226 
MALARIA 
Blood Salts 
Changes in the concentration of various 
salts in the blood plasma due to malarial 
infection appear to be limited to the period 
immediately after the rupture of large 
numbers of erythrocytes. The only salts 
which have a higher concentration within 
the erythrocytes than in the plasma are the 
potassium salts. The amounts of other 
salts are so much greater in the serum than 
in the erythrocytes that the addition of the 
amounts contained in ruptured erythro¬ 
cytes does not materially affect their per¬ 
centages in the plasma. 
Zwemer, Sims and Coggeshall (1940) 
studied the plasma potassium level in hu¬ 
man and monkey malaria. In eleven hu¬ 
man eases of P. vivax infection the plasma 
potassium was found to rise suddenly from 
an average of 22 mg per cent to an aver¬ 
age of 34 mg per cent at the time of the 
chill. It fell rapidly before the peak of 
fever was reached and attained its previous 
level in an average of 14 hours. This rapid 
fall was probably due to excretion through 
the kidneys. In monkeys infected with P. 
knowlesi, which undergoes schizogony every 
24 hours, it was more difficult to observe 
these sudden rises in plasma potassium, but 
they were observed when specimens were 
obtained exactly at the time of sporulation. 
When the infection became intense and the 
erythrocyte count became low the whole- 
blood potassium fell off to approximately 
33 per cent of the initial values, and the 
plasma potassium level showed a gradual 
decrease in the base line between periods 
of sporulation. The increase in potassium 
level at the time of sporulation was some¬ 
times too great to be accounted for by the 
potassium content of parasitized erythro¬ 
cytes, and the authors presumed that potas¬ 
sium might also have been released from 
body cells in general, due either to the toxic 
action of the released potassium or to cel¬ 
lular damage produced by the elevated 
temperature. These authors called atten¬ 
tion to the toxic effect of high plasma potas¬ 
sium on the adrenal cortex. 
Junior and Brandao (1937) described a 
series of cases of malaria which presented 
a syndrome of adrenal insufficiency, includ¬ 
ing the picture of Addison’s disease. 
Chessa (1938) studied cases which clini¬ 
cally suggested adrenal hypofunction and 
showed that 35 per cent of them had a 
hypersensitivity to insulin. Paisseau and 
Lemaire (1916) and Natali (1934) de¬ 
scribed profound changes in the adrenal 
cortex in autopsies on patients who had 
died of P. falciparum malaria. Natali also 
found similar changes in monkeys dying of 
infection with P. knowlesi. 
Blood Pigments 
Hematin (haemozoin). The composition 
of the pigment found in malaria parasites 
was the subject of discussion from the time 
the parasite was discovered. Its resem¬ 
blance to melanin and the fact that it did 
not give the ferrocyanide reaction for iron 
led many to believe that it was actually 
melanin. This was the basis of the use of 
melanin in the Henry reaction for diag¬ 
nosis. Brown (1911a) was the first to make 
an extensive chemical examination of ma¬ 
larial pigment and came to the conclusion 
that it was identical with hematin. Sinton 
and Ghosh (1934a, 1934b) and Ghosh and 
Sinton (1934) firmly established the iden¬ 
tity of the two substances, showing that 
haemozoin gave all the chemical and spec¬ 
troscopic reactions of hematin, that when 
purified it had the same rate of solution, 
and that its chloride and iodide salts were 
identical with similar salts of hematin. 
The hematin formed in the malaria 
parasites during their development in the 
erythrocytes apparently retains its chem¬ 
ical structure for some time after para¬ 
sitized erythrocytes which have been phag- 
ocytosed by the reticulo-endothelial cells 
are digested. Brown (1911b) showed that 
powdered hematin remained for weeks in 
tissue cells with but slight and slowly 
progressing alteration. It is also probable 
that much of the hematin liberated into the 
blood plasma with the fully developed 
schizonts remains in particulate form and 
is phagocytosed by the reticulo-endothelial 
cells, since these cells contain more hematin 
than can easily be explained by their phag- 
