28 The Rice Institute Pamphlet
amebae, but, when it is injured by virulent bacteria and their toxins, the
way is paved for the amebae, which then invade the tissues and produce
the characteristic lesions. On the other hand, there is some evidence at
present that the amebae take a more active part in this process, and some
authors even believe that penetration of the tissues can be effected by
their own unaided efforts (Meleney et al., 1939; Phillips & Bartgis, 1954;
Neal, 1957). Nevertheless, the available facts strongly support the view
that bacteria play an important contributory role in the production of
lesions in amebiasis (Porter, 1953; Phillips et al., 1955).
In addition to bacteria, it has been suggested that other causes of dis-
turbed gastro-intestinal function may expose the intestine to invasion by
E. histolytica, such as abnormal secretory function, temperature fluctua-
tions and irritant foodstuffs (Westphal, 1938), as well as inflammatory and
erosive processes manifested by colitis (Deschiens, 1950a). Some of these
factors are held to be responsible for the prevalence of clinical amebic
dysentery in the tropics, where inadequacies of diet and bacterial assault
commonly provoke gastro-intestinal disorders and a lowering of the host’s
resistance. It has also been shown that variation in the host’s diet and its
vitamin content may be predisposing factors in amebiasis (this question
has recently been fully reviewed by Porter, 1953; Frye, 1955; and Chan-
dler, 1955, 1957). These are the main conditions which are thought to in-
fluence the course of amebic infection, but the data are inconclusive and
it is obvious that the question of pathogenesis in this disease is in need of
further investigation.
A good illustration of the potential pathogenicity of carrier strains from
endemic areas of clinical amebiasis is provided by observations made
during the First World War. On the one hand, it was shown (Woodcock,
1917) that 20% of the normal population of India were symptomless car-
riers of E. histolytica. On the other hand, it was found that both in Egypt
(Woodcock, 1917) and in Mesopotamia (Ledingham, 1920) cases of ame-
bic dysentery were far more frequent among the Indian troops than
among British troops operating in these countries. In the light of our
present knowledge of the etiology of amebiasis, it is conceivable that the
Indians already harboured pathogenic strains, the dormant virulence of
which was activated when amebic carriers were exposed to unfavorable
conditions on the front. As regards the low incidence of disease among
the British, it was probably due to the fact that local invasive strains had
not yet succeeded in infecting many of them.
Attenuation of virulence. One of the puzzling phenomena in amebiasis
is the failure of virulent exotic strains to establish themselves in temperate
regions. Thus, after the First and Second World Wars, when troops which
had been exposed to infection with virulent strains of E. histolytica in