Giant Intestinal Roundworms: Ascaris lumbricoides
Round
worms
INTRODUCTION
•
Ascaris
lumbricoides
is
the
largest
nematode
(roundworm)
parasitizing
the
human
intestine.
•
Ascaris
lumbricoides
is
an
intestinal
worm
found
in
the
small
intestine
of
man
(mainly
in the
jejunum
and
upper
part
of
the
ileum).
•
They
are
more
common
in
children
than
in
adults
•
As
many
as
500
to
5000
adult
worms
may
inhabit
a
single
host.
Common
name:-
Giant Intestinal
round
worms.
Disease:-
Ascariaisis
Host
:-
The human is
intermediate
and
final
host.
Location in Definitive host
:-
the
adult
worm:
in
small intestines
.
larva:
in
lung
.
Infective
stage
:-
embryonated
eggs
Geographical
distribution
•
Worldwide
•
High
prevalence
in
underdeveloped
countries
that
have
poor
sanitation
(parts
of
Asia,
South
America
and
Africa)
•
Occurs
during
rainy
months,
tropical
and
subtropical
countries
•
Even
occurs
in
rural
areas
in
the
United
States
MORPHOLOGY
•
It
is
a
elongated,
cylindrical
and
tapering
at
both
ends.
•
Sexes
are
separate
•
The
female
is
longer
than
male
25
–
40
cm
long,
4-6
mm
in
diameter.
•
Male
is
smaller
being
15-30
cm
long,
2-4
mm
in
diameter.
•
The
posterior
end
of
male
is
curved
ventrally
in
the
form
of
a
hook
•
The
digestive
and
respiratory
organs
of
the
worm
float
inside
the
body
cavity
possessing
a
toxic
fluid
known
as
ascaron
The
Mouth
Parts
•
The
mouth
opens
at
the
anterior
end.
•
It
is
surrounded
by
three
finely
toothed
lips.
•
The
lips
are
one
dorsal
and
two
ventrolateral.
•
These
lips
bear
sensory
structures
called
labial
papillae
Adult
worms
of
A.
lumbricoides
A
mature
female
A.
lumbricoides
lays
enormous
number
of
eggs
(nearly
2,00,000
eggs
daily)
which
are
passed
in the
faeces
There
are
two
kinds
of
the
eggs.
They
are
fertilized
eggs,
and
unfertilized
eggs
We
usually
describe
an
egg
in
5
aspects:
size,
color,
shape,
shell
and
content
Decorticated
eggs:
Both
fertilized
and
unfertilized
eggs
sometimes
may
lack
their
outer
albuminous
coats
and
are
colorless
Fertilized
Egg
B
road
oval
in
shape,
brown
in
color,
an
average
size
60
×
45µm.
The
shell
is
thicker
and
consists
of
chitinous
layer,
and
mammillated
albuminous coat
stained
brown
by
bile.
The
content
is
a
fertilized
ovum.
There
is
a
new-moon(crescent)
shaped
clear
space
at
the
each
end
inside
the
shell.
Unfertilized
egg
Nar
r
o
w
er
a
n
d
lo
n
g
er
and
m
e
asu
r
e
9
0
µm
in
len
g
th
and
5
5
µm
in
breadth
They
are
bile
stained
and
brown
in
colour
The
chitinous
layer
and
albuminous
coat
are
thinner
and
irregular
than
those
of
the
fertilized
eggs
The
content
is made
of
small
atrophied
ovum
suurounded
by
many
refractable
granules
of
various
size.
Heaviest
of
all
the
helminthic
eggs
Decorticated
eggs
Both
fertilized
and
unfertilized
eggs
sometimes
may
lack
their
outer
albuminous
coats
and
are
colorless.
Modes
of
transmission
•
Occurs
mainly
via
ingestion
of
water
or
food
(raw
vegetables
or
fruits
in
particular)
contaminated
with
A.
lumbricoides
eggs.
