Circadian rhythms allow organisms to coordinate physiological processes to diel environmental variation. Circadian variation in epidemiologically relevant traits, such as behavior and immunity, could lead to circadian variation in infection outcomes. However, the link between circadian rhythms in host traits and infection outcomes is unclear, because trait variation may act synergistically or antagonistically. For example, if immunity and exposure risk vary together, infection outcomes may remain relatively constant over a diel cycle. To elucidate this link, we examined whether circadian rhythms in multiple host traits explain known variation in infection outcomes across four host genotypes. Specifically, we investigated circadian variation in feeding behavior of the zooplankton host, Daphnia dentifera, in response to its fungal pathogen, Metschnikowia bicuspidata. In nature, Daphnia are exposed to M. bicuspidata spores while feeding. We used individual feeding experiments to measure rhythms in feeding in the absence and presence of pathogens. Then, we compared pathogen present and absent feeding to test the hypothesis that infection outcomes are correlated with feeding rhythm plasticity.
Results/Conclusions
We find that in the absence of pathogens, host genotypes exhibit circadian rhythms in feeding that vary in amplitude and the time of peak feeding. In the presence of pathogens, some genotypes reduce feeding across the entire circadian cycle, whereas others only decrease feeding during specific phases, and others do not alter feeding rhythms. We find that healthy and exposed animals tend to eat less during their resting phase (day) than the active phase (night), but that infection prevalence is higher when exposed during the resting phase than the active phase. Moreover, counter to our hypothesis, genotypes with greater reduction in feeding exhibit the highest infection prevalence. These results suggest that reduced feeding may be a mechanism to compensate for poor immune function in highly susceptible genotypes, a hypothesis we are currently testing. Overall, our results indicate that genetic variation in the rhythms and plasticity of host feeding can explain both the probability of becoming infected and infection severity.