Commercial farming ventures rely on the western honey bee (Apis mellifera) for pollination, yet also rely on neonicotinoid insecticides to control sucking and chewing insects such as aphids and caterpillars. One such neonicotinoid, imidacloprid, was developed by Bayer CropScience in the early 1990s, introduced commercially in 1996 where itessentially replaced 3 other classes of insecticide, and is now the most common insecticide worldwide. Imidacloprid is rated as moderately toxic orally to mammals and extremely toxic to honey bees by ingestion and to a lesser degree by contact. It works by binding to nicotinic acetylcholine receptors in nerve cells, preventing normal nerve conduction and resulting in paralysis and eventually death. Farmers may try to protect bees from exposure by careful application. However, there is evidence that long-term exposure to even tiny amounts of neonicotinoids can impair bees' immune system, making them more susceptible to viral and fungal infections. Neonicotinoids are used on corn and soybeans and also on cotton, sorghum, sugar beets, apples, cherries, peaches, oranges, berries, leafy greens, tomatoes, potatoes, and almonds; they're present in yard and landscaping products and pet flea medications.
In the winter of 2005/2006, US commercial migratory beekeepers reported sharp declines in their honey bee colonies. This type of decline had happened before at rates of up to 20%, and had been attributed to mites, diseases, and management stress. Starting in 2005/2006, in what is now called colony collapse disorder (CCD), losses of 30% to 90% were reported in both migratory and nonmigratory beekeeping settings in the US, Canada, Europe, South and Central America, and Asia. CCD is characterized by the disappearance of adult bees (dead bees are not found in or near the hive). CCD continued steadily over the subsequent years, and in 2014 the Environmental Protection Agency and Department of Agriculture formed a task force to address the issue.
In 2014, an interesting Harvard study investigated the effects of sub-lethal doses of 2 neonicotinoids (imidacloprid or clothianidin). Six hives were set up similarly at each of 3 Massachusetts locations and were given imidacloprid or clothianidin (0.74 ng/bee/d) in either sucrose water or high-fructose corn syrup (HFCS) or sucrose water or HFCS alone (controls) for 13 weeks (July to September)1. The dose of 0.74 ng/d is well below the oral LD50 (dose required to kill 50% of a population of test animals) for clothianidin (3.4 ng) and imidacloprid (118.7 ng). Bees were allowed to freely forage during the study. Both active and control groups progressed almost identically with no acute morbidity or mortality until winter. Because results were similar between the different hive locations and between the sucrose and HFCS groups, data were pooled for analysis. Bee cluster size decreased in all colonies starting in late October. In January, this decline reversed in the control colonies, but not in the neonicotinoid-treated colonies.
Numbers of frames containing bees were similar for the active and control groups between late October and late December, but between early January and early April, significantly fewer frames contained bees in the neonicotinoid-treated colonies (one-way ANOVA, P <.0001). By the end of the experiment in April, 6 of the 12 neonicotinoid-treated colonies (50%) were lost, with symptoms resembling CCD; this comprised 4 of 6 (67%) of the imidacloprid-treated colonies and 2 of 6 (33%) of the clothianidin-treated colonies. One of the 6 control colonies (17%) was lost, exhibiting symptoms of an infection by the unicellular parasite, Nosema ceranae. Abandonment of the hive was a key finding in the active groups; masses of dead honeybees were not found at the hives in the active groups but were found in the one lost control colony.
Varroa mite counts were similar for the active and control groups, both before and after counts had been significantly reduced using Miteaway Quick strips. It's unclear why brood rearing was similar for both active and control groups until winter, but when the weather warmed again in the spring, the active groups failed to resume brood rearing.
The results of this study indicate that there is some relationship between administration of sub-lethal doses of neonicotinoids and the collapse of the studied bee colonies. The authors consider that the severity of CCD may be modulated by winter temperature; in another study previously conducted by the same authors during a longer, colder winter in 2010/2011 in central Massachusetts, a CCD mortality rate of 94% was reported.2 These studies add critical information to the body of research on neonicotinoids' effects on bees.
1 Lu C, Warchol KM, Callahan RA. Sub-lethal exposure to neonicotinoids impaired honey bees winterization before proceeding to colony collapse disorder. B Insectol 2014; 67(1): 125-30.
2 Lu C, Warchol KM, Callahan RA. In situ replication of honeybee colony collapse disorder. B Insectol 2012; 65(1): 99-106.
Image credit: CDC, Dr. Pratt
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