•
Occasionally
inhalation
of
contaminated
dust
•
Children
playing
in
contaminated soil
may
acquire
the
parasite
from
their
hands
•
Enhanced
by
the
fact
that
individuals
can
be
asymptomatically
infected
and
continues
to
shed
eggs
for
years
Stage I: Eggs in faeces
Sexually mature female produces as many as 200,000 eggs per day,
which are shed along with faeces in unembryonated form. They are
non infective.
Stage II: Development in soil
Embryonation occurs in soil as optimum temperature of 20-25C
with sufficient moisture and O2. Infective larva develops within egg
in about 3-6 weeks.
Stage III: Human infection and liberation of larvae
Human get infection with ingestion of embryonated egg
contaminated food and water
Within embryonated state inside egg, first stage larvae develops into
second stage larvae. This second stage larvae is known as
Rhabtitiform larvae
Second stage larvae is stimulated to hatch out by the presence of
alkaline pH in small intestine and solubilization of its outer layer by
bile.
Stage IV: migration of larvae through lungs
Hatched out larvae penetrates the intestinal wall and carried to liver
through portal circulation.
It then travels via blood to heart and to lungs by pulmonary circulation
within 4-7 days of infection.
The larvae in lungs molds twice, enlarge and breaks into alveoli.
Stage V: Re-entry to stomach and small intestine
From alveoli, the Larvae then pass up through bronchi and into trachea
and then swallowed.
The larvae passes down the oesophagus to the stomach and reached into
small intestine once again.
Small intestine is the normal habitat of
Ascaris
and it colonises here.
Within intestine parasite molds twice and mature into adult worm.
Sexual maturation occurs with 6-10 weeks and the mature female
discharges its eggs in intestinal lumen and excreted along with faeces,
continuing the life cycle.
The life span of parasite is 12-18 months
Pathogenesis
Infection of
A. lumbricoide
s in man is known
as Ascariasis. There are two phase in
ascariasis
.
Phase I: migrating larvae
The migrating larvae causes pathological
lesions. The severity of lesions depends upon
the sensitivity of host, nutritional status of host
and number of migrating larvae.
During migration and molding through lungs,
larvae may causes pneumonia with low grade
fever, cough and other allergic symptoms
.
Phase II: Adult worm
Few worm in intestine produce no major symptoms and but some time
give abdominal pain especially in children.
The adult worm produce trauma in host tissue and the wandering adults
may block the appendical lumen or common bile duct and even small
intestine.
Large number of adult worms affects the nutritional status of host by
robbing the nutrition leading to malnutrition and growth retardation in
children.
The metabolites of living or dead worm are toxic and immunogenic.
lumbricoides also produces various allergic toxin, which manifests fever,
conjunctivitis and irritation.
Clinical manifestation:
Most of the
Ascaris
infection is asymptomatic.
Sy
mptomatic ascariasis; two types:
Intestinal Ascariasis
Pulmonary Ascariasis
1. Intestinal ascariasis;
Nausea
Vomiting
Colicky abdominal pain
Abdominal distention
Weight loss and diarrhea
Malbasorption of nutrition
Growth retardation
Heavy worm in children leads to intussusception and total obstruction
Complications:
Appendicitis, Biliary colic and perforation of bile duct, Hepatomegaly
2. Pulmonary ascariasis;
Transient eosinophilic pneumonitis (loeffler’s disease); elevated IgE
Bronchospasm
Dyspnea and wheezing
Fever
Non-productive cough and chest pain
Laboratory
diagnosis
Done
by
following
methods
1.
Parasitic
diagnosis
a)
Demonstration
of
adult
worm
b)
Demonstration
of
eggs
c)
Demonstration
of
larvae
2.
Serodiagnosis
3.
