Intestinal Nematodes

Dr. Devika Iddawela

Dr. Devika ddawela
08/09 batch
 Helminthes

Nemathelminthes Platyhelminthes

Nematodes Cestodes Trematodes

(round worms) (tape worms ) (flukes )
 Flatten leaf-like
Elongated, Flattened tape-
cylindrical worms like segmented
Sexes are Sexes are not
Sexes are not
separate separate except
separate
Complete blood flukes
Alimentary canal + Alimentary canal Alimentary canal
Possess a body absent incomplete
cavity Body cavity
Body cavity absent
(psedocelome) absent
 word "nematode" came
Nematodes from a Greek
word nema that means "thread".

Nematodes have successfully

adapted to nearly every
ecological niche from marine to
fresh water, from the polar
regions to the tropics,
 Parasitize the intestinal tract, tissues,
tissue spaces, lymphatics
Body covered in a complex cuticle
Longitudinal muscle fibers present, No
circular muscle
Fluid filled body cavity present
Organs are suspended in the body
cavity
Reproduction & developmental stages:
egg, Egg fertilization,embryonated egg,
larva, 4 moults, adult
Small intestine - Nematode
parasites
Nematodes of small intestine
Ascaris lumbricoides
Ancylostoma duodenale/Necator

americanus
Strongyloides stercoralis
 Nematodes of the large
intestine

Trichuris trichiura - Whipworm

Enterobius vermicularis - Pinworm
Orally infected Intestinal nematodes

Ascaris lumbricoides (round worm)

Trichiuris trichiura ( Whip worm)

Enterobius vermicularis ( Pin worm)

Ascaris lumbricoides
(Round worm)
worm

Common intestinal parasite world

over but high prevalence in countries
with poor sanitation

Commonest age group affected

pre-school
children & young school children
Prevalence due to indiscriminate
defaecation in and around home gardens
Morphology -
Sexes are separate.
Female - 20 - 40 cm
Male - 15 - 30 cm with curved tails
No. of eggs /female/day - appr. 200,000
Location in host worms are found
free in the lumen of small intestine
Maintains position in lumen with muscular
movement against peristalsis. Can be temporarily
attached to mucosa for short periods

The anterior end of both sexes

shows three lips
 Eggs

Fertilized eggs: (corticated, decorticated)

Ovoid, 60 x 40 um.
Thick shell ( triple layered) inner non-permeable
layer, thick transparent middle layer and an outer
mammilated coat .
Unfertilized eggs - Larger, rectangular
(80 - 90 x 60 um) with disorganized,
vacuolated contents
 Male and female adults in the Fertilized eggs
small intestine ( non- infective
warm moist pass in the
Larva penetrate in to the clay soil 25- faeces
alveolus bronchioles 30C
trachea swallowed Infective L2 larva ( 2nd
oesophagus small stage larva)develop
intestine with in the egg ( 2-3
weeks )
Reaches
pulmonary Infective eggs swallowed
capillaries with contaminated water
and food
Heart
Larva penetrate
Larva enters eggs hatch in small
the Intestinal wall
portal vein intestine
and venules
Adults in the small intestine
 Pathogenesis & clinical features

Depends on
worm load
The host immune response
Effect of larval migration
Mechanical effects of adult worm
Nutritional deficiencies due to the
presence of adult worm
Majority of infections are clinically
asymptomatic
 Migrating Larvae( larval ascariasis)

Loefflers syndrome
Eosinophilic abscesses

Lungs - larval migration causes

pneumonitis (Lofflers syndrome) due
to immunological(hypersensitive)
reaction

CLINICAL FEATURERS: Fever, cough,

sputum, asthma, eosinophilia and
radiological infiltration
On reaching general circulation

Rarely larvae may wander in to the

brain, eye or retina causing
granuloma
 Adult worms
Adult worms in their normal habitat
cause little pathology
BUT(Severe disease
if worm burden 100 or >)
Heavy infections can cause intestinal colic
Aggregate masses of worms cause
Volvulous, Intestinal obstruction or
interssusception
Large worm load :Intestinal obstruction
Small bowel obstruction in kids >1000 in
worm ball
 Wandering ascarids
lone adults are prone to wandering habit
block/perforate ducts
cause acute symptoms
Blocking the duct orifices
Acute appendicitis
Pancreatic necrosis-
Obstructive jaundice
Ascaris liver abscess
Migrate out of the anus or come out the
mouth or nose
Immuno-pathological effects-

