Insecticide resistance to the microbial insecticides Bacillus thuringiensis subsp. israelensis (Bti) and Bacillus sphaericus (Bs) represents a serious threat to their success. Available evidence indicates that the risk for resistance to Bti is low due to the makeup of its parasporal crystal, which contains Cyt1A, Cry4A, Cry4B, and Cry11A toxic proteins. Disrupting the toxin complex in Bti enables resistance to evolve, especially in the absence of the key factor, the cytolytic toxin, Cyt1A. Cross-resistance is widespread among mosquitocidal Bacillus thuringiensis Cry toxins and the mechanisms of Cry resistance in mosquitoes are not known. Bacillus sphaericus (Bs) is at higher risk for resistance due to its singlesite action and field cases have been reported from a number of locations worldwide. Cross-resistance is reported among the various Bs isolates, although some isolates produce additional toxic proteins that can reduce cross-resistance and slow resistance evolution. Field and lab evolved resistant populations consistently show recessive and monofactorial inheritance of resistance. Resistant populations, however, have evolved a variety of molecular mechanisms causing that resistance. Traditional resistance management strategies with promise include rotations and mixtures of Bti and Bs, as well as untreated areas that provide natural refuges for susceptible alleles. Promising new strategies include genetic engineering to increase the toxin complexity targeted toward mosquito larvae, to enhance the host range of the mosquito control product, and to avoid the evolution of insecticide resistance. Regardless of the control strategy, a resistancemonitoring program alongside an integrative pest management approach is the best strategy to delay insecticide resistance.
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