Schistosoma in

Egypt
Prepared By:
407-417

Supervised By:
Professor Dr. Suzan Fathy El-Nasery
Dr. Safaa
 INTRODUCTION
Schistosomiasis, caused by a trematode helminth, infects over 200
million people,
with eighty percent of infections occurring in sub-Saharan Africa. It was
described in the mid-19th century by Theodor Bilharz; however,
symptoms characteristic
of the disease were described in antiquity and schistosome eggs have
been found in Egyptian and Chinese mummies.

Currently, most of the affected human population inhabit areas lacking

clean drinking water and adequate sanitation. Farmers and children can
be exposed from contact with infested water in irrigation ditches and
flooded fields; tourists may acquire
schistosomiasis after swimming or wading in infested freshwater.

History
A. Schistosomes were first described in Egypt by Theodor Bilharz in 1851,
and Wilhelm Griesinger associated the worms with the disease. They
named the worm Distoma haematobium, but the name didn’t stick.

B. In 1858 the genus Schistosoma was proposed, which did stick, but
there were Johnny-come-lately rivals: Gynaecophorus (1858), Bilhar-zia
(1859), and Thecosoma (1860). Schistosoma had precedence.

C. Fujiro Katsurada (1905) discovered schistosomes in Japan and named

them Schistosoma haematobium japonicum, later shortened to
Schistosoma japonicum.

D. In 1907 Louis Sambon discovered a second species in Egypt, which he

called Schistosoma mansoni.

E. “A long and testy controversy of the existence of two species in

Egypt…was finally resolved by Robert Leiper in 1915.”

F. The life cycle of Schistosoma japonicum was figured out in 1913 by

Keinosuke Miyairi and Masatsuga Suzuki, and Leiper rapidly confirmed a
similar cycle for the Egyptian schistosomes.

G. Early on antimony tartarate was used for therapy and copper sulfate
for killing the intermediate host snails.

H. The Rockefeller Foundation initiated an eradication program in Egypt

between 1929 and 1940, but it failed.

I. By 1950 schistosomiasis was recognized as the most important tropical

disease in the world, after malaria.
 J. In 1958, as part of the Great Leap Forward, the Chinese Communist
Party initiated an eradication campaign in China, which cut the
prevalence about four-fold.
Epidemiology and ecology
A. The ranges of Schistosoma haematobium and Schistosoma mansoni overlap,
but that of Schistosoma japonicum is distinct.
1. Distribution is critically dependent on the availability of suitable
intermediate snail hosts, i.e.
a) Bulinis spp. for Schistosoma haematobium
b) Biomphalaria spp. for Schistosoma mansoni
c) Oncomelania spp. for Schistosoma japonicum
2. Climate, water quality, sanitation, and patterns of human water
use also influence the range of the diseases.
B. Recent World Health Organization estimates indicate that 200 million people
are infected worldwide, with over 600 million people at risk of infection (this
suggests that one quarter of the population in endemic areas are infected).

C. Usually the infection is acquired in childhood, peaking in the age group of 15–
20 years

S.mekongi
Morphology

Adult schistosomes share all the fundamental features of the digenea.

They have a basic bilateral symmetry, oral and ventral suckers, a body
covering of a syncytial tegument, a blind-ending digestive system
consisting of mouth, oesophagus and bifurcated caeca; the area between
the tegument and alimentary canal filled with a loose network of
mesoderm cells, and an excretory or osmoregulatory system based on
flame cells. Adult worms tend to be 10-20 mm long and use globins from
their hosts' hemoglobin for their own circulatory system.

