Fisheries catches worldwide have shown no increase over the last two decades, while aquaculture has been booming. To cover the demand for fish in the growing human population, continued high growth rates in aquaculture are needed. A potential constraint to such growth is infectious diseases, as disease transmission rates are expected to increase with increasing densities of farmed fish. Using an extensive dataset from all farms growing salmonids along the Norwegian coast, we document that densities of farmed salmonids surrounding individual farms have a strong effect on farm levels of parasitic sea lice and efforts to control sea lice infections. Furthermore, increased intervention efforts have been unsuccessful in controlling elevated infection levels in high salmonid density areas in 2009–2010. Our results emphasize host density effects of farmed salmonids on the population dynamics of sea lice and suggest that parasitic sea lice represent a potent negative feedback mechanism that may limit sustainable spatial densities of farmed salmonids.

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Gyrodactylus salaris Malmberg, 1957 is an important pathogen in Norwegian populations of Atlantic salmon Salmo salar. It can infect a wide range of salmonid host species, but on most the infections are probably ultimately lim~ted by a host response. Generally, on Norwegian salmon stocks, infections grow unchecked until the host dies. On a Baltic salmon stock, originally from the Neva River, a host reaction is mounted, limltlng parasite population growth on those fishes initially susceptible. Among rainbow trouts Oncorhynchus mykiss from the sam.e stock and among full sib anadromous arctic char Salvelinus alpjnus, both naturally resistant and susceptible individuals later mounting a host response can be observed. This is in contrast to an anadromous stock of brown trout Salmo trutta where only innately resistant individuals were found. A general feature of salmonid infections is the considerable variation of susceptibility between individual fish of the same stock, which appears genetic in origin. The parasite seems to be generally unable to reproduce on non-salmonids, and on cyprinids, individual behavioural mechanisms of the parasite may prevent infection. Transmission occurs directly through host contact, and by detached gyrodactylids and also from dead fishes. Relative importance of these routes and of different host species in the epidemiology of the disease is discussed with reference to laboratory experiments and existing knowledge concerning the host-parasite ecology.

The susceptibility and resistance of hatchery‐reared salmon parr, native to the rivers Neva (U.S.S.R. Baltic Sea), Alta (northern Norway) and Lone (western Norway) (both eastern Atlantic Ocean), to Gyrodactylus salaris from Norway, was examined. The level of resistance to the parasite was assessed from counts, made on anaesthetized salmon, ofthe numbers of G. salaris after an initial experimental exposure (2 weeks) to G. salaris‐infected salmon. Three experiments, all in water at c. 12° C, were carried out: (1) 50 Alta and 50 Neva salmon, initial mean parasite intensity c. 12; (2) 50 Lone and 50 Neva salmon, initial mean parasite intensity c. 60; (3) 10 Lone and 10 Neva salmon individually isolated, initial intensity one gravid G. salaris. In both the Norwegian salmon stocks, the G. salaris infrapopulations steadily increased during the experimental period of 5 weeks, in contrast to a prominent decline in the Neva salmon stock, after, respectively: (Exp. 1) week 3, average peak intensity 32.6; (Exp. 2) week 2, average peak intensity 58.7; and (Exp. 3) week 3, average peak intensity 6.3. The hatchery‐reared Baltic Neva stock demonstrated both an innate and an acquired resistance towards G. salaris, in contrast to the highly susceptible, Norwegian Alta and Lone salmon stocks.

such Norwegian studies on Salmo salar provided a dataset for the time period 1996 to 2011 on 25 118 release groups comprising 657 624 fish released and 3 989 recaptured. The overall risk ratio 26 (RR), calculated as the probability of being recaptured in the treated group divided by the 27 probability of being recaptured in the control group, was estimated to be 1.18 (95 % CI: 1.07-281.30). The effect varied strongly between groups, quantified by Higgins measure of heterogeneity 29 (I 2 = 40.1%). Over 70% of this heterogeneity could be explained by the release location, time 30 period and baseline survival. The most important predictor variable was baseline survival. In 31 groups with low recapture in the control group (low baseline survival), the effect of treatment 32 was high (RR = 1.7), while in groups with high recapture in the control group (high baseline 33 survival), there was no effect of treatment (RR ~ 1.00). The most prevalent parasite in the region 34 affected by the drugs administered was Lepeophtheirus salmonis. Hence, the meta-analysis 35 supports the hypothesis that anti-parasitic treatment protects S. salar smolts from L. salmonis 36 during outward migration. However, the effect of treatment was not consistent, but was evidently 37 strongly modulated by other risk factors. The results suggest that the population level effects of 38 parasites cannot be estimated independently of other factors affecting the marine survival of 39Salmo salar. 40

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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