IMMUNITY TO HUMAN MALARIA 
237 
decision can be reached. Christophers 
(1924) was able to compare the suscepti¬ 
bility to infection in the same age groups 
but of different origin and of children who 
presumably had not been exposed to ma¬ 
laria. He found that in groups up to 6 
years of age the first 2 years of residence 
in malarial districts showed the highest rate 
of infection and the highest parasite count. 
There was only a slight difference in this 
age group in children born in the hyper¬ 
endemic community and those born else¬ 
where and moving into the area. However, 
in age groups over 6 years of age there 
appeared to be a marked resistance in chil¬ 
dren moving into the area. He was not 
able to preclude the possibility that the 
resistance shown by these children had not 
been acquired by exposure to malarial in¬ 
fections previous to entering the hyperen- 
demie center. 
Boyd and Stratman-Thomas (1933d) 
have very good evidence that the resistance 
to P. vivax found in negroes is a natural 
racial condition and not influenced by any 
previous exposure to this species of malaria. 
They have found it necessary to use P. 
falciparum in treating negro paretics. The 
few cases that show parasites have too few 
febrile attacks to be of therapeutic value. 
Two test cases each bitten by 16 mosquitoes 
infected with P. vivax failed to become in¬ 
fected. Twelve white patients each bitten 
by from 1 to 3 of the same mosquitoes all 
became infected. In another experiment a 
negro child 5 years of age was inoculated 
with P. vivax by allowing infected mos¬ 
quitoes to feed at two different times. No 
infection developed. Examinations over a 
long period of time previous to the test 
did not show any indication of an infection. 
Proof that the refractoriness of negroes to 
P. vivax is a natural resistance and not 
acquired as the result of infection is lack¬ 
ing, but this one case studied by Boyd is 
indicative that there is a natural racial 
tolerance in the negro to P. vivax infections. 
The aboriginal natives of one of the 
hyperendemic areas in India were no less 
susceptible than other tribes who were 
more recent immigrants to the commun¬ 
ity, according to observations made by 
Christophers (1924). 
In the absence of any marked resistance 
among the negroes to other species of ma¬ 
laria it appears that a racial tolerance must 
have been developed somewhere in the past 
and has become inherent in the race. It is 
possible that P. vivax has been endemic 
in the negro race for centuries and 
through long association the natural re¬ 
sistance shown by map to plasmodial in¬ 
fections has become enhanced to the degree 
of almost complete resistance. The fact 
that there is a preponderance of P. falci¬ 
parum in Africa at the present time lends 
credence to the hypothesis of the close asso¬ 
ciation of P. vivax and the negro race. 
Malarial infections have also been ob¬ 
served to reappear following accidents, 
operations and child-birth. Garnham 
(1938) believes the loss of large numbers 
of reticulo-endothelial cells with the pla¬ 
centa is responsible for the reappearance 
of malaria infections following child-birth. 
Likewise an accident or a major operation 
that requires the full component of the 
body’s resistance may leave the body with¬ 
out sufficient protection from the malaria, 
whereupon latent infections may become 
active. It is thought that diseases and 
similar factors may act in the same way as 
blockade of the reticulo-endothelial tissues. 
Effect of Drug Treatment on Immunity 
There is considerable disagreement on 
the question of the effect of drugs either 
directly or indirectly on the immunity to 
malaria. The most important factors ap¬ 
pear to be the period during the infection 
at which the drug is administered and the 
extent of the treatment. When the treat¬ 
ment is begun early in the development of 
the infection before the parasites have mul¬ 
tiplied to any considerable extent and is 
continued so long that the infection does 
not show up after the treatment is stopped, 
it has been found that no immunity devel¬ 
ops. On the other hand, if the infection is 
allowed to run its course the resultant im¬ 
munity is highly effective in preventing an¬ 
other infection. Yorke and Macfie (1924a) 
