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Schistosomiasis, which affects more than 200 million persons worldwide, leads to severe consequences in 20 million persons and about 100,000 deaths annually The disease is caused by five species of trematode blood flukes Four species cause intestinal schistosomiasis, with infection of mesenteric venules: Schistosoma mansoni, which is present in Africa, the Arabian peninsula, South America, and the Caribbean; Schistosoma japonicum, which is endemic in China and Southeast Asia; Schistosoma mekongi, which is endemic near the Mekong River in Southeast Asia; and Schistosoma intercalatum, which occurs in parts of Africa Schistosoma haematobium causes urinary schistosomiasis, with infection of venules of the urinary tract, and is endemic in Africa and the Middle East Transmission of schistosomiasis is focal, with greatest prevalence in poor rural areas Control efforts have diminished transmission significantly in many areas, but high level transmission remains common in sub-Saharan Africa and some other areas Prevalence of infection and illness typically peaks at about 15 20 years of age Humans are infected with schistosomes after contact with fresh water containing cercariae released by infected snails Infection is initiated by penetration of skin or mucous membranes After penetration, schistosomulae migrate to the portal circulation, where they rapidly mature After about 6 weeks, adult worms mate, and migrate to terminal mesenteric or bladder venules, where females deposit their eggs Some eggs reach the lumen of the bowel or bladder and are passed with feces or urine, while others are retained in the bowel or bladder wall or transported in the circulation to other tissues, in particular the liver Disease in endemic areas is primarily due to a host response to eggs, with granuloma formation and inflammation, eventually leading to fibrosis Chronic infection can result in scarring of mesenteric or vesicular blood vessels, leading to portal hypertension and alterations in the urinary tract In previously uninfected individuals, such as travelers with fresh water contact in endemic regions, acute schistosomiasis may occur, with a febrile illness 2 8 weeks after infection.



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Microscopic examination of stool or urine for eggs, evaluation of tissue, or serologic tests establish the diagnosis Characteristic eggs can be identified on smears of stool or urine, but filtration or concentration techniques can improve yields Quantitative tests that yield > 400 eggs per gram of feces or 10 mL of urine are indicative of heavy infections with increased risk of complications Diagnosis can also be made by biopsy of the rectum, colon, liver, or bladder Serologic tests include an ELISA available from the CDC that is 99% specific for all species The test is 99% sensitive for S mansoni, 95% sensitive for S haematobium, but < 50% sensitive for S japonicum Species-specific immunoblots can increase sensitivity In acute schistosomiasis, serologic tests may become positive before eggs are seen in stool or urine After therapy, eggs may be shed in stool or urine for months, and so the identification of eggs in fluids or tissue or positive serologic tests cannot distinguish past or active disease Tests for egg viability are available With a diagnosis of schistosomiasis, evaluation for the extent of disease is warranted, including liver function studies and imaging of the liver with intestinal disease and ultrasound or other imaging studies of the urinary system in urinary disease





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1 Cercarial dermatitis Following cercarial penetration, localized erythema develops in some individuals, which can progress to a pruritic maculopapular rash that persists for some days Dermatitis can be caused by human schistosomes and, in non-tropical areas, by bird schistosomes that cannot complete their life cycle in humans (swimmer s itch)

Treatment is indicated for all schistosome infections In areas where recurrent infection is common, treatment is valuable in reducing worm burdens and limiting clinical complications

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The drug of choice for schistosomiasis is praziquantel The drug is administered for 1 day at a dose of 40 mg/kg (in one or two doses) for S mansoni, S haematobium, and S intercalatum infections and a dose of 60 mg/kg (in two or three doses) for S japonicum and S mekongi Cure rates are generally > 80% after a single treatment, and those not cured have marked reduction in the intensity of infection Praziquantel is active against invading cercariae but not developing schistosomulae Therefore, the drug may not prevent illness when given after exposure and, for recent infections, a repeat course after a few weeks may be appropriate Praziquantel may be used during pregnancy Resistance to praziquantel has been reported Toxicities include abdominal pain, diarrhea, urticaria, headache, nausea, vomiting, and fever, and may be due both to direct effects of the drug and responses to dying worms Alternative therapies are oxamniquine for S mansoni infection and metrifonate for S haemotobium infection Both of these drugs currently have limited availability (they are not available in the United States), and resistance may be a problem No second-line drug is available for S japonicum infections The antimalarial drug artemether has activity against schistosomulae and adult worms and may be effective in chemoprophylaxis; however, it is expensive, and long-term use in malarious areas might select for resistant malaria parasites With severe disease, use of corticosteroids in conjunction with praziquantel may decrease complications Treatment should be followed by repeat examinations for eggs about every 3 months for 1 year after therapy, with re-treatment if eggs are seen

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Travelers to endemic areas should avoid fresh water exposure Vigorous toweling after exposure may limit cercarial penetration Chemoprophylaxis with artemether has shown efficacy but is not standard practice Community control of schistosomiasis includes improved sanitation and water supplies, elimination of snail habitats, and intermittent administration of treatment to limit worm burdens

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