MEDICAL HELMINTHOLOGY

This part deals with the study of helminths (worms) that parasitize man.
They belong to two main groups:
1- Platyhelminths 2- Nemathelminths
(flat worms) (round worms)
a- Class: Trematoda Class: Nematoda
b- Class: Cestoda

PLATYHELMINTHS
Class: Trematoda (Flukes)
General characters:
-The members of this class are commonly known as flukes.
-Adults are leaf-like, pear-shaped or elongated worms.
-All trematodes possess two suckers as organs of attachment.
-Covered externally by a cuticle that may be smooth, spiny or tuberculated.
- The body is made up of systems:
Starts by the mouth opening, found at the bottom of the oral
Digestive system sucker. The mouth leads to a pharynx, then a short oesophagus,
which bifurcates, into two long intestinal caeca.
Starts by a definite number of excretory cells called (flame
cells). Waste products pass from the cell to the excretory
Excretory system tubules➙excretory duct ➙excretory bladder which discharge
its contents through a pore situated at the posterior end of the
fluke.
Is simple. It consists of a ring of nerve ganglia, around the
Nervous system
pharynx, from which nerve fibers ramify
All the parasitic trematodes are hermaphrodites except
Schistosoma worms.
Reproductive
*The male reproductive organs consist of two or more testes.
system
*The female genital organs consist of a single ovary
situated in front of the two testes.
Parasitic trematodes feed on blood, intestinal contents, biliary
Nutrition and
secretions and tissue juices depending on their habitat. Adult
respiration
flukes are essentially anaerobic

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 Hepatic or Liver Flukes
Fasciola gigantica (Large liver fluke)
Geographical distribution: Human infection has been reported from many regions
including Egypt, Africa and Far East.
Morphology:
1. Large Fleshy leaf- like worm, measures 3 -7x1 cm.
2. Body formed of small anterior conical part (cephalic cone), shoulders with
parallel borders and posterior round end.
3. Suckers: small oral anterior sucker and large ventral sucker.
4. Digestive system: mouth leads to oesophagus with muscular pharynx, two long
intestinal caeca with lateral compound branches and medial T or Y-shaped
ones.
5. Genital system (reproductive system):
a. Common genital pore: anterior to the ventral sucker.
b. Testes: two highly branched, one behind the other, about
the middle third of the body
c. Ovary: branched at the right side in front of the testis.
d. Uterus: short and convoluted.
e. Vitelline glands: highly branched and extend along the lateral fields.

Life cycle:
-­‐Habitat: adult worms live in the bile ducts and gall bladder.
-Definitive host: man.
-Intermediate host: snail Lymnaea cailliaudi.
-Reservoir hosts: herbivorous animals as cattle, sheep, goat and camels.
-Infective stage: encysted metacercaria in water and on aquatic vegetations.
-Stages in the life cycle: egg à miracidium à sporocyst à 1st and 2nd
generation redia à cercariae àencysted metacercariaeà adult.

Egg: Size: 160x80 µ. Shape: oval.

Shell: thin. Color: light yellowish brown (bile stained).
Contents: immature (yolk cells).
Special character: operculated.
- Eggs are discharged with feces of infected host, in fresh water of canals, drains and
River Nile, hatch within 2 weeks into miracidium.

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 The life cycle of Fasciola spp.

Miracidium: a phototropic pyriform ciliated organism that can swim in water and
penetrates the snail intermediate host.
Sporocyst: Simple elongated sac in the snail.
Redia: Cylindrical larva in the snail.
Cercaria: Leptocercous cercaria formed of body (0.3mm) and simple tail (0.7mm).
-Body with 2 suckers (oral and ventral), primitive gut, excretory system of flame
cells, and cystogenous glands that secrete the cyst wall.
-Cercaria comes out from the snail and moves in water, gets attached to aquatic
vegetations, loses its tail and changes intoàencysted metacercaria.
Encysted metacercariae:
-Spherical 0.25mm. -Thick white cyst walls.
-They need about 12 hours after encystation to cause infection, and they live in
water for 6- 10 months.

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Mode of infection:
- By eating raw water vegetations or vegetables washed in infected water and by
drinking infected water polluted by the encysted metacercaria.
• In the duodenum, the cyst wall dissolves and the metacercaria penetrate the wall of
the intestine to reach peritoneal cavity.
• Metacercariae pass to the liver through it's capsule → through the liver tissue to
their final habitat in the bile duct, where they maturate to adult in about two
months after infection, eggs appear in the stool 3-4 months after infection.
Pathogenicity and clinical picture: Four Symptomatic Patterns
- Acute Phase
- Chronic Phase
- Halzoun
- Ectopic Infection
Acute Phase
- Rarely seen in humans.
- Fever, tender hepatomegaly, and abdominal pain are frequent symptoms.
- Vomiting, diarrhea, and anemia may be present.
Chronic Phase
- Symptoms include: Irregular fever ,biliary colic, abdominal pain, tender
hepatomegaly, and jaundice.
- In children: severe anemia and high eosinophilia are common.
- Inflammation of the bile ducts leads to fibrosis and a condition called “pipe-
stem liver”.
- Liver rot : mechanical and toxic destruction of liver tissue by passage of large
number of immature worms through the liver tissue leads to necrosis , fibrosis ,
hepatitis, and hepatomegaly
- Severe infections can lead to death.
Halzoun:
-Occurs when an individual consumes infected raw liver.
-The living Fasciola adult worm attach to the mucosa of the pharynx by its suckers.
This causes oedematous congestion of the pharynx and larynx resulting in dysphagia
and suffocation.
The case is treated by:
a) Gargling with alcoholic drink.
b) Giving emetic drugs.
c) Picking up of the worm by forceps.
- Tracheostomy in suffocation

