Sea lice (singular: sea louse) are copepods (small crustaceans) of the family Caligidae within the order Siphonostomatoida. They are marine ectoparasites (external parasites) that feed on the mucus, epidermal tissue, and blood of host fish. The roughly 559 species in 37 genera include around 162 Lepeophtheirus and 268 Caligus species.
The genera Lepeophtheirus and Caligus parasitize marine fish, in particular those species that have been recorded on farmed salmon. Lepeophtheirus salmonis and various Caligus species are adapted to salt water and are major ectoparasites of farmed and wild Atlantic salmon. Several antiparasitic drugs have been developed for control purposes. L. salmonis is the best understood in the areas of its biology and interactions with its salmon host.
Caligus rogercresseyi has become a major parasite of concern on salmon farms in Chile.[3] Studies are under way to gain a better understanding of the parasite and the host-parasite interactions. Recent evidence is also emerging that L. salmonis in the Atlantic has sufficient genetic differences from L. salmonis from the Pacific to suggest that Atlantic and Pacific L. salmonis may have independently co-evolved with Atlantic and Pacific salmonids respectively.[4]
The family Caligidae is estimated to contain around 559 species in 37 genera.[1] The largest of these are Caligus, with around 268 species,[5] and Lepeophtheirus with around 162 species.[6]
Most understanding of the biology of sea lice, other than the early morphological studies, is based on laboratory studies designed to understand issues associated with sea lice infecting fish on salmon farms. Information on sea lice biology and interactions with wild fish is sparse in most areas with a long-term history of open net-cage development, since understanding background levels of sea lice and transfer mechanisms has rarely been a condition of tenure license for farm operators.
Many sea louse species are specific with regard to host genera, for example L. salmonis, which has high specificity for anadromous fish including sticklebacks and salmonids including the widely farmed Atlantic salmon (Salmo salar). Lepeophtheirus salmonis can parasitize other salmonids to varying degrees, including brown trout (sea trout: Salmo trutta), Arctic char (Salvelinus alpinus), and all species of Pacific salmon. In the case of Pacific salmon, coho, chum, and pink salmon (Oncorhynchus kisutch, O. keta, and O. gorbuscha, respectively) mount strong tissue responses to attaching L. salmonis, which lead to rejection within the first week of infection.[7] Pacific L. salmonis can also develop, but not complete, its full lifecycle on the three-spined stickleback (Gasterosteus aculeatus).[8] This has not been observed with Atlantic L. salmonis.
How planktonic stages of sea lice disperse and find new hosts is still not completely known. Temperature, light, and currents are major factors and survival depends on salinity above 25 ‰.[9][10][11][12] L. salmonis copepodids migrating upwards towards light and salmon smolt moving downwards at daybreak have been hypothesized to facilitate finding a host.[13] 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,[11][14] including how their behaviour results in their being moved towards the coastline and mouth of estuaries[15]
The source of L. salmonis infections when salmon return from fresh water has always been a mystery. Sea lice die and fall off anadromous fish such as salmonids when they return to fresh water. Atlantic salmon return and travel upstream in the fall to reproduce, while the smolts do not return to salt water until the next spring. 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. Smolt get infected with sea lice larvae, or even possibly adults, when they enter the estuaries in the spring. How sea lice distribute between fish in the wild also is not known. Adult stages of Lepeophtheirus spp. can transfer under laboratory conditions, but the frequency is low. Caligus spp. transfer quite readily and between different species of fish, and are regularly found in the plankton.[11]
