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Examination of stool and/or urine for ova is the primary method 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.
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 portal hypertension.
S. haematobium eggs tend to lodge in the urinary tract causing damage that can lead to dysuria and hematuria. Chronic infections may increase the risk of bladder cancer. S. haematobium egg deposition has also been associated with damage to the female genital tract, causing female genital schistosomiasis that can affect the cervix, Fallopian tubes, and vagina and lead to increased susceptibility to other infections.
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.
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 examination at 1 to 2 months post-treatment is suggested to help confirm successful cure.
|Schistosoma species infection||Praziquantel dose and Duration|
|Schistosoma mansoni, S. haematobium, S. intercalatum||40 mg/kg per day orally in two divided doses for one day|
|S. japonicum, S. mekongi||60 mg/kg per day orally in three divided doses for one day|
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. Similarly, WHO reports that there is growing evidence that infected children as young as 1 year old can be effectively treated with praziquantel without serious side effects; however, the drug is commonly available in the form of large, hard-to-swallow pills, which puts young children at risk for choking and other difficulties swallowing the drug.
This information is provided as an informational resource for licensed health care providers as guidance only. It is not intended as a substitute for professional judgment.
Oral praziquantel is available for human use in the United States
Praziquantel is pregnancy category B. There are no adequate and well-controlled studies in pregnant women. However, the available evidence suggests no difference in adverse birth outcomes in the children of women who were accidentally treated with praziquantel during mass prevention campaigns compared with those who were not. In mass prevention campaigns for which the World Health Organization (WHO) has determined that the benefit of treatment outweighs the risk, WHO encourages the use of praziquantel in any stage of pregnancy. For individual patients in clinical settings, the risk of treatment in pregnant women who are known to have an infection needs to be balanced with the risk of disease progression in the absence of treatment.
Pregnancy Category B: Either animal-reproduction studies have not demonstrated a fetal risk but there are no controlled studies in pregnant women or animal-reproduction studies have shown an adverse effect (other than a decrease in fertility) that was not confirmed in controlled studies in women in the first trimester (and there is no evidence of a risk in later trimesters).
Praziquantel is excreted in low concentrations in human milk. According to WHO guidelines for mass prevention campaigns, the use of praziquantel during lactation is encouraged. For individual patients in clinical settings, praziquantel should be used in breast-feeding women only when the risk to the infant is outweighed by the risk of disease progress in the mother in the absence of treatment.
The safety of praziquantel in children aged less than 4 years has not been established. Many children younger than 4 years old have been treated without reported adverse effects in mass prevention campaigns and in studies of schistosomiasis. For individual patients in clinical settings, the risk of treatment of children younger than 4 years old who are known to have an infection needs to be balanced with the risk of disease progression in the absence of treatment.