Strongyloides stercoralis: Difference between revisions

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===Life Cycle===
===Life Cycle===
* Present in contaminated soil => larvae penetrate skin of hosts walking barefoot => enter venous circulation, migrate to lungs, then are expectorated to pharynx and swallowed => larvae develop into females that lay eggs asexually into GI tract, which hatch into larvae and are excreted into stool
* Present in contaminated soil larvae penetrate skin of hosts walking barefoot enter venous circulation, migrate to lungs, then are expectorated to pharynx and swallowed larvae develop into females that lay eggs asexually into GI tract, which hatch into larvae and are excreted into stool
* Larvae either become sexually reproducing males/females or filariform larvae that can reinfect host
* Larvae either become sexually reproducing males/females or filariform larvae that can reinfect host
* Autoinfection: Unique to Strongyloides; GI larvae can migrate from GI tract to venous system, then to lungs and proceed with life cycle
* Autoinfection: Unique to Strongyloides; GI larvae can migrate from GI tract to venous system, then to lungs and proceed with life cycle

Revision as of 10:18, 6 September 2015

Background

  • Intestinal nematode; roundworm
  • Endemic in tropical/subtropical areas such as Africa, Southeast Asia, Central/South America[1]

Life Cycle

  • Present in contaminated soil → larvae penetrate skin of hosts walking barefoot → enter venous circulation, migrate to lungs, then are expectorated to pharynx and swallowed → larvae develop into females that lay eggs asexually into GI tract, which hatch into larvae and are excreted into stool
  • Larvae either become sexually reproducing males/females or filariform larvae that can reinfect host
  • Autoinfection: Unique to Strongyloides; GI larvae can migrate from GI tract to venous system, then to lungs and proceed with life cycle
    • Can lead to dramatic increase in worm burden and hyperinfection in immunocompromised

Risk factors

  • Corticosteroid use, immunosuppression
  • Transplantation
  • Hematologic neoplasm
  • Human T-lymphotropic virus-1 infection (HTLV-1)
  • Malnutrition
  • Diabetes
  • Chronic renal failure
  • Chronic alcohol use

Clinical significance

  • Chronic infection in immunosuppressed can lead to fulminant dissemination with case fatality rate as high as 70%; strong index of suspicion is needed in such cases

Clinical Presentation

Dermatologic

  • Larva currens: rapidly progressive pruritic linear eruption due to migration of larvae
  • Perianal pruritis
  • Foot pruritus (“ground itch”)

Respiratory

  • Dry cough
  • Wheezing
  • Loeffler’s-like syndrome: fever, SOB, wheezing, pulmonary infiltrates

Immunocompromised patients

  • Respiratory and systemic symptoms such as fever will be more common[3]
  • Disseminated disease will invade multiple organ systems, including liver and brain

Differential Diagnosis

Diagnostic Evaluation

  • Establish possibility of infection (travel to endemic areas, etc)
  • Uncomplicated strongyloidiasis: 3 serial stool samples screened for ova and parasites, as well as ELISA for Strongyloides
    • Complicated strongyloidiasis: blood/sputum Cx, in addition to above
  • Notable eosinophilia in up to 70% of cases, though can be absent in immunosuppressed
  • Gram negative bacteremia may be present in immunocompromised

Management

Uncomplicated strongyloidiasis, normal immune system

  • Ivermectin 200 mcg/kg daily x 1-2d (drug of choice)

OR

  • Albendazole 400 mg BID x 7d
  • Can consider albendazole prophylaxis in immigrants from endemic regions with consistent clinical presentation

Immunosuppressed

  • Combination therapy: albendazole 400 mg BID x 7d AND ivermectin 200 mcg/kg daily x 1-2d[4]
  • Antibiotics may need to be continued until there is evidence that parasite is cleared[4]

Disposition

  • Discharge uncomplicated cases in those who are not immunosuppressed
  • Admit if immunocompromised or systemic symptoms

References

  1. Buonfrate D, Requena-Mendez A, Angheben A, Munoz J, Gobi F, Van Den Ende J, Bisoffi Z. Severe strongyloidiasis: a systematic review of case reports. BMC Infectious Diseases 2013, 13: 78. doi:10.1186/1471-2334-13-78
  2. Greaves D, Coggle S, Pollar C, Aliyu SH, Moore EM. Strongyloides stercoralis infection. BMJ 2013;347:f4610 doi: 10.1136/bmj.f4610 (Published 30 July 2013).
  3. Lim S, Katz K, Krajden S, Fuksa M, Keystone JS, Kain KC. Complicated and fatal Strongyloides infection in Canadians: risk factors, diagnosis and management. CMAJ 2004; 171 (5): 479-484.
  4. 4.0 4.1 Feely NM, Waghorn DJ, Dexter T, Gallen I, Chiodini. Strongyloides stercoralis hyperinfection: difficulties in diagnosis and treatment. Anaesthesia 2010; 65: 298-301.