Inheritance of resistance to acrinathrin in Frankliniella occidentalis (Thysanoptera: Thripidae).

BACKGROUND: The western flower thrips (WFT), Frankliniella occidentalis (Pergande), is an economically important pest. The genetic basis of acrinathrin resistance was investigated in WFT. RESULTS: The resistant strain, selected in the laboratory for acrinathrin resistance from a pool of thrips populations collected in Almeria (south-eastern Spain), showed a high resistance to acrinathrin (43-fold based on LC(50) values) compared with the laboratory susceptible strain. Mortality data from reciprocal crosses of resistant and susceptible thrips indicated that resistance was autosomal and not influenced by maternal effects. Analysis of probit lines from the parental strains and reciprocal crosses showed that resistance was expressed as a codominant trait. To determine the number of genes involved, a direct test of monogenic inheritance based on the backcrosses suggested that resistance to acrinathrin was probably controlled by one locus. Another approach, which was based on phenotypic variances, showed n(E), or the minimum number of freely segregating genetic factors for the resistant strain, to be 0.79. CONCLUSION: The results showed that acrinathrin resistance in WFT was autosomal and not influenced by maternal effects, and was expressed as a codominant trait, probably controlled by one locus.

Synergism studies with binary mixtures of pyrethroid, carbamate and organophosphate insecticides on Frankliniella occidentalis (Pergande).

The major mechanism of resistance to most insecticides in Frankliniella occidentalis (Pergande) is metabolic, piperonyl butoxide (PBO) suppressible, mediated by cytochrome-P450 monooxygenases and conferring cross-resistance among insecticide classes. The efficacy of insecticide mixtures of acrinathrin, methiocarb, formetanate and chlorpyrifos was studied by topical exposure in strains of F. occidentalis selected for resistance to each insecticide. The method consisted in combining increasing concentrations of one insecticide with a constant low rate of the second one as synergist. Acrinathrin activity against F. occidentalis was enhanced by carbamate insecticides, methiocarb being a much better synergist than formetanate. Monooxygenase action on the carbamates would prevent degradation of the pyrethroid, hence providing a level of synergism by competitive substrate inhibition. However, the number of insecticides registered for control of F. occidentalis is very limited, and they are needed for antiresistance strategies such as mosaics and rotations. Therefore, a study was made of the synergist effect of other carbamates not used against thrips, such as carbofuran and carbosulfan, against a susceptible strain and a field strain. Neither carbamate showed synergism to acrinathrin in the susceptible strain, but both did in the field strain, carbosulfan being a better synergist than carbofuran. The data obtained indicate that low rates of carbamates could be used as synergists to restore some pyrethroid susceptibility in F. occidentalis.

Esterase inhibition by synergists in the western flower thrips Frankliniella occidentalis.

BACKGROUND: Western flower thrips (WFT), Frankliniella occidentalis (Pergande), is among the most important crop pests in the south-eastern region of Spain. Its increasing resistance to insecticides constitutes a serious problem, and understanding the mechanisms involved is therefore of great interest. Use of synergists to inhibit the enzymes involved in insecticide detoxification is widely used to determine their responsibility for insecticide resistance. However, they do not always act as intended or expected, and caution must be exercised when interpreting synergist results. RESULTS: Laboratory-selected strains of WFT were used to analyse the effects of the synergists piperonyl butoxide (PBO), S,S,S-tributyl phosphorotrithioate (DEF) and methiocarb on total esterase activity. Significant differences were found, indicating esterase activity inhibition by DEF, a lower effect for methiocarb and a small inhibition of the activity by PBO. Esterase isoenzyme inhibition by these compounds showed a similar result; this assay revealed an extreme sensitivity of Triplet A (resistance-associated esterases) to DEF. In an in vivo assay carried out with these compounds at different incubation times, only DEF caused posterior in vitro esterase activity inhibition, with a maximum effect 1 h after treatment. CONCLUSION: In this work, only DEF shows true synergistic inhibition of WFT esterases.