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 - Ectopic Infection : In frequent, but can occur in peritoneal cavity, intestinal
wall, lungs, subcutaneous tissue, and very rarely in other locations.
N.B.:
} False fascioliasis: it is due to eating of infected animals liver and passage of
eggs in the stool. This must be excluded by repeated stool analysis one week
after liver free diet.
Diagnosis:
Clinical fever, hepatomegaly, habit of green salad consumption
1-Stool examination: for detection of eggs, after asking the patient to stop
eating liver for a few days before examination.
N.B.:Flukes do not begin to produce eggs until about 4 months after infection.
Prior to 4 months: serological tests can be used
Laboratory 2-Serological tests: are of value during the migratory stage of the worms and
ectopic infection for estimation of specific antibodies, as ELISA, IHA.
3-Examination of sample of aspirated duodenal contents.
4-Eosinophilia.
5-Ultrasound and CT

Treatment:
1. Bithionol (Bitin).
2. Triclabendazole (Fasinex).
3. Surgical removal of ectopic flukes.
Prevention and control:
1. Mass treatment of infected man and animal reservoir.
2. Snail control.
3. Sanitary disposal of feces.
4. Protection: - Pure filtered water supply.
-Proper washing or cooking of aquatic vegetation.
Fasciola hepatica
Pathogenicity:
-The adult worm can live in sheep for 5 year and cause liver cirrhosis and ascitis.
- In man; the young adults burrow through the liver tissue feeding on its cells
causing inflammation, necrosis (liver rot) and marked eosinophilia.
- The other pathological findings are similar to F. gigantica.

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It is similar to Fasciola gigantica but differs in:
Fasciola gigantica Fasciola hepatica
l) Size:3-7x 1cm. -Smaller, 2-3x1.3 cm.
2) Anterior cephalic cone: Is rather small. -Relatively big.
3) Lateral sides: parallel. -Converging.
4) Ventral sucker: bigger. -Oral and ventral suckers are equal.
5)Medial intestinal caeca :T or Y shaped. - Rudimentary.
6)Snail host :
In Egypt: Lymnea cailliaudi. -In Europe: Lymnea truncatula.
7) Reservoir host: Herbivorous animals as - Sheep.
cattle & buffalos.
Diagnosis, treatment, prevention and control are similar to F. gigantica.

Opisthorchis viverrini
(Southeast Asian liver fluke)

Geographical distribution: It is endemic in Southeast Asian countries including

Thailand, Laos, Vietnam and Cambodia.
- Although opisthorchiasis is not endemic in Egypt, imported cases may occur.
Morphology:
1-Adult
It is dorsoventrally flattened, lancet shaped, thin and transparent.
- Average size is 7 x 1.5 mm.
- Suckers: 2 suckers (oral sucker and the ventral sucker ).
- Testes: 2 in number, diagonal, deeply lobed, located near the posterior extremity.
- Ovary: single, multilobed in front of the anterior testes.
- The vitellaria consist of numerous follicles disposed in the lateral fields between
ventral sucker and testes.
2- Eggs :
Size : 27x15µ
Shape : oval
Shell : thick
Special character: opercular shoulder and
terminal knob
Colour : yellowish brown (bile stained)
Contents : mature (miracidium)

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 Opithorchis adult morphology

3. Cercaria (pleurolophocercus): formed of body and tail

- Body: have 2 suckers, primitive gut, 2 eye spots, 5 pairs of penetration glands,
cystogenous glands and excretory bladder.
- Tail: simple, longer than the body, provided with cuticular sheath .
Life cycle:
Habitat: adult worms live in the biliary tract of humans and other reservoirs,
attached to the mucosa by suckers.
Definitive host: man
Intermediate host (require 2 intermediate hosts) :
-1st I. H. : aquatic snails of genus Bithynia
- 2nd I.H. : freshwater fish (Cyprinoid fish)
Reservoir hosts: dogs, cats and other fish eating mammals
Infective stage: encysted metacercaria in muscles of fresh water fish
Stages in life cycle:
eggàingested by the snailàmiracidiumàsporocystsàrediaeàcercariae àencysted
metacercaria in fish muscles àexcysted metacercariaàadult

Mode of infection:
1- eating raw (dried or salted) or inadequately cooked freshwater fish.
2- infection can also occur through fingers or cooking utensils contaminated with the
metacercaria during preparation of fish for cooking.

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 life cycle of Opisthorchis viverrini

- Opisthorchis eggs are embryonated, pass out with faeces, ingested by the snail I.H.
and hatch inside into miracidium which then develop into sporocysts then rediae
stages to become cercariae.
- Cercariae then escape from the snail and swim in water waiting to get attached to
the 2ndI. H., lose their tails and encyst under the scales or in the flesh of fish to
become metacercariae in about 3 weeks.
-After ingestion of infected fish, metacercaria excyst in the duodenum, migrate
through the ampulla of vater to the biliary tract, where they mature into adult in
about 1 month.
- Eggs exit the bile ducts and are excreted in the feces.
Pathogenesis and symptomatology:
- The severity of the pathology appears to be associated with both intensity and
duration of infection.
1- Most infections are asymptomatic.
2- Patients in the early stage have high fever, epigastric pain, diarrhea and tender
hepatomegaly.
3- With chronic infection, the symptoms can be more severe, and hepatomegaly and
malnutrition may be present.

