232 
MALARIA 
the conditions for transfer become op¬ 
timum. By correlating these facts it has 
been possible to predict fairly accurately 
when and where an epidemic of malaria 
may be expected. Following an epidemic 
Christophers (1924) found a high spleen 
rate which began to fall off rapidly after 
about 2 years, if the infection rate was 
low. The average length of time before 
another epidemic may occur in the area 
is 6 years. Generally at the end of that 
time the spleen rate has fallen to about 
10 per cent. In hyperendemic centers 
where a constant infection rate is main¬ 
tained the resistance appears to be kept 
at a high degree and no epidemics occur. 
Not until Wagner-Jauregg introduced 
the malaria therapy of paresis were there 
any controlled experiments in immunity to 
human malaria. This technique has been 
used in various countries and has added 
much to our knowledge of malaria. 
Yorke and Macfie (1924a) first pointed 
out the fact that on recovery from an 
infection of P. vivax the patient showed a 
considerable degree of resistance to rein- 
ocUlation with the same strain of parasites. 
That recovery from normal attacks of in¬ 
duced malaria produces in the patient a 
resistance to further attacks of the same 
strain of parasite has been amply demon¬ 
strated by Antic (1925), James (1926), 
Plehn (1926), Ciuca, Ballif, and Chelar- 
escu-Vieru (1928), Boyd and Stratman- 
Thomas (1933c) and others. Most of these 
workers also observed that there was some 
resistance to infections with other strains 
of the same species of parasite, but none 
to other species. This fact is made use of 
in the malarial therapy of paretics where 
it is necessary to treat a patient more than 
once. 
Until mosquitoes were available for con¬ 
trolled transfers the inoculations were made 
by injecting a small amount of blood from 
an infected individual into a susceptible 
person. Following recovery from the sub¬ 
sequent attacks, provided the attacks were 
allowed to run their normal course, it was 
impossible in most cases to produce further 
attacks by inoculations with the same strain 
of parasite. In chronic eases showing a 
few parasites in the blood following re¬ 
covery from the primary attack a second 
inoculation generally produced an increase 
in the number of parasites in the periph¬ 
eral blood, but no further febrile at¬ 
tacks in the majority of cases. This led 
Sinton, Harbhagwan, and Singh (1931) to 
suggest that the resistance was manifested 
in two ways, an effect on the toxic products 
producing the symptoms, and a reduction 
in the number of parasites in the blood. 
The primary attack of P. vivax malaria is 
followed by one or more recrudescences. 
These attacks are light and generally end 
in spontaneous recovery. Then follows a 
period in which no parasites can be found. 
This period, however, lasts for only about 
8 to 10 months and a recurrence of fever 
and appearance of parasites follows. The 
recurrence generally ends spontaneously 
after one or more recrudescences within a 
period of 2 or 3 weeks. Rarely is the recur¬ 
rence as severe as the primary attack even 
though the parasite count may be almost 
as high. Febrile attacks are fewer in num¬ 
ber and occur for a period of only a few 
days. Previous to the recurrence a rein¬ 
oculation may result in a slight attack, but 
afterwards it is impossible in most cases 
to get any response from reinoculations 
with the same strain of parasites. 
Gill (1933) thinks that the immunity 
following induced malaria may not be 
analogous to the resistance produced in 
normal individuals since the subjects used 
in such experiments are syphilitic, and the 
treatment with arsenical drugs, and reac¬ 
tions produced both by these drugs and the 
disease may materially alter the reaction 
of the body to the malarial parasites. 
Development of Immunity 
As indicated above very little immunity 
follows a single infection unless that infec¬ 
tion is continued over a long period of time 
by relapse and' recrudescences. Termina¬ 
tion of the infection at an early stage by 
drug treatment has been found to interfere 
with the normal development of the im¬ 
munity. In controlled cases of therapeutic 
