Schistosoma mansoni, S. haematobium, S. japonicum and more rarely S. mekongi, S. malayensis, S. intercalatum and S. guineensis
Distribution
The risk of infection is greatest in Africa. Usually not encountered at altitudes higher than 1 800 m.
Schistosoma mansoni is encountered in Africa, the Middle East as well as Central and South America, S. haematobium in Africa and the Middle East and S. japonicum in the East and Southeast Asia. S. mekongi and S. malayensis (Southeast Asia) as well as S. intercalatum and S. guineensis (Africa) are rarer.
In endemic areas more common in the countryside than in cities.
Transmission
Human infection with Schistosoma species is acquired after swimming or wading in freshwater that harbours cercariae (larvae), which are able to penetrate intact human skin. Once inside the body, the cercariae travel to the lungs and further to the liver. From the liver the worms travel either to the venous plexus of the urinary bladder (S. haematobium) or to the mesenteric veins (other Schistosoma species). There they lay eggs and may live for prolonged periods. Some of the eggs remain in the tissues where they cause an immunological reaction that slowly damages the target tissue.
The parasite eggs are shed into freshwater via the urine and faeces of an infected human. After maturing inside freshwater snails, the parasites are released back into the water as infectious cercariae.
Children in endemic areas are repeatedly exposed as they swim or wade in water falls, lakes, streams and rivers. The worm load increases over the years; symptomatic disease is encountered often not earlier than in young adults.
Travellers may develop the disease after a single exposure; chronic disease is only rarely encountered in them.
Significance worldwide
Schistosomiasis is, after malaria, the second most prevalent tropical disease in the world.
More than 700 million people live in areas endemic for schistosomiasis.
The largest number of cases are in sub-Saharan Africa
Globally, more than 200 million cases and over 200 000 deaths annually
Symptoms
The majority of those infected will not get a symptomatic disease.
Cercarial dermatitis is a rare pruritic maculopapular allergic rash that may occur within a few hours of skin penetration.
Acute schistosomiasis (Katayama's fever) is associated with the first infection by S. mansoni and particularly by S. japonicum.
Acute schistosomiasis is a hypersensitivity reaction that occurs 4-6 weeks after infection, i.e. at the time of initial egg release.
The symptoms include: fever, generalised symptoms, asthmatic symptoms, urticaria and diarrhoea, enlarged lymph nodes, hepatosplenomegaly and severe eosinophilia.
Usually the symptoms disappear in a few weeks even without treatment, but S. japonicum infection may prove fatal without treatment.
Chronic schistosomiasis starts 3-6 months after infection. The character and severity of the symptoms depends on the one hand on the species of schistosome causing the infection and the location and number of the eggs and, on the other hand, on the immune response of the host. Repeated exposure increases the number of worms in persons living in endemic regions.
S. haematobium causes haematuria and urinary tract symptoms. The bladder wall will gradually become fibrosed and calcified, and its elasticity will diminish. Possible complications include hydroureter, hydronephrosis, renal failure and urinary bladder cancer. The infection may also cause different kinds of damage to the genital area.
Symptoms of S. mansoni infection include lethargy, abdominal pains and chronic, sometimes bloody diarrhoea. Hepatomegaly is possible, and some patients will develop an enlarged spleen, bleeding oesophageal varices or liver failure. Pulmonary fibrosis is also possible.
In S. japonicum infection the symptoms are comparable to those of S. mansoni infection. The disease progress, however, is faster and the risk of liver fibrosis is greater. In the Far East, schistosomiasis is an important cause of epilepsy.
Diagnosis
In screening of the disease, serology is utilized and urine and fecal samples are examined. In the initial phase of the disease the samples remain negative, which is why they should be repeated at a later point.
In travellers the parasite load is often low and consequently methods that are based on finding helminth eggs and detection of antigens have low sensitivity. Therefore, in travellers the diagnosis is often based on serology.
The diagnosis of acute schistosomiasis is based on clinical presentation and antibody detection from the blood; an antibody test will become positive over 4 weeks after infection.
Schistosoma antibodies are included in the serum screening test for anti-helminth antibodies that is used for investigating eosinophilia. No eggs are present in the acute phase.
The diagnosis of chronic schistosomiasis is usually based on identification of eggs in urine, faeces or an endoscopically obtained tissue biopsy. The Schistosoma species can be identified through microscopy or nucleic acid detection testing.
Haematuria is suggestive of an S. haematobium infection as are, in some cases, urinary tract ultrasound and x-ray findings; eggs may also be detected in the urine or a cystoscopically obtained biopsy sample.
In chronic S. mansoni and S. japonicum infection, eggs can be found in a stool parasite formalin sample or a rectal biopsy sample even when the mucous membranes appear macroscopically normal.
Eosinophilia is normal particularly in the early phases of the infection; it often disappears as the disease becomes chronic. After treatment, eosinophilia normally increases initially and disappears after a few months. This may be used both to confirm diagnosis and to monitor treatment response.
A specialist in infectious diseases should be consulted regarding treatment.
Acute schistosomiasis
Glucocorticoids in severe symptoms (e.g. prednisone 40 mg daily for 5 days)
Specific treatment with praziquantel (may require special license) only when eggs can be detected. It may be necessary to repeat the treatment even several times with 6-8-week intervals. In the initial phase praziquantel may even worsen the symptoms of the disease. Praziquantel is often administered with a glucocorticoid.
Chronic schistosomiasis
PraziquantelInterventions for Treating Urinary Schistosomiasis 40-60 mg/kg, in S. japonicum infection 60 mg/kg, as a single dose (divided into two portions administered at an interval of 4-6 hours). In a patient with severe symptoms the treatment is repeated after 2 weeks.
The result is checked after 3 months by examining a stool or urine sample for the presence of worm eggs, and possibly also a mucous membrane biopsy sample (urinary bladder or rectum). Blood eosinophilia concentration should also be checked. If esinophilia has not been corrected until then, the treatment is repeated and/or other underlying causes for eosinophilia are sought (e.g. other helminthic infections).
The changes are usually reversible when the treatment has been given early enough.
Prevention
Prevention of water contamination with human faeces
Destruction of the intermediate snail hosts
Reduction of contact with untreated fresh water in endemic regions
Regular treatment of disease carriers
Vigorous towel drying immediately after a brief exposure to water may help to reduce the risk of infection.