SCHISTOSOMIA

SIS
dr. Vera Diana Towidjojo, [Link]
Departemen Parasitologi
Fakutas Kedokteran
Universitas Tadulako
 INTRODUCTION

• Schistosomiasis or Bilharzia is
caused by schistosomes, which are
parasitic trematode worms of the
genus Schistosoma.

• Schistosomiasis is the third most

devastating tropical disease globally,
affecting mostly in developing
countries in Africa and Asia.

• Cental Sulawesi is the endemic of

Schistosomiasis in Indonesia,
located in Lindu Lake, Napu Valley,
and Bada Valler
Distribution of Schistosoma sp
Life Cycle
Stages
STADIUM
INFEKTIF

Cercaria
PATHO
PHYSIOLOG
I

HABITAT:
(A) Schistosoma
japonicum at Plexus
mesentericus
superior,

(B) Schistosoma
mansoni at plexus
venosus inferior

(C) Schistosoma
hematobium at
plexus venosus
vesicalis.
• Human or animal hosts (as with S. japonicum) get infected when they come in contact
with fresh water contaminated by cercariae, the infective stage of the parasite
• Upon host location, the cercariae attach to and penetrate the host skin via glandular
secretions. The parasites lose their tails as they penetrate the skin, and transform into
young schistosomes called schistosomula
• After spending at least two days in the skin, the parasites burrow through the dermis,
penetrate a blood vessel wall, and gain access into the circulatory system. The
parasites migrate to the lungs and remain there for several days before travelling to the
liver were they blood-feed on red blood cells, mature and mate within the liver vessels.
Afterwards, they emerge as male-female worm pairs, and inhabit either the portal or
pelvic vessels
• The female begins to lay eggs within the mesenteric or pelvic vessels. Most of the eggs
are carried upstream to the liver via the portal veins and its branches and get trapped in
the pre-sinusoidal portal venules
• Some of the eggs migrate and penetrate the intestines and shed in the stool. Eggs laid
in the pelvic venous plexus migrate towards the urinary bladder, pass through the
bladder wall, and are excreted in urine.
• When eggs contact water, they hatch into ciliated larval forms called miracidia that can
sense compatible intermediate snail hosts.
• Miracidia penetrate the snail by proteolytic activity and mechanical movement. Inside
the snail host, miracidia undergo asexual development and transform into cercariae
which emerge from the snails and seek out the definitive host.
PATHOLOGY AND SYMPTOMS
Acute Phase (Katayama Syndrome).
Clinical manifestations come out after 4 to 8
weeks of infection, similar to the time from
egg to adult worm (40 days)
• Egg Production
• Chills, fever, fatigue, headache, malaise
• Much exposure to antigens
• Granulomas surround eggs
• Eosinophils, neutrophils, macrophages
• 1-2 weeks fibroblasts enter granuloma
• Psuedotubercles-fibrous granulomas
• Schistosomula antigens/secretions
orchestrate a T helper type 1 (Th1)
(involving tumour necrosis factor,
interleukin-1, and interleukin-6 cytokines)
and cause febrile illness. As mature female
worms lay eggs, products of worm and egg
metabolism induce formation of immune
complexes resulting to a serum like-sickness
called Katayama syndrome
Acute infection
• Nonspesificdifficult to
diagnose
• “Swimmer itch/cercarial
dermatitis”inflammation&
pruritus penetration of
cercaria into the skin
• Febrile illnes,”snail fever or
Katayama fever”self
limiting febrile
• Arthralgia,myalgia,abdomin
al pain
• A history of exposure of
skin to water in endemic
areas
PATHOLOGY AND
SYMPTOMS

Chronic Phase
• S. japonicum, S. mansoni
Asymptomatic
S. haematobium
• Mild, chronic dysentery
• Blood in the
• Abdominal pain
urine • 8% infections develop liver
• Pain with fibrosis
urination • that impedes blood flow
• Loss of
• Cirrhosis of liver
bladder
• Long term problems
function
• Hepatosplenomeagly
• Long term: loss of tissue function
Symptom
Chronic infection
• body’s reaction to the worms'
eggs.
• Chronic pathologyadult worm
find in the portal circulation
• A mated pair of worms 300-
• 3,000 eggs/dayreleased into
the capillaries and portal veins
• Intestinal schistosomiasis 
abdominal pain, diarrhoea,
and blood in the stool.
• Splenomegaly,
ascites
• Egg must be insertedterminal vein within
the bowel wall and then be ulcerated (via
immune-mediated inflammation) through
the mucosa into the bowel lumenlocal
inflammation protein loss, iron loss, anemia
of chronic disease, diarrhea and intestinal
discomfort.
• Eggs become permanently trapped in host
tissues immune-mediated inflammatory
granulomaliver fibrosisportal
hypertensionascites,hepatosplenomegaly
TERMINAL STAGE OF
SCHISTOSOMIASIS
Liver cirrhosis is the prominent
syndrome of this stage

According to the
manifestations , it
can be divided into three
types:
• The type of giant spleen
• The type of ascites
• The type of dwarf
Diagnosis
Acute infection
• Acute infectionclinical symptoms are
nonspecificdifficult to diagnose
• Serologic testsantibody
• A history of exposure of skin to water in endemic
areas + suitable clinical syndrome
Chronic infection
• Direct stool examination (Kato-Katz technique)
 determining the presence of infection and the
associated egg density in affected humans.

• ELISA  soluble schistosome antigens

Treatment
• Prazikuantel / oral 60 mg/kgbbcure rate 80-90%
• In areas of high prevalencemass chemotherapy
(main control strategy)
• Environmental control (Oncomelania host snail)
• Improved sanitation
Roadmap Eradication Of Schistosomiasis In Indonesia