Swimmer's itch

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

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.

Since it was first described in Michigan in 1928,^[2] swimmer’s itch has been reported from around the world.

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.

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.

Orally adiministered hydroxyzine, an antihistamine, is sometimes prescribed to treat swimmer’s itch and similar dermal allergic reactions.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

Since it was first described in Michigan in 1928,^[2] swimmer’s itch has been reported from around the world.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

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.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

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.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

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. The length of time spent swimming is positively correlated with increased risk of infection in Europe^[2] and North America,^[3] and shallow inshore waters — snail habitat — undoubtedly harbor higher densities of cercariae than open waters offshore. Onshore winds are thought to cause cercariae to accumulate along shorelines.^[4] 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 bodies of water^[5] as well as instances where risk increases in endemic swimmer’s itch “hotspots.”^[6] 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.^[7] 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.

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