Main » Infectious diseases » Soil-mediated Helminthiases » Strongyloidiasis
Photo 1. Rhabditiform larvae of S. stercoralis in faeces.
The life cycle of Strongyloides stercoralis can follow one of several patterns: (1) Virtually identical to that of the hookworms, except that the rhabditiform larvae hatch in the colon and are passed as such in the faeces. (2) Involving a free-living adult stage in moist soil. Rhabditiform larvae developing from these also grow into infective filariform larvae which penetrate the skin of a new host. (3) Direct auto-infection of the original host by rhabditiform larvae which develop to the infective filariform stage before leaving the intestine. After invading the circulation through the intestinal mucosa the cycle continues in a normal fashion. The picture shows rhabditiform larvae in the faeces. The egg which is rarely seen in the faeces is very similar to that of hookworm. (x40)
Photo 2. Adult male and free-living larva in soil.
Photo 3. Migrating larvae of S. stercoralis in skin. Auto-infection can lead to severe 'creeping eruption' usually in the back. This may occur many years (30 or more) after initial infection. Deep migration of the larvae may be associated with an 'eosinophilic lung' type of syndrome.
Photo 4. Sections of parasitic female and eggs embedded in jejunal mucosa. Free living females (about one mm long) are smaller than the forms found in the intestine (up to 2.2 mm). Males are normally only found in the soil and are about 0.7 mm long. The parasitic females lying in the intestinal mucosa may reproduce partheno- genetically, the eggs filtering through to the intestinal lumen or first hatching in the mucosa. (x90)
Photo 5. Post-mortem appearance of colon. The incidental administration of steroids and immuno-suppressive agents may greatly enhance infection with S. stercoralis which may even be fatal as in this case. Note the multiple ulcerations and thickening of the wall of the colon.
Photo 5. Stronggyloides stercoralis.
Strongyloides stercoralis has two generations, one free-living and the other parasitic. I. The parasitic generation. Males are rare and the females are probably parthenogenetic, living in the mucosal glands of the small intestine (A). Eggs usually hatch in these glands into larvae which are passed in the faeces (B). These rhabditiform larvae can develop into filariform larvae (C) in the ground, the infective filariform larvae then penetrating the skin of a new host (D). The rest of the cycle in man is as in hookworm infections. II. Free-living generation. Rhabditiform larvae (B) may develop into free-living males and females (E) which lay eggs (F) that hatch in the soil into rhabditiform (G), then infective filariform larvae (H). These too can penetrate the skin (D) and recommence a parasitic cycle in man. III. Auto-infection. Rhabditiform larvae (B) can mature into filariform larvae in the intestine, and these can directly penetrate the peri-anal skin, causing auto-infection. IV. Hyperinfection. Rhabditiform larvae may penetrate the intestinal mucosa causing massive auto-infection, usually in people with diminished immune responsiveness (cycle not illustrated here).
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