Lakshmipathi Srigiriraju

Monitoring for imidacloprid resistance in the tobacco-adapted form of the green peach aphid, Myzus persicae (Sulzer) (Hemiptera: Aphididae), in the eastern United States.

BACKGROUND Imidacloprid is the primary insecticide for controlling the tobacco-adapted form of the green peach aphid (TGPA), Myzus persicae (Sulzer), a major pest of tobacco worldwide. This study used leaf-dip bioassays to assess TGPA resistance to imidacloprid in the eastern United States from 2004 through 2007. RESULTS When combined over the 4 year study, 18, 14 and 3% of the TGPA had imidacloprid resistance ratios (RRs) of 10-20-fold, 20-30-fold and 30-90-fold, respectively, compared with the most susceptible colony tested. This indicates that some colonies have developed moderate levels of resistance to imidacloprid. A colony collected near Clayton, North Carolina, had the highest RR of 91 (LC(50) value = 31 mg L(-1)). This resistance declined for six tests over a 3 year period in the laboratory culture from >130-fold RR (LC(50) = 48 mg L(-1)) to 40-fold RR (LC(50) = 15 mg L(-1)). Over the same period, the most susceptible colony and a standard colony not exposed to imidacloprid for over 7 years had consistently low LC(50) values. CONCLUSION Moderate levels of resistance to imidacloprid are noticed among TGPA colonies from the eastern United States. The variation in resistance indicates that the factors responsible are present in the populations at low frequencies and are just not enough to cause field failures yet.

Esterase-based resistance in the tobacco-adapted form of the green peach aphid, Myzus persicae (Sulzer) (Hemiptera: Aphididae) in the eastern United States.

Organophosphates and carbamates represent alternative insecticides in managing the tobacco-adapted form of the green peach aphid (TGPA), Myzus persicae (Sulzer), a major pest of tobacco in the United States and around the world. General esterases that detoxify these insecticides were assessed in green, red, and orange morphs of field-collected M. persicae. A total of 136 aphid colonies were collected from 2004 though 2007 and screened for total esterase activity. The green morphs had lower esterase levels, with a mean of 77+/-6.6 nmol/min/mg protein, as compared to red (84+/-2.9 nmol/min/mg protein) and orange morphs (172+/-16.5 nmol/min/mg protein). Overall esterase activities, and those for the red and green morphs, were positively correlated with LC(50) values for acephate (organophosphate) and methomyl (carbamate) assessed in leaf-dip bioassays. Esterase genes responsible for higher esterase activities were diagnosed by gene amplification studies. Twenty-three of 24 colonies tested had either the E4 or FE4 gene amplified, both known to confer esterase-based resistance. Fifteen out of the 24 colonies tested had amplified E4 gene and four colonies had FE4 gene amplification. All orange morphs and one green morph had both E4 and FE4 genes amplified. This unique phenotype, where two esterase genes were amplified had an 865-bp band characteristic of the FE4 gene and an additional 381-bp band characteristic of a deleted upstream region of the E4 gene. Changes that occurred in esterase-based resistance in the TGPA over the past two decades and their implications on insecticide resistance management are discussed.

Influence of Post-Exposure Temperature on the Toxicity of Insecticides to the Tobacco-Adapted Form of the Green Peach Aphid (Hemiptera: Aphididae)

Abiotic factors, such as temperature, are important in the activity and performance of insecticidal compounds, as they influence biochemical reactions that may either enhance or limit the insecticide effectiveness. The influence of these temperature-mediated factors on the toxicity of insecticides in red and green color morphs of the tobacco-adapted form of the green peach aphid, Myzus persicae (Sulzer), was evaluated using leaf-dip bioassays in laboratory incubators. Postexposure temperatures of 15, 20, and 25°C were evaluated for 4 classes of insecticides: organophosphate (acephate), carbamate (methomyl), pyrethroid (lambda-cyhalothrin), and neonicotinoid (imidacloprid). Except for lambda-cyhalothrin, all the insecticides had positive temperature coefficients that indicated increased toxicity to M. persicae at both 5 (15 - 20 and 20 - 25°C) and 10°C (15 - 25°C) temperature ranges. Postexposure temperature had similar effects on insecticide toxicity to both color morphs. A temperature increase of 5°C, from 15 - 20°C and 20 - 25°C, caused 1.3- to 3-fold increases in toxicity for methomyl, acephate, and imidacloprid in both color morphs. A change of 10°C (15 - 25°C) increased the toxicity of the three chemicals from 2.9- to 6.0-fold. In contrast, the toxicity of lambda-cyhalothrin decreased as the temperature increased, showing a negative temperature coefficient. Because laboratory bioassays are typically used for monitoring insecticide resistance, this study confirms that using standardized temperatures is necessary for diagnosing problems and making recommendations for resistance management programs in aphids.