Abstract

The salmon louse is an ectoparasitic copepod of salmonids in the marine environment, and represents a global challenge to salmon aquaculture. A major issue is the reliance of the industry on a limited number of chemicals to delouse salmonids on farms, and the high levels of resistance that lice have developed to all of these agents. However, for most of these chemicals, resistance and dispersal mechanisms are unknown. We recently demonstrated that the Phe362Tyr mutation is the primary cause of organophosphate resistance in lice collected on Norwegian farms. In the present study, we genotyped >2000 lice collected throughout the entire North Atlantic in the period 1998–2016, using Phe362Tyr and nine tightly linked SNPs. Our results showed that the Phe362Tyr mutation is strongly linked to lice survival following chemical treatment on farms located throughout the North Atlantic, demonstrating for the first time, that this mutation represents the primary mechanism for organophosphate resistance in salmon lice across the North Atlantic. Additionally, we observed multiple and diverse high frequency haplotypes linked with the allele conveying resistance to organophosphate. We, therefore, conclude that Phe362Tyr is not a de novo mutation, but probably existed in salmon lice before the introduction of organophosphates in commercial aquaculture.

Highlights

  • Lepeophtherius salmonis, commonly known as the salmon louse, is an ectoparasitic copepod that infects salmonids in the marine environment

  • Samples collected from the farms that were not treated with azamethiphos displayed a higher frequency of the SS genotype (Supplementary File S1). These results demonstrate the role of Phe362Tyr mutation in the survival of the salmon louse under azamethiphos treatment, confirming the association of this mutation with OPs resistance areas across the North Atlantic

  • Haplotype 6 appears to be both the most distant haplotype on the tree as well as a very singular haplotype that appears only in one of our samples (Canada 2009). This is the first study to investigate the presence of the Phe362Tyr, a mutation linked with azamethiphos resistance in L. salmonis from Norway[30], in salmon lice sampled across the entire North Atlantic

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Summary

Introduction

Lepeophtherius salmonis, commonly known as the salmon louse, is an ectoparasitic copepod that infects salmonids in the marine environment. A wide range of integrated pest management strategies have been developed to control salmon lice infections on farmed salmon These include cleaner fish[10], thermolicer[11] and alternative production forms limiting www.nature.com/scientificreports/. The industry is investigating the potential of breeding for increased resistance in host-fish[13,14], and attempting to develop vaccines[15,16] Despite this suite of control strategies, the industry is reliant on a limited number of chemical therapeutants applied as bath or in-feed treatments to control infections[17]. After nearly a decade of non-use, an OP (azamethiphos) was once again re-introduced to delouse farmed salmonids in 200825, due to the development of lice resistance to the other chemicals that were used extensively during this period[21,22,23]. In 2013 and 2014, a national surveillance program, using bioassays to test for resistance, revealed a widespread distribution of azamethiphos resistance on Norwegian fish farms[26,27]

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