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The relationship between pathogen proliferation and the cost of infection experienced by a host drives the ecology and evolution of host–pathogen dynamics. While environmental factors can shape this relationship, there is currently limited knowledge on the consequences of emerging contaminants, such as pharmaceutical pollutants, on the relationship between a pathogen's growth within the host and the damage it causes, termed its virulence. Here, we investigated how exposure to fluoxetine (Prozac), a commonly detected psychoactive pollutant, could alter this key relationship using the water flea Daphnia magna and its bacterial pathogen Pasteuria ramosa as a model system. Across a variety of fluoxetine concentrations, we found that fluoxetine shaped the damage a pathogen caused, such as the reduction in fecundity or intrinsic growth experienced by infected individuals, but with minimal change in average pathogen spore loads. Instead, fluoxetine modified the relationship between the degree of pathogen proliferation and its virulence, with both the strength of this trade-off and the component of host fitness most affected varying by fluoxetine concentration and host genotype. Our study underscores the potential for pharmaceutical pollution to modify the virulence of an invading pathogen, as well as the fundamental trade-off between host and pathogen fitness, even at the trace amounts increasingly found in natural waterways. [ABSTRACT FROM AUTHOR]

Pharmaceutical pollutants pose a threat to aquatic ecosystems worldwide. Yet, few studies have considered the interaction between pharmaceuticals and other chronic stressors contemporaneously, even though the environmental challenges confronting animals in the wild seldom, if ever, occur in isolation. Thermal stress is one such environmental challenge that may modify the threat of pharmaceutical pollutants. Accordingly, we investigated how fluoxetine (Prozac), a common psychotherapeutic and widespread pollutant, interacts with temperature to affect life-history traits in the water flea, Daphnia magna. We chronically exposed two genotypes of Daphnia to two ecological relevant concentrations of fluoxetine (30 ng l−1 and 300 ng l−1) and a concentration representing levels used in acute toxicity tests (3000 ng l−1) and quantified the change in phenotypic trajectories at two temperatures (20°C and 25°C). Across multiple life-history traits, we found that fluoxetine exposure impacted the fecundity, body size and intrinsic growth rate of Daphnia in a non-monotonic manner at 20°C, and often in genotypic-specific ways. At 25°C, however, the life-history phenotypes of individuals converged under the widely varying levels of fluoxetine, irrespective of genotype. Our study underscores the importance of considering the complexity of interactions that can occur in the wild when assessing the effects of chemical pollutants on life-history traits. [ABSTRACT FROM AUTHOR]