Unlike other trematodes, the schistosomes are dioecious - i.e., the sexes
are separate. The two sexes display a strong degree of sexual dimorphism,
and the male is considerably larger than the female. The male surrounds
the female and encloses her within his gynacophoric canal for the entire
adult lives of the worms, where they reproduce sexually.
 Morphology
-Adults -Eggs -Miracidium -Sporocyst -Cercaria
-schistosomule
s.hematobium s.mansoni
male female male female

-shape:

Flat elongated
Contain no body cavity
Same but no Same as male Same as female
Folded to form
g.canal hematobium hematobium
gyenchephoric canal to
carry female
Size: 10x1 mm 20x0.25 mm 8x1 mm 14x0.15 mm
Structure:
It is outer covering layer Mora coarsely
 Cuticle Smooth Smooth
Tuberculated tuberculated

 muscle layer 3 layers below cuticle same Same same

 spongy tissue Organs of attachment rudimentry

Same as male
contain Ventral and oral As female hematobium
hematobium
organs : Well developed
1- suckers
Mouth : at the bottom of
oral sucker
Same but the
2- digestive reunion of
Pharynx : not muscler The same Same as male
system intestinal ceaca
Osephegus
preequatorial
Intestinal ceaca:
Reunite post equatorial
Consist of :
Flame cells
Excretory tubules
3- excretory Excretory duct
same same same
system Excretory bladder
Genital pore:
At top of g.canal just below
v.sucker
Consist of :
4-nervous Nerve ganglia
same same same
system Nerve filaments

Testes:
Ovary:
Globular
Single
3-5 n Same as male H
5-genital Post equat.
Behind v.sucker but: Same as femal H but:
system Oviduct
Vasa efferentia Testes 6-9 Ovary pre equat.
Ootype
Vase deference Smaller in size
Uterus
Seminal vesicle
Vitelline gland
cirrus
 s.hematobium S,mansoni

 oval  Oval
 140x50 micron  150x65
 Faint yellow  Yellowish
 Non operculated  Non operculated
 Terminal spine  Lateral spine
 Contain fully mature  Contain fully mature
miracidium miracidium

Embryo (miracidium) :
 Piriform
 Covered with cilia
 Contain:
a) Non primitive gut
b) 1 or 2 pairs of lytic
penetrating glands
c) 1 or 2 pairs of flame cells
d) 2 execretory
tubules

Sporocyst
It is a sac:
• Elongated
• Blind
• Contain germ cells

cercaria:
Consist of :

• body→rsemble adult in organization

• tail→biforked

schistosomule:
• It is derived from cercaria after
penetrating body &leaving its tail
Life Cycle:
Schistosomes have a typical trematode vertebrate-invertebrate lifecycle, with
humans being the definitive host. The life cycles of all five human schistosomes
are broadly similar:
parasite eggs are released into the environment from the stool of infected
individuals, hatching on contact with fresh water to release the free-swimming
miracidium.

Miracidia infect fresh-water snails [Bulinus truncatus for

hematopium and Biomphalaria Alexandria for mansoni] by
penetrating the snail's foot. After infection, close to the site of penetration, the
miracidium transforms into a primary (mother) sporocyst. Germ cells within the
primary sporocyst will then begin dividing to produce secondary (daughter)
sporocysts, which migrate to the snail's hepatopancreas. Once at the
hepatopancreas, germ cells within the secondary sporocyst begin to divide again,
this time producing thousands of new parasites, known as cercariae, which are
the larvae capable of infecting mammals.

Cercariae emerge daily from the snail host in a circadian rhythm,

dependent on ambient temperature and light. Young cercariae are
highly mobile, alternating between vigorous upward movement
and sinking to maintain their position in the water. Cercarial
activity is particularly stimulated by water turbulence, by shadows
and by chemicals found on human skin.

Penetration of the human skin occurs after the cercaria have

attached to and explored the skin. The parasite secretes enzymes
that break down the skin's protein to enable penetration of the
cercarial head through the skin. As the cercaria penetrates the skin
it transforms into a migrating schistosomulum stage.
 So there are three factors for cercarial penetration:
1- Attachment of suckers and secretion of lytic glands.
2- Tail as a lever.
3- Presence of water film.

The newly transformed schistosomulum may remain

in the skin for 2 days before locating a post-capillary
venule; from here the schistosomulum travels to the
lungs where it undergoes further developmental
changes necessary for subsequent migration to the
liver. Eight to ten days after penetration of the skin,
the parasite migrates to the liver sinusoids. During
this period that the parasite begins to feed on red
blood cells.
The nearly-mature worms pair, with the longer female
worm residing in the gynaecophoric channel of the
shorter male.