L. salmonis tends to be about twice the size of most Caligus spp. (e.g. C. elongatus, C. clemensi, etc.). The body consists of four regions: cephalothorax, fourth (leg-bearing) segment, genital complex, and abdomen.[16] The cephalothorax forms a broad shield that includes all of the body segments up to the third leg-bearing segment. It acts like a suction cup in holding the louse on the fish. All species have mouth parts shaped as a siphon or oral cone (characteristic of the Siphonostomatoida). The second antennae and oral appendages are modified to assist in holding the parasite on the fish. The second pair of antennae is also used by males to grasp the female during copulation.[17] 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. Two egg strings of 500 to 1000 eggs (L. salmonis), which darken with maturation, are roughly the same length as the female's body. One female can produce 6-11 pairs of egg strings in a lifetime around 7 months.[11][13][18]
Sea lice have both free-swimming (planktonic) and parasitic life stages, all separated by moults.[16][17][19][20] The development rate for L. salmonis from egg to adult varies from 17 to 72 days depending on temperature. The lifecycle of L. salmonis is shown in the figure; the sketches of the stages are from Schram.[19]
Eggs hatch into nauplii I, which moult to a second naupliar stage; both naupliar stages are nonfeeding, depending on yolk reserves for energy, and adapted for swimming. The copepodid stage is the infectious stage and it searches for an appropriate host, likely by chemo- and mechanosensory clues. Currents, salinity, light, and other factors also assist copepodids in finding a host.[11] Preferred settlement on the fish occurs in areas with the least hydrodynamic disturbance, particularly the fins and other protected areas.[10][21] Copepodids once attached to a suitable host feed for a period of time prior to moulting to the chalimus I stage. Sea lice continue their development through three additional chalimus stages each separated by a moult. A characteristic feature of all four chalimus stages is that they are physically attached to the host by a structure referred to as the frontal filament. Differences in the timing, method of production, and the physical structure of the frontal filament are seen between different species of sea lice. With exception of a short period during the moult, the preadult and adult stages are mobile on the fish, and in some cases, can move between host fish. 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.[22]
The naupliar and copepodid stages until they locate a host are nonfeeding and live on endogenous food stores. Once attached to the host, the copepodid stage begins feeding and begins to develop into the first chalimus stage. Copepods and chalimus stages have a developed gastrointestinal tract and feed on host mucus and tissues within range of their attachment. Preadult and adult sea lice, especially gravid females, are aggressive feeders, in some cases feeding on blood in addition to tissue and mucus. Blood is often seen in the digestive tract, especially of adult females. L. salmonis is known to secrete large amounts of trypsin into its host's mucus, which may assist in feeding and digestion.[7][23] Other compounds such as, prostaglandin E2, have also been identified in L. salmonis secretions and may assist in feeding and/or serve the parasite in avoiding the immune response of the host by regulating it at the feeding site.[7][24] 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.[25]
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. Whether stressed fish are particularly prone to infestation is unclear. Sea-lice infection causes a generalized chronic stress response in fish since feeding and attachment cause changes in the mucus consistency and damage the epithelium resulting in loss of blood and fluids, electrolyte changes, and cortisol release. This can decrease salmon immune responses and make them susceptible to other diseases and reduce growth and performance.[26][27]
The degree of damage is also dependent on the species of sea lice, the developmental stages that are present, and the number of sea lice on a 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. This results in rejection of the parasite within the first week of infection in these species of salmonids.[7] Heavy infections of farmed Atlantic salmon and wild sockeye salmon (Oncorhynchus nerka) by L. salmonis can lead to deep lesions, particularly on the head region, even exposing the skull.
