Molecular evidence for a kdr‐like pyrethroid resistance mechanism in the malaria vector mosquito Anopheles stephensi

Medical and Veterinary Entomology - Tập 17 Số 2 - Trang 138-144 - 2003
Ahmadali Enayati1,2, Hassan Vatandoost3,4, H. Ladonni3,4, H. Townson5, Janet Hemingway5
1Mazandaran University of Medical Sciences, Iran
2Dr Ahmad Ali Enayati, Medical Entomology Group, School of Public Health, Mazandaran University of Medical Sciences, Amir Boulevard, Sari, Iran.
3Dr Hossein Ladonni & Dr Hassan Vatandoost, Medical Entomology Department, School of Public Health & Institute of Health Research, Teheran University of Medical Sciences, PO Box 6446-14155, Tehran, Iran.
4†Teheran University of Medical Sciences, Iran, and
5Liverpool School of Tropical Medicine U.K.

Tóm tắt

Abstract.  The mosquito Anopheles stephensi Liston (Diptera: Culicidae) is the urban vector of malaria in several countries of the Middle East and Indian subcontinent. Extensive use of residual insecticide spraying for malaria vector control has selected An. stephensi resistance to DDT, dieldrin, malathion and other organophosphates throughout much of its range and to pyrethroids in the Middle East. Metabolic resistance mechanisms and insensitivity to pyrethroids, so‐called knockdown resistance (kdr), have previously been reported in An. stephensi. Here we provide molecular data supporting the hypothesis that a kdr‐like pyrethroid‐resistance mechanism is present in An. stephensi. We found that larvae of a pyrethroid‐selected strain from Dubai (DUB‐R) were 182‐fold resistant to permethin, compared with a standard susceptible strain of An. stephensi. Activities of some enzymes likely to confer pyrethroid‐resistance (i.e. esterases, monooxygenases and glutathione S‐transferases) were significantly higher in the permethrin‐resistant than in the susceptible strain, but the use of synergists — piperonyl butoxide (PBO) to inhibit monooxygenases and/or tribufos (DEF) to inhibit esterases — did not fully prevent resistance in larvae (permethrin LC50 reduced by only 51–68%), indicating the involvement of another mechanism. From both strains of An. stephensi, we obtained a 237‐bp fragment of genomic DNA encoding segment 6 of domain II of the para type voltage‐gated sodium channel, i.e. the putative kdr locus. By sequencing this 237 bp fragment, we identified one point mutation difference involving a single A–T base change encoding a leucine to phenylalanine amino acid substitution in the pyrethroid‐resistant strain. This mutation appears to be homologous with those detected in An. gambiae and other insects with kdr‐like resistance. A diagnostic polymerase chain reaction assay using nested primers was therefore designed to detect this mechanism in An. stephensi.

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Medical and Veterinary Entomology

Tập 17 Số 2

138-144

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