.-...

wrt\JhOI t SI J br &--•-~

INTESTINAL HELMINTHIC INFECTIONS

Intestinal cestodes: Intestinal trematodes Small intestinal nematodes- Intestinal

Taenia saginata Intestinal flukes Ascaris nematodes of
T. solium Fasciolopsis buski hookworm lower animals
Hymenolepis nano Strongyloides rarely infect
Blood flukes such as man.
Schistosoma mansoni and Large intestinal nematodes
S. japonicum reside in such as Trichuris and
mesenteric venous plexus Enterobius.
of GIT, and cause various
GI symptoms including
dysentery.

INTESTINAL CESTODE INFECTIONS:

Cestodes are long, segmented, flattened dorsoventrally, tape like worms,
therefore also called as tapeworms.
Based on habitat, they are classified into two groups:
Intestinal cestodes: Somatic/tissue cestodes:
Adult worms inhabit in human Intestine. Larvae are found in human muscles or organs.
Examples include: Examples include: Taenia solium-causes
Taenia solium and Taenia saginata causing cysticercosis affecting CNS, muscle and eye
intestinal taeniasis Echinococcus species- agent of hydatid disease
affecting liver

MORPHOLOGICAL FORMS
Helminths exist in three morphological forms-
(1) Adult form (or the worm)
(2) Larval form
(3) Eggs.

Adult Worm Adult worm is long, segmented, dorsoventrally flattened; consists of

three parts:
Head or scolex: Neck: Strobila (body or trunk):
It is the organ of attachment, Next to head, the It consists of a number of segments
helps in attachment to intestinal portion is called as neck (or proglottids).
mucosa by virtue of bearing four from which the segments
cup like muscular structures called (proglottids) arise Based on reproductive organs they
suckers (or acetabula) bear, proglottids can further be
grouped into three types:
In some species like T. solium and i. Immature segments: Here, male
H. nana, scolex has a beak like and female reproductive organs are
apical protrusion called as not differentiated
rostellum, which may be armed with
hooklets (these species are called ii. Mature segments: Cestodes are
as armed tapeworms) hermaphrodites or monoecious, i.e. ,
contain male and female organs in
In Diphyllobothrium, the scolex the same segment, male organs
does not possess suckers but it appear first
bears a pair of longitudinal grooves·
called as bothria by which it iii. Gravid segments or fertilized
attaches to small intestine. segments: Following fertilization,
the uterus qets filled with eaas.
Hooklels on rostellum
---Sucker
- - - - Neck region

, ~ - - - - - Immature
proglottids

Mature
proglottlds Strobila

---Gravid
proglottids

Fig. 46.1: Adult worm of cestode (schematic diagram).

EGGS: LARVA :
Eggs formed following fertilization, fill gravid Embryonated eggs undergo further development
proglottids and subsequently released in feces to form larvae.
-> considered as the diagnostic form
Most cestodes have only one larval stage except
In most cestodes, eggs are round to oval, consist D. latum.
of an embryo (or oncosphere) with six hooklets, In T aenia, the larval stage is called as
surrounded by radially striated embryophore cysticercus
In Echinococcus, it is called as hydatid cyst
In D. latum, eggs are ovoid, and operculated

Operculum
Egg shell Three pairs of hooldets
l • . :•·:. •• •.•o Emb,yophore

\. _..._..~- Knob
Figs 46.2A to C: Schematic diagrams of eggs of cestodes: A. D. latum;
8. Other cestodes; C. Other cestodes after the loss of egg shell.
 INTESTINAL T AENIASIS

Two important pathogenic species are T. saginata and T. solium.

They cause two types ot manifestations in humans:
Intestinal taeniasis -> caused by both Cysticercosis -> caused by only T. solium.
T. saginata and T. solium It infects various tissues such as CNS, eyes and
muscles
MORPHOLOGY :
Taenia exists in three mor holo ical forms.
Adult worm Eggs Larvae
Comprises of head or scolex, neck and a contain embryo or oncosphere Cysticercus is the
body divided into several proglottids which contains three pair of larval stage of
The scolex bears four cup like muscular hooklets, surrounded by an Taenia.
suckers which hel s in attachment emb o hore
LIFE CYCLE {INTESTINAL T AENIASIS):
Ufe cycle of Taenia passes through two hosts
Man is the definitive host; whereas intermediate host is :
cattle for T. saginata (hence called beef tapeworm)
pigs for T. solium (hence called pork tapewormf
TRANSMISSION:
Man acquires infection by ingestion of contaminated undercooked beef or pork
containing larvae, i.e. cysticercus bovis (infective form)
Human GIT: Intermediate hosts (cattle or pigs):
The larvae develop into adult worms Eggs are ingested by cattle or pigs while grazing field.
(in 10-14 weeks) in human intestine, i
which undergo self fertilization within Eggs penetrate the intestinal wall and migrate to skeletal
the segments to produce eggs. that muscles via blood, where they transform into larvae
are rel~d into feces (diagnostic (cysticercus) that get encysted and deposited as cysts.
form) i
This is infective ..form and the cycle is repeated.
This takes around 7-10 weeks of time

