Are You Confident of the Diagnosis?
What you should be alert for in the history
Patients may present with tingling, burning, or itching of the skin occurring hours to days after water exposure; itching may be mild initially with progression of worsening intensity. Patients may have participated in shallow, fresh water activities during warm months. Friends and relatives participating in water activities may be symptomatic. Additionally, patients may have experienced similar episodes in the past. It is important to note that the initial reaction may be mild and go unnoticed by the patient. Subsequent reactions develop more rapidly and may be more severe.
Characteristic findings on physical examination
Patients may present in the first hours post-exposure with erythematous macules, which can progress to papules, with or without urticaria. Days to weeks post-exposure, the patient may exhibit purpuric lesions, vesicles, or pustules. The distribution of the rash only manifests where the patient has had direct contact with infested water.
The rash may appear diffusely (patient fully submerged) or may be localized to specific parts of body (patient wading legs in water). Of note, the rash is observed on areas not covered or protected by clothing (versus seabather’s eruption). Patient excoriation may lead to secondary skin infections and/or scarring. Systemic symptoms may include fever and local lymphadenopathy.
Expected results of diagnostic studies
Diagnosis of swimmer’s itch is based on clinical suspicion. Serologic tests are not commonly done, but the leukocyte differential may show peripheral eosinophilia. Histopathology may show spongiosis, dermal edema, and mixed inflammatory infiltrate. Rarely, cercariae can be observed.
Several conditions should be considered in the differential diagnosis of swimmer’s itch. Seabather’s eruption usually occurs after saltwater exposure and tends to affect areas of skin covered by clothing or hair (opposite to swimmer’s itch). Hot tub folliculitis generally occurs following recent exposure to hot tub, whirlpool, swimming pool, or waterslide water. The patient will have diffusely distributed follicular lesions.
Insect bites (mosquitoes, bed bugs, chiggers, scabies) present with patient history consistent with arthropod exposure. For contact dermatitis (poison ivy), patient reports history consistent with poison ivy or other similar exposure. Lesions are limited to areas which have been in contact with foliage. Skin manifestations of viral causes such as viral exanthems or more defined entities such as varicella/zoster, rubeola, rubella, herpes simplex, should be suspected if a patient is immunocompromised or has not received routine immunizations.
Who is at Risk for Developing this Disease?
Frequency and duration of open-water activity increases the incidence of swimmer’s itch. One study reports 6.8 episodes per 100 water exposure days. Swimmer’s itch occurs worldwide and is commonly observed in bodies of water with on-shore winds. Cases primarily occur in shallow freshwater; however, cases associated with saltwater exposure have also been reported.
Time of year also affects risk. Warm months may increase intermediate host snail populations leading to increased transmission. Presence of hosts is also an important factor. Resident or migratory birds (definitive hosts), snails (intermediate host), and humans (incidental host) must all be present in order for a person to contract swimmer’s itch. Children may be at a higher risk due to more exposure to shallow water and they may be less likely to towel dry.
What is the Cause of the Disease?
Swimmer’s itch is most often caused by non-human schistosomes (over 20 species), particularly avian schistosomes. The Trichobilharzia genus is commonly implicated. Cases are less often due to human schistosomes (e.g., Schistosoma haematobium, Schistosoma japonicum, Schistosoma mansoni, Schistosoma mekongi, Schistosoma intercalatum). Human schistosomes may additionally cause systemic schistosomiasis.
Swimmer’s itch occurs when free-swimming cercariae penetrate the skin of humans (incidental host) and cause an allergic skin reaction (types I and IV hypersensitivity). The life cycle begins as cercariae infect birds (definitive host), maturing into adult worms within blood vessels. Adult worms then produce eggs that are passed in avian feces.
The eggs hatch and liberate ciliated miracidia into the water, which infect snails (intermediate host). Miracidia mature within snails and produce free-swimming cercariae, which either reinfect birds or infect humans. Cercarie die upon penetration into human skin, thus halting the schistosome life cycle.
Systemic Implications and Complications
Possible complications include secondary bacterial skin infections. Patients are at an increased risk when lesions are excoriated or manipulated. Standard treatment is topical or oral antibiotics.
Treatment options are summarized in the Table I.
|• Calamine lotion|
|• Colloid oatmeal baths|
|• Cool compresses|
|• Baking soda|
|• Corticosteroids||Not applicable||Not applicable|
Optimal Therapeutic Approach for this Disease
Swimmer’s itch is a self-limiting process and is not contagious. Most cases only require symptomatic treatment. For very mild cases, treatment consists primarily of over the counter and home remedies including cool compresses and colloidal baths.
