Pesticides Found to Increase Bee Susceptibility to Colony Collapse Disorder

Since becoming common place in the mid 1980s, scientists have identified over sixty factors contributing to colony collapse disorder (CCD). This disease has the capacity to quickly decimate honey bee populations and posses a significant ecological and economic impact to the United States. Wu et al. tested the impact of common pesticides on worker honey bees (Apis mellifera) by raising three cycles of the species in combs treated with pesticide residue. The results demonstrated a number of sub-lethal effects to colonies such as reduced longevity, delays in the life cycle process such as larval development and adult emergence. These sub-lethal effects leave honey bee colonies more susceptible to pathogen infections which are known to cause colony collapse disorder.
Wu, J., Anelli, C., Sheppard, W., 2011. Sub-lethal effects of pesticide residue in brood comb on worker honey bee (Apis mellifera) development and longevity. PLoS One 6.

            Wu et al. used a relatively straightforward experimental design to test for the effects of pesticide in brood comb on worker honey bees. Using three colonies of similar strength from the USDA honey bee laboratory, researchers set up frames with a low pesticide residue control comb paired with a comb with high pesticide residue. For each pair of combs, queens were given access to both during a 24 hour period of egg laying. After eggs were laid, the combs were photographically monitored in patches to determine larval mortality on days 4, 8, 12, and 19. Beginning on day 19, both the control and test combs were incubated at 33°C and the emergence of adult bees was recorded as accounted-for adults were tagged with Testor’s enamel. After three generational cycles, the combs were sent to a lab to have their pesticide levels determined through spectrometry.
            While there was no statistical difference in larval mortality between the test and control broods, Wu et al. found delayed development at days 4 and 8 in the test combs. The lack of differential mortality rates in the larval stage may be due to cross-contamination of the control broods by bees from the infected comb. This seems especially plausible given that larval mortality increased in the control combs in the second and third generations. A chemical analysis of the control combs found that many pesticides from the test combs were present after the experiment, suggesting these chemicals can spread quickly to non-infected bee populations. In terms of adult emergence and longevity, Wu et al. found an average delay of about two days in adult emergence in test populations. In the control populations, there was a delay in adult emergence in the second and third cycles, suggesting that the impact of traveling pesticides. Furthermore, the results showed that bees from comb without pesticides lived an average of four days longer than the bees from the test populations.
            The results of Wu et al. point to pesticides as being responsible for sub-lethal effects on bee populations which can increase susceptibility to pathogens responsible for CCD. A drawn out life cycle provides a reproductive advantage for Varroa mites which feed on the hemolymph of pupating bees. The longer honey bees remain in a larval stage, the higher the level of mite reproduction, posing a serious threat to colony health. Furthermore, the researchers argue that the early death of adult worker bees in colonies with pesticide in the combs can lead to foraging and other responsibilities taken on by younger bees which negatively impact the overall health of the colonies. While further research is required, Wu et al. argue exposure to pesticide seems to be another plausible cause of colony collapse disorder. The paper argues that bee keepers should end the practice of reusing wax which can build up high levels of pesticides over a relatively short period of time. 

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