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Schistosome 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 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 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 Global Epidemiology Purple: S.mansoni Africa South America Blue: S.intercalatum Asia Africa Orange: S. haematobium Green: S. japonicum Red: S. mekongi S. japonicum still endemic in China 7 endemic provinces with 119 endemic counties Morphology “schisto-” means “split” Dioecious worms Gynecophoral canal in male – Pheromone from the male is necessary for the development of female worms Incomplete digestive system: mouth, esophagus , gut Some variations between species 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 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 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 Eggs Morphology Miracidium Morphology A ciliated, swimming larva Size about 99×35µm The germinal cells will become sporocysts Tropism – toward limpidity ; phototrophic Cercaria Free- swimming a forked tail penetrating glands Morphology C. sinensis F. buski S. japonicum P. westermani Cercariae of trematodes Life Cycle 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 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 Life Cycle Residing place (mesenteric vein ) Intermediate host Oncomelania hupensis Eggs in the vein 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) Ectopic migration – brain, lung 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). Papules caused by the penetration of cercariae Pathogenesis Egg granuloma in liver Fibrosis of portal vein Eggs of S. japonicum in brain 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 Clinical features Chronic schistosomiasis – immune modulation period Thickening of colon with tiny ulceration Liver and spleen enlargement Occasionally diarrhea, anemia,wizened 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 Advanced schistosomiasis patients ascites Splenomegaly 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 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 Man's arm showing positive skin test for schistosome Intracutaneous test 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