Strongyloides stercoralis is an intestinal parasitic nematode that can cause strongyloidiasis in humans. It has a unique life cycle involving both free-living and parasitic stages. In the parasitic stage, the worm resides in the small intestine and can spread throughout the body, potentially causing disseminated infection. Diagnosis is made by identifying larvae in stool samples or biopsy specimens. Transplant patients are at higher risk of severe hyperinfection due to immunosuppression. Screening and treatment prior to transplantation is important for prevention.

1. INSTITUTE OF PULIC HEALTH, DHAKA
Department of Laboratory Medicine
BSc in Health Technology (Laboratory)- 1st Year
HELMINTHOLOGY
Lecture No. 04 (Strongyloides stercoralis)
By
Sk. MIZANUR RAHMAN
Assistant Bacteriologist, MBL, IPH
MS in Biotechnology & Genetic Engineering (UODA)
MS in Microbiology (SU)
MPH in Epidemiology (SUB)

2. • Habitat: females live in the superficial tissues of the small
intestine (duodenum and jejunum)
• Definitive host: Human, dogs and cats
• Route of infection: Filariform larvae penetrate the skin of human.
• Infective stage: Third stage larvae ( filariform).
• Diagnostic stage: First stage larvae(Rhabditiform) in feces.
• Geographical distribution: - cosmopolitan parasite, mainly in
moist and warm areas of low hygiene
Introduction

3. Introduction cont……
• Human parasitic disease caused by nematode S. Stercoralis.
• Mostly in tropical, subtropical area and temperate climate.
• Affect 30-100 million annually.
• Has two unique life cycle: Free life cycle and Parasitic life cycle.
• Cause by direct contact with contaminated soil and recreational
activities.
• Children highly affected to bad sanitation.
• S. stercoralis is a 2 mm long intestinal worm

4. Epidemiology
• Relatively uncommon in the US
• BUT, endemic areas in the rural parts of the Southeastern
states and the Appalachian mountain area
– Certain pockets with prevalence 4%
• Usually found in tropical and subtropical countries
– Prevalence up to 40% in areas of West Africa, the Caribbean,
Southeast Asia
• Affects >100 million worldwide
• No sexual or racial disparities. All age groups.

5. Morphology cont……
Egg:
Size : 55 x 30 um.
Shape: oval . Clear, thin shelled Similar to hookworm but are
smaller.
Eggs are laid in the mucosa, hatch into rhabditiform larvae that
penetrate the glandular epithelium and pass into the lumen of
the intestine and out the feces
(Eggs are seldom seen in stools).

6. Morphology cont……

7. Morphology cont……
Adult:
Male (parasitic or free-living):
- 0.7 mm in length
- Rhabditiform oesophagus
- Posterior end curved ventrally with Spicules

8. Morphology cont……
Parasitic female:
- 2.2 mm in length
- Cylindrical oesophagus (1/3 body length)
- Posterior end straight
Free living female:
- 1 mm in length
- rhabditiform oesophagus
- posterior end straight

9. Morphology cont……
a) parasitic female
b) free-living male
c) free-living female

10. • 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.

12. Morphology cont……
Rhabditiform larvae
• 220 x 15 um.
• Short buccal cavity.
• Diagnostic stage
• appear in stools within 4weeks of infection.

13. Filariform larvae posterior part
Filariform larva with
notched tail.
Infective stage
Size 600 x 20 um.

14. Morphology cont……

15. Life Cycle
Free-living cycle
Parasitic cycle: In the parasitic stage, no male
form of this organism has been reliably
identified, and the female reproduce in a
parthinogenitic manner.

16. Life Cycle cont….
1. Free-living Phase
• Free living S. stercoralis dwell in moist soil in warm climates
• Copulation occurs in soil; sperm penetration merely activates
the oocyte to develop parthenogenetically with no contribution to
the genetic material of the developing embryo
• Following oviposition, eggs hatch in the soil and give rise to 1st
stage rhabditiform larvae
• These feed on organic debris, go through several molts and
become sexually mature adults
• This free-living heterogonic life cycle may continue indefinitely
• However, if the environment becomes inhospitable, the
rhabditform larvae molts to become a nonfeeding filariform larva
- the form infective to humans

