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Schistosomiasis: Diagnosis

Schistosomiasis: Diagnosis
Literature review current through: Jan 2024.
This topic last updated: Apr 03, 2023.

INTRODUCTION — Schistosomiasis is a disease caused by infection with parasitic blood flukes. The three major species are Schistosoma japonicum (East Asia), Schistosoma mansoni (Africa and South America), and Schistosoma haematobium (Africa and the Middle East). The two minor species are Schistosoma mekongi (Laos, Cambodia) and, within the Schistosoma haematobium group, Schistosoma intercalatum and Schistosoma guinéensis (West and Central Africa).

Genomic analysis has highlighted the importance of human infections with hybrids of the S. haematobium group with cattle schistosomes (Schistosoma bovis, Schistosoma mattheei, Schistosoma curassoni) and of introgressive gene transfer between species [1].

The parasites that cause schistosomiasis live in certain types of freshwater snails that are species-specific. Oncomelania spp snails host S. japonicum and Biomphalaria spp snails host S. mansoni, both causing intestinal (and liver) schistosomiasis. Bulinus spp are intermediate hosts for S. haematobium complex species, causing predominantly urogenital schistosomiasis. Emergence of cercariae (the infectious form of the parasite) from the snail leads to contamination of the water. Individuals can become infected when skin comes in contact with contaminated water and is penetrated by cercariae.

The diagnosis of schistosomiasis will be reviewed here. The epidemiology, pathogenesis, clinical features, treatment, and prevention of these infections are discussed separately. (See "Schistosomiasis: Epidemiology and clinical manifestations" and "Schistosomiasis: Treatment and prevention".)

DIAGNOSIS

Clinical approach

General principles — Schistosomiasis is diagnosed most frequently in asymptomatic individuals following exposure during travel to or residence in endemic areas. Antibody or antigen testing is the mainstay of diagnosis in this group.

Some individuals present with acute symptoms after primary recent exposure (“Katayama syndrome”), or chronic symptoms (eg, hematuria, hepatic fibrosis) that require a more specific diagnostic workup.

Neurologic complications are rare but require early diagnostic confirmation to guide appropriate management.

Asymptomatic screening — Screening for schistosomiasis may be pursued for asymptomatic individuals with freshwater exposure in endemic regions. This includes travelers as well as individuals with current or prior residence in an endemic area; the approach differs for each of these groups [2-8]:

Among travelers and migrants, the preferred screening tool is detection of schistosome antibodies in serum, since the parasite burden in these individuals is generally low. Serum antibody tests cannot distinguish ongoing from past infection nor measure the parasite burden. Serum antibody detection is much more sensitive than egg detection by microscopy or antigen detection in urine [8-10].

For individuals with a positive serum antibody screening test, subsequent evaluation consists of microscopy for detection of schistosome ova in urine and/or stool; this is important to demonstrate whether active infection is present, and if so, to establish the infective species and the parasite burden.  

In a retrospective study including 1020 cases of schistosomiasis among travelers and migrants, all cases were diagnosed by serology or microscopy; indirect tests such as urine dipstick test for hematuria and a serum white blood cell differential count for eosinophilia had low sensitivity. Schistosome ova were found in 25 percent of patients, with S. haematobium being the predominant species [10].

Among individuals in endemic areas, urinalysis for detection of circulating antigen released by adult schistosomes is becoming the standard (semi)quantitative screening method.

Symptomatic individuals — Diagnostic evaluation is warranted for patients with clinical manifestations suggestive of schistosomiasis in the setting of relevant epidemiologic exposure. (See "Schistosomiasis: Epidemiology and clinical manifestations".).

Among symptomatic individuals with symptoms of longstanding infection, schistosome serum antibody tests are a sensitive initial test. The parasite burden should be determined by microscopy for egg detection in feces and in urine, and if available, by schistosome circulating antigen (circulating anodic antigen [CCA], circulating cathodic antigen [CAA]) detection in urine or serum. The infecting species can be determined via microscopy and also by molecular tests (polymerase chain reaction [PCR]).

In the setting of early infection (<3 months), sensitivity of serum antibody tests and microscopy is low.

If microscopy is not diagnostic and suspicion for schistosomiasis persists, molecular testing using PCR to demonstrate schistosome DNA in serum, stool, and urine may be used; these are more sensitive than microscopy in the setting of early infection with low parasite burden (<3 months). Serum testing for schistosome circulating antigen (CAA, CCA) has comparable sensitivity but thus far is not commercially available.

