Resistance and metabolism of imidacloprid in Colorado potato beetle, Leptinotarsa decemlineata Say (Coleoptera: Chrysomelidae)

Since 1995, imidacloprid, a neonicotinoid compound and an agonist of nicotinic acetylcholine receptors, has been vital for the control of the Colorado potato beetle in many areas of the United States. High levels of resistance to this compound were detected in beetle populations collected in Long Island, NY after less than three years of use. In 1998, the imidacloprid resistance ratios ranged from 27-fold to 155-fold. Three imidacloprid resistant Long Island populations expressed very low levels of cross resistance to another neonicotinoid insecticide, thiamethoxam (resistance ratios ranged from 1.7-fold to 3.1-fold) and no cross resistance to bensultap, a nereistoxin derived compound, acting as an antagonist of the insect acetylcholine receptor. In 1999, significant survivals (17 to 80%) were found in populations from Long Island treated with a discriminating doses of 3.16 μg/beetle. High correlation was found between KD₅₀ and mortality 10 days after treatment (r = 0.90, p = 0.0007). The susceptible populations had faster knock down than resistant populations, and this fast knock down was significant correlated with high mortality 10 days after treatment. Mix of imidacloprid + the synergist piperonyl butoxide partially suppressed resistance in the Long Island strains.; Rapid penetration and excretion of 14C-imidacloprid were observed in a susceptible and a resistant strain of Colorado potato beetle. Comparison of the pharmacokinetics of 14C-imidacloprid in the resistant and susceptible strains treated with a low dose (16 ng/beetle) indicated a slightly lower rate of uptake in the resistant strain, but no significant difference was seen in the percentage of the dose excreted and present in the body. The pharmacokinetics in the resistant strain treated with a low dose and a high dose (900 ng/beetle) also indicated a similar pattern for the percent of external radioactivity, excretion and internal radioactivity of 14C-imidacloprid. Thus no significant differences were found between the susceptible strain and the resistant strain in either the metabolism or excretion of imidacloprid that could explain resistance, and the internal levels of imidacloprid were comparable in both strains. Both resistant and susceptible strains showed minimal metabolic conversion. Only a single major radioactive metabolite was formed. This was probably the olefine analog of imidacloprid. The resistant strain was also cross-resistant to the olefine compound which was less toxic than the parent imidacloprid.; The lack of differences in the pharmacokinetics and metabolism of imidacloprid observed in these experiments between resistant and susceptible beetles together with differences in intoxication symptoms suggest that resistance could be due to a modification of the target site, the nicotine AchRs. Further neurophysiology studies using the isolated nervous systems, together with studies of binding site competition of the nAChRs between resistant and susceptible strains of Colorado potato beetle are essential to determine if the target site modification is the mechanism of resistance to imidacloprid in the NY Selected strain.