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STRONGYLOIDES STERCORALIS
DR ARUNA RANI BEHERA
MD MICROBIOLOGY
History
Strongyloides stercoralis was first identified by
Normand in 1876 in the diarrhoeic feces of French
soldiers in Cochin-China
A/K/A the “Military worm”
Seen in patients with HIV infection and other
immunocompromised conditions.
Epidemiology
Prevalent in tropical regions.
Common in South East Asia (including India),
SubSaharan Africa, and South America (Brazil)
Morphology
Adult worm
Only female worms are seen in the human intestine,
male worms are rarely encountered.
 Size:
 2–3 mm X 0.03–0.05 mm broad (small and thin)
 Free living female worm is smaller and thicker (1 mm ×
80 μm)
 Alimentary tract: contains a cylindrical
esophagus occupying anterior third of
the body and intestine occupy
posterior 2/3rd .caudal extremity is
pointed and anus is situated ventrally
just before caudal tip.
 Female reproductive organs – paired
ovaries,oviduct and uteri leads to
vulval opening at the junction of middle
and posterior third of the body.
 The free living male worms are slightly
smaller, having two spicules at the
posterior end
Strongyloides stercoralis
(A) adult male (arrow shows
spicules);
(B) adult female
(containing single row of eggs);
Eggs
Eggs are conspicuous within the gravid female worm
and each uterus contains 5–10 eggs .
Oval, thin walled ,transparent and 50–70 μm long
Ovoviviparous, i.e they immediately hatch out to
larvae
Rhabditiform larva come out of mucus membrane
into lumen and excreted in feces.(eggs are not
detected in feces)
Larva
First stage or Rhabditiform
larva (L1): Eggs hatch out to
form L1 larvae in the human
intestine(250 μm × 16 μm).
They have a short mouth a
double bulb esophagus and
prominent, large genital
primordium.
Diagnostic form found in
human feces
Third stage or Filariform larva (L3):
In the environment, the L1 larva
molts twice(L2,L3) to form
filariform larva(L3).
Long, slender form 630 μm × 16
μm and bears a long cylindrical
esophagus and a notched tail.
Live in soil for about 12 days
Infective stage to human
Life Cycle
Host: only one host (Man).
Infective stage: L3 larva
(Filariform).
Mode of transmission:
-Penetration of skin by
the L3 larva (by walking
bare foot).
-Autoinfection (Internal
Autoinfection)
Migratory Phase
Following penetration, L3
larvae enter subcutaneous
small venules through the
venous circulation, they
reach to the right side of
heart and finally to the lungs.
Enter into the alveolar space
and migrate up to bronchi,
trachea and finally by
swallowing of sputum, they
enter GIT.
Intestinal Phase
Develop into adults
L3 larvae undergo third
molt to form L4 larvae
that reach the small
intestine where they
undergo the final molt to
develop into adult
females.
Adult males are not
found in human
intestine.
Laying eggs
Only the female worms are seen buried in the
intestinal mucosa.
 They can directly lay eggs without fertilization
(parthenogenesis)
Eggs soon hatch out liberating the rhabditiform (L1)
larvae into the intestinal lumen and are passed in
the feces
Autoinfection
Some times, the L1 larvae
released in the human
intestine don’t pass in the
feces but develop into
filariform larvae that
eventually penetrate the
intestinal wall or perianal
skin, enter the venous
circulation and reach lungs.
This is responsible for
maintaining the infection for
years.
Development in Environment
In moist and warm soil, the Rhabditiform (L1) larva
molts twice to form Filariform (L3) larva.
2 types of development takes place
1.Direct development
2. Indirect development
Direct
development
 L3 larva acts as the
infective form and
infects man through the
penetration of skin.
Indirect
development
 L3 larvae molt twice to develop
into the adult worms (male and
female) in the environment.
 Free living adult worms become
sexually matured; fertilization
takes place to lay eggs that hatch
to L1 larvae which molts twice to
form the infective L3 filariform
larvae.
Pathogenesis and Clinical Feature
Infection is K/A-Strongyloidiasis
Mostly asymptomatic
Symptomatic cases- Cutaneous, Pulmonary,
Intestinal
Effects Due to Migrating Larva
1.Cutaneous
Dermatitis,erythema,itching at site of penetration
Cutaneous larva migrans: pathognomonic
serpiginous urticarial rash called as larva currens
that advances 10 cm/hour
Rashes: recurrent maculopapular or urticarial
rashes involve buttocks, perineum, and thighs
2.Pulmonary symptoms
 uncommon compared to ascariasis and hookworm.
