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The Susceptibility of Liberians to the Madagascar Strain of Plasmodium vivax

Author(s): R. S. Bray
Source: The Journal of Parasitology, Vol. 44, No. 4, Section 1 (Aug., 1958), pp. 371-373
Published by: The American Society of Parasitologists
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Accessed: 15/01/2010 23:48

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The Liberian Institute of the American Foundationfor Tropical Medicine, Inc., Harbel, Liberia

The relative insusceptibility of Negroes to infection with Plasmodium vivax

has been reported by many observers (Mayne, 1932; Boyd and Stratman-Thomas,
1933; Young, Ellis and Stubbs, 1946; Becker, Kaplan, Read and Boyd, 1946;
Young, Eyles, Burgess and Jeffery, 1955). The only exception to these reports
of comparative insusceptibility has been that of Butler and Sapero (1947) who
found no difference in susceptibility between Negroes and white persons.
As P. vivax is rare or absent from large areas of Liberia (Bray, 1957) the
susceptibility of Liberians to infection with P. vivax was investigated to see if insus-
ceptibility is the dominant factor in the rarity of P. vivax. The Liberians infected
were living under natural conditions which include hyperendemic malaria due
largely to Laverania falciparum but also to P. malariae and P. ovale.

Thirty Liberian Nationals of all ages, either working at the Liberian Institute or living
close by, were exposed to the bites of Anopheles gambiae infected with the sporozoites of P.
The Madagascar strain of P. vivax1 employed was maintained in splenectomized chimpan-
zees and the A. gambiae employed were drawn from a laboratory colony.
The method of infection was "normal" in the sense that only 1 to 4 infective A. gambiae
were allowed to bite a subject. On the other hand the infection in A. gambiae was generally
heavy. All A. gambiae allowed to bite were dissected subsequently to ascertain if the salivary
glands contained sporozoites. Three separate batches of subjects were exposed to the bites of
infective A. gambiae at 3 different times and on 2 of these occasions non-immune whites2 were
similarly exposed as controls.
Following infection thick blood films were stained with Giemsa and examined from all in-
fected subjects from 9 days to 2 months after infection and again when possible 8 to 11 months
after infection. Examination was daily in the first period and twice weekly in the second.
Where P. ovale appeared the presence of this parasite was confirmed in thin quick-dried smears
after the method of Bray (1957).

The results are set out in Table I. They show a visible blood infection due to
P. vivax in only 1 Liberian subject among 30 exposed to infection. The subject
U. D. showed P. vivax in the blood 14 days after exposure and symptoms of ma-
laria occurred 15 days after exposure. A typical paroxysm occurred 17 days after
exposure. The infection was terminated by 1.5 grams of chloroquine base over
24 hours on the 17th day after exposure. No relapse occurred in the 11 months
following exposure.
On the 17th day after exposure, gametocytes of P. vivax appeared in the blood
of U. D. and A. gambiae fed at this time became infected. When sporozoites were
present these mosquitoes were allowed to bite subject F. 0. who failed to show
P. vivax in the blood.
Received for publication October 14, 1957.
1 The strain of P. vivax was received in Anopheles atroparvus kindly sent from London
by Mr. P. G. Shute.
2 My gratitude is extended to Dr. Max J. Miller and my wife; the non-immunes.

The subject R. D., who is the 1-year-old son of U. D., failed to show parasites
at any time after exposure to infection. The appearance of the parasites in U. D.
is worthy of note. Many thin films containing the generation of parasites seen
on the 14th and 15th days after sporozoite infection, were studied and the parasite
was at first glance thought to be P. ovale. Later it was shown definitely not to be
by the absence of oval host erythrocytes in quick-dried thin films. The rings were
small, compact and the vacuole was well defined, blank and white. The rings
resembled piroplasms.
The trophozoites were compact, sometimes 2-nucleated and the vacuole was
large and pronounced. The outline was usually round or oval with very few
TABLE I. The results of infecting Liberian subjects with the sporozoites of the
Madagascar strain of P. vivax.
Parasitest in the blood by months
Age* Number of after infection
Subject in infective
years bites 1st 2nd 8th 9th 10th 11th
month month month month month month