~1
,I§,

~evelops into
Man acquires ,infect.ion by
Ingestion of underoooked 4
beef/pork cont.ainlng
cystioercus la,vae Scolex exvaglnates
and anchors to Intestine

MAN
Adult worm in
amaU intestine

After
10-14 weeks
fertilization
occurs

Cysucercus
in skeletal muscle CATTLE/PIGS

c.-cu1auo\. Eggs In feces

.._ Eggsare /
·,___ingested
Oncosphere hatches out by cattlelptgs
and penetrates intestine
 CUNICAL MANIFESTATIONS:
Common symptoms include mild abdominal pain, nausea, loss of appetite and change
in bowel habit
Perianal discomfort or pruritus may be felt (when proglottids are discharged).
-.

LABORATORY DIAGNOSIS:
1. Stool Examination 2 .T aeni a Specific Antigen 3. Molecular Methods PCR
Wet mount examination of stool is Detection in Stool targeting mitochondrial
carried out to demonstrate EUSA has been developed to DNA followed by sequencing
characteristic eggs and less often detect Taenia specific antigen is available
proglottids of Taenia species. (coproantigen) in stool by using
polyclonal Taenia antibodies

INTESTINAL TREMATODE INFECTIONS

Trematodes (or flukes) are unsegmented, leaf-like and flat worms.

Based on the habitat, trematodes are classified as follows:
Intestinal flukes Blood flukes Hepatic flukes Lung flukes
e.g. Fasciolopsis buski. e.g. Schistosoma. e.g. Fasciola e.g.
It resides in intutine, They reside in venous plexus of various hepatica and F. Paragonimus
may cause various GI viscera gigantica in liver, westermani.
symptoms.
S. mansoni and S. japonicum - > reside It resides in
in venous plexus of GIT, cause various lungs, may
GI symptoms including dysentery. produce endemic
hemoptysis
S. haematobium - > resides in venous
plexus of bladder; causes urinary
schistosomiasis and carcinoma of
bladder
MORPHOLOGY
Trematodes exist in three mor holo ical forms-adult worm, e and larva.:
Adult worm: Eggs: Larvae:
Adult wo,,ns are unsegmented and flattened Trematodes are oviparous, Most trematodes
dorsoventrally but some have thick fleshy bodies i.e. they lay eggs; which have five larval
(schistosomes) develop into larvae later in forms such as
They ra~ from 1 mm to -60 mm, possess two environment miracidium,
suckers (as the organ of attachment), an sporocyst, redia,
incomplete digestive system, nervous system and The eggs of all trematodes cercaria, and
excretory system are characteristically metacercaria.
. operculated except that of
Most trematodes are hermaphrodites or schistosomes
monoecious (male and female organs present in
same worm), except schistosomes which are Schistosoma eggs are non-
diecious (sexes are se orate). o erculated and bear a s ine.
 SCHISTOSOMES

LIFE CYCLE OF SCHISTOSOMES

Schistosomes complete their life cycle in two different hosts-
one definitive host (man) and one intermediate host (fresh water snail).
There is no second intermediate host
form: Cercaria larvae are infective from, which are present freely in
water
of transmission: Humans acquire infection by skin penetration of
cercaria larvae (infective form) present freely in water.
Men acquire infection by
skin penetration of cercaria
Oral-----,L-.aA \ larvae present In water
sucker
\ Cercaria penetrates
Ventral_--.,....-...,_ / \ venous circulation
suc:ker
Cercarla \ \ Portal
Vllelaria
Uterus ---A~~,..~ \ circulation
Ovary-+.+½.-~~ \ Man Cercarla develops
/ \ into adult worm In liver
Oolype ~i:.-o,;;;;;;;5'"-:"C,.__- Sporocyst \
\ Adult worms sexually mature.
. \ migrate to their habitat
Wat.r \ (Venous plexuses of

