New Concepts Regarding the Pathogenesis of Amebiasis

Abstract

Our understanding of the pathogenesis of amebiasis has progressed significantly since Dr. Braude's description of the major clinical syndromes of amebic liver abscess. His hypothesis that invasive amebic strains must be resistant to complement-mediated lysis has been confirmed. We have also shown that Entamoeba histolytica activates complement by a unique mechanism, i.e., cleavage of C3 by an extracellular cysteine proteinase. Cysteine proteinases are important virulence factors encoded by at least three genes; one gene, acp1, is unique to invasive strains. The amebic cysteine proteinases are homologous to proteinases released by transformed cells and may represent a common mechanism of tissue invasion. The initial division of Entamoeba into invasive E. histolytica and noninvasive Entamoeba dispar by isoenzymes has been supported by genetic differences between amebae. Thus, a model of pathogenesis differentiating between two separate species of Entamoeba best explains the epidemiology, clinical syndromes, and pathology of amebiasis.

Intestinal parasitic infection and associated symptoms in children attending day care centres in Trujillo, Venezuela

“…1993). Entamoeba dispar , a protozoan morphologically identical to E. histolytica , is a non‐pathogenic gut commensal (Reed 1995). The clinical course of infection with larger parasites, such as the helminths, can vary widely from asymptomatic to severe secondary complications.…”

“…Among the protozoa, Giardia duodenalis and Entamoeba histolytica have been associated with persistent and acute diarrhoea (Utzinger et al 1999;Newman et al 2001), while Blastocystis hominis and Cryptosporidium parvum tend to cause marked symptoms primarily in immunocompromised hosts (Doyle et al 1990;Chacin-Bonilla et al 1993). Entamoeba dispar, a protozoan morphologically identical to E. histolytica, is a nonpathogenic gut commensal (Reed 1995). The clinical course of infection with larger parasites, such as the helminths, can vary widely from asymptomatic to severe secondary complications.…”

Molecular cloning and characterization of a cathepsin B from Angiostrongylus cantonensis

“…The cells were cultured in RPMI 1,640 medium supplemented with 25 ng/ml GM-CSF, 25 ng/ml IL-4, and 25 ng/ml Flt-3 ligand for 8 d, and were further cultured for 24 h untreated or treated with 1.0 μg/ml LPS, 1.0 μg/ml LPS+5.0 μg/ml rAcCPB. Non-adherent and loosely-adherent cells were then harvested and analyzed by flow cytometer 1995; Shenai et al 2000), molting (Tort et al 1999), and more importantly, host invasion (Dvorak et al 2008;Dolecková et al 2009;Que and Reed 2000;Reed 1995) and immune evasion (Alexander 1998;Draper 1998;Mckerrow et al 2006), suggesting key molecules in parasite-host interaction. These features validate cathespin Bs as prime strategic targets for parasite diseases control (Duschak and Couto 2009;Smooker 2010).…”

Primary cutaneous amoebiasis: case report with review of the literature

“…These include proteolytic enzymes, release of cell free cytotoxins, contact‐dependent cytolysis and phagocytosis 1 . It has also been postulated that a mutation in certain strains of amoebae and their resistance to complement mediated lysis is responsible for its virulence 30,31 . Recently, cases of cutaneous acanthamoebiasis have been reported in patients with AIDS, thereby suggesting vulnerability of immunocompromised patients 32 .…”

“…1 It has also been postulated that a mutation in certain strains of amoebae and their resistance to complement mediated lysis is responsible for its virulence. 30,31 Recently, cases of cutaneous acanthamoebiasis have been reported in patients with AIDS, thereby suggesting vulnerability of immunocompromised patients. 32 However, there is no such report regarding cutaneous amoebiasis, and our patient was HIV negative.…”