218 
MALARIA 
The facts of infectious disease, however, 
prove beyond a doubt that under the ordi¬ 
nary conditions of blood flow phagocytosis 
by endothelium is extremely uncommon. 
And even when there is some evidence that 
it may occur, the possibility cannot be ex¬ 
cluded that the infectious agents are merely 
passing through the endothelial cell rather 
than having been phagocytosed. In many 
infectious diseases, including malaria, 
numerous attempts have been made to 
demonstrate the role of endothelial phago¬ 
cytosis in common endothelium (Bruetsch 
1932a), but the evidence of the commonness 
or the importance of such activity is scanty 
and unconvincing. 
It is not surprising that this is so. Com¬ 
mon endothelium, as it lines capillaries, 
arterioles and larger blood vessels, consists 
of stretched-out cells with but little cyto¬ 
plasm available for phagocytic action. 
Maximow (1927b) described them as “fixed, 
highly differentiated cells” which belong 
to the group of fibrocytes. According to 
this eminent histologist “the role of the 
endothelium in the adsorption and neutrali¬ 
zation of toxins and in other general reac¬ 
tions combating infections or intoxications 
may be important, but it is not manifest 
in appreciable morphologic changes.” En¬ 
dothelium, therefore, may be thought of as 
a blood-tissue barrier which keeps formed 
elements constantly confined to the blood 
stream but which allows diffusion of oxy¬ 
gen, carbon dioxide and metabolites of the 
blood and tissues. So long as it remains 
uninjured, infectious agents in the blood 
stream may pass into and out of most 
organs until, in their passage through the 
liver, spleen or bone marrow, they en¬ 
counter altered conditions of blood flow and 
come into contact with t*he phagocytic cells. 
It is because of contact of the parasites with 
these specialized cells,' sometimes called 
“special endothelium,” and not because of 
contact with common endothelium, that 
they are engulfed and removed from the 
blood stream. This entire selective mecha¬ 
nism may well be regarded as a wise adapta¬ 
tion of nature, a specialization of organic 
function, whereby vital organs are shielded 
from many of the more serious vicissitudes 
of life. 
It is well to think, conversely, of what 
might happen if common endothelium were 
functionally active and participated ener¬ 
getically as a phagocytic tissue. In every 
bacteriemia, phagocytosis by common endo¬ 
thelium would interfere with the normal 
circulation of blood through many impor¬ 
tant organs; the ensuing circulatory dis¬ 
turbances and the resulting localized in¬ 
flammations would surely make common 
such conditions as thyroiditis, myocarditis, 
pancreatitis, myositis, adrenalitis, orchitis, 
oophoritis and the like. The fact that this 
does not happen constitutes excellent pre¬ 
sumptive evidence, therefore, that under 
ordinary conditions of blood flow, but little 
phagocytosis by endothelium occurs. 
Furthermore, under the usual conditions 
of blood circulation through capillaries and 
larger vessels, the rapidity of blood flow 
makes it unlikely that many opportuni¬ 
ties may be afforded endothelial cells for 
effective phagocytosis. And even under 
conditions of blood stasis, the extent of 
phagocytosis by endothelium is slight. In 
instances of extreme sluggishness of blood 
flow, as for example, in association with the 
hemoconcentration of shock (Moon 1939), 
some agonal phagocytosis by endothelium 
might contribute to the process of capillary 
occlusion, so prominent a feature of per¬ 
nicious malaria. 
This problem of capillary occlusion in 
pernicious malaria has been a perplexing 
one for many years. Although vascular 
occlusion by parasitized erythrocytes is par¬ 
ticularly common in the white matter of the 
brain, the fact that it may also occur in 
other organs, as for example, in the myo¬ 
cardium, gastrointestinal tract or elsewhere, 
suggests that local causes do not explain the 
condition adequately. These embolic oc¬ 
clusions cannot be attributed to the effects 
of swelling of the erythrocytes, because 
these cells tend to enlarge in infection with 
P. vivax, where such embolization does not 
occur, and tend often to shrink in infections 
with P. falciparum. 
One feature of pernicious malaria which 
