The virus is widespread in Norwegian salmon and rainbow trout aquaculture and is a significant cause of economic losses for the industry.
Pathogen and Transmission
IPNV belongs to the genus Aquabirnavirus within the family Birnaviridae. The virus particles are non-enveloped, and its genome consists of two segments of double-stranded RNA. IPNV is highly resilient, capable of surviving outside the host for extended periods. It shows strong resistance to both low pH and high temperatures, but it can be inactivated by disinfectants such as ozone, formalin, and iodine.
Transmission is believed to occur both horizontally (between fish) and vertically (via eggs). During an outbreak, infected fish excrete large quantities of virus through feces and urine. Many fish that survive an IPN outbreak remain persistently infected for long periods. These carriers can intermittently shed virus—particularly under stress—potentially leading to new outbreaks.
Clinical Signs
The disease primarily affects farmed salmonids, with aquaculture operations considered the main reservoir for the virus. While mortalities tend to be higher during the freshwater phase, economic losses are often greater during outbreaks in seawater due to the higher value of individual fish at that stage.
Mortality rates can vary significantly, from negligible to as high as 90%, with fry and post-smolts appearing most susceptible. In addition to fish age and developmental stage, mortality is influenced by viral strain, fish strain, and environmental and operational factors.
Diagnosis
A definitive diagnosis of IPN is made by histopathological examination of formalin-fixed tissue, showing characteristic necrosis in the liver and/or exocrine pancreas (the digestive enzyme-secreting portion of the pancreas). This is supported by positive immunohistochemical staining for IPNV in affected tissues.
The virus can also be detected in the kidney through cell culture or real-time RT-PCR. However, as many fish can carry the virus asymptomatically, diagnosis cannot be based on viral detection alone.
Other diseases, such as infections with Flavobacterium psychrophilum or Yersinia ruckeri, can mimic IPN in fry, so laboratory confirmation is critical.
Occurrence
IPN was first described as infectious enteritis in trout fry in Canada as early as 1941. The virus was identified in the 1950s in the USA, and first detected in Norway in 1975. Since the 1980s, IPN has been one of the most significant disease challenges in Norwegian aquaculture.
The virus has a broad tissue tropism and has been found in numerous fish species, as well as in mollusks, crustaceans, and cephalopods. The Norwegian Veterinary Institute publishes annual statistics on IPN outbreaks in the Fish Health Report, and a clear decline in reported cases has been observed in recent years.
Control Measures
Preventing the introduction of IPNV into hatcheries is essential. Efforts in recent years have focused on eradicating “house strains” of IPNV from the freshwater phase. These initiatives have led to a noticeable decline in IPN outbreaks in fry and post-smolt following sea transfer.
Long-term selective breeding has been conducted to enhance genetic resistance to IPN. New technologies, such as QTL (quantitative trait loci) mapping, have enabled the identification of salmon genes associated with resistance. These developments have contributed significantly to the reduction in annual IPN outbreaks.
A large proportion of Norwegian salmon are vaccinated against IPN. However, the efficacy of vaccination is considered less reliable compared to other preventive strategies. While vaccination likely helps reduce losses during outbreaks, it does not prevent infected fish from becoming virus carriers, which can lead to future outbreaks.
Despite advances in breeding, biosecurity, and vaccination, IPN continues to cause considerable losses. Outbreaks are often associated with stress. Therefore, maintaining good water quality, proper feeding, and sound operational practices is essential to minimize impacts.
Beyond direct losses, surviving fish may experience reduced resilience, increasing susceptibility to secondary diseases in the seawater phase. For example, significant mortality from HSMB and PD has been reported in groups that previously experienced IPN outbreaks.
