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

Abstract

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.