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4- In rare cases, cholangitis, cholecystitis, and cholangiocarcinoma (CCA) may
develop.
Opisthorchis viverrini is considered a group 1 carcinogen (known to cause
cancer in humans).
- The pathogenesis of O. viverrini-mediated hepatobiliary changes may be due to:
1. Mechanical irritation caused by the liver fluke suckers
2. Its metabolic products
3. Immunopathological process
Diagnosis
I. Clinical
II. laboratory:
1. Detection of eggs in stool samples or aspirated bile.
2.Detection of fecal Opisthorchis antigen has been reported .
3. Several serologic tests for the diagnosis of opisthorchiasis have been reported.
Treatment:
1. Praziquantel is the drug of choice.
2. Surgical intervention may become necessary in cases with obstructive jaundice.
Prevention and control
Health education, avoid eating raw fish, proper cooking of fish, treatment of infected
cases, snail control.

Case study:
A 36-year-old man suffering from intermittent fever, diarrhea, indigestion and
abdominal pain in the right hypochondrium. Upon examination, he had a slightly
enlarged tender liver and yellow colouration of the sclera. When questioned
regarding his eating habits, the patient admitted to having a fondness for un-
cooked water-cress and raw vegetables. Stool examination for ova& parasites was
ordered. Blood sample was collected for complete blood count and liver function
tests. Haematology results showed evidence of anaemia and eosinophilia (60%
eosinophils). The patient's liver enzyme levels were slightly elevated. The
diagnosis was made microscopically after the observation of large, oval, 160X80
u, yellowish-brown, operculated eggs in the concentrated stool specimen.
Questions:
1. Which parasite might be causing this infection?
2. Which other helminth lays eggs indistinguishable from the eggs
described in this specimen?
3. How does transmission of this parasite occur?
4. What are the usual symptoms of the disease in humans?
5. How the diagnosis of this infection is usually made?
6. How do you exclude false diagnosis?

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 Intestinal flukes
Heterophyes heterophyes
Geographical distribution: Common in Egypt in Nile Delta, especially around the
lakes of Manzala and Borollos, Turkey and Far East (Japan, China, Korea,
Philippine).
Morphology:
1. Size: 1.5-3mmx 0.5 mm.
2. Shape: Pear shape, the anterior end is more or less narrow, while the posterior
end is broadly rounded, some spines cover the cuticle especially anteriorly.
3. Suckers: three suckers
- Oral sucker: small around the mouth.
- Ventral sucker: large about the middle of the body.
- Genital sucker: postero- lateral to the ventral sucker.
4. Genital system:
- Testes: two oval, smooth, and opposite each other in the posterior part of
the body.
- Ovary: One ovary, smooth in front of the testes.
Life cycle:
-Habitat: adult lives between the villi of the small intestine.
-Definitive host: man.
-Intermediate host: -first is a snail, called Pirenella conica.
-Second is fish, Tilapia (Bolty) and Mugil (Boury).
-Reservoir host: cat, dog, and any fish eating animals.
-Infective stage: encysted metacercaria in the muscles of the fish (2nd I. H.).
-Stages in the life cycle: egg à miracidium à sporocyst à 1st and 2nd generation
redia à cercaria àencysted metacercaria à adult.

Egg: Size: 30xl5 µ.

Shape: Oval.
Shell: Thick with operculum at one pole and a small Knob at the other.
Colour: golden yellow.
Contents: Full mature embryo (miracidium).
-Eggs pass with the stool, which must reach to brackish water.
-In water, the eggs are ingested by the snail first intermediate host (Pirenella conica)
common in lakes Manzala and Borollos in Egypt.
-In the snail, the miracidium hatches into a sporocyst, that gives rediae then cercariae,
which escape from the snail in about 30 days and become free in water.

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 Life cycle of H. heterophyes

Cercaria: - Consists of body and tail.

- The body: is oval, has 2 suckers, primitive gut, 2 dark eye spots and 7 pairs of
penetration glands.
- The tail : is simple, covered from one side by membrane which reaches to the tip
of the tail then ascend to cover the distal 1/3 of the other side, it is called
lophocercous cercaria (pipe like).

- The cercaria in water searches for the second intermediate host, which is fish,
Tilapia (Bolty) and Mugil (Boury).
- It penetrates the tissue of fish and becomes encysted metacercaria under the scales
or in the muscles, and become infective within 20 days, it is spherical and 250 µ.
Mode of infection:   By   eating   insufficient   cooked,   roasted   or   salted   fish,   staked  
less   than   ten   days   (sweet   fesekh),   containing   the   infective   stage   (encysted  
metacercariae).    

-In the small intestine the cyst wall is dissolved, the metacercariae embedded between
the villi, maturate and the eggs appear in the stool 2-5 weeks after infection.

Pathogenicity and clinical picture:

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 Intestinal Attachment of the parasite to the mucosal membranes;
inflammation with superficial ulcers and necrosis occur.
*Mild infection with no symptoms
*Heavy infections cause:
-Abdominal colic. -Abdominal discomfort.
-Chronic intermittent diarrhea, sometimes with blood
Extra-intestinal The eggs may reach the general circulation to different
organs and form parasitic granuloma and fibrosis
Diagnosis: Stool examination for the characteristic eggs.
Treatment: 1. Praziquantel (Biltricid).
2. Niclosamide (Yomesan).
Prevention and control:
1. Sanitary disposal of feces.
2. Avoid eating raw, insufficient cooked fish or salted fish, salted less than 10
days (sweet fessekh), and proper grilling of fish.
3. Fried fish is safe as temperature needed for frying is high enough to kill
metacercariae.
4. Periodic examination of fishermen stool for Heterophyes eggs.
5. Mass treatment of infected cases.
6. Snail control.

