Susceptibility of First Instar Hippodamia convergens (Coleoptera: Coccinellidae) and Chrysoperla rufilabris (Neuroptera: Chrysopidae) to the Insecticide Sulfoxaflor

Abstract

The soybean aphid, Aphis glycines Matsumura (Hemiptera: Aphididae), continues to be the most economically important arthropod pest of soybean in the Midwest. Currently, management tactics for A. glycines rely on scouting and application of broad-spectrum insecticides. However, broadspectrum insecticides are toxic to most natural enemies of this aphid. Selective insecticides may provide an alternative strategy for suppressing A. glycines populations while conserving populations of its natural enemies. Therefore, the aim of this study was to evaluate the potential lethal and sublethal effects of sulfoxaflor (a relatively new selective insecticide), to 2 of this pest's natural enemies, Chrysoperla rufilabris (Burmeister) (Neuroptera: Chrysopidae) and Hippodamia convergens Guérin-Méneville (Coleoptera: Coccinellidae). Laboratory bioassays were performed on first instars of both predators with residual toxicity evaluated over time until adult emergence. Parameters evaluated were mortality and developmental time for larvae and pupae, and adult body size. Fecundity also was determined for C. rufilabris. We found that sulfoxaflor was not toxic to first instar C. rufilabris. However, developmental time to adult was significantly delayed after exposure to this insecticide, but fecundity and body size were not negatively affected. For H. convergens, sulfoxaflor at 25% of the field rate was toxic to first instars. No significant differences were found with regard to developmental time and body size. It is important to note that sulfoxaflor, though relatively less toxic than some insecticides, is not entirely without consequence if natural enemies are exposed. The present study emphasizes the importance of examining earlier life stages and potential sublethal effects when evaluating the toxicity of insecticides in the presence of natural enemies.

Toxicity assessment of two IGR insecticides on eggs and larvae of the ladybird Eriopis connexa

“…This result is in agreement with another study 45 that reported how cypermethrin caused an extension in the larval developmental time of different coccinellids. Also, other authors observed that λ‐cyhalothrin increased the developmental time of the 1 st and 2 nd larval instars of Chrysoperla rufilabris (Burmeister) (Neuroptera:Chrysopidae) 61 and deltamethrin lengthened the developmental time of 4 th instar larvae of Ceratomegilla undecimnotata (Schneider) (Coleoptera: Coccinellidae) 62 …”

Toxicity and Influence of Sublethal Exposure to Sulfoxaflor on the Aphidophagous Predator Hippodamia variegata (Coleoptera: Coccinellidae)

“…per insect significantly extended the duration of larval and pupal stages of H. variegata . Extended preadult developmental time has been found in many aphid predators, such as H. axyridis [ 28 ], Chrysoperla rufilabris (Neuroptera: Chrysopidae) [ 33 ], and C. carnea [ 34 ] after treatment with sulfoxaflor. These findings can be explained either by the antifeeding effect of sulfoxaflor on coccinellid predators [ 35 ] and the consequent reduced food intake or by the fact that affected larvae may use their metabolic energy for sulfoxaflor detoxification at expenses of their development and growth [ 10 , 32 , 36 ].…”

Lethal and Sublethal Effects of Conventional and Organic Insecticides on the Parasitoid Trissolcus japonicus, a Biological Control Agent for Halyomorpha halys

“…Sulfoxaflor was also toxic to T. japonicus in the first experiment (i.e., residual contact toxicity) with mean mortality of 55% (Figure 1). Sulfoxaflor is generally described as an insecticide with relatively low toxicity to predators (46)(47)(48), but higher toxicity to pollinators (47) and some parasitoids (49,50). Contrary to the first experiment (i.e., residual contact toxicity), the residual contact toxicity of sulfoxaflor (mortality <25%) was similar to that of pyrethrins, azadirachtin + pyrethrins, and clothianidin in the last experiment (i.e., different routes of exposure) (Figure 5A).…”