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
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.