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the parasite (
Mendis et al., 2001
;
Sattabongkot et al., 2004
;
Wells et al., 2010
);
in elimination settings,
P. vivax
is often the 'last parasite standing' (
Garnham,
1951
;
Yekutiel, 1960
;
Pampana, 1969
;
Wernsdorfer et al., 2009
;
Tatem et al.,
2010
).
Plasmodium vivax
gametocytes are present earlier in the progression
of a primary or recrudescent infection than
P. falciparum
(
Mendis et al., 2001
;
McKenzie et al., 2002
), such that the majority of patients have sufficient
gametocytaemia to allow transmission before the infection is diagnosed or
treated (
Ratcliff et al., 2007
;
Awab et al., 2010
;
Douglas et al., 2010
).
Plasmodium vivax
gametocytes are transmitted more efficiently to
Anopheles
mosquito vectors (
Boyd and Kitchen, 1937
;
Collins et al., 2002
) than those
of
P. falciparum
and are transmissible at lower parasite densities (
Sattabongkot
et al., 2004
). Within the mosquito, vivax sporozoites develop faster than
P.
falciparum
and with slightly wider viable temperature ranges, allowing for a
greater geographical distribution (
Gething et al., 2011b
). In addition, due
to vector bionomics in regions where
P. vivax
is most prevalent, methods of
control that are broadly effective in reducing
P. falciparum
transmission, such
as insecticide-treated bed nets (ITNs), show far less success in the control of
P. vivax
(
Luxemburger et al., 1994
;
Bockarie and Dagoro, 2006
).
Plasmodium
vivax
malaria is typically carried with lower levels of parasitaemia, making it
relatively difficult to diagnose (
Mendis et al., 2001
). However, there is evi-
dence that, despite lower blood parasite loads,
P. vivax
immunity is acquired
more rapidly than
P. falciparum
and may result in an earlier age-prevalence
peak in areas of high transmission (
Mueller et al., 2009a
,
2009b
). Detailed
reviews regarding the biology (Chapter 2, Volume 80), control (Chapter 6,
Volume 80), and acquired immunity (Chapter 3, Volume 81) of
P. vivax
are
available elsewhere in this thematic issue of
Advances in Parasitology
.
Perhaps the most important feature of
P. vivax
biology is its ability to relapse
in the weeks and months following a primary parasitaemia, via a dormant liver
stage known as the hypnozoite (
James, 1931
;
Coatney, 1976
;
Garnham, 1989
;
Prudencio et al., 2006
;
Chen et al., 2007
;
Imwong et al., 2007
;
White, 2011
). It
has long been known that there is significant geographical variation in the rate
at which a 'strain' of
P. vivax
may relapse (
Coatney and Cooper, 1948
;
Winckel,
1955
;
Garnham et al., 1975
). The exact mechanism through which hypnozo-
ite relapses are triggered is unknown (
Cogswell, 1992
;
Prudencio et al., 2006
;
Baird, 2009
;
Mueller et al., 2009a
). One theory is that the mechanism is an
adaptive trait of the parasite to sequester or 'hibernate' during times when cli-
matic conditions would be inhospitable to the
Anopheles
vector of the disease
(
Shute et al., 1976
;
Baird and Rieckmann, 2003
;
White, 2011
). This theory is
supported by observations that temperate strains of the parasite tend to exhibit
