INFECTION OF THE INTERMEDIATE HOST 
169 
TABLE YII 
Strain Variations in the Length of the Intrinsic Incubation Period of P. falciparum . 
Strain 
Days to first fever of 100° F 
Mean 
0 7 8 9 
10 
11 
12 
13 
14 
15 16 17 
18 + 
Tot. 
Coker . 
1 . 1 
4 
1 
14 
4 
7 
7 1 . 
2 
42 
13.1 
Long . 
1 1 1 ... 
11 
3 
34 
9 
24 
6 5 1 
3 
100 
12.9 
TABLE VIII 
Strain Variation in the Length of Intrinsic Incubatton Period of P. vivax 
Strain 
Days to first fever of 100° F 
Mean 
6 7 8 
9 
10 
11 
12 
13 
14 
15 
16 
17 
18 
19 
20 
21 + 
Tot. 
Madagascar* 
3 8 16 
34 
60 
59 
96 
99 
109 
78 
62 
50 
29 
16 
13 
14 
746 
13.6 
McCoy . 
. 3 
7 
12 
40 
33 
43 
32 
23 
23 
15 
10 
5 
4 
4 
254 
13.6 
* After James (1931). 
nance are equal. On the other hand, the 
indigenous Dutch strain previously men¬ 
tioned is stated to have a “normal” incu¬ 
bation of from 15 to 30 days, with an 
average length of 21 days (de Buck 1936). 
The number of merozoites formed at 
schizogony varies with these different 
strains of P. vivax as follows: 
Madagascar Av. 17-18 (Swellengrebel and de Buck 
1938) 
Dutch Av. 12-13 (Swellengrebel and de Buck 
1938) 
McCoy Av. 16.1 
Simultaneous Inoculation with Two 
Species of Parasites 
A period of intensified malaria transmis¬ 
sion is not infrequently followed by two 
epidemic waves. The first wave, consisting 
largely of recognized infections with P. 
falciparum, is closely connected chronologi¬ 
cally with the transmission period; the sec¬ 
ond wave, occurring in the following year, 
is less obviously related, and consists of 
infections with P. vivax. This is exempli¬ 
fied by the data presented in Fig. 1. 
It has been shown (Boyd and Kitchen 
1937f) that anopheline mosquitoes may be 
simultaneously infected with both P. vivax 
and P. falciparum, and can simultaneously 
transmit both species. Neither species of 
parasite present in a simultaneous infection 
appears to exercise a significantly injurious 
or inhibitory effect upon the other (Boyd, 
Kitchen and Kupper 1937). 
While both species of parasites are de¬ 
tectable in the blood of patients simul¬ 
taneously infected at about the same time 
after the lapse of a “normal” incubation 
period, the center of the stage is soon as¬ 
sumed by falciparum, as it is the first to 
increase to densities in excess of the mini¬ 
mal microscopical level, while the first 
clinical reaction displays the characteristics 
of the disease which it initiates. The ex¬ 
hibition of quinine at this period, so neces¬ 
sary to restrain the exuberant multiplica¬ 
tion of P. falciparum, has a more destruc¬ 
tive effect on the lagging P. vivax, which is 
driven down to submicroscopic levels. In 
some individuals who did not receive a 
great deal of quinine, a return of P. vivax 
is noted after several weeks, during which 
time P. falciparum may markedly decline. 
Thereupon clinical activity displays all the 
characteristics of vivax malaria. P. falci¬ 
parum may later return to clinical levels 
while P. vivax is still abundant, in which 