Lung fluke
Paragonimus westermani
Geographical distribution: Heavily infected areas are found primarily in the Far
East including Japan, Korea and Taiwan; it is also found in central Africa.
Adult morphology:
Shape Ovoid, thick, reddish brown, rounded anteriorly and tapering posteriorly.

Size 0.5 - 1.5 cm in length

Suckers the oral and ventral suckers are equal
Genital a) Testes: deeply lobed situated nearly side by side midway
system between the ventral sucker and posterior end.
b) Ovary: large, lobed and situated behind the ventral sucker,
the uterus coils opposite to it
Life cycle:

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Habitat worms generally live in pairs encapsulated in pockets of the
lungs
Definitive host Man
Intermediate hosts 1st I.H.à snail Melania& Semisulcospira.
2nd I.H.à crabs and crayfish
Reservoir host Carnivores as dog, fox, wolf, tiger and pig
Infective stage Encysted metacercaria in muscles, gills, legs and viscera of
crabs and crayfish.
Stages in the life cycle: egg à miracidium à sporocystà rediaà cercaria à
metacercaria →adult.
• The life cycle is completed in 6-8 months.

Paragonimus westermani life cycle

Egg:
Size 100 x 50 µ Color Golden brown
Shape Ovoid Content Immature miracidium
Shell Thick shell Special characters With flat operculum
-The eggs escape from the pulmonary pockets through the bronchioles and are
coughed out with sputum, or swallowed and pass immature with feces.
-Eggs require from 15 days to several weeks in water to complete embryonation then

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hatch and miracidia escape.
Miracidium: enters the snail first I.H. then develops into sporocysts à rediae à
cercariae in 3-5 months.
Cercaria: Microcercous with a knob like tail. The released cercariae penetrate the
crustaceans 2nd I.H. then develop into metacercariae.
Metacercaria: requires 6-8 weeks to become infective.
Mode of infection:
• Human and mammals’ infection occur by eating raw or insufficiently cooked
crabs or crayfish infected with the encysted metacercariae.
• Metacercariae excyst in the small intestine pass through the intestinal wall,
grow for about one week into young flukes, penetrate the diaphragm and pleural
cavity and come to rest in the lung, forming cystic cavities then get mature.

Pathogenicity and clinical picture:

1. The worms provoke granulomatous reactions leading to fibrotic
encapsulations of the parasites with a picture of generalized or localized
diffuse fibrosis, pneumonia and tubercles like abscesses.
2. Clinically: The disease is insidious in onset.
-There may be initial episodes of chills and fever with
persistent cough and haemoptysis.
-The sputum is viscous and flecked with dark golden brown
particles and may be bloody.
3. Eosinophilia (20 - 25 %).
4. Pleural effusion may occur.
Diagnosis:
1. By finding the characteristic eggs in sputum, feces or in aspirated pleural effusion.
2. Plain x-ray chest and computerized tomography show nodular shadows & cavities.
3. Immunodiagnostic tests as ELISA to detect early & chronic infection.
Treatment: Praziquantel.
Prevention and control:
1. Avoid eating raw, inadequately cooked or freshly salted crabs or crayfish.
2. Treatment of cases.
3. Snail control.

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 Blood flukes
(Schistosomes)
Human beings are infected with three main species of schistosomes:
1. Schistosoma haematobium: causing urinary schistosomiasis. (present in Egypt)
2. Schistosoma mansoni: causing intestinal schistosomiasis. (present in Egypt)
3. Schistosoma japonicum: causing oriental schistosomiasis.
(not present in Egypt)
Schistosoma haematobium
(Urinary schistosomiasis)
Geographical distribution:
Africa: scattered areas. In Egypt, it is prevalent all over the Nile Valley.
Asia: Syria, Palestine, Iraq, Iran, Saudi Arabia, Yemen, India.
Europe: Cyprus and South Portugal.
Adult morphology:
Male Female
Size 1 -2cm x l mm long (2 - 2.5 cm x0.25mm)
Shape flattened, lateral margins are folded cylindrical (round in cross
ventrally to form the gynaecophoric section)
canal
Tegument provided with fine tubercles on the smooth.
dorsal surface
Suckers sub-terminal oral sucker around the weakly developed
mouth and a larger ventral sucker
some distance behind
Digestive mouth, oesophagus without muscular like male but union of intestinal
system pharynx, two simple intestinal caeca caeca occurs at the posterior
that unite in the middle into single third.
blind caecum
Genital Testes :4-5 separate testes, smooth, Ovary :oval, smooth lies just in
system globular arranged in one line postero- front of the intestinal union.
lateral to the ventral sucker. Uterus: long, straight,
Male genital pore :behind the ventral terminates at the genital pore,
sucker. contains one raw of 20 - 30 ova
Vitelline glands: extend from
behind the ovary till the
posterior end.