Worm pairs migrate to inferior mesenteric veins where S.mansoni settle but s.
hematopium migrate to rectal veins and cross porto systemic shunts through
inferior rectal vein to reach the vesical and pelvic venous plexus where they
settle.
They begin to produce eggs which are laid immature in the very fine capillaries
then acquire maturity in submocosa.

Then the eggs escape to fall in the lumen by effect of :

1- miracidial antigens.
2- Egg shell spine.

3- Contraction of the muscles.

Adult S. mansoni pairs residing in the mesenteric vessels may produce up to 300
eggs per day during their reproductive lives. Many of the eggs pass through the
walls of the blood vessels, and through the intestinal wall, to be passed out of the
body in faeces. S. haematobium eggs pass through the ureteral or bladder wall
and into the urinebut5%of eggs can pass through stool. Up to half the eggs
released by the worm pairs become trapped in the mesenteric veins.
Secreting antigens that elicit a vigorous immune response. The eggs themselves
do not damage the body. Rather it is the cellular infiltration resultant from the
immune response that causes the pathology classically associated with
schistosomiasis.

DAMS Dams and irrigation projects can either increase or decrease the prevalence of
disease.
With the construction of the Aswan Dam in Egypt, S. haematobium in the Nile Delta
decreased but S. mansoni in Upper Egypt increased. Dams built in the 1980s in the Senegal
River Basin caused a great increase in schistosomiasis 2. In contrast, when the Ertan Dam
in China was built, precautions were taken to ensure the prevalence of
schistosomiasis did not increase: concrete irrigation canals and piping systems for the
water supply were installed to eliminate the snails, molluscicides were used, sanitary
facilities were built for the workers, and infected people and cattle were treated with
praziquantel. Currently, the Three Gorges dam project in China is being monitored for
schistosomiasis.
Pathogenesis and pathology:
Schistoso Schistoso Schistoso
Schistoso
Schistosoma ma ma ma
Species ma
mansoni haematobi intercalat japonicu
mekongi
um um m
Bulinus
Biomphalaria glabrata Oncomela
truncatus Tricula
Intermediat B. alexandrina Bulinus nia
Bulinus aperta
e host B. pfeifferi forskali hupensis
globosus a.o.
a.o. a.o.
a.o.
East Asian
Form of the urogenital intestinal intestinal
intestinal bilharziasis intestinal
disease bilharziasis bilharziasis bilharziasis
bilharziasis
Gabun,
East Asia,
Endemic South America, the Carribean, Africa, the Cameroon,
South East Indochina
Areas Africa, the Middle East Middle East Tschad,
Asia
Zaire

Schistosomiasis is one of the most important communicable diseases, both

for public health and because of its socio-economic impact in the
developing world. Currently, 200 million people are infected worldwide,
among which 120 million are symptomatic and 20 million have severe
disease.

Different species of Schistosoma are known to infect humans. Infection

with Schistosoma mansoni, S. japonicum, S. mekongi and S. intercalatum
is associated with chronic hepatic and intestinal fibrosis. Schistosoma
haematobium infection results in fibrosis, structuring and calcification of
the urinary tract.

Schistosomiasis results from the host’s immune responses to schistosome

eggs, including a granulomatous reaction evoked by the antigens they
secrete. Most granulomas develop at the sites of maximal accumulation of
the eggs, which are the intestine and the liver for S. mansoni, since worms
locate in the portal mesenteric system.
Testicular schistosomiasis caused by S. mansoni is exceedingly rare; till
now only 11 cases have been reported in PubMed/Medline.

The pathology and pathogenesis of bilharzial infection are related to 3

stages.

