Bioassays of nicotine and imidacloprid against clones of Myzus persicae (Sulzer) and Myzus nicotianae (Blackman) from around the world demonstrated that some had low levels of resistance to both compounds. This was (expressed not only as a reduced mortality, but more markedly as differential inhibition of feeding by imidacloprid concentrations in the parts per billion range. Such concentrations also reduced aphid fecundity by inhibiting the production and viability of nymphs, and this effect was more marked for susceptible aphids than for those showing reduced direct lethal and antifeedant effects.

: The peach-potato aphid Myzus persicae (Sulzer) can resist a range of insecticides by over-producing detoxifying esterase and having mutantinsensitive forms of the target proteins, acetylcholinesterase (AChE), and the sodium channel. Using a combination of bioassays, biochemical and DNA diagnostics, it is now possible to diagnose all three mechanisms in individual aphids, and thereby establish their spatial distributions and temporal dynamics. A survey of 58 samples of wide geographic origin showed that all 46 resistant clones had ampliÐed esterase genes (E4 or FE4) conferring broad-spectrum resistance to pyrethroids, organophosphates and carbamates. These occurred in combination with insensitive AChE (11 clones), conferring resistance to pirimicarb and triazamate, and/or mutant sodium channel genes (25 clones), conferring knockdown (kdr) resistance to pyrethroids and DDT. AmpliÐed esterase genes were in linkage disequilibrium with both insensitive AChE and the kdr mutation, reÑec-ting tight physical linkage, heavy selection favouring aphids with multiple mechanisms, and/or the prominence of parthenogenesis in many M. persicae populations. An ability to monitor individual mechanisms with contrasting cross-resistance proÐles has important implications for the development of resistance management recommendations.

The well-established carboxylesterase-based resistance to insecticides in Myzus persicae Sulzer has recently been accentuated by the appearance of aphids with a modified acetylcholinesterase (MACE) insensitive to pirimicarb and the novel aphicide, triazamate. This target site resistance mechanism was found in M. persicae from crops in the UK for the first time in 1996, together with especially large proportions of aphids with R 2 and R 3 levels of carboxylesterases, a combination that was associated with serious insecticide failures. This paper describes the incidence of both mechanisms and discusses the implications for future recommendations for aphid control in the UK.

Bioassays of nicotine and imidacloprid against clones of Myzus persicae (Sulzer) and Myzus nicotianae (Blackman) from around the world demonstrated that some had low levels of resistance to both compounds. This was expressed not only as a reduced mortality, but more markedly as differential inhibition of feeding by imidacloprid concentrations in the parts per billion range. Such concentrations also reduced aphid fecundity by inhibiting the production and viability of nymphs, and this effect was more marked for susceptible aphids than for those showing reduced direct lethal and antifeedant effects.

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