ABRC2010 Effects of a Miticide on Honeybee Memory - is the Cure Worse than the Disease

Bee Health August 13, 2013 Print Friendly and PDF

The following was presented at the 2010 American Bee Research Conference in Orlando, FL.

13. Frost, E.H., D. Shutler & K. Hillier - EFFECTS OF A MITICIDE ON HONEYBEE MEMORY: IS THE CURE WORSE THAN THE DISEASE? - Significant mortality from Varroa destructor has occurred in wild and managed honeybee populations. Although mortality is the clearest indicator of negative consequences, Varroa may have other subtle effects. For example, chemical treatments used to eliminate Varroa may interfere with the honey bees’ ability to properly integrate stimuli that elicit feeding, mating, colony defense, and communication behaviors.

We assessed learning and memory of honey bees exposed to tau-fluvalinate, the active ingredient in Apistan®, using a standardized Pavlovian insect-learning paradigm (proboscis extension reflex [PER]), that mimics learning in the natural environment. Honey bees are presented with a neutral stimulus, usually an odor, followed by a positive reward such as sugar water. Honey bees learn to extend their proboscis when exposed to the odor, in the absence of a reward, because the odor predicts the presence of food. Stressors, such as pesticides may reduce the frequency of PER, suggesting impaired learning (e.g., Abramson et al., 2004 Environ. Entomol. 33:378-388; Decourtye et al., 2005 Arch. Environ. Contam. Toxicol. 48:242-250).

Forager honey bees were collected in Nova Scotia, Canada in August/September 2009 and immobilized with only their antennae and mouthparts free. Tau-fluvalinate, dissolved in 1.25 µL of acetone, was applied dermally (thorax) or orally (proboscis) at concentrations of 0.125 µg (estimated to be daily exposure per bee in treated hives [Johnson et al., 2009 J. Econ. Entomol. 102:474-479]) or 1.25 µg. Controls were treated with 1.25 µL of acetone. Bees were trained to perform PER (training trials), and then tested for retention of odor memory 24 hours later (extinction trials).

Lower dose treatments had no significant effect on mortality or PER during training or extinction. At the 1.25 µg dermal dose, mortality was significantly higher in treated honey bees than controls at both 3 and 24 hours post treatment (p = 0.001 and p < 0.0001, respectively). Controls had a significantly higher average number of PER responses to odor cues during training (p = 0.05); there was no significant effect during extinction trials (p = 0.08).

We are also quantifying how tau-fluvalinate is partitioned within the honey bee body, and the relative concentrations. Chemical residues are evaluated using gas chromatography mass spectrophotometry by isolating the head and thorax and placing them in hexane to extract tau-fluvalinate. Quantities of tau-fluvalinate are measured by the size of the peaks on the chromatography output relative to a standard curve. Preliminary results suggest tau-fluvalinate enters the honey bee circulatory system after dermal contact. Honey bees with a dermal application (thorax) of tau-fluvalinate also have traces of the chemical in their head. Detoxification may also occur over time, with decreasing levels of tau-fluvalinate present in honey bee tissues over a 24 hour period.

Ultimately, this research will lead to standardized methods to evaluate suitability of mite treatment programs and potential sublethal effects of chemicals on honeybees. Bees worldwide are exposed to both mite and acaricide stressors, so results of this research will be applicable globally.

More presentations from this conference can be found at Proceedings of the American Bee Research Conference 2010