Detection And Characterization of Insecticide Resistance Mechanisms in Culex Tarsalis

Insecticide resistance in disease-transmitting arthropods has become a serious hindrance for successful vector control. Mosquitoes, in particular, are notorious vectors of potentially deadly diseases like malaria, dengue fever, and West Nile virus. Anopheles gambiae and Culex quinquefasciatus are just two examples of mosquito vectors that possess genetic mutations (denoted kdr and ace-1 ) and/or enhanced detoxifying enzymes (oxidases, esterases, and glutathione-s-transferases) that confer insecticide resistance. Culex tarsalis, a primary vector for West Nile virus among other arboviruses in Northern California, is a target for insecticide application and is under constant insecticide pressure, making it likely to adapt resistance mechanisms like kdr or ace-1 or increased detoxifying enzymes. Culex tarsalis adult females were collected from Yolo and Sutter counties. A bottle bioassay was completed to determine prevalence of resistance to Sumithrin (a pyrethroid; N=217) and Naled (an organophosphate; N=154). A susceptible lab-reared colony was used for comparison. Microplate assays were completed to investigate elevated levels of detoxification enzymes present as well as AChE. PCR was used to amplify the VGSC and ace-1 genes. Amplicons were sequenced and aligned to determine if mutations were present. No evidence of the ace-1 mutation was found in any mosquitoes, but the kdr mutation was seen in all semi-resistant and resistant individuals exposed to Sumithrin. Microplate data revealed significant differences between certain detoxifying enzymes within mosquitoes collected from Sutter and Yolo Counties exposed to both Sumithrin and Naled. The data obtained from this study suggests that resistance to Sumithrin in both populations is carried out by both metabolic and target site insensitivity, while resistance to Naled is caused by metabolic resistance only