sensitivity to ascaris ag-

conjunctivitis, urticaria, asthma

Indirect effects - Micro organisms can

by carried by the adult worms on their
migration from bowel
 Effect of Ascariasis on Growth & Nutrition
Protein Energy Malnutrition [PEM]
Due to consumption by the worm
Act as a mechanical barrier to absorb
nutrients
children with 13-40 worms
loose 4g protein/day from a daily intake of 35-50g
[1 egg only 6g protein]
Kwashiorkor swelling due to low albumin [low
serum proteins]
Vitamin A deficiency Night blindness
AFFECTS NORMAL GROWTH & EDUCATIONAL
DEVELOPMENT
CHRONIC MALNUTRITION STUNTING
Stunting linked to impaired intellectual development
UNICEF State of the Worlds Children
The same factors that lead to stunting cause learning deficits

Malnutrition early in life is

linked to deficits in children's
intellectual development
that persist in spite of schooling
and impair their learning ability

Stunting = low height for age

Height difference in 2 girls of 5 years age
40% of worlds children are stunted

growth retardation, poor cognitive & scholastic

achievements
 Diagnosis

Demonstrating characteristic eggs in faeces

Identification worm
Concentration techniques are useful
Eosiniphilia Larval ascariasis high
eosinophilia
In Adult infection little or none
Radiography: 4 -6 hours after opaque meal
displays worm as cylindrical filling defect
Long, tubular filling defects,
especially in distal small
bowel
The worm ingests barium and
the barium may be seen as a
thin line of contrast in the
center of the worm
Especially after the remainder
of the barium exits the small
bowel
Epidemiology
Common backyard infection
Maintained by young children
Transmission occurs through
infective eggs Contaminated food
and water

In Sri Lanka prevalence is highest

among school children
 Prevention & Control
Prevention of ingestion of infective
eggs

Wash raw vegetables and fruits thoroughly

( preferably with running water)

Wash hands with soap and water

before eating and after soil contact

Drink boiled cool water

Prevention of indiscriminate
Defaecation by Providing sanitary
latrines
.
Provision of safe drinking
water

Treatment of infected patients

 Trichuris trichiura
Geographical distribution -Parasite of
warmclimates
Morphology - 3 - 5 cm. Posterior 2/5th of
the body is thick (whip handle). Anterior
3/5th thin and is threaded into the
mucosa of the large intestine. Posterior
end of male is curved.
Egg - Paddy seed shape with
two polar plugs 50 x 20 um
 Life cycle

Adults - attached to the colon from their

anterior site embedded in mucous
between intestinal villi
Eggs are laid unsegmented require
embryonation in the soil

No lung migration
 Life cycle of whipworm

Adults in large
Eggs in stools
intestine

Penetrate and mature in Moist Eggs

intestinal mucosa
clay mature
No lung migration 25 -30 C in soil
Larva hatches in
intestine
Eggs ingested with contaminated fruits,
vegetables
etc.
 Pathology

Few worms little damage

Heavy infection- spread
throughout the colon to the rectum
causing
Haemorrhages
Muco-purulent stools, dysentery
and rectal prolapse
clinical features

Mild infections are asymptomatic

Heavy infection cause blood and mucus
diarrhoea
due to mucosal damage & rectal prolapse
Children may get Trichuris dysentery
syndrome resulting in severe diarrhoea,
malnutrition, growth retardation and
impairment of cognitive functions
 Diagnosis
Finding the characteristic eggs in
stool by direct smear or by
concentration methods

Proctoscopy in cases of dysentery, show

numerous worms attach to the mucosa which is
redden and ulcerated
Epidemiology
Trichuris trichiura is primary a human
infection but Trichuris suis of pig also
can infect man
Common in areas of high rain fall, high
humidity, dense shade and poor
sanitation.
High prevalence in children of primary
school age
Often associated with ascariasis
Enterobius vermicularis

Geographical distribution -worldwide high

prevalence in cold climates.
Location in host - Adults are loosely
attached to the mucosa of the large
intestine
Morphology - creamy white, 1cm, spindle
shaped
Eggs - Plano-convex 50 x 25 um,
double walled with outer
albuminous layer and an inner
lipoid layer
The cervical alae extend right down
the sides of the body so in cut section
seen as projection in either side of the
body
 Life cycle

