Schistosomiasis, also known as bilharzia or snail fever, is caused by parasitic flatworms of the genus Schistosoma. The disease infects the urinary tract and intestines through parasite eggs. There are several species of Schistosoma that cause disease in humans, including S. haematobium, S. mansoni, and S. japonicum. The parasites have complex life cycles involving freshwater snails and human hosts. Symptoms vary depending on the species and stage of infection, but often include abdominal pain, diarrhea, bloody stool or urine. Diagnosis is made by detecting parasite eggs in stool or urine samples under microscopy. Treatment involves praziqu

1. Presenter – Insha jan
Schistosomiasis

2. Schistosomiasis, also known as
Bilharzia
Snail fever
Katayama fever
It an acute & chronic disease that is caused by parasitic flatworms called Schistosomes
This disease may infect urinary tract & intestinal system

3. Trematodes
Intestinal
trematodes
F. buski
Lung
trematodes
P. westermani
Blood
trematodes
Schistosomes
Hepatic
trematodes
Clonorchis
Phylum : Platyhelminthes
Class : Trematoda
Order : Prosostomata
Superfamily: Schistosomatoidea
Genus : Schistosoma
Species : S.haematobium
S. mansoni
S. japonicum
S. intercalatum
S. menkongi

4. Obligate intravascular parasites
Unisexual (dioecious) - males are
shorter & stouter than females
Males possess a gynaecophoric
canal
Muscular Pharynx is lacking.
Suckers are armed with delicate
spines

5. Eggs are non – operculated & fully
embryonated when laid.
Cercariae have bifid tails & penetrate into
the definitive host through the unbroken skin.
Encysted meta cercarial stage is absent. Adult
worm lives in the lumen of the portal vein and its
radicles.
Females laurer’s canal (vestigial
vagina) is absent, in males 4-8 testes
present.
Intestinal caeca reunite behind the
ventral sucker to form a single canal.

6. 1847
Funjii mentioned about
the katayama disease
1851
Bilharz discovered the adult
worm of S. haematobium
from the mesenteric vein of a
native of Cairo.
1903
Manson observed lateral –
spined eggs in the faeces
1904
Funjiami recovered an
adult female of S.
japonicum in the portal
vein of a man at autopsy.
1904
Katsurada observed the eggs
of S. japonicum in the human
faeces.

7. 1907
Sambon pointed out that the
lateral – spined eggs belonged
to a separate species , S.
mansoni
Miyairi and suzuki
worked out the life
cycle of S. japonicum
1913-1914
1915
Leiper worked out the life
cycle of s. haematobium
in bulinus in Egypt .
1910
Schistosome eggs were found by
Ruffer in the renal pelvis of a
mummy of the twentieth dynasty
( 1250-1000 B.C).

8. Common name : Vesical blood fluke
Geographical distribution :Various parts of Africa and middle East.
 Gadgil and Shah (1952) reported a few cases from India ( Ratnagiri in
Maharashtra state).
 200 million persons are at a risk of infection & 90 million are infected by S.
haematobium globally.

9. Adult worm (Males)
 10–15 mm long & 1mm thick.
 Covered by a finely tuberculated cuticle.
 Possesses two muscular suckers- oral
sucker & ventral sucker
 Gynecophoric canal is located behind
the ventral sucker and extending to a
caudal end.

10.  Long and slender, 20 mm × 0.25 mm
with the cuticular tubercles confined to
the two ends.
 Gravid worm contains 20–30 eggs in its
uterus at one time & may pass up to 300
eggs a day.
Adult female

11. Egg
 Ovoid
 120–170 μm in length & 40–70 μm in
breadth.
 Non-operculated with a brownish yellow
transparent shell carrying a terminal spine
at one pole.

12. Miracidium
 First larval stage
 Ciliated larva develops in all trematode eggs & is
infective to molluscs only
Sporocyst
 Thin walled sac containing masses of proliferating
cells (germ cells)
 Asexual reproduction
 Primary Sporocyst & secondary Sporocyst
Larva
 S. haematobium has many larval stages
 miracidium
 sporocyst and cercaria.

