As a foundation species in shallow-water ecosystems, the mussel Mytilus edulis exposed to abiotic and biotic stressors. In particular, heat stress can have detrimental effects on mussel performance and biotic interactions with parasites may exacerbate those effects. This study explores the metabolic responses of mussels to infections with the trematode Renicola roscovita, under mild and transient heat exposures. Using controlled laboratory infections, a first experiment investigated the responses of infected and uninfected small mussels (2 cm), to a 24-hour exposure to a mild temperature followed by an acute heat ramp and subsequent cooling. The results indicated that trematode infections reduced mussel filtration by, on average, 13%, and that infections exacerbated the impact of the transient heat exposure, as indicated by a larger difference (33%) between infected and uninfected mussels in the post-heat recovery phase. However, these differences were statistically not significant, owing to generally large variation among mussels and low sample sizes. In a second experiment, we further investigated how mussel size (2 and 4 cm) affected infection impacts on mussel performance under constant exposure to a mild temperature. We found that infections reduced mussel filtration at similar rates (11% and 12% for small and large mussels, respectively) compared to the first experiment, albeit statistically significant only for large mussels. In both experiments, no discernible impact on the mussel respiration rate was found. Interestingly, we found positive relationships between mussel filtration capacity and infection intensity, suggesting that mussel phenotypes with generally higher filtration capacity may be more prone to infections. Overall, our results suggest that R. roscovita metacercariae infections can lower the ability of hosts to sustain optimal energy supply, which in turn may exacerbate the negative effects of heat stress. The role of mussel phenotypic variation in filtration capacity in driving infection levels and subsequent effects warrants further investigation.

Concomitant predation, which occurs when parasites are consumed and digested along with their hosts, has previously been suggested as a profound factor determining food web structure. Few studies have adressed the impact of concomitant predation in research on behaviourally parasite-modified prey or in biological control studies. However, empirical evidence of concomitant predation effects on hosts infected with multiple parasite taxa is lacking. We investigated the importance of concomitant predation on digenean trematodes by examining the degree of snail (Radix balthica, first intermediate host) seasonal predation by Arctic charr (Salvelinus alpinus) and brown trout (Salmo trutta) by contrasting infection rates of free-living snails obtained from a lake vs predated snails retrieved from fish stomachs and intestines. The fish consumed infected snails nearly at all seasons, demonstrating that concomitant predation in the model subarctic lake is common, likely indirectly affecting trematode transmission by reducing host and parasite populations. The overall trematode prevalence in both snail groups was season-independent, being however substantially higher in free-living compared to predated snails. The net effects of underlying mechanisms related to prey availability, fish feeding ecology, continuous presence of dominant trematodes and, most importantly, size of fish and snails drove the strength of predator-prey interactions and infection patterns in both snail groups. Larger fish preying upon larger snails, which simultaneously harboured more infections, may induce a substiantial negative effect of concomitant predation on snail and parasite population dynamics, with serious implications for food web structure and ecosystem functioning. This study contributes to a better understanding of the role of non-host predators in regulating trematode infection, community structure and transmisison patterns, biomass transfer and energy flow in food webs. Our findings also highlight the importance of studying the impact and extent of concomitant predation in terms of parasite seasonal dynamics and biological control of infectious diseases.

Ecological communities can affect transmission pathways of parasites and pathogens, ultimately affecting disease dynamics. While the community composition of less competent decoy hosts is known to affect diseases in focal hosts, it remains poorly understood whether such diversity effects also exist when non-host organisms remove free-living parasite stages, e.g. by predation. In response surface design laboratory experiments, we investigated non-host diversity effects on the removal of cercarial stages of trematodes, ubiquitous parasites in aquatic ecosystems. In all three combinations of two non-hosts at four density levels, the addition of a second non-host did not generally result in increased parasite removal but neutralised, amplified or reduced the parasite removal exerted by the first non-host, depending on the density. These complex non-host diversity effects were probably driven by intra- and interspecific interactions and suggest the need to integrate non-host diversity effects in understanding the links between community diversity and disease risk.