MALARIA AND THE COMMUNITY 
155 
chronic malaria in the individual and en¬ 
demic malaria in the community. Endemic 
malaria is malaria which is constantly pres¬ 
ent in a degree to give a measurable amount 
of morbidity or splenomegaly. Any rapid 
increase of acute cases is called an epidemic 
and may take the form of an outbreak in a 
small community, or the expected seasonal 
wave of morbidity in temperate climates, 
or a widespread regional exacerbation of 
the disease on a large scale. Almost al¬ 
ways, the epidemic manifestations have an 
endemic basis. 
It is possible of course to have pure epi¬ 
demic malaria, caused by the advent of a 
carrier or carriers into an uninfected area 
where there are anopheline vectors. This 
happens once in a while in the northern 
states. However, where periodic epidem¬ 
ics occur, the sources of infection are usu¬ 
ally present, widely though often sparsely 
distributed throughout the population. If 
there is little evidence of malaria in the 
interepidemic season, this is called hypo- 
endemic malaria. Such a situation comes 
about through a very low transmission rate 
or a very short transmission season. Still, 
the malaria may have a certain intensity in 
summer and carry -on from year to year. 
In western Spain the summer epidemic may 
involve 30 per cent of the population, yet 
the winter parasite and spleen rates may 
be nearly zero. The inhabitants have al¬ 
most but not quite time enough to recover 
between seasons. 
At the other extreme, where transmission 
is constant at a higher or lower level, we 
may have pure endemic malaria, although 
this too is rare. It is approached in such 
tropical places at Laos in Indo-China where 
malaria prevails everywhere without inter¬ 
mission, and with little seasonal or annual 
variation. Epidemics are unknown, though 
hospital returns indicate an increased prev¬ 
alence during the rains. Where the trans¬ 
mission rate is very high and constant, com¬ 
plete im m unity may be established, as in 
certain Bantu tribes on the East African 
coast, described by D. B. Wilson (1939). 
Everyone is infected a dozen times a year 
and there is little illness after 2 or 3 years 
of age. No ill effects in older children or 
adults are seen which can be attributed to 
malaria. The parasite counts in such a 
population are very interesting. They 
range from 8,000 per cc in infants to less 
than 200 in the age group 9-25. The toler¬ 
ance is like immunity to sunburn, obtained 
only by frequent and prolonged exposure. 
Between these extremes lies the broad 
field of endemic malaria with periodic epi¬ 
demic waves. Transmission is seasonal, 
and if it is high, we have overlapping in¬ 
fections and chronic cases, while if it is low. 
the infections are widely spaced and the 
cases are mainly acute. The malaria is 
called hyperendemic if the spleen rate is 
constantly above 50, and sporadic or hypo- 
endemic if the winter spleen rate is insig¬ 
nificant. 
Within these limits two general situa¬ 
tions occur, depending on the transmission 
rate, which are not sharply divided from 
each other, but grade from one into the 
other. One of these is characterized by 
poorly developed group immunity, and the 
type is chiefly epidemic, with a permanent 
and measurable endemic seed-bed. Such 
malaria can be identified by: 
(a) Its high seasonal peaks. 
(b) Little adult immunity to infection. 
(c) No pronounced tendency to restrict spleno¬ 
megaly, high parasite densities and car¬ 
rier incidence to the early age groups. 
The high seasonal and periodic increases 
in malaria may have several causes: a sea¬ 
sonal increase in anopheline production 
due to rain or lack of rain depending on the 
species; the introduction of a new anoph¬ 
eles, as in Calcutta and northeastern Bra¬ 
zil, which can build up serious epidemics 
on the foundation of a mild pre-existing 
endemic malaria; or possibly a wave of 
gametocyte production in the population 
provoked by some environmental cause. 
Gill (1938a) has recently called attention to 
this phenomenon in connection with the 
great Ceylon epidemic of 1934. He be¬ 
lieves this began with a simultaneous out¬ 
break of relapses in latent cases due to un¬ 
usual meteorological conditions, and cites 
in support of his theory the low incidence 
among babies and unimportant mortality 
in the population during the first weeks of 
