Timing acaricide treatments to prevent Varroa destructor (Acari: Varroidae) from causing economic damage to honey bee colonies

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AbstractThis study consisted of two field experiments designed to assess the effects of acaricide treatment timing on the mean abundance of the mite Varroa destructor Anderson and Trueman and its impact on honey production and colony survival in honey bees, Apis mellifera L. (Hymenoptera: Apidae). In the first experiment, replicated colonies with different levels of infestation by V. destructor were given one of six treatments: untreated, with a low level of infestation by V. destructor; untreated, with a moderate level of infestation by V. destructor; exposed to fluvalinate for 42 days; exposed to two applications of Perizin®; or exposed to four applications of a pour-on formulation of formic acid at 4- or 10-day intervals. The six treatments were applied in either spring or fall. In experiment two, replicated colonies with a high level of infestation by V. destructor were left untreated, exposed to fluvalinate for 42 days, exposed to five applications of formic acid at 7-day intervals, or exposed to an equivalent amount of formic acid applied as a slow-release formulation. For each experiment, V. destructor densities, measured by alcohol wash, and colony survival were monitored for 1 year, and honey production was assessed in the year in which the spring treatment was applied. The results showed that all of the acaricide treatments were effective in reducing the mean abundance of V. destructor. However, efficacy varied with season. Fluvalinate was effective in controlling varroa under either spring or fall treatment conditions. Fall applications of Perizin® provided better control than spring applications. Formic acid provided consistent control of V. destructor in spring applications, regardless of the interval between treatments or whether pour-on or slow-release formulations were used, but was ineffective in the fall. Honey production was improved by spring acaricide treatments in both years. When the mean abundance of V. destructor was 0.02 ± 0.005 mites per bee (2 mites per 100 bees) in mid-April, honey production increased from 66 ± 17 kg per colony in untreated colonies to up to 116 ± 23 kg per colony in colonies treated with acaricide. When V. destructor levels were 0.21 ± 0.02 mites per bee (21 mites per 100 bees) in mid-May, spring acaricide treatments increased honey production from 1.3 ± 2.3 kg per untreated colony to up to 48 ± 17 kg per acaricide-treated colony. For the prairie region of Canada, producers will need to assess colonies in both spring and fall and treat when the mean abundance of V. destructor is more than 0.02 mites per bee (2 mites per 100 bees) in spring to prevent losses in honey production. Producers should treat when the mite level is greater than 0.04 mites per bee (4 mites per 100 bees) in late August to early September to prevent fall or winter colony loss. In this study, tracheal mite (Acarapis woodi (Rennie)) (Acari: Tarsonemidae) levels were very low, so interactions between mites were not studied. If both tracheal and varroa mites are present, lower fall thresholds might be required. In the absence of tracheal mites, colonies with varroa mite levels of more than 0.17 mites per bee (17 mites per 100 bees) in late fall experienced significant winter loss.