Topical application of the synergists piperonyl butoxide (PB) and S,S,S‐tributyl phosphorotrithioate (DEF) to second‐instar larvae of a standard laboratory strain (FS) and an unselected Malaysian field strain (CH) of the diamondback moth Plutella xylostella had no significant effect on the toxicity of the acylurea insecticides, chlorfluazuron and teflubenzuron, in a subsequent leafdip bioassay. In contrast, pre‐treatment with PB or DEF in acylurea‐selected subpopulations of the CH strain with varying levels of cross‐resistance to chlorfluazuron and teflubenzuron significantly increased (up to 34‐fold and 28‐fold, respectively) the toxicity of both compounds, suggesting that microsomal monooxygenases and esterases may be involved in resistance. The addition of a mineral oil, ‘Sunspray 6E’, to topically‐applied chlorfluazuron consistently reduced its LD50 value, and the effect of the oil appeared to be greatest on the most resistant population of P. xylostella. However, the effects of the oil were not significant (P > 0·05) and further studies are necessary to determine whether a penetration factor is present in the CH strain.

The activities of the acylurea insect growth regulators, chlorfluazuron, teflubenzuron and difubenzuron, and the neurotoxic macrocyclic lactone, abamectin were assessed against a laboratory susceptible (FS) strain and a field (Cameron Highlands, Malaysia (CH)) strain of the diamondback moth, Plutella xylostella L. using a leaf‐dip bioassay at 20°C. The time taken to achieve end‐point mortality was found to vary considerably (9–17 days), being fastest with abamectin against the FS strain and slowest with difubenzuron against the CH strain. The order of activity (LC50 at F6/7) against second‐instar larvae of both strains was: abamectin > chlorfluazuron = teflubenzuron ⋙ difubenzuron. Subsequent assays (F14) with the acylureas, flufenoxuron and hexaflumuron against the FS strain suggested that the former was slightly more active than chlorfluazuron or teflubenzuron, the latter slightly less active. The CH population was found to be 12.6‐, 6.7‐, 6.4‐ and 2.3‐fold less sensitive to difubenzuron, teflubenzuron, chlorfluazuron and abamectin respectively than the FS strain. Selection of sub‐populations of the CH strain with chlorfluazuron (CHL‐SEL) and teflubenzuron (TEF‐SEL) for six generations (F6‐11), resulted in LC50 resistance ratios of 109‐ and 315‐fold respectively when compared with the FS strain, equivalent to an 18‐ and a 46‐fold increase in resistance compared with the unselected CH strain. Marked cross‐resistance was also demonstrated between chlorfluazuron and teflubenzuron in both sub‐populations. However, there was no evidence of cross‐resistance to dijlubenzuron and abamectin and little or no cross‐resistance to flufenoxuron and hexaflumuron. Resistance to chlorfluazuron and teflubenzuron appeared to be relatively unstable in the TEF‐SEL compared with the CHL‐SEL sub‐population (over 6–9 generations). However, reselection of the TEF‐SEL population with chlorfluazuron (F18–20) led to a very rapid increase in resistance to chlorfluazuron and particularly teflubenzuron. For the latter compound, resistance factors of about 1000000 were obtained (F19, 21). Such values are probably only semi‐quantitative, as above a certain level of resistance feeding bioassays with acylureas (compounds which are active to a significant extent by ingestion) are likely to become rate‐limiting.

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