Sea Lice

Sea lice are an ectoparasite found on wild and farmed salmon in British Columbia, and around the world. Lice can create open sores on their host, the salmon. Salmon contained in high densities amplify lice levels can carry introduced and native fish pathogens between the salmon.

Lice at natural levels are benign, but at amplified population levels and/or hosts encountering lice at unnatural life stages (ie salmon smolts without fully developed scales), they can induce increased vulnerability to other pathogens or mortality.

Principles of Salmon and Sea Lice Ecology

Salmon farms in British Columbia can be found along the southern coast of the mainland, on the central coast near Klemtu and along both coastlines of Vancouver Island, occupying the same coastal areas that wild Pacific salmon fry use to migrate out to the open ocean or return back to spawn. High-density farm tenures with large populations of farmed fish acquire naturally occurring ectoparasites, whose populations then grow substantially and are transferred through the water column to juvenile and adult wild fish as they migrate past (Morton et al. 2004). Pathogen amplification has been a well-documented phenomenon in finfish aquaculture worldwide (Ford and Myers 2008; Anderson and May 1978).

The main ectoparasites transferred from farmed to wild salmonids are commonly known as sea lice (Boxapen 2006). Research in Scotland, Norway and British Columbia indicate that incidence of sea lice infection on wild fish is more prevalent in areas that contain fish farms, which support and concentrate the lice populations (Krkošek et al. 2007).

Sea lice are a parasitic copepod (Johnson and Albright 1991). They are crustaceans that occur naturally in coastal and open ocean populations of fish, as well as in freshwater environments (Brooks and Jones 2008). There are over 300 species of lice, most of which are parasitic on fish. Various species of sea lice occur in the Atlantic and Pacific populations of farmed and wild salmonids (Intervet 2009).

Lice can be host-specific* to salmonids or not:

  • Western North Pacific – Caligus clemensi, Lepeophtheirus salmonis*
  • Eastern North Pacific (Japan and China) – Caligus rogercresseyi
  • Southern Pacific – Caligus rogercresseyi, Caligus teres
  • Eastern North Atlantic – Lepeophtheirus salmonis*
  • Western North Atlantic – Lepeophtheirus salmonis*, Caligus elongatus

Life Cycle

Sea lice have a free swimming and parasitic stage in their life cycle (Johnson and Albright 1991). As they grow throughout these stages, they continue to molt. These distinct stages make the amplification and transmission of sea lice relatively simple to monitor spatially and temporally in migratory wild smolts.

Napulius – free swimming: In the free swimming part of their life cycle, nauplii hatch out of eggs. They are free swimming in the water column. Nauplii have two growth stages – I & II. They have very noticeable appendages and patterning, and so it is possible to differentiate between species.

Copepidid – free swimming: As they mature, the lice associate themselves with a host, living on but not attached to the fish. This stage is known as the copepidid stage, where the lice are still free swimming. At this point, they are just visible to the naked eye. It is possible to differentiate between species at this point.

Chalimus – parasitic: Upon further maturation, the lice enter the parasitic stage of their life cycle known as the chalimus stage. Chalimus lice attach themselves with their mouths to the host, like a tether. There are I-IV parts of this stage, whereby the louse continues to grow and develop. It is very difficult to distinguish between species with the naked eye at this life stage.

Adult – parasitic: Lice develop from tethered chalimus into mobile pre-adult lice. At this stage, it is possible to distinguish between sex and species. Eventually, they molt into the adult, or motile, stage. Adults are free swimming and feed on the fish’s mucous with mouth appendages, often leaving scars. Females tend to remain on one host, while males are more prone to take risks and find new hosts. Once a male finds a host that also houses a female louse, it will guard the female from other males (Connors et al. 2008).

Gravid females extrude their eggs on egg strings. These strings contain an average of 250-500 eggs, where the nauplii larvae develop. Hatching time for the eggs varies with temperature and salinity, taking less time at higher temperatures and higher salinities (Bricknell et al. 2006).


The high host density of salmon farms is a classic example of pathogen amplification (Anderson and May 1978). Farms, containing hundreds of thousands of fish each with 1 or 2 female lice, can create high-density areas of lice larvae in the water column (Morton et al. 2004). This high density of larval lice disrupts the temporal refugia migrating wild salmon smolts normally experience in the spring in nearshore environments, and it is this age class that is particularly vulnerable (Krksoek 2009; Krkošek et al. 2006).

The survival and success of lice populations are generally correlated to salinity and temperature, although previous research is not conclusive on how the range of salinities which could impact how lice infect juvenile chum and pink salmon (Brooks 2005; Jones et al. 2007). Salinities in the nearshore Broughton environments range are normally 20-30ppt in the springtime, but fluctuate with glacial melt and precipitation (Conners et al. 2008). Rapid louse mortality occurs in freshwater, but lice can tolerate salinities from 7-21 ppt for short terms (Conners et al. 2008). Lice infection models should take salinity fluctuations into account, and therefore our understanding of both the accurate range of salinity and the response of sea lice must be better understood.