It occurs only secondary to underlying chronic
obstructive lung disease.
Hemorrhages in lung alveoli
Bronchopneumonia
Chronic bronchitis ,asthmatic symptoms
Rhabditiform larva found in sputum
Effect Due to worm and Filariform Larva
3.Intestinal
Mild to moderate worm load: epigastric pain
(resembling peptic ulcer), nausea, diarrhea, and blood
loss, symptoms resemble malabsorption syndrome
Heavy larva load:
Hyperinfection syndrome
Complications
1.Hyperinfection syndrome
Repeated autoinfection cycles lead to generation of large number
of worms in intestine and lungs and filariform larvae in tissues
and organs.
Risk factor:
Impaired host immunity
Glucocorticoid therapy
Diabetes or other debilitating chronic diseases
C/F
Depends on sites involved
Complications
Brain abscess, meningitis, peritonitis
Laboratory diagnosis
1.Microscopy
Freshly passed Stool ,
duodenal aspirate, sputum—
detects rhabditiform larvae
Hyperinfection syndrome-
body fluids, tissues
Concentration of larva in feces
done by Baermann funnel
technique Baermann technique
2.Stool culture-when larva are
scanty in feces
 Harada Mori filter paper tube
method
 Petridish (slant culture) technique
 Charcoal culture method
 Agar Plate technique (more
sensitive)
 Large number of free living larva
and adults seen after 7-10 days
(A) Harada-Mori filter paper strip culture;
(B) (B) petri dish/slant culture method;
Agar plate method:
The agar plate method carried out in Petri
dishes containing water or solid agar is the
sensitive method.
3.Serology-ELISA, CFT, IHA
4.Molecular Diagnosis- Realtime PCR
5.Non specific tests- Eosinophillia
Treatment
Even in the asymptomatic stage, strongyloidiasis must
be treated because of the potential for subsequent fatal
hyperinfection
Ivermectin (2 days)
Disseminated strongyloidiasis: Prolonged course of
Ivermectin for 5–7 days or until the parasites are
eradicated.
Prevention
Improved personal hygiene
Proper disposal of feces
Improved nutrition with dietary iron
Treatment of infected persons
Use of sanitary latrines.
Health education.
Strongyloides stercoralis

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Strongyloides stercoralis

  • 1. STRONGYLOIDES STERCORALIS DR ARUNA RANI BEHERA MD MICROBIOLOGY
  • 2. History Strongyloides stercoralis was first identified by Normand in 1876 in the diarrhoeic feces of French soldiers in Cochin-China A/K/A the “Military worm” Seen in patients with HIV infection and other immunocompromised conditions.
  • 3. Epidemiology Prevalent in tropical regions. Common in South East Asia (including India), SubSaharan Africa, and South America (Brazil)
  • 4. Morphology Adult worm Only female worms are seen in the human intestine, male worms are rarely encountered.  Size:  2–3 mm X 0.03–0.05 mm broad (small and thin)  Free living female worm is smaller and thicker (1 mm × 80 μm)
  • 5.  Alimentary tract: contains a cylindrical esophagus occupying anterior third of the body and intestine occupy posterior 2/3rd .caudal extremity is pointed and anus is situated ventrally just before caudal tip.  Female reproductive organs – paired ovaries,oviduct and uteri leads to vulval opening at the junction of middle and posterior third of the body.  The free living male worms are slightly smaller, having two spicules at the posterior end
  • 6. Strongyloides stercoralis (A) adult male (arrow shows spicules); (B) adult female (containing single row of eggs);
  • 7. Eggs Eggs are conspicuous within the gravid female worm and each uterus contains 5–10 eggs . Oval, thin walled ,transparent and 50–70 μm long Ovoviviparous, i.e they immediately hatch out to larvae Rhabditiform larva come out of mucus membrane into lumen and excreted in feces.(eggs are not detected in feces)
  • 8. Larva First stage or Rhabditiform larva (L1): Eggs hatch out to form L1 larvae in the human intestine(250 μm × 16 μm). They have a short mouth a double bulb esophagus and prominent, large genital primordium. Diagnostic form found in human feces
  • 9. Third stage or Filariform larva (L3): In the environment, the L1 larva molts twice(L2,L3) to form filariform larva(L3). Long, slender form 630 μm × 16 μm and bears a long cylindrical esophagus and a notched tail. Live in soil for about 12 days Infective stage to human
  • 10. Life Cycle Host: only one host (Man). Infective stage: L3 larva (Filariform). Mode of transmission: -Penetration of skin by the L3 larva (by walking bare foot). -Autoinfection (Internal Autoinfection)
  • 11. Migratory Phase Following penetration, L3 larvae enter subcutaneous small venules through the venous circulation, they reach to the right side of heart and finally to the lungs. Enter into the alveolar space and migrate up to bronchi, trachea and finally by swallowing of sputum, they enter GIT.