Some evidence indicates that sea lice flourishing on salmon farms can spread to nearby wild juvenile salmon and devastate these populations.[28] 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][29] 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.[30][31][32] Large numbers of highly populated, open-net salmon farms can create exceptionally large concentrations of sea lice. When exposed in river estuaries containing large numbers of open-net farms, mathematical models have suggested that many young wild salmon may be infected [33][34] Adult salmon may survive otherwise critical numbers of sea lice, but small, thin-skinned juvenile salmon migrating to sea are highly vulnerable. Sea trout populations in recent years may have seriously declined due to infestation by sea lice,[35] and Krkosek et al. have claimed that on the Pacific coast of Canada the louse-induced mortality of pink salmon in some regions is over 80%.[28] A few studies indicated no long-term damage to fish stocks in some locations,[36] and a population decline in wild salmon that occurred in 2002 was caused by "something other than sea lice".[37] 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.[38] Field sampling of copepodids, and hydrographic and population models, show how L. salmonis from farms can cause mass infestations of seaward-migrating salmonids, and this effect can occur up to 30 km (19 mi) from the farms.[15]
Several scientific studies have suggested that caged, farmed salmon harbour lice to a degree that can destroy surrounding wild salmon populations.[34] Other studies have shown that lice from farmed fish have relatively no effect on wild fish if good husbandry and adequate control measures are carried out (see section: Control on salmon farms).[39] Further studies to establish wild-farmed fish interactions are ongoing, particularly in Canada, Britain (Scotland), Ireland, and Norway. A reference manual with protocol and guidelines for studying wild/cultured fish interactions with sea lice has been published.[40]
This has been reviewed by Pike & Wadsworth,[20] McVicar,[41] and Costello.[11] Integrated pest management programs for sea lice are instituted or recommended in a number of countries, including Canada,[42][43] Norway,[39] Scotland,[44] and Ireland.[45] Identification of epidemiological factors as potential risk factors for sea lice abundance[46] with effective sea lice monitoring programs have been shown to effectively reduce sea lice levels on salmon farms.[47]
Cleaner fish, including five species of wrasse (Labridae), are used on fish farms in Norway and to a lesser extent in Scotland, Shetland and Ireland.[48] Their potential has not been researched in other fish farming regions, such as Pacific and Atlantic Canada or Chile.
Good husbandry techniques include fallowing, removal of dead and sick fish, prevention of net fouling, etc. Bay management plans are in place in most fish farming regions to keep sea lice below a level that could lead to health concerns on the farm or affect wild fish in surrounding waters. These include separation of year classes, counting and recording of sea lice on a prescribed basis, use of parasiticides when sea lice counts increase, and monitoring for resistance to parasiticides.
Early findings suggested genetic variation in the susceptibility of Atlantic salmon to Caligus elongatus.[49] Research then began to identify trait markers,[50] and recent studies have shown that susceptibility of Atlantic salmon to L. salmonis can be identified to specific families and that there is a link between MHC Class II and susceptibility to lice.[51]
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. [52]
In 2017, salmon prices in Norway increased by 15% over a 3-month period because of a sea lice outbreak. [53]
Freshwater is sometimes adequate to kill the sea lice and as salmon eventually swim in fresh water, they are not harmed.[54]
The range of therapeutants for farmed fish was limited, often due to regulatory processing limitations. All drugs used have been assessed for environmental impact and risks.[55][56] The parasiticides are classified into bath and in-feed treatments as follows:
There are both advantages and disadvantages to using bath treatments. Bath treatments are more difficult and need more manpower to administer, requiring skirts or tarpaulins to be placed around the cages to contain the drug. Prevention of reinfection is a challenge since it is practically impossible to treat an entire bay in a short time period. Since the volume of water is imprecise, the required concentration is not guaranteed. Crowding of fish to reduce the volume of drug can also stress the fish. 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. The major advantage to bath treatments is that all the fish will be treated equally, in contrast to in-feed treatments where amount of drug ingested can vary due to a number of reasons.
Organophosphates are acetylcholinesterase inhibitors and cause excitatory paralysis leading to death of sea lice when given as a bath treatment. Dichlorvos was used for many years in Europe and later replaced by azamethiphos, the active ingredient in Salmosan, which is safer for operators to handle.[57] Azamethiphos is water-soluble and broken down relatively quickly in the environment. Resistance to organophosphates began to develop in Norway in the mid 1990s, apparently due to acetylcholinesterases being altered due to mutation.[58] Use has declined considerably with the introduction of SLICE, emamectin benzoate.
Pyrethroids are direct stimulators of sodium channels in neuronal cells, inducing rapid depolarization and spastic paralysis leading to death. The effect is specific to the parasite since the drugs used are only slowly absorbed by the host and rapidly metabolized once absorbed. Cypermethrin (Excis, Betamax) and deltamethrin (Alphamax) are the two pyrethroids commonly used to control sea lice. Resistance to pyrethroids has been reported in Norway and appears to be due to a mutation leading to a structural change in the sodium channel which prevents pyrethroids from activating the channel.[59] Use of deltamethrin has been increasing as an alternate treatment with the rise in resistance observed with emamectin benzoate.
