Cross-Resistance to Imidacloprid in Strains of German Cockroach (Blattella germanica) and House Fly (Musca domestica)

The toxicity of a promising new insecticide, imidacloprid, was evaluated against several susceptible and resistant strains of German cockroach and house fly. 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 houseflies were immobilized more slowly than treated cockroaches, with the maximum effect observed after 72 h, and there was no recovery. Based upon 72‐h LD50 values imidacloprid was moderately toxic to German cockroaches (LD50 values were 6–8 ng mg‐1) and had only low toxicity to house flies (LD50 140 ng mg‐1). Piperonyl butoxide (PBO) blocked the observed recovery in German cockroaches. PBO also greatly enhanced the 72‐h LD50 of imidacloprid from 43‐ to 59‐fold in cockroaches and 86‐fold in house flies. 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 ‘basal’ level of monooxygenase‐mediated detoxication of imidacloprid is quite variable between strains of German cockroach. The AVER and LPR strains of house fly showed significant cross‐resistance to imidacloprid. PBO reduced the level of cross‐resistance in AVER from >4·2‐fold to 0·5‐fold (i.e. the AVER strain LD50 was half that of the susceptible strain when both were treated with PBO), but PBO did not suppress the cross‐resistance in LPR. These data suggest monooxygenases are the mechanism responsible for cross‐resistance to imidacloprid in AVER, but not in the LPR strain. © of SCI.