Strongyloides stercoralis

INSTITUTE OF PULIC HEALTH, DHAKADepartment of Laboratory Medicine

BSc in Health Technology (Laboratory)- 1st Year

HELMINTHOLOGYLecture No. 04 (Strongyloides stercoralis)

By

Sk. MIZANUR RAHMANAssistant Bacteriologist, MBL, IPH

MS in Biotechnology & Genetic Engineering (UODA)MS in Microbiology (SU)

MPH in Epidemiology (SUB)

• 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

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

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.

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).

Morphology cont……

Morphology cont……

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

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

Morphology cont……

a) parasitic female

b) free-living male

c) free-living female

• 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.

Morphology cont……

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

Filariform larvae posterior part

Filariform larva withnotched tail. Infective stageSize 600 x 20 um.

Morphology cont……

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.

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

Life cycle

of

S. stercoralis

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

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

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

Pathology

• Invasive : Skin Penetration.

• Pulmonary: During Cycle or Immigration.

• Intestinal: Tissue Destruction

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)

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

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)

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

Transmission

• Direct penetration of unbroken skin by larva

• Autoinfection - internal (larva becomes infectious in intestinal tract) & external

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

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.

• 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…..

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

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…..

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

Laboratory Diagnosis cont…..

Diagnosis:String Test Baermann concentration

Serology & Bacterial agar plate

Strongyloides stercoralis

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

Strongyloides stercoralis

Morphology:Larvae 0.2-0.3 nm

Strongyloides stercoralis in transplant patients

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)

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)

Prevention

• Good sanitation with specific care of human waste disposal.

• Wearing permanent shoes.• screening prior to transplantation• Education Program for community.

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Thank you for attention!