Pediatric Schistosomiasis 

Updated: Dec 15, 2020
Author: Vinod K Dhawan, MD, FACP, FRCPC, FIDSA; Chief Editor: Russell W Steele, MD 



Pediatric schistosomiasis is principally caused by one of the following 6 species of parasitic worms:

  • Schistosoma haematobium

  • Schistosoma intercalatum

  • Schistosoma japonicum

  • Schistosoma malayensis

  • Schistosoma mansoni

  • Schistosoma mekongi

Other species of animal schistosomes cause human infection, including schistosomes of birds and small mammals that cannot mature in the human host but die in the skin where they cause dermatitis.

Schistosomes are blood flukes and belong to the class Trematoda. Unlike other trematodes, schistosomes are elongated but become round as they adapt to residing in blood vessels of the genitourinary or gastrointestinal (GI) tract. They require a vertebrate and an intermediate water-dwelling snail host to complete their life cycle. Geographic distribution and maintenance of human infection by schistosomes depends on and is limited by the presence of a suitable snail host.

Clinical features of human schistosomiasis depend on the species, developmental stage, and site of infection in the body. Schistosomiasis comprises the following 3 major syndromes:

  • Cercarial dermatitis

  • Acute schistosomiasis or Katayama fever

  • Chronic fibro-obstructive disease


Schistosomes are digenetic, which means that mature adult worms reproduce sexually in the definitive human host with asexual reproduction in the larval forms (common to all trematodes or flukes). They are also diecious, which means that adults are sexually distinct and that male and female genitals do not occur within the same individual (a characteristic that separates them from other flukes).

Life cycle of human schistosomes

The life cycle of schistosomes differs from that of other trematodes in that humans become infected through penetration of the skin by cercariae rather than through oral ingestion. Human schistosomes can infect other vertebrates and provide an animal reservoir of infection, though this is of epidemiologic significance only for S japonicum and, possibly, S mekongi. Snails of the genera Biomphalaria, Bulinus, Neotricula, and Oncomelania are the principal intermediate hosts for S mansoni, S haematobium, S mekongi, and S japonicum, respectively.

Once cercariae have entered the human body through the skin, they are referred to as schistosomula. These organisms migrate through the tissues to invade blood vessels. They are transported to the lungs and then to the liver, where they mature into adult worms within 6 weeks before descending to their final positions in the venous circulation.

Adult S haematobium organisms are mostly found in the venous plexuses of the bladder, prostate, and uterus, whereas adult S intercalatum, S japonicum, S mansoni, and S mekongi organisms are observed in the portal, inferior, and superior mesenteric veins. The maturity of female worms depends on the presence of a mature male because the 2 worms are paired, with the female lying enclosed within a groove formed by the male.

Adult worms have a mean life span of 5-10 years, with females releasing 300-3000 eggs per day. Eggs are deposited in the terminal venules of the bladder (S haematobium), intestine, and rectum (S intercalatum, S japonicum, S mansoni, and S mekongi), where they mature over the next 10 days into a larval form known as a miracidium. The miracidium releases proteolytic enzymes, which facilitate larval movement through the tissues into either the genitourinary tract or the GI tract.

Schistosome eggs contain spines in various positions, depending on the species (see the images below). Eggs are passed in human urine and excrement, and motile miracidia are released upon contact with fresh water. Miracidia then actively seek out snail hosts, in which they develop first into mother and daughter sporocysts by asexual division and then into cercariae over 4-6 weeks. Cercariae then leave the snail and penetrate the human skin on contact, with the assistance of their glandular secretions.

Egg of Schistosoma japonicum from a fecal smear is Egg of Schistosoma japonicum from a fecal smear is shown. Note lateral umbilicated spine on the right side of the egg.
Egg of Schistosoma mekongi (53 X 45 μm) in the fec Egg of Schistosoma mekongi (53 X 45 μm) in the feces of a woman from Laos.
Egg of Schistosoma mansoni from a fecal smear. Egg of Schistosoma mansoni from a fecal smear.
Egg of Schistosoma haematobium from a fecal smear. Egg of Schistosoma haematobium from a fecal smear.
Eggs of Schistosoma japonicum within the intestina Eggs of Schistosoma japonicum within the intestinal mucosa.
Eggs of Schistosoma haematobium isolated from urin Eggs of Schistosoma haematobium isolated from urinary sediment.
Eggs of Schistosoma haematobium detected in the bl Eggs of Schistosoma haematobium detected in the bladder.

Immune response and granuloma formation

Not all schistosome eggs are excreted from the body. As many as 50% can embolize to other body areas, leading to a host immune reaction and granuloma formation (see the images below). Granulomas begin to form with maturation of the miracidium at 6 days and are focal within 2 weeks. The most common sites are the liver for S intercalatum, S japonicum, and S mansoni and the bladder for S haematobium. Other areas less commonly affected include the lungs, central nervous system (CNS), and kidneys.

Liver granulomata secondary to Schistosoma japonic Liver granulomata secondary to Schistosoma japonicum infestation.
Granuloma within the intestinal mucosa secondary t Granuloma within the intestinal mucosa secondary to Schistosoma mansoni infestation.

The immune response to schistosomiasis is highly regulated and of the delayed hypersensitivity type, including type 1 (Th1) and type 2 (Th2) helper T cell responses with local cytokine production. Granulomata are notable for the presence of eosinophils and lead to the development of widespread collagen deposition and scar tissue. This causes major lesions of chronic schistosomiasis with blood flow obstruction in affected tissues.

Human skin appears to be a critical site where the initial events of the host and parasite interaction occur and where the immune response is commenced. Induction and modulation of granuloma formation is under the control of clones of CD4 and CD8 T cells. Cytokines produced in response to the parasite, such as interleukin (IL)–7 in the skin and interferon-gamma (IFN-γ) in the liver, also seem to influence the development of schistosomal immunity.


The diagnosis of schistosomiasis should be considered in any individuals who have resided in endemic areas with significant freshwater contact.

S mekongi is thought to be the principal human schistosome pathogen of Cambodia and Laos. It has smaller eggs than S japonicum does, as well as a different intermediate snail host (Neotricula aperta). Hepatosplenomegaly, portal hypertension, or both are the main clinical findings in infected individuals.

S intercalatum (localized to West and Central Africa) is of less epidemiologic importance in these regions than S haematobium and S mansoni are. Observed symptoms include abdominal pain and bloody diarrhea.

Cercarial dermatitis is more commonly observed in human infection with avian schistosomes, cercarial demise, and immediate hypersensitivity reactions occurring at skin invasion sites.

Katayama fever occurs with the onset of egg production. The syndrome includes lymphadenopathy and diarrhea, with symptoms and signs similar to those of a serum sickness reaction. Katayama fever is commonly associated with S japonicum infection and is probably due to the larger number of eggs released by this species. It is less common with S mansoni infestation and is rare with S haematobium. Onset of symptoms is 20-40 days after exposure, and temperatures may reach 105°F. Fevers spontaneously subside 2-10 weeks after onset.

During infection by S haematobium, eggs are deposited in the mucosa and submucosa of the bladder and lower ureters. Granulomas are highly cellular and form intraluminal polyploidal lesions that can lead to hydronephrosis. Lesions tend to necrotize, ulcerate, and bleed.

With age, the lesions become acellular, fibrose, and calcify and are termed sandy patches. Calcification may lead to bladder deformation, ureteric obstruction, secondary infections, hydronephrosis, chronic pyelonephritis, and renal failure. Carcinoma of the bladder is a long-term sequela of chronic infection.

In acute schistosomiasis, the enlarged liver and spleen are initially soft as a result of passive venous congestion and granuloma cellular proliferation. In chronic disease, the liver and spleen remain large, nodular, and nontender. Stigmata of liver disease and cirrhosis (eg, ascites, spider nevi, peripheral edema, testicular atrophy, and feminization) are usually absent. However, a small number of patients decompensate and show the above signs of chronic liver disease.

Focal epilepsy is secondary to a localized brain granuloma or generalized encephalopathy. It constitutes 3% of the complications of chronic disease. In transverse myelitis, spinal cord lesions are the result of the retrograde flow of eggs and granuloma formation in either S mansoni or S haematobium infection.

Pulmonary involvement (ie, cor pulmonale) is most commonly observed with S haematobium infection because ectopic egg deposition can occur more readily from the vesical plexus to the lungs via the inferior vena cava, bypassing the liver. Pulmonary complications with S japonicum and S mansoni are usually observed only after the development of collateral circulation secondary to severe hepatosplenic disease.[1]


United States statistics

The prevalence of schistosomiasis in the United States has been estimated to exceed 400,000 persons, principally as a consequence of immigration from endemic areas. Transmission of the disease cannot occur in the United States, because of the lack of suitable snail hosts. Epidemics of acute schistosomiasis have been reported in Americans traveling in or returning from endemic areas.[2] Cercarial dermatitis due to avian schistosomes has been reported in the Great Lakes region of the United States.

International statistics

Worldwide, human schistosomes currently infect more than 200 million people in 74 countries, including the endemic areas of Africa, the Caribbean, Central America, South America, East Asia, and the Middle East.[3, 4] The prevalence of schistosomiasis is thought to be increasing. A meta-analysis found that more than 4 million school-aged children in Zambia have schistosomiasis. The disease primarily affects those living in rural communities, owing to unsafe water and inadequate sanitation facilities.[5]

The most severely affected countries in Africa include Angola, Chad, Congo, Egypt, Ghana, Kenya, Madagascar, Malawi, Mali, Mozambique, Nigeria, Senegal, Sudan, Tanzania, Uganda, Zambia, and Zimbabwe. Yemen has the most infected people in the Middle East. Brazil is the most severely affected country in the Americas, with 25 million people living in endemic areas and an estimated 3 million infected.

S mansoni is found in 54 countries, including the Arabian Peninsula (especially Yemen), Egypt, Libya, Mauritania, Somalia, Sudan, sub-Saharan Africa, Brazil, the Caribbean (except Antigua, Guadeloupe, Martinique, Montserrat, and St. Lucia), Suriname, and Venezuela.

S haematobium is endemic in 53 countries in the Middle East and most of the African continent, including the islands of Madagascar and Mauritius. The infection is unlikely to be of public health significance in Lebanon, Mauritius, Oman, Syria, Tunisia, and Turkey, because transmission is low or nonexistent. A disputed and ill-defined focus is noted in India and requires further confirmation.

S japonicum is endemic in China, the Sulawesi province of Indonesia, and the Philippines. China is the most severely affected country, with an estimated 900,000 people infected. The parasite has been eradicated from Japan since 1982.

S intercalatum has been reported in 10 countries in central and western Africa. S mekongi is confined to Cambodia and Laos, where the borders run along the Mekong River. Neotricula snails have been reported in southern China, but S mekongi has not been reported in these areas. S malayensis has been reported among aboriginal people in a small jungle focus in Malaysia.

Age-related demographics

People of all ages are susceptible. Immune responses are heightened and more intense with secondary and subsequent exposures to schistosome cercariae. Surveys in endemic areas have demonstrated that severity and prevalence of infection takes several years to peak in children and that both decrease with age.

Most manifestations of disease occur in the second decade of life, apparently related to peak egg output. Evidence points to a partial and acquired immunity to schistosomes that is determined by specific antibodies and eosinophils, and the immunity targets immature adult worms.

Sex-related demographics

The 2 sexes are equally susceptible to schistosomiasis. Because of different local and cultural work and social practices, either sex may be more exposed to infection.


Cure rates for oral medical treatment range from 70-100%, depending on the drug used. Mortality from human schistosomiasis is related to complications of fibro-occlusive disease (secondary to the immune stimulus of schistosome eggs) and end-organ damage.

The morbidity of schistosomiasis correlates well with the worm burden as calculated by fecal and urinary egg counts. The disease significantly disrupts the nutritional status and growth from middle childhood to adolescence. Prevalence of infection in endemic communities demonstrates a negative binomial distribution, with most infected individuals having low worm burdens and only a small percentage with heavy infestations.

A possible genetic link has been observed between human leukocyte antigen (HLA) antigens and the occurrence of end-stage liver disease in S japonicum and S mansoni infections.




Symptoms of schistosomiasis depend on the species of the schistosome and the stage of disease. Most infected individuals are asymptomatic or have only mild nonspecific symptoms. Only 5-10% of infected individuals develop severe clinical symptoms, which are usually associated with heavy infestations.

Edema and pruritus are symptoms of cercarial dermatitis and are rarely observed in primary exposure (see the image below).

Cercarial dermatitis secondary to avian schistosom Cercarial dermatitis secondary to avian schistosomes is shown. Photography taken by A. Joseph Bearup and provided by John Walker, MD.

High fever or Katayama fever is described in heavy primary infections. Nausea is observed in acute schistosomiasis and at the onset of fevers. Vomiting may be experienced in acute schistosomiasis. Generalized lymphadenopathy is described as part of the Katayama fever syndrome. Profuse diarrhea or dysentery is associated with Katayama fever.

Hematemesis or melena is the usual presenting symptom of chronic schistosomiasis due to S japonicum and S mansoni. Abdominal pain may be observed with acute and chronic schistosomiasis secondary to liver and splenic enlargement (see following image).

Two 10-year-old boys with abdominal distension sec Two 10-year-old boys with abdominal distension secondary to chronic Schistosoma japonicum infection.

Urticaria may occur with cercarial dermatitis or may be more extensive, affecting large body areas in acute schistosomiasis. Malaise, generalized fatigue, and weakness are sometimes observed with acute schistosomiasis.

Focal epilepsy is a recognized complication of chronic S japonicum infection in East Asia (see the image below). Spinal cord lesions due to S mansoni or S haematobium can cause a myelopathy.

CT scan of the brain reveals a right cerebral hemi CT scan of the brain reveals a right cerebral hemisphere lesion due to Schistosoma japonicum. The patient presented with focal motor seizures.

A dry cough (with or without hemoptysis) secondary to inflammation in the lungs can be experienced in acute schistosomiasis and is associated with migration of schistosomula through the lungs. Cough is also a symptom of cor pulmonale resulting from chronic pulmonary schistosomiasis. The subsequent pulmonary hypertension may lead to hemoptysis.

Palpitations may be felt as a complication of cor pulmonale in chronic pulmonary schistosomiasis. Shortness of breath may be observed in both acute and chronic pulmonary schistosomiasis as a result of cor pulmonale in chronic cases. Acute pulmonary symptoms of cough and dyspnea may occur 3-6 weeks after exposure and occur without fever.

Weight loss may be experienced as a consequence of vomiting and profuse diarrhea.

Urinary frequency is regularly associated with acute S haematobium infection. Dysuria is a common feature of acute S haematobium infection. Terminal hematuria is also a regular presenting symptom for S haematobium infection or bilharzia. Referred suprapubic or perineal pain may be associated with S haematobium infection.

Physical Examination

Physical findings vary with the species and the stage of the disease.

Urticaria may be observed in cases with cercarial dermatitis or acute schistosomiasis with Katayama fever. Papular lesions may develop from cercarial dermatitis and remain for 5-7 days and up to 10 days after water exposure. However, this is more often observed with avian schistosomiasis.

General enlargement of lymph nodes may be detected in acute schistosomiasis with Katayama fever.

Areas of moist crackles may be heard over both lung fields in acute schistosomiasis.

Hepatosplenomegaly is often detected in acute and chronic schistosomiasis with S japonicum and S mansoni. Jaundice is a rare clinical finding. Purpura resulting from thrombocytopenia is observed with hypersplenism.

Hematuria with S haematobium typically progresses from microscopic to frank bloody urine as the bladder mucosa ulcerates.

A transverse myelitislike syndrome may be observed with S mansoni or S haematobium disease. Focal neurologic deficits may be found due to cerebral granulomas in cases with seizures and chronic S japonicum infection.

Clinical signs of right ventricular hypertrophy are observed in cases with cor pulmonale and chronic schistosomiasis. This includes palpable sternal heave and increased and delayed pulmonary second heart sound.


Possible complications of schistosomiasis include fibro-occlusive disease secondary to the immune stimulus of schistosome eggs, end-organ damage, end-stage liver disease, and others.

Possible complications of female genital schistosomiasis (defined as the presence of schistosome eggs or worms in the upper or lower genital tract) include hypogonadism, retarded puberty, infertility (primary and secondary), ectopic and tubal pregnancy, tubal abortion, hemoperitoneum, anemia due to chronic blood loss, metaplasia, miscarriage and preterm delivery, carcinoma, increased risk for sexually transmitted diseases, destruction of the hymen or clitoris, and vesicovaginal fistula.

Persistent bacteremia with Salmonella typhi and other Salmonella species has been reported in persons chronically infected with S mansoni, S japonicum, S intercalatum, and S haematobium. Chronic Salmonella bacteria may be noted in patients infected with S haematobium.

Immune complexes formed in response to schistosomal infection may be deposited on glomerular capillaries and renal basement membranes, leading to mesangioproliferative glomerulonephritis, nephrosclerosis, and renal failure. The severity of renal disease is related to the worm burden and to the extent and duration of hepatic fibrosis and collateral circulations.

Schistosomiasis has been associated with high HIV viral loads and a theoretical risk of increased progression of HIV disease.[6]



Diagnostic Considerations

Potentially serious asymptomatic infections are common in travelers returning to developed countries. A detailed freshwater exposure history, symptom history, and physical examination may add little in detecting cases. Stool microscopy, schistosomal serology, and the eosinophil count tend to be the best tools for evaluating suspected disease.

Patients with schistosomiasis are, by default, at risk for other parasitic infections because areas that are endemic for schistosomiasis are also endemic for other parasites. After treatment, patients should be monitored for other symptomatology characteristic of parasitic infections.

In addition to the conditions listed in the differential diagnosis, other problems to be considered include the following:

  • Bacterial or viral gastrointestinal (GI) infection in the acute presentation

  • Idiopathic epilepsy

  • Postinfectious viral transverse myelitis

  • Congenital hydronephrosis

  • Congenital heart disease and cor pulmonale

  • Renal disease

Differential Diagnoses



Laboratory Studies

Definitive diagnosis of schistosomiasis depends on detection of specific schistosome eggs excreted in stool and urine. This occurs from 5-13 weeks after infection and is determined by worm burden. Blood and urine studies may be helpful. Hepatitis screening is indicated in some cases.

A study that assessed genome-wide identification of diagnostic protein markers for schistosome infection found that the application of this sensitive, specific, and affordable rSP13-ELISA method should help reduce schistosomiasis transmission through targeted treatment of individuals, particularly with low intensity infections, and therefore support schistosomiasis control and elimination strategies.[7]

Egg detection

For detection of schistosome eggs, thick smears of feces, nucleopore filtration of urine, and formalin-ether concentration techniques for stool or urine are recommended. Collection of urine is usually recommended between noon and 2:00 PM, when excretion of ova is greatest.

Multiple examinations may be required in light or chronic infections. If infections are active, schistosome eggs contain live and mature miracidia. Studies suggest that adult HIV-1–related immunodeficiency does not impair the ability to excrete eggs in low-intensity infection with S haematobium, S mansoni, or both and that infection with HIV-1 may not have major implications for diagnosis and surveillance of schistosomiasis.

Do not attempt detection of schistosome eggs in feces or urine until after the incubation period of the infection, which is usually 3 months since the last known freshwater contact.

Blood and urine studies

Eosinophilia is prominent in acute schistosomiasis. The complete blood count (CBC) may reveal thrombocytopenia, anemia, or prolonged prothrombin times in severe chronic schistosomiasis.

Hematuria is common with S haematobium infections, and screening for blood in urine with dipsticks may be useful in diagnosing this disease in endemic areas.

Serum bilirubin and transaminase levels are usually within the reference range or only mildly elevated. Hyperglobulinemia may be evident in chronic schistosomiasis.

Serologic tests for antibodies to schistosomes are available at some reference laboratories, including the Centers for Disease Control and Prevention (CDC). Serologic tests cannot distinguish active from past infections.

The CDC uses a combination of tests with purified adult worm antigens. The Falcon assay screening test enzyme-linked immunosorbent assay (FAST-ELISA) is 99% specific for all species and has a sensitivity of 99% for S mansoni, 95% for S haematobium, and 50% for S japonicum. Because of false negative results with the FAST-ELISA, immunoblots using species-specific antigens are performed in cases of potential exposure to S haematobium and S japonicum infections.[8]

Hepatitis screening

In some endemic areas, S japonicum, S mansoni, and viral hepatitis are the most common causes of chronic liver disease. The hepatitis B surface antigen (HBsAg) carrier state has been noted to be 4 times higher in patients with schistosomiasis; the significance of this finding is uncertain. Different explanations have been proposed for the association of S mansoni with hepatitis B, including the following:

  • Impaired cell-mediated immunity, which reduces host resistance

  • Low socioeconomic conditions and educational levels, which increase the risk of exposure

  • Repeated treatments in the past with intravenous (IV) or parenteral drugs or blood transfusions

Patients with coexisting hepatitis C virus (HCV) and hepatic schistosomiasis have more advanced liver disease, higher HCV titers, predominance of HCV genotype 4, higher histologic activity, and higher frequency of cirrhosis and hepatocellular carcinoma.[9]

Culture and skin testing

Routine cultures of feces and urine exclude common infections of the gastrointestinal (GI) and genitourinary tracts. Cultures of blood may reveal Salmonella species or other pathogens that explain persisting fevers.

Crude antigenic extracts of schistosomes and eggs are used in skin testing. The sensitivity and specificity are poor and provide no indication of the intensity of infection.

Radiography, CT, Ultrasonography, and MRI

In both acute and chronic disease, abnormalities may be detected on chest radiography, including findings ranging from multiple nodules to diffuse interstitial infiltrates. Computed tomography (CT) may be helpful in the evaluation of pulmonary disease.[10] Head, chest, abdominal, and spinal CT scanning or magnetic resonance imaging (MRI) is useful in viewing granulomas of the brain, lungs, liver, or spinal cord; if granulomas are present, they are revealed as ring-enhancing lesions with contrast studies.

Ultrasonography is well established for the staging of schistosomiasis-related solid organ pathology and is especially useful in monitoring its status after chemotherapy or cessation of exposure to schistosomes.[11] Ultrasonographic changes in acute schistosomiasis are nonspecific and include hepatosplenomegaly and enlarged abdominal or perihilar lymph nodes. Ultrasonography for the assessment of urinary schistosomiasis has also been validated with concurrent cystography, pyelography, and CT scanning.

IV pyelography and voiding cystourethrography may reveal hydronephrosis, bladder calcification, and filling defects.

Endoscopy and Biopsy

Endoscopy, bronchoscopy, and sigmoidoscopy or colonoscopy may be indicated.[12] Esophageal varices are often present in patients with hematemesis and/or melena. They are visualized with barium swallow or endoscopy. Cystoscopy for S haematobium reveals bleeding mucosal points, ulcers, and polyps in acute cases and calcified patches in chronic disease.

Eggs incite a granulomatous response in the small intestine and colon, causing inflammation and edema of the mucosa with papular lesions, small hemorrhages, and ulcers. A diffuse transmural fibrosis occurs with continued oviposition.

Liver biopsy is not usually indicated unless schistosomal eggs are undetected or the diagnosis is unclear. Rectal biopsy is useful in cases with light, chronic, or inactive infections. It is also beneficial in assessing the response to chemotherapy.