Neuroschistosomiasis — Neuroschistosomiasis develops as a result of embolization of adult worms to the spinal cord or cerebral microcirculation, with subsequent release of eggs leading to an intense inflammatory reaction with local tissue destruction and scarring. It can cause cerebral disease or myelopathy; the latter is more common. Clinical manifestations are discussed further separately. (See "Schistosomiasis: Epidemiology and clinical manifestations", section on 'Neuroschistosomiasis'.)

The diagnosis of neuroschistosomiasis requires laboratory detection of infection at an extraneural site (as described above) together with clinical and radiographic evidence of neurologic involvement. Alternatively, neuroschistosomiasis may be diagnosed via direct evidence of central nervous system (CNS) infection such as biopsy of a CNS lesion and/or a positive antibody titer or PCR in the cerebrospinal fluid [11].

Computed tomography and magnetic resonance imaging (MRI) of the brain generally demonstrate nonspecific contrast-enhancing infiltrates suggestive of tumors; a characteristic arborization pattern has occasionally been described (image 1) [12-16]. MRI of the spine may demonstrate extradural or intramyelitic lesions; the findings are not specific and include increased volume of medullar cone, linear radicular thickening, or a nodular (often pseudotumoral) appearance [17].

Histopathology of CNS lesions typically demonstrates granuloma formation around eggs embedded in the affected tissue [16].

Diagnostic tools

Laboratory tests — The diagnosis of schistosomiasis requires detection of infection; some assays also measure parasite burden. Diagnostic tools include direct assays (demonstration of eggs in the stool or urine via microscopy, or demonstration of schistosome antigen or DNA in the blood, urine, and/or stool) and indirect assays (demonstration of antibody in blood via serology) (table 1) [18]. Antigen tests use CAA and CCA excreted in urine or detected in a blood sample.

Species diagnosis is mainly based on egg morphology by microscopy; the egg of each species has a characteristic shape (picture 1). Laboratory diagnosis lacks sensitivity in the setting of early infection and/or low-grade infection. More sensitive tests are needed to demonstrate active infection in strategies to eliminate of schistosomiasis in endemic regions.

Use of genomic tests targeting schistosome DNA sequences in a blood sample (PCR) enables species-specific diagnosis even in the absence of excreted eggs [19,20].

Microscopy — Identification of schistosome eggs in a stool or urine sample via microscopy remains the standard technique for diagnosis of active schistosomiasis. Microscopy can also be used for species identification and to measure the parasite burden (picture 1). The sensitivity of microscopy is low in light infections and in acute infection. Eggs from hybrid species may differ in shape and therefore may be more difficult to identify correctly.

Eggs of S. mansoni, S. japonicum, S. haematobium, S. mekongi, and S. intercalatum can be found in stool (although S. haematobium is principally found in urine). In endemic settings, the Kato-Katz method is a common thick-smear technique using 5 mg of stool examined with a low-power microscope lens; it is relatively easy to perform but lacks sensitivity in light infections. At best, the detection threshold is 20 eggs per gram of stool for a single slide; the Kato-Katz method is good for epidemiologic studies in areas of high endemicity but is not as useful in the setting of light infection in an individual patient.

Most travel clinics use stool concentration techniques to improve sensitivity to a detection threshold of 10 eggs per gram of stool [21]. The FLOTAC stool concentration method has been proven more sensitive for S. mansoni egg detection than the Kato-Katz and yields at least as good results as the formol-ether extraction techniques, with a detection threshold of two eggs per gram [22]. The mini-FLOTAC method is a further development that can be used in population surveys [23]. Approximately 3000 to 6000 eggs per day must be excreted to reach this detection threshold. Egg production begins about 6 to 12 weeks after infection. Egg production and detection may be reduced in the setting of malaria chemoprophylaxis with mefloquine or with atovaquone-proguanil [24,25].

Eggs of S. haematobium are usually found in urine. The sensitivity of urine microscopy is highest in samples collected between 10:00 AM and 2:00 PM [26]. Sensitivity can be much improved by examining the precipitate after centrifugation or filtration of urine (minimum volume 10 mL).

In individuals with pulmonary involvement, eggs may be detected in bronchoscopic washings or transbronchial biopsies [27,28].

