Intestinal nematodes

Intestinal Nematodes
Dr. Devika Iddawela
08/09 batch
Dr. Devika
ddawela

Helminthes
Nemathelminthes Platyhelminthes
Nematodes
(round worms)
Cestodes
(tape worms)
Trematodes
(flukes)

Elongated,
cylindrical worms
Flattened tape-
like segmented
Flatten leaf-like
Sexes are
separate
Sexes are not
separate
Sexes are not
separate except
blood flukesComplete
Alimentary canal + Alimentary canal
absent
Alimentary canal
incompletePossess a body
cavity
(psedocelome)
Body cavity
absent
Body cavity absent

Nematodes
Nematodes have successfully
adapted to nearly every
ecological niche from marine to
fresh water, from the polar
regions to the tropics,
word "nematode" came from a Greek
word nema that means "thread".

Nematodes
Long cyndrical body
No segmentation
Males and females separate. Females larger then
male.
Similar to each other but vary in size
Eg: round worm-size of a pencil
hook worm-size of a pin
Pin worm- smaller than the above
DO NOT MULTIPLY IN HUMANS

• 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
Ascaris lumbricoides
Ancylostoma duodenale/Necator
americanus
Strongyloides stercoralis
Nematodes of small intestine

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

The anterior end of both sexes
shows three lips
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

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
small intestine
Fertilized eggs
( non- infective
pass in the
faeces
Infective L2 larva ( 2nd
stage larva)develop
with in the egg ( 2-3
weeks )
Infective eggs swallowed
with contaminated water
and food
eggs hatch in small
intestine
Larva penetrate
the Intestinal wall
and venules
Larva enters
portal vein
Heart
Reaches
pulmonary
capillaries
Larva penetrate in to the
alveolus bronchioles
trachea swallowed
oesophagus small
intestine
warm moist
clay soil 25-
30C

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)
Loeffler’s syndrome
Eosinophilic abscesses
• Lungs - larval migration causes
pneumonitis (Loffler’s 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

• 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
Effect of Ascariasis on Growth & Nutrition

Stunting = low height for age
Height difference in 2 girls of 5 years age
40% of world’s children are stunted
CHRONIC MALNUTRITION STUNTING
Stunting linked to impaired intellectual development
UNICEF – State of the World’s 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
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 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 & Control

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

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.
Trichuris trichiura

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

Adults in large
intestine
Eggs in stools
Eggs
mature
in soil
Moist
clay
25 -30 C
Eggs ingested with contaminated fruits,
vegetables
etc.
Life cycle of whipworm
Larva hatches in
intestine
Penetrate and mature in
intestinal mucosa
No lung migration

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

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
Life cycle

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

Adults
Eggs are usually collected in the folds of
skin around the anus. Rarely appear in
the stools

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

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
Female
Male
The caudal expansion of certain
male nematodes that functions as a
claspers during copulation.

Egg – Oval ,60 x 40 µm with a thin
glass like shell. Embryo usually
segmented when pass out with
the faeces

Shade,warmth, sandy
soil
24 hours
L1
L3 5th
day
L2
rhab.larva
(3rd
day)
Free
living,actively
feeding
Non feeding,move
on to top soil
Obligatory lung
migration

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

500-1000 worms
• Anaemia even if adequate dietary iron
intake
• If dietary iron deficient – anaemia even
with light infection
Iron deficiency Anaemia
Hb related to worm burden

Severe iron deficiency anaemia,
hypoproteinaemia, oedema with
associated circulatory problems
Hypoalbuminaemia - reduced albumin
synthesis &Protein loss > RBC loss
Related to worm load
Hookworm
disease

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

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 in
soil
Follow free
living cycle
in the soil
Penetrate the
intact skin and
initiate the
infection
Filariform larvae
develop before
leaving the patient
Enter perianal
skin & initiate
autoinfection
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)

HOOK WORM TREAD WORM
Attach to small
intestine
Embedded in
small intestine
Both male and
female
Male short living
parasitic cycle parasitic and
free living cycles
no autoinfection Autoinfection+
Differences between hookworms and
threadworms

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

Both species - Males have
expanded tails to form the
copulatory bursa
Female
Male
The caudal expansion of
certain male nematodes that
functions as a clasper during
copulation.

Egg - Ovoid,60 x 40 µm with a
thin glass like shell. Embryo
usually segmented when pass
out with the faeces

Life cycle
Adults in small
intestine
Eggs passed in faeces
Eggs hatch in 24
hours into 1st stage
rhabditiform
larva
Moults into 2nd rhab.
larva on the 3rd day
Moults into 3rd stage
infective filariform larva
Penetrates skin, enters
circulation, carried to
the lungs
Breaks into alveoli
move along bronchioles,
trachea, swallowed
Shady warmth
sandy soil

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.

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

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

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

In hyperinfection: larvae can found in
sputum
Hookworm L3
larvaS. Stercoralis L3 larva

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

Intestinal nematodes

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