Lepeophtheirus salmonis and various Caligus species are adapted to salt water and are major ectoparasites of farmed and wild Atlantic salmon.

[10][11][12][13] L. salmonis copepodids migrating upwards towards light and salmon smolt moving downwards at daybreak have been hypothesized to facilitate finding a host.

[14] Several field and modeling studies on L. salmonis have examined copepodid populations and have shown that planktonic stages can be transported tens of kilometres from their source,[12][15] including how their behaviour results in their being moved towards the coastline and mouth of estuaries.

Pacific salmon return to the marine nearshore starting in June, and finish as late as December, dependent upon species and run timing, whereas the smolts typically outmigrate starting in April, and ending in late August, dependent upon species and run timing.

Sea lice possibly survive on fish that remain in the estuaries or they transfer to an as yet unknown alternate host to spend the winter.

[18] The adult females are always significantly larger than males and develop a very large genital complex, which in many species makes up the majority of the body mass.

Adult females, being larger, occupy relatively flat body surfaces on the posterior ventral and dorsal midlines and may actually outcompete preadults and males at these sites.

Copepods and chalimus stages have a developed gastrointestinal tract and feed on host mucus and tissues within range of their attachment.

Pre-adult and adult sea lice, especially pregnant females, are aggressive feeders, in some cases feeding on blood in addition to tissue and mucus.

[8][25] Whether sea lice are vectors of disease is unknown, but they can be carriers of bacteria and viruses likely obtained from their attachment to and feeding on tissues of contaminated fish.

[26] Sea lice cause physical and enzymatic damage at their sites of attachment and feeding, which results in abrasion-like lesions that vary in their nature and severity depending upon a number of factors, including host species, age, and general health of the fish.

Little evidence exists of host tissue responses in Atlantic salmon at the sites of feeding and attachment, regardless of the development stage.

In contrast, coho and pink salmon show strong tissue responses to L. salmonis characterized by epithelial hyperplasia and inflammation.

[29] Sea lice, particularly L. salmonis and various Caligus species, including C. clemensi and C. rogercresseyi, can cause deadly infestations of both farm-grown and wild salmon.

[3][30] Sea lice migrate and latch onto the skin of wild salmon during free-swimming, planktonic nauplii and copepodid larval stages, which can persist for several days.

[29] A few studies indicated no long-term damage to fish stocks in some locations,[37] and a population decline in wild salmon that occurred in 2002 was caused by "something other than sea lice".

[38] However, the repeated epizootics of lice on wild fish have only occurred in areas with salmon farms in Ireland, Britain (Scotland), Norway, Canada (British Columbia), and Chile.

[12] Integrated pest management programs for sea lice are instituted or recommended in a number of countries, including Canada,[43][44] Norway,[40] Scotland,[45] and Ireland.

Good husbandry techniques include fallowing, removal of dead and sick fish, prevention of net fouling, etc.

[52] In October 2012, the grocery chain Sobeys pulled whole Atlantic salmon from 84 store locations in the Canadian Maritimes after concerns were raised over sea lice.

Recent use of well-boats containing the drugs has reduced both the concentration and environmental concerns, although transferring fish to the well boat and back to the cage can be stressful.

Organophosphates are acetylcholinesterase inhibitors and cause excitatory paralysis leading to death of sea lice when given as a bath treatment.

Pyrethroids are direct stimulators of sodium channels in neuronal cells, inducing rapid depolarization and spastic paralysis leading to death.

Avermectins belong to the family of macrocyclic lactones and are the major drugs used as in-feed treatments to kill sea lice.

Ivermectin was toxic to some fish, causing sedation and central nervous system depression due to the drug's ability to cross the blood–brain barrier.

Avermectins act by opening glutamate-gated chloride channels in arthropod neuromuscular tissues, causing hyperpolarization and flaccid paralysis leading to death.

It has been used only sparingly in sea lice control, largely due to concerns that it may affect the moult cycle of non-target crustaceans, although this has not been shown at the concentrations recommended.

Two published studies have tested vaccine candidate antigens against salmon lice, which resulted in a reduced infection rate.