13. Cercaria
 Elongated & oval with 400 μm length (including tail) & 60 μm breadth.
 Body is covered with minute spine like projection on the surface.
 Two suckers, i.e. anterior & ventral & has bifurcated tail.
 life span of 24–72 hours

14.  S. heamatobium passes its life cycle in 2 hosts.
 Definitive host: Humans. No animal reservoir is known.
 Intermediate host: Fresh water snails.
 Infective form: Cercarial larva

16. An individual bathing in an
infected pool or coming in contact
with contaminated water
cercariae
Cercariae stick to the
surface of the skin of the
swimmers or bathers, by
means of their ventral
suckers
Terminal – spined
eggs of S.
haematobium may
erode blood vessels
& cause
haemorrhages
Tissue reaction in connective
tissue hyperplasia produces
“pseudotubercle ’’ around the
egg (egg granuloma).
Pathogenicity of S. haematobiumPathogenicity of S. haematobium

17.  Disease caused by infection with S.haematobium is referred as schistosomiasis
haematobia ( urinary schistosomiasis or bilharziasis )
 Clinical features depend on the stages in the evolution of the infection,
 By the cercariae at the site of entrance.
 By the toxic metabolites.
 At the time of laying eggs.

18. Cercarial Dermatitis
 After 2 or 3 days of cercarial invasion, an itchy
maculopapular rash develops on the affected areas
of the skin called as cercarial dermatitis
(swimmer’s itch).
 Particularly seen with the cercariae of non human
Schistosomes.

19.  Liberated during the growth of schistosomulae in the portal blood of the liver
 General anaphylactic reaction characterised by
 Fever, urticaria
 Eosinophilic Leucocytosis
 Enlarged tender liver
 Palpable spleen
 Symptoms appear between the 4th and the 5th week of the infection

20.  Regarded as a localising symptom, generally occurring within 3 to 9 months of the
infection.
 Characteristic manifestation is a painless terminal haematuria.
 Adjacent structures of uro-genital apparatus are involved
 At first by the reversible granulomatous inflammatory reaction to eggs
 Later by the irreversible fibrosis and calcification.
 Squamous cell carcinoma of urinary bladder has been seen to be associated
with urinary schistosomiasis.

21.  Geographical distribution: various parts of Africa and South America. No cases
are reported from India so far.
 S. mansoni produces intestinal schistosomiasis in humans.
 Habitat: Adult worm lives in the inferior mesenteric vein.
Common name: Manson’s blood fluke

22. Morphology
 Adult worms are similar to other Schistosomes
 Gravid female - the uterus contains very few eggs,
usually 1–3 only.
 Prepatent period is 4–5 weeks.
 Nonoperculated eggs have characteristic lateral
spine.
 Measures 110–175 μm × 45–70 μm

23.  Definitive host: Humans are the only natural definitive hosts, though in endemic
areas monkeys and baboons have also been found infected.
 Intermediate host: Planorbid fresh-water snails of the genus Biomphalaria.
 Infective form: Fork-tailed cercaria.
Life cycle

24.  In humans, the schistosomulae mature in the liver & the adult worms move against
the blood stream into the venules of the inferior mesenteric group in the
sigmoidorectal area.
 Eggs penetrate the gut wall, reach the colonic lumen, & are shed in feces.
Life cycle

25. Pathogenesis of mansonian schistosomiasis occurs in three stages.
 Cercarial Dermatitis
 Acute Schistosomiasis (Katayama Fever)
 Chronic schistosomiasis

26.  Characterized by
 Fever
 Generalized lymphadenopathy and
 Hepatosplenomegaly.
Acute Schistosomiasis (Katayama Fever)
 Acute phase of disease occurs within 4–8 weeks of infection, especially when the
Schistosomes start producing eggs.
 Antigens (released from eggs) & adult worms stimulate the host humoral response,
leading to the formation of immune complexes & serum sickness like illness called
Katayama fever.

27. Chronic Schistosomiasis
 After eggs are produced, they are trapped in the small venules & are carried into
the intestine (or less commonly to bladder) & are excreted in feces. Some are
carried through portal circulation into liver and other parts of the body.
 Intestinal disease
 The eggs are deposited in the intestinal wall.
 Soluble antigens liberated from eggs induce inflammatory reactions that lead to
granuloma formation around the eggs in the intestine.

28. Hepatosplenic disease
 Granuloma formation and fibrosis in liver (Symmers pipe stem fibrosis)
seriously impedes the portal blood flow leading
 Portal hypertension,
 Hepatomegaly (seen in 15–20%),
 Splenomegaly and
 Gastric varices.

29. Other body sites
 Pulmonary involvement occurs when eggs are carried & lodged in the lungs by
collateral circulation.
 Egg sequestration and granuloma formation may cause
 pulmonary emboli formation,
 Pulmonary hypertension and
 right sided heart failure(cor pulmonale).
 Spinal cord schistosomiasis & myelopathy
 Nephrosclerosis & kidney failure due to circulating immune complexes deposited
in glomerular membrane
 Secondary bacterial infection especially with Salmonella species.