', , I
\ \ intestine or bladder)
Miracidlum
penetrates Into
snail \ Fertilized female
', worm lays eggs
Figs 46.11 A and 8: Adult worm of: A. Fasciolopsis buski (schematic); \ (in urine/feces)
B. Schistosoma (The thin female worm resides in the gynecophoric
canal of the thicker male worm). Free living •-------<n water
miracidium
Fig. 46.13: Life cycle of schistosomes.
In man (develop into adult worms):
After penetrating intact epidermis, cercariae develop into next stage larvae,
schistosomula.
!
They travel via dermal veins to lungs, later to ~.systemic circulation and finally
enter portal circulation.
In liver sinusoids they develop into adult worms.
!
Adult worms sexually mature (as male and female) and migrate to their habitat
(venous plexuses of intestine or urinary bladder)
Intestine (for S. mansoni and S. japonicum) Kidney and bladder (for S.
hematobium).

In man (produce eggs): Fertilized female worms lay eggs in these venous plexuses.
Eggs are the diagnostic form; passed either in feces (for S. mansoni and S.
japonicum) or urine (for S. hematobium) .
!
In water: The eggs mature and hatch to release miracidium larvae which infect
the snails
!
In inte-rmediate host (snails): The miracidium larvae develop into sporocyst larvae
-+ finally into cercaria larvae, which are infective form to man and thus the life
cycle continues.
 ASCARIASIS

Ascoriosis is on infection of small intestine caused by Ascaris lumbricoides .

It is largest nematode parositizing human intestine.
It is commonly called as roundworm.
M9m1Hated
MORPHOLOGY: albuminous
Atrophied ovum
coat
Ascaris exists in three forms:
adult, larvae ( four stages) and egg. Unsegmented
ovum
Adult worm is cylindrical and measures 15-31 cm.
Crescentlc
The female worms liberate two types of eggs- space
Fertilized Unfertilized Decorticated
(1) fertilized eggs, and (2) unfertilized eggs. cor11cated egg egg rertilized egg

UFE CYCLE : Fig. 46.22: Eggs of Ascaris lumbr/coldes (schematic diagram).

Ascaris involves only one host (man).

Embryonated eggs containing the L2 larvae are infective form.
Mode of transmission:
Ingestion of embryonated eggs from contaminated soil, food and water.
MIGRATORY PHASE: INTESTINAL PHASE: DEVELOPMENT IN SOIL:
Following ingestion, eggs hatch out The L4 larvae undergo final Fertilized eggs molt twice become
to liberate L2 larvae, which molt molt to develop into a·dult embryonated (carrying L2 larvae),
once to form L3 . worms in the small intestine which is infective to man and the
! ! life cycle continues.
L3 larvae penetrate the intestine, Following fertilization, the
reach right side of the heart via female worms start laying It occurs within 2 weeks under
portal circulation, then enter lungs the fertilized eggs which suitable conditions such as warm
via pulmonary capillaries, where are passed in the feces. and clay soil, 22-30°C and 40%
they molt once to form L4 humidity
! Sometimes, before mating,
L4 larvae in lungs migrate up to the female worms may The unfertilized eggs cannot
reach pharynx and finally are directly lay the unfertilized develop further, are not infective
swallowed to re-enter the eggs . and disintegrate in some time
intestine.

Man acquires intection by

ingestion of contaminated
soil, food and water "-.
.
with embryonated egg )&
/ Rhabditlform
Embryonated egg larva (L,) hatches
containing larva out from egg

f Embryonation \ MolUng
Unembryonated eggs Larva penetrates
passed in feces Intestinal wall
t Venous
FertiJization ) circulation

'
Develops into
adult worm
\
Small intestine
Right side of heart
)

Lungs
Pulmonary
capillary

Swa~Phary~
Fig. 46..21: Life cycJe of Ascaris lumbricoides.
 PATHOGENESIS AND CLINIC AL FEATURE:
Pulmonary Phase: Intestin al Phase
It results from migrating larvae in lungs, which
It results due effect of adult worm in the
provoke an immune-mediated hypersensitivity intestine.
response.
Most people with mild Ascaris
infections are asymptomatic
Symptoms are observed in second week after the
ingestion of eggs; characterized by non-productive Intestin al complications: A large bolus of
cough, chest discomfort and fever entangled worms can cause intestinal obstruction,
rarely perforation, intussusception, or volvulus.
Eosinophilic pneumonia (Loeffle r's syndrome):
In severe cases, patients develop dyspnea and a
complications: Larger worms can
transient patchy infiltrat es seen in the chest X- enter and occlude the biliary tree, causing biliary
ray along with transient peripheral eosinophilia. colic, cholecystitis, pancreatitis, or (rarely)
intrahepatic abscesses.

