Biology Reference
In-Depth Information
of drug development and use in
P. vivax
malaria). Chloroquine was first
synthesised in Germany in 1934 and subsequently tested by Sioli in four
neurosyphilis patients treated with vivax malaria. Due to perceived toxicity,
it did not become widely available until the end of the Second World War.
By the 1950s, chloroquine was being used increasingly as a reliable prophy-
lactic and blood schizontocidal treatment for both
P. vivax
and
P. falciparum
malaria. It remains the mainstay of
P. vivax
blood-stage treatment in most
parts of the vivax-endemic world (
Douglas et al., 2010
).
The anti-relapse properties of primaquine were recognised in the 1950s
following observations of its ability to prevent late recurrences of vivax
malaria in troops returning from the Korean War (
Alving et al., 1953
).
Remarkably, anti-relapse treatment is still reliant on primaquine, a drug
that is contraindicated in infants and pregnant women and can cause
life-threatening haemolysis in those with glucose-6-phosphate dehydro-
genase (G6PD) deficiency. The pipeline for new, safer hypnozoitocidal
alternatives is dismally bare (
Medicines for Malaria Venture, 2011
;
Anthony
et al., 2012
). This situation is compounded by a lack of point-of-care tests
for G6PD deficiency, as well as the poor sensitivity of rapid diagnostic tests
for
P. vivax
(
Arevalo-Herrera et al., 2010
;
World Health Organization et al.,
2009
). Currently
P. vivax
attracts less than 5% of the US National Institutes
of Health malaria research budget (
Carlton et al., 2011
).
It is time to re-focus research efforts on
P. vivax
and, perhaps most
urgently, on the optimal means of reducing transmission of this highly
evolved parasite. Decreasing the interaction between humans and mosquito
vectors will play a crucial role in this endeavour. Anti-malarial drugs will
also be critically important components of the elimination arsenal. In this
chapter we focus on how best to use currently available anti-malarials to
reduce transmission of
P. vivax
including in the management of symptom-
atic malaria due to both
P. vivax
and
P. falciparum
and in mass drug adminis-
tration (MDA) campaigns.
2. TRANSMISSION OF
P.VIVAX
Mosquito transmission of
P. vivax
begins when a female anopheline
ingests mature gametocytes from an infected human. Once inside the
insect's midgut, the male
Plasmodium
gamete fertilises the female gamete
initiating the process of sporogony. Assuming a mean ambient temperature
of 25 °C, sporozoites concentrate in the mosquito's salivary glands within
9 days (the shortest sporogonic period of any of the
Plasmodium
species that
