Journal : Aquaculture , vol. 535 , p. 1–10 , 2021
Publisher : Elsevier
International Standard Numbers
Printed : 0044-8486
Electronic : 1873-5622
Publication type : Academic article
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A transmission trial was carried out using 420 Atlantic salmon (Salmo salar L., parr stage) to simultaneously test the impact of vaccination and selective breeding on the transmission of Infectious salmon anemia virus (ISAV). Genetic difference in disease resistance was based on mortality differences across 15 families (defined by a genomic breeding value (GEBV)) and organised into three groups (low GEBV (LBV), mid GEBV (MBV) and high GEBV (HBV)). Three different shedder groups were infected with ISAV before being placed in tanks (T1 – T18) with naive contact fish (n = 15), one representative from each of the 15 families. The shedder groups included LBV vaccinated (LBVv), LBV not vaccinated (LBVnv) and HBV not vaccinated (HBVnv). The trial was run with two consecutive sets of nine tanks so the infectiousness of the shedder fish could be tested at different stages in their infection process (early (3–9 days post-infection (dpi) versus late (9–15 dpi)). Infection and mortality data of the contact fish were analysed using a Generalised Linear Mixed Model (GLMM) and a Bayesian epidemiological model. Neither vaccination nor genetic resistance prevented transmission, but both lowered the probability of infection in contact fish. Though not statistically significant, the effect of genetic resistance was larger (LBVNV vs HBVNV: odds ratio: 8.35 (0.75–93.36)) than vaccination (LBVNV vs LBVV: odds ratio: 4.52 (0.43–46.99)). There was no difference in the susceptibility of fish with different resistance breeding values, however, significant differences were found in their endurance to ISAV infection, with LBV fish dying 14 days earlier than HBV fish. Mortality as a resistance phenotype in breeding programmes appears to simultaneously improve survival of ISAV infected fish and reduce ISA transmission. However, it would be beneficial to evaluate mucus viral load (MVL) as an additional phenotype to more effectively reduce ISA transmission.