Researchers and the salmon industry have been debating whether fingerling (young fish) from freshwater farms can be a source of the virus that causes pancreas disease (PD): salmonid alfavirus (SAV). The results of a new doctoral study show that this is not the case: pancreas disease transmits horizontally in the seawater phase and infection in fresh water has little bearing on how the disease spreads.
During her doctoral research, Mona Dverdal Jansen has followed the progression of pancreas disease (PD) in Norwegian farmed salmon from the fresh water phase and throughout the entire seawater phase. The research involved testing 46 different fish populations of farmed salmon from 6 counties for SAV in the fresh water phase, before the fish were released into seawater. SAV was not found to occur in any of these populations.
The 46 salmon populations were transferred to 51 seawater locations, where they were tested for SAV three times during the production phase, including when they were slaughtered. 36 of the 51 locations were situated within the infected zone and 23 (64%) of these 36 were shown to be affected by the SAV virus during the seawater phase. The fish populations were infected during the entire seawater phase, and the risk of infection increased, the longer the fish were in the seawater.
With the exception of three populations, where SAV was detected when the salmon were slaughtered, all the infected populations developed PD. In contrast, no SAV was detected during the production phase amongst the populations released into the 15 uncontaminated seawater locations.
Jansen investigated a number of potential risk factors for infection, but the only factor shown to have any significance was the location within the infected zone. These findings confirm earlier discoveries: that PD infects horizontally from population to population in the seawater phase and that the fresh water phase is insignificant as a source of SAV.
Furthermore, Jansen's thesis describes how, once a population is infected, it remains infected until the time of slaughter. She observed a very varying time lapse between the detection of the SAV virus and the outbreak of PD in some populations. In addition, she found that mortality rates resulting from PD also varied greatly from population to population. She found no signs that the SAV virus was reactivated when the fish were stripped in the one broodstock population she examined.
Dying and thin fish had a higher risk of testing positive in one or more of the diagnostic trials, compared to apparently healthy fish from the same population. This indicates that current routines for taking samples and studying the disease, where dying and clinically abnormal fish are given priority, ought to be continued. The degree of observed conformity between the diagnostic tests employed varied according to which stage of the disease the fish were in.
Jansen carried out genetic analyses of SAV sequences. All belonged to SAV subtype 3 -- the only subtype identified in Norway so far. The sequence variation was found to be somewhat larger than previously reported in the case of one of the genetic fragments studied.
A model based on a stochastic scenario tree indicated that there was an extremely high probability that SAV infection would be absent within the uncontaminated area in the model year of 2007, and this tallied with the results of the field studies.
Jansen carried out her research at the Centre for Epidemiology and Biostatistics at The Norwegian School of Veterinary Science (NVH) and at The National Veterinary Institute from 2006-2010.
Cite This Page: