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Pediatric Schistosomiasis Workup

  • Author: Vinod K Dhawan, MD, FACP, FRCPC, FIDSA; Chief Editor: Russell W Steele, MD  more...
Updated: Feb 26, 2015

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.[6]

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.[7]

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.[8]

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.[9] 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.[10] 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.[11] 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.[12] 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.

Contributor Information and Disclosures

Vinod K Dhawan, MD, FACP, FRCPC, FIDSA Professor, Department of Clinical Medicine, University of California, Los Angeles, David Geffen School of Medicine; Chief, Division of Infectious Diseases, Rancho Los Amigos National Rehabilitation Center

Vinod K Dhawan, MD, FACP, FRCPC, FIDSA is a member of the following medical societies: American College of Physicians, American Medical Association, American Society for Microbiology, Infectious Diseases Society of America, Royal College of Physicians and Surgeons of Canada

Disclosure: Received honoraria from Pfizer Inc for speaking and teaching.

Chief Editor

Russell W Steele, MD Clinical Professor, Tulane University School of Medicine; Staff Physician, Ochsner Clinic Foundation

Russell W Steele, MD is a member of the following medical societies: American Academy of Pediatrics, American Association of Immunologists, American Pediatric Society, American Society for Microbiology, Infectious Diseases Society of America, Louisiana State Medical Society, Pediatric Infectious Diseases Society, Society for Pediatric Research, Southern Medical Association

Disclosure: Nothing to disclose.


Leslie L Barton, MD Professor Emerita of Pediatrics, University of Arizona College of Medicine

Leslie L Barton, MD is a member of the following medical societies: American Academy of Pediatrics, Association of Pediatric Program Directors, Infectious Diseases Society of America, and Pediatric Infectious Diseases Society

Disclosure: Nothing to disclose.

Michael D Nissen, MBBS, FRACP, FRCPA, Associate Professor in Biomolecular, Biomedical Science & Health, Griffith University; Director of Infectious Diseases and Unit Head of Queensland Paediatric Infectious Laboratory, Sir Albert Sakzewski Viral Research Centre, Royal Children's Hospital

Michael D Nissen, MBBS, FRACP, FRCPA is a member of the following societies : American Academy of Pediatrics, American Society for Microbiology, Pediatric Infectious Diseases Society,Royal Australasian College of Physicians, Royal College of Pathologists of Australasia

Disclosure: Nothing to disclose.

Robert W Tolan Jr, MD Chief, Division of Allergy, Immunology and Infectious Diseases, The Children's Hospital at Saint Peter's University Hospital; Clinical Associate Professor of Pediatrics, Drexel University College of Medicine

Robert W Tolan Jr, MD is a member of the following medical societies: American Academy of Pediatrics, American Medical Association, American Society for Microbiology, American Society of Tropical Medicine and Hygiene, Infectious Diseases Society of America, Pediatric Infectious Diseases Society, Phi Beta Kappa, and Physicians for Social Responsibility

Disclosure: GlaxoSmithKline Honoraria Speaking and teaching; MedImmune Honoraria Speaking and teaching; Merck Honoraria Speaking and teaching; Sanofi Pasteur Honoraria Speaking and teaching; Baxter Healthcare Honoraria Speaking and teaching; Novartis Honoraria Speaking and teaching

John Charles Walker, MSc, PhD Head, Department of Parasitology, Center for Infectious Diseases and Microbiology, Westmead Hospital, Westmead, Australia; Senior Lecturer, Department of Medicine, University of Sydney, Australia

Disclosure: Nothing to disclose.

Mary L Windle, PharmD Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Nothing to disclose.

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Cercarial dermatitis secondary to avian schistosomes is shown. Photography taken by A. Joseph Bearup and provided by John Walker, MD.
Two 10-year-old boys with abdominal distension secondary to chronic Schistosoma japonicum infection.
CT scan of the brain reveals a right cerebral hemisphere lesion due to Schistosoma japonicum. The patient presented with focal motor seizures.
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 feces of a woman from Laos.
Egg of Schistosoma mansoni from a fecal smear.
Egg of Schistosoma haematobium from a fecal smear.
Eggs of Schistosoma japonicum within the intestinal mucosa.
Liver granulomata secondary to Schistosoma japonicum infestation.
Granuloma within the intestinal mucosa secondary to Schistosoma mansoni infestation.
Eggs of Schistosoma haematobium isolated from urinary sediment.
Eggs of Schistosoma haematobium detected in the bladder.
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