The following was presented at the 2010 American Bee Research Conference in Orlando, FL.
36. Williams, G.R., D. Shutler, C.M. Little, K.L. Burgher-MacLellan & R.E.L. Rogers, – NOSEMA CERANAE IN NORTH AMERICA: NASTY, NICE, OR NEITHER? - A variety of emerging pathogens threaten western honey bees (Apis mellifera), including the microsporidian Nosema ceranae. Since jumping from the Asian (Apis cerana) to the western honey bee in the latter half of the 20th century (Chen et al., 2008 J. Invertebr. Pathol. 97:186-188), N. ceranae has become distributed nearly globally and has displaced western honey bees’ historical Nosema parasite, Nosema apis, in many regions (Klee et al., 2007 J. Invertebr. Pathol. 96:1-10).
Very little is known about the epizootiology and control of N. ceranae in western honey bees because of its recent detection. Infection resulted in sudden collapse of apparently asymptomatic colonies in Spain (Higes et al., 2008 Environ. Microbiol. 10:2659-2669), whereas multiple stressors, rather than N. ceranae alone, are implicated as the cause of Colony Collapse Disorder in the United States (van Engelsdorp et al., 2009 PLoS One 4: e6481-e6497). Numerous control methods exist for N. apis in western honey bees, including fumigation, heat treatment, and replacement of aging equipment (Fries, 1992 Bee World 74:5-19); however, most common in North America is oral administration of the antibiotic Fumagilin-B® with sugar syrup in fall and spring. In our preliminary investigation (Williams et al., 2008 J. Invertebr. Pathol. 99:342-344), Fumagilin-B® applied in the fall at the recommended dosage for N. apis controlled N. ceranae for at least 6 months; however, we did not account for potential variation among beekeeping operations.
Here we investigated effects of Fumagilin-B® on N. ceranae and on western honey bee colony strength (i.e., size of adult worker population, and amount of capped and uncapped brood, honey, and pollen) using colonies over-wintered in a single apiary, as well as investigated effects of N. ceranae on colony mortality. We also repeated our previous study using colonies over-wintered by seven different beekeepers to incorporate variation arising from beekeeping practices.
N. ceranae did not affect colony winter mortality (all P > 0.56) or any colony strength measure (all Ps > 0.17). There are a number of possible explanations for this, including false recovery of colonies (Higes et al., 2008 Environ. Microbiol. 10:2659-2669), sub-damaging N. ceranae intensities, or non-significant differences in N. ceranae intensity between treatment groups for colonies whose strength was measured (i.e., P = 0.07). Similar to our previous study, fall Fumagilin-B® treatment generally lowered N. ceranae the following spring (all Ps ≤ 0.05), although results were highly variable both within and among beekeepers. Differences in N. ceranae intensities and fumagillin effectiveness among beekeeping operations could be due to a number of factors, including beekeeper management and weather.
Understanding factors influencing colony-level pathology of N. ceranae is crucial, particularly due to conflicting data on pathogenicity of the parasite. Significant recent increases in honey bee colony losses globally are likely caused by multiple factors, including recently-introduced parasites, nutritional deficiencies, and exposure to pesticides intrinsic and extrinsic to beekeeping. Until influences of all important stressors are known, both singly and in combination, it may be difficult to understand differences in strength and mortality among western honey bee colonies.
More presentations from this conference can be found at Proceedings of the American Bee Research Conference 2010