Parasitology: Hook worm and Stronglyoides stercoralis

University of Duhok
College of Health Sciences
Dep. of Medical Laboratories
Parasitology Theory
3rd stage
Lecture 10
Lecturer: Dr. Shameeran S. Ismael
BVM & S, M.Sc Medical Microbiology(Parasitology),
PhD Molecular Parasitology
Dr. Shameeran S. Bamarni, Medical
Parasitology, Health Sciences

Hookworms
The family Ancylostomidae, whose
members are commonly called hookworms
because of the characteristic hook posture of
their anterior ends.

The most relevant medical species are:
1.Ancylostoma duodenale known as the old
world hookworm.
2.Necator americanus known as the american
killer also known the new world hookworm.

1.Ancylostoma duodenale

Keys
Kingdome: Animalia
Phylum: Nematohelminthes
Class: Nematoda
Order: Rhabditida
Suborder: Strongylida
Superfamily: Ancylostomatoidea
Family: Ancylostomatidae

Genus: Ancylostoma
Species: duodenale
Common name: Old world hook worm
Final host: Human
Site of infection: Small intestine
Infective stage: L3
Disease: Hookworm disease or ancylostomiasis

Infection: occur by the accidental drinking of water
contaminated with filariform larvae (L3) or this occurs
when man walks bare foot on the fecally contaminated
soil. The L3 penetrate directly through the skin with
which they come in contact.

Morphology
• It is small, greyish white, cylindrical worm. It appears
reddish brown when freshly passed in feces due to
ingested blood in its intestinal tract
• The anterior end is bent sharply backwards giving
them a hooked appearance, about 10 mm in length

•The buccal cavity is armed with two pairs of marginal teeth
and two knob like plates
•Posterior end of females is taper and pointed, while male
have a copulatory bursa

Adult worm

• The eggs have an ovoid shape and a thin wall and
contain already 4 to 16 cells when shed with the feces

Life Cycle
• Ancylostoma worms have a direct life cycle
• Eggs pass with the feces complete development to L2
larvae inside the egg in 2 to 9 days after shedding.
• Hatching of eggs occurs and L3 release.
• The L3 infect the final hosts through the mouth (after
ingestion of contaminated water, food or soil)
or through the skin.

• Some ingested larvae reach the gut, attach and
complete development to adult worms. Other larvae
penetrate the gut's wall and undertake a migration
through various organs that brings them to the lungs,
the trachea and the mouth, where they are again
swallowed. These larvae than reach the gut, complete
development to adults, attach to the gut's wall and
start producing eggs

• Larvae that penetrate the skin (often between the
footpads) reach a blood vessel and are carried to the
lungs, from where they reach trachea, the mouth and
are subsequently swallowed. These larvae reach the
intestine, complete development to adults, attach to
the gut's wall and start producing eggs.

Life cycle

Pathogenesis
• Adult worms in the gut are blood suckers and change
frequently the site, up to six times a day. They
produce anticoagulants that prevent blood clotting. When they
leave the place to bite elsewhere the bleeding continues.
A single worm can consume up to 0.1 ml blood within 24 hours.
100 worms consume up to 10 ml just in one day and leave about
600 injuries that continue bleeding.
• Migrating larvae can cause skin inflammation (dermatitis) at
the points of entry that can become infected with secondary
bacteria. Allergic reactions can also occur along the migration
paths.

Clinical signs
• Clinical signs of hookworm infection can include pale
gums due to anemia; diarrhea which can be bloody,
dark or tarry looking; weakness; weight loss; and
sudden death in severely infected puppies and kittens.
Sometimes the hookworm larvae cause itching due to
burrowing into the skin of the animal
• Damage to the lungs causes coughing and can lead
to pneumonia.

Diagnosis:
• Diagnosis requires microscopic examination of stool
sample for detection of the characteristics eggs
Treatment:
• Albendazole 400mg once
• Ferrous sulphate 400mg thrice daily.
• Folic acid and vit. B12

Keys
Kingdome: Animalia
Phylum: Nematohelminthes
Class: Nematoda
Order: Rhabditida
Suborder: Strongylida
Family: Strongylidae
Genus: Strongyloides
Species: stercoralis

Site of infection: females live in the superficial tissues of
the small intestine (duodenum and jejunum)
Definitive host: Human
Infective stage: L3 ( filariform).
Diagnostic stage: L1 (Rhabditiform) in feces.
Route of infection: L3 penetrate the skin of host.

Adult:
Male (parasitic or free-living):
- Size is about 0.7 mm in length
- Have a rhabditiform oesophagus
- Posterior end curved ventrally with Spicules
Morphology

Parasitic female:
- Size is about 2.2 mm in length
- Have a cylindrical oesophagus (1/3 body length)
- Posterior end straight
Free living female:
- Size is about 1 mm in length
- Have a rhabditiform oesophagus
- Posterior end straight
Adult female

Morphology of Strongyloides stercoralis
a) parasitic female
b) free-living male
c) free-living female

Egg:
Size : 55 x 30 um.
Shape: oval . Clear, thin shelled Similar to hookworm
but are smaller.

Rhabditiform larvae
• 220 x 15 um.
• Short buccal cavity.
Diagnostic stage
• Appear in stools within 4weeks of infection.

Filariform larvae posterior end:
Filariform larva with notched tail.
Infective stage
Size 600 x 20 um.

Two types of cycles exist:
1. Free-living cycle
2. Parasitic cycle:.
Life Cycle:

1.Free-living cycle :The rhabditiform larvae passed with feces "can either
become infective filariform larvae (direct development or free living)
adult males and females that mate and produce eggs from which
rhabditiform larvae release and eventually become infective filariform
larvae . The L3 penetrate the human host skin to initiate the parasitic
cycle

Life cycle
of
S. stercoralis

2. Parasitic Phase:
In the parasitic stage, no male form of this organism has
been reliably identified, and the female reproduce in a
parthinogenitic manner
• When L3 encounter A suitable host, they penetrate the
skin and are carried by cutaneous veins to the vena cava.
They enter the right side of the heart and are carried to the
lungs via the pulmonary artery
• In the lungs, L3 molt to L4 and cough up, L4 swallowed
and reach to the small intestine and where they undergo a
final molt and become sexually mature females

• Females produce embryonated eggs parthenogenetically
• These eggs hatch in the mucosa of small intestine into L1
and L1 pass with feces.
• L1 become established in the soil, undergo several molts
and become free-living adults
• Under adverse conditions they can revert to being
filariform larvae

• Since the parasitic females live in the superficial tissues
of the small intestine, and can be present in high numbers,
they can cause significant pathology.

3. Autoinfection
• During passage through the host digestive system,
rhabditiform larvae (L1) may undergo 2 molts to
filariform larvae and by penetrating the intestinal mucosa,
enter the circulatory system and continue their parasitic
lives without leaving the host

Clinical Signs:
•Cutaneous reaction due to skin penetration “ ground itch
Dermatologic manifestations include urticarial rashes in the
buttocks and waist areas.
•Pulmonary symptoms (including Loeffler’s syndrome) can
occur during pulmonary migration of the L3.
•Gastrointestinal symptoms include abdominal pain,
vomiting, diarrhea, weight loss, mala-bsorption,.
•

Laboratory Diagnosis
• Direct stool examination for detection of larvae
• Coproculture for identification of Genus and Species of
L3
• Histological examination of duodenal or jejunal biopsy
specimens obtained by endoscopy can demonstrate adult
worms embedded in the mucosa.

Parasitology: Hook worm and Stronglyoides stercoralis

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