (Salmo salar L) after vaccination against Piscirickettsia salmonis (EM90‐like)

“…All macro‐ and microscopic pathological changes observed in this study were consistent with those previously described after both natural and experimental outbreaks (Almendras, Fuentealba, Markham, & Speare, ; Evensen, ; Fryer & Hedrick, ; Meza et al, ; OIE, ).…”

Comparative pathogenesis of piscirickettsiosis in Atlantic salmon (Salmo salar L.) post‐smolt experimentally challenged with LF‐89‐like and EM‐90‐like Piscirickettsia salmonis isolates

“…The systemic nature of the infection has been demonstrated by the presence of infected macrophages in blood smears from infected fish (Cvitanich et al, 1991). Almendras, Fuentealba, Markham, and Speare (2000) described the development of liver lesions in Atlantic salmon infected with P. salmonis through intraperitoneal (i.p. ), oral and gill infections.…”