46 
MALARIA 
vary secretion is delivered through a duct 
in a structure adjacent to the sucking tube. 
It is assumed that at least some of the sporo¬ 
zoites so injected find their way into the 
blood stream. Concerning what takes place 
between the time of injection of the sporo¬ 
zoites and the first appearance of tropho¬ 
zoites in the inoculated person’s peripheral 
circulation, there is a gap in our knowledge 
of the pathogenesis which is not satisfac¬ 
torily explained on the basis of time needed 
for the parasites to reach a detectable den¬ 
sity. Schaudinn (1902) claimed to have 
observed the penetration of an erythrocyte 
by a sporozoite, but no one has been able to 
support this observation and it is not gen¬ 
erally accepted as the usual course of events. 
Recently considerable work has been done 
on a fixed tissue stage of the asexual cycle 
in bird malaria. If such a stage were 
proved to exist between the sporozoite and 
merozoite in human infections it might 
explain several vexing problems. 
Physiology 
Relatively little is known regarding tl^e 
physiology of the plasmodia in general. 
Presumably the trophozoite obtains all its 
nourishment from the erythrocyte it occu¬ 
pies. Whether a parasite exhausts the 
available food of more than one red cell 
during its growth is not known, although it 
seems unlikely that migration from one ery¬ 
throcyte to another takes place. Of inter¬ 
est is the tendency of P. vivax and P. ma¬ 
larias to invade erythrocytes of a certain 
age, in comparison with the indifference 
exhibited by P. falciparum. 
The growing parasite utilizes the hemo¬ 
globin of the red cell and deposits the char¬ 
acteristic pigment, hemozoin, in its own 
cytoplasm. The pigment in this species is 
much darker than that of P. vivax. It is at 
first deposited in the form of fine, dust-like 
granules which, as they are added to, be¬ 
come coarse clumps or blocks. Though the 
pigment was called melanin for some years, 
it is actually more closely related to hema- 
tin. It is soluble in alkalies, and iron has 
not been satisfactorily demonstrated in it. 
In P. falciparum infections it is commonly 
seen in the monocytes of peripheral blood 
smears and at autopsy in the fixed tissue 
phagocytes, sometimes in large quantities 
so that it may impart a characteristic slate 
grey appearance to certain organs. 
In its early stages the unstained, non- 
con'traetile vacuole that is enclosed by the 
ring of cytoplasm is considered to be of im¬ 
portance in the matter of the parasite’s 
nutrition. This function was attributed to 
it by Marchiafava and Bignami (1901). 
The vacuole appears to be of less conse¬ 
quence to the older forms, however, since 
it gradually disappears with the increase in 
size of the parasite. The amoeboid stage, 
even with its limited activity, doubtlessly 
facilitates the nourishment of the organism. 
Presumably hemoglobin is taken in through 
the pseudopodia to be broken down subse¬ 
quently by enzymic action. 
Some writers have hypothesized the pro¬ 
duction of a hemolytic toxin by this para¬ 
site. They feel that the blood destruction 
is too great to be accounted for by multipli¬ 
cation of the parasite alone. We do not, 
however, have any proof of such a hemolytic 
toxin. It has been assumed, furthermore, 
that the parasite secretes a specific toxin 
which is released at the time of sporulation 
and which is responsible for the paroxysm. 
Of this we do not have any proof either. 
The paroxysm may be due wholly to the 
release of the foreign protein into the host’s 
circulation at the time of sporulation. It 
has been evident, according to our observa¬ 
tions, that the toxic effect of this species 
per se is not particularly marked; the high 
parasite densities attained are probably the 
most important factor. 