30.  Habitat
 Adult worms are seen typically in the venules of the superior mesenteric vein
draining the ileocecal region.
 Seen in the intrahepatic portal venules and hemorrhoidal plexus of veins.
 Common name: Oriental blood fluke
 Distribution
 S. japonicum is found in the far east, Japan, China, Taiwan, Philippines, and
Sulawesi.

31. Morphology
 similar to the schistosomes except
 Adult male is comparatively slender (0.5
mm thick) & does not have cuticular
tuberculation's.
 Gravid female - the uterus contains as many as 100 eggs at one time & up to 3,500
eggs may be passed daily by a single worm.
 Prepatent period is 4–5 weeks. Eggs are smaller & more spherical than those of S.
haematobium and S. mansoni.
 No spine, but shows a lateral small rudimentary knob.

32. Life Cycle
 Life cycle of S. japonicum is similar to S. haematobium with the following
exceptions.
 Definitive host: Man is the definitive host but in endemic areas, natural infection
occurs widely in several domestic animals & rodents,
 Intermediate host: Amphibian snails of the genus Oncomelania.
 Infective form for humans: Fork tailed cercaria.

33.  Eggs deposited in the superior mesenteric venules penetrate the gut wall and
are passed in feces.
 They hatch in water and the miracidia infect the intermediate hosts, amphibian
snails of the genus Oncomelania.
 Fork-tailed cercaria, which escapes from the snails is the infective form for
men and other definitive hosts.
Life Cycle

34.  Pathogenesis is similar to that caused by S. mansoni.
 Disease is more severe because of the higher egg production and smaller size of
the eggs (easy dissemination).
 Cercarial dermatitis
 Katayama fever: Seen after 40 days of infection.
 More severe and sometimes leads to death.

35. Intestinal disease: Deposition of egg granulomas in the intestinal wall leads to
 Mucosal hyperplasia,
 Ulcers,
 Micro abscess formation &
 Pseudopolyposis with blood loss
Hepatosplenic disease: Seen due to granulomatous response surrounding the eggs

36.  Parietal lobe is the most common site.
 Symptoms include Jacksonian convulsions & grand mal seizures
 Carcinoma: Both colorectal carcinoma & liver carcinoma (& cirrhosis) are reported
from people of China and Japan infected with S. japonicum
 Chronic secondary infection with Salmonella species and hepatitis B virus has been
associated with S. japonicum.
Central nervous system (CNS) infection: Occurs in 2–4% of cases.

37.  First recognized in 1934 is found in West-
Central Africa.
 Eggs are fully embroyonated without any
operculum having terminal spines, but are
passed exclusively in stools. The eggs are acid
fast.
 Produces few symptoms involving the
mesenteric portal system.
 Diagnosis is established by detection of the egg in feces and rectal biopsy.

38.  First recognized in 1978 is found in Thailand
and Cambodia, along the Mekong river.
 Closely related to S. japonicum but are slightly
smaller and round.
 Man and dog are the definitive host.
 Man acquires infection in the same way as in S. Japonicum.
 Hepatosplenomegaly and ascites are the common clinical finding.

39. Urine Microscopy
 Detection of nonoperculated terminal spined eggs in the urine or rarely in feces.
 Terminal hematuria portion of urine is collected between 12 pm & 3 pm,
concentrated by centrifugation or by membrane filtration.
 Observed under microscope

40.  Eggs with lateral spine can be demonstrated in stool or rarely in urine.
 Chronic cases or in patients with low worm burden,
the number of eggs excreted in stool is less &
intermittent.
 Multiple stool specimens should be examined.
 Stool concentration techniques - Gravity or centrifugal
sedimentation

41.  Hatching test
 Quantitation of eggs in stool specimens can be done by Kato thick smear
technique.
Rectal Biopsy Specimen
 Lateral spined eggs in biopsy material from rectal mucosa confirms the diagnosis
of schistosomiasis.
 Egg shell of S. mansoni is acid fast & can be stained by modified ZiehlNeelsen
stain.

42. Antigen Detection
 Detection of circulating antigen indicates recent infection
 Used for monitoring the treatment response.
 Useful when urine microscopy fails to detect eggs (chronic & ectopic cases).
 Circulating cathodic antigen (CCA) & circulating anodic antigen (CAA) in serum
and soluble egg antigen (SEA) in serum.