Increased temperatures also support greater lice populations (Brooks 2005). This supports Morton and Krkošek’s belief in the temporal refugia of nearshore waters in winter and early spring months. Temperature also influences sea louse abundance, but not even the combination of salinity and temperature can solely account for lice infection levels – host density is equally if not more important (Morton et al. 2005). Generalizations about louse populations and temperature, or any other environmental factor for that matter, are difficult to make because each population and its environment presents a unique combination of factors (Costello 2006).

Implications for Migratory Wild Smolts

Field and lab experiments in recent years have conflicted in just how much of the pink and chum juveniles’ mortality can be attributed to sea lice from the salmon farms (Krkošek et al. 2006; Beamish et al. 2006). However, it is clear that pink and chum salmon fry did not evolve to encounter sea lice parasitism at the beginning of their juvenile migration at the amplified levels induced by year-long populations of hosts of farmed salmon along their nearshore migration routes (Morton et al. 2005).

Research over the past five years by Krkošek et al. indicates that the amplification of L. salmonis populations by salmon farms is enough to significantly disrupt the natural relationship between sea lice and Pacific salmon (Krkošek 2009). This disruption eventually leads to decline in some wild salmon populations (Krkošek 2009). One of the most explosive papers on sea lice came out in a 2007 issue of Science by Krkošek et al. (2007), claiming that exposure to lice was correlated to a 99% reduction in the population of specific runs of pink salmon in B.C., while not in others. By examining historic DFO escapement records, Krkošek et al. were able to monitor pink salmon population fluctuations in 64 rivers along the central coast and seven rivers in the Broughton Archipelago that were exposed to fish farms along their juvenile migration routes. The degree to which lice infections caused mortality in juvenile pink salmon was estimated to be between 16-97%. If infection levels remained consistent, Krkošek et al. (2007) predicted a collapse within exposed populations in four generations if infection rates remained at 2003 levels.

Secondary infection and mortality is not the only impact of sea lice on salmonids. Sublethal effects of L. salmonis have been demonstrated in Atlantic salmon smolts, where S. salar infected with lice grew less than those protected from lice via pesticide treatments on the farms (Skilbrei and Wennevik 2006). In experimental conditions, Krkošek et al. (2006) found that those juveniles infected with lice were more vulnerable to predation, as their ability to swim was compromised.

De-lousing the Marine Environment

Fallowing farms, or treating cultured fish with pesticides, greatly reduces host density for sea lice in nearshore environments.

It has been shown that those years which had a combination of fallowing and drug treatments reduced the numbers of lice both on fish farms and in wild populations (Morton et al. 2005; Krkošek et al. 2007; Brooks 2005). For example, louse infection levels were lower in 2003 than in previous years in Broughton juveniles. Farms were fallowed in 2003, which could be a major contributing factor as it reduced the host presence for the sea lice (Morton et al. 2005).

Pathogen amplification on salmon farms has proven to be problematic from its inception due its’ high host density (CAFSAC 1986; Anderson and May 1978). Controlling sea lice populations on farms is very important,  because in addition to the subsequent impact to wild fish, lice can damage the salmon product, transmit and amplify other pathogens or, if highly concentrated, induce mortality (Marine Harvest 2010). Drug usage can be coordinated to control lice populations to mimic the migratory allopatry that wild salmonids once had to ectoparasites in the nearshore environment. A number of pesticides have been employed to control lice populations in farms. The current drug being used in Canada is emamectin benzoate, which is commercially known as SLICE™ (Lees et al. 2008; Ministry of Agriculture and Lands 2009).

SLICE™ has been proven to be very effective in the marine environment in both Atlantic and Pacific water with strains of L. salmonis, if applied correctly (Lees et al. 2008). Use of SLICE™ has been shown to greatly reduce sea lice populations, although it is unlikely it is the only factor affecting those population levels (Jones 2007). Survival and growth of Atlantic smolts protected with SLICE™ have been shown to have higher survivorship and growth than those not protected, demonstrating not only the effectiveness of the drug but also that sea lice have sublethal effects on the growth of S. salar smolts (Skilbrei and Wennevik 2006). SLICE™ is currently part of the management plan to protect the migration route of juvenile salmon in the Broughton. It is used to manage sea lice on farms throughout British Columbia.

Like any drug, improper or long-term use of SLICE™ does incur resistance in lice populations (Lees et al. 2008). This has occurred in Europe and has now emerged in Eastern Canada and on farms on the west coast of Vancouver Island (pers. comm. Morton 2010). Strategic rotation of drug therapeutants and fallowing for sea lice should be required to maintain efficacy of drugs and control of lice populations (Lees et al. 2008). Currently, SLICE™ is the only pesticide approved for use in salmon farming in British Columbia.


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