MORPHOLOGY, LIFE CYCLE AND PHYSIOLOGY OF P. MALARIAE 
29 
established that P. malariae requires the 
longest time of any of the human parasites 
to complete its sporogonous cycle. As indi¬ 
cated in the discussion of the developmental 
forms, the time reported for the complete 
development of the extrinsic cycle in the 
mosquito varies widely. 
Kligler and Mer (1937) found it required 
27 days at 24° C and 24 days at 27° C to 
complete the cycle in A. elutus. Iyengar 
(1932) found sporozoites in glands after 
infective feedings as follows: A. ludlowi 
var. sundaica, 21 days; A. stephensi, 10, 14 
and 19 days. 
Hylkema (1920) found the developmen¬ 
tal period in A. ludlowi to be 11 to 13 days. 
De Buck (1935) found glands infected with 
sporozoites in 15 days at 27° C and a rela¬ 
tive humidity of 90. Mayne (1932) found 
sporozoites the twenty-fifth day after feed¬ 
ing; Marotta and Sandicchi (1939) in 24 
days. 
Transfer to Man. After the sporozoites 
of P. malariae pass into the tissues of man 
by the bite of an infected mosquito, the 
development of the disease usually requires 
a longer period than in the other species. 
Knowles and Senior-White (1927) give this 
as to 18 to 21 days. Boyd (1935, 1940) 
found the prepatent period of the para¬ 
sites to be from 28. to 37 days, the parox¬ 
ysms occurring a few days later. De Buck 
(1935) found the “intrinsic” incubation 
period to be from 24 to 25 days in several 
cases. Usually the symptoms occurred a 
few days later. Mer (1933) found that 
parasites appeared in the blood stream from 
26 to 31 days after the bite of infected 
mosquitoes. Hylkema (1920) gave 12 days 
as the incubation period in a self-inflicted 
infection. However, as he was bitten on 
successive days, there seems to be some ques¬ 
tion as to the accuracy of this estimate. 
Marotta and Sandicchi (1939) found the 
incubation period in two experimentally 
infected patients to be 23 and 29 days. 
Physiology 
This is probably the most neglected field 
in human malariology, with the result that 
very little is known about the life functions 
of these important disease producers. 
There are general statements that resi¬ 
dues result from the metabolic processes of 
the parasites and that these, when released 
into the blood stream, contribute to the 
paroxysmal attack. There is little real evi¬ 
dence to support this view. There is still 
uncertainty whether the parasites produce 
toxins at all, and that if they do, these 
toxic products initiate the paroxysm. 
Comes (1922) concludes that in P. vivax 
and P. malariae the pigment is formed by 
the activity of the alimentary vacuole under 
the influence of the adjacent nucleus. If it 
can be assumed that the malarial pigment 
of P. knowlesi and of the human parasites 
are similar, it would appear from the work 
of Sinton and Ghosh (1934a and 1934b), 
Ghosh and Sinton (1934), and Ghosh and 
Nath (1934) that the pigment of the P. 
malariae parasite originates from the hemo¬ 
globin of the infected red blood cell by 
direct metabolic action of the parasite. 
