ABSTRACT
Ocean temperatures continue to rise annually due to the ever-growing consequences of global climate change. These temperature changes can have an impact on the immunological robustness of cultured fish, especially cold-water species such as Atlantic salmon. The salmon farming industry already loses hundreds of millions of dollars each year to infectious and non-infectious diseases. One particularly important and WOAH reportable disease is infectious salmon anemia caused by the orthomyxovirus ISAv. Considering the changing environment, it is necessary to find ways to mitigate the effect of diseases on the industry. For this study, 20 Atlantic salmon families were housed in each of 38 different tanks at the AVC, with half of the fish being kept at 10 °C and half being kept at 20 °C. Donor Atlantic salmon IP- injected with a highly virulent ISAv isolate (HPR4; TCID50 of 1 × 105/mL) were added to each tank as the source of co-habitation infection. Both temperatures were sampled at onset of mortality in co-habited fish and at resolution of mortality. Family background and temperature significantly impacted ISAv load, as assessed by qPCR, time to mortality and overall mortality. Mortality was more acute at 20 °C, but overall mortality was higher at 10 °C. Based on percent mortality calculated over the course of the study, different families demonstrated different levels of survival. The three families that demonstrated the highest percent mortality, and the three families with the lowest percent mortality were then assessed for their antiviral responses using relative gene expression. Genes significantly upregulated between the unexposed fish and ISAv exposed fish included mx1, il4/13a, il12rb2, and trim25, and these were further impacted by temperature. Understanding how ISAv resistance is impacted by temperature can help identify seasonal risks of ISAv outbreaks as well as ideal responses to be targeted through immunopotentiation.
ABSTRACT
Variance components were estimated for 2 body size traits of Atlantic cod at 2 time points. Wild-caught founders from 3 regions off eastern North America were spawned and their progeny were reared at 2 locations in 2 consecutive years. Full-sib families (n = 148) were kept separate until individuals achieved a size large enough to be tagged. At that time (220 d of age), BW and length of 47,637 offspring from 90 sires and 89 dams were recorded. The juveniles were then transferred to sea cages at 3 sites, where they grew further for more than a year. A second set of measurements was collected on 11,839 fish (634 d of age). Dispersion parameters were estimated using REML in bivariate analyses. Models included fixed degree-days (covariate), year × location subclasses, and genetic groups composed of connected families within region of origin. Random factors were animal (additive genetic effects), considering known relationships among the fish; dam (maternal effects); and family (effects common to full-sibs). At tagging, heritability estimates were small to moderate (0.15 and 0.24 for BW and length, respectively; SE = 0.14), similar to or somewhat larger than the proportions of variation ascribed to dams and families (11 to 16%). Later, heritability estimates were greater (0.27 ± 0.08 and 0.31 ± 0.09 for BW and length, respectively), whereas dam and family variance proportions were very small (3 to 4%). Omitting maternal or family components substantially increased the values obtained for heritability at both time points. At the later point, failure to account for maternal effects inflated heritability estimates by about 24% for both traits; ignoring family effects had double the impact. These effects persisted even though endogenous feeding lasts only a couple of weeks in this species and the fish had been pooled since tagging. Discarding data from parents that were completely confounded with their mates decreased heritability estimates slightly (by 0.04, for both traits) at the second point, with no loss of precision despite 15% fewer records and 34% fewer parents; the improved design seemed to have more fully disentangled the additive genetic effects. Estimates of genetic correlations between traits and between time points were very large (>0.89). The results imply that genetic variation exists for body size of cod at both stages. Poor data structure and inadequate models can potentially lead to overstatement of heritability, and thus also of the predicted selection response.
