Biology Reference
In-Depth Information
for ≥48 days (
Boyd, 1947
;
Boyd et al., 1936
). Importantly, asymptomatic
parasitaemia (and gametocytaemia) tended to persist for weeks as disease
controlling immunity was acquired.
During the malaria therapy experience, it became clear that both the
incubation period and the number of relapses per infection were determined
by the numbers of sporozoites inoculated (
Boyd, 1940b
). Low-sporozoite
inocula often resulted in an extended incubation period of 7-10 months.
The more sporozoites that were inoculated, the more likely was an early
infection (incubation period - 2 weeks), and the more relapses that fol-
lowed - provided that prompt anti-malarial treatment (quinine) was given
each time. In order to ensure that there was a short incubation period pre-
ceding the malaria illness, malaria therapy infections were produced typi-
cally by the bites of 5-10 infected mosquitoes, and either no treatment or
partial suppressive treatment was given. Theories that seasonal influences
were important determinants of relapse were largely rejected as the inter-
vals from primary illness to relapse in neurosyphilis patients were generally
similar, whichever month the infection started.
Until the end of the Second World War, the long-latency infection was
regarded as the 'usual'
P. vivax
phenotype. Throughout the endemic areas of
Europe, vivax malaria peaked in the late spring and early summer (largely
from inoculations the previous year) (
Swellengrebel and De Buck, 1938
;
Winckel, 1955
;
Gill, 1938
;
Hackett, 1937
). In southern Europe, there was
often a bimodal pattern with a late summer peak of falciparum malaria
(aestivo-autumnal malaria). During the Second World War observations on
soldiers fighting in Europe and temperate areas of Asia, all pointed clearly
to long-latency
P. vivax
with similar illness patterns to the Madagascar and
St. Elizabeth strains (
Findlay, 1951
;
Höring, 1947
;
Eyles and Young, 1948
;
Ebisawa, 1973
;
MRC, 1945
;
Mowrey, 1963
;
Wilson and Reid, 1949
). In
contrast, soldiers fighting in the Indo-Burman and South Pacific cam-
paigns encountered vivax malaria with a very different relapse pattern. The
relapse rate was very high - relapses were frequent and recurrent. Infections
occurred at 3-week intervals if quinine was given, and 7-week intervals fol-
lowing treatment with mepacrine (quinacrine, atebrine) (
Most, 1963
;
Noe
et al., 1946
;
Bianco et al., 1947
;
Whorton et al., 1947
;
Craige et al., 1947
;
Jeffery, 1956
). Initially, this disease pattern was thought simply to reflect the
very high sporozoite inocula that the soldiers were exposed to but it soon
became apparent that the phenotype was fundamentally different. Multiple
relapses were very common and there was no evidence of long latency. The
'type strain' for this tropical frequent relapse
P. vivax
phenotype was the
