Swimmer’s itch


Swimmer’s itch

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Swimmer’s itch
Cercarial dermatitis lower legs.jpg
Cercarial dermatitis on lower legs, four days after spending a day in the shallows of a lake
Specialty Infectious disease Edit this on Wikidata

Swimmer’s itch or cercarial dermatitis, is a short-term allergic immune reaction occurring in the skin of humans that have been infected by water-borne schistosomes. Symptoms, which include itchy, raised papules, commonly occur within 1–2 days of infection and do not generally last more than 2–3 weeks. However, people repeatedly exposed to cercariae develop heavier symptoms with faster onset.[1] Cercarial dermatitis is common in freshwater, brackish and marine habitats worldwide.[2] Incidence may be on the rise, although this may also be attributed to better monitoring. Nevertheless, the condition has been regarded as emerging infectious disease.[3]

There are no permanent effects to people from this condition.[4] Orally administered hydroxyzine, an antihistamine, is sometimes prescribed to treat swimmer’s itch and similar dermal allergic reactions. In addition, bathing in oatmeal, baking soda, or Epsom salts can also provide relief of symptoms.[5]


Swimmer’s itch probably has been around as long as humans. The condition was known to exist as early as the 1800s, but it was not until 1928 that a biologist found that the dermatitis was caused by the larval stage of a group of flatworm parasites in the family Schistosomatidae.[6] The genera most commonly associated with swimmer’s itch in humans are Trichobilharzia[1] and Gigantobilharzia. It 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. In marine habitats, especially along the coasts, swimmer’s itch can occur as well.[7]

These parasites use both freshwater snails and vertebrates as hosts in their parasitic life cycles as follows:

  1. 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 freshwater snail.
  2. 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.
  3. Cercariae use a tail-like appendage (often forked in genera causing swimmer’s itch) to swim to the surface of the water; and use various physical and chemical cues in order to locate the next and final (definitive) host in the life cycle, a bird. These larvae can accidentally come into contact with the skin of a swimmer. The cercaria penetrates the skin and dies in the skin immediately. The cercariae cannot infect humans, but they cause an inflammatory immune reaction. This reaction causes initially mildly itchy spots on the skin. Within hours, these spots become raised papules which are intensely itchy. Each papule corresponds to the penetration site of a single parasite.

    Life-cycle of swimmers itch

  4. After locating a bird, the parasite penetrates through the skin (usually the feet), dropping the forked tail in the process. Inside the circulatory system, the immature worms (schistosomula) develop into mature male and female worms, mate and migrate through the host’s circulatory system (or nervous system in case of T. regenti) to the final location (veins feeding the gastrointestinal tract) within the host body. There they lay eggs in the small veins in the intestinal mucosa from which they make their way into the lumen of the gut, and are dumped into the water when the bird defecates. One European species, Trichobilharzia regenti, instead infects the bird host’s nasal tissues and larvae hatch from the eggs directly in the tissue during drinking/feeding of the infected birds.[8]

Risk factors[edit]

Image of infectious cercariae

Humans usually become infected 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[9] and North America,[10] and shallow inshore waters may harbour higher densities of cercariae than open waters offshore. Onshore winds are thought to cause cercariae to accumulate along shorelines.[11] 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[9] as well as instances where risk increases in endemic swimmer’s itch “hotspots”.[11] 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.[12] 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.


Mechanical removal of snails in Lake Annecy, France

Various strategies targeting the mollusc and 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 sulfate 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[13]

More importantly, perhaps, copper sulfate 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.[14] Work on schistosomiasis showed that water-resistant topical applications of the common insect repellent DEET prevented schistosomes from penetrating the skin of mice.[15] Public education of risk factors, a good alternative to the aforementioned interventionist strategies, can also reduce human exposure to cercariae.

