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peripheral parasitaemia below patent levels requires an extended period of
persistent parasitaemia, in many cases longer than 200 days ( Coatney et al.,
1950 ). Sterilising immunity does eventually develop ( Van den Eede et al.,
2011 ) but probably follows suppressive immunity by a substantial period of
time. Since even sub-patent P. vivax infections can be transmitted relatively
efficiently, asymptomatic individuals are likely to be a very important source
of P. vivax transmission in endemic settings ( Bousema and Drakeley, 2011 ;
Jeffery, 1952 ; Bharti et al., 2006 ).
Unlike P. falciparum gametocytes, P. vivax gametocytes are short-lived. In
the absence of anti-malarial treatment, vivax gametocytes are estimated to
circulate in the peripheral bloodstream for a maximum of 3 days ( Bousema
and Drakeley, 2011 ). Therefore, P. vivax gametocytaemia does not persist
for any significant length of time following clearance of asexual parasitae-
mia by anti-malarial drugs. The mathematical relationship between asexual
parasite density and gametocyte density does not appear to differ between
primary and recurrent infections (Douglas et al., in submission). The factors
that determine the presence of gametocytaemia and, therefore, the overall
likelihood of transmission of a P. vivax inoculum, are those that determine
the presence of asexual parasitaemia. The most important of these determi-
nants are the relapse pattern of the particular P. vivax strain, the strength of
homologous immunity and the anti-malarial drug regimen received. Since
P. vivax gametocytaemia mirrors asexual parasitaemia, one would assume
that the impact of anti-malarial treatment on the total area under the asexual
parasitaemia-time curve for a given inoculation could be used as a primary
indicator of a regimen's potential to reduce transmission of P. vivax .
All patients with patent P. vivax monoinfections or mixed species infec-
tions involving P. vivax will have hypnozoites and are, therefore, at risk of
multiple future relapses. Even in low-transmission areas, a significant pro-
portion of those without patent P. vivax parasitaemia will also harbour
P. vivax hypnozoites. Acute infection with P. falciparum is a strong risk fac-
tor for activation of hypnozoites in these individuals ( Looareesuwan et al.,
1987 ). Table 5.1 shows the risk of P. vivax parasitaemia following treat-
ment of P. falciparum infection with artemether + lumefantrine in several
co-endemic regions ( Ratcliff et al., 2007 ; Hasugian et al., 2007 ; Douglas
et al., 2011 ; Smithuis et al., 2010 ; Karunajeewa et al., 2008 ; McGready et al.,
2008 ; Hutagalung et al., 2005 ; Lefevre et al., 2001 ; van Vugt et al., 1998,
1999 ; Mayxay et al., 2004 ; Stohrer et al., 2004 ; Denis et al., 2006 ; Thriemer
et al., 2010 ; van den Broek et al., 2005 ; Haque et al., 2007 ; Thapa et al.,
2007 ; Assefa et al., 2010 ; Hwang et al., 2011 ). This particular artemisinin
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