Difference between revisions of "Sea Lice"
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Revision as of 21:56, 29 September 2011
Caligidae | |
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Kingdom | Metazoa |
Phylum | Arthropoda |
Super-class | Crustacea |
Class | Copepoda |
Order | Siphonostomatoida |
Family | Caligidae |
Species | Caligus spp. and Lepeotheirus spp. |
Also Known As: Caligidae infection
Caused By: Lepeotheirus salmonis — L. Pectoralis — L. Thompsomni — L. Europaensis — Caligus elongatus — C. orientalis — C. teres — C. rogercresseyi — C. punctatus — C. epidemicus
Introduction
Sea lice are parasites of the Caligidae family of arthropods and are among the most notorious pests affecting cultured marine fish. They have a particularly large impact upon salmonid fish production. The parasites feed on body mucus, epidermal tissues and blood from their hosts, causing significant superficial damage and consequent impact upon circulatory volume.
The lice are brown-red in colour, have 5 pairs of legs and the female is considerably larger than the male (10mm and 6mm respectively) with a long egg sac. Three leg pairs are for swimming and the other two adapted for eating.
Lifecycle
Eggs are released into the aquatic environment from long egg sacs. There are two non-parasitic larval stages that include copepod, chalimus and pre-adult. Larval migration may exceed 1km and they may be carriers of bacteria and viruses as they migrate from fish to fish.
Seven parasitic larval stages follow including copepod, chalimus and pre-adult. The larvae damage the fish’ skin by penetrating the epidermis an dermis with first their antennae followed by their cephalothoracic shield which causes separation from the basement membrane. They then secrete a substance which hardens to form their frontal filament and moult into the first chalimus stage.[1]
The chalimus then typically attaches to the dorsal or pectoral fin and anus. They are <4mm long and require microscopy for identification.
Pre-adult and adult stages move freely over their hosts and can also move between hosts. They attach by suction generated by their cephalothorax.
Dependent on temperature, the life cycle can take 3 weeks to 4 months to complete. Adults then live for up to three weeks.
Distribution
Most sea lice infections occur in tropical and temperate waters. Infection is thought to occur as the parasites rise to the shallows during the day and sink at night, thus crossing the path of the salmon migrating in the opposite direction.
L. salmonis is the exception, affecting Atlantic salmon in the colder waters of the Northern hemisphere. It also infects salmonids is Japan.
C. orientalis is also found on rainbow trout in Japan. C. elongatus is the most common species in British waters, C. teres and C. rogercresseyi in Chile, C. epidemicus, C. punctatus and C. orientalis in Asia and L. pectoralis occurs in the north-east Atlantic Ocean, Balic Sea and White Sea.
No significant problems appear to occur in the Southern hemisphere except for C. elongatus in Australia which originated from wild fish and is thought to have been introduced by ballast water translocated from northern Asia.
Signalment
L. salmonis is the most host specific of the sea lice while C. elongates is cosmopolitan and has been found in over 80 species of fish.
L. pectoralis affects pleuronectids (flatfish) such as plaice and flounder.
Many factors including breed, location and immune status will affect susceptibility to sea lice.
Clinical Signs
Infected fish have skin erosions, often near the head. These often begin as whitish spots, becoming open wounds in advanced disease. Erosion may be deep enough to expose the underlying bones. Secondary infection is common, which may be fungal if the fish is returned to freshwater.[2] Erosion of the eyes can lead to corneal ulceration and secondary infection causing blindness and cataract formation. The fins may also be damaged by the parasites and the body is often covered in mucus. Malaise and interference with feeding behaviour lead to loss of condition and anorexia.
Even when not feeding, the presence of the parasites is stressful to the fish and therefore reduces condition and productivity/breeding performance.
Mortalities can be significant in heavily infected fish. The principal cause is thought to be osmoregulatory failure due to extensive skin damage. Osmotic balance is also affected when anaemia results from a large parasite burden.
Diagnosis
The large female caligoids, although well camouflaged, are usually visible to the naked eye and are usually on the gills, fins or in the buccal or opercular cavities on the fish. They can then be identified microscopically.
Treatment
Ectoparasiticides (e.g. organophosphates, pyrethroids, hydrogen peroxide) are available in a variety of formulations but not all are approved for food fish so care should be taken when selecting. Resistance is also an issue.
In-feed treatments include coating the feed with drugs (e.g. avermectins) or with growth inhibitors (e.g. Teflubenzuron).
Control
Ectoparasiticides can also be used prophylactically.
Biological control has also been investigated, in a search for feeder species such as wrasse (natural predator) which may decrease louse numbers.
Management improvements are imperative, and an all-in-all-out system is ideal.
Selective breeding from resistant breeds is also advised but difficult.
Good animal husbandry including fallowing, removal of dead and sick fish, and preventing net fouling help in preventing serious outbreaks.
Sea Lice Learning Resources | |
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Flashcards Test your knowledge using flashcard type questions |
Sea Lice Flashcards |
References
- ↑ Bron, J. E., Sommerville, C., Jones, M., Rae, G. H (1991) The settlement and attachment of early stages of the salmon louse, Lepeophtheirus salmonis (Copepoda: Caligidae) on the salmon host, Salmo salar. J Zoology, 224:201-212
- ↑ Hastein, T., Bergsjo, T (1976) The salmon lice Lepeophtheirus salmonis as the cause of disease in farmed salmonids. Revista Italiana Piscicoltura e Ittiopatologia, II:3-5
Burka, J.F., Fast, M.D. Revie, C.W. (2011). Lepeophtheirus salmonis and Caligus rogercresseyi. In: Fish Parasites: Pathobiology and Protection (eds. P.T.K. Woo and K. Buchmann), CABI, Wallingford, U.K. pages 350-370
This article was originally sourced from The Animal Health & Production Compendium (AHPC) published online by CABI during the OVAL Project. The datasheet was accessed on 11 July 2011. |
This article has been expert reviewed by Prof Patrick Woo MSc PhD Date reviewed: 20 September 2011 |