Aphicidal activity of imidacloprid against a tobacco feeding strain of Myzus persicae (Homoptera: Aphididae) from Japan closely related to Myzus nicotianae and highly resistant to carbamates and organophosphates

Abstract

We investigated the resistance potential of a red-coloured Japanese strain (JR) of a tobacco feeding form of Myzus persicae (Sulzer) of the M. persicae species complex closely related to the tobacco aphid Myzus nicotianae Blackman. Bioassays were performed with a range of insecticides, imidacloprid, nicotine and cartap, thought to act on nicotinic acetylcholine receptors in vivo, as well as with two conventional insecticides, pirimicarb and oxydemeton-methyl, acting on acetylchol-inesterase (AChE). Compared to a susceptible strain, JR showed high resistance to pirimicarb and oxydemeton-methyl, but was far less resistant to nicotine, cartap and imidacloprid. Imidacloprid was, among the insecticides tested, the most active compound in contact and ingestion bioassays. Compared to the susceptible strain, JR showed four-to seven-fold resistance to imidacloprid depending on the type of bioassay. Resistance factors for other insecticides tested in an oral ingestion bioassay were: cartap five-fold, nicotine nine-fold, oxydemeton-methyl 107-fold and pirimicarb > 385-fold. JR showed high carboxylesterase activity. Polyacrylamide gel electrophoresis indicated esterase FE4 as the major carboxylesterase. As for most M. persicae strains and some Greek strains of M. nicotianae, JR was monomorphic for glutamate oxalacetate transaminase. Studies with pirimicarb showed a marked insensitivity of AChE to inhibition by this chemical, whilst such insensitivity could not be detected with the organophosphate insecticide oxydemeton-methyl. Receptor binding assays with [³H]-imidacloprid in aphid homogenates revealed I₅₀-values of 0.4 to 0.8 nM and no statistical difference between the JR and susceptible strain.