IPNV

The growth of the salmon farming industry in the last couple decades has stimulated interest in the diseases of farmed Atlantic salmon, Salmo salar L. Infectious pancreatic necrosis (IPN) has become of particular concern because of the increasing prevalence of IPN virus (IPNV) in salmon farms. IPN has been identified in nearly all trout and salmon producing countries. In Norwegian salmon farms, losses of millions of dollars annually in Atlantic salmon have been due to outbreaks of IPN. In 1995, it was estimated that 5% of Atlantic salmon set to sea in Norwegian fish farms were lost due to IPN, giving economic losses of about 60 million USD yearly (Christie, 1997).

IPNV occurs in salmonids in both freshwater and marine environments. The disease can be acquired through horizontal transmission, from feces of infected fish, and by vertical transmission, from parent to progeny via reproductive products (Wolf, 1988). The virus causes acute infection, primarily in the liver, but it is also found in high concentrations in the kidney and spleen (Smail & Munro, 1995).

In Atlantic salmon, IPN virus can cause significant chronic mortality in larger fish, particularly after the stress of smoltification and saltwater introduction. Losses of up to 60% have been reported shortly after seawater transfer. The discrepancy between experimental results and the actual disease situation have given rise to speculation as to the cause of the outbreaks of IPN in post-molts and the impact of management and environmental factors (Taksdal, 1998). Stresses such as handling and transport from hatchery to the sea site, may have a cumulative effect on the fish, leading to an increased susceptibility to disease during the first months of the seawater stage.

Salmo salar L., post-smolts by stress exposure, by injection of IPN virus

Low temperature is found to have a sparing effect on fry. Mortality rate in fry has been considerably lowered or prevented, when held between 4-6°C (Frantsi, 1971, Dorson, 1981). Cold temperatures would decrease the rate of virus production by infected cells, as well as slow the production of antibodies. Frantsi & Savan (1971) emphasized that low ambient temperatures could account for the low mortalities caused by IPN. The cold-water temperatures in spite of affecting a slow rate of growth may be beneficial in terms of preventing disease mortality. The mechanism for such sparing has not been demonstrated, but would likely be related to the maturation of vulnerable cells to a stage where they would not be sensitive to the virus (Sadasiv, 1995).

Sadasiv et al (1993), found that Atlantic salmon kept at 6°C were able to develop a good antibody response to IPNV, although somewhat more slowly than those at higher temperatures. Sadasiv et al (1993) concluded immune suppression would have been due to low temperatures (Bly and Clem, 1993). Late-occurring fish deaths, some noted to be related to increasing water temperatures, could be explained by antibody-mediated processes (Sadasiv, 1993). Disease resistance or immune responses appear to be optimized at higher temperatures (16°C).

It is generally accepted that stress is a very important factor in outbreaks of infectious diseases of fishes (Snieszko, 1974). Immune response may be compromised due to stress allowing the disease to proliferate. The exact epidemiology is not yet well established but factors such as age, temperature and the strain of fish play a part in the development of the disease.

The primary defense against IPNV currently is avoidance. Raising stock in IPN-free environments has proved to be difficult, since live fish, fish eggs, and fish farm wastes pose a high risk for spread of IPNV. Fish with latent infection appear to be healthy, which can increase the possibility of giving rise to infected eggs. Selection for IPN-free brood stock is key. Brood stock could also be selected for resistance, although there is no evidence of transferred immunity, resistance appears to be heritable and can be enhanced by selective breeding.

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