1. Stage of Invasion and maturation:-

 considered as the incubation period prior to egg deposition. This includes
cercarial penetration, schistosomular migration and maturation.
Mild maculopapular skin lesion may develop in a cute infection within
hours after exposure to cercaria.

katayama Syndrome :
Fever, cough, fatigue, splenomegaly, lymphadenopathy Eosinophilia
(Sometimes PIE…pulmonary infiltrates and eosinophilia)

• Clinical picture of this stage:

Cercarial penetration manifestal by
papular rash-pruritis.

Schistosomular migration manifested

by
-Fever.
-Cough.
-Marked peripheral eosinophilia and circulating immune complexes.
-Lethargy.
-Eruption of pale temporary bumps associated with severe itching
(urtecaria).

2. Stage of Established infection:

Correspond to stage of ovi-deposition and egg extrusion.
Most of pathologic lesions in bilharziasis are due to deposition of
schistosomal eggs. The soluble schistosomal antigens from the eggs
initiate in the tissue an inflammatory granulomatous reaction. Which is
an example of a cell- mediated immunity.

Living adult worms produce no tissue damage because they acquire a

coating of host antigen on their cuticle, while dead adults produce a local
inflammatory reaction because the schistosomal antigen will come in
contact with the tissue.

• Clinical picture of this stage:

 i- terminal haematuria, dysuria, frequency in schistosoma
haematobium due to egg retention and granulome formation.

ii- dysentery - in the form of diarrhea accompanied by tenesmus

with mucus and blood in stools – cramping in schistosoma mansoni
due to egg retention and granulome formation.

3. Stage of late infection and complications:

progressive formation of fibrous tissue which prevents extrusion of eggs
resulting in complications according to the organ involved.

A) Complications of (schistosoma haematobium).

i- Urinary complication:
* Urinary bladder:
- congestion and haemorrhage due to the spine of the ova and its
traumatization to the mucosa.
- Sandy patches: The commonest lesion in urinary bladder (60-
70%) due to deposition of large number of bilharzial ova
(calcified).
- Ulcer in the bladder: healing by fibrosis usually occur.
- Finally bladder carcinoma due to squamous metaplasia.
(Transitional epithelium of the bladder
transformed to squamous one).
* Ureter: hydroureters- pyourter- sticture.
* kidney: hydronephrosis- pyonephrosis.
* genital organs: pseudo-elephantiasis of the penis –
granuloma in prostate- ovary- uterus- vulva.
ii- Extraurinary complications:
Ova of S. haematobium may reach the lung as emboli through
branches of IVC. Ova will reach pulmonary artery and impacted in its
branches leading to necrotizing arteriolitis leading to bilharzial
corpulmonale which is a condition of right side heart failure secondry
to fibrosis and sclerosis of the pulmonary artery branches.

B) Complications of S. mansoni:
i- Intestinal lesions:
 - oedema and pin point haemorrhages due to escape of ova from
blood vessels to the lumen of the intestine.
- Sandy patches due to deposition of large number of calcified ova.
- bilharzial polypi: large mass of bilharzial granulomatous reaction is
formed in submucosa.
- Fissures and perianal sinuses.
ii- Hepatic affection in the form of hepatic fibrosis and this lead
to :
a- portal hypertension - hepatic dysfunction.
b- Splenomegaly- ascites.
N.B. Co-infiction with hepatitis B or C can
accelerate hepatic dysfunction and raise risk for
hepato-celluler carcinoma beyond that seen
with hepatitis alone.
c- Haematemesis: due to portal hypertension that
open portosystemic shunts leading to oesophageal varicose venis
rupture of these veins leading to haemorrhage and vomting of blood.
iii- pulmonary complications:
Ova of S. mansoni carried from the portal circulation to the systemic
circulation and reach the lung. (Due to portal hypertension.)
Diagnosis:
Microscopic identification of eggs in stool or urine is the most practical
method for diagnosis. The stool exam is the more common of the two.
For the measurement of eggs in the feces of presenting patients the
scientific unit used is epg or eggs per gram. Stool examination should be
performed when infection with S. mansoni or S. japonicum is suspected,
and urine examination should be performed if S. haematobium is
suspected.

