The incidence, influencing factors and mechanisms of resistance to insecticides from a range of chemical groups were examined in UK and European populations of the glasshouse whitefly, Trialeurodes vaporariorum (Westwood). Toxicological assessments of populations from a range of plant production glasshouses and comparisons with the responses of a laboratory susceptible strain disclosed levels of resistance to pyrethroid, organophosphate, insect growth regulator (IGR) and neonicotinoid insecticides. Responses to conventional compounds indicated varying levels of resistance, potentially reflecting disparate usage between collection sites. All strains examined possessed resistance to the IGR, buprofezin; some populations were virtually immune to this commonly used control agent. Selection experiments demonstrated reciprocal crossresistance between buprofezin and a further IGR, teflubenzuron, both of which are frequently incorporated into integrated pest management (IPM) programmes for this species. Results for the leading neonicotinoid, imidacloprid, revealed resistance in both UK and European strains, representing the first documented cases of neonicotinoid resistance in this species worldwide, and the first in any insect species within the UK. The lethal effects of vapour emitted by applications of buprofezin and the anti-feedant effects of imidacloprid were demonstrated in T. vaporariorum for the first time. The potential consequences of these factors for both the control and selection of resistance were highlighted. Mechanistic studies using electrophoresis and kinetic spectrophotometer readings showed that neither non-specific esterases nor modified acetylcholinesterases were involved with resistance to either pyrethroid or specific organophosphate insecticides.

The whitefly Trialeurodes vaporariorum Westwood (Hemiptera: Aleyrodidae) is a serious pest of protected vegetable and ornamental crops in most temperate regions of the world. Neonicotinoids, pymetrozine (a feeding blocker), spiromesifen (a tetronic acid derivative), bifenthrin (a pyrethroid), and pyriproxyfen (a juvenile hormone mimic) are among the most important insecticides used to control this species. Bioassays were used to quantify responses of recently-collected strains of T. vaporariorum to three neonicotinoids (imidacloprid, thiamethoxam, and acetamiprid), pymetrozine, spiromesifen, bifenthrin, and pyriproxyfen. 454 pyrosequencing was exploited to generate the first transcriptome for this species. PCR-sequencing was used to identify mutations in the target proteins of spiromesifen and bifenthrin potentially associated with resistance to these compounds. Microarray sequencing technology was employed to investigate differences in gene expression associated with pyriproxyfen resistance. Resistance to neonicotinoids was age-specific in expression and consistently associated with resistance to pymetrozine, supporting a hypothesis of metabolic resistance analogous to that in the tobacco whitefly, Bemisia tabaci. Bioassays also showed moderate to high level resistance to spiromesifen, bifenthrin and pyriproxyfen in some strains. Analysis of the transcriptome identified genes encoding enzymes involved in the detoxification of xenobiotics (cytochrome P450s, carboxyl/cholinesterases, and glutathione-s transferases) and ones encoding insecticide targets: acetyl-coA carboxylase (ACCase), the target of spiromesifen and the voltage-gated sodium channel protein targeted by pyrethroids. PCR-sequencing revealed a single nucleotide polymorphism in the ACCase gene, which was consistently associated with spiromesifen resistance. Three amino-acid substitutions in the sodium channel of pyrethroid-resistant T. vaporariorum were found in positions previously implicated in pyrethroid resistance in B. tabaci. Microarray sequencing disclosed that a cytochrome P450 gene (CYP4G61) was overexpressed in a strain selected for increased pyriproxyfen resistance. The implications of these results and opportunities for further work are discussed.

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