We describe the finding of a novel viral haemorrhagic septicaemia virus (VHSV) Genotype III strain that caused disease of both a neurological and septicaemic nature in seawater-farmed rainbow trout Oncorhynchus mykiss in Storfjorden, Norway. In November 2007, an outbreak of VHS associated with slightly elevated mortality was confirmed at a seawater site rearing rainbow trout (90 to 440 g). Within 3 to 4 mo, the disease was recognised in 3 neighbouring sea sites with ongrowing rainbow trout. The clinical, gross pathological and histopathological findings were in accordance with VHS, and the diagnosis was confirmed by the detection of VHSV in brain and internal tissues by immunohistochemistry, cell culture and reverse transcriptase PCR (RT-PCR). Sequence analysis of the G-gene revealed that the isolated virus clustered with VHSV Genotype III and that the Norwegian isolate represents a unique strain of VHSV. The pathogenicity of the virus strain to rainbow trout and Atlantic salmon Salmo salar was examined using infection experiments. In immersion trials, the Norwegian isolate produced a cumulative mortality of 70% in rainbow trout, while nearly 100% mortality was obtained after intraperitoneal injection of the virus. For Atlantic salmon, no mortality was observed in immersion trials, whereas 52% mortality was observed after intraperitoneal injection. The Norwegian isolate thus represents the first VHSV of Genotype III pathogenic to rainbow trout.

Infectious salmon anaemia (ISA) is an important infectious disease in Atlantic salmon farming causing recurrent epidemic outbreaks worldwide. The focus of this paper is on tracing the spread of ISA among Norwegian salmon farms. To trace transmission pathways for the ISA virus (ISAV), we use phylogenetic relationships between virus isolates in combination with spacetime data on disease occurrences. The rate of ISA infection of salmon farms is modelled stochastically, where seaway distances between farms and genetic distances between ISAV isolates from infected farms play prominent roles. The model was fitted to data covering all cohorts of farmed salmon and the history of all farms with ISA between 2003 and summer 2009. Both seaway and genetic distances were significantly associated with the rate of ISA infection. The fitted model predicts that the risk of infection from a neighbourhood infectious farm decreases with increasing seaway distance between the two farms. Furthermore, for a given infected farm with a given ISAV genotype, the source of infection is significantly more likely to be ISAV of a small genetic distance than of moderate or large genetic distances. Nearly half of the farms with ISA in the investigated period are predicted to have been infected by an infectious farm in their neighbourhood, whereas the remaining half of the infected farms had unknown sources. For many of the neighbourhood infected farms, it was possible to point out one or a few infectious farms as the most probable sources of infection. This makes it possible to map probable infection pathways.

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We suggest that a single HPR-deleted genotype of ISAV has spread between salmon farms in the North-cluster. Furthermore, we find that HPR0/F (Q(266)) genotypes are frequently present in farmed populations of Atlantic salmon. From this, we anticipate a population dynamics of ISAV portrayed by low virulent genotypes occasionally transitioning into virulent genotypes, causing solitary outbreaks or local epidemics through local transmission.

Infectious salmon anaemia (ISA) is a severe disease in farmed Atlantic salmon Salmo salar that has caused epidemic outbreaks in most salmon-producing countries worldwide. The disease is caused by virulent ISA virus (ISAV). Low virulent variants of the virus, characterised by a full-length sequence in the highly polymorphic region of segment 6 in the virus genome, have been reported with increasing frequencies. These variants of the virus, termed HPR0, have been proposed to be ancestors of virulent ISAV. We examined this idea through studies of the phylogeographic and environmental distribution of ISAV-HPR0, as well as phylogeographic associations between virulent ISAV and ISAV-HPR0. Samples from 232 fish groups were screened for ISAV. Real-time RT-PCR was used for detection of ISAV, and the ISAV haemagglutinin esterase (HE) gene was characterised for positive samples. A Mantel test was used to test phylogeographic associations between pairs of ISAV-HPR0 HE gene sequences. A rank test was used to test associations between HE gene sequences from virulent ISAV and ISAV-HPR0. ISAV-HPR0 was detected in fish groups both in freshwater and marine environments, and in juveniles, on-grown marine salmon and broodstock salmon. Genetic and geographic distances between pairs of ISAV-HPR0 HE gene sequences were positively correlated, suggesting that the population of ISAV-HPR0 is geographically structured. Finally, we found a spatial association between fish groups with virulent ISAV (n = 21) and fish groups with ISAV-HPR0 (n = 27), supporting the hypothesis that ISAV-HPR0 may undergo a transition to virulent ISAV. KEY WORDS: Infectious salmon anaemia virus · ISAV · HPR0 · Atlantic salmon · NorwayResale or republication not permitted without written consent of the publisher OPEN PEN ACCESS CCESS