Bronchoscopy with transbronchial biopsy may be used to detect an eosinophilic pneumonitis if diffuse chest radiography findings are observed.

Laparoscopy in patients with chronic S japonica may reveal yellowish small speckles sparsely clustered over the liver surface; these correspond to subcapsular calcified ova of S japonica.[13] These areas correspond with abnormalities observed on ultrasonography, CT scanning, and histology.

Histologic Findings

Histology of liver biopsies is unique for schistosomiasis. Hepatic granulomas and thrombophlebitis destroy hepatic radicals of the portal system but are replaced by newly formed thinner blood vessels. This process maintains normal blood flow but contributes to portal hypertension.

A progressive increase in fibrous tissue eventually surrounds and compresses the hepatic venules. Portal vascular and fibrotic changes lead to a pipestem fibrosis appearance, which differs from other forms of cirrhotic liver disease. Hepatocyte damage and necrosis are rare but may be observed in severe cases of chronic schistosomiasis.


Determination of the severity of schistosomiasis and disease staging are accomplished through combining the investigations described above, including includes serology, abdominal and perihilar ultrasonography, body CT scanning, endoscopy, cystoscopy, laparoscopy, and histology.

Changes detected on ultrasonographic studies in acute schistosomiasis (Katayama fever) include focal liver hypoechogenicities that may reflect secondary abscess formation with bacterial superinfection, pleural effusions, and pericardial effusions. Enlarged lymph nodes may reveal an echodense center surrounded by an echopolar halo.

With mild schistosomiasis, laparoscopy reveals that the liver surface is mostly smooth, although multiple whitish markings and irregular wide grooves are observed with more advanced disease.

With chronic schistosomiasis, ultrasonographic features are characteristic and include echogenic thickening of the walls of portal branches and of the portal vein, which frequently extends to the gall bladder and ligamenta.

With moderate schistosomiasis, ultrasonography reveals areas of high echogenicity, and CT scanning reveals network patterns and lineal calcified spots.

With severe schistosomiasis, laparoscopy reveals a liver surface distorted with blocklike formations of variable size separated by grooved depressions, which yields a turtle shell–like appearance. Ultrasonography reveals areas of high echogenicity, and CT scanning reveals network patterns and lineal calcified spots.



Approach Considerations

Praziquantel is currently the main antischistosomal agent. Other oral agents are oxamniquine and metrifonate, but these have limited parasite specificity. Artemether appears to be beneficial in some settings.

Surgery may be necessary in severe or chronic schistosomiasis. Patients who have chronic liver disease or are experiencing further episodes of gastrointestinal (GI) bleeding or bacterial sepsis should be admitted for further inpatient care.

No special diet is required for acute disease. Individuals with chronic liver disease may benefit from a high-protein, low-salt diet. Limit activity for patients with acute GI bleeding or severe thrombocytopenia.

As a preventive measure, patients should be advised to avoid further freshwater contact in endemic areas if possible. An improved understanding of the immune response to schistosome infection suggests that development of a vaccine may be possible in the future.[14]

Pharmacologic Therapy

Praziquantel remains the drug of choice for treating all species of schistosomes.[15, 16] Typical dosages are 20 mg/kg orally twice daily on day 1 for S haematobium, S intercalatum,andS mansoni and 20 mg/kg orally 3 times daily on day 1 for S japonicumandS mekongi. Cure rates range from 65-90% after a single treatment.[17] Egg excretion is reduced by more than 90% in persons not cured.

Praziquantel appears to be safe during pregnancy, as demonstrated in a prospective study carried out in eastern Sudan involving 25 pregnant women with S mansoni infection.[18] The drug was given to 6 (24%), 12 (48%), and 7 (28%) of the women during the first, second, and third trimesters of their pregnancies, respectively. No stillbirths or congenital abnormalities were reported among the newborns. One patient aborted (3 weeks after treatment), but this rate of abortion was considered typical in the local community.

