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Evaluation of resistance, cross-resistance and synergism of abamectin and teflubenzuron in a multi-resistant field population of Plutella xylostella (Lepidoptera: Plutellidae)

  • M. Iqbal (a1) and D.J. Wright (a1)


The efficacy of abamectin (AgrimecR) and teflubenzuron (NomoltR) was assessed by leaf-dip bioassay against larvae of the diamondback moth, Plutella xylostella Linnaeus from a population (SERD3) collected originally in lowland Malaysia in December 1994. Evidence for resistance to both abamectin and teflubenzuron was found in the F7 generation (LC50 ratio of 60 and 24 respectively compared with a laboratory, insecticide-susceptible strain). Selection of sub-populations of SERD3 (F7–F9) with abamectin and teflubenzuron increased the LC50 ratio to 220 and 360 respectively and estimates of realized heritability [h2] were high (c. 0.8 and 0.9) for both compounds. There was no cross-resistance between these compounds in the abamectin and teflubenzuron-selected sub-populations but some indication of negatively-correlated resistance. Topical application of the synergists piperonyl butoxide, S,S,S-tributylphosphorotrithioate and maleic acid diethyl ester to the laboratory strain had no significant effect on the toxicity of abamectin or teflubenzuron in subsequent leaf-dip assays. In contrast, pre-treatment with piperonyl butoxide and S,S,S-tributylphosphorotrithioate significantly increased the toxicity of abamectin (c. 4- and 3-fold) and teflubenzuron (c. 7- and 19-fold) in the abamectin and teflubenzuron-selected sub-populations of SERD3, suggesting that microsomal monoxygenases and/or esterases may be involved in resistance. Pre-treatment with maleic acid diethyl ester only increased the toxicity of abamectin by c. 2-fold and had no significant effect on the toxicity of teflubenzuron, providing limited evidence for the involvement of glutathione-S-transferases in resistance to the former compound alone.


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