Abstract

This article reports the current status of ethiprole resistance in Nilaparvata lugens Stal in the central region of Thailand, together with the associated resistance mechanisms. A resistance survey found that a field population had developed 308.5-fold resistance to ethiprole. Further selection with ethiprole for nine generations in the laboratory led to 453.1-fold ethiprole resistance. However, following this selection procedure, the resistance of N. lugens to other insecticides decreased to about one-third of its original resistance. This result implies that there is no cross-resistance between ethiprole and other kinds of insecticides in this pest. In an in vivo study of synergisms, triphenyl phosphate (TPP) exhibited a strong synergism (SR 4.2) with ethiprole in the resistant hoppers, piperonyl butoxide (PBO) also showed significant synergistic effects with ethiprole (1.6), but diethyl maleate (DEM) did not show any obvious synergism with ethiprole (1.2). An in vitro biochemical study indicated that esterase activity increased with ethiprole resistance in N. lugens, that P450 monooxygenase activity also increased significantly with high resistance, but that glutathione S-transferase activity did not. These results reveal that increases in esterase activity and P450 monooxygenase activity cause the ethiprole resistance observed in the field populations of N. lugens. Whether the mechanisms for ethiprole resistance involve target-site sensitivity is not yet known; further molecular analysis is required. However, an analysis of insecticide cross-resistance and the insecticide application history of the resistant populations indicated that target resistance was present and that rotation between insecticides with different modes of action will provide a key countermeasure to maintain the efficacy of ethiprole.

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