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Special Issue Review
INTRODUCTION
Strongyloidiasis, the disease caused by the infection with Strongyloides stercoralis, and to a lesser extent by Strongyloides fuelleborni fuelleborni and S. fuelleborni kelleyi, is a soil-transmitted helminthiasis with an estimated 30-100 million people infected worldwide (Genta, 1989; Schar et al. 2013). Although the burden of the disease has been felt to be underestimated (Viney and Lok, 2007; Olsen et al. 2009; Schar et al. 2015, 2014), S. stercoralis infections in humans range from asymptomatic light infections to chronic symptomatic strongyloidiasis. However, uncontrolled multiplication of the parasite (hyperinfection) and potentially life-threatening dissemination of larvae in immunocompromised patients result in mortality rates of up to 85% (Keiser and Nutman, 2004; Mejia and Nutman, 2012).
The parasite, occurring naturally in dogs, primates and humans, is endemic to the tropics and subtropics; foci of infection occur in temperate regions as well (Genta, 1989; Schar et al. 2013) where poor sanitation or other factors facilitate the transmission through fecal contamination. In parts of Africa and in Papua New Guinea, human infections caused by S. fuelleborni fuelleborni and S. fuelleborni kelleyi respectively have been reported (Pampiglione and Ricciardi, 1971; Hira and Patel, 1977; Vince et al. 1979; Crouch and Shield, 1982; Evans et al. 1991; Freedman, 1991; Ashford et al. 1992). In Africa, S. fuelleborni fuelleborni is primarily a parasite of primates, but in Papua New Guinea no animal host has been demonstrated for S. fuelleborni kelleyi (Ashford et al. 1992; Viney and Lok, 2007).
Strongyloides stercoralis is unique among nematodes infectious for humans in that larvae passing in the feces can give rise to a free-living generation of worms which, in turn, give rise to infective larvae. This so-called heterogonic development process serves as an amplification mechanism that allows for increased numbers of infective larvae in the external environment. The infective larvae are active skin penetrators; infection per os, while possible, is probably of limited importance. Because the parasitic female's eggs hatch often within the gastrointestinal tract, the potential for autoinfection exists when precociously developing larvae attain infectivity while still in the host. When the rate of autoinfection escapes control by the host, massive re-penetration and larval migration may result.
LIFE CYCLE
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