  • 12. Intestinal Phase Develop into adults L3 larvae undergo third molt to form L4 larvae that reach the small intestine where they undergo the final molt to develop into adult females. Adult males are not found in human intestine.
  • 13. Laying eggs Only the female worms are seen buried in the intestinal mucosa.  They can directly lay eggs without fertilization (parthenogenesis) Eggs soon hatch out liberating the rhabditiform (L1) larvae into the intestinal lumen and are passed in the feces
  • 14. Autoinfection Some times, the L1 larvae released in the human intestine don’t pass in the feces but develop into filariform larvae that eventually penetrate the intestinal wall or perianal skin, enter the venous circulation and reach lungs. This is responsible for maintaining the infection for years.
  • 15. Development in Environment In moist and warm soil, the Rhabditiform (L1) larva molts twice to form Filariform (L3) larva. 2 types of development takes place 1.Direct development 2. Indirect development
  • 16. Direct development  L3 larva acts as the infective form and infects man through the penetration of skin. Indirect development  L3 larvae molt twice to develop into the adult worms (male and female) in the environment.  Free living adult worms become sexually matured; fertilization takes place to lay eggs that hatch to L1 larvae which molts twice to form the infective L3 filariform larvae.
  • 17.
  • 18. Pathogenesis and Clinical Feature Infection is K/A-Strongyloidiasis Mostly asymptomatic Symptomatic cases- Cutaneous, Pulmonary, Intestinal Effects Due to Migrating Larva 1.Cutaneous Dermatitis,erythema,itching at site of penetration Cutaneous larva migrans: pathognomonic serpiginous urticarial rash called as larva currens that advances 10 cm/hour Rashes: recurrent maculopapular or urticarial rashes involve buttocks, perineum, and thighs
  • 19. 2.Pulmonary symptoms  uncommon compared to ascariasis and hookworm. It occurs only secondary to underlying chronic obstructive lung disease. Hemorrhages in lung alveoli Bronchopneumonia Chronic bronchitis ,asthmatic symptoms Rhabditiform larva found in sputum
  • 20. Effect Due to worm and Filariform Larva 3.Intestinal Mild to moderate worm load: epigastric pain (resembling peptic ulcer), nausea, diarrhea, and blood loss, symptoms resemble malabsorption syndrome Heavy larva load: Hyperinfection syndrome
  • 21. Complications 1.Hyperinfection syndrome Repeated autoinfection cycles lead to generation of large number of worms in intestine and lungs and filariform larvae in tissues and organs. Risk factor: Impaired host immunity Glucocorticoid therapy Diabetes or other debilitating chronic diseases C/F Depends on sites involved Complications Brain abscess, meningitis, peritonitis
  • 22.
  • 23. Laboratory diagnosis 1.Microscopy Freshly passed Stool , duodenal aspirate, sputum— detects rhabditiform larvae Hyperinfection syndrome- body fluids, tissues Concentration of larva in feces done by Baermann funnel technique Baermann technique
  • 24. 2.Stool culture-when larva are scanty in feces  Harada Mori filter paper tube method  Petridish (slant culture) technique  Charcoal culture method  Agar Plate technique (more sensitive)  Large number of free living larva and adults seen after 7-10 days (A) Harada-Mori filter paper strip culture; (B) (B) petri dish/slant culture method;
  • 25. Agar plate method: The agar plate method carried out in Petri dishes containing water or solid agar is the sensitive method.
  • 26. 3.Serology-ELISA, CFT, IHA 4.Molecular Diagnosis- Realtime PCR 5.Non specific tests- Eosinophillia
  • 27. Treatment Even in the asymptomatic stage, strongyloidiasis must be treated because of the potential for subsequent fatal hyperinfection Ivermectin (2 days) Disseminated strongyloidiasis: Prolonged course of Ivermectin for 5–7 days or until the parasites are eradicated.
  • 28. Prevention Improved personal hygiene Proper disposal of feces Improved nutrition with dietary iron Treatment of infected persons Use of sanitary latrines. Health education.