Adults live in the large intestine; females

migrate out of the anus for oviposition:
Worm attached to the mucosa of large intestine,
they are not blood suckers
A gravid female carries about 10,000 eggs.It dies
after oviposition
No lung migration of larvae
No development in the soil. Therefore it is not a
soil transmitted helminthe infection
Eggs become infective within 6
hours
of laying
 clinical features

Very little tissue damage

Rarely penetrates the gut wall causing
granulomatous reactions in the liver,
ovary, kidney
Can co-exist with amoebiasis
Causes intense perianal pruritis especially at
night when gravid female moves on and lay eggs
on the perianal skin
 In children this leads to insomnia
Female worms may enter vagina
urethra, can cause vulvitis, pruritis
vulvi

Loss of appetite, loss of weight

,irritability, enuresis
 Diagnosis
Demonstration of eggs:NIH (National
Institute of Health, USA) swab and
Scotch Tape method a clear adhesive
cellulose tape is applied to the anal area
early in the morning before bathing or
defecation
A simple cello-tape
Cotton wool swab
Eggs are usually collected in the folds of
skin around the anus. Rarely appear in
the stools
Adults
 Transmission and
epidemiology
1.Direct transmission from the perianal and
anal region to mouth by figure nail
contamination due to scratching of perianal
region and by soiled night cloths ( hand to
mouth)
2. Exposure to viable eggs from soiled bed
linen and other contaminated objects in the
environment.
3. Via mouth or nose from contaminated dust
4. Retro-infection where eggs hatch in the
perianal skin and larvae migrate up the bowel
 It is a household infection and is common in
overcrowded houses and institutions like
hostels, prisons, refugee camps, orphanages
etc
Prevention

Cut figure nails short

Wash hand with soap and water regularly
Treat every one in the household
Following treatment all bed linen & personal
cloths should be washed and dried in hot sun
 Intestinal nematodes

Infection via skin penetration

Hook worms- Ancylostoma duodenale

Necator americanus

Tread worm- Strongyloides stercoralis

HOOK WORMS
 Hookworms

Necator americanus - Sri Lanka,

S.Asia,Africa,
Pacific region and America
Ancylostoma duodenale -
E.Europe,N.Africa,
India, N.China, Japan
Both species overlap in S.E.Asia,
Pacific, W.Africa
Morphology
N.americanus - 1 cm, head sharply bent
backwards. Buccal capsule has a pair of
ventral cutting plates
 A.duodenale
slightly larger
head bent backwards in a
smooth curve.
Buccal capsule has two pairs
of teeth
 Both species - Males have expanded
tails to form the copulatory bursa

The caudal expansion of certain

male nematodes that functions as a
claspers during copulation.

Female

Male
Egg Oval ,60 x 40 m with a thin
glass like shell. Embryo usually
segmented when pass out with
the faeces
 L3 5th
day Obligatory lung
migration
Non feeding,move
on to top soil
L2
rhab.larva
(3rd day)
Free
living,actively
feeding

L1 Shade,warmth, sandy
soil

24 hours
Life cycles of Ancylostoma and Necator
are similar except that
A.duodenale can infect by ingestion as
well as via the skin
N. americana infects only through skin
Migrating larvae of N.americana grow and
develop in the lungs, where as
ancylostoma do not
Pathogenesis
Larvae
Larvae at the site of entry vesiculation and
pustulation (ground itch)
Can be secondarily infected due to severe itching
Asthma and bronchitis during migration, can
cause pneumonitis but less severe than ascariasis

Adults:
Hook worm Anaemia
Symptoms- mucous surface & skin become pale. Palpitation,
breathlessness
Chronic blood loss is due to
active suction impulse 120- 200 times/min
Habitual blood sucker and need serum
Secrete anticoagulant substance and
may move from spot to spot increasing the
damage and blood loss
Blood loss
N. Americarnus -0.03ml /day/worm
A. Duodenale 0.15/day/worm
 Iron deficiency Anaemia
Hb related to worm burden

500-1000 worms
Anaemia even if adequate dietary iron
intake
If dietary iron deficient anaemia even
with light infection
 Hookworm
disease
Severe iron deficiency anaemia,
hypoproteinaemia, oedema with
associated circulatory problems

Hypoalbuminaemia - reduced albumin

synthesis &Protein loss > RBC loss
Related to worm load
 Laboratory Diagnosis
By demonstrating characteristic eggs
in faeces.
In old stool samples
Rhabditiform larvae may be found
( distinguish them from those
of Strongyloides stercoralis).
Concentration techniques are helpful
Eggs can be cultured into infective larvae
(Harada Mori culture)
 Transmission

Normally acquired via the skin from

filariform larvae in the soil contaminated by
the human faeces or
Orally via the ingestion of contaminated
food ( A. duodenale)
Migrating infective filariform larvae of
A.duodenale are arrested in their
development and migrate to the mammary
gland and are excreted via milk and infect
the child
Epidemiology

varies in different parts of the world.

