Abstract
Anopheles gambiae Giles (Diptera: Culicidae) is the most prolific malaria vector in sub-Saharan Africa, where widespread insecticide resistance has been reported. An. gambiae laboratory strains are commonly used to study the basic biology of this important mosquito vector, and also in new insecticide discovery programs, where insecticide-susceptible and -resistant strains are often used to screen new molecules for potency and cross-resistance, respectively. This study investigated the toxicity of permethrin, a Type-I pyrethroid insecticide, and etofenprox, a non-ester containing pyrethroid insecticide, against An. gambiae at three life stages. This characterization was performed with susceptible (G3; MRA-112) and resistant (Akdr; MRA-1280) An. gambiae strains; the Akdr strain is known to contain the L1014F mutation in the voltage-sensitive sodium channel. Surprisingly, etofenprox displays a lower level of resistance than permethrin against all stages of mosquitoes, except in a headless larval paralysis assay designed to minimize penetration factors. In first-instar An. gambiae larvae, permethrin had significant resistance, determined by the resistance ratio (RR50 = 5), but etofenprox was not significantly different (RR50 = 3.4) from the wild-type strain. Fourth-instar larvae displayed the highest level of resistance for permethrin (RR50 = 108) and etofenprox (RR50 = 35). Permethrin (PC50 = 2 ppb) and etofenprox (PC50 = 9 ppb) resulted in headless larval paralysis (5-h), but resistance, albeit lower, was still present for permethrin (RR50 = 5) and etofenprox (RR50 = 6.9). In adult female mosquitoes, permethrin displayed higher resistance (RR50 = 14) compared to etofenprox (RR50 = 4.3). The level of etofenprox resistance was different from that previously reported for a similar Akron An. gambiae laboratory strain (MRA-913). The chemical synergists piperonyl butoxide (PBO) and diethyl maleate (DEM) were able to synergize permethrin, but not etofenprox in the resistant strain (Akdr). In conclusion, multiple mechanisms are likely involved in pyrethroid resistance, but resistance profiles are dependent upon selection. Etofenprox is an effective insecticide against An. gambiae in the lab but will likely suffer from resistance in the field.
Highlights
The African malaria mosquito, Anopheles gambiae Giles (Diptera: Culicidae), is the most efficient vector of malaria in Sub-Saharan Africa [1], and insecticide treated bed nets (ITNs) and/or indoor residual spraying (IRS) are used to decrease its populations
An. gambiae were reared from eggs obtained from pyrethroid susceptible (G3, MRA-112) and pyrethroid-resistant (Akron-kdr (Akdr), MRA-1280) colonies maintained by the Malaria Research and Reference Reagent Resource Center (MR4), part of the Biodefense and Emerging Infections (BEI) Research Resources Repository at the Center for Disease Control and Prevention (CDC), Atlanta, GA, USA
The toxicity of permethrin and etofenprox was examined against susceptible (G3) and resistant (Akdr) first-instar An. gambiae larvae (Table 1)
Summary
The African malaria mosquito, Anopheles gambiae Giles (Diptera: Culicidae), is the most efficient vector of malaria in Sub-Saharan Africa [1], and insecticide treated bed nets (ITNs) and/or indoor residual spraying (IRS) are used to decrease its populations. Insects 2018, 9, 146 endemic with An. gambiae report resistance to at least a single class of insecticide, and more than 60%. Of these countries reported resistance to two or more insecticide classes [1]. Protection of military personnel from arthropod-vectored diseases is often achieved with the use of insecticide-treated combat and work uniforms [3,4], and permethrin, a Type-I pyrethroid insecticide, has long been approved for this use. According to the Insecticide Resistance Action Committee’s (IRAC’s) mode of action classification system, pyrethrum and pyrethroid insecticides (Group 3) modify the insect voltage-sensitive sodium channel (VSSC) [6]. VSSCs are transmembrane proteins that function in the movement of sodium ions into the cell, resulting in membrane depolarization during an action potential. Different classes of pyrethroid insecticides differently affect the VSSC causing depolarization of resting membrane potential, and/or repetitive nerve firing [9]
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