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Resistance and cross‐resistance to neonicotinoid insecticides and spinosad in the Colorado potato beetle, Leptinotarsa decemlineata (Say) (Coleoptera: Chrysomelidae)
Author(s) -
MotaSanchez David,
Hollingworth Robert M,
Grafius Edward J,
Moyer Dale D
Publication year - 2006
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.1120
Subject(s) - imidacloprid , colorado potato beetle , neonicotinoid , spinosad , biology , leptinotarsa , acetamiprid , clothianidin , thiamethoxam , cross resistance , toxicology , methomyl , pest analysis , agronomy , botany , pesticide , microbiology and biotechnology
The Colorado potato beetle, Leptinotarsa decemlineata (Say), has developed resistance to many insecticides used for its control, recently including imidacloprid, a neonicotinoid compound. Other neonicotinoids are now being deployed to control this pest. A key point in the strategies of resistance management is the monitoring of resistance and cross‐resistance. In the summer of 2003, imidacloprid‐resistant adult Colorado potato beetles collected from Long Island, New York, USA were bioassayed using topical applications of imidacloprid and nine other neonicotinoids. Compared to a standard susceptible strain, the Long Island beetles showed 309‐fold resistance to imidacloprid, and lower levels of cross‐resistance to all other neonicotinoids, despite these never having been used in the field, i.e., 59‐fold to dinotefuran, 33‐fold to clothianidin, 29‐fold to acetamiprid, 28‐fold to N ‐methylimidacloprid, 25‐fold to thiacloprid, 15‐fold to thiamethoxam, 10‐fold to nitenpyram, but less than 2‐fold to nicotine. In injection bioassays, high resistance to imidacloprid was also found (116‐fold). Piperonyl butoxide partially suppressed resistance to imidacloprid, but the resistance level was still over 100‐fold, indicating that other mechanisms were primarily responsible for resistance. Low levels of resistance (8‐ to 10‐fold) were found to the nicotinic activator, spinosad, in an imidacloprid‐resistant strain collected from the same field in 2004. The cross‐resistance seen with all the neonicotinoids tested suggests that the rotation of imidacloprid with other neonicotinoids may not be an effective long‐term resistance management strategy. Rotation with spinosad also carries some risk, but it is unlikely that spinosad resistance in this case is mechanistically related to that for the neonicotinoids. Copyright © 2005 Society of Chemical Industry

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