The Study Population
In the Swiss Aegelsee pond, D. magna and P. ramosadynamics have been monitored for the last 10 years (Andras and Ebert 2013, Ameline et al. 2020, Ameline et al. 2021). D. magna hatch from ephippia in early Spring (March or April), when water temperatures are around 10 oC. Strong seasonal epidemics have been observed every year, with parasite prevalence increasing in May, when water temperatures are about 15 oC (Ameline et al. 2020). Prevalence peaks in midsummer and declines in the Fall (as does temperature). Concurrently, as a consequence of natural selection, the proportions of susceptible D. magna decline throughout the course of the season, and the proportion of resistant clones increases as the epidemic progresses (Ameline et al. 2020). D. magna and P. ramosa populations overwinter through resting stages (ephippia) and dormant parasite stages in the spore bank (endospores), resulting in cycles of epidemics and host demographic dynamics each year. The parallel dynamics of P. ramosa prevalence, temperature andD. magna population size in Spring prevent us from understanding if P. ramosa outbreaks are limited by temperature, the availability of the susceptible hosts or other factors. Previous work has demonstrated that warmer temperatures are more favourable for infections from the water column (Vale et al. 2008). However, this work did not include the natural means of spore uptake from the pond sediments, nor did it consider that D. magna hatchlings from ephippia resting stages might differ in behaviour, physiology and/or resistance to parasites from D. magna bred as clonal lines in preparation of the experiment. It is therefore unknown whether spore bank transmission is triggered or accelerated by temperature increase, or simply by the presence of susceptible D. magna , which activate the spores upon contact (Duneau et al. 2011).
The objectives of this study were thus to 1) disentangle whether the onset of P. ramosa epidemics (defined as when infections are first observed in the population) is independently driven by temperature, or simply by the presence of susceptible D. magna , and 2) determine how temperature influences the speed/timing of initial infections, and to thereby 3) ascertain how temperature contributes to the seasonality of P. ramosa epidemics. We hypothesized the development of both the host and the parasite depends on temperature, and that the parasite is limited by temperature beyond its need for available hosts. We therefore predicted that the acceleration of development of P. ramosa (time to visible infection) with increasing temperature is faster than that of the host, such that relative development is faster for hosts at low temperature and faster for the parasite at high temperatures. Support for this hypothesis would indicate that the seasonality of the epidemics, especially the timing of outbreaks in Spring, are driven by temperature effects on the parasite rather than solely the presence of susceptible hosts. It would also indicate that the effects of temperature on the parasite are different from those on the host.
Methods