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Life cycle:
-Habitat: Schistosoma haematobium adults live in the vesical and pelvic venous
plexuses in man surrounding the kidney, pelvis, urinary bladder, urethra, prostate,
seminal vesicles, lower 1/3 of uterus and vagina.
-Definitive host: man.
-Intermediate host: snail Bulinus truncatus in Egypt.
-Reservoir host: no reservoir host.
-Infective stage: furcocercus cercaria.
-Stages in life cycle: egg àmiracidiumà sporocystà furcocercous cercariaàadult.

Life cycle of Schistosoma species

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Egg: Eggs sweep out in urine and rarely with feces.
Size 120 x 60 µ.
Shape oval.
Shell thin with terminal spine.
Colour translucent.
Contents mature miracidium.
Miracidium: -In fresh water the miracidium hatches.
- It is distributed homogeneously in water.
- It penetrates the soft tissue of the snail intermediate host (Bulinus truncates)
where it develops into first and second generation sporocysts then cercariae that
escape into water. Each miracidium gives rise to 250.000 cercariae.
Cercaria: (furcocercus cercaria)
a. Body: 200 u in length with 2 suckers, primitive gut and 5 pairs of
penetration glands.
b. Tail: 300 µ in length, bifid or bi-forked Forked cercaria is the infective stage.
- The cycle inside the snail takes 1-2 months.
-It survives in canal water for 48 hours and is attracted to man by the body
temperature.
Mode of infection:
1. Infection occurs by skin penetration within minutes up to half an hour as water
begins to dry, after bathing, washing or playing in infected canals. Penetration
is helped by the penetration glands and mechanically by the tail activity.
2. Drinking water may lead to infection when cercaria penetrates the mucous
membrane above the gastric acidity that kills it.
- The body of cercaria enters the skin or mucous membrane leaving the tail
(schistosomulum). It is carried by the blood à left side of the heart à
systemic circulation à intestinal capillary bed à intra-hepatic branches of the
portal vein where it matures in 7 weeks.
- Then male carries the female in the gynaecophoric canal and migrates out of
the liver in the portal vein against the blood stream to reach the vesical and
pelvic plexuses to deposit the eggs.
- Eggs appear in urine 10 weeks after infection.

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Pathogenicity and clinical picture:
Disease: schistosomiasis haematobium, vesical or urinary bilharziasis:
There are four progressive stages:
Stage of Skin reaction due to cercarial penetration in the form of
invasion local dermatitis, itching (bather's itch), irritation and papular rash.

Stage of Due to circulating schistosomules

migration a- Lung: verminous pneumonitis (small patches of inflammation) &
hemorrhage, with cough, sputum & heamoptysis.
b- Liver and spleen: hepatosplenomegaly.
c- Metabolic products of maturing parasites à toxic and allergic
manifestations e.g. urticaria, fever, headache, cough, wheezes,
muscle pain, leucocytosis & eosinophilia.

Stage of egg Active egg deposition with escape of eggs in urine à tissue damage
deposition and hemorrhage that manifest with:
and a- Terminal haematuria (blood in the last part of micturation)
extrusion which is due to increased contraction of bladder à injury of
(early-acute venules by egg spine à drops of blood in urine.
stage) b- Frequency of micturation.
c- Dysuria (burning pain during micturation).
Stage of -Eggs trapped in the wall of blood vessels stimulate both humoral and
tissue cellular immune response to miracidial antigenàaggregation of
proliferatio inflammatory cells around eggs (granulomas) and fibrosis with the
n, repair formation of sandy patches, bilharzial nodules, papillomata which
and fibrosis may ulcerate.
(chronic- - Inflammatory reaction heals by fibrosis :
late stage) a- Urinary bladder: polyps, ulcers, cystitis, contracted bladder,
calcified bladder, diverticulosis, malignancy (due to parasite toxic
secretions).
b- Ureters: stricture, hydroureter.
c-Kidneys: hydronephrosis,2ry infection(pyonephrosis)&renal failure.
d-Urethra: stricture, fistula.
e-Genital organs: pseudo-elephantiasis of the penis, granuloma in
prostate, seminal vesicle, spermatic cord, ovaries, uterus and vagina.
-Embolic lesions: Schistosoma eggs are swept by blood to reach
various organs (liver, lungs, brain or other organs).
Eggs swept from the pelvic and vesical plexuses toà the pulmonary
artery branches produce granulomata and fibrosis with obliteration of
blood flow à pulmonary hypertension, right ventricular hypertrophy
and right sided heart failure (Bilharzial cor-Pulmonale).

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Diagnosis:
I. Clinical: history of terminal haematuria & dysuria in endemic area is suggestive.
In mild infection, haematuria manifests only after muscular activity. Infection of
seminal vesicle manifests by blood in seminal fluid.
II. Laboratory:
a. Direct methods:
1. Detection of eggs in urine: microscopical examination of last drop of urine
sample for the eggs after sedimentation or centrifugation (concentration
method).
2. Cystoscopy: in chronic cases when eggs cannot be detected in urine, for
histopathological lesions as well as eggs.
*Eggs should be examined for viability by the hatching test to differentiate between
living and dead eggs: fresh water is added to the urine sediment and examined after
30 minutes by a hand lens to demonstrate swimming miracidia.

Living egg Dead egg

Translucent Opaque
Intact moving miracidium Dead miracidium (not motile or
Contracting and relaxing. silent)
Surrounded by R.B.Cs. No R.B.Cs
Hatches in fresh water (Positive Does not hatch (Negative
hatching test) hatching test)

3. Urine precipitin test: for detection of schistosomal antigens excreted in

patient's urine. Hyper immune serum + patient's urine à precipitate forms in
+ve cases.
4. ELISA for circulating antigens.
b- Indirect methods: Serological tests for detection of antigen antibody reaction.
1. Indirect haemagglutination test (IHA).
2. Indirect fluorescent antibody test (IFA).
3. Enzyme-linked immunosorbent assay (ELISA): for antibodies detection.
Treatment:
1. Praziquantel (Biltricide or Distocide).
2. Metrifonate (Bilarcil).

