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Diversity of insecticide resistance mechanisms and spectrum in European populations of the codling moth, Cydia pomonella
Author(s) -
Reyes Maritza,
Franck Pierre,
Charmillot PierreJoseph,
Ioriatti Claudio,
Olivares Jérôme,
Pasqualini Edison,
Sauphanor Benoît
Publication year - 2007
Publication title -
pest management science
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.296
H-Index - 125
eISSN - 1526-4998
pISSN - 1526-498X
DOI - 10.1002/ps.1421
Subject(s) - spinosad , codling moth , thiacloprid , biology , toxicology , population , pesticide resistance , chlorpyrifos , emamectin , novaluron , pest analysis , pesticide , larva , botany , thiamethoxam , agronomy , imidacloprid , medicine , environmental health
Only a few of the registered insecticides against Cydia pomonella L. are still effective in areas where insecticide resistance has emerged in this pest. Resistance mechanisms are multiple, and their lone or cumulative effects in a single population are not completely understood. A detailed estimation of resistance spectrum is still required to define the suitable insecticides to use against a given population. The efficacy of ten insecticides was therefore investigated together with the resistance mechanisms expressed in four laboratory strains and 47 field populations of C. pomonella from five countries. Bioassays were performed using topical applications of diagnostic concentrations on diapausing larvae, and resistance mechanisms were analysed on adults emerging from control insects. All populations exhibited a reduced susceptibility to at least one insecticide when compared with the susceptible laboratory strain. Cross‐resistances were observed between azinphos‐methyl or phosalone and more recent compounds such as spinosad and thiacloprid. Resistances to azinphos‐methyl, diflubenzuron, spinosad, tebufenozide and thiacloprid were significantly correlated with mixed‐function oxidase activity, while increased glutathione‐ S ‐transferase and reduced non‐specific esterase activities were correlated with resistance to azinphos‐methyl and emamectin, respectively. Conversely, resistances to azinphos‐methyl, tebufenozide and thiacloprid were negatively correlated with increased esterase activity. None of the observed mechanisms explained the loss of susceptibility of populations to chlorpyrifos‐ethyl, and no significant correlation was detected between resistance to deltamethrin and the presence of the kdr mutation. The suitability of such non‐target instars to monitor insecticide resistance in field populations is discussed. Copyright © 2007 Society of Chemical Industry