An experienced microscopist can distinguish between viable eggs (containing a living miracidium) and nonviable eggs (empty egg shells) that may be found in a tissue biopsy or are excreted for some time after successful treatment [29]. Eggs can be "hatched" by putting them in water, proving their viability.

Infection intensity — Determining the intensity of infection is important in endemic settings, since parasite burden correlates with the likelihood of complications. The intensity of intestinal schistosomiasis is classified as light (up to 100 eggs per gram), moderate (100 to 400 eggs per gram), or severe (>400 eggs per gram). The intensity of urinary schistosomiasis is classified as light to moderate (up to 50 eggs/10 mL) or severe (>50 eggs/10 mL) [30].

Species morphology — Schistosomiasis eggs have characteristic spines that can be seen on microscopy and usually allow easy species differentiation for the three major species (picture 1). Eggs from schistosome hybrids have been described in endemic populations and travelers [31]. Identification of these aberrant egg morphologies may be more difficult and require parasite genome sequencing [32,33]. Species identification may also be facilitated by epidemiologic information. (See "Schistosomiasis: Epidemiology and clinical manifestations".)

Serology — Serologic tests are a useful diagnostic tool in the absence of egg detection via microscopy, particularly for travelers, who generally have a low parasite burden. In general, serologic tests are negative during acute infection and turn positive 4 to 12 weeks or more after exposure [34]. Antibodies are usually detectable before eggs are detectable.

The assays available include ELISA, radioimmunoassay, indirect hemagglutination, immunofluorescent antibody test, Western blot, and complement fixation [35,36]. Serologic tests use a broad array of schistosome antigens including extracts of adult worms, cercarial antigens, or egg extracts such as the S. mansoni soluble egg antigen (SmSEA). Most commercially produced antibody test assays are not species specific; therefore, these assays are generally used as screening tests for schistosome infection.

The sensitivity and specificity are variable and depend on the serologic technique, the antigen used, the stage and the intensity of infection, and the infecting species [37-41]. Sensitivity can be improved by combining the results of two different serologic assays targeting distinct antigens, such as adult worm antigen and egg antigen [40-42]. The adult worm antigen immunofluorescent immunoglobulin (Ig)M antibody assay (AWA-IFA) is the most sensitive test used in exposed travelers [43], but thus far is not commercially available.

In general, antibody titer does not correlate with parasite burden. A negative antibody test is useful for ruling out infection in endemic settings. None of the tests can distinguish between prior infection and active disease. Antibodies persist for many months to years even after successful treatment, so serologic tests are not reliable for post-treatment follow-up [44].

Antigen detection — Techniques to detect parasite antigens in urine are already used qualitatively and are commercially available in a point-of-care format. These tests are particularly useful for schistosome eradication programs in low-endemic settings and in travelers with low parasite burden [45,46].

Soluble schistosome antigen titers correlate well with infection intensity and with clinical severity of disease [47-50]. They can also be used to assess treatment efficacy, since loss of excreted antigens indicates cure. Antigen tests become negative soon after successful therapy [50-52].

Two gut-associated genus-specific schistosome glycoproteins, CAA (sensitive for detection of all schistosome species) and CCA (only sensitive in S. mansoni infection), are present in the blood and excreted in the urine during active infection [53-55]. Detection of these water-soluble antigens is a sure way to identify active infection [56]; CAA is detectable early after exposure [54]. In most assays, these antigens are measured via a sandwich ELISA using monoclonal antibodies, which allows quantitation of infection intensity. Sensitivity is highest in serum, even when parasite burden is low; the detection threshold is 30 pg CAA/mL serum, which is equivalent to about 10 worm pairs. The schistosome circulating antigen test using an up-converting phosphor reporters lateral flow chromatography (UCP-LF-CAA) is even more sensitive in urine and in serum [57]. These test formats are restricted to research and reference laboratories.

Qualitative assays that measure parasite antigens in stool and/or urine have also been developed for field use. A commercially produced urine dipstick test to detect CCA (POC-CCA) is a much more sensitive alternative to the Kato-Katz method to measure spread of infection and posttreatment cure in settings where S. mansoni is endemic [45,57,58]. The sensitivity of antigen detection is superior to stool or urine concentration methods for egg detection; combining these techniques and/or concentrating these soluble antigens improves sensitivity in low-intensity infections [51,59]. Urine antigen detection by POC-CCA and UCP-LF-CAA outperforms PCR techniques [60].

