If infected as adults, older fish may undergo subclinical infection, unapparent infection or mount an immune response and clear the infection. Juvenile fish, which survive infection, tend to become carriers, with stress-precipitated re-activation later in life leading to virus shedding and clinical disease. Up to 90% of survivors carry the virus and shed it in their feces for the remainder of their life.
The infectious pancreatic necrosis virus (IPNV) is a member of the Birnaviridae family, which are naked icosahedral viruses having a genome consisting in two molecules of double stranded RNA. The diameter of the virus is around 60 nm and it is built up of two RNA proteins: Vp2 and Vp3. Vp2 is known to contain an epitope, which is the target for fish neutralizing antibodies. There are estimates that 3-12 different serotypes exist. The degree of pathogenicity of the disease is related to the serotype of the viral isolate, the age fish and the species of fish. The occurrence of the disease is thought to be a complex interaction between the IPN virus and the physiological status of the fish (Reno, 1978).
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. .
Discussion.
Two aspects have been examined to minimize and control outbreaks of IPNV. The first is that older fish should be more tolerant to IPNV having a developed immune system and the second that higher temperature should lower the rates of IPNV infection. .
Age immune response has been demonstrated on numerous occasions to have a nearly linear decrease of mortality with increasing age. This has been shown in brook trout fry (Wolf, 1988, Frantsi, 1971) and rainbow trout fry of different ages (Dorson, 1981).
