Schistosomiasis is a parasitic disease caused by the Schistosoma genus, primarily affecting individuals in poor sanitation areas, particularly school-age children in sub-Saharan Africa. The disease's life cycle involves freshwater snails, leading to significant morbidity and mortality through various clinical manifestations such as abdominal pain, hematuria, and chronic organ damage. Diagnosis relies on geographic history and the detection of schistosome eggs in stool or urine, with praziquantel as the main treatment and prevention through community health measures and education.

1. SCHISTOSOMIASI
S
By ; Dhanani Ynarah

2. TOPIC OUTLINES
■ Introduction
■ Epidemiology
■ Etiology and life cycle
■ Pathogenesis
■ Clinical manifestations
■ Diagnosis and Laboratory tests
■ Treatment
■ Prevention and Control

3. INTRODUCTION
■ Schistosomiasis is a parasitic disease caused by flukes ( trematodes) of the
Genus Schistosoma.
■ Schistosomiasis or ( Snail Fever ) is an important cause of disease in many
parts of the world, most commonly in places with poor sanitation. School-age
children who live in these areas are often most at risk because they tend to
swim or bath in water containing infectious cercariae.
■ After malaria and intestinal helminthiasis, Schistosomiasis is the Third most
devastating tropical disease in the word.
■ Schistosomiasis is a major source of morbidity and mortality For developing
countries in Africa, the Middle East and Asia.
■ Most human Schistosomiasis is caused by S. haematobium, S. mansoni, S.
japonicum.

4. EPIDEMIOLOGY
■ It is estimated that 230 million people are infected
globally, with ~800 million people living in areas where
there is a risk of infection.
■ More than 70% of infected people live in sub-Saharan
Africa.
■ It is a poverty-related disease.
■ Infection is prevalent in areas where adequate water
supplies and sanitary facilities are lacking.
■ A characteristic feature of schistosomiasis infection in
human populations is a convex age–prevalence curve:
A. with low prevalence in very young children
B. higher prevalence in older children with a peak at
10–15 years of age
C. and declining prevalence in adults.

5. ETIOLOGY
■ Human schistosomiasis is caused by five species of
the parasitic genus Schistosoma:
 S. mansoni, S. japonicum, S. mekongi, and S.
intercalatum cause intestinal disease
 S. haematobium causes urogenital disease.
■ The infection may cause considerable intestinal,
hepatic and genitourinary morbidity.
■ RISK FACTORS
1. wading or swimming in lakes, ponds and other
bodies of water which are infested with the
snails
2. Fishing (both men and women)
3. Women washing clothes in infested water are at
risk

6. LIFE CYCLE
■ LIFE CYCLE
■ 1.Diagnostic stage
■ 2. INFECTIVE
STAGE

7. PATHOGENESIS
 Schistosomiasis is characterized by there distinct syndromes:
A. Cercarial Dermatitis
B. Acute Schistosomiasis
C. Chronic Schistosomiasis
 When People become infected when larval parasites(released by
freshwater snails)
penetrate their skin during contact with infested water.
the larvae develop into adult schistosomes.
Adult schistosomes live in the blood vessels where the females
release eggs.
Some of the eggs are passed out of the body in the faeces or
urine to continue the parasite life-cycle.
Others become trapped in body tissues (intestinal and urinary
system), causing an immune reaction and progressive damage
to organs.

8. CLINICAL MANIFESTATIONS
■ Schistosomiasis occurs in three stages that vary
by species, intensity of infection, and host factors
(e.g., age, genetics).
■ Cercarial dermatitis causes a pruritic
maculopapular rash (“swimmers’ itch”) that lasts
for 1–2 weeks.
■ Acute schistosomiasis (Katayama fever)-
Caused by S.japonicum and presents between
2 weeks and 3 months after parasite exposure
with fever, myalgia, general malaise, fatigue,
headache, cough, abdominal tenderness,
eosinophilia, and transient pulmonary infiltrates.

9. CLINICAL MANIFESTATIONS
■ Chronic Schistosomiasis: It is largely associated with
the granulomatous & fibrotic responses to Schistosoma
ova during mature infections and mainly include:
A. Intestinal schistosomiasis
B. Urinary Schistosomiasis.
A. Intestinal schistosomiasis( S. Mansoni and S.
Japonicum)- Cause due to parasite eggs passing
through or becoming trapped in intestinal tissue,
lead to mucosal granulomatous inflammation with
microulcerations, superficial bleeding.
1. Symptoms:
1. Abdominal pain
2. Diarrhea
3. Blood in stool, fresh or melena
4. Hematemesis and Liver enlargement.