There are geographical variations
too. In Sri Lanka it is an infection of
the adults due to indiscriminate
defaecation in shady areas away
from dwellings.
Prevention & Control
avoidance of indiscriminate defaecation & use
of foot wear

provision of hygienic latrines, treatment of

infected persons& health education
Strongyloides stercoralis
Distribution - Worldwide but more
common in warm climates. Major
opportunistic infection among
immunocompromised persons.

Morphology - Females are about 2mm.

Male is very small , short life span in
parasitic life cycle or non- exsistant
Male exist but disappear from the bowel
soon after oviposition. Eggs can be
produced parthenogenetically
Worm - embedded in the small
intestinal mucosa

Egg output
low and asynchronous ( not
occurring at regular interval)
Eggs hatch in the mucosa itself and
1st stage rhabditiform larvae are
passed in faeces
 Life cycle
Two life cycles
Parasitic cycle ( if the external
conditions are unfavorable)
Free living cycle( if conditions are
favorable )
 Rabditiform larvae

Develop in to Filariform larvae

filariform larvae in develop before
soil leaving the patient

Penetrate the
Follow free Enter perianal
intact skin and
living cycle skin & initiate
initiate the
in the soil autoinfection
infection

Enter intestinal mucosa,

migrate to lung & initiate
autoinfection
Multiplication in the host by two ways

1. Filariform larvae do not pass out in

the stool but reinvade bowel or skin

2. Filariform larvae lodge in the

bronchial epithelium and produce
further progeny (offspring)
 Differences between hookworms and
threadworms
HOOK WORM TREAD WORM

Attach to small Embedded in

intestine small intestine
Both male and Male short living
female
parasitic cycle parasitic and
free living cycles

no autoinfection Autoinfection+
 clinical features

Vast majority of infections in endemic

areas are symptomless
Primary infection
a pruritic erythematous eruption Ground
itch at the site of entry to larvae, last about
3 weeks
Pneumonitis due to lung migration not
common
 Intestinal nematodes

Infection via skin penetration

Hook worms- Ancylostoma duodenale

Necator americanus

Tread worm- Strongyloides stercoralis

HOOK WORMS
 Hookworms

Necator americanus - Sri Lanka,

S.Asia,Africa,
Pacific region and America
Ancylostoma duodenale -
E.Europe,N.Africa,
India, N.China, Japan
Both species overlap in S.E.Asia,
Pacific, W.Africa
Morphology
N.americanus - 1 cm, head sharply bent
backwards. Buccal capsule has a pair of
ventral cutting plates
 A.duodenale
slightly larger
head bent backwards in a
smooth curve.
Buccal capsule has two pairs
of teeth
 Both species - Males have
expanded tails to form the
copulatory
The caudal bursa
expansion of
certain male nematodes that
functions as a clasper during
copulation.

Female

Male
Egg - Ovoid,60 x 40 m with a
thin glass like shell. Embryo
usually segmented when pass
out with the faeces
 L3 5th
day Obligatory lung
migration
Non feeding,move
on to top soil
L2
rhab.larva
(3rd day)
Free
living,actively
feeding

L1 Shade,warmth, sandy
soil

24 hours
Life cycle Eggs passed in faeces
Adults in small Shady warmth Eggs hatch in 24
intestine sandy soil hours into 1st stage

rhabditiform
larva
Breaks into alveoli
move along bronchioles,
trachea, swallowed
Moults into 2nd rhab.
larva on the 3rd day
Penetrates skin, enters
circulation, carried to
the lungs Moults into 3rd stage
infective filariform larva
Life cycles of Ancylostoma and Necator
are similar except that
A.duodenale can infect by ingestion as
well as via the skin
N. americana infects only through skin
Migrating larvae of N.americana grow and
develop in the lungs, where as
ancylostoma do not
Pathogenesis
Larvae
Larvae at the site of entry vesiculation and
pustulation (ground itch)
Can be secondarily infected due to severe itching
Asthma and bronchitis during migration, can
cause pneumonitis but less severe than ascariasis

