Stay informed with the latest updates on coronavirus (COVID-19). Find out more >>


  • Background

    Schistosomiasis is a complex of several acute and/or chronic infections cause by the flatworm Schistosoma spp. (S. haematobium, S. guineensis, S. intercalatum, S. mansoni, S. japonicum, and S. mekongi).1 It has a low mortality rate but causes significant chronic illness and may lead to growth delay and cognitive impairment in children. 


    Worldwide 200 million (or 1 in 30 individuals) are estimated to have schistosoma infection.2 Schistosomes are widespread in tropical and subtropical areas (see map).

    • S. mansoni sub-Saharan Africa, Middle East, South America, Caribbean. 
    • S. haematobium North Africa, sub-Saharan Africa, Middle East, Corsica, Turkey, India. 
    • S. japonicum occurs only in Asia, particularly China, Philippines, Indonesia. 
    • S. intercalatum and S. guineensis occur only in rainforest areas of central and West Africa 
    • S. mekongi occurs only in Laos and Cambodia.3

    Over the period 2005 - 2010, the rates of positive Schistosoma serology in new refugee arrivals to Australia varied from 5-40%,4-7 with positive serology more common in people from African source countries.4

    Life cycle

    • Schistosoma has a complex life cycle
    • The infection is acquired from fresh water sources in endemic areas (e.g. when a person walks bare foot in lakes or wetlands). There is no endemic Schistosoma infection in Australia (and no intermediate snail host), and transmission does not occur in salt water.
    • Different species cause human disease depending on their location e.g. the mesenteric venules of the bowel (S. mansoni, S. japonicum, S. mekongi, S.intercalatum, S. guineensis) or the bladder (S. haematobium). CNS disease, while rare, is associated with S. japonicum, S. mekongi, and spinal cord lesions have been reported (S. japonicum, S. mansoni, S. haematobium).


    Most Schistosoma spp. infection are asymptomatic

    • Early symptoms - mild itching/papular dermatitis may occur at the site of penetration of the schistosoma larvae (‘swimmer’s itch’) 12-24 hours after infection
    • Later symptoms - infection can cause a serum sickness like response (systemic hypersensitivity reaction) a few weeks after initial infection (‘Katayama fever’). This is more common in travellers from non-endemic countries, where infestation results in a more severe immune response.8 Symptoms include abdominal pain, diarrhoea, cough, fever, and fatigue. Hepatosplenomegaly and lymphadenopathy may be present. Symptoms usually resolve spontaneously over weeks. 
    • Chronic symptoms tend to occur in persons from endemic areas and be related to a high burden of infection. They are a response to egg deposition and depend on the location of the schistosome. 
      • Urinary tract schistosomiasis can cause cystitis and haematuria. Chronic infection can lead to ureteral obstruction and hydronephrosis, and is associated with bladder cancer in adults
      • Bowel schistosomiasis: can cause abdominal pain and bloody diarrhoea. Infestation may lead to colonic polyposis, ulcers, portal hypertension and, less commonly, pulmonary hypertension. 
      • Other: Portal, pulmonary and central nervous system (CNS) schistosomiasis may also occur. Schistosoma infection can cause transverse myelitis or CNS lesions - and can cause focal deficits, seizures, raised intracranial pressure. Schistosomes are also a common cause of oesophageal varices worldwide. They may also rarely cause genital sores (examination should be completed if S. haematobium is identified) and be associated with increased risk of sexually transmitted infection (STI) acquisition.


    All recent immigrants from endemic areas (see also from ASID guidelines) should be screened for schistosomiasis infection by history, examination and investigation


    • Schistosoma serology - antibody detection is usually by enzyme immunoassay (EIA) or indirect haemagglutination of antibodies (IHA). Serology has greater sensitivity for S. mansoni (93%) and S. haematobium (around 90%) than S. mekongi and S. japonicum (around 50%).
    • Eosinophilia in peripheral blood is common (FBE is also part of refugee health screening). In Katayama fever, serology and microscopy are usually negative, and eosinophilia may be the only feature. 
    • If any clinical symptoms suggest schistosomiasis - collect specimens relevant to the suspected infection 
      • Midday end urine (10am - 2pm) large volume (>20mL, not mid-stream) looking for haematuria and microscopy for ova
      • Stool in SAF for faecal OCP
    • If Schistosoma serology is positive also collect stool for microscopy and check urine for haematuria (and examine for ova if positive).
    • Patients with positive stool or urine microscopy should have further evaluation for end-organ damage
      • Urinary schistosomiasis – renal/bladder ultrasound
      • Intestinal schistosomiasis – liver ultrasound for portal hypertension/ hepatic fibrosis.
    • Consider (and screen for) co-infections including malaria, HIV, hepatitis B and hepatitis C.9
    • Consider cerebral imaging prior to treatment in individuals with seizures (to consider neurocysticercosis as a differential diagnosis, and treatment options - praziquantel may worsen seizures in this situation).


    • All patients with evidence of schistosoma infection should be treated (including those with positive serology), even if asymptomatic, to prevent chronic complications
      • Praziquantel (pregnancy category B1) is the treatment of choice,10 and usually very well tolerated with few adverse effects (mild potential adverse effects include dizziness, headache, vomiting, abdominal pain, diarrhoea, and pruritus). It is only effective against adult worms, and usually most effective at least 4-6 weeks after exposure - so it is less useful in early infection (e.g. Katayama fever – see below).
      • Praziquantel 40mg/kg total in 2 divided doses, given 4 hours apart (i.e. 20 mg/kg/dose x 2 doses) or 40 mg/kg stat dosing in children (for all spp.) Seek specialist advice for children <12 months of age. Tablets come in 600 mg strength and divide into quarters.
    • Treatment is curative in ~ 85%.10,11 Treatment is not necessarily effective in treating late stage complications such as oesophageal varices or cor pulmonale. 

    Follow up

    • Patients with positive urine or stool samples should have samples repeated 2-3 months (not less) after treatment, to confirm eradication. If stool or urine remains positive after 8 weeks, the treatment course should be repeated.
    • FBE can be checked >12 weeks after therapy to ensure eosinophilia has resolved. Persistent eosinophilia after treatment may also indicate another parasitic infection. 
    • Repeat serology 12 months after infection may be reassuring if antibody response has converted to negative; the value of routine serology as a test of cure is unclear at this stage.12-14

    Note: Katayama fever - treatment is mainly supportive and may include glucocorticoids (+/- praziquantel or antimalarials). The patient should be retreated with praziquantel 2-3 months later to eliminate any remaining worms. Seek specialist advice.


    Immigrant health clinic resources. Author: Vanessa Clifford and Georgie Paxton. Last updated June 2020. Contact