Project Summary/Abstract: 30 lines
Although Plasmodium vivax causes more than 7 million malaria cases each year, it has typically been
excluded from malaria control programming in sub-Saharan Africa (SSA) due to the absence of reported cases
and the assumption that the predominantly Duffy-negative population is invulnerable to P. vivax infection.
However, there is growing evidence that P. vivax is indeed present in SSA and that Duffy-negative individuals
can be infected, albeit at lower rates than their Duffy-positive counterparts. In addition, the recent
documentation of Anopheles stephensi, a highly competent vector for both P. vivax and P. falciparum, in the
Horn of Africa raises the possibility that P. vivax transmission may be enhanced by this emerging vector as it
spreads southward into SSA. As Kenya approaches pre-elimination phase in its fight against malaria, it
is facing the dual threat of the invasive An. stephensi vector and an unknown burden of the largely
neglected P. vivax species. While models have shed some light on the potential spread of An. stephensi into
SSA, these predictions and their potential impact on P. vivax transmission remain to be confirmed or
quantified. Here, we focus on Turkana, a semi-arid region of northern Kenya where we recently documented
low levels of year-round P. vivax for the first time. Turkana county borders Ethiopia, where P. vivax is endemic
and An. stephensi presence has recently been confirmed. Across the border in Kenya, there is little to no
information available on P. vivax prevalence, clinical burden, or its relationship with Duffy blood groups.
Furthermore, An. stephensi surveillance has not been mounted in Turkana, despite the fact that it is predicted
to have the highest risk of An. stephensi invasion. First, we propose to measure the clinical burden of P. vivax
and its relationship with Duffy blood groups through passive case detection. By working with select health
facilities across the county to screen and test patients seeking malaria treatment, we can measure the
prevalence of P. vivax in suspected malaria cases and compare the rate of infections in different Duffy blood
groups. Second, by conducting follow-ups with treated patients, we will quantify the rate at which P. vivax
infections relapse due to dormant hypnozoite presence following the clearance of P. falciparum parasites, a
phenomenon that has been well documented in many areas where P. falciparum and P. vivax are co-endemic.
This will allow us to estimate the underlying silent reservoir of liver-stage P. vivax infection. Third, we will
identify vectors likely involved in P. vivax transmission by collecting and classifying the species of mosquitoes
and/or larvae from the homes of P. vivax cases, with particular emphasis on detecting An. stephensi. Evidence
from this study will provide the foundation for understanding the conditions in which P. vivax could potentially
spread from Turkana across Kenya and would have broad application, informing malaria surveillance and
control strategies in Kenya and other areas across SSA where P. vivax and An. stephensi may have an
increasing impact.