Adults:
Hook worm Anaemia
Symptoms- mucous surface & skin become pale. Palpitation,
breathlessness
Chronic blood loss is due to
active suction impulse 120- 200 times/min
Habitual blood sucker and need serum
Secrete anticoagulant substance and
may move from spot to spot increasing the
damage and blood loss
Blood loss
N. Americarnus -0.03ml /day/worm
A. Duodenale 0.15/day/worm
 Iron deficiency Anaemia
Hb related to worm burden

500-1000 worms
Anaemia even if adequate dietary iron
intake
If dietary iron deficient anaemia even
with light infection
 Hookworm
disease
Severe iron deficiency anaemia,
hypoproteinaemia, oedema with
associated circulatory problems

Hypoalbuminaemia - reduced albumin

synthesis &Protein loss > RBC loss
Related to worm load
 Laboratory Diagnosis
By demonstrating characteristic eggs
in faeces.
In old stool samples
Rhabditiform larvae may be found
( distinguish them from those
of Strongyloides stercoralis).
Concentration techniques are helpful
Eggs can be cultured into infective larvae
(Harada Mori culture)
 Transmission

Normally acquired via the skin from

filariform larvae in the soil contaminated by
the human faeces or
Orally via the ingestion of contaminated
food ( A. duodenale)
Migrating infective filariform larvae of
A.duodenale are arrested in their
development and migrate to the mammary
gland and are excreted via milk and infect
the child
Epidemiology - varies in different parts
of the world. There are geographical
variations too. In Sri Lanka it is an
infection of the adults due to
indiscriminate defaecation in shady areas
away from dwellings.
Prevention & Control
avoidance of indiscriminate defaecation & use
of foot wear

provision of hygienic latrines, treatment of

infected persons& health education
Strongyloides stercoralis
Distribution - Worldwide but more
common in warm climates. Major
opportunistic infection among
immunocompromised persons.

Morphology - Females are about 2mm.

Male is very small , short life span in
parasitic life cycle
Male exist but disappear from the
bowel soon after oviposition. Eggs
can be produced
parthenogenetically
Worm - embedded in the small
intestinal mucosa
Egg output
low and asynchronous ( not
occurring at regular interval)
Eggs hatch in the mucosa itself and
1st stage rhabditiform larvae are
passed in faeces
 Life cycle
Two life cycles
Parasitic cycle ( if the external
conditions are unfavorable)
Free living cycle( if conditions are
favorable )
 Rabditiform larvae

Develop in to Filariform larvae

filariform larvae in develop before
soil leaving the patient

Penetrate the
Follow free Enter perianal
intact skin and
living cycle skin & initiate
initiate the
in the soil autoinfection
infection

Enter intestinal mucosa,

migrate to lung & initiate
autoinfection
Multiplication in the host by two ways

1. Filariform larvae do not pass out in

the stool but reinvade bowel or skin

2. Filariform larvae lodge in the

bronchial epithelium and produce
further progeny
 Differences between hookworms and
threadworms
HOOK WORM TREAD WORM

Attach to small Embedded in

intestine small intestine
Both male and Male short living
female
parasitic cycle parasitic and
free living cycles

no autoinfection Autoinfection+
 clinical features

Vast majority of infections in endemic

areas are symptomless
Primary infection
a pruritic erythematous eruption
Ground itch at the site of entry to larvae,
last about 3 weeks
Pneumonitis due to lung migration not
common
Chronic uncomplicated strongyloidiasis
Epigastric pain, anorexia, chronic
diarrhoea due to mucosal damage, weight
loss
Skin rashes
Two types
Larva currens: Occur around the anus and
anywhere on the trunk. larvae migrate
under the skin
causes itchy rash which is not indurate &
has a red flare at the edge
Urticaria
Allergy to larval penetration in already
sensitized patient
Occur in the buttocks with pruritus ani&
around the waist

Last 1-2 days and can recurs at regular

intervals
 Severe complicated
strongyloidiasis
Severe disease with hyper-infection in persons
with immunosupression
severe watery diarrhoea, often with
malabsorption, hypoalbuminaemia.
Generalized oedema, Fever,

