Phenotypic effects of concomitant insensitive acetylcholinesterase ( ace-1 R ) and knockdown resistance ( kdr R ) in Anopheles gambiae : a hindrance for insecticide resistance management for malaria vector control

Abstract

Background: Malaria is endemic in sub-Saharan Africa with considerable burden for human health. Major insecticide resistance mechanisms such as kdr R and ace-1

Evidence of multiple insecticide resistance mechanisms in Anopheles gambiae populations in Bangui, Central African Republic

“…Accordingly, these data can justify the slow effect of fenitrothion on mosquito populations in the absence of the Ace-1 R mutation. The same results have been observed in Cameroon by Nwane et al [15] and in Benin by Assogba et al [13]. …”

“…Consequently, the emergence of resistance in natural populations of A. gambiae to various classes of insecticides used in malaria vector control strategies has been reported in many African countries [10]. Consequently, multiple mechanisms of resistance to insecticides have been observed in anopheline populations, including target site mutation ( kdr , Ace-1 R ) [11–13] and increased metabolic detoxification [overproduction of esterases, cytochrome P450 monooxygenases and glutathione-S-transferases (GST)] [14, 15]. …”

An ace-1 gene duplication resorbs the fitness cost associated with resistance in Anopheles gambiae, the main malaria mosquito

“…This would select for resistance to the new IRS and ITN, and could be quite disastrous. In high PYR resistance areas, ace-1 D would spread in populations with high frequencies of the kdr allele; yet previous studies showed that kdr and ace-1 R ( ace-1 D -kdr interaction has not been investigated so far) act in synergy for both resistance levels and fitness costs 61 62 . Furthermore, a recent study showed that ace-1 duplication associated with enzyme detoxification seems to confer a very high bendiocarb resistance to An.…”

A genetic model of the effects of insecticide-treated bed nets on the evolution of insecticide-resistance

“…We assume, e.g. that the resistance allele gives a similar level of resistance to larvae and adults and that the level of dominance is similar in the two life stages, as observed in insecticide bioassays conducted with larval and adult mosquitoes of various genotypes [ 41 , 42 ]. In our model, we talk about a lethal concentration but in the natural setting, this will also depend on the exposure length (compare a short contact with an ITN to a more prolonged contact in the larval environment) as well as the concentration of the insecticide in a given environment (potentially a stronger concentration on an ITN).…”