Infection with S. stercoralis (see Figure 18c.l) are initiated from skin penetration by infective (L3 or filariform) larvae, although they may be established following ingestion of these larvae (Grove, 1996). Larvae enter the circulation and lymphatics and are carried to the lungs. They break out of the alveoli, ascend the bronchial tree and are eventually swallowed, enter the wall of the proximal duodenum and moult to become adult worms (Figure 18c.5).
Recent evidence using radiolabelled L3 larvae to track the route of migration in an animal model shows that not all larvae reach the intestinal tract via the lungs. A significant number were seen to be able to do so by other routes (Aikens and Schad, 1989; Mansfield et al., 1995; Schad et al., 1989). Clinically, this is important because absence of larvae from the lungs may not necessarily rule out disseminated disease.
Parasitic females (Figure 18c.7) produce eggs by parthenogenesis and these hatch in the crypts of Lieberkuhn soon after they are deposited to release first-stage (L1) rhabditiform larvae. This accounts for the presence of L1 larvae rather than eggs in the stool. L1 larvae are well suited for a microbivorous life and thrive on organisms in faeces-enriched soil.
It appears that a proportion of these larvae are destined to undergo two moults, giving rise to infective larvae (L2 rhabditiform, and then L2 filariform). This is the homogonic route of development; the resulting infective larvae will live for about 1-2 weeks, as judged by their survival in laboratory cultures (Grove, 1989b, 1996). This is a rapid mode of development and may result in infective larvae in about 24 hours.
Those L1 larvae that do not undergo homo-gonic development will moult to rhabditiform L2, then to rhabditiform L3 larvae, then to free-living male and female adults, retaining their rhabditi-form morphology. Free-living females contain 5-45 eggs and will mate with the smaller males (Hammond and Robinson, 1994). Pseudofertilisation is believed to take place and this results in egg production. All L1 larvae hatched from the eggs of free-living females are destined to become infective L3 (filariform) larvae, since heterogonic development occurs over a single generation only (Yamada et a/., 1991; Schad, 1989).
Factors determining the mode of development of S. stercoralis in the free-living phase are not well understood. A simplified view is that a hostile host environment and/or a favourable external environment drives the heterogonic development of larvae. Conversely, a favourable host and/or an unfavourable external environment results in homogonic development (Moncol and Triantaphyllou, 1978). In the related species S. ratti, the direction of external development can be determined by factors such as ambient temperature, and generally tropical strains are more likely to undergo heterogonic development than temperate strains in coproculture (Viney, 1996). Furthermore, strains of S. ratti have been selected to develop homogonically or heterogoni-cally (Wertheim and Lengy, 1965). Manipulation of the host immune status may also result in clonal larvae, which are more likely to develop heterogonically in response to specific immunity (Gemmill et al, 1997).
S. stercoralis infections are notoriously chronic: infections lasting for more than four decades are not uncommon (Gill and Bell, 1979; Pelletier, 1984). These long-lasting infections are due to autoinfection, and this parasite is almost unique among intestinal nematodes because of its ability to replicate and multiply within the host in the absence of external sources of infection.
Autoinfection in strongyloidiasis results from the moulting of more L1 larvae into infective L3 larvae while they are in the intestine or on the perineum. These larvae will penetrate the wall of the intestine or perineum and establish as adults in the gut. The factors that regulate autoinfection are not well understood but host immunologic factors appear to play an important role in its regulation. However, by this method infections can be sustained for very long periods and have the potential to increase the parasite burden in the absence of external sources of re-infection.
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