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 Schistosoma mansoni
(Intestinal schistosomiasis)
Geographical distribution:
It is widespread in Africa.
In Egypt, it was prevalent in the region of the Nile delta, but after construction of the
high dam, it invaded upper Egypt.
Also S. mansoni is found in Saudi Arabia, Yemen and Tropical America.
Morphology: similar to S. haematobium with few differences listed below:
1. Male: -size: shorter, 8-10mm x l mm.
-Cuticle: more coarsely tuberculated.
-Digestive system: intestinal caeca unite at the anterior third.
-Testes: 6-9 as a mass.
2. Female:-size: shorter, 14-22mm x0.15mm.
-Digestive system: union of intestinal caeca occurs at the anterior third.
-Ovary: at the anterior third.
-Uterus: short with 1-4 ova.
3. Egg: size: 140 x 70 µ.
Shape: oval.
Shell: thin with lateral spine.
Colour: translucent.
Contents: mature miracidium.
Eggs sweep out with feces and rarely in urine.
4. Miracidium: found in the upper layer of water, has fused penetration glands.
5. Cercariae: provided with 6 pairs of unicellular penetration glands.
Life cycle:
-Habitat: radicals of the inferior mesenteric vein draining the large intestine, and in
the portal system.
-Definitive host: man.
-Intermediate host: snail Biomphalaria alexandrina in Egypt.
-Reservoir host: monkeys and rodents.

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Pathogenicity and clinical picture:
Disease: schistosomiasis mansoni, intestinal bilharziasis.
Pathogenicity of Schistosoma mansoni is similar to that of Schistosoma
haematobium with the following variations:
-Stage of egg deposition and extrusion (early or acute stage):
Active egg deposition especially in the pelvic colon and rectum leads to
erosion of submucosa and villous tissue followed by inflammation, tissue
damage and hemorrhage. The patient suffers from:
a. Dysentery with mucous and blood in the stool.
b. Abdominal pain.
c. Frequent stool.
-Stage of tissue proliferation, repair and fibrosis (chronic or late stage):
a. Eggs trapped in the wall lead to formation of sandy patches, nodules and
papillomata. The wall becomes thickened, fibrosed and may be complicated
with strictures, sinuses, fistulae and prolapse.
b. Embolic lesions: female S. mansoni produces about 300 eggs / day. 50% are
swept by blood and reach the liver. They block the presinusoisal capillaries and
the soluble egg antigen (SEA) elicits T-cell dependent granulomas around each
egg à periportal fibrosis and portal hypertension à splenomegaly, ascitis and
oesophageal varices due to opening of the porto-systemic shunts at the cardiac
end of the oesophagus.
c. Haematemesis: due to ruptured oesophageal varices.
d. Melena: digested blood after ruptured oesophageal varices.
e. Eggs directed to the lungs by collateral circulation lead to cor-Pulmonale.
f. Renal involvement occurs due to precipitation of immune complexes in the
glomerular vascular bed leading to end-stage renal failure.
Diagnosis:
I. Clinical:
a- Early: diarrhea and dysentery with mucus and blood in stool.
b- Late:
• Anal fissures and perianal sinuses.
• Bilharzial hepatic fibrosis causing:
- Portal hypertension.
- Splenomegaly &ascitis.

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 - Hepatic dysfunction.
• Portal hypertension, haematemesis and melena.
• Blood loss, leading to iron deficiency anaemia.
II. Laboratory:
a. Direct methods:
1. Stool examination: detection of the characteristic eggs in stool (lateral spine).
2. Rectal swab using a gloved finger lubricated with soap to palpate the
pathological lesion in the rectum and the fecal sample are then examined on a
slide for Schistosoma mansoni eggs.
3. Sigmoidoscopy and rectal biopsy to visualize the mucosa of sigmoid colon for
pathological lesions and Schistosoma eggs.
4. ELISA for circulating antigens.
b. Indirect methods: as schistosomiasis haematobium.
Treatment:
1. Praziquantel: a single oral dose is effective against all Schistosoma species
infecting man.
2. Oxamniquine (Vansil).
3. Chemotherapy followed by surgical interference in portal hypertension.
N.B.: urine and stool examination should be done after 3 months of treatment for
Schistosoma eggs. The viability test should be done to decide whether the patient is
cured or not.

Schistosoma japonicum
(Oriental schistosomiasis)
Geographical distribution: in Far East (Japan, China, Philippines, Formosa, Korea).
Morphology: similar to other Schistosomes with few differences.
1. Male:
-Size: 9-22 mm x 0.5 mm.
-Cuticle: smooth.
-Intestinal caeca unite very late posteriorly.
-Testes: 6-8 small testicles in a single column.
2. Female:
-Size: 12-26 mm x 0.3 mm.
-Intestinal caeca unite at the posterior two fifths.
-Ovary: posterior.
-Uterine tube: long, contain 50 - 100 eggs.