Eosinophilia
and
Ultrasonography
and CT scan
Demonstration
of
adult
worms
Worm
may
be
passed
through
anus,
mouth,
nose
and
rarely
through
ear
Barium meal
may
occasionally
reveal
the
presence
of
adult
worms
in the
small
intestine
Demonstration
of
eggs
Eggs
may
be
detected
in
stool
or
duodenal
bile
aspirate
by
direct
microscopy
or
after
concentration
of
faeces
Eggs
may
not
be
seen
if
only
male
worms
are
present
Demonstraion
of
larvae
Ascaris
larvae
may
be
detected
in
the
sputum
during
the
stage
of
migration
2.
Serodiagnosis
Ascaris
antibody
can
be
detected
by
indirect
haemagglutination
(IHA)
And
immunofluorescence
antibody
(IFA)
test
These
tests
are
useful
for
the
diagnosis
of
extraintestinal
–
ascariasis
like
Loeffler’s
syndrome
3.
Eosinophilia
It
is
seen
in
larval
invasion
stage
Treatment
•
Pyrantel
pamoate,
in
a
single
dose
of
11
mg
per
kilogram
body
weight
(maximum
1
gm)
•
Mebendazole
in
a
dose
of
100
mg
twice
daily
for
3
days,
and
piperazine
citrate
in
a
dose
of
75
mg
per
kg
body
weight
daily
for
2
days
•
Keeping good sanitation
conditions
is
the only
way
to prevent
the
infection of
Ascaris.
•
Pollution
of soil
with
human
faeces
should
be
avoided.
•
Vegetable
should be
thoroughly
washed
in a mild
solution of
Pottasium
permanganate
and
properly
cooked before
use.
•
Finger nails should be regularly
cut
to avoid
the
collection of
dirt
and
eggs
below
them.
•
Hands should be
properly
washed
with
some antiseptic soap
before
touching
edibles
or
eating.
Prophylaxis
Ascariasis can
be
prevented
by
•
Proper
disposal
of
human
faeces
•
Avoidance
of
eating
raw
vegetables
and
salads
•
Periodic
treatment
with
an
effective
anthelminthic,
in
communities
that
lack
sanitary
facilities
Larva
Migrans
•
This
is
a
term
used
to
describe
human
infections
with
helminth
larvae,
which
are
not
adapted
to
human
beings
•
The
condition
is
usually
caused
by
animal
parasites,
man
being
an
abnormal
host,
these
larvae
are
not
able
to
reach
the
normal
habitat
and
keep
wandering
in
the
abnormal
host
(man),
hence,
known
as
larva
migrans
Divided
into
2
types
1)
Cutaneous
larva
migrans
(CLM)
also
known
as
creeping
eruption
2)
Visceral
larva
migrans
(VLM)
Common
points
between
CLM
and
VLM
•
Man
always
acquires
the
infection
as
an
accidental
host
•
The
causative
agents
are
usually
zoophilic
helminths
•
The
host mounts
an
inflammatory
response
directed
against
somatic
antigens
of
parasites
•
Both
diseases
affect
primarily
the
children
•
Both
are
widespread
in
tropical
and
temperate
countries
of
the
world
Ascaris lumbricoides, also known as the Giant Intestinal Roundworm, is a common parasitic nematode infecting the human intestines, especially prevalent in underdeveloped regions with poor sanitation. Found in the small intestines, this worm can cause significant health issues. Learn about its morphology, geographical distribution, life cycle, and impact on human health.
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Presentation Transcript
Round Round worms worms
INTRODUCTION Ascaris lumbricoides is the largest nematode (roundworm) parasitizingthe human intestine. Ascaris lumbricoides is an intestinal worm found in the small intestine of man(mainly in the jejunum and upperpart of theileum). They are more commonin children than inadults As many as 500 to 5000 adult worms may inhabit a single host.
