Aedes-borne diseases are on the rampant rise despite continued application of chemical insecticide-based interventions. The appearance of high degree of insecticide resistance in Aedes species and noxious effects on environment and non-targets have raised further concerns. Among new chemical interventions, neonicotinoids are considered a safe and effective approach. The present study investigated the control potency of acetamiprid and development of resistance in Aedes aegypti larvae; and the involvement of CYP450 monooxygenases in inducing resistance. The early fourth instars of Ae. aegypti parent susceptible strain (PS) were selected with acetamiprid for 15 generations (ACSF strain) increasing the resistance to 19.74-fold in ACSF-10 and 36.71-fold in ACSF-15. The ACSF-10 larvae were assayed with acetamiprid combined with piperonyl butoxide (PBO) in three different ratios (1:1, 1:5 and 1:10) and selected for next five generations with 1:10 combination. Selection with synergized acetamiprid (APSF strains) reversed as well as reduced the rate of resistance development resulting in only 1.35-fold resistance in APSF-15. The APSF strains showed %monooxygenase dependency ranging from 86.71 to 96.72%. The estimation of the monooxygenases levels in parent and selected larvae showed increased monooxygenase level in the ACSF strains by 2.42–2.87-fold. The APSF-15 strains exhibited 57.95% lower enzyme production than ACSF-15 strain. The reduction and reversion of resistance by using PBO and the elevated levels of monooxygenases in ACSF and reduction in APSF strains recommend the involvement of CYP450-mediated mechanism in the development of acetamiprid resistance in Ae. aegypti. These studies could help in devising resistance management strategies in order to preserve the efficiency of pre-existing insecticides.
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.
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.
Dysdercus koenigii is a major global pest of cotton that causes severe economic loss. Among several control measures, pyrethroids are frequently used toxicants because of high efficacy at low dosages and relative safety. Since haemocytes are biomarkers of the physiological response and immunity of insect which determine the insecticide efficacy, the current study assessed the effect of a pyrethroid, β-cyfluthrin, on the total and differential haemocyte counts of D. koenigii. Haemolymph was collected from the fifth instars after the topical application of β-cyfluthrin (0.8, 1.6, 3.2, 6.4 and 12.8 mg/L) on the thoracic tergum. The haemolymph of control nymphs revealed 5270 haemocytes/mm3 which decreased instantly by 1.4-3.1-fold on β-cyfluthrin exposure; more reduction observed at lower dosages. Increase in exposure duration and β-cyfluthrin dosages fluctuated the count considerably, eventually raising them at lower dosages and diminishing at higher dosages. Among five kinds of haemocytes recorded in the haemolymph, the β-cyfluthrin exposure increased %prohaemocytes count; diminished %granulocytes and %plasmatocytes count while spherulocyte and oenocyte counts were inconsistent. The alterations in haemocyte counts indicate the immunity response trigger in D. koenigii due to β-cyfluthrin-induced stress. Further investigations may decipher the mechanisms involved and help to formulate the strategies for its management in fields.
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