Strongyloides
Morning Report
Dec 14th, 2009
Nicole Cullen
What is Strongyloides?
• Parasitic infection
– with a predilection for the
intestines
• 2 most common and clinically
relevant species are:
– Strongyloides stercoralis
– Strongyloides fuelleborni
• Limited to Africa and Papua New
Guinea
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.
How Do You Get It?
• Penetration of intact skin by filiariform
larvae in the soil, or ingestion through
contaminated food or water
• Larvae enter the circulation
– Lungs  alveoli  ascension up
tracheobronchial tree  swallowed  molt
in the small bowel and mature into adult
female
• Females enter the intestinal mucosa
and produce several eggs daily through
parthenogenesis (hatch during transit
through the gut)
Clinical Presentation
• Acute infection:
– Lower extremity itching (mild
erythematous maculopapular rash at
the site of skin penetration)
– Cough, dyspnea, wheezing
– Low-grade fevers
– Epigastric discomfort, n/v/d
Clinical Presentation
• 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 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
Larva Currens
Clinical Presentation
•
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, TNF modulators,
tacro, etc – all BUT cyclosporine)
– Malignancy
– Malabsorptive state
– ESRD
– DM
– Advanced age
– HIV
– HTLV1
– Etoh
Clinical Presentation
• Can replicate in the host for
decades with minimal or no sx
• High morbidity and mortality when
progresses to hyperinfection
syndrome or disseminated
strongyloidiasis
– Usually in immunocompromised
hosts (pregnancy?)
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
Laboratory Findings
• 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
Diagnostic Testing
• Stool 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)
Wet Mount
Larva seen via direct examination of stool
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
Imaging
• CXR – patchy alveolar infiltrates, diffuse
interstitial infiltrates, pleural effusions
• AXR – Loops of dilated small bowel,
ileus
• Barium swallow – stenosis, ulceration,
bowel dilitation
• Small bowel follow-through – worms in
the instestine
• CT abdomen/pelvis – nonspecific
thickening of the bowel wall
Procedures
• EGD – duodenitis, edematous mucosa, white
villi, erythema
• Colonoscopy – colitis
• Duodenal aspiration – examine for larvae
• Sputum sample, bronchial washings, BAL –
show larvae
• Sputum cx
– Nl respiratory flora organisms pushed to the outside
in groups as a result of migrating larvae
– Characteristic pattern can be diagnostic of
S.Stercoralis infection
• If CNS involved, LP – gram stain, cell count/diff
( protein, ↓ glu, poly predominance), wet
mount prep
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
Treatment
• Antihelminitic therapy
– Ivermectin
– Albendazole
– Thiabendazole
• Abx directed toward enteric pathogens if
bacteremia or meningitis (2-4wks)
• Minimize immunosuppression as possible
• Directed supportive tx
– Transfusions if GI bleed, antihistamines for itching,
surgery if bowel perf, etc
• Repeat course of antihelminitic therapy if
immunocompromised, as relapse common
Follow-Up
• Repeat stool exams or duodenal
aspirations in 2-3 mos to document cure
• Repeat serologies 4-8 mos after therapy
– Ab titer should be low or undetectable 6-18
mos after successful tx
• If titer not falling, additional
antihelminitic tx
• Precautions for travelers to endemic
areas, but no prophylaxis or vaccine
available
References
• Arch EL, Schaefer JT and Dahiya A. Cutaneous
manifestation of disseminated strongyloidiasis in a
patient coinfected with HTLV-1. Dermatology Online
Journal. 2008;14(12):6.
• Chadrasekar PH, Bharadwaj RA, Polenakovik H,
Polenakovik S. Emedicine: Strongyloidiasis. April 3,
2009.
• Concha R, Harrington W and Rogers A. Intestinal
Strongyloidiasis. Recognition, Management and
Determinants of Outcome. Journal of Clinical
Gastroengerology. 2005;39(3):203-211.
• Greiner K, Bettencourt J, and Semolic C.
Strongyloidiasis: A Review and Update by Case
Example. Clinical Laboratory Science. 2008;21(2):82-8.
• Siddiqui AA, Berk SL. Diagnosis of Strongyloides
stercoralis infection. Clin Infect Dis. October 1,
2001;33:1040-7.
• Zeph, Bill. Strongyloides stercoralis Infection Can Be
Fatal. American Family Physician. March 15, 2002.