Bathing fish with hydrogen peroxide (350–500 mg/L for 20 min) will remove mobile sea lice from fish. It is environmentally friendly since H2O2 dissociates to water and oxygen, but can be toxic to fish, depending on water temperature, as well as to operators.[60] It appears to knock the sea lice off the fish, leaving them capable of reattaching to other fish and reinitiating an infection.
In-feed treatments are easier to administer and pose less environmental risk than bath treatments. Feed is usually coated with the drug and drug distribution to the parasite is dependent on the pharmacokinetics of the drug getting in sufficient quantity to the parasite. The drugs have high selective toxicity for the parasite, are quite lipid-soluble so that there is sufficient drug to act for approximately 2 months, and any unmetabolized drug is excreted so slowly that there are little to no environmental concerns.
Avermectins belong to the family of macrocyclic lactones and are the major drugs used as in-feed treatments to kill sea lice. The first avermectin used was ivermectin at doses close to the therapeutic level and was not submitted for legal approval for use on fish by its manufacturer. 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. Emamectin benzoate, which is the active agent in the formulation SLICE,[61] has been used since 1999 and has a greater safety margin on fish. It is administered at 50 µg/kg/day for 7 days and is effective for two months, killing both chalimus and mobile stages. Withdrawal times vary with jurisdiction from 68 days in Canada[62] to 175 degree days in Norway. Avermectins act by opening glutamate-gated chloride channels in arthropod neuromuscular tissues, causing hyperpolarization and flaccid paralysis leading to death. Resistance has been noted in Chalimus rogercresseyi in Chile and L. salmonis on North Atlantic fish farms. The resistance is likely due to prolonged use of the drug leading to up-regulation of P-glycoprotein,[63] similar to what has been seen in nematode resistance to macrocyclic lactones.[64]
Teflubenzuron, the active agent in the formulation Calicide,[65] is a chitin synthesis inhibitor and prevents moulting. It thus prevents further development of larval stages of sea lice, but has no effect on adults. 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.[55]
A number of studies are underway to examine various antigens, particularly from the gastrointestinal tract and reproductive endocrine pathways, as vaccine targets, but no vaccine against sea lice has been reported to date. Two published studies have tested vaccine candidate antigens against salmon lice, which resulted in a reduced infection rate.[66][67]
A more recent advance in the delousing strategy is to use pulsed lasers operating at the wavelength of 550 nm to delouse.[68]
Branchiurans, family Argulidae, order Arguloida are known as fish lice and parasitize fish in freshwater.
Sea lice (singular: sea louse) are copepods (small crustaceans) of the family Caligidae within the order Siphonostomatoida. They are marine ectoparasites (external parasites) that feed on the mucus, epidermal tissue, and blood of host fish. The roughly 559 species in 37 genera include around 162 Lepeophtheirus and 268 Caligus species.
The genera Lepeophtheirus and Caligus parasitize marine fish, in particular those species that have been recorded on farmed salmon. Lepeophtheirus salmonis and various Caligus species are adapted to salt water and are major ectoparasites of farmed and wild Atlantic salmon. Several antiparasitic drugs have been developed for control purposes. L. salmonis is the best understood in the areas of its biology and interactions with its salmon host.
Caligus rogercresseyi has become a major parasite of concern on salmon farms in Chile. Studies are under way to gain a better understanding of the parasite and the host-parasite interactions. Recent evidence is also emerging that L. salmonis in the Atlantic has sufficient genetic differences from L. salmonis from the Pacific to suggest that Atlantic and Pacific L. salmonis may have independently co-evolved with Atlantic and Pacific salmonids respectively.
Les Caligidae sont une famille de crustacés copépodes de l'ordre des Siphonostomatoida.
Les Caligidae sont une famille de crustacés copépodes de l'ordre des Siphonostomatoida.
Kutu laut adalah sekelompok spesies hewan copepoda dari ordo Siphonostomatoida, yaitu famili Caligidae. Terdapat sekitar 559 spesies di 37 genera, termasuk 162 spesies Lepeophtheirus dan 268 spesies Caligus. Kutu laut merupakan ektoparasit yang memakan lendir, jaringan epidermis, dan darah dari ikan laut inangnya.
