Abstract

The magnitude of the genetic variation in the susceptibility of Atlantic salmon to Lepeophtheirus salmonis was estimated through a controlled infestation test of 2206 individually tagged post-smolts of 154 full-sib families, i.e. the offspring of 78 sires and 154 dams. The infestation test took place in two replicated tanks with seawater. On average 74 and 36 copepodids per fish were added to tanks 1 and 2, respectively. The number of sessile lice (chalimus II–II stage) per fish (LC) was counted ten days after infestation at which the average body weight of the fish was 260 g in each of the two tanks. The average LC per fish was 27.1 (SD = 16.4) and 13.9 (SD = 13.2) in tanks 1 and 2, respectively while the lice density per fish, calculated as LD = LC/Body weight 2/3, was 0.66 (SD = 0.38) and 0.34 (SD = 0.29). Observed LC was found to increase with increasing body weight, while LD was seemingly independent of body weight. These relationships explain the lower heritability for LD (0.26 ± 0.05) than for LC (0.33 ± 0.05), and a genetic correlation between LC and LD (r g = 0.89 ± 0.03) different from unity. The magnitude of the heritability estimate for LD together with the large phenotypic variation of the trait, and a genetic correlation close to unity between LD in the two replicated tanks, shows that there is substantial additive genetic variation in resistance to L. salmonis in Atlantic salmon, and thus a great potential for increasing the resistance through selective breeding. The genetic correlation between LD and harvest body weight recorded on two subsamples of sibs of the lice infected fish reared at two farms was close to and not significantly different from zero (0.06 ± 0.12 and − 0.13 ± 0.11). Hence, the increasing lice problem in the salmon industry during the last years is most likely caused by other factors than the selection that has been practised for increased growth rate over the last 3–4 decades.

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