The name is absent

Host-Parasite Relations in Amebiasis 31
serological response, which is weak in the case of intestinal involvement
and stronger in the case of amebic hepatitis (Hussey & Brown, 1950;
Heinz et al., 1956; Meleney, 1957).

Among other reactions for the demonstration of immune bodies in
amebiasis, should be mentioned an intradermal test (Leal, 1953), and
tests in which the presence of antibody in immune serum is revealed by
immobilization of the amebae (Cole & Kent, 1953; Brown & Whitby, 1955;
Valentino, 1956) or by their fluorescence when combined with fluorescein-
tagged antibody (Goldman, 1953).

If the foregoing data on immunity in amebiasis are examined in the
light of our present knowledge of the host-parasite relations, most of them
will not stand the test of critical analysis. And, indeed, individual variation
in susceptibility to infection with virulent strains of E. histolytica is prob-
ably due mainly to diversity in the intestinal flora, rather than to disparity
in the innate immunity of different persons (as already suggested by
Nauss & Rappaport, 1940, and Porter, 1953). It would seem, however, that
in endemic areas the indigenous population might possess a degree of
racial immunity. Thus, according to Boyd (1957), in 1930-1935 the in-
cidence of amebic dysentery among British troops serving in India was
higher than among Indian troops, in spite of the prevalence in that coun-
try of pathogenic strains of E. histolytica. Likewise, the absence of symp-
toms may be due either to infection with the avirulent race or to a lack
of factors capable of activating the dormant virulent race. There is also
fairly convincing evidence that the human host does not acquire immu-
nity in the course of his infection. There remain the serological reactions,
which do seem to point to some immunological response to amebic in-
fection. Furthermore, the absence of inflammatory reactions to invasion
by the amebae also indicates that the mechanism of defense is repre-
sented by humoral rather than cellular factors (Anderson et al., 1953).

Since no complement-fixing rection is produced in infections restricted
to the lumen of the gut, it would seem that the great majority of cases of
amebiasis develop no specific immunity against E. histolytica. As regards
cases in which invasion of the tissues has taken place, only a slight im-
mune response is detectable in them by serological reactions. From these
facts it can be inferred that the amebic antigen is too weak to stimulate
appreciable antibody formation in the human organism. In this respect
E. histolytica is like many other pathogenic protozoa, the antigenicity of
which is of a low grade, producing only transient immunity. The anti-
genic lability of protozoa has been attributed to the predominance in
their body of lipid haptens, which are unable to induce lasting immunity,
in contrast to carbohydrate haptens in bacteria, which provide powerful

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