Authors
CJ Sutherland1; HP Fuehrer2; OJ Watson1; S Campino1; 1 London School of Hygiene & Tropical Medicine, UK; 2 Med Vet University, Wien, Austria Discussion
The advent of molecular genetic and genomic analyses over the past 25 years has greatly increased our understanding of the parasites that cause ovale malaria in humans.
It is now widely accepted that these comprise two distinct, non-recombining but fully sympatric species, a hypothesis first presented at the BSP Spring Meeting in Edinburgh in 2009. It has become clear also that, across the African continent, ovale malaria is ubiquitous yet under-reported, most frequently occurring as asymptomatic and/or mixed species infections with Plasmodium falciparum. In these mixed infections, ovale parasites are invariably the minor species in terms of peripheral blood densities, and so easily over-looked. There is also a growing body of compelling data supporting the view that the two species differ in the latency period exhibited by putative quiescent hypnozoite forms residing in the liver following primary infection. Finally, new genomic studies utilising bespoke selective amplification protocols are beginning to shed comprehensive light on the degree of gene diversity within and between the dimorphic forms of ovale parasites.
We present a summary of recent clinical, epidemiological and genomic studies of Plasmodium ovale curtisi and P. ovale wallikeri and, in response to the incontrovertable weight of evidence that these parasites represent two distinct species, propose a new binomial nomenclature. 
