Swimmer's itch
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| Cercarial dermatitis on lower legs, four days after spending a day in the shallows of a lake. |
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Synonyms and keywords: Rice paddy itch, kubure; kobanyo; sawah; hoi con; duckworms itch; clam digger's itch; duck itch; cercarial dermatitis
Overview
Swimmer’s itch is a short-term, immune reaction occurring in the skin of humans that have been infected by water-borne trematode parasites. Symptoms, which include itchy, raised papules, commonly occur within hours of infection and do not generally last more than a week.
The trematodes that cause swimmer’s itch are parasitic schistosomes that use both snails and vertebrates as hosts in their life cycles. Most cases are caused by parasites that use waterfowl as the vertebrate host. These avian schistosomes cannot complete their life cycles in mammals, but can accidentally infect humans, giving rise to mildly itchy spots on the skin. Within hours, these spots become raised papules that are more intensely itchy. The papules are caused by localized inflammatory immune reactions, each corresponding to the penetration site of a single parasite, which dies in the skin within hours.
The schistosomes that give rise to swimmer’s itch should not to be confused with those of the genus Schistosoma, which infect humans and cause the serious human disease schistosomiasis, or with larval stages of thimble jellyfish (Linuche unguiculata), which give rise to seabather's eruption.
Since it was first described in Michigan in 1928[2], swimmer's itch has been reported from around the world. Some suggest incidence may be on the rise[3], although this may also be attributed to better monitoring.
Etiology
The genera most commonly associated with swimmer’s itch in humans are Trichobilharzia and Gigantobilharzia. Trematodes in these groups normally complete their life cycles in birds. However, swimmer’s itch can also be caused by schistosome parasites of non-avian vertebrates, such as Schistosomatium douthitti, which infects snails and rodents. Other taxa reported to cause the reaction include Bilharziella polonica and Schistosoma bovis.
Life cycles of non-human schistosomes
The non-human schistosomes use two hosts in their life cycles. One is a snail, the other is a bird or mammal. Schistosomes are gonochoristic and sexual reproduction takes place in the vertebrate host. In genera that infect birds, adult worms occur in tissues and veins of the host’s gastrointestinal tract, where they produce eggs that are shed into water with host feces. One European species, Trichobilharzia regenti, instead infects the bird host’s nasal tissues, where its eggs are shed with lachrymal secretions.
Once a schistosome egg is immersed in water, a short-lived, non-feeding, free-living stage known as the miracidium emerges. The miracidium uses cilia to follow chemical and physical cues thought to increase its chances of finding the first intermediate host in its life cycle, a snail. After infecting a snail, it develops into a mother sporocyst, which in turn undergoes asexual reproduction, yielding large numbers of daughter sporocysts, which asexually produce another short-lived, free-living stage, the cercaria. Cercariae use a tail-like appendage (often forked in genera causing swimmer’s itch) to swim to the surface of the water, as well as other physical and chemical cues, in order to locate the next and final (definitive) host in the life cycle, a bird. After infecting a bird, the parasite develops into a schistosomulum and migrates through the host’s circulatory system (or nervous system in case of T. regenti) to the final location within the host body where it matures and, if it encounters a mate, sheds eggs to begin the cycle anew.
Risk factors
Humans usually become infected with avian schistosomes after swimming in lakes or other bodies of slow-moving fresh water. Some laboratory evidence indicates snails shed cercariae most intensely in the morning and on sunny days, and exposure to water in these conditions may therefore increase risk. Duration of swimming is positively correlated with increased risk of infection in Europe[4] and North America[5], and shallow inshore waters -- snail habitat -- undoubtedly harbour higher densities of cercariae than open waters offshore. Onshore winds are thought to cause cercariae to accumulate along shorelines.[6] Studies of infested lakes and outbreaks in Europe and North America have found cases where infection risk appears to be evenly distributed around the margins of water bodies[7] as well as instances where risk increases in endemic swimmer's itch "hotspots"[8]. Children may become infected more frequently and more intensely than adults but this probably reflects their tendency to swim for longer periods inshore, where cercariae also concentrate.[9] Stimuli for cercarial penetration into host skin include unsaturated fatty acids, such as linoleic and linolenic acids. These substances occur naturally in human skin and are found in sun lotions and creams based on plant oils.
Control measures and treatment
Various strategies, targeting either the mollusc or avian hosts of schistosomes, have been used by lakeside residents in recreational areas of North America to deal with outbreaks of swimmer's itch. In Michigan, for decades authorities used copper sulphate as a molluscicide to reduce snail host populations and thereby the incidence of swimmer's itch. The results with this agent have been inconclusive, possibly because
- snails become tolerant
- local water chemistry reduces the molluscicide's efficacy
- local currents diffuse it
- adjacent snail populations repopulate a treated area. [10]
More importantly, perhaps, copper sulphate is toxic to more than just molluscs, and the effects of its use on aquatic ecosystems are not well understood. Another method targeting the snail host, mechanical disturbance of snail habitat, has been also tried in some areas of North America[11] and Lake Annecy in France, with promising results. Some work in Michigan suggests that administering praziquantel to hatchling waterfowl can reduce local swimmer's itch rates in humans.[12] Work on schistosomiasis showed that water-resistant topical applications of the common insect repellent DEET prevented schistosomes from penetrating the skin of mice.[13]
Public education of risk factors, a good alternative to the above-mentioned interventionist strategies, can also reduce human exposure to cercariae.
Orally adiministered hydroxyzine, an antihistamine, is sometimes prescribed to treat swimmer's itch and similar dermal allergic reactions.