10. CLINICAL MANIFESTATIONS CONTd.
■ Urogenital schistosomiasis(S. haematobium):
1. Hematuria (terminal)
2. Dysuria
3. Frequent need to urinate (polykauria)
4. In females; genital lesions, vaginal bleeding, pain during
sexual intercourse and nodules on the vulva, irregular
menstruation
■ Pulmonary disease (e.g., pulmonary hypertension, cor
pulmonale) and CNS disease (e.g., seizures, encephalopathy,
transverse myelitis) can occur and are due to granulomas
and fibrosis.
■ Hepatosplenic Schistosomiasis(s.mansoni and s.
Japonicum)-caused by schistosome eggs trapped in liver
tissue; lead to early inflammatory hepatosplenomegaly and
late hepato- splenic disease with periportal fibrosis.

11. DIAGNOSIS
■ Diagnosis is based on geographic history,
clinical presentation, and presence of
schistosome ova in excreta.
■ The definitive diagnosis depends on the
pathogen examination.
1. Stool examination:
1. (i) Direct fecal smear for acute stage
2. (ii) Concentration method: Water
sedimentation method and miracidia
hatching test can be done at same
time; nylon net method may be used
2. Biopsy can be done by proctoscope for
terminal stage.
3. Immunological tests are subsidiary for
reference only.

12. DIAGNOSIS AND LABORATORY
TESTS
 SAMPLES
 STOOL
 URINE
 SERUM
 Macroscopic:
 Stool speciment ( may be dysenteric )
 Urine speciment ( may be terminal
hematuria ).

13. DIAGNOSIS AND LABORATORY TESTS
■ Microscopically:
 Demonstration of parasite eggs in stool or urine
i s g o l d s t a n d a r d t e s t f o r d i a g n o s i n g
Schistosomiasis.
 The sensitivity maybe low especially with light
infection & take 6 weeks for eggs to be detect
after the initial infection.
 S.Haematobium eggs are usually found in urine
but my also be present in stool.
 S.Mansoni & the other intestinal schistosomes,
S.japonicum, S.Merangi & S.Intercalatum are
found in stool.

14. DIAGNOSIS AND LABORATORY TESTS
■ THE EGGS ARE VERY CHARACTERISTICS AND CONFIRM
DIAGNOSIS

15. DIAGNOSIS AND LABORATORY TESTS
■ URINE DIPSTICK: S.Haematobium infections are
usually associated with hematuria on dipstick testing.
■ Full blood count:
1. May show an eosinophilia which is frequently
marked during the acute stage of infection.
2. Anemia patient may also be seen due to chronic
blood loss from the urinary or intestinal tract.
3. Pation with hepatosplenic Schistosomiasis my
have thrombocytopenia secondary to splenic
sequestration.
■ Diagnosis can also be made by demonstrating eggs in
tissue biopsy specimens from the rectum, liver,
bladder or cervix depending on the site of infection.

16. DIAGNOSIS AND LABORATORY
TESTS ■ Antigen detection:
 Schistosoma the antigen weaks are present in the serum
& urine.
 To antigen referred to as circulating anodic antigens
(CCA) & circulating cathodic antigens ( CCA ) can be
detected in laboratory sensitivity of these test depend on
largely & intensity of infection.
■ Antibody test:
 Schistosoma antibodies can be detected by enzyme
linked lmmunosorbent assay ( ELISA ).
 it is application is limited as these antibodies will only
appear after 4-6 weeks.
 present of IgE antibody is marked of chronic active
disease.
■ Polymerase chain reaction:
 Specific & highly sensitive detection of Schistosoma.
 DNA in urine, stool & serum.
 Advantage able to diagnosis Schistosomiasis in all stage

17. TREATMENT
■ Praziquantel(DOC):
A. 20 mg/kg bid)-S. mansoni, S. intercalatum, and S.
haematobium.
B. 20 mg/kg tid for S. japonicum and S. mekongi infections)
■ In failures of initial treatment, the same dose can be repeated
at weekly intervals for 2 weeks.
■ In young migrating schistosome stages, treatment may need
to be repeated in 6–12 weeks if eosinophilia or symptoms
persist.
■ Glucocorticoids can be added in Katayama fever to suppress
the hypersensitivity reaction.
■ Late established manifestations, such as severe fibrosis, do
not improve with treatment.

18. TREATMENT

19. PREVENTION AND CONTROL
■ Mass treatment of entire communities and targeted treatment of school-age
■ Environmental sanitation(Improved sanitation could reduce or eliminate
transmission of this disease)
■ Safety of supply water
■ snail control with spraying & drip feeding. Molluscisciding drip feeding
■ Swimming in adequately chlorinated pools.
■ Vigorous towel drying after accidental exposure.
■ Topical application of the insect repellent DEET can block penetrating cercariae.
■ Education-the risk of getting infected by bathing in fresh water lakes and
ponds/dams.
■ Heating bathing water to 50°C (122°F) for 5 minutes or filtering water with fine-
mesh filters.
■ Allow bathing water to stand for 2 days because cercariae rarely remain
infective longer than 24 hrs.