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Once rhabditiform larvae mature in the host, autoinfection occurs and the filariform larvae are now free to reinfect.
The major immunologic action against incoming L3 larvae (infective filariform larvae) and L4 larvae (final larval stage within the intestine) is regulated by the infection itself (28).
S stercoralis has the unusual property that rhabditiform larvae may develop into infective filariform larvae and be passed in the feces.
2,4] Immunocompromised hosts with Strongyloides infections may develop autoinfection and disseminated strongyloidiasis as a result of direct transformation of rhabditiform larvae to filariform larvae within the gastrointestinal tract.
The larvae can develop into filariform larvae, which can penetrate the human skin and migrate through circulation to the lungs before settling in the intestine.
26) Patients infected with Strongyloides develop a specific immunoglobulin E (IgE) response to the invasive filariform larvae.
Sources of infection are filariform strongyloid larvae present in soil contaminated by infected feces; the larvae penetrate through the skin of a human host.
If first stage juveniles molt twice during transit down the intestinal tract, they become infective filariform larvae that can penetrate the lower gut mucosa (internal autoinfection) or perianal skin (external autoinfection) and begin migration to the lungs and up the respiratory tree to the pharynx, ultimately returning to the small intestine.
Initial infestation occurs when the infectious form, the filariform larva, enters the human host through skin that was in contact with infected fecal material or contaminated soil.
Rhabditiform and filariform larvae were isolated by stool culture (Figure, panel B).
Patients who have recently had their skin penetrated by the filariform larvae may acquire an itchy cutaneous eruption of pruritic papulovesicular lesion.