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Pathogenesis and immune response in Atlantic salmon (Salmo salar L.) parr experimentally infected with salmon pancreas disease virus (SPDV) Desvignes, L.; Quentel, C.; Lamour, F.; Le Ven, A. (2002). Pathogenesis and immune response in Atlantic salmon (Salmo salar L.) parr experimentally infected with salmon pancreas disease virus (SPDV). Fish Shellfish Immunol. 12(1): 77-95. https://dx.doi.org/10.1006/fsim.2001.0356 In: Fish & Shellfish Immunology. Academic Press: London; New York. ISSN 1050-4648; e-ISSN 1095-9947

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Beschikbaar in	Auteurs
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Trefwoorden

Complement Defence mechanisms > Phagocytosis Diseases Fishes > Osteichthyes > Salmoniformes > Salmonidae > Salmon > Salmo > Diadromous fishes > Atlantic salmon Fluids > Body fluids > Serum > Antibodies Immunological factors > Complement Immunological factors > Cytokines > Immunological factors > Animal proteins > Proteins > Antiviral agents > Interferon Interferon Lysozyme Microorganisms > Viruses Pathology > Histopathology Peptides > Proteins > Animal proteins > Egg proteins > O-glycoside hydrolases > Antiviral agents > Lysozyme Secretory organs > Glands > Exocrine glands > Digestive system > Digestive glands > Pancreas Symptoms > Viraemia Salmo salar Linnaeus, 1758 [WoRMS] Marien/Kust

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Auteurs		Top
Desvignes, L. Quentel, C., correspondent Lamour, F. Le Ven, A.

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Abstract

Atlantic salmon parr were injected intraperitoneally with salmon pancreas disease virus (SPDV) grown on CHSE-214 cells. The viraemia, the histopathological changes in target organs and some immune parameters were taken at intervals up to 30 days post-infection (dpi). The earliest kind of lesion was necrosis of exocrine pancreas, appearing as soon as 2 dpi. It progressed towards complete tissue breakdown at 9 dpi before resolving gradually. Concurrent to this necrosis, a strong inflammatory response was in evidence from 9 dpi in the pancreatic area for a majority of fish. A necrosis of the myocardial cells of the ventricle occurred in infected fish mainly at 16 dpi and it faded thereafter. The monitoring of the plasma viral load showed a rapid haematogenous spreading of SPDV, peaking at 4 dpi, but also the absence of a secondary viraemia. No interferon (IFN) was detected following the infection of parr with SPDV, probably owing to an IFN activity in Atlantic salmon below the detection level of the technique. Neutralising antibodies against SPDV were in evidence from 16 dpi and they showed a time-related increasing titre and prevalence. The phagocytic activity in head-kidney leucocytes was always significantly higher in the infected fish than in the control fish, being particularly high by 9 dpi. Lysozyme and complement levels were both increased and they peaked significantly in the infected fish at 9 and 16 dpi respectively. These results demonstrated that an experimental infection of Atlantic salmon parr with SPDV provoked a stimulation of both specific and non-specific immunity with regards to the viraemia and the histopathology.

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