Entamoeba histolytica, a protozoan parasite, is the etiologic agent of
amoebiasis in humans. It exists in two forms--the trophozoite which i
s the active, dividing form, and the cyst which is dormant and can sur
vive for prolonged periods outside the host. In most infected individu
als the trophozoites exist as commensals. In a small percentage of inf
ections, the trophozoites become invasive and penetrate the intestinal
mucosa, causing ulcers. The trophozoites may reach other parts of the
body--mainly liver, where they cause tissue necrosis, leading to life
-threatening abscesses. It is thought that pathogenesis of infection b
y Entamoeba histolytica is governed at several levels, chief among the
m are (i) adherence of trophozoite to the target cell, (ii) lysis of t
arget cell, and (iii) phagocytosis of target cell. Several molecules w
hich may be involved in these processes have been identified. A lectin
inhibitable by galactose and N-acetyl-D-galactosamine is present on t
he trophozoite surface. This is implicated in adherence of trophozoite
to the target cell. Various amoebic pore-forming proteins are known,
of which 5 kDa protein (amoebapore) has been extensively studied. Thes
e can insert into the lipid bilayers of target cells, forming ion-chan
nels. The phagocytic potential of trophozoites is directly linked to v
irulence as measured in animal models. Factors like association of bac
teria with trophozoites also influence virulence. Thus, pathogenesis i
s determined by multiple factors and a unifying picture taking into ac
count the relative contributions of each factor is sought. Recent tech
nical advances, which includes the development of a transfection syste
m to introduce genes into trophozoites, should help to understand the
mechanism of pathogenesis in amoebiasis.