Eggs can be present in the stool in infections with all Schistosoma

species. The examination can be performed on a simple smear (1 to 2 mg
of fecal material). Since eggs may be passed intermittently or in small
amounts, their detection will be enhanced by repeated examinations
and/or concentration procedures (such as the formalin-ethyl acetate
technique). In addition, for field surveys and investigational purposes, the
egg output can be quantified by using the Kato-Katz technique (20 to 50
mg of fecal material) or the Ritchie technique.

Eggs can be found in the urine in infections with S. japonicum and with S.
intercalatum (recommended time for collection: between noon and 3
PM). Detection will be enhanced by centrifugation and examination of the
sediment. Quantification is possible by using filtration through a
nucleopore membrane of a standard volume of urine followed by egg
counts on the membrane. Investigation of S. haematobium should also
include a pelvic x-ray as bladder wall calcificaition is highly characteristic
of chronic infection.

Recently a field evaluation of a novel handheld microscope was

undertaken in Uganda for the diagnosis of intestinal schistosomiasis by a
team led by Dr. Russell Stothard who heads the Schistosomiasis Control
Iniative at the Natural History Museum, London. His report abstract found
here:
Tissue biopsy (rectal biopsy for all species and biopsy of the bladder for
S. haematobium) may demonstrate eggs when stool or urine
examinations are negative.
The eggs of S. haematobium are ellipsoidal with a terminal spine, S.
mansoni eggs are also ellipsoidal but with a lateral spine, S. japonicum
eggs are spheroidal with a small knob.

Antibody detection can be useful in both clinical management and for

epidemiologic surveys.
• intestinal schistosomiasis
1. History of freshwater exposure
2. Stool for O&P (egg counts and viability)
3. Serology-- Elisa and Western Blot
4. Antigen capture
5. Eosinophilia
6. Rectal snips or biopsies
7. Liver biopsy
8. Ultrasound or CT of abdomen
• urinary schistosomiasis
1. History of freshwater exposure
2. Screening for blood and protein in urine
3. Urine for eggs (9am to 3pm collection concentration, egg counts &
viability)
4. Ultrasound, CT or IVP
5. Serology-- Elisa and Western Blot
6. Antigen capture
7. Eosinophilia
8. Cystoscopy-trigone appearance

Procedures
Rectal biopsy or bladder mucosal biopsy
o Mucosal biopsy is effective for visualizing eggs.
o Biopsy is helpful when stool sample findings are negative or
in light infection.
o Obtain multiple biopsy samples and crush them between
slides (to increase egg-detecting sensitivity).
• Sigmoidoscopy/proctoscopy
o To obtain mucosal biopsies (including rectal)
o For diagnosis and to identify complications such as
pedunculated and sessile polyps
• Upper endoscopy
o Assess for esophageal varices.
o Treat upper intestinal bleeding with endoscopic
sclerotherapy.
• Cystoscopy
o To obtain mucosal biopsy for diagnosis
o To assess complications such as bladder cancer
• Surgical biopsy findings may be used to diagnose ectopic
schistosomiasis.
 Treatment
Antimony has been used in the past to treat the disease. In low doses, this
toxic metalloid bonds to sulfur atoms in enzymes used by the parasite and
kills it without harming the host. This treatment is not referred to in
present-day peer-review scholarship.

Mirazid, an Egyptian drug, was under investigation

for oral treatment of the disease up until 2005. The
efficacy of Praziquantel was proven to be about 8
times that of Mirazid and therefore it was not
recommeded as a suitable agent to control schistosomiasis.

