Floral nectar, produced by plants to attract pollinators, is primarily composed of sugars.  However, some nectar may also contain secondary compounds such as alkaloids, normally produced by plants to defend themselves against herbivores.  The function of this so-called “toxic nectar” is not fully understood, but one hypothesis is that it may prevent the microbial degradation of nectar.  Given that these compounds will be ingested by floral visitors, could nectar alkaloids have antimicrobial properties that inhibit pollinator pathogens?  We examined how gelsemine, the primary alkaloid found in the nectar of Gelsemium sempervirens, affects the pathogenicity of the gut protozoan Crithidia bombi.  C. bombi has well-documented effects on bumble bee behaviour, but is of particular interest because it can be horizontally transmitted via floral nectar.  To test the direct effect of gelsemine on pathogenicity, we inoculated artificial nectar with C. bombi and let the solution rest for either 0, 60, or 120 minutes before infecting bumble bee workers, simulating the possible time lag before contaminated nectar is consumed by naïve bees.  We also examined how continuous consumption of gelsemine altered pathogen load by feeding bees a high-gelsemine nectar diet for ten days post-infection. 

Results/Conclusions

Overall, the presence of gelsemine did inhibit Crithidia bombi infections in bumble bees in all treatments.  The direct effect of gelsemine on C. bombi was weak, with a marginal reduction in pathogen load at any of the three delay periods, although the effect did increase throughout the duration of the infection.  In contrast, there was a 20-30% reduction in standardized infection intensity after the continuous consumption of gelsemine. Taken together these results suggest that while direct exposure to nectar alkaloids has a marginal antimicrobial effect, the repeated consumption of putatively toxic nectar can significantly reduce C. bombi infections in bumble bees.  It remains to be seen whether infected bees self-medicate by actively seeking toxic nectar, but our results do provide a potential mechanism for the function and maintenance of secondary compounds in floral nectar.