This document summarizes the key characteristics of Strongyloides stercoralis, including its morphology, life cycle, pathogenicity, clinical manifestations, diagnosis and treatment. It is a parasitic nematode commonly found in warm, moist tropical regions. The adult worms inhabit the small intestine and larvae can disseminate throughout the body. It has a complex life cycle involving both free-living and parasitic stages that allows it to persist long-term in human hosts through autoinfection. While often asymptomatic, it can cause skin, pulmonary or intestinal symptoms and severe disseminated infection in immunocompromised individuals. Diagnosis involves microscopic identification of larvae in stool or biopsy samples. Treatment involves antihelminthics like ivermect
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Strongyloides_stercoralis.ppt
1. Strongyloides stercoralis
• Also called thread worm.
• The smallest nematode & is aetiologic agent
of Strongylodiasis.
• Found mainly in the warm moist tropics but
may also occur in the temperate regions.
Habitat:
1. Adults in wall of intestine(duodenum &
jejunum)
2. larvae can be found throughout the body
3. Parasitic females may invade lung epithelium
and reproduce.
2. MORPHOLOGY
1. Both male & female worms have a well
devt digestive & reproductive systems.
2. Females are thin, transparent & about 2.5
mm long .
3. The female reproductive system contains
paired uteri, vagina & vulva. Gravid
female uteri contain thin walled
transparent ovoid eggs.
3. • The worm is ovoviviparous(lay eggs within
them, incubate & produce larvae or eggs that
hatch immediately after being layed).
• Individual worm has a lifespan of 3 or 4
months.
• However, the infection may persist for years
due to autoinfection.
4. • Male worms are shorter & broader than
females measuring 0.6–1 mm in length.
• They have copulatory spicules which
penetrate the female during copulation.
• They do not invade the intestinal wall &
usually not seen in human infection.
6. Eggs
• Are oval & measure 50–60 µm in length.
• Eggs are seen within the uterus of gravid
female.
• Eggs hatch out to rhabditiform larva (1st stage
larva) soon after being layed.
• Hence it is the larva & not the egg which is
excreted in feces & detected during stool
examination.
7. Larva
1. Rhabditiform Larva (L1 stage)
• Eggs hatch out to form L1 larva in the small
intestine.
• Most common form of the parasite found in
the feces.
• L1 larva migrates into the lumen of the
intestine & excreted in feces.
8. 2. Filariform Larva (L3 stage)
• L1 larva moults twice to become the L3 larva.
• It is the infective stage of the parasite to man.
10. Life Cycle
• S. stercoralis has a complex life cycle due to
multiplicity of pathways thru which it can
develop.
• Has a parasitic cycle & a free-living soil cycle
where it can persist for long periods in soil.
• Natural host: Man but dogs & cats are found
infected with morphologically similar strains.
11. • Infective form: Filariform larva(L3 larva).
• Mode of infection:
1. Penetration of skin by filariform larva when a
person walks barefoot in contaminated soil.
2. Internal autoinfection in colon – L3 penetrate
mucosa of colon.
3. External autoinfection: L3 penetrate perianal,
and perineal area.
12. • Female adult worms are found in the
intestines embedded in the mucosa of the
duodenum & upper jejunum.
• Males not seen in human infections because
they do not invade the intestinal wall .
• Are eliminated from the bowel soon after the
females begin to oviposit(lay eggs).
• However, the majority of females are probably
parthenogenetic ( lay fertilized eggs without
males).
13. • Eggs laid in mucosa hatch immediately
releasing rhabditiform larva which migrates
into intestinal lumen & gets released in feces.
• The L1 larva may even transform into filariform
larva in the bowel.
• L3 larva may penetrate colonic mucosa or
perianal skin without leaving the host ( auto-
infection).
• This leads to persistence of the infection in
patients for long periods(even 30–40 years).
14. • The L1 larva undergo two types of devt in the
soil.
1. Direct development
2. Indirect development
• Direct devt: L1 larva on reaching the soil
moults twice to become the infective L3 larva.
• Free-living phase/indirect devt: The L1 larva
passed in stools develop into free-living males
& females in moist soil.
15. • These mate in the soil & fertilized female lay
eggs which hatch to release L1 larvae.
• These may repeat the free-living cycle or may
develop into the filariform larvae which infect
humans & initiate the parasitic phase.
19. Pathogenicity & Clinical Features
• S. stercoralis generally cause benign &
asymptomatic disease.
• Blood eosinophilia & larvae in stool may be
the only indications of infn.
• Severe & even fatal disease may occur in
those with defective immune response.
• Clinical disease may have skin, pulmonary &
intestinal manifestations.
20. Skin manifestations
• Dermatitis with erythema & itching at site of
penetration of L3 larva occur.
• In sensitized individuals, there may be an allergic
response.
• Pruritus & urticarial lesions particularly around
the perianal skin & buttocks are symptoms of
chronic strongyloidiasis.
• larva migrans do occur = larva currens or racing
larva, 10cm/hour.
21.
22. Pulmonary Manifestations
• Small hemorrhages may occur in the alveoli &
bronchioles as larva escape pulmonary
capillaries .
• Bronchopneumonia may be present, which
may progress to chronic bronchitis &
asthmatic symptoms in some patients.
