What is autoinfection in stage 3 of the life cycle of Strongyloides stercoralis in strongyloidiasis?

Updated: Jun 20, 2019
  • Author: Pranatharthi Haran Chandrasekar, MBBS, MD; Chief Editor: Michael Stuart Bronze, MD  more...
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Autoinfection involves premature transformation of noninfective larvae (rhabditiform, 0.25 mm × 0.015 mm) into infective larvae (filariform, 0.5 mm × 0.015 mm), which can penetrate the intestinal mucosa (internal autoinfection) or the skin of the perineal area (external autoinfection), thus establishing a developmental (parasitic) cycle within the host. Infection can be maintained by repeated migratory cycles for the remainder of the host’s life.

Millions of filariform larvae reach the skin by means of the circulation or direct invasion from body cavities; they can migrate through all levels of the dermis and involve the subcutaneous tissue. The infective filariform larvae reenter the circulation by 1 of 3 methods: (1) The larvae penetrate the mucosa of the colon and cause indirect endoautoinfection; (2) the larvae penetrate the mucosa of the upper small intestine and cause direct endoautoinfection; or (3) the larvae penetrate the perianal skin and cause exoautoinfection. The last method has been associated with the development of larva currens.

After entering the circulation, the larvae are carried to the lungs, where the cycle repeats itself. This mechanism accounts for the chronicity and frequent recurrence of the disease in patients who no longer live in areas in which the disease is endemic.

Autoinfection is kept in check by a normal host immune response. However, in patients with impaired cell-mediated immunity, autoinfection may give rise to the 2 most severe forms of strongyloidiasis: hyperinfection syndrome (stage 4) and disseminated strongyloidiasis (stage 5).

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