Nauen_1998_Pest.Sci_53_133

It is known from laboratory studies that tobacco-associated forms of Myzus persicae (Sulzer) and the closely related tobacco aphid Myzus nicotianae (Blackman) are often somewhat less susceptible to imidacloprid than non-tobacco strains of M. persicae. Choice tests (floating leaf technique) showed that tobacco aphids were also less susceptible to the antifeedant potential of imidacloprid in contact bioassays. Synergists like piperonyl butoxide or DEF did not enhance the susceptibility of tobacco-associated morphs of Myzus ssp. to imidacloprid, thus providing evidence that neither oxidative detoxication nor hydrolytic metabolization took place. However, in an attempt to study the influence of endosymbiotic bacteria on the efficacy of imidacloprid, we allowed small populations of tobacco aphids to feed on diets containing the antibiotic chlortetracycline prior to imidacloprid treatment. While the effectiveness of imidacloprid, i.e. lower LC50 values, could be improved in all strains, including the susceptible reference strain, there was no change in overall tolerance factors. In order to investigate any possible alteration of the target site, the affinity of imidacloprid and nicotine to nicotinic acetylcholine receptors in whole-aphid homogenates was measured. All strains (and clones) showed the same high-affinity binding sites and no detectable difference. Studies using the FAO dip method revealed that the lower susceptibility of M. nicotianae is not restricted to chloronicotinyls like imidacloprid or acetamiprid, because other insecticides with different modes of action such as pymetrozine and fipronil were also affected in laboratory studies. It is considered that the observed tolerance to chloronicotinyls in certain strains of Myzus ssp. is a natural variation in response, probably not coupled with any known mechanism of resistance in this species complex.