Abstract
Resistance to the knockdown effect of pyrethroid insecticides occurs due to mutations at target sites of pyrethroids, meaning the voltage-gated sodium channels gene (VGSC) in the membrane of the neurons. In fleas, this mutation occurs at two sites in the sodium channel in neurons: one is the replacement of leucine with phenylalanine (L1014F) and the other is the replacement of threonine with valine (T929V). In this study, 81 Pulex irritans and 47 Ctenocephalides canis fleas were collected from five provinces in the west and northwest of Iran. Adult fleas were exposed to cypermethrin 0.75%, and the mortality rate was calculated after 1 and 8 hr, and the mutation sites in the VGSC gene were investigated. The lethality of cypermethrin 0.75% for P. irritans was 40.00 - 57.14% after 1 hr and 60.00 - 73.91% after 8 hr. The lethality of this dose for C. canis after 1 and 8 hr of exposure was 33.33 - 41.17% and 66.66 - 80.33%, respectively. The VGSC sequence analysis indicated two mutation sites in the resistant and one mutation site in the susceptible fleas. The VGSC sequence analysis of susceptible P. irritans showed that 5.50% of them were homozygous susceptible and 94.45% were hetero-zygous susceptible. Susceptible C. canis were 5.26% homozygous and 94.73% heterozygous susceptible. All the resistant fleas were homozygous. The development of pyrethroid resistance and high-frequency L1014F mutation in fleas suggest that pyrethroids are likely to be ineffective in controlling fleas. Therefore, monitoring pyrethroid resistance and its underlying mechanisms are necessary for controlling fleas and finding new alternative control methods.