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[Strongyloides stercoralis]

 Filariform (L3) larva of S. stercoralis in a sputum specimen, stained with Giemsa. Image taken at 200x magnification.

Filariform (L3) larva of S. stercoralis in a sputum specimen, stained with Giemsa. Image taken at 200x magnification.

Rhabdititoid larvae of S. stercoralis.

’Rhabditiform (L1) larva of S. stercoralis.

Causal Agents

The nematode (roundworm) Strongyloides stercoralis. Other Strongyloides include S. fülleborni, which infects chimpanzees and baboons and may produce limited infections in humans.

Life Cycle

Life cycle of Strongyloidiasis

The Strongyloides life cycle is more complex than that of most nematodes with its alternation between free-living and parasitic cycles, and its potential for autoinfection and multiplication within the host. Two types of cycles exist: Free-living cycle: The rhabditiform larvae passed in the stool The number 1(see "Parasitic cycle" below) can either become infective filariform larvae (direct development)The number 6, or free-living adult males and females The number 2 that mate and produce eggs The number 3 from which rhabditiform larvae hatch The number 4and eventually become infective filariform larvae The number 5. The filariform larvae penetrate the human host skin to initiate the parasitic cycle (see below) The number 6. Parasitic cycle: Filariform larvae in contaminated soil penetrate the human skin The number 6, and by various, often random routes, migrate to the small intestine The number 7. Historically it was believed that the L3 larvae migrate via the bloodstream to the lungs, where they are eventually coughed up and swallowed. However, there is also evidence that L3 larvae can migrate directly to the intestine via connective tissues. In the small intestine they molt twice and become adult female worms The number 8. The females live threaded in the epithelium of the small intestine and by parthenogenesis produce eggsThe number 9, which yield rhabditiform larvae. The rhabditiform larvae can either be passed in the stool The number 1 (see "Free-living cycle" above), or can cause autoinfection The number 10. In autoinfection, the rhabditiform larvae become infective filariform larvae, which can penetrate either the intestinal mucosa (internal autoinfection) or the skin of the perianal area (external autoinfection); in either case, the filariform larvae may disseminate throughout the body. To date, occurrence of autoinfection in humans with helminthic infections is recognized only in Strongyloides stercoralis and Capillaria philippinensis infections. In the case of Strongyloides, autoinfection may explain the possibility of persistent infections for many years in persons who have not been in an endemic area and of hyperinfections in immunodepressed individuals.

Geographic Distribution

Tropical and subtropical areas, but cases also occur in temperate areas (including the South of the United States). More frequently found in rural areas, institutional settings, and lower socioeconomic groups.

Clinical Presentation

Frequently asymptomatic. Gastrointestinal symptoms include abdominal pain and diarrhea. Pulmonary symptoms (including Loeffler’s syndrome) can occur during pulmonary migration of the filariform larvae. Dermatologic manifestations include urticarial rashes in the buttocks and waist areas. Disseminated strongyloidiasis occurs in immunosuppressed patients, can present with abdominal pain, distension, shock, pulmonary and neurologic complications and septicemia, and is potentially fatal. Blood eosinophilia is generally present during the acute and chronic stages, but may be absent with dissemination.

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  • Page last reviewed April 13, 2015
  • Page last updated April 13, 2015
  • Content source: Global Health - Division of Parasitic Diseases and Malaria
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