43. Antibody Detection
 ELISA
 Complement fixation test
 Immunofluorescence
 Indirect heamagglutination test
 Latex agglutination test
 RIA

44. Intradermal skin test ( fairley’s test )
 Allergic reaction , positive in all the varieties of schistosomiasis
Imaging
 X-ray –bladder and ureteral calcification
USG- hydroureter & hydronephrosis.
Other tests
 Blood examination
 Eosinophilic count – increased in early cases
 Aldehyde test – often positive (due to globulin value)

45.  Treatment of schistosomiasis depends
 stage of infection
 clinical presentation.
 Therapy for acute schistosomiasis or Katayama syndrome needs to be adjusted
appropriately for each case.
 Severe acute schistosomiasis management in an acute-care setting is necessary, with
supportive measures & consideration of glucocorticoid treatment to reduce
inflammation.
 Once the acute critical phase is over, specific chemotherapy is indicated for parasite
elimination.

46.  Drug of choice is praziquantel, depending on the infecting species is administered
PO as a total of 40 or 60 mg/kg in two or three doses over a single day.
 Praziquantel treatment results in parasitologic cure in ~85% of cases and reduces
egg counts by >90%.
 Metriphonate is the alternative drug of choice in schistosomiasis due to S.
haematobium. (7.5 mg/kg. weekly for 3 weeks).
 Oxamniquine ( 15- 20 mg/kg as a single dose) is also effective for S.mansoni

47.  Prophylactic measures include:
 Eradication of the intermediate molluscan hosts.
 Prevention of environmental pollution with urine and feces.
 Effective treatment of infected persons.
 Avoid swimming, bathing, and washing in infected water.
 Vaccination.

48. 1. Antigenic modification
 Antigen disguise:
 Adult Schistosoma cover themselves with host proteins to be considered as self &
will not be attacked by the immune factors.
 Surface turnover :
 Schistosoma mansoni shed their teguments in abundance can neutralize antibody
response at a distance away from the parasite.
 Antigen mimicry:
 Schistosoma produce antigens similar to host antigens so they are not recognized
by the host’s immune system.
1. Antigenic modification
2. Production of blocking antibodies
3. Inhibition of Immune Factors

49. 2- Production of blocking antibodies

Antibodies of little protective effect.
 Schistosoma produce blocking Abs that combine with Schistosoma Ags making
them unavailable for antibodies of high protective effect .
3- Inhibition of Immune Factors
Schistosoma larva , inactivates the complement system through protease activity .The
mechanism of immune evasion is not resolved completely till now.

50.  Vaccine strategies represent an essential component as an adjunct to chemotherapy
for the future control of Schistosomiasis.
 An improving understanding of immune response to Schistosome infection suggest
the development of vaccine is possible .
 Vaccination against Schistosome can be targeted towards prevention of infection and
reduction in worm burden.

51.  Existance of immunity in the presence of active adult
infection is considered by Smithers and Terry (1969),to be an example of
Concomitant immunity.
 Phenomena of concomitant immunity is studied in baboon, mice, rats and humans.

52.  Live cercariae or Schistosomulae as well as attenuated forms are used to immunize
experimental animals in which they induce immunity.
 Such immunized animals are substantially protected from pathogenic effect and
shows 60-70% lower worm count and tissue egg count than non –vaccinated
animals.

53. Tetraspanin (Sm-tsp-1& Sm-tsp-2)
 Important vaccine candidate .
 Present at apical syncytial surface of S. mansoni.
 Used in a defined vaccine formulation & upon administration provided :
 Protection 29-61 %
 Reduction in egg burden 50-61 %

54.  Sm-28-GST (Glutathione S- transferase)
Expressed in subtegumental tissues of developmental stages of parasite.
 Used as the potential vaccine candidate against human Schistosome infection.
 Successfully tested at primate level and ready for human trial.

55.  Sm-p80 (calpain)
 First vaccine antigen identified on the basis of T-cell activity.
 Sm-p80 – based vaccine formulation have three protective effects:
 Worm reduction .
 Antifecundity effect .
 Protection against acute Schistosomiasis .
 worm reduction 60-70%

56.  A number of recent studies, have utilised plasmid DNA vaccines.
 Generate both T-cell and B-cell immune responses.
 Particularly appealing for Schistosome vaccines development.

57.  An effective, protective Schistosomiasis vaccine would be of immense public
importance.
 The apical membrane proteins, help in immune evasion are the logical vaccine
targets.
 All mentioned candidate vaccines are based on this idea.
 One successful human trial is yet to be completed, the vaccine will be available
for commercial product in next few years time.