IMMUNITY TO HUMAN MALARIA 
235 
gous but little heterologous immunity to 
the latter species. 
Thomson (1934) reports that in the dis¬ 
trict around Kisumu “Immunity to quar¬ 
tan malaria develops early and rapidly 
becomes well-nigh perfect.” Ciuca states 
that quartan malaria is less likely to recover 
spontaneously than benign tertian and 
although 36 per cent of cases become im¬ 
mune after the first infection, seven rein¬ 
oculations are necessary to increase the 
number to 100 per cent. Young and 
Coatney (1940) report almost complete 
protection against a second inoculation of 
quartan malaria. In one or two cases a 
few parasites were observed, but no clin¬ 
ical attack appeared. 
Reinoculations of P. knowlesi following 
recovery from primary attacks in man in¬ 
dicate that a good homologous immunity 
is developed. Ciuca, Tomescu, and Baden- 
ski (193?) had only one febrile attack in 
20 reinoculations; Milam and Coggeshall 
(1938) reported no febrile attack following 
a second inoculation. In five of Ciuca’s 
patients a slight rise in the parasite count 
was noted. Although James and Ciuca re¬ 
ported that infections of P. knowlesi pro¬ 
duced a heterologous immunity to P. vivax, 
the reciprocal cross is evidently not pro¬ 
tective. Milam and Kusch (1938) inocu¬ 
lated 7 paretic patients with P. vivax that 
had been previously treated with infections 
of P. knowlesi. They did not state the 
nature of the resulting infections but in¬ 
dicated that they were normal. 
Comparison op Immunity in Infections 
Initiated with Sporozoites and 
with Trophozoites 
Sinton (1939b) inoculated 22 patients 
with sporozoites and compared the primary 
attacks with those following blood inocu¬ 
lations. There appeared to be very little 
natural resistance to the sporozoite infec¬ 
tions. On the other hand the primary at¬ 
tacks of the patients inoculated with in¬ 
fected blood were much shorter and less 
intense. Later he (1940b) compared the 
immunity resulting from the two methods 
of infection and found that the patients 
with sporozoite inoculations acquired a 
greater degree of resistance than those with 
blood inoculations. Likewise, when the re¬ 
inoculating dose was sporozoites the result¬ 
ing infection was more pronounced than 
when' infected blood was used. James, 
Nicol and Shute (1932) could not differ¬ 
entiate between infections of P. falciparum 
one group of which was inoculated with 
sporozoites and the other with trophozoites. 
Resistance to reinfection appears to be 
against the trophozoite stage of the para¬ 
sitic cycle of P. vivax and has very little 
effect on the sporozoites. According to 
Boyd and Kitchen (1936b) a reinoculation 
with sporozoites results in the usual incu¬ 
bation period before the resistance comes 
into play, but the resulting trophozoites in 
the erythrocytes are as susceptible as those 
following blood inoculations. Jeraee(1934) 
says that P. vivax infections induced by 
sporozoites are more likely to produce 
quotidian febrile attacks than when in¬ 
duced by trophozoite inoculations. These 
observations have led some workers to 
adopt the sporozoite inoculation method of 
giving infections to their patients, either 
by allowing infected mosquitoes to transfer 
the sporozoites by feeding on the patients 
to be infected or by injecting the sporozoites 
obtained from the mosquitoes. 
Duration op Immunity 
A very important question regarding ma¬ 
larial immunity is its duration. The im¬ 
munity to avian malaria has been estab¬ 
lished as lasting while the infection remains 
latent. If the bird loses the infection the 
immunity very soon disappears. Thomson 
(1933) states that immunity to human ma¬ 
laria, likewise, is associated with a latent 
infection. Others have failed to find a 
latent infection in cases that proved to be 
immune. In numerous cases subinocula¬ 
tions have been made with the idea of de¬ 
termining the presence or absence of a 
latent infection. If the subinoculated in¬ 
dividual becomes infected this establishes 
the infection in the case, but on the other 
hand no infection does not prove the ab¬ 
sence of a latent infection. Splenectomy 