Experiments have shown medicinal Castor oil as an oral anti-penetration

agent to prevent Schistosomiasis
.A. Praziquantel (Biltricide®) is the drug of choice
:Description -
Usually well tolerated. Mechanism of action is complex. Damages
the tegument membrane (the natural
covering of the worm body) and exposes the
worm to the body's immune response, which
leads to worm death. Cure rate is equal to or
greater than 85%. In persons not cured, the
.egg burden is markedly decreased

:Adult Dose -
S haematobium and S mansoni: 40 mg/kg/d PO divided bid for 1 d
S japonicum and S mekongi: 60 mg/kg/d PO divided tid for 1 d

:Pediatric Dose -
S haematobium and S mansoni: 40 mg/kg/d PO divided bid for 1 d
S japonicum and S mekongi: 60 mg/kg/d PO divided tid for 1 d

:Contraindications -
Documented hypersensitivity; ocular cysticercosis

:Interactions -
Hydantoins may reduce serum praziquantel concentrations, possibly
leading to treatment failures

:Pregnancy -
B - Fetal risk not confirmed in studies in humans but has been
shown in some studies in animals

:Precautions -
Destruction of parasite within the eyes can cause irreparable lesions
(ocular cysticercosis should not be treated with praziquantel);
caution while driving or performing other tasks requiring alertness
on the day of and following treatment; minimal increases in liver
enzyme levels reported; when schistosomiasis or fluke infection is
associated with cerebral cysticercosis, hospitalize patient for
duration of treatment

.B. Metrifonate works well on Schistosoma haematobium

:Description -
It is organophosphate compound and its metabolites cause the
schistosomes to detach from the vessel wall, forcing the worms to
.travel downstream with the blood flow
Intestinal schistosomes that are detached in this way can migrate
back to the portal vein after the effect of the drug has passed, but in
S. haematobium the adult worms pass from the vesical plexus
through the right side of the heart into the pulmonary vasculature,
.where they are trapped and die
.Clinical tolerance to this drug is good
:Dosage -
mg/kg every 2 weeks x 3 doses 7.5-10
:Contraindications -
There are no contraindication to retreatment

.C. Oxamniquine (Vansil®) works well on Schistosoma mansoni

:Description -
Mechanism of action is complex. Metabolized into an ester by
schistosomes. Damages tegument surface of male schistosome
worms so that the immune system is able to kill the worm. Stops
female from producing eggs. Only effective against S mansoni. Cure
.rate is 60-90%

:Adult Dose -
mg/kg PO as single dose 15

:Pediatric Dose -
mg/kg PO divided bid for 1 d 20

:Contraindications -
Documented hypersensitivity

:Interactions -
None reported; food may delay absorption

:Pregnancy -
D - Fetal risk shown in humans; use only if benefits outweigh risk to
fetus

:Precautions -
Use caution and closely monitor in patients with history of seizures
because they may experience epileptiform convulsions; EEG
abnormalities may develop in patients with normal pretreatment
recordings

(D. Artesunate (anti-schistosomule

:Dosage -
mg/kgm weekly x 3 6

:Contraindications -
The drug is contraindicated in patients with prior hypersensitivity to
.artesunate or artemisinin derivatives
Oral artesunate should not be used during the first trimester of
.pregnancy
 - Interactions:
Artesunate has a minimal effect on hepatic cytochrome P450
activity and does not appear to influence the metabolism of
mefloquine, a drug likely to be used in combination with artesunate.
Artersunate does not inhibit the formation of carboxy-primaquine, a
metabolite of primaquine.

- Pregnancy:
Little experience has been gained with the use of artesunate in
pregnancy, but the parenteral preparation should not be withheld if
it is considered life-saving to the mother. Oral artesunate should not
be used during the first trimester of pregnancy.

:Precautions -
Parenteral artesunate should be used for the treatment of severe
falciparum malaria only where there is evidence that the
.antimalarial efficacy of quinine is declining

.E. Nothing else works very well on Schistosoma japonicum

The World Health Organization has developed guidelines for community

treatment schistosomiasis based on the impact the disease has on
children in endemic villages:

• When a village reports more than 50 percent of children have blood

in their urine, everyone in the village receives treatment.
• When 20 to 50 percent of children have bloody urine, only school-
age children are treated.
• When less than 20 percent of children have symptoms, mass
treatment is not implemented.

