The distribution of S. stercoralis parallels that of the hookworms, although it is less preva-lent in all but tropical areas. It infects 90 million individuals worldwide, including 400,000 throughout the rural areas of Puerto Rico and the southeastern sections of the continental United States. Although, like hookworm infection, it is generally acquired by direct con-tact of skin with soil-dwelling larvae, infection may also follow ingestion of filariform-contaminated food. Transformation of the rhabditiform larvae to the filariform stage within the gut can result in seeding of the perianal area with infectious organisms. These larvae may be passed to another person through direct physical contact or autoinfect the original host. In debilitated and immunosuppressed patients, transformation to the filariform stage occurs within the gut itself, producing marked autoinfection or hyperinfection.
Invasion of the intestinal epithelium may accelerate epithelial cell turnover, alter intesti-nal motility, and induce acute and chronic inflammatory lesions, ulcerations, and abscess formation, all of which may play a role in the malabsorptive syndrome that frequently characterizes clinical disease. Steroid- or malnutrition-related immunosuppression ap-pears to accelerate the metamorphosis of rhabditiform to filariform larvae within the bowel lumen, enhancing the frequency and intensity of autoinfection. There is little evi-dence that protective immunity develops in the infected host.