Social Fever or General Immune Response? Revisiting an Example of Social Immunity in Honey Bees.

Abstract

Simple SummaryBehavioral, or social fever in honey bees is frequently cited as a form of social immunity—the behavioral, organizational, and physiological mechanisms that social organisms use to defend against parasites and pathogens to maintain group health. It has been shown previously that colonies elevate brood nest temperature as a response to challenge with the fungal pathogen, Ascosphaera apis, the causative agent of chalkbrood disease in honey bees. Our objective was to test whether we could replicate social fever and its effect on reducing signs of chalkbrood disease in colonies using methods similar to previous reports. We affirmed that honey bees increase the temperature of the brood nest after exposure to A. apis. However, the magnitude of temperature increase was insufficient at preventing infection, as all colonies showed signs of chalkbrood post-exposure. We conducted additional studies to explore alternative hypotheses related to the cause and effect of behavioral fever. We found that challenge with A. apis resulted in an increased immune response of adult bees, but this activation was not due to thermal and other stress, as measured by expression of the heat stress and nutritional genes, Hsp 70Ab-like and vitellogenin, respectively. We proposed additional hypotheses that could be tested.Honey bees use several strategies to protect themselves and the colony from parasites and pathogens. In addition to individual immunity, social immunity involves the cumulative effort of some individuals to limit the spread of parasites and pathogens to uninfected nestmates. Examples of social immunity in honey bees that have received attention include hygienic behavior, or the removal of diseased brood, and the collection and deposition of antimicrobial resins (propolis) on interior nest surfaces. Advances in our understanding of another form of social immunity, social fever, are lacking. Honey bees were shown to raise the temperature of the nest in response to temperature-sensitive brood pathogen, Ascosphaera apis. The increase in nest temperature (−0.6 °C) is thought to limit the spread of A. apis infection to uninfected immatures. We established observation hives and monitored the temperature of the brood nest for 40 days. This observation period was broken into five distinct segments, corresponding to sucrose solution feedings—Pre-Feed, Feed I, Challenge, Feed II, and Post-Feed. Ascosphaera apis was administered to colonies as a 1% solution of ground sporulating chalkbrood mummies in 50% v/v sucrose solution, during the Challenge period. Like previous reports, we observed a modest increase in brood nest temperature during the Challenge period. However, all hives presented signs of chalkbrood disease, suggesting that elevation of the nest temperature was not sufficient to stop the spread of infection among immatures. We also began to explore the molecular mechanisms of temperature increase by exposing adult bees in cages to A. apis, without the presence of immatures. Compared to adult workers who were given sucrose solution only, workers exposed to A. apis showed increased expression of the antimicrobial peptides abaecin (p = 0.07) and hymenoptaecin (p = 0.04), but expression of the heat shock response protein Hsp 70Ab-like (p = 0.76) and the nutritional marker vitellogenin (p = 0.72) were unaffected. These results indicate that adult honey bee workers exposed to a brood pathogen elevate the temperature of the brood nest and initiate an immune response, but the effect of this fever on preventing disease requires further study.