It is prevalent in East Africa, east of the rift valley. This because of the loss of the duffy receptor in most African populations. Plasmodium vivax requires the duffy receptor to invade reticulocytes. Ref: http://www.plosntds.org/article/info:doi/10.1371/journal.pntd.0000774?imageURI=info:doi/10.1371/journal.pntd.0000774.t002

and it is also prevalent in the west African countries where the duffy blood group is prevalent(1) , may be this might be explained by mixing between different ethnic groups or disease evolution but by any means , there remains a bad need for an estimate to the burden of vivax malaria on Africa . Ref

PLoS Negl Trop Dis. 2011 June; 5(6): e1192.

Published online 2011 June 21. doi: 10.1371/journal.pntd.0001192

PMCID: PMC3119644

Duffy Negative Antigen Is No Longer a Barrier to Plasmodium vivax – Molecular Evidences from the African West Coast (Angola and Equatorial Guinea)

Cristina Mendes,1 Fernanda Dias,1,2 Joana Figueiredo,1 Vicenta Gonzalez Mora,3 Jorge Cano,3 Bruno de Sousa,4 Virgílio E. do Rosário,1 Agustin Benito,3 Pedro Berzosa,3 and Ana Paula Arez1,*

Since this study checked the duffy phenotype for the individuals and they were negative, it would suggest that the mechanism is disease evolution. You are correct, there is a need for better estimates of vivax burden in Africa.

Knowing exactly what is the situation with vivax in Sub-Saharan Africa is essential for planning malaria control programmes as falciparum is brought under better control. Fortunately ACTs also are effective in acute vivax but do not act on relapses. If a programme manager believes that he/she only has falciparum in his/her country and malaria fevers keep being recorded, then the obvious conclusion is that control is not working as well as was thought. If however a proportion of the fevers are due to vivax, then the control measures may be working well. The new fevers are not due to reinfections (and so to a failure in the vector control measures) but to the relapses from the initial infection. This then introduces the complexity of introducing primaquine and testing for G6PD deficiency into the design of the control programmes.

Dear Ian ,Thank you very much for directing attention towards this important point concerning relapse, the need for the use of Primaquine and G6PD deficiency among Africans , where the Prevalence of G6PD deficiency is estimated to be around 32.5% in the sub-saharan African region and hence this might well be one of the challenges to be considered in the battle against malaria.

The G6PD incidence is a big challenge. In Asia-Pacific, where primaquine has been used for a long time, doctors are aware of the risks of using it and so look out for the symptoms of haemolysis. In Africa, with no such history, the risk of doctors missing the symptoms early in treatment (when the drug can be stopped) is a major risk factor. Newer 8-aminoquinolines (e.g. tafenoquine) with much shorter dosage regimens (3-days) increase this risk as all the drug will have been taken on board by the patient before symptoms of haemolysis become apparent.hence the critical need for a G6PD RDT to add more complexity to the treatment regimens in the control programme.