Atlantic salmon post-smolts were given an intraperitoneal (ip) injection of tissue homogenate of Atlantic salmon fry from an outbreak of infectious pancreatic necrosis (IPN), and cohabitants were given an ip injection of Earle's balanced salt solution (EBSS). Parallel treatment groups were exposed to recurrent episodes of environmental stress by water drainage twice a week. Fish injected with EBSS and non-injected fish were exposed to water drainage. The control fish were left untreated. Mortality due to IPN started 3 weeks after challenge in non-injected and EBSS-injected fish that had been exposed to water drainage. This showed that the fish used in the experiment were covertly infected with IPN virus (IPNV) prior to challenge, although no virus was detected in the fish sampled before the experiment. In fish that received an injection of IPNV, mortality started 5-6 days after challenge, regardless of the presence or absence of stress exposure. The EBSS-injected cohabitants started to die after an additional 5-6 days, also regardless of the presence or absence of stress exposure. The final cumulative mortality in the IPNV-injected fish was significantly lower than in the EBSS-injected cohabitants, thus suggesting that the secondary immune response after injection of IPNV provided more protection than the response after a water-borne infection. No disease outbreak was observed in the control fish.

ABSTRACT. Thirteen week old Atlantic salmon Salmo salar fry and 15 wk old brook trout Salvelinus fontinalis with average weights of 0.19 and 0.17 g, respectively, were bath challenged with infectious pancreatic necrosis virus (IPNV), serotype Sp, NI strain. The virus had been isolated from a clinical outbreak of infectious pancreatic necrosis (IPN) in Atlantic salmon parr. Cell culture supernatant after a first passage of virus was used as the infective material. Approximately 400 fry of each species were divided into 2 parallel tanks with challenged fish and 2 parallel tanks with non-challenged fish. At 69 d after challenge, cumulative mortalities of Atlantic salmon were 76 and 82 % for the challenged groups and 6 and 15% for the non-challenged groups. The corresponding values for brook trout were 42 and 4 3 % for the challenged groups and 8 and 10% for the non-challenged groups. The onset of mortality in challenged Atlantic salmon was delayed compared with the onset in brook trout. IPNV was reisolated from the fry of all challenged groups. Histological examination of sampled moribund fish showed hepatic degeneration or necrosis and exocrine pancreatic necrosis in fry from all challenged groups. The presence of IPNV in the lesions was demonstrated immunohistochemically. Virological, histological and immunohistochemical examinations of fry sampled prior to challenge and of non-challenged fry gave negative results. This study represents, to our knowledge, the first report of an experimental induction of clinical IPN in Atlantic salmon fry.

Atlantic salmon post-smolts were given an intraperitoneal (ip) injection of tissue homogenate of Atlantic salmon fry from an outbreak of infectious pancreatic necrosis (IPN), and cohabitants were given an ip injection of Earle's balanced salt solution (EBSS). Parallel treatment groups were exposed to recurrent episodes of environmental stress by water drainage twice a week. Fish injected with EBSS and non-injected fish were exposed to water drainage. The control fish were left untreated. Mortality due to IPN started 3 weeks after challenge in non-injected and EBSS-injected fish that had been exposed to water drainage. This showed that the fish used in the experiment were covertly infected with IPN virus (IPNV) prior to challenge, although no virus was detected in the fish sampled before the experiment. In fish that received an injection of IPNV, mortality started 5-6 days after challenge, regardless of the presence or absence of stress exposure. The EBSS-injected cohabitants started to die after an additional 5-6 days, also regardless of the presence or absence of stress exposure. The final cumulative mortality in the IPNV-injected fish was significantly lower than in the EBSS-injected cohabitants, thus suggesting that the secondary immune response after injection of IPNV provided more protection than the response after a water-borne infection. No disease outbreak was observed in the control fish.

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