202 
MALARIA 
enlargement of the spleen is a constant 
occurrence during the paroxysm. It tends 
to become smaller during the interval, how¬ 
ever, and may not be palpable during the 
first few paroxysms in a primary infection. 
As the course of the infection progresses the 
swelling increases and a relatively large 
volume may be attained. The usual ten¬ 
dency is for the tip of the enlarging spleen 
to swing diagonally across the abdomen to¬ 
ward the lower right quadrant. Pain is 
sometimes complained of and may be due to 
perisplenitis or stretching of the capsule. 
Tenderness on palpation, particularly dur¬ 
ing the paroxysm, is commonly experienced. 
Bupture of the engorged spleen has been 
met with but it is usually consequent upon 
trauma. 
It has been our experience that the 
splenomegaly in primary P. falciparum at¬ 
tacks does not reach the proportions that 
may be noted in vivax malaria in highly 
susceptible individuals. Probably this is 
largely due to the fact that primary P. falci¬ 
parum attacks are of shorter duration than 
those caused by P. vivax. In negroes the 
attacks have been relatively brief and 
splenomegaly has seldom been evident. Our 
white patients have experienced longer at¬ 
tacks, but here the degree of enlargement 
has not exceeded the Number 2 size of 
Boyd’s classification (1930a). 
Anemia. The great densities which P. 
falciparum may quickly attain undoubtedly 
accelerate the development of anemia. Too, 
as the writer pointed out, their tendency to 
invade both mature and immature erythro¬ 
cytes may be a factor of importance. We 
do not definitely know of destruction of the 
erythrocytes other than by direct action of 
the parasite, although some authors feel 
that circumstances necessitate the hypothe¬ 
sis of some additional factor, such as a hemo¬ 
lytic toxin. It must be remembered, how¬ 
ever, that we only see the parasitized cells 
that appear in the peripheral circulation. 
It is not uncommon to note that in the 
course of a week of infection a patient may 
lose from one to two million erythrocytes 
per cmm and from two to five grams of 
hemoglobin per 100 cc of blood. There is 
not necessarily a correlation between the 
blood destruction and the apparent clinical 
severity of the infection. It is noteworthy, 
furthermore, that as the degree of anemia 
increases the rate of its development 
slackens. It is remarkable how quickly the 
blood restoration becomes evident follow¬ 
ing the termination of an attack. In some 
instances we have noted that the destruc¬ 
tion is more than compensated for as the 
number of parasites is decreasing and per¬ 
haps just before the paroxysms have ceased. 
Leucocytic reaction. The total leucocyte 
count is altered both in relation to the indi¬ 
vidual paroxysm and to the course of the 
infection. It is generally agreed that a leu- 
copenia exists during the paroxysm; it 
probably becomes evident prior to the onset 
of the latter. This reaction, however, may 
be of the same general type as the usual 
body response to the introduction of a 
foreign protein and therefore relatively 
non-specific, in so far as the malarial infec¬ 
tion is concerned. James (1922) states that 
“a true leucoeytosis is by no means infre¬ 
quent during the very early stage of an 
ordinary acute attack (especially in malig¬ 
nant tertian infections) and for a longer 
period in pernicious eases while the fever is 
rising.” Marchiafava and Bignami (1901) 
quote Kelsch as observing a leucoeytosis in 
the pernicious infections. Craig (1909) 
agrees on this point. We have noted a leu- 
copenia in our falciparum infections, 
though not a very marked one as Fig. 7 
shows. In this chart the means of the leuco¬ 
cyte counts for ten patients have been 
plotted over a period of from 3 days before 
until 12 days after the first appearance of 
parasites. It will be noted that the leuco- 
penia begins to appear before we are able 
to detect parasites in thick smears and that 
the lowest point in the curve occurs 6 days 
after parasites were first detected. Fre¬ 
quently a low count persists for some time 
after the onset of the infection. We have 
occasionally observed a greater degree of 
leucopenia to occur, as a result of a relapse 
with its accompanying increase in parasite 
density, than there was evident during the 
primary infection. 
