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