Effect of Synergists on Organophosphate and Permethrin Resistance in Sweetpotato Whitefly (Homoptera: Aleyrodidae)

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Abstract
A field strain of Bemisia tabaci (Gennadius) from California, resistant to malathion, methyl parathion, sulprofos, permethrin, and DDT, showed increases in resistance levels (ranging from 1.1- to 8.9-fold) in a subsequent survey. Selective synergists were used to study the involvement of hydrolytic or oxidative enzymes (or both) in the resistance mechanism of the resistant strain. Resistance levels were decreased markedly when DEF (S,S,S-tributyl phosphorotrithioate) synergized three organophosphate (OP) compounds (malathion, methyl parathion, and sulprofos) and one pyrethroid (permethrin), suggesting the involvement of increased detoxication by esterases as part of the resistance mechanism. In addition, malathion was synergized by triphenyl phosphate (TPP), indicating the influence of carboxylesterases in malathion resistance. No highly active esterases were associated with organophosphate (OP) resistance. Piperonyl butoxide (PB) synergized the three OPs, permethrin, and DDT to different degrees in both susceptible and resistant strains, thus indicating the importance of enhanced oxidative metabolism in B. tabaci resistance. Because use of DEF, PB, and TPP did not increase the toxicity in the resistant strain to that of the susceptible strain, an unidentified resistance factor, possibly insensitive acetylcholinesterase, may be of importance in OP resistance. DEF antagonized DDT toxicity in the resistant strain, which increased the resistance ratio from 12.0- to 16.7-fold. DDT was synergized to a limited extent by diethyl maleate (DEM), thus suggesting limited metabolism by DDT-dehydrochlorinase in the resistant strain. A nonmetabolic knockdown resistance mechanism (kdr) may be a factor in DDT resistance because neither PB nor DEM supressed resistance completely.