Schistosomiasis is caused by helminth parasites of the genus Schistosoma. Other helminth infections are discussed in the Helminths, Soil-Transmitted section earlier in this chapter.
Waterborne transmission occurs when larval cercariae, found in contaminated bodies of freshwater, penetrate the skin.
An estimated 85% of the world’s cases of schistosomiasis are in Africa, where prevalence rates can exceed 50% in local populations. Schistosoma mansoni and S. haematobium are distributed throughout Africa; only S. haematobium is found in areas of the Middle East, and S. japonicum is found in Indonesia and parts of China and Southeast Asia (Map 3-12). Although schistosomiasis had been eliminated in Europe for decades, transmission of S. haematobium was reported in Corsica in 2014, when cases were identified among travelers who had bathed in the Cavu River. Two other species can infect humans: S. mekongi, found in Cambodia and Laos, and S. intercalatum, found in parts of Central and West Africa. These 2 species are rarely reported causes of human infection. Many countries endemic for schistosomiasis have established control programs, but others have not. Countries where development has led to widespread improvements in sanitation and water safety, as well as successful schistosomiasis control programs, may have eliminated this disease. However, there are currently no international guidelines for certification of elimination.
All ages are at risk for infection from freshwater exposure in endemic areas. Swimming, bathing, and wading in contaminated freshwater can result in infection. Human schistosomiasis is not acquired by contact with saltwater (oceans or seas). The distribution of schistosomiasis is very focal and determined by the presence of competent snail vectors, inadequate sanitation, and infected humans. The specific snail vectors can be difficult to identify, and whether snails are infected with human schistosome species can only be determined in the laboratory.
The geographic distribution of cases of schistosomiasis acquired by travelers reflects travel and immigration patterns. Most travel-associated cases of schistosomiasis are acquired in sub-Saharan Africa. Sites in Africa frequently visited by travelers are common sites of infection. These sites include rivers and water sources in the Banfora region (Burkina Faso) and areas populated by the Dogon people (Mali), Lake Malawi, Lake Tanganyika, Lake Victoria, the Omo River (Ethiopia), the Zambezi River, and the Nile River. However, as visitors travel to more remote sites, it is important to remember that most freshwater surface water sources in Africa are potentially contaminated and can be sources of infection. A local claim that there is no schistosomiasis in a body of freshwater is not necessarily reliable.
The types of travelers and expatriates potentially at increased risk for infection include adventure travelers, Peace Corps volunteers, missionaries, soldiers, and ecotourists. Outbreaks of schistosomiasis have occurred among adventure travelers on river trips in Africa.
1 The distribution of schistosomiasis is very focal; however, surveillance for schistosomiasis is limited in most countries. Therefore, this map shades entire countries where schistosomiasis transmission has been reported. The exception to this is France, where schistosomiasis has been reported on several islands, such as Guadeloupe, Martinique, and Corsica.
The incubation period is typically 14–84 days for acute schistosomiasis (Katayama syndrome), but chronic infection can remain asymptomatic for years. Penetration of cercariae can be associated with a rash that develops within hours or up to a week after contaminated water exposures. Acute schistosomiasis is characterized by fever, headache, myalgia, diarrhea, and respiratory symptoms. Eosinophilia is often present, as well as painful hepatomegaly or splenomegaly.
The clinical manifestations of chronic schistosomiasis are the result of host immune responses to schistosome eggs. Eggs, secreted by adult worm pairs living in the bloodstream, become lodged in the capillaries of organs and cause granulomatous reactions. S. mansoni and S. japonicum eggs most commonly lodge in the blood vessels of the liver or intestine and can cause diarrhea, constipation, and blood in the stool. Chronic inflammation can lead to bowel wall ulceration, hyperplasia, and polyposis and, with heavy infections, to periportal liver fibrosis. S. haematobium eggs typically lodge in the urinary tract and can cause dysuria and hematuria. Calcifications in the bladder may appear late in the disease. S. haematobium infection can also cause genital symptoms and has been associated with increased risk of bladder cancer. As with acute schistosomiasis, eosinophilia may be present during chronic infection with any species.
Rarely, central nervous system manifestations of schistosomiasis may develop; this is thought to result from aberrant migration of adult worms or eggs depositing in the spinal cord or brain. Signs and symptoms are related to ectopic granulomas in the central nervous system and can present as transverse myelitis.
Diagnosis is made by microscopic identification of parasite eggs in stool (S. mansoni or S. japonicum) or urine (S. haematobium). Serologic tests are useful to diagnose light infections because egg shedding may not be consistent such as in travelers and in others who have not had schistosomiasis previously. Antibody tests do not distinguish between past and current infection. Immunologic test sensitivity and specificity vary, depending on the antigen preparation used and how the test is performed. Health care providers should consider screening asymptomatic people who may have been exposed during travel and may benefit from treatment.
Schistosomiasis is uncommon in the United States, and clinicians unfamiliar with management of schistosomiasis should consult an infectious disease or tropical medicine specialist for diagnosis and treatment. Praziquantel is used to treat schistosomiasis. Praziquantel is most effective against adult forms of the parasite and requires an immune response to the adult worm to be fully effective. Host immune response differences may affect individual response to treatment with praziquantel. Although a single course of treatment is usually curative, the immune response in lightly infected patients may be less robust, and repeat treatment may be needed after 2–4 weeks to increase effectiveness.
No vaccine is available. No drugs for preventing infection are available. Preventive measures are primarily avoiding wading, swimming, or other contact with freshwater in disease-endemic countries. Untreated piped water coming directly from freshwater sources may contain cercariae, but filtering with fine-mesh filters, heating bathing water to 122°F (50°C) for 5 minutes, or allowing water to stand for ≥24 hours before exposure can prevent infection.
Swimming in adequately chlorinated swimming pools is safe, even in disease-endemic countries, although confirming adequate levels of chlorination is difficult. Vigorous towel-drying after accidental exposure to water has been suggested as a way to remove cercariae before they can penetrate, but this may only prevent some infections and should not be recommended as a preventive measure. Topical applications of insect repellents such as DEET can block penetrating cercariae, but the effect depends on the repellent formulation, may be short-lived, and cannot reliably prevent infection.
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