Characterization of abamectin resistance in Iranian populations of European red mite, Panonychus ulmi Koch (Acari: Tetranychidae)

The European red mite, Panonychus ulmi Koch is one of the most important pests in apple orchards and was introduced to Iran by apple seedlings from Europe. The insecticide/acaricide abamectin for example has been used extensively against P. ulmi and some other pests in apple orchards. To evaluate abamectin resistance in field-collected populations of P. ulmi, 12 populations were collected from commercial apple orchards of East Azarbaijan, West Azarbaijan, and Isfahan provinces. The abamectin toxicity was determined by a leaf disc spray method. The LC₅₀ values of abamectin ranged from 0.11 mg a. i.L⁻¹ to 5.50 mg a. i.L⁻¹. All field populations were resistant to abamectin (RR ranged from 11- to 46-fold) in comparing with PSR-TK, a reference susceptible population for abamectin. The Mahabad population was identified as the most resistant population. The glutamate-gated chloride channels (GluCls) are well-known target site of abamectin in mites and it was demonstrated that amino acid substitutions in GluCls can confer abamectin resistance. The partial channels PuGluCl1, PuGluCl2, and PuGluCl3 were sequenced in Mahabad population, but the previously reported point mutations associated with abamectin resistance in Tetranychus urticae Koch were not found. In contrast, the cytochrome P450 monooxygenase inhibitor piperonyl butoxide (PBO) significantly increased abamectin toxicity in Mahabad (synergistic ratio SR= 64), a moderately resistant population, and Shahin Dej (SR = 2) population. Also, pretreatment of triphenylphosphate (TPP) resulted in reduced LC₅₀ values of abamectin in Shahin Dej (SR = 4.79) and Mahabad (SR = 8.91) populations. The second highest synergism ratio (SR = 22.13) against abamectin was observed in the resistant population of Mahabad with the glutathione S-transferase inhibitor diethylmaleate (DEM). Although quantification of activity of detoxification enzymes with model substrates did not support the role of detoxification enzymes, the synergism assays and the lack of target-site resistance suggested that multiple metabolic mechanisms are involved in abamectin resistance.