Biorational insecticides: Mechanism and cross‐resistance

Potency and cross-resistance of various biorational insecticides, exemplified by the whitefly Bemisia tabaci, have been studied. Bemisia tabaci were exposed to the juvenile hormone mimic pyriproxyfen for the past 12 years resulting in an over 2,000-fold resistance, but there was no appreciable cross-resistance with the benzoylphenyl urea novaluron. Similarly, no cross-resistance was found between pyriproxyfen and the two neonicotinoids, acetamiprid and imidacloprid. On the other hand, a slight cross-resistance of 5-13-fold was observed with another neonicotinoid thiamethoxam. Among the neonicotinoids, a resistant strain of B. tabaci to thiamethoxam (approximately 100-fold) showed no appreciable cross-resistance to either acetamiprid or imidacloprid, while another strain 500-fold resistant to thiamethoxam resulted in a mild of 4-6-fold resistance to acetamiprid and imidacloprid. In other assays, B. tabaci strain resistant to thiamethoxam (approximately 100-fold) had no cross-resistance to pyriproxyfen. Our findings indicate that no appreciable cross-resistance was observed between the benzoylphenyl urea novaluron, the juvenile hormone mimic pyriproxyfen, and the neonicotinoids acetamiprid and imidacloprid. Hence, these compounds could be used as components in insecticide resistance management programs.