Prevalence of kdr mutations and insecticide susceptibility among natural population of Aedes aegypti in West Bengal

Abstract

Background Aedes albopictus and Aedes aegypti are the major vectors of arboviral diseases. As effective vaccines are not available for most of the arboviral diseases, vector control by using insecticides play the key role to reduce the disease transmission. The emergence and spread of resistance to different classes of insecticides by the vectors is a major obstacle to control the disease transmission. Information about vector susceptibility to different insecticides and their mechanisms are very important for formulating proper vector control measures. The present study was designed to assess the susceptibility of Ae . aegypti against three different classes of adulticides, one larvicidal agent available and polymorphisms in the voltage-gated sodium channel ( VGSC ) gene related to insecticide resistance. Methods Immature stages of Ae . aegypti were collected from three dengue endemic municipal areas of West Bengal and reared in the laboratory. Larvae and adults (F1 progeny) were used for insecticide bioassay as per WHO protocols. Knock down resistance gene ( kdr ) mutations were assessed by direct sequencing of PCR products. Results The Ae . aegypti population was found to be susceptible to type II pyrethroids and malathion but highly resistant to DDT. A high rate of polymorphisms in the VGSC gene was observed among the collected mosquitoes. A double mutant V1016 G + F1534 C was found to be associated with DDT resistance but neither V1016 G nor F1534 C alone showed the same association. Association between the kdr mutations and the susceptibility status of pyrethroids could not be established due to very small sample size. A low to moderate level of resistance was noticed against temephos among the larval population based on WHO criteria. Conclusion The replacement of DDT by type II pyrethroids for the management of dengue vectors is an appropriate decision taken by the national program which is supported by the findings of a higher level of resistance to DDT. Persistence of polymorphisms in the VGSC gene might be an indication of emergence of resistance against pyrethroid insecticides that should be monitored at a regular interval. Attempts should be made to determine the effectiveness of other larvicides for replacement of temephos if needed in future. Along with the chemical insecticides different biological vector control methods as well as biopesticides should also be used in vector control programmes.

Molecular Resistance Status of Aedes aegypti to the Organophosphate and Pyrethroid Insecticides in Central Sulawesi and East Nusa Tenggara Provinces, Indonesia

“…In addition, larvicide plays an important role to manage and control larval stages of Ae. aegypti [10]. The selection of active ingredients with an appropriate dose is very important for this purpose.…”

“…In the absence of specific medications against dengue and an effective vaccine still under research, the control of mosquitoe vector is the sole strategy to prevent and control the transmission of dengue [4,10] .The government of Indonesia, through the Ministry of Health and local govenments, have carried out vector control activities for more than five decades. In the early 1990s, the Ministry of Health issued a series of legislations concerning the National DF/DHF prevention and control program and the implementation of the control program.…”

“…The second mechanism is mutations in insecticide target proteins in the central nervous system that leads to these protein to susceptibly decrease to coresponding insecticides [15][16][17][18]. The third and fourth are behavioral changes and thickening of the cuticle, respectively [10,16,17]. The first two mechanisms are most studied [10,18,19] Increased production of three main metabolic enzymes, i.e.…”

“…The third and fourth are behavioral changes and thickening of the cuticle, respectively [10,16,17]. The first two mechanisms are most studied [10,18,19] Increased production of three main metabolic enzymes, i.e. cytochrome P450 monooxygenases or mixed-function oxydases (P450 or MFOs), glutathione Stransferases (GST), and esterases are reported to be associated with metabolic resistance [10,15,16,20].…”

“…The first two mechanisms are most studied [10,18,19] Increased production of three main metabolic enzymes, i.e. cytochrome P450 monooxygenases or mixed-function oxydases (P450 or MFOs), glutathione Stransferases (GST), and esterases are reported to be associated with metabolic resistance [10,15,16,20]. The most common target site resistance mechanism is associated with mutations of a target protein at the voltage-gated sodium channel (VGSC) gene, which is the target of pyrethroid (PY) insecticide and point mutation at the acetylcholinesterase (AchE) gene that is the target of OP and carbamate insecticides.…”