Strongyloidiasis

Strongyloidiasis, caused by the nematode Strongyloides stercoralis ( S. sterocralis, threadworm), is prevalent in Asia, Africa, Oceania, South America, Southern Europe, and southeastern states of the United States (Kentucky, Virginia, Tennessee, and North Carolina). In the United States, the predisposing factors for the infection include immigrants and military veterans who have lived in endemic areas, and patients with malnutrition, chronic obstructive pulmonary disease (COPD), chronic renal failure, alcoholism, or underlying malignancies. The mode of infection is by contact with contaminated soil with free living larvae that penetrate the skin and migrate throughout the body prior to the lungs and finally to the small intestine. The larvae from the lungs are coughed up and swallowed, and reach the small intestine. Here they mature into the adult female worm, which can produce rhabditiform larvae by means of parthenogenesis. Larvae are also found in the heart, liver, gallbladder, brain, genitourinary organs, and nervous system ( Fig. 120.1 ). The larvae are then swallowed and enter the duodenum, where the adults attach to or penetrate the wall. The female worm is tiny—no more than 2 mm in length. It enters the small bowel mucosa, where it can extrude eggs (see Fig. 123.1 ). A sexual cycle of development then occurs in which the rhabditiform larvae develop into males and females, and pass eggs into the soil, which then form filariform larvae that can restart the cycle.

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Strongyloidiasis: Life Cycle of Strongyloides stercoralis.

However, a short life cycle can occur in which the rhabditiform larvae mature and penetrate the skin in the perianal area and autoinfect the host. Parasitologists debate these varieties in the life cycle. Autoinfection is well documented, and rhabditiform larvae do develop adult sexual forms in soil.

Hyperinfection can occur if large numbers of organisms enter the host, usually in an immunocompromised patient or when one is treated with corticosteroids. The worms are able to regulate their own populations, but when a host is treated with corticosteroids, the eggs produce increased amounts of ecdysteroid substances (a steroid structurally similar to androgens) in host tissue, which allow proliferation of adult female worms and eggs and a massive number of larvae. Hyperinfection has been associated with millions of adult worms or filarial larvae in the mucosa of the small and large intestines.