LABORATORY DIAGN OSIS:

1 . Detection of Parasite egg: 2.Adult Worm Detection: 3.Larva
Detection (Stool examination) Both Adult worms may be detected in stool Detection
f ertili.zed and unfertil ized eggs can be or sputum of patients by naked eye During early
detected by stool ~amina tion by saline
pulmonary
and iodine wet mount. Barium meal X-ray of the GIT may migrato ry phase,
demonstrate the adult worms in the larvae can be
Concentration techniques by sedimentation intestine. found in sputum
method should be done if direct stool
or gastric
microscopy is negative Ultrasound should be done to detect aspirates before
Floatation tMthod for stool concentration adult worms in extraintestinal sites the eggs appear
is not preferTed as unfertil ized eggs do - in the stool.
not f loot on saturat ed salt solution.

4.Eqqs of Ascaris:
Fertilize d eggs Unfertil ized eggs
to ovat measure 45-75 • 35-50 measure 85-95 ~m •. 43-47
coat is thin, distorte d and scanty
Surrounded by a thick mamillated, albuminous an unsegmented, small atrophied owm
coat with a mass of disorganized highly refractile
a large unsegmented owm of granules and no crescentic space at poles
granular mass with clear crescentic space at appear golden brown in saline
both pol~ mount
appear golden brown in saline Does not f Ioat in saturated salt solution
mount
in saturated salt solution
 5. Serology Antibody detection (by 6. Molecular Method 7. Other Methods Eosinophilia is
EUSA and other formats) though PCR assay has been prominent during the early lung
sensitive developed targeting stage, but disappears later
internal transcribed Presence of Charcot-Leyden
spacer region (ITS1) or crystals in sputum and stool, a
cytochrome oxidase-1 of nonspecific finding seen in
Ascaris egg in the stool. ascariasis.

Figs 46.23A to C: Eggs of Ascaris lumbricoides: A. Fertilized eggs; B. Unfertilized eggs; C. Decorticated eggs.

HOOKWORM INFECTION

Hookworm is one of important causes of iron deficiency anemia in both tropics and
temperate countries.
It is one of the soil-transmitted helminths.

Hookworm comprises of several species, which infect humans and animals; out of
which only two species are human pathogens; cause intestinal disease.
Ancylostoma duodenale or old world hookworm -.
Necator americanus or new world hookworm or American hookworm.

MORPHOLOGY
Hookworm hos three mor holo ical forms: adult, larvae (four sta es) and e .
Ancylostoma and Necator The adult worm of Ancylostoma and Ll larva is called as
can be differentiated by Necator can be differentiated by rhabditiform larva whereas
morphology of adult worm buccal capsule with teeth or cutting
and third stage 'larva. . plate (present in the anterior end) and L3 stage larva is called as
copulatory bursa (present in the f ilariform larva.
sterior end)

LIFE CYCLE
Hookworm involves only one host (man).
Third stage filariform (L3 ) larva is infective form.
 MODE OF TRANSMI SSION:
Throu h enetration of skin b L3 larva; duri • barefoot in dam en soil.
Migratory phase: Intestinal phase: Development in soil:
Following peMtratio n, L3 larvae The L3 larvae molt twice in Eggs released in feces are
enter into subcutaneous venules small intestine to develop into immature, which become
and are carried to lungs through adult worms, which attach to embryonated in moist, shady,
venous circulation. the intestinal mucosa by their warm soil Ll (rhabditifo rm)
! teeth in buccal capsule larvae hatch out from eggs
they enter into the alveolar ! and then molt twice to
space and migrate up to Following fertilizatio n, female develop into L3 larvae L3
pharynx and finally by worms lay eggs, which are larvae remain viable in the
swallowing of sputum, they excreted in feces soil for several weeks and
enter GIT ! are infective to man.
A gravid female of A.
duodenale can lay 25, 000-
35,000 eggs/day, whereas that
of N. americanus can_ lay
6,000-20, 000 e s/da .

