Interactive Effects of Temperature and Available Hosts on
Infection
Among live D. magna treatments, the more resistant clones were
less likely to become infected and had a longer time to infection than
the more susceptible ones. Moreover, host resistotype interacted with
temperature to influence infection prevalence, with most observed
infections at low temperature being among the more susceptible clones.
As our broadly resistant clones are susceptible to at least one of the
known P. ramosa strains in the spore bank, it is not surprising
that they still became infected. However, that fewer individuals did so
compared to the more susceptible clones (especially at low temperatures)
and that they also took longer to become infected could be due either to
the frequency of P. ramosa strains within the mud that are able
to infect them, or the possibility that these strains indeed take longer
to cause visible infection (i.e. reproduce inside the host slower than
other strains). Although we are unable to elucidate which of these two
hypotheses is more likely with these data, these findings nevertheless
suggest an important interactive effect of host resistance with
temperature on outbreak timing and dynamics. Similar
temperature-by-genotype interactions have been found in D. magnaresistance to other parasites (Bruijning et al. 2022, Santos and Ebert
2022) and in many other host-parasite systems (Judelson and Michelmore
1992, Gsell et al. 2013). Our results imply that the host-parasite
relationships in this system are strongly linked to temperature, and
that changes in temperature may alter the infection and host demographic
cycles we have repeatedly observed.
Prevalence in the ephippia treatments at the end of the experiment was
at all temperatures considerably lower than in the treatments with liveD. magna (compare Figure 2c,d). Moreover, within ephippia
treatments no infection was observed below 15 oC a
finding consistent with dynamics observed at the field site (Ameline et
al. 2020). Although we do not know the resistotypes of animals used in
this treatment, it is unlikely that this result is due to resistotype
composition, as the known resistotypes used in the live treatment are
also known to hatch from ephippia (Ameline et al. 2020, Ameline et al.
2021). It is possible that females hatching from resting stages behave
differently than asexually produced females and that this reduces the
likelihood of encountering the parasite. Sediment-borne parasite stages,
like the spores of P. ramosa , are picked up when the host browses
over the sediment surface, to enrich its food (Arbore et al. 2016). We
do not know if this behaviour differs among the two types of females,
but if so, it might partially explain these observed differences and
possibly why Spring epidemics of P. ramosa are delayed, because
all D. magna in early Spring hatch from ephippia. This hypothesis
could further explain why infections are not observed in nature at lower
temperatures, since the time for the first generation of asexual females
to be born compounded with the impacts of temperature on development
would further prolong the time until outbreak.