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Intestinal Invasion by Entamoeba histolytica

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Molecular Mechanisms of Parasite Invasion

Part of the book series: Subcellular Biochemistry ((SCBI,volume 47))

Abstract

Entamoeba histolytica is a protozoan parasite that infects humans and causes the disease amebiasis. The spectrum of intestinal amebiasis varies from colonization without symptoms to fulminating diarrhea and intestinal hemorrhage. The dissemination of the parasite via invasion of the intestinal epithelium allows the trophozoites to invade extra-intestinal sites, most usually the liver. Without treatment, the amebic liver abscesses may continue to enlarge and, if ruptured, cause mortality owing to acute peritonitis. Cases of clinical amebiasis have been reported worldwide, in particular in under-developed and developing counties in Africa, South America, the Indian subcontinent, and Mexico. It has been estimated that approximately 50 million individuals are infected with E. histolytica and about 100,000 people die of invasive amebiasis annually, making it the third leading parasitic cause of death, after malaria and schistosomiasis.1 The host-parasite interaction in human amebiasis is very complicated, and different aspects of innate immunity of the human host against the parasite still are unknown. New insights into the pathogenesis of amebic infections have come from development of in vitro and in vivo models of disease, new molecular and genetic approaches, the identification of key factors in E. histolytica pathogenesis, recognition of the mechanisms of evasion from the host’s harmful responses, and detection of crucial elements of the host immune responses both innate and acquired. In this chapter, we discuss the innate immunity of human hosts against the parasite and the most important parasite virulence factors and survival strategies that are implicated in pathogenesis.

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Solaymani-Mohammadi, S., Petri, W.A. (2008). Intestinal Invasion by Entamoeba histolytica . In: Burleigh, B.A., Soldati-Favre, D. (eds) Molecular Mechanisms of Parasite Invasion. Subcellular Biochemistry, vol 47. Springer, New York, NY. https://doi.org/10.1007/978-0-387-78267-6_18

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