Mechanisms of carbamate resistance in the malaria vector: Anopheles gambiae

Abstract

In Africa, the female <i>Anopheles gambiae</i> is the primary malaria vector and a key target of vector control measures. The four principal classes of insecticides used in the control of these vectors are pyrethroids, organophosphates, carbamates and organochlorines. Historically, pyrethroids were the main type of insecticides employed to impregnate insecticide-treated nets because they are less toxic to humans and more effective against mosquitoes. The effectiveness of these interventions is however currently challenged by the development of pyrethroid-resistant mosquito populations. The World Health Organization recommends alternative or rotational use of carbamate insecticides in pyrethroid-resistant areas. The mechanism of action of carbamates is to inhibit acetylcholinesterase reversibly to trigger the build-up of acetylcholine in mosquito nerves and consequent paralysis and death of the mosquito. However, carbamate resistance is also on the rise, and poses significant issues to malaria control systems. Notably, the mechanisms of carbamate resistance in <i>Anopheles gambiae</i> are target site mutations in the acetylcholinesterase gene and increased detoxification of carbamate by enzymes, including esterases and cytochrome P450s. This review presents a synthesis of existing information on the molecular and metabolic pathways of carbamate resistance in the <i>Anopheles gambiae</i> and discuss their consequences for the control of malaria vector. Understanding these resistance mechanisms is crucial for sustaining the effectiveness of IRS, informing insecticide resistance management strategies, and guiding malaria control policies in areas where pyrethroid resistance is increasing. Keywords: Carbamate, Insecticide Resistance, female <i>Anopheles gambiae</i>, Malaria Vector.