INFECTION OF THE INTERMEDIATE HOST: VIVAX 
187 
Malaria in infancy. Young infants are 
early infected with, malaria in endemic 
localities. In a highly endemic region, as 
Leopoldville in the Belgian Congo, one-half 
of the infant mortality in 1928 was due to 
malaria. In Cyprus was observed that 
nearly 100 per cent of infants over a month 
old had malaria and exhibited enlarged 
spleens of malarial origin, occasionally 
reaching to the symphasis pubis when they 
were two months old. The splenic enlarge¬ 
ment is proportionately greater in infants 
under 6 months of age. 
The clinical symptoms of malaria and the 
classic paroxysm is seldom observed in 
children under 6 years. In infants and 
young children, the clinical attack is ush¬ 
ered in suddenly. Fretfulness, refusal to 
nurse, and vomiting may be the first sign. 
The malarial chill, which is uncommon in 
children under 6 years of age, is repre¬ 
sented by a paleness of nails and lips; the 
hands and feet show the same pallor and 
there is a shrinking of the skin of the pads 
of the toes and fingers as is seen in adults 
during a malarial chill. The skin of the 
hands and feet is cold to touch and a slight 
degree of cyanosis may be present. 
In infants and young children the fever 
due to P. vivax infection is continuous or 
remittent in type, rather than of a well de¬ 
fined intermittent form. 
A clinical diagnosis of malaria in infants 
and young children is far more difficult to 
make than in the adult, but examination of 
a blood smear on 3 consecutive days will 
show whether the fever is due to malaria. 
Obscure symptoms and convulsions can 
be attributed to P. falciparum, rather than 
to P. vivax and will not be discussed here. 
Likewise, such sequelae as cachexia, “pasty 
appearance, ’ ’ secondary anemia and mental 
dullness, if they ever do follow an acute 
attack of malaria, are more probably at¬ 
tributable to concurrent hookworm infec¬ 
tion or malnutrition. 
Malaria in pregnancy. In countries 
where the endemicity of malaria is high 
this disease is credited with causing a 
large number of maternal, fetal, and neo¬ 
natal deaths, and there is no doubt that 
an acute attack of P. vivax malaria during 
pregnancy is prejudicial to women already 
in a poor physical condition because of 
hookworm, malnutrition, etc. 
Spontaneous interruption of a pregnancy 
before term is stated to be common, re¬ 
peated clinical attacks are credited with 
bringing about miscarriages or premature 
labor, and death of the fetus in utero is 
described. 
In cases where there is a marked degree 
of anemia due to P. vivax malaria, the 
resistance to intercurrent infection may be 
so lowered that the patient develops puer¬ 
peral sepsis. It has been stated that women 
with grave anemia seldom reach term, and 
if so, fetal deaths due to anemia may be 
ascribed to P. vivax. It must be borne in 
mind, however, that it is only the acute 
clinical attack and not a chronic P. vivax 
infection that can be incriminated in hav¬ 
ing a harmful effect on either pregnancy 
or the puerperium. It is very doubtful that 
a P. vivax infection is a predisposing factor 
in the toxemia of pregnancy. Likewise, 
there are no data to show that such infec¬ 
tions prolong the time of labor or predis¬ 
pose to hemorrhage after delivery. 
There is good reason to believe that child¬ 
birth may precipitate an attack of acute 
clinical malaria in a woman with a latent 
P. vivax infection. However, the difficulty 
of finding adequate data on this point is 
almost insuperable. In the South it is not 
uncommon to find a well informed prac¬ 
titioner who routinely administers quinine 
to the mother shortly before labor and 
during the puerperium in order to prevent 
the development of an acute clinical re¬ 
lapse. As in the case of P. falciparum in¬ 
fections, P. vivax can be demonstrated in 
placental smears when no parasites are to 
be found in the peripheral blood of the 
mother. It has been stated that malarial 
parasites persist in the placenta and so 
generate a relapse. This reasoning is not 
quite clear, except that pregnancy itself 
may conceivably protect the mother from 
an acute clinical attack of malaria, just as 
we have observed in experimental trypano¬ 
somiasis that pregnant female rats survive 