Strongyloides and Hookworm

Environment Environment
(soil) Trans mission : Skin penetration (soif}
Infective from : L3 (Filariform larva)••-- --
i Penetrates '-
Venous circulation
i
"'
4

Lay !
Lungs
Swallowing of sputum
\

eggs Reach G~T L,

g La larvae mig,ate to
I
if
various organs to cause
hyperinfection syndrome
[ Intestine ) \
Adult __r Male
WOOll 4 Female Direct
development C
0 Larvae develop into larvae develop
-c Mate

l
; II)

e
.g 0 Indirect
u·-
a, J!?
-c:--·a:I
adult female worms into adults Female
-
O·c II)
(I) -
C: s development - a,
Parthenogenesis Fertilization
Cl) a,
:, f?
g~ Unembryonated eggs in
a, e
L, g>>- Female worms lay eggs feces (diagnostic form)

!
~.o containing larva
w
Transfo~ L, Molting
into rm'\.
L 1 (Rhabdiliform larvae) in feces
L, (diagnostic form)

Transform into
 CLINICAL FEATURES:
Affect due to Migrating Larva Cutaneous Affect due to Adult Worm in Intestine Clinical
lesions: spectrum produced by adult hookworm depends
This may occur in previously sensitized persons upon the worm load.
Infecti ve larvae may provoke pnritic
maculopapular dermat itis and rashes ("ground Asymptomatic: Most hookworm infections are
itch") at site of skin penetration asymptomatic Early intestinal phase
(less worm load):
Mild transient pneumonitis: Migrating larvae
through lungs occasionally cause mild transient Infected persons may develop epigastric pain,
pneumonitis, asthma and bronchitis inflammatory diarrhea, or other abdominal
symptoms, accompanied by eosinophilia

LABORATORY DIAGN OSIS:

1.Stool Microscopy: 2. Stool Culture 3. Molecular Diagnosis
The diagnosis is established by finding The freshly passed PCR and real-tim e PCR based
of charac teristic eggs in feces. stool samples can be assays have been developed
cultured so that the targeting genes such as
Stool concentration procedures may be eggs hatch out to mitochondrial cytochrome
required to detect lighter infections. develop to L3 stage oxidase genes.
eggs of hookworm f ilariform larvae
Hookworm eggs are oval, meas&.re 60 •
40 pm, sWTOUl'lded by thin eggshell.
Not bile stained, appear colorless· in
saline mount
Ovum (embryo) is segmented; comprises
of 4-32 blastomeres
~.
There is a clear space between egg
shell and the embryo

Floats in sanrat ed salt solution

 AMOEBIC LIVER ABSCESS

Amoebic liver abscess (A_~A) is an important cause of space occupying lesion of

liver, occurs mainly in developing countries; caused by a protozoan parasite, E.
histolytica.

PATHOGENESIS:
Transmission occurs through ingestion of food and water contaminated with cysts
of E. histolytica
!
Attachment: Cysts develop into trophozoites, which adhere to intestinal mucosa by
virtue of Gal/NAG lectin antigen (major virulence factor)
!
Invasion: The trophozoites secrete cysteine proteases and hydrolytic enzymes,
which help in the invasion of intestinal mucosa
i
Spread: In few cases, erosion and necrosis of small intestine are so extensive that
the trophozoites gain entry into the portal venous system and carried to
extraint~inal sites
!
Survival: Resistance to complement-mediated lysis (mediated by Gal/NAG lectin
antigen) is a crucial property of E. histolytica, critical for its survival in the
bloodstream Liver is the most common extraintestinal site; followed by lungs,
brain, enitourin tract and s leen
MICROSCOPICALLY I Anchovy sauce pus:
Abscess wall is comprised of: Liver abscess pus is thick chocolate brown in
Inner central zone of necrotic hepatocytes color.
without amoeba
zone of degenerative hepatocytes, The fluid is acidic and pH 5. 2-6. 7 and is
RBC, few leukocytes and occasionally amoebic comprised of necrotic hepatocytes without any
trophozoites pus cells and occasionally amoebic trophozoites
zone comprised of healthy (mainly found in last few drops of pus) as
hepatocytes invaded with amoebic amoebae multiply in the wall of abscess
tro hozoites.

Figs 49.1 A and 8: A. Cross section of the liver showing amoebic

liver abscess (right side); 8. Anchovy sauce pus aspirated from
amoebic liver abscess.
 HUMAN ECHINOCOCCOSIS

Human echinococcosis is a- zoonotic disease that is caused by a cestode of genus

Echinococcus.
CYSTIC ECHINOCOCCOSIS
It is caused by Echinococcus granulosus; also called as dog tapeworm.

