The salmon louse Lepeophtheirus salmonis has been a substantial obstacle in Norwegian farming of Atlantic salmon for decades. With a limited selection of available medicines and frequent delousing treatments, resistance has emerged among salmon lice. Surveillance of salmon louse sensitivity has been in place since 2013, and consumption of medicines has been recorded since the early 80’s. The peak year for salmon lice treatments was 2015, when 5.7 times as many tonnes of salmonids were treated compared to harvested. In recent years, non-medicinal methods of delousing farmed fish have been introduced to the industry. By utilizing data on the annual consumption of medicines, annual frequency of medicinal and non-medicinal treatments, the aim of the current study was to describe the causative factors behind salmon lice sensitivity in the years 2000–2019, measured through toxicity tests–bioassays. The sensitivity data from 2000–2012 demonstrate the early emergence of resistance in salmon lice along the Norwegian coast. Reduced sensitivity towards azamethiphos, deltamethrin and emamectin benzoate was evident from 2009, 2009 and 2007, respectively. The annual variation in medicine consumption and frequency of medicinal treatments correlated well with the evolution in salmon louse sensitivity. The patterns are similar, with a relatively small response delay from the decline in the consumption of medicines in Norway (2016 and onward) to the decline in measured resistance among salmon louse (2017 and onward). 2017 was the first year in which non-medicinal treatments outnumbered medicinal delousing treatments as well as the peak year in numbers of cleanerfish deployed. This study highlights the significance of avoiding heavy reliance on a few substance groups to combat ectoparasites, this can be a potent catalyst for resistance evolution. Further, it demonstrates the importance of transparency in the global industry, which enables the industry to learn from poor choices in the past.

Resistance towards antiparasitic agents in the salmon louse (Lepeophtheirus salmonis) is a widespread problem along the Norwegian coast, reducing treatments efficacies and slowing down the envisioned expansion of Norwegian salmon production. The present study was conducted in order to assess the efficacies of two of the most widely used anti-parasitic substances–azamethiphos and deltamethrin–as well as assessing the benefit of having a resistant genotype compared to being fully sensitive when exposed to one of these substances. Atlantic salmon were exposed to a mix of salmon lice copepodids from a fully sensitive, a double resistant and a multi-resistant strain. Once the lice reached pre-adult stages, one group was exposed to 100 μg/L azamethiphos for 60 minutes, the other to 2 μg/L deltamethrin for 30 minutes, and the last was kept in a seawater control. Detached lice were collected at a series of time points following exposure, and all lice (immobilized and surviving) were analysed for both pyrethroid (sensitive “S” and resistant “R”) and azamethiphos (fully sensitive “SS”, heterozygous resistant “RS” and fully resistant “RR”) resistance markers. We found that the efficacies of deltamethrin on parasites with genotype S and R were 70.3 and 13.2%, respectively. The overall efficacy of the deltamethrin treatment was 32.3%. The efficacies of azamethiphos on parasites with genotype SS, RS and RR were 100, 80 and 19.1%, respectively. The overall efficacy of the azamethiphos treatment was 80.4%. Survival analyses revealed that the median survival time in deltamethrin-sensitive and–resistant parasites were 16.8 and >172 hours, respectively. The differences were even more pronounced in the azamethiphos-treated group, where SS, RS and RR parasites survived for 0.26, 6.6 and >172 hours, respectively. The substantial differences in survival between sensitive and resistant lice following treatment demonstrate the ability of medicinal treatments to drive genetic selection towards a much more resistant salmon lice population within a very short time span if there is no influx of sensitive genotypes.