Intestinal Nematodes: PARASITOLOGY

Soil-Transmitted
Helminths (STH)
 Trichuris
Common name: Whipworm
trichiura
Classification:

Phylum: Nematoda (roundworms)

Class: Adenophorea
Subclass: Enoplia
Order: Trichocephalida
Family: Trichuridae
Genus: Trichuris
 I.Distribution Trichuris
trichiura
- distributed globally

- more common: tropics &

subtropics

- infection is widespread in tropical

Africa, South America and South-
East Asia

- infection is found throughout India

I.Distribution Trichuris
trichiura
- Two conditions needed for
spreading of T. trichiura:
poor sanitation
environmental conditions

- 800 million people are estimated to

be infected
II. Habitat

large intestine
(mainly in the caecum)
 III. Morphology

Adult whipworm
Color: Flesh-colored
Shape: whip-like
Structure:

anterior portion (3/5): - thin and thread-like;

- esophagus and mouth;

posterior portion (2/5): - thick and fleshy;

- intestines and reproductive organs
 III. Morphology

Adult (Male) Adult (Female)

Length: 30–45 mm Length: 40–50 mm

Posterior end: coiled Posterior end: straight

and rounded
ventrally
 III. Morphology
Egg

Color: brown (bile-stained)

Shape: barrel-shaped
Structure:

bipolar plugs:
contains unsegmented ovum when passed in faeces
located at each pole
Unembryonated egg
triple shell:
dense and thick Length: 50 μm
Width: 25 μm
 IV. Life cycle

2 main stages: egg and adult

Natural host: Infective form: Diagnostic form:

Embryonated egg Unembryonated egg

No intermediate host is required.
(rhabditiform larva) (unsegmented ovum)
IV. Life cycle

Mode of transmission:

Fecal- oral transmission

Location:

Large intestine (caecum)

IV. Life cycle
V. Pathogenesis and Clinical features

Trichuriasis - infection caused by T. trichiura

- Asymptomatic
- Heavy and chronic infection

Iron deficiency amemia acute appendicitis

V. Pathogenesis and Clinical features

Trichuriasis - infection caused by T. trichiura

- Asymptomatic
- Heavy and chronic infection
Mucous diarrhea

Rectal prolapse

Iron deficiency
anemia
Trichuris dysentery syndrome (TDS) Finger clubbing
V. Pathogenesis and Clinical features

Children with severe infection:

Growth retardation impaired mental development

and cognitive function
VI. Diagnosis

Microscopic examination

Stool test

Counts:

< 10 eggs – Light infection

> 50 eggs - Heavy infection
Unembryonated eggs in stool
sample under light microscope.
VI. Diagnosis

Blood examination Sigmoidoscopy

- differential leukocyte count

(DLC) may show up to 25%
eosinophila

Adult worms in
sigmoid colon.
VII. Treatment

Albendazole Sigmoidoscopy

Mebendazole Ivermectin

400 mg (3 days)
100 mg twice/day (3 days)
200 micrograms/kg
(3 days)
VIII. Prevention and Control
Ascaris
lumbricoides
CN: Roundworm

Classification:
Phylum: Nematoda
Class: Chromodorea
Subclass: Secementea
Order: Ascaridida
Family: Ascarididae
Genus: Ascaris
 Distribution Climate
- distributed worldwide - tropical and subtropical
regions, and in other humid
areas.
Incidence
-approximately 1.2 billion
people are infected.
- 80- 100% in rural areas
with poor sanitation.

I.Distribution
II. Habitat

Small Intestine
- 85% in jejunum

-15% in ileum

A. lumbricoides is the
largest nematode parasite
in the human intestine.
 III. Morphology

Adult roundworm
Color:
- Flesh-colored in fresh stool
- White outside host
Shape:
- Cylindrical, with tapering ends

Anterior end: three finely toothed

lips, one dorsal and two
ventrolateral
 III. Morphology

Adult (Female) Adult (Male)

Length: 20-40 cm Length: 15-30 cm
Width: 3-6 mm
Width: 2-4 mm
Posterior end: straight and
conical Posterior end: hooked, and
Vulva: carries two copulatory
- situated mid-ventrally spicules
- leads to a single vagina
Vulvar waist: distinct groove at
the level of vulva
Vagina: branches into a pair of (A) Adult female and male worms; (B)
genital tubules Anterior end of worm; (C) Posterior end
of female; (D) Posterior end of male
Genital tubules: contain eggs; 27
million at a time
 III. Morphology
Fertilized Egg
Length: 40- 75 μm
Diameter: 35- 50 μm
Egg
Shape: Ovoid
Color: Golden- brown
Structure:
Lecithin granules
Three layers: vitelline membrane,
chronic layer, albuminoid layer

