Background. Strongyloidiasis is an infection caused by Strongyloides stercoralis (and rarely S. fülleborni), live in the small intestine of humans. The helminth presents mainly in tropical and subtropical regions but also in temperate climates. Some 30–100 million people are estimated to be infected worldwide. Although strongyloidiasis has a similar route of infection as the other soil-transmitted helminthiases, it needs different diagnostic tools and different treatment.
Infection. Strongyloidiasis is transmitted through direct penetration of human skin by infective larvae when in contact with soil; walking barefoot is, therefore, a major risk factor for acquiring the infection. Strongyloides spp. larvae penetrate the human host and reach the intestine where they mature into adults and produce eggs; the eggs hatch in the gut lumen and yield larvae that are evacuated in feces. The peculiarity of this worm is that some larvae are not excreted but reinvade the intestine or perianal skin to perpetuate the infection (“autoinfection cycle”).
Morphology. The parthenogenic females from the gut are 2.1 – 2.7 mm long. Their buccal capsule is small and their pharynx is filariform. Free-living females are about 1 mm long, the males slightly shorter. Both have a rhabditiform pharynx. Both types of females are didelphic, with the vulva of the parasitic female two-thirds along the body length and that of the free-living female at the midpoint of the body. The infective filariform L3 is 490–630μm long, the rhabditiform L1 passed in the stool is 180–240μm long. Eggs of the parasitic females are thin-shelled and embryonated when shed. They measure 54×32μm.
Development. S. stercoralis has no intermediate host. The parasitic phase starts when filariform L3 from contaminated soil invade the body, usually the feet. The larvae are carried via circulation to the lungs and trachea, penetrate the pulmonary alveoli, and are coughed up and swallowed. In the duodenum and jejunum, they molt twice and give rise to parthenogenetic females. Rhabditiform L1 hatch from the eggs in the intestine and are excreted with the feces. Eggs are rarely found in the feces. The free-living phase starts with first-stage larvae hatching in the gut and excreted with the stool. They can follow two pathways: either molt twice and become infective female third-stage larvae (filariform L3) or molt four times, thereby going through the stage of a rhabditiform L3 and become free-living adult males and females, which can propagate again in the open.
Pathology In a heavy infection, pneumonia-like symptoms with dry cough may occur during the passage of larvae through the lungs. Intestinal symptoms are usually not present or are only slight in the chronic phase. Anal pruritus, though, may occur, when L1 invades the perianal skin. The major concern is hyperinfection. This does not necessarily occur as often assumed in individuals that are immunocompromised due to HIV infection, for example. The large number of females and the larval migration through the body during a hyperinfection induces watery diarrhea, digestive problems, edema, heavy pneumonia, occasionally meningitis, and even death, as available therapies are rarely successful.
References:
Chernin, J. Parasitology – Lifeline (Modules in life sciences). CRC Press, London: 2000.
Lucius R., Brigitte Loos-Frank, Richard P.L., Robert P., Craig W.R., and Richard K.G. The Biology of Parasites. Wiley-VCH Verlag GmbH and Co. KGaA, Weinheim, German: 2017.
World Health Organization. Strongyloidiasis[WHO; 2019]. Available from: https://www.who.int/intestinal_worms/epidemiology/strongyloidiasis/en/