Molecular tests — Molecular testing of specific DNA sequences of the parasite genome via PCR is a promising qualitative diagnostic assay but thus far largely remains a scientific tool restricted to research laboratories. PCR assays for stool, urine, and serum have been developed for diagnosis of schistosomiasis [61-65]. A genus-specific schistosome PCR assay can be combined with PCR assays for other helminths ("multiplex PCR"), with better sensitivity than microscopy [66]. In endemic settings, a PCR assay can measure the parasite burden and can be combined with antigen tests to improve sensitivity to monitor eradication progress [67,68].

The relative sensitivity and specificity of PCR in early infection and nonendemic settings is promising [69]; some [70] assays may be useful for early diagnosis of recent infection [63,64,69,71,72].

Some PCR assays facilitate species identification [73]. One study of PCR on urine samples noted sensitivity and specificity of 94 and 100 percent, respectively; use of an assay specific for S. mansoni was notable for sensitivity and specificity of 100 and 90 percent, respectively [62]. Another assay for S. haematobium is promising for use with serum, urine, or stool [71]. PCR on dried blood samples lacked sensitivity, which makes it less attractive for field studies [74].

Promising developments include LAMP (loop-mediated isothermal amplification) and RPA (recombinase polymerase amplification) molecular techniques. Sample preparation and DNA extraction are limiting factors for field use [75]. Genome sequencing of schistosome DNA extracted from blood and ova has been used for species determination when other tests remained inconclusive [20,31]. Schistosome genome sequencing techniques are also used to determine the epidemiology of schistosome hybrids occasionally found in humans [76].

PCR on cerebrospinal fluid for diagnosis of neuroschistosomiasis, even during the acute infection phase, may also be useful [77,78].

Imaging — Issues related to imaging are discussed separately. (See "Schistosomiasis: Epidemiology and clinical manifestations", section on 'Chronic infection'.)

Biopsy — Biopsy is useful as a diagnostic tool in the setting of ectopic disease manifestations and in the absence of demonstrative laboratory diagnostic tools.

In the setting of intestinal schistosomiasis, biopsy of rectal or higher intestinal tract mucosa, even in the absence of polyps, may demonstrate characteristic granulomas surrounding eggs embedded in the mucosa (picture 2). Histopathology of superficial rectal biopsies ("rectal snips") is more sensitive than stool microscopy and may demonstrate eggs even when multiple stool specimens are negative. In one study of 135 British expatriates with S. mansoni infection, eggs were detected on rectal biopsy in 61 percent of patients and on stool examination in 39 percent of patients [29].

In the setting of genitourinary schistosomiasis, cystoscopy with bladder biopsy is not needed in most cases but can be performed if the diagnosis is suspected and eggs are not found in urine [79]. Biopsy of urinary tract polyps may demonstrate characteristic granulomas with eosinophils surrounding eggs embedded in the mucosa.

Species-specific PCR assays have been used to confirm schistosomiasis as the cause of genital lesions in biopsies and in cytological scrapings [80].

Monitoring control efforts — Control and prevention of schistosomiasis via snail control and repeated mass treatment require careful monitoring with sensitive diagnostic tests such as the schistosome gut-associated antigen tests (CCA, CAA) in urine or serum, and with schistosome DNA assays by PCR in blood, feces, or urine [81,82]. (See "Schistosomiasis: Treatment and prevention", section on 'Control and prevention'.)

DIFFERENTIAL DIAGNOSIS — The differential diagnosis of schistosomiasis is broad. Most entities can be distinguished on analysis of the stool for ova and parasites. Some require additional evaluation with imaging of the affected organ system and/or serologic testing. The specific entities included in the differential diagnosis vary based upon the clinical presentation (see "Approach to stool microscopy"):

Acute febrile illness – Acute schistosomiasis with fever must be differentiated from malaria, typhoid fever, and other Salmonella infections. Other illnesses that must be distinguished from schistosomiasis include gastroenteritis, brucellosis, leptospirosis, and appendicitis. (See "Evaluation of fever in the returning traveler".)

Eosinophilia – Eosinophilia and fever can occur in the setting of fluke infections such as clonorchiasis and fascioliasis, as well as trichinosis, tropical eosinophilia, visceral larva migrans, and infections with Opisthorchis and Paragonimus. Eosinophilia can also occur in the setting of strongyloidiasis and infections due to Ancylostoma, Necator, or Ascaris. (See "Approach to the patient with unexplained eosinophilia".)