Lungs- hypereosinophilia, pneuminitis, diffuse

crepitation, pulmonary abscess and gross
respiratory failure
 Diagnosis
Demonstration of 1st stage rhab.
larvae in stools
Diffentiate from hookworm 1st stage larvae
Ss 1st stage rhab larva has a short buccal
capsule compared to that of Hw

 Diagnosis
Microscopic identification of larvae
(rhabditiform and occasionally filariform) in the
stool or duodenal
Examination of serial samples is necessary and
not always sufficient, because stool examination
is relatively insensitive.
stool can be examined in wet mounts:
directly
after concentration (formalin-ethyl acetate)
after culture by the Harada-Mori filter paper
technique
after culture in agar plates
 Culture faeces by /Modified agar plate
Harada-Mori technique
obtain 3rd stage filariform larvae. Ss
has a
triradiate tip of the tail while Hw has a
pointed tail
Larvae may be obtained by endoscopy
or by Entero test

ELISA to detect parasite specific IgG

 Antibody detection
Indications When the infection is suspected
: and the organism cannot be
demonstrated by duodenal
aspiration, string tests, or by
repeated examinations of stool.
Enzyme immunoassay (EIA) is currently recommended
because of its greater sensitivity (90%).
Antibody test results cannot be used to differentiate
between past and current infection

Serological test is useful in follow up of treated patients

 Hookworm L3
S. Stercoralis L3 larva larva
In hyperinfection: larvae can found in
sputum
 Examination of faeces for
intestinal parasites

Collection of faeces
Into a dry, clean, leakproof container
using wooden spatula
Avoid contamination with urine, water,
soil
Label the sample
Delivery and transportation :
Formed faecal sample without blood and
mucous should be examined during the
day of passage
Preservation methods:
Allow faecal sample to be examined
after delay in delivery
Commonly used preservatives: 10%
aqueous formalin and PVA (polyvinyl
alcohol)
Microscopic examination of faeces

Direct wet smear (saline/iodine)

Quantitative faecal examination:

Kato Katz thick smear to calculate
the worm burden
 Concentration techniques
separate parasites from faecal debris and
increase the chances of detecting parasitic
organisms when these are in small numbers.
Methods
flotation techniques and
sedimentation techniques
Sedimentation techniques
use solutions of lower specific gravity than
the parasitic organisms, concentrating the
latter in the sediment
Eg: formalin-ethyl acetate technique

Flotation techniques :
use solutions which have higher specific
gravity than the organisms to be floated so
that the organisms rise to the top and the
debris sinks to the bottom.

most frequently used: zinc sulfate ,

Sheather's sugar
Objectives:

List the different groups of parasitic helminthes.

List the major characteristics of parasitic nematodes.
List the common intestinal nematodes in humans.
Outline the life cycles (LC) with stages and events.
Write a comparative account of the different LSs(SGL)
State the stages that cause pathogenic effects and identify those
stages of diagnostic importance.
Describe the pathogenesis and clinical features of parasitic
nematodes
Outline laboratory methods of visualization/identification.
Identify points in the life cycle where preventive matures are
applicable.
Soil is essential for complete the life
cycles of following
A.A. lumbricoides
B.Hook worms
C. Enterobius vermicularis
D.Strongyloides stercoralis
E. Trichuris trichiura
Regarding transmission of intestinal
nematodes
A.A. lumbricodes is by ingestion of
contaminated food and water
B. Hook worms by faeco oral route
C. S. stercoralis is by skin penetration of
infective larva
D.T. trichiura by transplacental rout
E.E. vermicularis is by retro infection
Match the infective stage with the
organism
A.E. vermicularis infective larva
containing egg
B. A. lumbricoides L2 larvae
C.Hook worms Filariform larvae
D. T. Trichiura Infective larva
containing egg
True/ false
1.Hook worm infection causes blood and
mucous diarrhoea
2.S. stercoralis causes sever disease in
immunocompromised patients
3.A.lumdricoides infection is common
among adults in SL
4. Hookworm infection is common
among children In SL
5. Whipworm infection is known cause
of rectal prolapse in children
6. Trichiuris trichiura and A.
lumbricoides infections co-exist
Hook worm anemia is microcytic
hypoochromic
Ascaris lumbricoides infection causes
stunting
S. Stercoralis infection can be diagnosed
by detecting eggs in faeces
S. Stercoralis is known to cause watery
diarrhoea