Diagnosis

Examination of stool and/or urine for ova is the primary methods of diagnosis for suspected schistosome infections. The choice of sample to diagnose schistosomiasis depends on the species of parasite likely causing the infection. Adult stages of S. mansoni, S. japonicum, S. mekongi, and S. intercalatum reside in the mesenteric venous plexus of infected hosts and eggs are shed in feces; S. haematobium adult worms are found in the venous plexus of the lower urinary tract and eggs are shed in urine.

Careful review of travel and residence history is critical for determining whether infection is likely and which species may be causing infection. It is important to remember that both S. mansoni and S. haematobium are endemic in some areas of sub-Saharan Africa; patients with freshwater exposures in those areas should have both stool and urine samples examined for eggs. Testing of stool or urine can be of limited sensitivity, particularly for travelers who may have lighter burden infections. To increase the sensitivity of stool and urine examination, three samples should be collected on different days. For S. haematobium, presence of hematuria can suggest infection but this test is more useful for population studies in Africa and is not sufficiently sensitive or specific for individual patient diagnosis. The eggs are shed intermittently and in low amounts in light-intensity infections.

Serologic testing for antischistosomal antibody is indicated for diagnosis of travelers or immigrants from endemic areas who have not been treated appropriately for schistosomiasis in the past. Commonly used serologic tests detect antibody to the adult worm. For new infections, the serum sample tested should be collected at least 6 to 8 weeks after likely infection, to allow for full development of the parasite and antibody to the adult stage. Serologic testing may not be appropriate for determination of  active infection in patients who have been repeatedly infected and treated in the past because specific antibody can persist despite cure. In these patients, serologic testing cannot distinguish resolved infection from active infection. An antigen test has been developed that can detect active infection based on the presence of schistosomal antigen, but this test is not commercially available in the United States and at this time is undergoing field evaluations for accurate diagnosis of low-intensity infections.

Disease

The incubation period for patients with acute schistosomiasis is usually 14-84 days; however, many people are asymptomatic and have subclinical disease during both acute and chronic stages of infection. Persons with acute infection (also known as Katayama syndrome) may present with rash, fever, headache, myalgia, and respiratory symptoms. Often eosinophilia is present with hepato- and/or splenomegaly.

Clinical manifestations of chronic disease result from host immune responses to schistosome eggs. 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 liver fibrosis and periportal hypertension.

S. haematobium eggs tend to lodge in the urinary tract causing damage, dysuria and hematuria. Chronic infections may increase the risk of bladder cancer.

Central nervous system lesions have been reported, but are rare. Disease is the result of ectopic deposition of eggs in the spinal cord (S. mansoni or S. haematobium) or brain (S. japonicum) and inflammatory reactions, typically the formation of granulomas that act as space occupying lesions.

Treatment

Infections with all major Schistosoma species can be treated with praziquantel. The timing of treatment is important since praziquantel is most effective against the adult worm and requires the presence of a mature antibody response to the parasite. For travelers, treatment should be at least 6-8 weeks after last exposure to potentially contaminated freshwater. One study has suggested an effect of praziquantel on schistosome eggs lodged in tissues. Limited evidence of parasite resistance to praziquantel has been reported based on low cure rates in recently exposed or heavily infected populations; however, widespread clinical resistance has not occurred. Thus, praziquantel remains the drug of choice for  treatment of schistosomiasis. Host immune response differences may impact 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 to 4 weeks to increase effectiveness.  If the pre-treatment stool or urine examination was positive for schistosome eggs, follow up examinations at 1 to 2 months post-treatment is suggested to help confirm successful cure.

There is a lack of safety trial data for the use of praziquantel in children less than 4 years of age or pregnant women. However, this drug has been  distributed widely in mass drug administration programs and WHO now recommends that pregnant women should be treated as part of those campaigns based on extensive experience with the drug and review of the veterinary and human evidence.

Oxaminiquine, which has been used to treat S. mansoni infections in the past, is not commercially available in the United States and is no longer routinely used in other countries for treatment of schistosomiasis. More recently, artemesinin derivatives, either alone or in combination with praziquantel, have been shown to be effective against immature stages of S. mansoni, S. haematobium, and S. japonicum in laboratory studies and limited field studies. Further evaluation is needed to document effectiveness of artemisinin derivative monotherapy or combination therapy and possible impact on malaria control efforts.