Eosinophilia, fever, and meningeal signs – The differential diagnosis of eosinophilia, fever, and meningeal signs includes neuroschistosomiasis, eosinophilic meningitis, neurocysticercosis, and coccidiomycosis. These may be distinguished from one another based on clinical history, radiography, and cerebrospinal fluid examination. (See "Eosinophilic meningitis".)

Hematuria – Urinary schistosomiasis due to S. haematobium must be distinguished from other causes of hematuria, including urinary tract infection, acute nephritis, renal tuberculosis, and cancer of the urogenital tract. The differential diagnosis of genital schistosomiasis also includes alternative causes of infertility. Hematuria (presence of whole red blood cells in urine) must be distinguished from hemoglobinuria (free hemoglobin in urine) by microscopy. (See "Urogenital tuberculosis" and "Clinical presentation, diagnosis, and staging of bladder cancer" and "Overview of infertility".)

Abdominal symptoms – Abdominal symptoms that occur in the setting of S. mansoni or S. intercalatum infection may suggest peptic ulcer, biliary disease, or pancreatitis. Lower abdominal conditions to be excluded include the various forms of dysentery, giardiasis, and ulcerative colitis.

Hepatosplenomegaly – The differential diagnosis of hepatosplenic disease includes tropical splenomegaly, a chronic illness that can occur in the setting of repeated bouts of malaria and an exaggerated immune response. The marked splenic enlargement of portal hypertension due to periportal fibrosis must be distinguished from visceral leishmaniasis, chronic leukemia, myeloproliferative syndromes, and thalassemia. (See "Splenomegaly and other splenic disorders in adults".)

Pruritic rash – Swimmer's itch should be distinguished from other dermatologic entities including seabather's eruption, hot tub folliculitis, cutaneous larva migrans, varicella, and contact dermatitis. (See "Skin lesions in the returning traveler".)

Noninfectious etiologies include drug reaction or other toxin ingestion, adrenal insufficiency, and rheumatologic diseases such as dermatomyositis and systemic lupus erythematosus. Allergic and hematologic disorders should also be considered. The clinical approach to these entities is discussed separately.

SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Schistosomiasis".)

SUMMARY

Schistosomiasis is a disease caused by infection with parasitic blood flukes. The parasites that cause schistosomiasis live in certain types of freshwater snails. Individuals can become infected when skin comes in contact with freshwater containing the infective larval stage (cercariae). (See 'Introduction' above.)

The approach to diagnosis for returned travelers differs from the approach to diagnosis in endemic settings. Among returned travelers, serology is the most useful test, but it does not reflect definitive evidence of ongoing infection. Among individuals living in endemic areas, the parasite burden should be determined by microscopy for egg detection and antigen detection. Microscopy (of stool or urine) and antigen detection (in urine) can be used to determine the burden of infection, although these are less helpful in the setting of early infection. Microscopy and polymerase chain reaction (PCR) assays are also used to determine the infecting species. (See 'Clinical approach' above.)

The diagnosis of schistosomiasis requires detection of infection and measurement of parasite burden. Diagnostic tools include direct assays (demonstration of eggs in the stool or urine via microscopy, or demonstration of antigen or DNA in the blood, urine, and/or stool) and indirect assays (demonstration of antibody in blood via serology) (table 1). Species diagnosis is based on egg identification; the egg of each species has a characteristic shape (picture 1). (See 'Laboratory tests' above.)

Biopsy is useful as a diagnostic tool in the setting of ectopic disease manifestations and in the absence of demonstrative laboratory diagnostic tools. Biopsy of polyps in the intestinal tract or bladder may demonstrate characteristic granulomas surrounding eggs embedded in the mucosa. (See 'Biopsy' above.)

The diagnosis of neuroschistosomiasis requires laboratory detection of infection at an extraneural site (as described above) together with clinical and radiographic evidence of neurologic involvement. Alternatively, neuroschistosomiasis may be diagnosed via direct evidence of central nervous system (CNS) infection such as biopsy of a CNS lesion and/or a positive antibody titer or PCR in the cerebrospinal fluid. (See 'Neuroschistosomiasis' above.)

ACKNOWLEDGMENT — The UpToDate editorial staff acknowledges Karin Leder, MD, who contributed to an earlier version of this topic.

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Topic 5682 Version 21.0

References

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