M.J.M. F
(control) A 2 V
A A 1 F F, 0 F F F F
S.L. A F 0 F F
H A 1 F, M F
K A 1 F, M F F
C A 11 F, M F, M F F F F
T A 2 F F
(control) A 1 V
U.D. A 3 V - F
N A 2 F F
B A 4 F F, O F
F.O. A 4 F F, M
W 1-10/12 1 0
J 2- 4/12 2 F
0 7 F F F F F
S 3 22 F, M F, M, O F F F F
M .S 0 F, M F, M F F F F
H 5 4 F F F
L 3 1 F 0
R.D. 1 4
J A 1
V A 1
R A 1 F
G A 1
S A 1 F
T A 1 F F
A A 1 F
P A 1
W A 1
M A 2 F F
G A 1
* A-Adult.
t V-P. vivax, F-L. falciparum, M-P. malariae, O-P. ovale.

amoeboid forms. The cytoplasm was collected into a very dense thin line around
the periphery of the vacuole. The nucleus of many of the old trophozoites appeared
unable to divide, resulting in a number of parasites which filled four-fifths of the
cell and displayed a pale cytoplasm with a diffuse pink nucleus which possessed
long strands running through it. Although these parasites looked like poorly
stained microgametocytes, it is believed that they were degenerating trophozoites.
The schizonts had a pale cytoplasm and large oval nuclei. The number of mero-
zoites was 8-12. The pigment was yellow-brown and scattered in the schizonts.
The host erythrocyte of the trophozoite was enlarged and pale. Heavy staining
showed very pale fine Schiiffner's dots to be present but these were invisible when
stained normally. The host erythrocyte of the schizonts was greatly enlarged and
fine pale Schiiffner's dots could be seen when normally stained.

The second generation of parasites studied on the 16th and 17th days after
infection was completely typical of P. vivax. The parasites stained normally and
produced 18-28 merozoites.

It is obvious that Liberians of all ages are highly resistant to infection with the
Madagascar strain of P. vivax, as was to be expected from the results of previous
work. This factor is obviously the main cause of the absence or rarity of P. vivax
in Liberia.
The result presented here of a 3% susceptibility is less than the 7.4% sus-
ceptibility reported by Young et al (1955). Under the conditions of malarial hy-
perendemicity however, it might be expected that susceptibility would be lower in
Liberia than was found in the U.S.A.
The inability to infect F. O. with the line of P. vivax taken from U. D. bears
out the statement of Young et al (1955) that the infection in 1 Negro is not infec-
tive to Negro recipients. Similarly inability to infect R. D., the son of the suscepti-
ble U. D., would indicate that susceptibility is not a family characteristic though
more evidence is needed to establish the point.
The morphology of the first generation of P. vivax studied in U. D. is that of
P. wilsoni Roberts, 1940. It is possible that P. wilsoni is merely P. vivax slightly
modified by sojourn in a Negro host.


Of 30 Liberian Nationals aged 1-35 years exposed to infection by sporozoites

of the Madagascar strain of P. vivax only 1 showed a patent infection due to P.
vivax in the blood. The 1-year-old son of this subject exposed at the same time
failed to show a patent infection. The line of P. vivax isolated from the susceptible
Liberian failed to produce an infection in another Liberian.
The first generation of P. vivax studied in the blood of the susceptible Liberian
showed the characteristics of P. wilsoni. The succeeding generation was typical of
P. vivax.
BECKER,F. T., KAPLAN,L. I., READ,H. S., AND BOYD,M. F. 1946 Variation in susceptibility
to therapeutic malaria. Am. J. Med. Sci. 211: 680-683.
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On the refractoriness of Negroes to the inoculation with Plasmodium vivax. Am. J.
Hyg. 18: 485-489.
BRAY,R. S. 1957 Studies on Plasmodium ovale in Liberia. Am. J. Trop. Med. Hyg. 6:
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