See also[edit]


  1. ^ Jump up to:a b Macháček, Tomáš; Turjanicová, Libuše; Bulantová, Jana; Hrdý, Jiří; Horák, Petr; Mikeš, Libor (2018-10-09). “Cercarial dermatitis: a systematic follow-up study of human cases with implications for diagnostics”. Parasitology Research. 117 (12): 3881–3895. doi:10.1007/s00436-018-6095-0. ISSN 0932-0113. PMID 30302587.
  2. ^ “Avian Schistosome Biodiversity”. www.schistosomes.net. Retrieved 2016-03-07.
  3. ^ Horák, Petr; Mikeš, Libor; Lichtenbergová, Lucie; Skála, Vladimír; Soldánová, Miroslava; Brant, Sara Vanessa (January 2015). “Avian schistosomes and outbreaks of cercarial dermatitis”. Clinical Microbiology Reviews. 28 (1): 165–190. doi:10.1128/CMR.00043-14. ISSN 1098-6618. PMC 4284296. PMID 25567226.
  4. ^ “With warm weather, Swimmers Itch makes annual appearance”. dnr.wi.gov. Retrieved 2016-03-07.
  5. ^ In CDC. “Swimmers Itch FAQS.” retrieved May 12, 2014
  6. ^ “Swimmer’s Itch in Michigan” (PDF). State of Michigan. 2014. Retrieved 5 March 2015.
  7. ^ Brant S, Cohen A, James D, Hui L, Hom A, Loker E (2010). “Cercarial Dermatitis Transmitted by Exotic Marine Snail”. Emerging Infectious Diseases. 16 (9): 1357–65. doi:10.3201/eid1609.091664. PMC 3294964. PMID 20735918.
  8. ^ Horák P., Kolářová L., Dvořák J. (1998). Trichobilharzia regenti n. sp. (Schistosomatidae, Bilharziellinae), a new nasal schistosome from Europe” (PDF). Parasite. 5 (4): 349–357. doi:10.1051/parasite/1998054349. PMID 9879557.
  9. ^ Jump up to:a b Chamot E, Toscani L, Rougemont A (1998). “Public health importance and risk factors for cercarial dermatitis associated with swimming in Lake Leman at Geneva, Switzerland”. Epidemiol. Infect. 120 (3): 305–14. doi:10.1017/S0950268898008826. PMC 2809408. PMID 9692609.
  10. ^ Lindblade KA (1998). “The epidemiology of cercarial dermatitis and its association with limnological characteristics of a northern Michigan lake”. J. Parasitol. 84 (1): 19–23. doi:10.2307/3284521. JSTOR 3284521. PMID 9488332.
  11. ^ Jump up to:a b c Leighton BJ, Zervos S, Webster JM (2000). “Ecological factors in schistosome transmission, and an environmentally benign method for controlling snails in a recreational lake with a record of schistosome dermatitis”. Parasitol. Int. 49 (1): 9–17. doi:10.1016/S1383-5769(99)00034-3. PMID 10729712.
  12. ^ Verbrugge LM, Rainey JJ, Reimink RL, Blankespoor HD (2004). “Prospective study of swimmer’s itch incidence and severity”. J. Parasitol. 90 (4): 697–704. doi:10.1645/GE-237R. PMID 15357056.
  13. ^ Blankespoor, H. D., Reimink, R. L. (1991). “The control of swimmer’s itch in Michigan: Past, present, and future”. Michigan Academician. 24 (1): 7–23.
  14. ^ Blankespoor, C. L., Reimink, R. L., Blankespoort, H. D. (2001). “Efficacy of praziquantel in treating natural schistosome infections in common mergansers”. Journal of Parasitology. 87 (2): 424–6. doi:10.1645/0022-3395(2001)087[0424:EOPITN]2.0.CO;2. PMID 11318576.
  15. ^ Salafsky, B., Ramaswamy, K., He, Y. X., Li, J., Shibuya, T. (November 1999). “Development and evaluation of LIPODEET, a new long-acting formulation of N, N-diethyl-m-toluamide (DEET) for the prevention of schistosomiasis”. Am. J. Trop. Med. Hyg. 61 (5): 743–50. PMID 10586906.

External links[edit]



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