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INTRODUCTION

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In 1876, a nematode was observed during microscopic examination of stool from a number of French soldiers suffering from severe diarrhea while stationed in French colonial Vietnam. The condition was known as Cochin-China diarrhea, named after the southern region of today’s Vietnam. Within 12 years, the etiologic agent and its complex life cycle were defined. The diagnosis of strongyloidiasis can be challenging, and it is frequently overlooked. Adding to the challenging diagnosis is the fact that a large proportion of cases are asymptomatic. The scenario of missed infection leading to chronicity is common in immunocompetent children, and devastating, life-threatening infection can occur in the immunocompromised host. The World Health Organization has recognized the importance of strongyloidiasis by placing it on its official list of neglected diseases.

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PATHOGENESIS AND EPIDEMIOLOGY

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Strongyloidiasis is a generally chronic infectious disease caused by the intestinal nematode, Strongyloides stercoralis. The phases of development of Strongyloides are distinctive and complex. Beginning at the point of human infection, filariform larvae penetrate exposed skin using a lytic protease mechanism. They subsequently gain access to the bloodstream by way of lymphatics and venules at their point of entry. Next the larvae are transported by the intravascular circulation to the lungs and break through alveolar walls in order to travel up the trachea to the pharynx where they are swallowed to enter the small bowel. There the larvae mature into adult worms. After successfully mating, the adult female deposits eggs into the intestinal mucosa. In this way, Strongyloides is unique among helminths because its eggs are not meant to be secreted in stool. During confinement in the mucosa, eggs develop into noninfective rhabditiform larvae (Fig. 325-1). These larvae then take 2 possible paths. They are either excreted from the body in the stool, or they transform into filariform larvae in the intestine (Fig. 325-2). In this way, any larvae becoming filariform within the gut are infectious to the host and can penetrate the intestine, reenter the blood circulation, and go to the lungs just like the initial infecting larvae. This is called the autoinfection portion of the cycle. Such multiplication in the host is also exclusive among nematodes to Strongyloides. The cycle external to the host begins with the rhabditiform larvae that were excreted in the stool into moist soil. From there, this external cycle splits into 2 directions: transformation of rhabditiform larvae into the infective filariform larvae to infect the next human, as described earlier, or maturation of the filariform larvae into free-living adult male and female worms in the soil that mate. Fertilized eggs are laid in the soil, where they eventually hatch as new rhabditiform larvae that, in turn, mature into infective filariform larvae that will await the next human skin contact, and on it goes (Fig. 325-3). The 2 life cycles of Strongyloides within the host then predict the potential clinical presentations.

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