17. Life cycle
of
S. stercoralis

19. Life Cycle cont….
2. Parasitic Phase
• When filariform larvae encounter a human or another suitable
host (e.g. cats and dogs), 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, following a 3rd molt, the larvae rupture from the
pulmonary capillaries and enter the alveoli
• From the alveoli, the larvae move up the respiratory tree to the
epiglottis
• Abetted by coughing and subsequent swallowing by the host, they
migrate over the epiglottis to the esophagus and down into the
small intestine, where they undergo a final molt and become
sexually mature females

20. Parasitic Phase cont.
• Females produce embryonated eggs
parhenogenetically
• These eggs hatch in the mucosa into 1st stage
rhabditiform larvae
• These exit the intestine with the feces, feeding down
the length of the intestine
• Larvae become established in the soil, undergo
several molts and become free-living adults
• Under adverse conditions they can revert to being
filariform larvae

21. 3. Autoinfection
• During passage through the host digestive system, rhabditiform
larvae 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
•Autoinfection can also occur when larvae remain on and penetrate
the perianal skin.
• Autoinfection often leads to very high worm burdens in humans

22. Pathology
• Invasive : Skin Penetration.
• Pulmonary: During Cycle or Immigration.
• Intestinal: Tissue Destruction

23. Clinical Presentation/ Aspects
• Acute infection:
– Lower extremity itching (mild erythematous
maculopapular rash at the site of skin
penetration)
– Cough, dyspnea, wheezing
– Low-grade fevers
– Epigastric discomfort, nausea, vomiting, diarrhea
(n/v/d)

24. Clinical Presentation/Aspects cont….
• Chronic Infection
– Can be completely asymptomatic
– Abdominal pain that can be very vague, crampy, burning
• Often worse after eating
– Intermittent diarrhea
• Can alternate with constipation
– Occasional nausea, vomiting (n/v)
– Weight loss (if heavy infestation)
– Larva currens (“racing larva” – a recurrent maculopapular or
serpiginous rash)
• Usually begins perianally and extends up the buttocks, upper thighs,
abdomen
– Chronic urticaria

25. Clinical Presentation/Aspects cont….
• Severe infection
– Can be abrupt or insidious in onset
– N/v/d, severe abdominal pain, distention
– Cough, hemoptysis, dyspnea, wheezing, crackles
– Stiff neck, headache, MS changes
• If CNS involved
– Fever/chills
– Hematemesis, hematochezia
– Rash (petechiae, purpura) over the trunk and proximal extremities
• Caused by dermal blood vessel disruption brought on by massive migration
of larvae within the skin
• Risk factors for severe infection
– Immunosuppressant meds (steroids, chemo, tumor necrosis factor
(TNF ) modulators, tacro, etc)
– Malignancy
– Malabsorptive state
– end-stage renal disease (ESRD)
– Diabetes mellitus (DM)
– Advanced age
– human immunodeficiency virus (HIV)
– human T-cell lymphotropic virus (HTLV1)
– ethyl alcohol (Etoh)

26. Dangerous Complications
• Hyperinfection Syndrome
– Acceleration of the normal life cycle, causing excessive
worm burden
– Autoinfection (turn into infective filariform larva within
the lumen
– Spread of larvae outside the usual migration pattern of GI
tract and lungs
• Disseminated strongyloidiasis
– Widespread dissemination of larvae to extraintestinal
organs
• CNS (meningitis), heart, urinary tract, bacteremia, etc
– Can be complicated by translocation of enteric bacteria
• Travel on the larvae themselves or via intestinal ulcers
– Mortality rate close to 80%
• Due to delayed diagnosis, immunocompromised state of
the host at this point

29. Transmission
• Direct penetration of unbroken skin by
larva
• Autoinfection - internal (larva becomes
infectious in intestinal tract) & external

30.  Direct stool smears (larvae)
 Cultivation of stool. (Damp charcoal or Harada-Mori
mediums).
 Eosinophilia, is present in uncomplicated strongyloidiasis,
but is lost in hyper infection
 Histological examination of duodenal or jejunal biopsy
specimens obtained by endoscopy can demonstrate adult
worms embedded in the mucosa.
 For population screening in endemic areas, an ELISA for IgG
anfi-Strongyloides antibodies is effective.
Laboratory Diagnosis

31. Laboratory Diagnosis cont…..
• Diagnosis rests on the microscopic identification of
larvae (rhabditiform and occasionally filariform) in
the stool or duodenal fluid.
• Examination of serial samples may be necessary, and
not always sufficient, because stool examination is
relatively insensitive.

