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The constant rise in cases of Zika, Dengue and Chikungunya worldwide has made control of Aedes aegypti a principal concern. The most recommended plan to control mosquito-borne diseases primarily lies on vector management and disturbing their disease-transmission cycle. Wide-ranging use of different classes of organic insecticides for mosquito control has led to the development of high levels of resistance making them less operative at safe dosages imposing us to explore novel insecticides. Present study investigates the bioefficacy of a neonicotinoid, acetamiprid on the Ae. aegypti larvae, development of resistance after subjecting acetamiprid selection pressure for 10 successive generations and biochemical characterization of the resistance developed. Acetamiprid exposure of the parent population of Ae. aegypti early fourth instars resulted in respective LC 50 and LC 90 values of 0.188 ppm and 1.315 ppm. Selection with acetamiprid for 10 successive generations (ACSF-10) reduced its efficacy by 20-fold. Involvement of four enzymes; alphaesterases, beta-esterases, glutathione-S-transferases and acetylcholinesterases in development of acetamiprid resistance was investigated to uncover mode of action of acetamiprid. An elevation of 1.4-fold and 2.1-fold was observed in alpha-esterases and beta-esterases activity in ACSF-10 as compared to ACSF-5. However, activity of glutathione-S-transferases decreased in ACSF-5 which rose to 12-fold in ACSF-10. Similarly, the activity of acetylcholinesterases was found to be much higher in resistant generations as compared to the parental strains. The results indicated individual/synergistic contribution of different enzymes leading to acetamiprid detoxification. Further research is being conducted to identify the role of target site mutations in resistance development.

Despite the continuous use of chemical interventions, Aedes-borne diseases remain on the rise. Neonicotinoids are new, safer, and relatively effective pharmacological interventions against mosquitoes. Neonicotinoids interact with the postsynaptic nicotinic acetylcholine receptors (nAChRs) of the insect central nervous system, but the absence of nAChR polymorphism in resistant phenotypes makes their involvement in neonicotinoid resistance uncertain. Thus, an investigation was carried out to understand the role of metabolic detoxification and target site insensitivity in imparting acetamiprid resistance in Aedes aegypti larvae. Studies were conducted on the parent susceptible strain (PS), acetamiprid-larval selected strain for five generations (ACSF-5; 8.83-fold resistance) and 10 generations (ACSF-10; 19.74-fold resistance) of Ae. aegypti. The larval selection raised α-esterase and β-esterase activities by 1.32-fold and 1.34-fold, respectively, in ACSF-10 as compared to PS, while the corresponding glutathione-S-transferase and acetylcholinesterase activity increased by 22.5 and 2%. The ace-1 gene in PS and ACSF-10 showed four mismatches in the 1312—1511 bp region due to mutations in the Y455C codon (tyrosine to cysteine) at the 1367th position (TAC→TGC); I457V codon (isoleucine to valine) at 1372 bp and 1374 bp (ATA→GTG); and R494M codon (arginine to methionine) at 1484 bp (AGG→ATG). The R494M mutation was the novel and dominant type, observed in 70% ACSF-10 population, and has not been reported so far. The studies evidenced the combination of metabolic detoxification and target site mutation in imparting acetamiprid resistance in Ae. aegypti.

Chemical control of dengue vector, Aedes aegypti is impaired due to development of resistance to conventional insecticides. Insect Growth Regulators (IGRs) are considered more suitable and effective vector control agents as they specifically inhibit chitin biosynthesis, a process absent in vertebrates, and impose less adverse effects on beneficial insects and the environment. Present study investigates Lufenuron, a Chitin Synthesis Inhibitor (CSI), as a control agent of Ae. aegypti. Different instars of Ae. aegypti were exposed to a range of concentrations of Lufenuron as per WHO protocol. The investigations showed the effective hormone-mimetic effect of Lufenuron resulting in the formation of a significant number of larval-pupal and pupal-adult intermediates with the maximum number observed on exposure to L3 (L-P=17%, P-A=21%). Approximately 20% of L2 instars either could not moult and remained trapped inside the new exuviae or possessed bulged abdomen while some showed ruptured exoskeleton. The results showed increase in IE 30 from L1 (0.00010 ppm) to L4 stage (0.00013 ppm); the L2 stage exhibiting maximum IE 30 (0.00025 ppm). The median emergence suppression (IE 50 ) doses of the Lufenuron were found to be 0.00057 ppm for L1, 0.00047 ppm for L2, 0.00050 ppm for L3 and 0.00096 ppm for L4. The results also revealed increased duration of larval development and inability of pupae to develop into adults, as compared to the controls. The investigations indicate the potential use of Lufenuron as the control agent of Ae. aegypti. Further research is being conducted to understand its mode of action to develop effective control strategies.

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