Submitted to: Pesticide Biochemistry and Physiology
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 10/18/1999
Publication Date: N/A
Citation: N/A Interpretive Summary: Insecticide resistance has been estimated to cost the U.S. $133 million annually and perhaps $1 billion worldwide. The German cockroach has developed resistance to all of the traditional insecticides and cross resistance has been reported among many new insecticides. Elucidation of the biochemical and molecular mechanisms responsible for insecticide resistance in the German cockroach will provide possible methods to preven or delay its development. Scientists at the Center for Medical, Agricultural and Veterinary Entomology in Gainesville, Florida, and Michigan State University have identified several key mechanisms responsible for cypermethrin resistance in the German cockroach, including a previously unknown detoxification esterase(s) located in the endoplasmic reticulum. Slower insecticide penetration rate, enhanced detoxification (oxidative and hydrolytic) and a mutation resulting in insecticide insensitivity were also identified. This fundamental information will be used to conduct future studies that may provide a means to detect insecticide resistance in the German cockroach (and possibly other insects) before insecticide treatments are chosen or dispensed or methods to subvert the resistance. This information would allow the most efficacious insecticide to be chosen which would prevent unnecessary insecticide use and minimize the associated risks.
Technical Abstract: The level of resistance to cypermetrin and the mechanisms responsible for the resistance were investigated in a strain (Aves) of German cockroach, Blattella germanica (L.), collected recently from a Gainesville, Florida, residence. Topical bioassay data revealed that the Aves strain was highly resistant to cypermethrin, exhibiting a resistance ratio of 93-fold which was reduced to 29-fold when cockroaches were pretreated with piperonyl butoxide (a cytochrome P450 inhibitor) and 18-fold when pretreated with S,S,S-tributyl phosphorotrithioate (an esterase inhibitor). The synergist data implicated enhanced oxidative and hydrolytic metabolism as resistance mechanisms in the Aves German cockroach strain. This conclusion was further supported by significantly higher oxidative (2.4- to 4.2-fold) and hydrolytic (1.6- to 3.6-fold) detoxification enzyme activities toward surrogate substrates and significantly higher in vitro [14C]cypermethrin metabolism. Microsomal NADPH-dependent (1.8-fold) and NADPH-independent (2.2-fold) [14C]cypermethrin metabolism were significantly greater in the Aves strain as compared with Orlando. To examine whether target-site insensitivity was a contributing resistance mechanism in the Aves strain, we amplified and sequenced a PCR fragment of 0.9 kb that encodes the IIS4-IIS6 region of the Para sodium channel protein. The G to C mutation at nt 2979 resulting in a leucine to phenylalanine amino acid substitution and shown previously to be associated with knockdown resistance (kdr) was present in the Aves strain. It is concluded that the high level of cypermethrin resistance in the Aves German cockroach strain was due to enhanced oxidative and hydrolytic metabolism of the insecticide, target site insensitivity (kdr) and reducced cuticular penetration.