Selective breeding provides an approach to increase resistance of rainbow trout (Onchorhynchus mykiss) to the diseases, enteric redmouth disease, rainbow trout fry syndrome, and viral haemorrhagic septicaemia

In this study, we reasoned that if we challenged rainbow trout with the causative agents of enteric redmouth disease (ERM), rainbow trout fry syndrome (RTFS), and viral haemorrhagic septicaemia (VHS), we would: 1) detect additive genetic variation for resistance to ERM, RTFS, and VHS; and 2) find that resistance of the trout to ERM and RTFS are favourably correlated genetically, while resistance to VHS is unfavourably correlated with resistance to ERM and RTFS. We tested these premises by challenging 63 full-sib families of rainbow trout (50 sires, 38 dams) with Yersinia ruckeri, Flavobacterium psychrophilum, and VHS virus, the causative agents of ERM, RTFS, and VHS. Resistance to each disease was assessed as both a binary trait (i.e., died/survived) and a longitudinal trait (i.e., time until death following challenge). Additive genetic variation and genetic correlations for resistance to ERM, RTFS, and VHS were estimated by fitting a threshold liability model to resistance assessed as a binary trait. As a longitudinal trait, additive genetic variation and genetic correlations were estimated by fitting a Weibull frailty model to the times until death. Our findings support the first of our premises as we detected additive genetic variation for resistance to ERM, RTFS, and VHS. The heritability for resistance to ERM, RTFS, and VHS ranged between 0.42 and 0.57 on the underlying liability scale when resistance was assessed as a binary trait. As a longitudinal trait, the heritabilities ranged between 0.07 and 0.21 for time until death on the logarithmic-time scale. We were, however, unable to support our second premise as we found that resistance to each of the diseases tended to be weakly correlated genetically. The genetic correlations between the resistances ranged between −0.11 and 0.15 when resistance was assessed as a binary trait, and between −0.23 and 0.16 when resistance was assessed as a longitudinal trait. These findings are encouraging for commercial trout production. The additive genetic variation detected for resistance demonstrates that selectively breeding trout for resistance to ERM, RTFS, and VHS will be successful, providing a complementary approach to control these diseases. The weak genetic correlations suggest that it should be relatively easy to improve resistance to each of the diseases simultaneously.