S. japonicum
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Transcript S. japonicum
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