Salah satu spesiesnya yaitu Caligus rogercresseyi menjadi parasit utama di pembudidayaan salmon di Cile,[3]. Penelitian telah dilaksanakan untuk memperoleh pemahaman lebih lanjut dari interaksi antara parasit ini dengan inangnya. Bukti-bukti terkini menunjukkan bahwa L. salmonis di Samudra Atlantik memiliki beberapa perbedaan genetik dibandingkan dengan L. salmonis dari Samudra Pasifik, menunjukkan bahwa L. salmonis Atlantik dan Pasifik kemungkinan secara independen berevolusi bersama salmon di Atlantik dan Pasifik.[4]
Famili Caligidae diperkirakan beranggotakan 559 spesies pada 37 genera.[1] Genus yang terbesarnya ialah Caligus, dengan anggota sekitar 268 spesies,[5] dan Lepeophtheirus yang beranggotakan sekitar 162 spesies.[6]
Kebanyakan spesies kutu laut dispesifikasi berdasarkan makhluk inangnya. Contohnya adalah L. salmonis yang menunjukkan kecenderungan tinggi untuk salmonid, termasuk spesies salmonid yang banyak dibudidayakan yaitu salmon Atlantik (Salmo salar). Lepeophtheirus salmonis dapat menjadi parasit dari beberapa spesies salmonid pada tingkat yang bervariasi, termasuk spesies trout coklat (trout laut: Salmo trutta), char Arktik (Salvelinus alpinus), dan seluruh spesies salmon Pasifik. Untuk Salmon Pasifik, coho, chum, dan salmon merah jambu (O. kisutch, O. keta, dan O. gorbuscha) memiliki jaringan yang kuat melindunginya dari L. salmonis sehingga dapat terjadi penolakan dari tubuh ikan pada minggu pertama infeksi.[7] L. salmonis Pasifik juga dapat berkembang pada daur hidup penuhnya walaupun tidak sempurna pada Gasterosteus aculeatus sebagai inangnya.[8] Hal ini belum diteliti untuk L. salmonis Atlantik.
Bagaimana tahapan hidup dari kutu laut menyebar dan menemukan inang baru masih belum sepenuhnya diketahui. Suhu, intensitas penyinaran Matahari, dan arus laut merupakan faktor utama yang mempengaruhi. Salinitas yang dibutuhkan kutu laut agar dapat bertahan hidup adalah di atas 25 ‰.[9][10][11][12] Terdapat sebuah hipotesis bahwa L. salmonis copepoda bermigrasi ke laut bagian dekat permukaan menuju cahaya dan ikan salmon yang bergerak ke arah laut dalam saat dini hari memfasilitasinya untuk mencari inang.[13] Beberapa penelitian dan pemodelan lapangan terhadap L. salmonis meneliti populasi copepodid dan berhasil diketahui bahwa tahapan hidup planktionnya dapat berpindah puluhan kilometer dari sumbernya.[11][14], termasuk bagaimana tingkah laku mereka ketika berpindah ke dekat pantai atau muara sungai.[15]
Sumber dari infeksi L. salmonis ketika ikan salmon kembali dari perairan tawar menuju laut masih belum diketahui. Kutu laut mati dan lepas dari inang salmonidnya ketika mereka kembali ke perairan tawar. Salmon Atlantik kembali dan pergi melawan aliran sungai pada musim gugur untuk berkembang biak dan tidak kembali ke perairan garam hingga musim semi berikutnya. Salmon Pasifik kembali ke laut di dekat daratan mulai bulan Juni dan selesai paling lambat bulan Desember, tergantung pada spesiesnya dan waktu perjalanannya; sementara salmon mudanya umumnya akan pergi mulai bulan April dan berkahir pada penghujung Agustus, tergantung spesies dan waktu perjalanannya.
