Strongyloides is a soil-transmitted helminth. The principal definitive hosts of S stercoralis are humans, but infection in dogs can also occur. Infection is contracted via direct contact with contaminated soil during agricultural, domestic, and recreational activities. Filariform larvae penetrate the skin of the host, enter a venous or lymphatic channel. These larvae then migrate to the lungs, where they break out of the capillaries into the alveoli and move to the trachea as they mature. Eventually these larvae gets coughed up and swallowed. Parthenogenetic female worms reside in the lamina propria of the duodenum and the proximal jejunum, where they lay eggs. The eggs hatch into rhabditiform larvae. These larvae migrate into the intestinal lumen and ultimately exit the body with the feces. The free-living rhabditiform larvae may either directly molt into infective (parasitic) filariform larvae that are capable of penetrating the skin of a suitable host or shift to a free-living cycle. In this latter indirect (heterogonic) cycle, molts result in the development of adult male and female worms that mate and produce a generation of offspring whose filariform stage will have the ability to re-enter parasitic life. A small percentage of the rhabditiform larvae molt within the host's intestine into the filariform stage. These tissue-penetrating infective larvae may penetrate the colonic wall or the perianal skin, completing an internal cycle, maturing into adult females in the small intestine. This process is known as autoinfection and may be the mechanism by which S stercoralis can persist indefinitely in infected hosts. This is a unique characteristic of S stercoralis.
Strongyloidiasis pathophysiology
Ascariasis pathophysiology
Schistosomiasis pathophysiology
Ischemic colitis pathophysiology
Stomatitis pathophysiology
Campylobacteriosis pathophysiology
Irritable bowel syndrome pathophysiology
Cyclosporiasis pathophysiology