The toxicity of a promising new insecticide, imidacloprid, was evaluated against several susceptible and resistant strains of German cockroach and house Ñy. Imidacloprid rapidly immobilized German cockroaches followed by a period of about 72 h during which some cockroaches recovered. After 72 h there was no further recovery. Imidacloprid-treated houseÑies were immobilized more slowly than treated cockroaches, with the maximum e †ect observed after 72 h, and there was no recovery. Based upon 72-h values imidacloprid was mod-LD 50 erately toxic to German cockroaches values were 6È8 ng mg~1) and had (LD 50 only low toxicity to house Ñies 140 ng mg~1). Piperonyl butoxide (PBO) (LD 50 blocked the observed recovery in German cockroaches. PBO also greatly enhanced the 72-h of imidacloprid from 43-to 59-fold in cockroaches and LD 50 86-fold in house Ñies.
Two strains of German cockroach (Baygon-R and Pyr-R) showed [4-fold cross-resistance to imidacloprid. This cross-resistance could not be suppressed by PBO, suggesting that P450 monooxygenase-mediated detoxication is not responsible for this cross-resistance. Variation in the level of synergism observed with PBO (between strains) suggests the "basalÏ level of monooxygenase-mediated detoxication of imidacloprid is quite variable between strains of German cockroach.
The AVER and LPR strains of house Ñy showed signiÐcant cross-resistance to imidacloprid. PBO reduced the level of cross-resistance in AVER from [4É2-fold to 0É5-fold (i.e. the AVER strain was half that of the susceptible strain LD 50 when both were treated with PBO), but PBO did not suppress the crossresistance in LPR. These data suggest monooxygenases are the mechanism responsible for cross-resistance to imidacloprid in AVER, but not in the LPR strain.