If itching is moderate, a combination of topical steroid, oral anti-histamine, and calamine lotion may be used:
Table II. Optimal Therapeutic Approach for Swimmer’s Itch – Moderate Cases
|Medication||Dose, Route, Frequency|
|Mometasone:||Children more than 2 years of age and adults:|
|(0.1%) apply topically sparingly to the affected area(s) once daily|
|5mg/kg daily orally given in divided doses every 6-8 hours when required, maximum 300mg daily|
|25-50mg orally every 4-6 hours when required, maximum 300mg daily|
|Calamine Lotion:||Children and adults:|
|apply topically to the affected area(s) as required|
Severe or refractory cases may require oral corticosteroids:Table III: Optimal Therapeutic Approach for Swimmer’s Itch – Severe or Refractory Cases
|Medication||Dose, Route, Frequency|
|Prednisone:||Children and adults:|
|1mg/kg daily orally for 1 week, followed by 0.5mg/kg daily for 1 week, followed by 0.25mg/kg daily for 1 week|
Patients should be followed days to weeks after initial presentation to monitor possible complications and assess response to symptomatic therapy. Patient and community education is paramount in the prevention of swimmer’s itch.
People in endemic areas should avoid prolonged activity in areas where swimmer’s itch has been reported. One should also avoid shallow, marshy areas where exposure to snails and schistosomes is likely.
If one has swum in a high-risk environment, the person should remove swimsuits, towel dry the exposed skin, and shower immediately after water exposure to potentially reduce risk of parasite penetration into the skin. One should check with the local health department regarding reported cases of water-borne illnesses, including swimmer’s itch, prior to water activity.
Unusual Clinical Scenarios to Consider in Patient Management
When evaluating swimmer’s itch in a patient, one must also consider other more treacherous culprits. The clinician must contemplate the possibility of swimmer’s itch as an early sign of systemic schistosomiasis caused by human schistosomes. This is highly suspect if the patient’s history includes recent travel to endemic areas.
Diagnosis of systemic schistosomiasis is supported by the presence of eggs in urine or stool samples. Anti-schistosomal antibodies may also be evident on serological testing. It is widely accepted that non-human schistosomes die in human epidermis. While dissemination of non-human schistosomes has not been reported in humans, studies in murine models have reported migration of avian schistosomes past the epidermis and into the lungs.
What is the Evidence?
Parasites – Cercarial Dermatitis (also known as Swimmer’s Itch). 2012. (General overview of the biology of cercarial dermatitis and frequently asked questions for patients and healthcare professionals.)
Mulvihill, CA, Burnett, JW. “Swimmer’s itch: a cercarial dermatitis”. Cutis. vol. 46. 1990. pp. 211-3. (Short review article focusing on life cycle, epidemiology, and clinical presentation.)
Baird, JK, Wear, DJ. “Cercarial dermatitis: the swimmer’s itch”. Clin Dermatol. vol. 5. 1987. pp. 88-91. (Detailed review article discussing background, disease, biology, diagnosis, and treatment.)
Verbrugge, LM, Rainey, JJ, Reimink, RL, Blankespoor, HD. “Swimmer’s itch: incidence and risk factors”. Am J Public Health. vol. 94. 2004. pp. 738-41. (Prospective survey conducted at Lake Douglas in Michigan, U.S.A. Discusses incidence, human and geographical risk factors at this location.)
Tremaine, AM, Whittemore, DE, Gewirtzman, AJ, Bartlett, BL, Mendoza, N, Rapini, RP. “An unusual case of swimmer’s itch”. J Am Acad Dermatol. vol. 60. 2009. pp. 174-6. (Case report demonstrating cercarial dermatitis of the face. Illustrates that patient interaction with environment may affect disease presentation. Excellent histologic image of cercariae in stratum corneum.)
Jacobson, CC, Abel, EA. “Parasitic infestations”. J Am Acad Dermatol. vol. 56. 2007. pp. 1026-43. (Review article of multiple parasitic infestations. Gives a brief review of swimmer’s itch and outlines five key takehome points)
(Article provides therapeutic approach to cercarial dermatitis.)
Horák, P, Kolárova, L. “Bird schistosomes:do they die in mammalian skin?”. Trends in Parasitology. vol. 17. 2001. pp. 66-69. (Article reviews avian schistosome lifecycle and discusses the potential that these parasites may penetrate mammalian epidermis and cause additional symptoms.)
Horák, P, Kolárová, L. “Survival of bird schistosomes in mammalian lungs”. Int J Parasitol. vol. 30. 2000. pp. 65-8. (Article discusses experimental murine model demonstrating avian schistosoma migration to mammalian lungs.)
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