Within-farm spread of infectious salmon anemia virus (ISAV) in Atlantic salmon Salmo salar farms in Chile.

Spread of infectious salmon anemia virus (ISAV) at the cage level was quantified using a subset of data from 23 Atlantic salmon Salmo salar farms located in southern Chile. Data collected from official surveillance activities were systematically organized to obtain detailed information on infectious salmon anemia (ISA) outbreaks. Descriptive statistics for outbreak duration, proportion of infected fish, and time to secondary infection were calculated to quantify the magnitude of ISAV incursions. Linear and multiple failure time (MFT) regression models were used to determine factors associated with the cage-level reproduction number (Rc) and hazard rate (HR) for recurrent events, respectively. In addition, the Knox test was used to assess if cage-to-cage transmissions were clustered in space and time. Findings suggest that within farms, ISA outbreaks, on average, lasted 30 wk (median = 26 wk, 95% CI = 24 to 37 wk) and affected 57.3% (95% CI = 47.7 to 67.0%) of susceptible cages. The median time to secondarily diagnosed cages was 23 d. Occurrence of clinical ISAV outbreaks was significantly associated with increased Rc, whereas increased HR was significantly associated with clinical outbreaks and with a large number of fish. Spatio-temporal analysis failed to identify clustering of cage cases, suggesting that within-farm ISAV spread is independent of the spatial location of the cages. Results presented here will help to better understand ISAV transmission, to improve the design of surveillance programs in Chile and other regions in which salmon are intensively farmed, and to examine the economic impact of ISAV and related management strategies on various cost and demand shifting factors.

Use of molecular epidemiology to trace transmission pathways for infectious salmon anaemia virus (ISAV) in Norwegian salmon farming.

BACKGROUND: Infectious Salmon Anaemia (ISA) is a disease affecting farmed Atlantic salmon, and most salmon producing countries have experienced ISA outbreaks. The aim of the present study was to use epidemiological and viral sequence information to trace transmission pathways for ISA virus (ISAV) in Norwegian salmon farming. METHODS: The study covers a period from January 2007 to July 2009 with a relatively high rate of ISA outbreaks, including a large cluster of outbreaks that emerged in Northern Norway (the North-cluster). Farms with ISA outbreaks and neighbouring salmon farms (At-risk-sites) were tested for the presence of ISAV, and epidemiological information was collected. ISAV hemagglutinin-esterase (HE) and fusion (F) protein genes were sequenced and phylogenetic analyses were performed. Associations between sequence similarities and salmon population data were analysed to substantiate possible transmission pathways. RESULTS: There was a high degree of genetic similarity between ISAV isolates within the North-cluster. ISAV was detected in 12 of 28 At-risk-sites, and a high proportion of the viruses were identified as putative low virulent genotypes harbouring the full length highly polymorphic region (HPR); HPR0 of the HE protein and the amino acid glutamine (Q) in the F protein at position 266. The sequences from HPR0/F (Q(266)) genotypes revealed larger genetic variation, lower viral loads and lower prevalence of infection than HPR-deleted genotypes. Seaway distance between salmon farms was the only robust explanatory variable to explain genetic similarity between ISAV isolates. DISCUSSION: 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.

Modelling the spread of infectious salmon anaemia among salmon farms based on seaway distances between farms and genetic relationships between infectious salmon anaemia virus isolates.

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 space-time 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.

Lack of evidence for vertical transmission of SAV 3 using gametes of Atlantic salmon, Salmo salar L., exposed by natural and experimental routes.

Pancreas disease (PD) is an important cause of losses in farmed salmonids in Norway, the United Kingdom and Ireland. As the spread of salmonid alphavirus (SAV), the causal agent, to naïve populations is of major concern to the farming industry, it is important to uncover the transmission routes of the virus. This study was conducted to investigate the potential for vertical transmission of SAV subtype 3. Progeny of broodstock with signs of late-stage PD and persistent RT-PCR signals for SAV were followed from fertilization to smoltification in an experimental facility. Fertilized ova were either not disinfected or taken through one of three different disinfection regimes. Also, ova and milt from uninfected broodfish from a different population were exposed to a cell-cultured strain of SAV 3 immediately before fertilization to simulate a viraemic phase in parent fish. A group of uninfected controls were also included in the study. Fertilized ova from bath exposed and negative control groups were double disinfected. Following fertilization, experimental fish went through a normal freshwater phase. However, fry were stressed at first feeding to enhance replication of possibly latent virus. Smoltification was induced by an artificial light regime, and experimental fish were followed to the late smoltification phase. Selected samples were investigated by real-time RT-PCR for SAV, by histology for evidence of PD and by serology for neutralising antibodies against SAV. All analysed samples of progeny were negative. This result shows that SAV 3 is not readily transmitted vertically from parents to offspring. Additional negative PCR results from salmon sampled in commercial hatcheries support these findings. Also, recent studies have shown that risk factors for the horizontal transmission route explain the vast majority of PD outbreaks in Norway. It is concluded that if it happens at all, vertical transmission is of minor importance in the spread of SAV 3.

Outbreak of viral haemorrhagic septicaemia (VHS) in seawater-farmed rainbow trout in Norway caused by VHS virus Genotype III.

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.

Risk factors associated with the presence of Campylobacter species in Norwegian broiler flocks.

A case-control study was conducted in 2005 to identify risk factors for the presence of Campylobacter spp. in Norwegian broiler flocks. A total of 131 broiler farms (44 cases and 87 controls) were included in the study, and 1 flock from each farm was included in the statistical analyses. Data on farm and flock level were collected by means of a questionnaire designed for the present study. The relationship and strength of association between the presence of Campylobacter spp. in the broiler flocks and several factors were investigated by unconditional logistic regression. The following factors were found to be associated with an increased risk of testing positive for Campylobacter spp.: water from a private water source, swine holdings closer than 2 km, a specific slaughterhouse, a hired animal caretaker, transport personnel passing through the hygiene barrier when delivering day-old chickens, less than 9 d between depopulation and restocking, and multiple broiler houses on the farm.

Epidemiological investigation of infectious salmon anaemia (ISA) outbreaks in Norway 2003-2005.

Epidemiological information was summarized from 32 outbreaks of infectious salmon anaemia (ISA) on salmon farming sites in Norway in 2003-2005. Virus isolates from the outbreak sites were genotyped, and the genotyping was used to assess possible associations between outbreak sites due to adjacent location, sharing fish farming authorisation, sharing smolt suppliers or sharing broodfish origin of the fish. The ISA outbreaks were distributed along most of the Norwegian coast and showed a variable clinical picture. The virus genotypes clustered into three genogroups. Pairs of outbreak sites matched for adjacent location or registered under the same authorisation, all shared genogroup, which was a significantly higher number of corresponding genogroups than expected by chance. For outbreak sites sharing smolt suppliers, corresponding genogroups appeared in 7 out of 12 matched pairs, which was not significant. An evaluation of broodfish origin associated with genogroups did not support transmission linked to broodfish origin. In conclusion, genotyping of virus isolates from ISA outbreaks supports associations between adjacent outbreaks. This is consistent with horizontal transmission. The present study failed to find evidence for vertical transmission (patterns of genogroups related to smolt suppliers or broodfish companies were not identified).