32. • Stool ova and parasite (O&P)
– Microscopic ID of S. sterocoralis larvae is the definitive
diagnosis
– Ova usually not seen (only helminth to secrete larva in the
feces)
• Stool wet mount (direct exam)
– In chronic infection, sensitivity only 30%, can increase to
75% if 3 consecutive stool exams
– Can enhance larvae recovery with more obscure methods
(Baermann funnel, agar plate, Harada-Mori filter paper)
Laboratory Diagnosis cont…..

33. Laboratory Diagnosis cont…..
• CBC
– WBC usually wnl for acute and chronic cases, can
be elevated in severe cases
– Eosinophilia common during acute infection, +/- in
chronic infection (75%), usually absent in severe
infection

34. Serology
ELISA
• Most sensitive method (88-95%)
– May be lower in immunocompromised patients
• Cannot distinguish between past and present
infections
• Can cross-react with other nematode infections
• If results are positive, can move on to try and
establish a microscopic dx
Laboratory Diagnosis cont…..

35. Laboratory Diagnosis cont…..
Histology
• Larvae typically found in proximal portion of
small intestine
– Embedded in lamina propria
• Cause edema, cellular infiltration, villous
atrophy, ulcerations
• In-long standing infections, may see fibrosis

36. Laboratory Diagnosis cont…..

38. Diagnosis:
String Test Baermann concentration
Serology & Bacterial agar plate
Strongyloides stercoralis

39. Microscopy
Rhabditiform larvae of Strongyloides stercoralis The rhabditoid esophagus is clearly visible in this larva; it consists of a
club-shaped anterior portion, a postmedian constriction, and a posterior
bulb .
Larva seen via direct examination of stool
Morphology:
Adult females 2-3 mm

40. Strongyloides stercoralis
Morphology:
Larvae 0.2-0.3 nm

45. Strongyloides stercoralis in
transplant patients

46. Transplant patients
• S. stercoralis has been reported in kidney
(n=54), liver (n=3), lung (n=1), heart (n=3)
and stem cell (n=7) transplant patients
• More common for transplant patients to
have hyperinfection, though more mild
presentations have been reported
• 0.7% of the renal transplant recipients
between 1971-1984 at Vanderbilt had
strongloidiasis (Morgan 1986)

47. Transplant patients
• Strongloidiasis can be transmitted by solid
organs and it has been documented in people
who have not left the US
• presentation more likely after transplantation
or after treatment of acute rejection
– associated with steroid use
– cyclosporine may be protective
• mortality rate in kidney transplant patients:
49% (Roxby 2009)

48. Prevention
• Good sanitation with specific care of human
waste disposal.
• Wearing permanent shoes.
• screening prior to transplantation
• Education Program for community.

49. References
1. Neva FA. Biology and immunology of human strongyloidiasis. J. Infect. Dis. 1986 Mar ;153(3):397-406.
2. Siddiqui AA, Berk SL. Diagnosis of Strongyloides stercoralis infection. Clin. Infect. Dis. 2001 Oct 1;33(7):1040-
1047.
3. Segarra-Newnham M. Manifestations, diagnosis, and treatment of Strongyloides stercoralis infection. Ann
Pharmacother. 2007 Dec ;41(12):1992-2001.
4. DeVault GA, King JW, Rohr MS, Landreneau MD, Brown ST, McDonald JC. Opportunistic infections with
Strongyloides stercoralis in renal transplantation. Rev. Infect. Dis. 1990 Aug ;12(4):653-671.
5. Morgan JS, Schaffner W, Stone WJ. Opportunistic strongyloidiasis in renal transplant recipients. Transplantation.
1986 Nov ;42(5):518-524.
6. Marty FM. Strongyloides hyperinfection syndrome and transplantation: a preventable, frequently fatal infection.
Transpl Infect Dis. 2009 Apr ;11(2):97-99.
7. Vilela EG, Clemente WT, Mira RRL, Torres HOG, Veloso LF, Fonseca LP, et al. Strongyloides stercoralis
hyperinfection syndrome after liver transplantation: case report and literature review. Transpl Infect Dis. 2009
Apr ;11(2):132-136.
8. Roxby AC, Gottlieb GS, Limaye AP. Strongyloidiasis in transplant patients. Clin. Infect. Dis. 2009 Nov 1;49(9):1411-
1423.
9. Mandell G, Bennett J, Dolin R. Principles and Practice of Infectious Diseases. 6th ed. Philadelphia, PA: Elsevier;
10.Center for Disease Control and Prevention. CDC surveillance summaries. MMWR. 1991 ;40(SS):

50. Thank you for attention!