Michael Christopher Otterstatter

The conservation of insect pollinators is drawing attention because of reported declines in bee species and the ‘ecosystem services’ they provide. This issue has been brought to a head by recent devastating losses of honey bees throughout North America (so called, ‘Colony Collapse Disorder’); yet, we still have little understanding of the cause(s) of bee declines. Wild bumble bees (Bombus spp.) have also suffered serious declines and circumstantial evidence suggests that pathogen ‘spillover’ from commercially reared bumble bees, which are used extensively to pollinate greenhouse crops, is a possible cause. We constructed a spatially explicit model of pathogen spillover in bumble bees and, using laboratory experiments and the literature, estimated parameter values for the spillover of Crithidia bombi, a destructive pathogen commonly found in commercial Bombus. We also monitored wild bumble bee populations near greenhouses for evidence of pathogen spillover, and compared the fit of our model to patterns of C. bombi infection observed in the field. Our model predicts that, during the first three months of spillover, transmission from commercial hives would infect up to 20% of wild bumble bees within 2 km of the greenhouse. However, a travelling wave of disease is predicted to form suddenly, infecting up to 35–100% of wild Bombus, and spread away from the greenhouse at a rate of 2 km/wk. In the field, although we did not observe a large epizootic wave of infection, the prevalences of C. bombi near greenhouses were consistent with our model. Indeed, we found that spillover has allowed C. bombi to invade several wild bumble bee species near greenhouses. Given the available evidence, it is likely that pathogen spillover from commercial bees is contributing to the ongoing decline of wild Bombus in North America. Improved management of domestic bees, for example by reducing their parasite loads and their overlap with wild congeners, could diminish or even eliminate pathogen spillover.

In socially living animals, individuals interact through complex networks of contact that may influence the spread of disease. Whereas traditional epidemiological models typically assume no social structure, network theory suggests that an individual’s location in the network determines its risk of infection. Empirical, especially experimental, studies of disease spread on networks are lacking, however, largely due to a shortage of amenable study systems. We used automated video-tracking to quantify networks of physical contact among individuals within colonies of the social bumble bee Bombus impatiens. We explored the effects of network structure on pathogen transmission in naturally and artificially infected hives. We show for the first time that contact network structure determines the spread of a contagious pathogen (Crithidia bombi) in social insect colonies. Differences in rates of infection among colonies resulted largely from differences in network density among hives. Within colonies, a bee’s rate of contact with infected nestmates emerged as the only significant predictor of infection risk. The activity of bees, in terms of their movement rates and division of labour (e.g., brood care, nest care, foraging), did not influence risk of infection. Our results suggest that contact networks may have an important influence on the transmission of pathogens in social insects and, possibly, other social animals.

The success of a pathogen depends not only on its transmission to new hosts, but also on its ability to colonize and persist within its current host. Studies of within-host dynamics have focused on only a few diseases of humans, whereas little is known about the factors that influence pathogen populations as they develop inside non-human hosts. Here, we investigate pathogen dynamics occurring within bumble bees (Bombus impatiens) infected by the gut trypanosome Crithidia bombi. Infection by C. bombi showed several features characteristic of vertebrate diseases, including a rapid initial increase in infection intensity, marked oscillations in parasitaemia, and the stimulation of a systemic immune response in infected bees. Within-host dynamics generated substantial variation in the infectiousness and flower-visiting behaviour of bumble bees. Changes in bee foraging that arise from infection may influence the probability of C. bombi transmission between bees at flowers.

The effects of host size and host species on the prevalence and fitness of conopid flies (Diptera: Conopidae) parasitizing bumblebees (Hymenoptera: Apidae) were investigated. Field data from nine sites across south‐western Alberta, Canada, showed that conopids parasitized, on average, 12.3% of workers and 3.5% of male bees. In general, bee mass was a better predictor of host use and conopid offspring size than bee species. Host mass could not, however, explain the very low prevalence of conopids in the long‐tongued bumblebee, Bombus californicus Smith, or in male bees in general. Conopids predominately infested bees of intermediate size, and as a result, occurred most commonly in the intermediately sized species, B. flavifrons Cresson. Host quality, in terms of conopid offspring size, increased as a non‐linear function of bee size. The results are discussed with respect to the impact of conopids on bumblebee populations, and the relation between host quality and patterns of host use.