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Toxicological and mechanistic studies on neonicotinoid cross resistance in Q-type Bemisia tabaci (Hemiptera: Aleyrodidae)


  • Based on a presentation at the Meeting ‘Resistance 2001’, organised by IACR, SCI and BCPC and held at IACR, Rothamsted, Harpenden, UK, on 24–26 September 2001


The tobacco whitefly, Bemisia tabaci Gennadius (Homoptera: Aleyrodidae) is a serious pest in numerous cropping systems and has developed a high degree of resistance against several chemical classes of insecticides. One of the latest group of insecticides introduced to the market were the neonicotinoids (chloronicotinyls), acting agonistically on insect nicotinic acetylcholine receptors. Resistance to neonicotinoid insecticides has recently been shown to occur, especially in Q-type B tabaci in some places in Almeria, Spain, whereas control of B-type B tabaci in many other intense cropping systems worldwide has remained on high levels. Our study revealed that neonicotinoid-resistant Q-type strains from Almeria were often more than 100-fold less susceptible to thiamethoxam, acetamiprid and imidacloprid when tested in discontinuous systemic laboratory bioassays. The resistance factors were generally 2- to 3-fold lower in leaf-dip bioassays. In addition to the Spanish strains, we obtained two other highly neonicotinoid-cross-resistant B tabaci greenhouse populations, one from Italy (December 1999) and one from Germany (June 2001). A molecular diagnostic analysis revealed that both strains also belong to the (Spanish) subtype Q of the B tabaci species complex. The resistance levels of Q-type whitefly strains derived from Almeria greenhouses in 1999 remained stable for at least two years, even when maintained in the laboratory without any selection pressure. The biochemical mechanisms conferring resistance to neonicotinoids have not yet been elucidated in detail, but synergist studies suggested a possible involvement of microsomal monooxygenases. Furthermore, we checked two Almerian strains of B tabaci isolated in 1998 and 1999 and demonstrated that neonicotinoid resistance is not due to an altered [3H]imidacloprid binding site of nicotinic acetylcholine receptors.

© 2002 Society of Chemical Industry