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3. Egg: sweep out with feces.
Shape rounded.
Size 70-100x50 µ.
Shell thin, spineless but has curved tubercle-like projection in
shallow depression
Colour translucent.
Contents mature miracidium.
4. Miracidium: similar to S. mansoni miracidium.
5. Cercaria: provided with 5 pairs of penetration glands.
Life cycle:
-Habitat: Schistosoma japonicum lives in mesenteric veins of large & small intestine.
-Definitive host: man.
-Reservoir hosts: cats, dogs, cattle, horses, pigs, rodents, sheep and goats.
-Intermediate host: snail Oncomelania.
Pathogenicity:
It causes oriental schistosomiasis.
The disease caused by Schistosoma japonicum is similar to that caused by
Schistosoma mansoni with the following differences:
- The mesenteric lymph nodes are affected. Adhesions and thickening of mesentery
and omentum occur.
- Liver fibrosis and splenomegaly are common; the condition is called "Katayama
Syndrome".
The pathogenesis is more dangerous than other schistosomes due to:
1. It inhabits the small intestine, affecting the absorption process, leading to retarded
growth in children.
2. Many reservoir hosts makes control difficult.
3. Intermediate host is amphibian (lives in mud for long time).
4. Female lays 3000 eggs/day, with high metabolism and more antigens excreted.
4. Absence of a spine and the rounded contour of the eggs allow their dispersion in
the body with CNS and spinal cord affection.
Clinical picture: The clinical manifestations of schistosomiasis japonica are
similar to that of schistosomiasis mansoni (intestinal schistosomiasis) but:
1. The incubation period is short.
2. The disease is serious and fatal.
3. Diarrhea is common due to the pathological lesions of the small intestine.

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 4. Katayama disease is more sever and is characterized by :
a. Acute onset of fever, headache, weakness, cough, abdominal pain, diarrhea,
eosinophilia (40%), hepato-splenomegaly and involvement of the CNS (2-
3%).
b. Symptoms of katayama disease coincide with the maturation of the adult
worms and beginning of oviposition i.e. 5-7 weeks after infection.
c. The disease is frequently seen in heavy infection with S. mansoni and
rarely occurs in S. haematobium infection.
Diagnosis:
1. Stool examination for the characteristic eggs.
2. Detection of circulating antigens and antibodies by different immuno-
diagnostic assays.
Treatment:
- Schistosoma japonicum is resistant to treatment.
-Praziquantel is the only effective drug for this infection.

Schistosoma intercalatum
• Common in central and West Africa.
• Adults are found in intestinal venous plexuses of man.
• Intermediate host: snail Bulinus africanus.
• Eggs : 170× 60µ
-With terminal spine as Schistosoma haematobium eggs and are Zeihl-
Neelsen positive.
-Eggs are detected in stool.
• Usually cause benign disease and hepatomegaly is not marked.
Control: (for all species of schistosomes)
(1) Protection (prophylaxis from infection):
A) Health education -should be directed mainly for school children.
-prevention of urination or defecation in or near
water streams.
B) Personal prophylaxis By wearing of boots and gloves, use of repellents
e.g. dimethyl phthalate.

C) Quick and thorough drying of exposed wet skin

D) Pure water supply and Sanitary disposal of excreta
E) Treatment of canals water to e.g. storage more than 48 hours, boiling or
become safe addition of chemicals like chlorine to render it
free from living cercariae.

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(2) Treatment of cases: mass treatment by Praziquantel.
(3) Reservoir hosts: should be controlled.
(4) Snail control:
a) Physical methods - Dryness of canals e.g. double canalization system (one
used and one dried).
- Periodic clearance of canals from vegetations and weeds.
- Pitching canal banks with concrete to prevent growth of
aquatic plants.
- Wire screens at inlets of canals to prevent & collect snails
b)Biological methods - Natural enemies of snails e.g. birds (ducks, geese) or snails
(Marisa).
- Certain toxic plants e.g. Balanites aegyptica and Ambrosa
maritima (Damsisa) whose leaves and fruits are toxic to
snails.
- Pathogens: infection of snails by miracidia of avian
schistosomiasis to decrease its vitality.

c)Chemical methods chemical substance used to kill snails (molluscicides)

- Copper sulphate : 10-20 p.p.m., widely used in
Egypt, but it is not effective against eggs of snails, should
be reapplied every 3 months to kill the newly hatched
snails or applied as a chemical barrier at the inlet of canal
to give a concentration of 0.5 p.p.m.
- Sodium pentachlorophenate : 5- 10 p.p.m.
- Baylucide: 2 p.p.m.

Cercarial dermatitis
Swimmer's itch, Bather's itch
- It is caused by cercariae of non-human schistosomes (bird and animal
schistosomes) in fresh water or marine water.
- Cercariae penetrate the human skin, but cannot proceed beyond the germinal layer,
and rapidly destroyed in the skin by the host defense mechanism.
Clinically - Dermatitis,itching, urticarial wheels and 2ry bacterial infection.
- Formation of macules & papules occur by subsequent exposures
Diagnosis History of contact with water followed by skin rash
Treatment - Local antihistamines, antipruritis, antibiotics for 2ry bacterial
infection.
Prevention - Rapid drying of the skin to prevent cercarial penetration.
and - Snail control. -Avoid polluted water
control