Common name:- Giant Intestinal round worms. Disease:-Ascariaisis Host :- The human is intermediate and final host. Location in Definitive host :- the adult worm: in small intestines . larva: in lung . Infective stage :- embryonated eggs
Geographicaldistribution Worldwide High prevalence in underdeveloped countries that havepoor sanitation(partsof Asia,South America andAfrica) Occurs during rainy months, tropicaland subtropicalcountries Even occurs in rural areas in the UnitedStates
MORPHOLOGY It is a elongated, cylindricaland tapering at bothends. Sexes areseparate The female is longer than male25 40 cm long, 4-6 mmin diameter. Male is smaller being 15-30cm long, 2-4 mm indiameter. The posterior end of male is curvedventrallyintheformofa hook The digestive and respiratory organs of the worm float inside the body cavity possessing atoxic fluid known asascaron
The Mouth Parts The mouth opens at theanterior end. It is surrounded by threefinely toothed lips. The lips are one dorsal andtwo ventrolateral. These lips bear sensorystructures called labialpapillae
A mature female A. lumbricoides lays enormous number ofeggs (nearly 2,00,000 eggs daily) which are passed in thefaeces There are two kinds ofthe eggs. They are fertilized eggs, and unfertilized eggs We usually describe an egg in 5 aspects: size, color,shape, shell andcontent Decorticated eggs: Both fertilized and unfertilized eggs sometimes may lack their outer albuminous coats andare colorless
Fertilized Egg Broad oval in shape,brown in color, anaveragesize60 45 m. The shell is thicker and consists of chitinous layer, and mammillated albuminous coat stained brown by bile. The content is a fertilizedovum. There is a new-moon(crescent) shaped clear space at the each end insidetheshell.
Unfertilizedegg Narrower and longer and measure 90 m in length and 55 m in breadth They are bile stained and brown in colour The chitinous layer and albuminous coat are thinner and irregular than those of the fertilizedeggs The content is made of atrophied ovum many refractable granules of various size. Heaviest of all the helminthiceggs small suurounded by
Decorticatedeggs Both fertilized and unfertilized eggs sometimes may lack their outer albuminous coats and arecolorless.
Modes oftransmission Occurs mainly via ingestion of water or food (raw vegetablesorfruitsinparticular)contaminatedwithA. lumbricoideseggs. Occasionally inhalation of contaminateddust Children playing in contaminated soil may acquirethe parasite from theirhands Enhanced by the fact that individuals can be asymptomatically infected and continues to shedeggs for years
Stage I: Eggs in faeces Sexually mature female produces as many as 200,000 eggs per day, which are shed along with faeces in unembryonated form. They are non infective. Stage II: Development in soil Embryonation occurs in soil as optimum temperature of 20-25C with sufficient moisture and O2. Infective larva develops within egg in about 3-6 weeks. Stage III: Human infection and liberation of larvae Human get infection with ingestion of embryonated egg contaminated food and water Within embryonated state inside egg, first stage larvae develops into second stage larvae. This second stage larvae is known as Rhabtitiform larvae Second stage larvae is stimulated to hatch out by the presence of alkaline pH in small intestine and solubilization of its outer layer by bile.
Stage IV: migration of larvae through lungs Hatched out larvae penetrates the intestinal wall and carried to liver through portal circulation. It then travels via blood to heart and to lungs by pulmonary circulation within 4-7 days of infection. The larvae in lungs molds twice, enlarge and breaks into alveoli.
Stage V: Re-entry to stomach and small intestine From alveoli, the Larvae then pass up through bronchi and into trachea and then swallowed. The larvae passes down the oesophagus to the stomach and reached into small intestine once again. Small intestine is the normal habitat of Ascaris and it colonises here. Within intestine parasite molds twice and mature into adult worm. Sexual maturation occurs with 6-10 weeks and the mature female discharges its eggs in intestinal lumen and excreted along with faeces, continuing the life cycle. The life span of parasite is 12-18 months
Pathogenesis Infection of A. lumbricoides in man is known as Ascariasis. There are two phase in ascariasis. Phase I: migrating larvae The migrating larvae causes pathological lesions. The severity of lesions depends upon the sensitivity of host, nutritional status of host and number of migrating larvae. During migration and molding through lungs, larvae may causes pneumonia with low grade fever, cough and other allergic symptoms.
