Cross‐resistance,inheritance and biochemical mechanisms of imidacloprid resistance in B‐biotype Bemisia tabaci

BACKGROUND: The B‐type Bemisia tabaci (Gennadius) has become established in many regions in China, and neonicotinoids are extensively used to control this pest. Imidacloprid resistance in a laboratory‐selected strain of B‐type B. tabaci was characterised in order to provide the basis for recommending resistance management tactics. RESULTS: The NJ‐Imi strain of B‐type B. tabaci was selected from the NJ strain with imidacloprid for 30 generations. The NJ‐Imi strain exhibited 490‐fold resistance to imidacloprid, high levels of cross‐resistance to three other neonicotinoids, low levels of cross‐resistance to monosultap, cartap and spinosad, but no cross‐resistance to abamectin and cypermethrin. Imidacloprid resistance in the NJ‐Imi strain was autosomal and semi‐dominant. It is shown that enhanced detoxification mediated by cytochrome‐P450‐dependent monooxygenases contributes to imidacloprid resistance to some extent in the NJ‐Imi strain. Results from synergist bioassays and cross‐resistance patterns indicated that target‐site insensitivity may be involved in imidacloprid resistance in the NJ‐Imi strain of B. tabaci. CONCLUSION: Although oxidative detoxification mediated by P450 monooxygenases is involved in imidacloprid resistance in the NJ‐Imi strain of B‐type B. tabaci, target‐site modification as an additional resistance mechanism cannot be ruled out. Considering the high risk of cross‐resistance, neonicotinoids should be regarded as a single group when implementing an insecticide rotation scheme in B. tabaci control. Copyright © 2009 Society of Chemical Industry