THE PHYSIOLOGICAL PATHOLOGY OP MALARIA 
225 
presence of parasites' in the peripheral 
blood. They suggested that the clinical 
phenomena were evidences of hypersensi¬ 
tivity to the parasites and that spontaneous 
remission was an evidence of desensitiza¬ 
tion. 
Kehar and Harbhagwan (1937), report¬ 
ing observations made by Mulligan, found 
a considerable increase in the sedimentation 
rate during the acute phases of human in¬ 
fections with both P. vivax and P. falci¬ 
parum. 
Blood Lipoids 
Cholesterol and lecithin have been mea¬ 
sured in a few instances in both human 
and monkey malaria. Kehar (1937) found 
an increase in cholesterol in human malaria 
during the rigor stage and a decrease to 
below normal during the afebrile periods 
before and after the paroxysm as well as 
in chronic infections. There was a high 
correlation between the cholesterol content 
and the temperature but the fall in choles¬ 
terol preceded the fall in temperature. In 
monkeys infected with P. hnowlesi he found 
a slight fall in cholesterol during the pri¬ 
mary acute attack. Since this infection is 
not characterized by paroxysms of fever, 
as in human malaria, the relation of the 
cholesterol to such episodes could not be 
determined. In monkeys dying of over¬ 
whelming infection without hemoglobinuria 
the cholesterol continued to fall until death. 
In monkeys in which hemoglobinuria oc¬ 
curred as a terminal event there was a 
sharp terminal rise in cholesterol. Lecithin 
determinations demonstrated a close corre¬ 
lation between the amount of this substance 
and the amount of cholesterol in the serum 
both before and during malaria infections. 
Krishnan, Ghosh and Bose (1936) also 
studied the cholesterol changes in monkeys 
infected with P. hnowlesi. They found 
wide fluctuations during the early period 
of parasitemia and a distinct tendency 
toward a decrease when the infection be¬ 
came intense. If the cholesterol remained 
normal or rose to normal or above after the 
occurrence of hemoglobinuria the hemoglo¬ 
binuria invariably disappeared. These 
authors concluded that cholesterol was 
capable of exerting an inhibiting influence 
on hemolysis and hemoglobinuria resulting 
from intense infection in monkeys. Kehar 
(1937), however, was unable to protect 
monkeys from the onset of hemoglobinuria 
by the administration of cholesterol. 
Blood Sugar 
Sinton and Kehar (1931) reviewed the 
literature on the blood sugar in malaria and 
made observations on human cases of P. 
vivax and P. falciparum infections. There 
was always a rise during fever, sometimes 
to a level slightly above normal limits 
(maximum 149 mg per cent) and a fall 
after the fever to a level usually slightly 
higher than before the fever. In three 
patients followed at short intervals during 
the febrile period it was found that the 
peak of the blood sugar level was reached 
slightly before the peak of temperature, 
and began to decline slightly before the 
temperature. In one case of P. falciparum 
similarly studied the rise in blood sugar 
was much greater than in the P. vivax 
cases, reaching 206 mg per cent. The rise 
in temperature was not so marked as in 
the vivax cases but was of longer dura¬ 
tion, and the blood sugar began to fall be¬ 
fore the maximum rise of temperature was 
attained. The authors discussed the pos¬ 
sible causes of the rise in blood sugar and 
concluded that it was chiefly due to an 
increased glycogenolysis following an in¬ 
creased activity of the adrenal glands with 
an increased secretion of adrenalin. They 
called attention to the similarity of this 
mechanism to that occurring in protein 
shock. 
An interference with the storage of gly¬ 
cogen in the liver has been emphasized by 
a number of workers who studied the func¬ 
tional capacity of the liver in malaria. 
Sinton and Hughes (1924) found a de¬ 
crease in levulose tolerance and Ruge 
(1935, 1939) a decrease in galactose toler¬ 
ance in human subjects, indicating a dis¬ 
turbance of the glycogenetic function of 
the liver. 