MORPHOLOGY
It is a tissue cestode, exits in three morphological forms-
Adult, Larva (called hydatid cyst), and EQQ:
The adult worm resides in dog's The larval form is called Eggs: E. granulosus eggs are
intestine. It measures 3-6 mm as hydatid cyst. It is the morphologically similar to Taenia
long, consists of head, neck and a pathogenic form, forms eggs, consists of an embryo with six
strobila or body made up of three cystic lesions in liver and hooklets surrounded by an
proglottids/segments other viscera of man and embryophore.
other herbivores

UFE CYCLE:
Host: E. granulosus passes its life cycle through two hosts:
Intermediate hosts: Sheep and other herbivores Definitive host: Dogs and other canine animals
are the usual intermediate host.
Man acts as an accidental intermediate host
(dead end).
Infective form: Eggs are .infective form.
Mode of transmission: Man (and other intermediate hosts) acquires the infection
b i tion of food contaminated with do ·s feces containi E. ranulosus e s.
Development in Man/Sheep Development in Dog :
In duodenum, embryo or oncosphere is released, Dog and other canine animals acquire infection
which penetrates intestinal wall, enters the portal by consumption of the contaminated viscera of
circulation and carTied to the liver (60-70% of intermediate hosts (sheep) containing mature
cases) or lungs or rarely to other organs hydatid cysts.
i The hydatid cyst (larva) transforms into adult
Although majority of embryo are destroyed by worm in dog's intestine.
host irntnl.l\e response, few escape and develop The adult worms sexually mature,. self fertilize
into fluid filled bladder-like cyst called as to produce eggs which are passed in feces and
hydatid cysts are ,infective to man

Rost.ellum with two iI , ..

rows of hooklets
~Suckers
·--Scolex

Neck
.I~ i,
I l:i I '

. Immature proglottid

....
..
: •. Mature proglottid

Gravid proglottid

El
Figs 49.2A and I! Edllnococcus granulosus: A. Adult worm
(schematic); B. Hydatld cyst. gross specimen. ~ltw<IM-

4. ~11'91
 HYDATID CYST
It is a fluid-filled bladder-like cyst; unilocular, subspherical in shape
Cyst wall consists of three layer$: Hydatid sand: Some of brood capsules break off
outer pericyst (host derived), middle ectocyst and get deposited at bottom as hydatid sand
inner endocyst
Brood capsule: The inner side of the endocyst Fate: Hydatid cyst may undergo
gives rise to brood capsule, and also secretes (i) spontaneous resolution
the hydatid fluid. (ii) rupture of cyst, which may lead to either
Hydatid fluid: It is clear, pale yellow colored formation of secondary cysts (carried to other
fluid, which is antigenic, toxic and anaphylactic organs) or anaphylactic reaction to the hydatid
fluid antigens.

Figs 49.sA to C: Microscopy d hydatid cyst: A. Schematic I and C. Histopathological section (hematoxylin and eosin stain) showing Fig. 49.4: Surgiuly rM«ted ~tid cyst from r_,._
CB) all t h ~ ~ d cyst wall--pericy$t. ectocyst ind ~ndocyst. (Cl endocyst with attached brood capsules.

CLINICAL FEATURES :
Infection usually occurs in childhood but gets manifested in adult life.
Site: Most common site of the cyst is liver (60-70%, right lobe) or lung (20%t
followed by kidney, muscle, spleen, soft tissue, brain, bone and others

Asymptomatic: The cysts grow up to 5-10 cm in size within first year and can
survive for years or even decades, without any symptoms

Symptoms: Few patients develop symptoms whi~h may be due to:

Pressure effect of enlarging cyst: Leads to palpable abdominal mass,
hepatomegaly, abdominal tenderness, portal hypertension and ascites
Secondary bacterial infection, causing pyogenic abscess in liver
LABORATORY DIAGNOSIS :
1. Histological examination:
Surgically removed cysts can be subjected to histopathological stains like Giemsa,
hematoxylin and eosin (H & E) ,and periodic acid-Schiff (PAS) stain to demonstrate
the three layers of the cyst wall and attached brood capsules

2.Antibody detection -> ELISA (using 82t antigen), DIGFA (dot immunogold
filtration assay) and western blot

3.Imaging methods -> X-ray, USG (demonstrates Water lily sign), CT scan, MRI

4.Molecular methods -> PCR, PCR-RFLP and molecular typing