Unfertilized Egg
Length: 88- 94 μm
(A) Unfertilized egg of Ascaris; and (B) Fertilized egg of Ascaris
Diameter: 44 μm
Shape: Elliptical
Structure: Two layers
chronic layer, albuminoid layer
 IV. Life cycle

2 main stages: egg and adult

Natural host: Infective form: Diagnostic form:

Embryonated egg All

No intermediate host is required.
(rhabditiform larva) Stages
IV. Life cycle

Mode of transmission:

Fecal- oral transmission

Location:

Small Intestine
 IV. Life cycle
Soil
a period of incubation
eggs are resistant to adverse
conditions
A heavy clayey soil and moist shady
location, with temperature between
20°c and 30°C are optimal for rapid
development of the embryo.
10-40 days of development
embryo moults twice and becomes
the infective rhabditiforrn larva
 IV. Life cycle
Host
ingestion
larvae hatch in the duodenum
penetrate the intestinal mucosa
reach the liver via portal vessels
reach the lungs after 4 days of infection;
develop for 10- 15 days (moult twice)
invade alveoli; carried to the throat
swallowed and enter the small intestine.
Develop into adults, and become
sexually- mature in about 6-12 weeks
adult worm lifespan: 12-20 months
V. Pathogenesis and Clinical features

Ascariasis
- disease caused by A. lumbricoides

- clinical manifestations in ascariasis can be

caused either by the migration of larvae, or by
adult worms
 V. Pathogenesis and Clinical features

Symptoms: Larvae Migration

initially asymptomatic
intense cellular reaction
allergic reaction

Ascaris pneumonia
low- grade fever, dry cough,
asthmatic wheezing, urticaria, Pneumonic infiltration at the upper lobe of the left lung
eosinophilia and mottled lung
infiltration
Loejfler's syndrome
blood- tinged sputum with Charcot-
Leyden crystals.
hypersensitivity

generally clear in 1 or 2 weeks Loejfler's syndrome; sputum

 V. Pathogenesis and Clinical features

Symptoms: Adult Worm

asymptomatic infection
pathological effects
spoliative effects
heavy worm burden
protein-energy malnutrition and vitamin A
deficiency.
toxic effects
hypersensitivity to the worm antigens
fever, urticaria, angioneurotic edema,
wheezing and conjunctivitis.
mechanical effects
luminal occlusion
infiltration of vital area
volvulus, intussusception, or intestinal
obstruction and intestinal perforation.
 V. Pathogenesis and Clinical features

Symptoms: Adult Worm

Ectopic ascariasis (Wanderlust):

movement enhanced as a result of illness

febrile host; above 39°C.
acute biliary obstruction or pancreatitis
liver abscesses.
respiratory obstruction or lung abscesses
obstructive appendicitis
peritonitis
 VI. Diagnosis
Detection
Adult Worm
barium meal
plain abdominal film
ultrasound (more than 50% sensitive) and
endoscopic retrograde
cholangiopancreatography (ERCP; 90%
sensitive).
Larvae
demonstration in sputum and gastric
washings
presence of Charcot-Leyden crystals in
sputum and an attendant eosinophilia
supports the diagnosis.
patchy pulmonary infiltrates in X- rays
 VI. Diagnosis
Detection

Egg

fecal examination
three eggs per mg of feces.
saline emulsion
Both fertilized and unfertilized eggs are
usually present
fertilized eggs may sometimes appear
decorticated
unfertilized eggs are not detectable by salt
floatation.
eggs may be demonstrative in the bile
obtained by duodenal aspirates
 VI. Diagnosis
Serological Tests
Indirect hemagglutination (IHA)
Indirect fluorescent antibody (IFA)
Enzyme-linked irnmunosorbent
assay (ELISA)
Serodiagnosis is helpful in
extraintestinal ascariasis like Loeffler's
syndrome
Indirect fluorescent
antibody (IFA)
0n A. lumbricoides
Blood Examination larvae
detection of eosinophilia
VII. Treatment
Pyrantel Pamoate

Albendazole Sigmoidoscopy

Mebendazole

(11 mg/ kg once; maximum 1 g)

(400 mg once)

(100 g twice daily for 3 days or 500

mg once)
 VIII. Prevention and Control

Prevention of soil fecal contamination

disuse of night manure

Treatment of vegetables and crops

iodine 200 ppm for 15 minutes

Avoidance of raw vegetable consumption

Improvement of personal hygiene.

