Total mortalities in fry infected with IPNV and held at 10°C regularly decreased from 70% in fish infected when 1 to 2 weeks old to a negligible percent in fish infected when 20 weeks old (Dorson, 1981). Typically the juvenile stage is most affected, resulting in high mortality, especially during the summer (Espinoza & Kuznar, 1997).
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. .
Host response and viral replication seem to be influenced by temperature. Swings in water temperature are commonly encountered after transfer to seawater. Disease usually occurs under conditions of virus exposure accompanied by additional stress. Changes in temperature are important in outbreaks or reduction of fish diseases, as the temperature affects the response of fish to an invasion by pathogens (Snieszko, 1974). .
Salmonids can live at a fairly large range of temperature. IPN can also occur over a wide temperature range, but it tends to be most acute at 10 to 15°C. Under certain conditions the course of the disease may be more chronic with lower mortality. Acute infections normally occur in 1-4 month old salmonids. Mortality typically begins 3 to 10 days following infection and peaks in 10 to 20 days. Total mortality from acute infection may reach 70% or more over 2 to 4 weeks (Wolf, 1988).