Abstract

IntroductionRecent surge ofAnophelesresistance to major classes of World Health Organization (WHO)-approved insecticides globally necessitates the need for information about local malaria vector populations. It is believed that insecticide efficacy loss may lead to operational failure of control interventions and an increase in malaria infection transmission. We investigated the susceptibility levels of malaria vectors to all classes of WHO-approved vector control insecticides and described the dynamics of malaria transmission in a peri-urban setting.MethodsFit 3–5-day-old adults that emerged fromAnopheleslarvae collected from several different sites in the study area were subjected to the WHO bioassay for detecting insecticide resistance. The knockdown resistance gene (kdr) mutations within the vector populations were detected using PCR. Entomological inoculation rates were determined using the human landing catch technique andPlasmodium falciparumcircumsporozoite ELISA.ResultsThe malaria vectors from the study area were resistant to all classes of insecticides tested. Out of the 284Anophelescomplex specimen assayed for the resistance study, 265 (93.30%) were identified asAnopheles gambiae s.s.The kdr gene was detected in 90% of theAnopheles gambiae s.s.assayed. In an area whereAnopheles coluzziiresistance to insecticides had never been reported, the kdr gene was detected in 78% of theAnopheles coluzziisampled. The entomological inoculation rate (EIR) for the dry season was 1.44 ib/m/n, whereas the EIR for the rainy season was 2.69 ib/m/n.ConclusionsThis study provides information on the high parasite inoculation rate and insecticide resistance of malaria vectors in a peri-urban community, which is critical in the development of an insecticide resistance management program for the community.

Highlights

  • Recent surge of Anopheles resistance to major classes of World Health Organization (WHO)-approved insecticides globally necessitates the need for information about local malaria vector populations

  • Recent malaria data provided by the World Health Organization (WHO) show that targets for reductions in the death and disease caused by malaria may have stalled due to the rapid emergence of malaria vector control insecticide resistance [3]

  • Target site insensitivity is caused by gene mutation of target proteins that interact with vector control insecticides

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Summary

Introduction

Recent surge of Anopheles resistance to major classes of World Health Organization (WHO)-approved insecticides globally necessitates the need for information about local malaria vector populations. Recent malaria data provided by the World Health Organization (WHO) show that targets for reductions in the death and disease caused by malaria may have stalled due to the rapid emergence of malaria vector control insecticide resistance [3]. The commonest target site insensitive mechanisms are the acetylcholinesterase G119S mutation and the voltagegated sodium channel L1014F mutation that causes resistance to pyrethroids [5]. The insecticidal effect of pyrethroids and organochlorines is due to the insecticide chemical binding to the sodium ion channel of the vector These chemicals act on the gating properties of the vector and keep it open [7]. Knockdown resistance (kdr) occurs when the amino acid sequences in voltage-gated sodium channels of the vector get mutated, resulting in the reduction of channel sensitivity to pyrethroid and organochlorine insecticides

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