Schistosomiasis aetiology and management
Schistosomiasis aetiology and management
Schistosomiasis aetiology and management
Infection with digenetic flukes of the genus Schistosomaaffects the bladder and urinary tract (S. haematobium) orintestine (S. mansoni, S. japonicum). These worms causedisease because of the host's response to eggs retained inthe tissues. The severity of disease relates to the number ofeggs in the tissues, which is proportional to the wormburden.
Aetiology Eggs are passed in stools or urine; those deposited in stillor slow-flowing fresh water hatch to release the ciliatemiracidium, which can survive for up to 48 hours before itdies. During this time it must find an aquaticsnail of the appropriate genus: Biomphalaria for S. mansoni,Bulinus for S. haematobium, and Oncomelania forS. japonicum.Cercariae are released from the snail and these penetratethe skin of a suitable host, almost always human, becomingschistosomules during penetration. These migratevia the blood vessels to the pulmonary vasculature, wheresome traverse the pulmonary circulation to enter thesystemic circulation.Schistosomules of mansoni and japonicum mature in thehepatic branches of the portal vein, and by 6 weeks afterinfection they are mature. They migrate out of the liveragainst the flow of blood in the portal vein to small veinsaround the colon and small intestine. The colon is mainlyinvolved in mansoni infections, and both colon and smallintestine are involved in japonicum infections.The lifecycle of S. haematobium is similar, but maturationtakes place in pelvic veins. The worm pairs migrateinto small branches of the internal iliac vein, principally370 around the bladder, although other pelvic structures suchas the prostate and seminal vesicles in men, and the uterusand adnexal structures in women, may be involved. Adultworms survive for about 7 years on average, but survivalof over 30 years has been reported.
Distribution and incidence There is considerable overlap in the endemic areas of haematobium and mansoni, but japonicum has a distinct Asian distribution.The prevalence and incidence of infection vary considerably,with rates up to 70% or more in the endemic areas.Infection rates tend to be highest in children and declinewith increasing age.
Transmission and epidemiology Freshwater contact is the major factor in infection andmaintenance of transmission. Children are infected earlyin life by playing in infected water. They are also likely tourinate and defecate in and around pools and streams,further enhancing the local intensity of transmission. Thehighest rates and intensities of infection are found in thesecond and third decades of life.
Pathology and pathogenesis The pathological changes relate to the presence of eggs inthe tissues. Eggs laid in the small branches of veins may: pass through the wall of the viscus to reach the exteriorin faeces or urinebe retained in the tissues embolize through vessels to lodge in presinusoidalbranches of the portal vein in mansoni and japonicuminfections, or in pulmonary arterioles in haematobiuminfections.The egg excites a granulomatous response with macrophages,lymphocytes, plasma cells and eosinophils.Granuloma formation is important for the transition of theegg through the mucosa to the lumen of the viscus. Thechronic inflammation they may cause in the epitheliummay be a factor in carcinogenesis of the bladder (haematobium).Eggs retained in the tissues within granulomas graduallybreak down until all that may remain is remnants of the eggcase. The granuloma heals by fibrosis. Early in the course ofinfection exuberant granuloma formation can cause colonicpolyps in mansoni and japonicum infections, and bladderpolyps in haematobium infection. These resolve after treatmentand may also resolve spontaneously.Fibrotic polyps and strictures are not often seen inmansoni infection, although they are more common injaponicum infection. Haematobium infection causes fibrosisof the bladder, which is often shrunken, with a thickwall. Bladder stones may form and cystitis is common. Unilateralor, less commonly, bilateral ureteric strictures causeobstructive uropathy. Stones may form in the dilatedureters. Distortion of the ureterovesical junction may allowvesicoureteric reflux of urine with associated recurrentpyelonephritis.Squamous cell carcinoma of the bladder is common inhighly endemic S. haematobium areas. It is suggested thatschistosomiasis acts with dietary factors to produce malignancy.This has not been found in S. mansoni infection orin S. japonicum, despite earlier reports from China.Mansoni and japonicum eggs embolize to the liver. Thegranulomas that form around eggs add to the volumeof the liver and increase its size, and obstruct the flow ofblood through the portal circulation in the liver, causingcongestive hepatosplenomegaly in those with heavy wormburdens. Granulomas resolve with local fibrosis, and whenthis process goes on over years periportal fibrosis results,causing irreversible portal hypertension. The anatomy andarchitecture of the hepatic lobules are not altered andthere are no regenerating nodules, therefore cirrhosis is notcaused. In the lungs granulomatous reactions in the vesselscause fibrosis and pulmonary hypertension.Involvement of the CNS occurs in S. japonicum, S.mansoni and S. haematobium, in descending order offrequency. Disease of the central nervous system is mostprobably the result of an ectopic worm pair laying eggs inor around the brain or spinal cord. Mansoni and haematobiuminfections are associated with spinal cord and caudaequina lesions.
Clinical features Cercarial invasion of the skin may cause a local irritantpapular eruption, but this is uncommon. Most patientshave no symptoms related to the phase of migration and maturation. Occasionally non-immune people develop theKatayama syndrome with the phase of worm migration.There is malaise and lethargy, and fever, profuse sweats,muscle pain, abdominal pain, joint aches, unproductivecough, urticaria, swollen eyelids and hepatosplenomegalyoccur in more severely affected patients. These symptomsbegin 3-4 weeks after exposure and persist for up to 3months, with reducing severity.Chest X-rays may show coin lesions caused by wormsdying in vessels and evoking local inflammatory reactions.Marked eosinophilia is common. Eggs are not found until3-6 weeks after infection.S. mansoni and S. japonicumMany infected patients go through life without any symptomsrelated to this infection. Rectal examination is normal;sigmoidoscopy is normal or shows scattered mucosalhaemorrhages. Occasional patients present with anaemiaand oedema because of bleeding and protein loss fromschistosomal polyps.The most common physical sign in infected patients inendemic areas is hepatomegaly, which correlates with theintensity of infection in the first two decades but not inolder age groups. Similar findings are noted in S. japonicuminfection. Abdominal pain and subacute intestinalobstruction occasionally occur in the rare patient whodevelops fibrotic strictures in the colon or, less often, thesmall intestine.Hepatosplenomegaly with congestive splenomegalysuggests end-stage schistosomal hepatofibrosis. Thesepatients often present with haematemesis and ascites.Portosystemic encephalopathy is not a usual feature aftervariceal bleeding in schistosomiasis. Severe pain over agrossly enlarged spleen may indicate splenic infarction.
Management Three safe, effective drugs are available for use in schistosomiasis. Their safety in pregnancy has notbeen confirmed, and so treatment should be delayed untilafter delivery unless there are urgent indications forprompt treatment. All cases should be treated, even theadvanced ones, as further ovideposition causes furtherurinary tract, intestinal, liver or pulmonary damage.Ideally, stools and rectal snips should be examined forviable ova 3 months after treatment.
Prevention and control Control measures are expensive and require a change inthe behaviour pattern of the exposed population. Educationregarding the reasons for the measures is essential.Dams and irrigation projects for the improvement of theeconomy of an area may create new habitats for snail hostsof schistosome parasites. Molluscicides can be used, but areexpensive and may have detrimental effects on other watercreatures. Regular, community-based treatment withpraziquantel has reduced morbidity.
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