Spinosad resistance

A single gene may be responsible for the resistance, and in these cases the level of resistance can be quite high. Well-known examples are the 2000-fold resistance to organophosphates in spider mites, spinosad resistance in western flower thrips, DDT resistance in houseflies, and dieldrin resistance in several Diptera. In other cases, multiple genes are clearly involved in the resistance. Examples are carbaryl resistance in houseflies (Georghiou, 1972), carbaryl resistance in fall army worms (Yu et al., 2003), and malathion resistance in oriental houseflies (Yeoh et al., 1981). 

In contrast to the mammalian and avian studies, the available information on the metabolism of the spinosyns by insects suggests that metabolism of the spinosyns (e.g., spinosyn A) is very limited. Studies of spinosyn A metabolism in tobacco budworm Heliothis virescens) larvae show that the only component detected (within the limits of detection, up to 24 h post treatment) in larval homogenates of topically treated larvae was the parent, spinosyn A [53, 54]. In contrast, these same larvae readily metabolized the acaricide fenazaquin [3, 53], clearly demonstrating that H. virescens larvae have the capacity to metabolize xenobiotics. Further, studies with H. virescens larvae highly resistant to spinosad [55] also found no evidence for metabolism of spinosyn A [56, 57]. 

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