156 
MALARIA 
the epidemic. The epidemic, according to 
Gill, broke out everywhere on virtually the 
same day all over the epidemic area, and 
could not therefore have been built up by 
an unusual prevalence of anopheles. This 
is characteristic, however, of malaria epi¬ 
demics which are always explosive and do 
not spread centrifugally from a few foci 
of infection, as in many diseases. The 
seedbed is scattered far and wide and the 
epidemic is limited to the area in which 
conditions of spread are favorable. It can 
not spread beyond this area, and it does not 
actually spread within it, since the new 
cases arise in every part of it at once, giv¬ 
ing a static character to the epidemic. 
We have no good proof that the observed 
phenomena cannot be produced by the ordi¬ 
nary gametocyte prevalence, through the 
agency of an enormously increased anophe- 
line population. 
We have been discussing a malaria situ¬ 
ation which is mainly epidemic in char¬ 
acter with an endemic seedbed. Under 
more intense transmission, this is converted 
into a type of malaria which is chiefly 
endemic, but with periodic waves of in¬ 
creased incidence. Mixed infections pre¬ 
vail with a consequent preponderance of 
chronic cases. Such malaria is character¬ 
ized by: 
(a) Reduced epidemic manifestations. 
(b) Adult immunity well developed. 
(c) Splenomegaly, high parasite densities and 
high carrier incidence restricted to the 
earlier age groups. 
This well-established group immunity is 
the result of a high transmission rate dur¬ 
ing a long season. 
The commonest measure of endemicity 
is the spleen rate. However, Wilson and 
Wilson (1937) point out that frequency of 
infection in the non-immune portion of the 
population—that is in early life—is the 
most accurate index of endemicity. A re¬ 
duction in the parasite count reveals devel¬ 
oping immunity. Variation with age in 
spleen and parasite rates is the best basis 
for classification of communities according 
to the degree of developed immunity. It 
is clear that in localities with seasonal 
transmission, the spleen and parasitic rates 
taken during the interepidemic period will 
measure the importance of the endemic 
component of the local malaria, while those 
secured during or immediately after the 
transmission season will indicate the extent 
of the epidemic oscillation. 
Summary 
Malaria in the community derives its 
character from the rate and constancy of 
transmission, and from the immunological 
diversity of the parasites. The frequency 
of infection depends on the one hand, on 
the density and efficiency of the anopheline 
vectors, and particularly their host-rela¬ 
tionship to man, and on the other, on the 
incalculable fluctuations in the source of 
infection, the gametocyte carriers. At 
every level, the transmission rate, thus 
determined, creates a corresponding toler¬ 
ance which is made up of highly specific 
reactions to the numerous and immuno- 
logically independent strains and species 
of the parasite. The picture is one of 
growing multiplicity of mixed infections, 
resulting in chronic malaria and the atten¬ 
dant phenomenon of mutual parasite an¬ 
tagonisms. The mass effect, however, of 
group immunity at high levels of intensity 
is one of powerful protection of the older 
age groups and the shifting of the struggle 
to childhood or even infancy. The blood 
picture of the individual and the parasite 
formula of the group are resultants of com¬ 
plex factors arising from the biological 
diversity of the plasmodia and the differ¬ 
ential immune reactions of the human host. 
The discontinuity of transmission due to 
seasonal influence is responsible for the 
epidemic waves characteristic of endemic 
malaria. Only very rarely do we find pure 
epidemics without an endemic seedbed, or 
a hyperendemic situation without seasonal 
or annual exacerbations. The rate of trans¬ 
mission is best measured by the frequency 
of inoculation among infants, and the de- 
gree of endemicity is indicated by the de¬ 
veloped immunity which determines the 
proportion of acute cases, the scope of the 
epidemic manifestations, and the age dis¬ 
tribution of splenic enlargement, parasite 
densities and gametocyte carriers. 