Treatment of infected persons

Strongyloides
stercoralis

Classification:

Class: Chromadorea
Subclass: Secementea
Order: Rhabditida
Superfamily: Rhabdiasoidea
Family: Strongylidae
Genus: Strongyloides
Species: S. stercoralis
I.Distribution

It is found mainly in the warm

moist tropics, but may also
occur in the temperate regions.

It is common in Brazil,
Columbia, and in the Far East-
Myanmar, Thailand, Vietnam,
Malaysia and Philippines.
II. Habitat

Small Intestine
- jejunum

- ileum

S. stercoralis is the
smallest nematode parasite
in the human intestine.
 III. Morphology

Adult female

Color: transparent
Size: 2.5 mm x 0.05mm
Digestive system:
cylindrical esophagus (anterior 1/3)
intestines (posterior 2/3)
anus
Reproductive system:
paired uteri
vagina
vulva
Ovoviviparous
Lifespan: 3- 4 months
Present in human infection
 III. Morphology

Adult male

Color: transparent
Size: 0.6- 1 mm x 40-50 mm
Reproductive system:
copulatory spicules
Absent in human infection
 III. Morphology

Eggs

conspicuous; 8- 10 eggs
arranged antero-posteriorly
in a single row
Shape: oval
Size: 50-60 μm x 30-35 µm
Shape: Oval
Hatch into rhabditiform
larva as soon as laid
 III. Morphology

Rhabditiform Larva

first larval stage

hatch out in the small intestine;
and migrates into lumen
most common form
observed in feces
Size: 0.25 mm in length
short
double- bulb esophagus
 III. Morphology

Filariform Larva

third larval stage

larva molts twice
Shape: long and slender
Size: 0.55 mm in length
long esophagus of uniform width
notched tail
infective stage to man
IV. Life cycle

Mode of transmission:

skin penetration
autoinfection
external
internal
 IV. Life cycle

Direct life cycle (Parasitic)

Natural Host: Man
Infective form: Filariform larva
Adult female in the mucosa of small intestine
Eggs laid immediately hatch into rhabditiform larva.
may be released in feces into moist soil
autoinfection
Filariform larva
skin penetration
circulation
migrate into small intestine
mature in 15- 20 days
 IV. Life cycle

Indirect life cycle (Free-living)

Rhabditiform larva released in
feces into soil
Develop in soil
Mate in soil
May repeat continuously
V. Pathogenesis and Clinical features

Strongyloidiasis
- infection caused by Strongyloides stercoralis

Benign
Asymptomatic
Severe and fatal – immunocompromised persons

Clinical diseases:
cutaneous manifestations
pulmonary manifestations
intestinal manifestations
 V. Pathogenesis and Clinical features
Clinical diseases:

1. Cutaneous manifestations

Dermatitis Larva currens

 V. Pathogenesis and Clinical features
Clinical diseases:
2. Pulmonary manifestations:

Loeffler’s syndrome
Bronchopneumonia

A radiographic image of the

patient's lungs with Loeffler's
syndrome.
 V. Pathogenesis and Clinical features
Clinical diseases:
3. Intestinal manifestations:

Malabsorption
syndrome

 V. Pathogenesis and Clinical features

Clinical diseases:
Other manifestations:

Protein losing
Paralytic ileus
enteropathy

 V. Pathogenesis and Clinical features

Clinical diseases:
Hyperinfection
- Immunocompromised patients
- Internal autoinfection takes place resulting in a large number of worms in
the intestine and lungs

Disseminated strongyloidiasis

- filariform larvae may enter blood circulation and lodge in various

organs.
 VI. Diagnosis
Microscopic examination Stool culture
Direct wet mount of stool Agar plate culture
Concentration methods of stool Charcoal culture
examination
Formol-ether concentration method
Baermann's test

(A) Modified agar plate culture and

(B) Strongyloides stercoralis larvae
groove.
L1 rhabditiform larva of S. stercoralis in
unstained wet mounts of stool.
VI. Diagnosis

Serodiagnosis
Complement fixation, indirect hemagglutination and enzyme-linked
immunosorbent assay (ELISA) have been reported.

Imaging
Radiological appearances in intestinal and pulmonary infection are said
to be characteristic and helpful in diagnosis

Others
Peripheral eosinophilia (>500/cumL of blood) is a constant finding
Total serum immunoglobulin (Ig)E antibody level is elevated in more than half
of the patients
VII. Treatment

Sigmoidoscopy

Albendazole Ivermectin

200 μg/kg daily (2 days)

400 mg daily (3 days)
VIII. Prevention and Control