• Larva of Stongyloides may be found in the
sputum of these patients.
23. Intestinal Manifestations
• Epigastric pain & hunger pangs in acute stage
resembling peptic ulcer or malabsorption
syndrome.
• Mucus diarrhea is often present.
• Extensive sloughing of mucosa causing
dysenteric stools occur in heavy infn.
• Other manifestations include protein-losing
enteropathy and paralytic ileus.
24. Hyperinfection
• Refers to extensive internal reinfection leading
to large numbers of adult worms in intestines,
lungs & larvae in various tissues & organs.
• Common in immunosuppressed persons e.g
Severe malnutrition, malignancies, AIDS etc.
• Defective cell-mediated immunity predispose
to this condition.
25. • Filariform larvae may enter arterial circulation
& lodge in various organs e.g. heart, lungs,
brain, kidney, pancreas, liver & lymph nodes.
• CNS involvement lead to brain abscess &
meningitis.
• Peritonitis is also a major fatal complications.
• Circulating larvae may carry intestinal bacteria
causing septicemia.
26. Appearance of colon at post mortem examination Note the multiple
ulcerations and thickening of the wall of the colon in S.stercoralis
27.
28. Diagnosis of Strongylodiasis
1. Clinical – diarrhoea with epigastric pain,
high eosinophilia.
2. Definitive diagnosis – Microscopy
• Direct wet mount of stool: Demonstration
of L1 larvae in freshly passed stools most
important for specific diagnosis.
• Concentration methods: formol ether
concentration method or Baermann’s
funnel gauze method.
29. • Larvae may be present in sputum, duodenal
aspirates & jejunal biopsies.
• Stool Culture esp when larvae are scanty using
Agar plate culture & Charcoal culture method.
• Serological tests e.g ELISA although has a
downside of extensive cross-reactions with
other helminth infns.
30. Treatment
• All cases whether symptomatic or not need to
be treated to prevent severe invasive disease.
• Ivermectin (200 mg/kg daily for 2 days) more
effective than Albendazole.
• Disseminated disease need extended
treatment with Ivermectin for atleast 5–7
days.
• Absence of eosinophilia is a poor prognostic
sign in hyperinfection.
31. Prevention of Strongyloidiasis
1. Sanitary disposal of human excreta
- long voided feces or surface water
specially dangerous.
2. Treat all cases specifically
3. Rule out Strongylodiasis before treatment
with immunosuppressives.
4. 30 year old infection in absence of
exposure reported – autoinfection.
32. ZOONOTIC Strongyloidiasis
• Wild or domestic animals as definitive
/natural hosts.
• Do not cause patient infections.
• Causes cuteneous larva migrans and
urticaria in man.
33. Strongyloides fuellerborni
Parasite of Old World monkeys, Zoonotic
First human case – Zimbabwe
Papua New Guinea.
Zambia
Hira P.R., and Patel B.G. 1977. Strongyloides
fuellerborni infections in man in Zambia. Am. J.
Trp. Med. Hyg. 26: 640 –643
Hira and Patel, 1980. Trop. Geog. Med. 32: 23 - 29
34. Biology of S.fuellerborni
1. Eggs in stool, not larvae
2. Eggs resemble hookworm eggs.
3. Freeliving female with post vulvar
constriction
36. Pathogenesis of S.fuellerborni
1. Similar to S.stercoralis
2. Abdominal symptoms with oedema –
“swollen belly sickness”as a result of
protein loss.
3. Respiratory distress and abdominal
distension symptoms.
37. .
Eggs of Strongyloides fullerborni in faeces. Strongyloides frulleborni,
a common intestinal nematode in can and Asian primates, is found in
humans in several countries, including Zambia where 10% of human
Strongyloides infections may be caused by this species. Massive
infections with a subspecies of this nematode, S.fullerborni kellyi,
cause an often fatal illness in infants in the West of Papua New Guinea,
a country from which monkeys absent. This condition, known as
'swollen belly sickness “ characterised by respiratory distress, abdominal
distention and generalised oedema. Very heavy egg loads, as seen here
38. Diagnosis of S. fuellerborni
1. Demonstration of ova in feces
2. Copro culture of eggs to adults, and their
identification.
40. Prevention of S.fuellerborni
1. Sanitary disposal of human excreta
2. Control of monkey populations
3. Treat all cases specifically
41. Diploscasper coronata
1. Lives in decaying matter and sewage beds
2. Facultative parasite of man
3. Males rarely found – parthenogenesis
reproduction
4. Worms found in human urine and stomach
contents
5. Worms acquired from decaying vegetation.
42. Rhabditis
1. Resemble free-living Strongyloides
2. Life cycle free-living – but no fllariform
larval form
3. Can live in ulcerated damaged skin and
organs
4. Contaminators of food and drink
5. In human larvae found in itching
cutaneous papules- resemble craw-craw,
female urine.
43. Meloidogyne javanica
Syn Heterodera incognita
1. Plant parasitic Nematodes found in roots
and stem of many edible plants
2. Eggs and larvae in feces after ingestion of
infected plants
3. Eggs thin shelled, elongate ovoid,
flattened on one side
4. Mistaken for infertile eggs of Ascaris or
hookworm eggs.