Phase II: Adult worm Few worm in intestine produce no major symptoms and but some time give abdominal pain especially in children. The adult worm produce trauma in host tissue and the wandering adults may block the appendical lumen or common bile duct and even small intestine. Large number of adult worms affects the nutritional status of host by robbing the nutrition leading to malnutrition and growth retardation in children. The metabolites of living or dead worm are toxic and immunogenic. lumbricoides also produces various allergic toxin, which manifests fever, conjunctivitis and irritation.
Clinical manifestation: Most of the Ascaris infection is asymptomatic. Symptomatic ascariasis; two types: Intestinal Ascariasis Pulmonary Ascariasis 1. Intestinal ascariasis; Nausea Vomiting Colicky abdominal pain Abdominal distention Weight loss and diarrhea Malbasorption of nutrition Growth retardation Heavy worm in children leads to intussusception and total obstruction Complications:Appendicitis, Biliary colic and perforation of bile duct, Hepatomegaly 2. Pulmonary ascariasis; Transient eosinophilic pneumonitis (loeffler s disease); elevated IgE Bronchospasm Dyspnea and wheezing Fever Non-productive cough and chest pain
Laboratorydiagnosis Done by followingmethods 1. Parasiticdiagnosis a) Demonstration of adultworm b) Demonstration ofeggs c) Demonstration oflarvae 2. Serodiagnosis 3. Eosinophilia and Ultrasonography and CT scan
Demonstration of adultworms Worm may be passed through anus, mouth, nose andrarely through ear Barium meal may occasionally reveal the presence ofadult worms in the smallintestine Demonstration ofeggs Eggs may be detected in stool orduodenal bile aspirate by direct microscopyor after concentrationof faeces Eggs may not be seen if only male worms arepresent
Demonstraion oflarvae Ascarislarvaemaybedetectedinthesputumduringthestage ofmigration 2.Serodiagnosis Ascaris antibody can be detected by indirecthaemagglutination (IHA) And immunofluorescence antibody (IFA)test Thesetestsareusefulforthediagnosisofextraintestinal ascariasis like Loeffler ssyndrome 3.Eosinophilia It is seen in larval invasionstage
Treatment Pyrantel pamoate, in a single dose of 11mg per kilogram body weight (maximum 1gm) Mebendazolein adoseof 100mgtwice daily for 3 days,and piperazine citrate in adoseof 75mgper kgbody weight daily for 2days
PREVENTION Keeping good sanitation conditions is the only way to prevent the infection of Ascaris. Pollution of soil with human faeces should be avoided. Vegetable should be thoroughly washed in a mild solution of Pottasium permanganate and properly cooked before use. Finger nails should be regularly cut to avoid the collection of dirt and eggs below them. Hands should be properly washed with some antiseptic soap before touching edibles or eating.
Prophylaxis Ascariasis can be prevented by Proper disposal of humanfaeces Avoidance of eating raw vegetables andsalads Periodic treatment with an effective anthelminthic, in communities thatlack sanitary facilities
LarvaMigrans This is a term used to describe human infections with helminth larvae, which arenot adapted to humanbeings The condition is usually caused by animal parasites, man being an abnormal host,these larvae are not able to reach the normal habitat and keep wandering in the abnormal host (man), hence, known as larvamigrans
Divided into 2types 1) Cutaneous larva migrans (CLM) also known as creeping eruption 2) Visceral larva migrans(VLM)
Common points between CLM andVLM Man always acquires the infection asan accidentalhost The causative agents are usually zoophilic helminths The host mounts an inflammatory response directed against somatic antigens ofparasites Both diseases affect primarily thechildren Both are widespread in tropical andtemperate countries of theworld
