Pyrethroids resistance in Pulex irritans and Ctenocephalides canis in west and northwest Iran

سال انتشار: 1401
نوع سند: مقاله ژورنالی
زبان: انگلیسی
مشاهده: 39

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شناسه ملی سند علمی:

JR_VRFAN-13-4_011

تاریخ نمایه سازی: 25 آبان 1402

چکیده مقاله:

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 (L۱۰۱۴F) and the other is the replacement of threonine with valine (T۹۲۹V). In this study, ۸۱ Pulex irritans and ۴۷ Ctenocephalides canis fleas were collected from five provinces in the west and northwest of Iran. Adult fleas were exposed to cypermethrin ۰.۷۵%, and the mortality rate was calculated after ۱ and ۸ hr, and the mutation sites in the VGSC gene were investigated. The lethality of cypermethrin ۰.۷۵% for P. irritans was ۴۰.۰۰ - ۵۷.۱۴% after ۱ hr and ۶۰.۰۰ - ۷۳.۹۱% after ۸ hr. The lethality of this dose for C. canis after ۱ and ۸ hr of exposure was ۳۳.۳۳ - ۴۱.۱۷% and ۶۶.۶۶ - ۸۰.۳۳%, 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 ۵.۵۰% of them were homozygous susceptible and ۹۴.۴۵% were hetero-zygous susceptible. Susceptible C. canis were ۵.۲۶% homozygous and ۹۴.۷۳% heterozygous susceptible. All the resistant fleas were homozygous. The development of pyrethroid resistance and high-frequency L۱۰۱۴F 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.

کلیدواژه ها:

Ctenocephalides canis ، Pulex irritans ، Pyrethroid ، resistance ، Voltage-gated sodium channels gene

نویسندگان

Shahin Seidy

Department of Pathobiology, Faculty of Veterinary Medicine, Urmia University, Urmia, Iran

Mousa Tavassoli

Department of Pathobiology, Faculty of Veterinary Medicine, Urmia University, Urmia, Iran

Farnaz Malekifard

Department of Pathobiology, Faculty of Veterinary Medicine, Urmia University, Urmia, Iran

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