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Chemical Methods of Vector Control
Published in Jacques Derek Charlwood, The Ecology of Malaria Vectors, 2019
Alterations in the target site that cause resistance to insecticides are often referred to as knockdown resistance (kdr) in reference to the ability of insects with these alleles to withstand prolonged exposure to insecticides without being ‘knocked down’. The target site for OP and carbamate insecticides is acetylcholinesterase (AChE) in the nerve cell synapses. Several mutations in the gene encoding for an acetylcholinesterase have been found in insects, which result in reduced sensitivity to inhibition of the enzyme by these insecticides. There is cross-resistance between pyrethroids and DDT for kdr. Kdr resistance was first noted in areas where cotton was grown and where pyrethroids were used for pest control.
Permethrin
Published in M. Lindsay Grayson, Sara E. Cosgrove, Suzanne M. Crowe, M. Lindsay Grayson, William Hope, James S. McCarthy, John Mills, Johan W. Mouton, David L. Paterson, Kucers’ The Use of Antibiotics, 2017
Richard Speare, Deon V. Canyon, Jorg Heukelbach, Essam S. Shaalan
Permethrin has excellent activity against head lice (Pediculus humanus var. capitis), except where resistance has emerged (Frankowski, 2004; Burgess, 2005; Durand et al., 2012). It was first trialed for treating pediculosis in a randomized double-blind controlled trial in 1983 in Panama (Taplin et al., 1986). In its initial formulations, permethrin showed some ovicidal effect (Ares Mazas et al., 1985; Taplin et al., 1986). However, this appeared to be lost in subsequent formulations (Burgess, 1995). A systematic review of randomized trials from the twentieth century found that 1% permethrin cream rinse was the only topical treatment to have efficacy above 90% (see section 7, Clinical uses of the drug) (Vander Stichele et al., 1995). From the mid-1990s, reports of reduced efficacy began to appear, and these were subsequently shown to be a result of increasing permethrin resistance (see section 2b, Emerging resistance and cross-resistance). A Cochrane systematic review acknowledged that although permethrin was comparable to other neurotoxic pediculicides (malathion and synergized pyrethrin), local resistance patterns negated any general recommendations (Dodd, 2000; 2001). The frequency of resistance conferred by the “knockdown resistance gene” has increased progressively in the North American head lice population; in 2009 resistance was greater than 97% (Yoon et al., 2014), in some locations in 2015 it had reached 100% (Gellatly et al., 2016). The rapidly changing situation makes the conclusions of the systematic reviews about the efficacy of permethrin in treating pediculosis outdated. Dimeticones/cyclomethicones are now more effective than permethrin (Feldmeier, 2014). This has been recognized by many public health authorities who now recommend dimeticones as the treatment for pediculosis rather than permethrin, especially in areas where permethrin resistance is common.
Exploring insecticide resistance mechanisms in three major malaria vectors from Bangui in Central African Republic
Published in Pathogens and Global Health, 2018
Basile Kamgang, Williams Tchapga, Carine Ngoagouni, Claire Sangbakembi-Ngounou, Murielle Wondji, Jacob M. Riveron, Charles S. Wondji
Despite the remarkable efforts in controlling malaria during the last 10 years, this disease continues to have a negative impact on people’s health and livelihoods in Africa. The World Health Organization (WHO) estimates that 216 million cases occurred globally in 2016, leading to 445,000 deaths, most of which were in children aged under 5 years in Africa [1]. In the Central African Republic (CAR), malaria is the most important disease responsible for 58% of all hospital consultation and a principal cause of death among children [2]. Malaria prevention mainly relies on insecticide-based interventions notably long lasting insecticidal nets (LLINs) and indoor residual sprays (IRS) [3]. However, the emergence of insecticide resistance in malaria vectors can compromise these control efforts. In Africa, several Anopheles species are implicated in malaria transmission. Among them, species such as An. gambiae sensu stricto (s.s.), An. arabiensis and An. coluzzii belonging to An. gambiae complex and An. funestus s.s. belonging to An. funestus group are implicated as major malaria vectors [4]. All these vectors have been found to be resistant to several insecticides belonging to four main classes (organophosphates, carbamates, organochlorines and pyrethroids) used in public health [5–7]. It has also been show on that several resistance mechanisms are involved in insecticide resistance to malaria vectors such as the target-site resistance and metabolic resistance. The most commonly reported target-site mutation described in An. gambiae s.s. and An. coluzzii, is the knockdown resistance (kdr) mutation which has two variants; L1014F (kdr-w) and L1014S (kdr-e) and confers resistance to pyrethroids and (dichlorodiphenyltrichloroethane) DDT [8,9]. Another mutation, the Ace1RG119S, confers resistance to carbamates and organophosphates [10]. In both An. gambiae s.s and An. coluzzii, metabolic resistance has been shown to be driven by multiple genes belonging to the cytochrome P450 monooxygenases (P450s) such as CYP6M2 and CYP6P3 [11–13] and glutathione S-transferases (GSTs) [14]. Contrary to An. gambiae s.s. or An. coluzzii, no kdr mutations have been reported in An. funestus s.s. despite the presence of some non-synonymous substitutions [7,15–17]. However, two target-site resistance markers have been described in this species, the N485I Ace-1 in southern African populations [18] and the Rdl A296S mutation mainly in West, Central and East Africa populations [19]. Metabolic resistance has been shown as the main mechanism driving pyrethroid and DDT resistance in this species [20–23]. The cytochrome P450s CYP6P9a, CYP6P9b and CYP6M7 and the glutathione S-transferases GSTe2 are the main resistance genes implicated in An. funestus s.s. [21,23,24]. It was notably demonstrated that the single amino acid change L119F in an up-regulated glutathione S-transferase gene, GSTe2, confers high levels of metabolic resistance to DDT and pyrethroids in the malaria vector An. funestus s.s. [23].