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 Human schistosomes
S. haematobium S. mansoni S. japonicum
Male: Length 1-2 cm 0.8-1 cm 0.9-2.2 cm
Breadth 1 mm 1 mm 0.5 mm
Surface Fine Coarse Non tuberculated
(smooth)
Union of intestinal At the middle At the anterior Very late posteriorly
caeca third
Testes 4-5 separate 6-9 as a mass 6-8 compressed
Female: Length 2-2.5 cm 1.4-2.2 cm 1.2-2.6 cm
Breadth 0.25 mm 0.15 mm 0.3 mm
Union of intestinal At posterior third At anterior third At posterior two
caeca fifths
Ovary position Posterior Anterior Posterior
Uterine tube Long, contains Short, contains few Long, contain 100
20-30 eggs eggs eggs
Vitelline glands Occupy the Occupy the Occupy the posterior
posterior third posterior two third two fifths
Egg : Size 120 × 60 µ 140 × 70 µ 100 × 50 µ
Spine Terminal Lateral Lateral, short, curved
tubercle
Exit Urine, rarely Feces, rarely urine Feces
feces
Miracidium Found in all Found in the upper As S. mansoni
levels of water layer of water.

Cercaria 5 pairs of 6 pairs 5 pairs

penetration glands
I.H. Bulinus truncatus Biomphalaria Onchomelania
alexandrina
R.H. No Monkeys & rodents Horses, cattle, dogs,
cats and rodents

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Case study:
A 13-year-old male, from a village near Mansoura, presented to the Out-Patient
Clinic of Mansoura University Hospital with complaints of painful urination, the
presence of blood in his urine, fatigue, fever and general body aches. Upon
examination, the physician ordered a urine analysis and urine culture to rule out a
urinary tract infection.
Culture results were negative for pathogenic bacteria. Microscopic
examination of the urine sediment revealed proteinuria, many RBCs (haematuria)
and few white blood cells. Oval, translucent eggs with prominent terminal spines
were also detected.
Questions:
1. Which parasite is the cause of this patient's infection?
2. How is this infection transmitted?
3. Mention the complications of this parasitic infection.
4. Describe the detected egg.
5. Compare this egg with those of other members of this genus.
6. Which types of specimens should be collected for diagnosis?
7. How is this infection diagnosed?
8. Describe the "hatching test" and mention its value.
9. What is the association of this infection with bladder cancer?
10. How is this infection treated?
11. How is infection with this parasite prevented and controlled?

Case study :
A 22-year-old Egyptian woman was visiting American relatives and developed
fever, malaise, dysentery and abdominal pain. Her relatives brought her to the
family doctor for examination. Upon examination, she was noted to have liver
tenderness. Blood was drawn for complete blood count and liver enzyme analysis.
Three stool specimens were submitted for examination for ova and parasites.
The patient was noted to be mildly anaemic and had slightly elevated liver
enzyme levels. Two of the 3 stool specimens revealed a small number of eggs.
Each is oval, translucent, 140X70 p with a prominent lateral spine.
Questions :
1) Which parasite is causing this patient's infection?
2) Give an account on Katayama syndrome?
3) What are the possible complications of this parasitic infection?
4) How is this infection diagnosed?
5) Do bird species in this genus cause human disease?
6) How is this infection treated?

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 Snails (Mollusca)
§ Snails may be aquatic, amphibians or land snail.
§ Their life span ranges from few months up to 2 years.
The snail consists of:
(1) Shell: the hard - Whorls (segments): separated by sutures (grooves).
part of the snail, and - Apex: the top of the snail.
each shell composed - Body whorl: the big whorl above the aperture
of: - Siphon: the outside eversion of the lower margin of snail.
- Umbilicus: the margin of the opening may be inverted
towards the body forming a groove called umbilicus.
The aperture: may be right-sided (dextral) or left-sided
(sinistral).
(2) Body It is the soft part of the snail, which gets its shelter inside the
snail. It is composed of head, foot and viscera

To identify a snail the following points should be considered:

1. Apex: whether sharp or blunt.
2. Aperture: whether directed to the right side (dextral) or to the left sides
(sinistral).
3. Shell: its shape, color, presence of tubercles & the depth of the sutures.

Classification of some Egyptian snails:

I- Dextral (right- sided snails)
1. Snails with conical spire (conical):
Melania tuberculata Pirenella conica

1st I.H. of H. heterophyes. Resembles

No medical importance.
Melania except in:
1- Dextral, long spire 1- Whorls less oblique provided
2- Shell ornamented with fine with coarse tubercles arranged in 1-4
tubercles arranged in numerous rows.
rows. 2- The presence of siphonal notch.
3- No siphonal notch.
4- Sharp apex.
5- Oblique whorls.

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2.Snails with medium spire: all are of no medical importance
Cleopatra bulimoides Cleopatra cyclostomoides Vivipara unicolor

3. Fragile snails:
Lymnea cailliaudi Lymnea truncatula

I.H. of Fasciola gigantica I.H. of Fasciola hepatica

- Dextral, prominent spire. - Resembles L. cailliaudi except in
- Thin fragile shell. smaller size.
-Oval aperture half the length of the
snail.
-Large body whorl (first whorl above
the aperture).
II - Sinistral (left - sided snails)
Bulinus truncatus Physa acuta

I.H. of Schistosoma haematobium No medical importance

-Sinistral, short spire. - Resembles B. truncatus except in:
-Small or medium sized. - Sharp apex.
-Blunt apex and shoulder. - Sutures less deep.
-Deep sutures.
-Comparatively large body whorl.

Biomphalaria alexandrina Lanistes bolteni

I.H of Schistosoma mansoni No medical importance

-Sinistral. -Large with short spire.
-Discoidal shell (button shape). -Blunt apex.
-Flat upper surface. -Large umbilicus.

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