186 
MALARIA 
occurs, however, the patient usually ‘‘ knows 
he is going to have his chill,” but a lucid 
description of the subjective symptoms 
which give him this information is difficult 
to obtain. A sense of giddiness, nausea 
and feeling of cold is about all that is 
present within 15 to 30 minutes before the 
paroxysm occurs, although some hours 
earlier the headache and the muscle and 
joint pains may be experienced. 
During the rigor the outstanding sensa¬ 
tion is that of cold. The patient’s mind 
is not greatly disturbed and he can think 
clearly. When the chill is over there is a 
pleasant feeling of warmth. When the 
fever rises, however, there is present eu¬ 
phoria and a considerable amount of mental 
dissociation as evidenced by the patient’s 
conversation and inability to put his 
thoughts on paper. The latter may be 
aggravated by a certain degree of muscular 
incoordination which exists at the height 
of the febrile attack. 
The stage of defervescence commences as 
the temperature begins to drop, which it 
usually does rather rapidly. Perspiration 
occurs during this stage and may become 
so profuse as to saturate the bed clothes. 
Often the patient will fall into a refresh¬ 
ing sleep. As a rule subjective symptoms 
disappear a few hours after the tempera¬ 
ture has returned to normal and the patient 
feels quite well again. 
It is important to note that there are 
no subjective symptoms in a chronic or 
latent P. vivax infection. After the clin¬ 
ical attack of benign tertian malaria has 
terminated, either spontaneously or by the 
use of quinine, the patient “enjoys good 
health” unless he experiences a relapse of 
which there are few warning symptoms 
more than a few hours before the paroxysm 
occurs. 
Characteristics of the Infection 
The method of inoculation (natural or 
artificial) appears to have some influence on 
subsequent events. Boyd (1940b) pointed 
out that in artificially induced attacks: (1) 
the incubation period is usually shorter 
and may even be eliminated if the dosage 
of trophozoites be large enough, (2) the 
detection of parasites in the peripheral 
blood smears more frequently precedes the 
initial fever, (3) renewed clinical activity 
occurs only within eight weeks of the 
termination of the primary attack, and (4) 
when the donor of the trophozoites had been 
naturally inoculated, the subsequent attacks 
in the recipients were usually briefer than 
when ‘the donor had been artificially in¬ 
oculated. 
Other factors may also influence the 
course of the attack. These are race, resi¬ 
dential environment and season of the year. 
Boyd (1934) noted that negroes show a high 
degree of tolerance for P. vivax. He ob¬ 
served that but 5 of 14 colored patients 
developed infection following their inocu¬ 
lation with this parasite. Furthermore, 
only 3 of the 5 developed pyrexia. This 
was light in degree and of less than a week’s 
duration. These results were in marked 
contrast to those observed in white patients 
inoculated with the same mosquitoes. 
In areas where P. vivax infections are 
endemic the likelihood of a resident con¬ 
tracting the disease varies directly with the 
constancy of his exposure. It is quite 
common for persons who have spent their 
lives in such areas to exhibit some degree 
of immunity toward this parasite, and when 
reinfected with other strains of the same 
species the resulting illness may be quite 
mild. 
It was observed by Boyd, Kitchen and 
Muench (1936) that inoculations made dur¬ 
ing the winter quarter of the year were 
followed by a lower proportion of takes; 
the latter had longer incubation periods, 
shorter courses, and renewal of clinical 
activity was confined to an eight-week 
period following termination of the pri¬ 
mary attack. On the other hand, inocula¬ 
tions made in the other quarters of the 
year, and particularly those in the summer 
quarter, were characterized by the largest 
proportion of takes, the shortest incubation 
periods, the longest clinical attacks and the 
greatest likelihood of renewed clinical ac¬ 
tivity as late as 24 weeks after termination 
of the primary attack. 