Patients should be monitored during therapy for any seizures or other neurologic consequences of dying cysticerci. Corticosteroid therapy has been used to reduce inflammation and mitigate reactions that develop in response to killing the parasites. Maturing schistosomes are less susceptible to chemotherapy than adult worms; therefore, a second course of therapy should be given several weeks after the first.

Oxamniquine has been used for treatment of S mansoni infections with equally good results, but this agent is no longer available in the United States.

Metrifonate is effective only against urinary schistosomes; it requires 3 doses administered 2 weeks apart and is not currently available in the United States.

Artemether can kill schistosomula during the first 3 weeks of infection and has been shown to be effective for prophylaxis in areas of high endemicity. Used as an antimalarial, artemether is also active against schistosome parasites (mainly schistosomula). Trials involving the combination of artemether and praziquantel show beneficial effect.

Surgical Management of Associated Conditions

Surgery may be necessary in severe or chronic schistosomiasis. Procedures that may be indicated include the following:

  • Resection of bladder and colonic polyps

  • Correction of obstructive uropathy

  • Partial colectomy for GI polyposis and fibrosis

  • Placement of a distal splenorenal shunt for reversal of portal hypertension

  • Resection of cerebral cortical granulomas after failure of chemotherapy


Consultations may be indicated with the following specialists:

  • Infectious diseases specialist

  • Gastroenterologist

  • General surgeon

  • Nephrologist

  • Neurologist

  • Neurosurgeon

  • Urologist

Long-Term Monitoring

Patients who have been treated with antischistosomal chemotherapy should be monitored for treatment effectiveness. Stool and urine samples should be examined for 1 year after therapy. Successful therapy results in decreased in egg excretion.

Newer tests that measure antigens may help assess therapeutic response. Persistent circulating antigen and continued excretion of eggs indicate residual infection and the need for retreatment with praziquantel.

It should be kept in mind that serologic tests may remain positive for several years after successful treatment and thus may not be helpful as a test of cure.



Medication Summary

Praziquantel (a pyrazinoquinolone) has become the main antischistosomal agent because it is effective against all human pathogens and is well tolerated orally. Other oral compounds available are oxamniquine (a nitroquinolone that is no longer available in the United States) and metrifonate (an organophosphorus cholinesterase inhibitor that is also unavailable in the United States), but these have limited parasite specificity.


Class Summary

Parasite biochemical pathways are different from those of the human host; thus, toxicity is directed to the parasite, egg, or larvae. The mechanism of action varies within the drug class. Antiparasitic actions may include the following:

- Inhibition of microtubules, causing irreversible block of glucose uptake

- Tubulin polymerization inhibition

- Depolarizing neuromuscular blockade

- Cholinesterase inhibition

- Increased cell membrane permeability, resulting in intracellular calcium loss

- Vacuolization of the schistosome tegument

- Increased cell membrane permeability to chloride ions via chloride-channel alteration

Praziquantel (Biltricide)

Animal studies report that praziquantel induces rapid contraction of schistosomes by exerting a specific effect on the permeability of the cell membrane. The drug further causes vacuolization and disintegration of the schistosomal tegument. It has a more marked effect on adult worms than on young worms. After oral administration, praziquantel is rapidly absorbed (80%). It is subject to a first-pass effect and extensive metabolism.


Oxamniquine is no longer available in the United States. It is active only against S mansoni. Oxamniquine is effective in disintegrating the schistosome tegument to which phagocytes attach, causing death.

The drug is well absorbed and is metabolized extensively to inactive metabolites that, in turn, are excreted in urine. The plasma half-life is approximately 1-2.5 hours, and a peak in drug concentrations is usually reached in 1-1.5 hours after oral administration.


Metrifonate, an organophosphate derivative with anthelmintic and anticholinesterase activity, is not available in the United States. It is used as an alternative to praziquantel for treatment of S haematobium infections; it is not effective for S japonicum or S mansoni infections. The drug is well absorbed from the gastrointestinal (GI) tract, with peak levels occurring 1 hour after administration.