Life Cycle
The strongyloid's life cycle is heterogonic - it is more complex than that of most nematodes, with its alternation between free-living and parasitic cycles, and its potential for autoinfection and multiplication within the host. The parasitic cycle is homogenic, while the free-living cycle is heterogonic. The heterogonic life cycle is advantageous to the parasite because it allows reproduction for one or more generations in the absence of a host.
In the free-living cycle, the rhabditiform larvae passed in the stool can either molt twice and become infective filariform larvae (direct development) or molt four times and become free-living adult males and females that mate and produce eggs from which rhabditiform larvae hatch. In the direct development, first-stage larvae (L1) transform into infective larvae (IL) via three molts. The indirect route results first in the development of free-living adults that mate; the female lays eggs, which hatch and then develop into IL. The direct route gives IL faster (three days) versus the indirect route (seven to 10 days). However, the indirect route results in an increase in the number of IL produced. Speed of development of IL is traded for increased numbers. The free-living males and females of S. stercoralis die after one generation; they do not persist in the soil. The latter, in turn, can either develop into a new generation of free-living adults or develop into infective filariform larvae. The filariform larvae penetrate the human host skin to initiate the parasitic cycle.
The infectious larvae penetrate the skin when it contacts soil. While S. stercoralis is attracted to chemicals such as carbon dioxide or sodium chloride, these chemicals are not specific. Larvae have been thought to locate their hosts via chemicals in the skin, the predominant one being urocanic acid, a histidine metabolite on the uppermost layer of skin that is removed by sweat or the daily skin-shedding cycle. Urocanic acid concentrations can be up to five times greater in the foot than any other part of the human body. Some of them enter the superficial veins and ride the blood flow to the lungs, where they enter the alveoli. They are then coughed up and swallowed into the gut, where they parasitise the intestinal mucosa (duodenum and jejunum). In the small intestine, they molt twice and become adult female worms. The females live threaded in the epithelium of the small intestine and, by parthenogenesis, produce eggs, which yield rhabditiform larvae. Only females will reach reproductive adulthood in the intestine. Female strongyloids reproduce through parthenogenesis. The eggs hatch in the intestine and young larvae are then excreted in the feces. It takes about two weeks to reach egg development from the initial skin penetration. By this process, S. stercoralis can cause both respiratory and gastrointestinal symptoms. The worms also participate in autoinfection, in which the rhabditiform larvae become infective filariform larvae, which can penetrate either the intestinal mucosa (internal autoinfection) or the skin of the perianal area (external autoinfection); in either case, the filariform larvae may follow the previously described route, being carried successively to the lungs, the bronchial tree, the pharynx, and the small intestine, where they mature into adults; or they may disseminate widely in the body. To date, occurrence of autoinfection in humans with helminthic infections is recognized only in Strongyloides stercoralis and Capillaria philippinensis infections. In the case of Strongyloides, autoinfection may explain the possibility of persistent infections for many years in persons not having been in an endemic area and of hyperinfections in immunodepressed individuals.
Read more about this topic: Strongyloides Stercoralis
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