Kemungkinan yang dapat terjadi adalah bahwa kutu laut bertahan di ikan yang tetap berada di lingkungan muara sungai atau mereka berpindah ke inang lain yang belum diketahu selama musim dingin. Bagaimanapun, salmon muda bahkan dewasa akan terinfeksi degngan larva kutu laut ketika mereka memsuki perairan muara pada musim semi. Tidak diketahui pula bagaimana kutu laut menyebar di antara ikan-ikan di alam liar. Tahap dewasa dari Lepeophtheirus spp. dapat menyebar dalam kondisi laboratorium namun frekuensinya rendah. Caligus spp. menyebar relatif lebih cepat dan pada beberapa spesies ikan yang berbeda, dan biasanya ditemukan dalam bentuk.[11]
Lepeophtheirus salmonis cenderung berukuran 2 kali lebih besar daripada Caligus spp. pada umumnya (seperti C. elongatus, C. clemensi). Tubuhnya terdiri dari 4 bagian: cefalotoraks, ruas penyangga kaki, abdomen, dan area kemaluan.[16] Cefalotoraksnya membentuk sebuah pelindung yang lebar yang merangkul seluruh bagian tubuhnya hingga sepertiga ruas penyangga kakinya. Cafalotoraksnya bertindak seperti sebuah mangkuk penyedot untuk bertahan di tubuh ikan. Seluruh spesies kutu laut memiliki bagian mulut yang berbentuk seperti sifon atau kerucut (ciri-ciri dari Siphonostomatoida). Antena sekunder dan anggota mulut termodifikasi untuk membantunya bertahan di tubuh ikan. Sepasang antena sekundernya juga digunakan oleh pejantan untuk merangkul betina ketika pembuahan.[17] Betina dewasanya selalu lebih besar daripada pejantannya dan menumbuhkan area kemaluan yang besar yang berpengaruh ke pada massa tubuh keseluruhannya di mayoritas spesies kutu laut. 2 rantaian telur yang terdiri atas 500 hingga 1000 telur (L. salmonis), yang akan menjadi semakin gelap seiring perkembangannya, kira-kira memiliki panjang yang sama dengan tubuh kutu laut betina. Seekor betinanya dapat memproduksi 6 hingga 11 pasang rantaian telur selama usia hidup 7 bulan.[11][13][18]
Pada fase naupliar dan copepodid hingga kutu laut hinggap di inangnya, kutu laut tidak menerima makanan dari luar dan hidup dari simpanan nutrisi dari dalam. Setelah hinggap di inangnya, pada fase copepodid pencarian makanan dimulai dan kutu laut mulai berkembang ke fase chalimus. Fase copepodid dan chalimus mengembangkan sistem pencernaan dan mengonsumsi lendir dan jaringan inangnya ayng ada dalam jangkauannya. Kutu laut muda dan dewasa, terutama betina yang hamil, pada beberapa kasus juga memakan darah. Darah seringkali terlihat pada saluran pencernaannya, terutama di betina dewasa. Lepeophtheirus salmonis dikenal mensekresikan tripsin ke lendir inangnya yang dapat membantunya untuk mencernanya.[7][19] Senyawa lain seperti prostaglandin E2 telah ditemukan dari sekresi L. salmonis dan kemungkinan membantunya untuk untuk memangsa dan/atau membantu kutu laut untuk melindunginya dari respon imunitas inangnya dengan mengaturnya di tempat ia memangsa.[7][20] Tidak diketahui apakah kutu laut merupakan perantara dari penyakti, namun kutu laut yang membawa bakteri dan virus kemungkinan mendapatkannya dari inangnya dan mengkonsumsi jaringan ikan yang terkontaminasi.[21]
|chapter= akan diabaikan (bantuan)Pemeliharaan CS1: Banyak nama: authors list (link) 
. PMID 19586950. Kutu laut adalah sekelompok spesies hewan copepoda dari ordo Siphonostomatoida, yaitu famili Caligidae. Terdapat sekitar 559 spesies di 37 genera, termasuk 162 spesies Lepeophtheirus dan 268 spesies Caligus. Kutu laut merupakan ektoparasit yang memakan lendir, jaringan epidermis, dan darah dari ikan laut inangnya.
