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Understanding Schistosomiasis: A Comprehensive Look at the Blood Fluke Infection

Learn about schistosomiasis caused by the Schistosome parasite, its global impact, morphology, life cycle, pathogenesis, and clinical features. Get insights into the six species affecting humans and the significant medical importance of three species.

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Understanding Schistosomiasis: A Comprehensive Look at the Blood Fluke Infection

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  1. Schistosome

  2. Introduction • Schistosome (blood fluke) causes schistosomiasis • first discovered by the German parasitologist Theodor Bilharz in 1852 in Egypt • Dated back to ancient Egypt and about 2000 years ago in China • over 200 million people in the world infected • 600 million people are at risk

  3. Introduction • Six species affecting human being • Schistosoma japonicum • S.mansoni • S.haematobium • S.intercalatum • S.mekongi • S.malayensis : parasite of humans (rarely) and other animals. A recently described 'new' species

  4. Introduction • Three species of significant medical importance : • S. mansoni: Africa, Arabia, S. America, Caribbean • S. haematobium: Africa, Middle East • S. japonicum: China, the Philippines, southern Japan, Central Sulawesi (Indonesia) • Different homing orientation : • S. mansoni: Mesenteric veins • S. haematobium: Vesical plexus • S. japonicum: Superior mesenteric veins

  5. Global Epidemiology Africa South America Purple:S.mansoni Blue:S.intercalatum Asia Africa Orange:S. haematobium Green:S. japonicum Red:S. mekongi

  6. S. japonicum still endemic in China 7 endemic provinces with 119 endemic counties

  7. Morphology • “schisto-”means “split” • Dioecious worms • Gynecophoral canalin male – • Pheromone fromthe male is necessary for the development of female worms • Incomplete digestive system: mouth, esophagus , gut • Some variations between species

  8. Morphology • The male adult worm of S. japonicum is slightly larger than the other 2 species at ~ 1.2cm by 0.5mm • Two suckers • maintains its position in the blood vessels－－ the ventral, and larger oral suckers

  9. Female adult worm Morphology • S.japonicum female parasite is about 2cm by 0.4mm • Eggs in the uterus • S. mansoni: a single egg is shown, usually 1 - 3 • S. haematobium: many more are seen (between 20 - 30) • S. japonicum: 50 or more eggs • Dark grey color because of the metabolic RBC in the digestive duct

  10. Eggs of S.japonicum Morphology • Average size 89×67µm • Oval or sub-spherical • Pale yellow or yellow brown • Small lateral spine • No operculum • Embryonated, contains mature miracidium when discharged

  11. Eggs Morphology

  12. Miracidium Morphology • A ciliated, swimming larva • Size about 99×35µm • The germinal cells will become sporocysts • Tropism – toward limpidity ; phototrophic

  13. Cercaria Morphology • Free- swimming • a forked tail • penetrating glands

  14. C. sinensis F.buski S.japonicum P. westermani Cercariae of trematodes

  15. Life Cycle

  16. Life Cycle • Mode of infection: penetration of the skin • Migration: stay in skin(5-10h) convert to schistosomula  subcutaneous venules pulmonary circulation  heart  systemic circulation  portal vein  mesenteric vein • Diagnostic stage: egg • One intermediate host -- Oncomelania hupensis (S. japonicum) Biomphalaria (S. mansoni) Bulinus (S. haematobium) • Infective stage: Cercaria • Lack of metacercaria stage • no redia • two generations of sporocyst

  17. Life Cycle • Reside in portal system, superior mesenteric vein or vesical plexus • Tissue-residing ova (the main result for pathology) – 15-63% in tissue (liver and intestine) • Instant hatching of the discharged egg in water • A variety of reservoir hosts -- zoonosis

  18. Residing place (mesenteric vein ) Life Cycle Intermediatehost Oncomelania hupensis Eggs in the vein

  19. Pathogenesis • Schistosomiasis is an immune disease • All stages in host may be pathogenic: cercaria, schistosomulae, egg and adult • The main pathogenic factor is the egg • Deposit in important organs – liver, intestine,etc • Formation of egg granuloma • Accumulation of eggs (thousands of eggs per day) • Ectopicmigration – brain, lung

  20. Pathogenesis • Skin - “swimmer’s itch” just for a short period after cercaria penetration –type I & IV allergic reaction • Transient fever and coughing -- mechanically damage and allergic reaction to the metabolic materials of schistosomulae • Phlebitis caused by adult worm (rarely) and glomerulonephritis caused by the type III hypersensitivity to the metabolic materials to adult worms • The eggs induced granuloma formation is a Delayed Type Hypersensitivity (Type IV Hypersensitivity) reaction • Although eventually resulting in severe pathology, appears to be a necessary protective host response against hepatotoxic components of Soluble Egg Antigen (SEA).

  21. Papules caused by the penetration of cercariae

  22. Egg granuloma in liver Pathogenesis

  23. Fibrosis of portal vein

  24. Eggs of S. japonicum in brain

  25. Clinical features • Acute schistosmiasis • May occur 5-8 weeks after the initial infection • Allergic reaction to first release of the eggs called Katayamu fever • Enlarged spleen and tender liver

  26. Clinical features • Chronic schistosomiasis – immune modulation period • Thickening of colon with tiny ulceration • Liver and spleen enlargement • Occasionally diarrhea, anemia,wizened

  27. Clinical features • Advanced schistosomiasis – hepatosplenic schistosomiasis -- usually happens 5 years after infection • Irreversible liver and spleen enlargement with abnormal function of these organs • Increased pressure in veins that drain upper intestine with risk of bursting of these veins. upper gastrointestinal bleeding may cause death • Cerebral granulomatous disease may be caused by ectopic S. japonicum eggs in the brain • In child, it may cause nanoid

  28. Advanced schistosomiasis patients • ascites • Splenomegaly

  29. Immunity • Non-sterilized immunity • Concomitant immunity:Concomitant immunity has long been considered a feature of schistosome infections and describes the phenomenon where by the adult worms can survive happily in the mesenteric veins where as the host seems to be resistant to secondary infection. • Age-related immunity in human

  30. Diagnosis • Etiological diagnosis • Sedimentation hatching method – first choice • Kato’s smear method for EPG • Rectal biopsy – must distinguish live or dead egg • Immunological diagnosis • COPT – CircumOval Precipitation Test • Intracutaneous test • ELISA, IHA, etc

  31. Man's arm showing positive skin test for schistosome Intracutaneous test

  32. Control methods • Treat both human and the reservoir animals, such as buffalo, swine etc ---praziquantel • Feces (egg) control—avoid being discharged into water • Snail control---molluscicides • Ask people to avoid contacting with water that contained the snails and cercariae

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