Detection and biochemical characterization of insecticide resistance in the diamondback moth

Abstract

A strain of the diamondback moth, Plutella xylostella (L.), collected from cabbage in north Florida in 1991, was examined for insecticide resistance. When compared with a laboratory strain, resistance to pyrethroids (permethrin, cypermethrin, fenvalerate, esfenvalerate, cyhalothrin, and fluvalinate) ranged from 2132- to 82,475-fold; the highest resistance level observed was to fenvalerate. Resistance to organophosphates (chlorpyrifos, methyl parathion, malathion, methamidophos, and diazinon) ranged from 20- to 73-fold and was highest to diazinon. Resistance to the carbamates methomyl and carbofuran was 409- and 405-fold, respectively. Resistance to the cyclodiene endosulfan was 25-fold. Synergist studies showed that piperonyl butoxide (microsomal oxidase inhibitor) greatly reduced the resistance. No resistance to Bacillus thuringiensis var. kurstaki was observed in the field strain. Detoxication enzyme assays revealed that activities of microsomal oxidases (epoxidases, hydroxylase, sulfoxidase, N-demethylase, O-dealkylases), glutathione transferases (DCNB and CDNB), esterase (acetylcholinesterase), and reductases (juglone reductase and cytochrome c reductase) were 1.4- to 20.7-fold higher in the field strain than in the susceptible strain. In addition, the bimolecular rate constants for inhibition of acetylcholinesterase by dichlorvos, carbaryl, and methomyl ranged from 1.7- to 2.8-fold higher in the susceptible strain than in the field strain. The results indicated that the broad spectrum of insecticide resistance observed in the field strain was due to multiple resistance mechanisms, including increased detoxication of these insecticides by microsomal oxidases, glutathione transferases and reductases, and target site insensitivity (insensitive acetylcholinesterase).