Salah satu spesiesnya yaitu Caligus rogercresseyi menjadi parasit utama di pembudidayaan salmon di Cile,. Penelitian telah dilaksanakan untuk memperoleh pemahaman lebih lanjut dari interaksi antara parasit ini dengan inangnya. Bukti-bukti terkini menunjukkan bahwa L. salmonis di Samudra Atlantik memiliki beberapa perbedaan genetik dibandingkan dengan L. salmonis dari Samudra Pasifik, menunjukkan bahwa L. salmonis Atlantik dan Pasifik kemungkinan secara independen berevolusi bersama salmon di Atlantik dan Pasifik.
Caligidae vormen een familie binnen de orde Siphonostomatoida.
Deze parasitaire roeipootkreeftjes hebben een vergrote kop met aangepaste aanhangsels om de gastheer vast te grijpen. Ze hebben een gereduceerd achterlijf. Sommigen hebben een rode verkleuring door de aanwezigheid van hemoglobine in hun lichaam.
De soorten van deze familie komen in zowel zoet als zout water voor als parasiet op vissen.
De volgende geslachten zijn bij de familie ingedeeld:
Caligidae vormen een familie binnen de orde Siphonostomatoida.
Multimedia w Wikimedia Commons Caligidae – rodzina pasożytniczych widłonogów z rzędu Cyclopoida powodujących zachorowania ryb słodkowodnych i morskich. W rozwoju tego pasożyta występują larwy: nauplius, kopepodit oraz chalimus. Ryby są żywicielem ostatecznym oraz żywicielem stadium larwalnego zwanego chalimus.
Przedstawicielami tej rodziny są:
Caligidae – rodzina pasożytniczych widłonogów z rzędu Cyclopoida powodujących zachorowania ryb słodkowodnych i morskich. W rozwoju tego pasożyta występują larwy: nauplius, kopepodit oraz chalimus. Ryby są żywicielem ostatecznym oraz żywicielem stadium larwalnego zwanego chalimus.
Przedstawicielami tej rodziny są:
Rodzaj Caligus – obejmuje ponad 200 gatunków. Caligus lacustris – Samica wielkości 4–7 mm. Pasożytuje na skórze i płetwach ryb słodkowodnych. Głównym żywicielem jest leszcz (Abramis brama). Caligus bonito Caligus curtus Caligus germoi Caligus kala海蝨是橈腳類下的魚虱科生物。其下共有36個屬，當中最著名的瘡痂魚虱屬及魚虱屬就分別約有42和300個物種。[2]它們是水生的 體外寄生蟲，吃寄主的黏液、表皮組織及血液。其下的瘡痂魚虱屬及魚虱屬會寄生在海魚身上，尤其對飼養的鮭魚造成很大的問題。