Prevention
A. Treatment of cases to reduce egg loads may be the cheapest
.solution
B. Reduction or elimination of snail intermediate hosts
C. Elimination of snail habitats
D. Sanitation measures
E. Protective footwear
!F. Don’t swim in the Nile

Egypt treatment campaign and Hepatitis C

• Schistosomiasis is endemic in Egypt, exacerbated by the
country's dam and irrigation projects along the Nile. From the late
1950s through the early 1980s, infected villagers were treated with
repeated shots of tartar emetic. It has been hypothesized that this
campaign unintentionally spread the Hepatitis C virus via unclean
needles. Egypt has the world's highest Hepatitis C infection rate,
and the infection rates in various regions of the country closely
track the intensity of the Schistosomiasis campaign.
• EGG female discharges up to 300 eggs per day singly (not in batches as
Schistosoma japonicum); into mesenteric venule of definitive host (human); the
eggs eventually obstruct blood flow in the venule causing a partial necrosis in the
intestinal wall; hence, the eggs are dropped of into the lumen of the intestine, and
passed to feces; eggs measure ~140 X 60 µm in diameter (bigger than eggs of
Schistosoma japonicum)

• MIRACIDIUM a free-swimming larva; once the egg is released into

environment, miracidium hatches immediately and starts swimming; if it happened
to swim into a snail of species Biomphalaria sp., it enters the snail and starts its
first life as a parasite

• SPOROCYST a sac-like secondary larval stage; miracidium transforms into a

primary (mother) sporocyst; germ cells within the primary sporocyst begin dividing
to produce secondary (daughter) sporocysts, which migrate to the snail
hepatopancreas; once at the hepatopancreas, germ cells within the secondary
sporocyst begin to divide again, this time producing thousands of new parasites,
known as cercariae, which are the larvae capable of infecting mammals

• CERCARIUM an infectious form of Schistosoma which infects their hosts by

direct skin penetration; cercariae emerge daily from the snail host; they are highly
motile, alternating between vigorous upward movement and sinking; cercarium
attaches to the human skin and secretes proteolytic enzymes helping it to enter
into cuteneous capillary vessel; upon the penetration the cercarium sheds its tail
and transforms into schistosomulum

• SCHISTOSOMULUM a tailless cercarium; after penetration and spending a few

days in the skin, schistosomula migrate to the lungs (in 3-4 days), and after
passing through the pulmonary capillaries, enter the systemic circulation and,
eventually, are carried to the mesenteric vein of the host; there they mature into
adult schistosomes in a month; female schistosomes do not maturate without a
mature male and females schistosomes from single sex infections are
underdeveloped and exhibit immature reproductive system; male schistosome
holds female between its gynecophoral canal; at this time, the infection of the final
host is complete and sexual reproduction of the parasite begins

• ADULT adult males are approximately 1 cm long and 0.11 cm wide; adult
females are approximately 1.4 cm long and 0.016 cm wide; the adults can live for
years; male and female are always hugged together; up to half the eggs released
by the worm pairs become trapped in the mesenteric veins, or will be washed back
into the liver, where they will become lodged; trapped eggs mature normally,
secreting antigens that elicit a vigorous immune response
 References
- Principles and Practice of Clinical Parasitology Edited By
S.Gillespie & Richard D. Pearson, Copyright © 2001 John Wiley &
Sons Ltd
- J Dick MacLean, McGill Centre for Tropical Diseases, Montreal
- NovaTec, Immunodiagnostica GMBH v 04.2007
- CMPT Connections “on-line” Volume 11 Number 3—Fall 2007
- Bulletin of the World Health Organization 2003, 81 (3)
http://www.bioportfolio.com/indepth/Schistosomiasis_Haematobia.ht
ml
http://en.wikipedia.org/wiki/Schistosoma_haematobium
http://en.wikipedia.org/wiki/Schistosoma_mansoni
http://www.emedicine.com/radio/topic621.htm
http://en.wikipedia.org/wiki/Schistosomiasis
http://www.cartercenter.org/health/schistosomiasis/treatment.html

Supervised
By:
Professor Dr. Suzan Fathy El-