就海蝨的認識主要是來自對飼養鮭魚的感染。不過，就其生物學及與寄主間的關係所知甚少。
很多海蝨都有特有的寄主，例如鮭瘡痂魚虱就特別喜歡寄生在鮭魚當中，尤其是飼養的大西洋鮭。鮭瘡痂魚虱也可以寄生在其他鮭魚，但程度各有不同。太平洋的鮭魚，如銀大麻哈魚、大麻哈魚及駝背大馬哈魚等對於鮭瘡痂魚虱會產生強烈的組織反應，在感染的首週就會將之排出。[3]太平洋的鮭瘡痂魚虱也可以發展到寄生到三刺魚[4]，不過大西洋的則沒有出現這種情況。
海蝨在浮游階段如何擴散及尋找寄主仍然是迷。溫度、光線及水流都是主因，其生存倚賴25‰以上的鹽度。[5][6][7][8]有指鮭瘡痂魚虱會向著光源向上遷徙，正好會遇到向下游的鮭魚魚秧。[9]在潮間帶浮游階段的海蝨可以被送到幾十公里以外的地方。[7][10][11]
海蝨會從溯河的魚類身體上掉下及死去，例如回到淡水河流中繁殖的鮭魚。不過這些鮭魚回到海中重新受感染的原因則不明。有指海蝨可能是在河口生活的魚類身體上存活下來，或是轉往其他的寄主。至於海蝨如何在野外魚類之間傳播也不詳。成年的瘡痂魚虱屬在實驗室環境下可以在不同魚種間傳播，但並不頻繁；而魚虱屬則隨時可以傳播。
鮭瘡痂魚虱的大小較魚虱屬大一倍。它們的身體有4個部份，包括頭胸部、第四足體節、生殖部份及腹部。[12]頭胸部是一塊闊板，當中包含了頭三足的體節，可以像吸盤般將它們吸在寄主魚類的身體上。所有的海蝨都有像吸管的口器。第二觸角及口附肢都進化到可以幫助將它們找著寄主。雄蝨也會用第二觸角來找住雌性進行交配。[13]成年雌性比雄性大，生殖部份也非常大。鮭瘡痂魚虱會生兩串共500-1000顆卵，成熟後卵會變深色。一隻雌蝨一生可以產6-11對卵串，估計壽命只有7個月。[7][9][14]
海蝨有浮游及寄生的階段。所有階段之間都會脫殼。[12][13][15][16]其中鮭瘡痂魚虱只要17-72日就可以由卵成長到成年。
海蝨的卵會孵化出第一期無節幼體，繼而脫殼成長至第二期無節幼體。兩期的無節幼體階段都不會進食，只靠卵黃供應能量，而且懂得游泳。到了成年階段就會尋找寄主。水流、鹽度、光線等都可以幫助它們尋找寄主。[7]海蝨多會寄生在魚類身體受水流影響較少的地方，特別是鰭及其他受保護的地方。[6][17]當幼體附在寄主身上後，就會覓食一段時間脫殼成第一期的附著幼體。海蝨會繼續發育成另外的3期附著幼體。所有四個附著幼體階段都有一個前部絲體的結構，用來附著在寄主身上。不同的海蝨有不同的繁殖時間及方法。亞成體及成體可以在魚類的身體上移動，有時甚至可以在寄主之間轉移。雌性成體的身體較大，也較為扁平。[18]
無節幼體及幼體期都是不會進食的。當附在寄主身上時，它們就會發育到附著幼體階段。附著幼體都有胃腸道，且會吃寄主的黏液及組織。亞成體及成體都是主動覓食者，有時甚至會吃寄主的血液。鮭瘡痂魚虱會分泌大量胰蛋白酶到寄主的黏液，幫助覓食及消化。[3][19]其他的物質包括前列腺素E2，可以幫助覓食及避開寄主的免疫反應。[3][20]海蝨是否疾病媒介則不明，但它們肯定是帶有細菌及病毒。[21]
海蝨會在附著的位置對寄主造成物質及酶促的破壞。它們在吃食的時候會造成像割開的傷口，嚴重程度會受到幾個因素所影響，如寄主物種、年齡及健康。海蝨感染會對寄主魚造成慢性壓力，包括破壞其表皮出現失血、電解質的改變及釋放皮質醇。這樣會降低寄主魚的免疫反應，令它們易於染病。[22][23]
不同海蝨的物種、發育階段及數量也會造成不同程度的破壞。大西洋鮭的組織似乎對海蝨沒有任何反應。相反，銀大麻哈魚及駝背大馬哈魚對於鮭瘡痂魚虱則有強烈的反應，包括表皮增生及炎症。在感染後的第一周就會排斥海蝨。[3]鮭瘡痂魚虱可以令飼養的大西洋鮭及野生的紅大馬哈魚出現深深的損傷，尤其是在頭部，嚴重的程度可以見到頭顱骨。
有指受到海蝨感染的飼養鮭魚會將病傳播到周邊野生的幼魚，令它們的數量大減。[24]海蝨，尤其是鮭瘡痂魚虱及多種魚虱屬都會令飼養及野生的鮭魚致命。[25][26]海蝨會遷徙及附在野生鮭魚的皮膚上達幾日之久。[27][28][29]大量受感染的鮭魚可以令海蝨的濃度攀升，游經此地的野生幼鮭魚就會受到感染及死亡。[30][31]在加拿大的太平洋海岸，差不多有80%的駝背大馬哈魚死於海蝨的感染。[24]
多項研究都指飼養鮭魚會積聚海蝨，並會破壞周邊的野生鮭魚群落。[31]其他研究卻指飼養鮭魚所感染的海蝨，並不會對野生群落造成影響。[33]
