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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.

Human activity is changing global environments at an unprecedented rate, imposing new ecological and evolutionary ramifications on wildlife dynamics, including host-parasite interactions. Here we investigate how an emerging concern of modern human activity, pharmaceutical pollution, influences the spread of disease in a population, using the water flea Daphnia magna and the bacterial pathogen Pasteuria ramosa as a model system. We found that exposure to different concentrations of fluoxetine-a widely prescribed psychoactive drug and widespread contaminant of aquatic ecosystems-affected the severity of disease experienced by an individual in a non-monotonic manner. The direction and magnitude of any effect, however, varied with both the infection outcome measured and the genotype of the pathogen. By contrast, the characteristics of unexposed animals, and thus the growth and density of susceptible hosts, were robust to fluoxetine. Using our data to parameterize an epidemiological model, we show that fluoxetine is unlikely to lead to a net increase or decrease in the likelihood of an infectious disease outbreak, as measured by a pathogen's transmission rate or basic reproductive number. Instead, any given pathogen genotype may experience a twofold change in likely fitness, but often in opposing directions. Our study demonstrates that changes in pharmaceutical pollution give rise to complex genotype-by-environment interactions in its influence of disease dynamics, with repercussions on pathogen genetic diversity and evolution. This article is part of the theme issue 'Infectious disease ecology and evolution in a changing world'.

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.

Environmental pollution is an increasing problem for wildlife globally. Animals are confronted with many different forms of pollution, including chemicals, light, noise, and heat, and these can disrupt critical biological processes such as reproduction. Impacts on reproductive processes can dramatically reduce the number and quality of offspring produced by exposed individuals, and this can have further repercussions on the ecology and evolution of affected populations. Here, we illustrate how environmental pollutants can affect various components of reproduction in wildlife, including direct impacts on reproductive physiology and development, consequences for gamete quality and function, as well as effects on sexual communication, sexual selection, and parental care. We follow with a discussion of the broader ecological and evolutionary consequences of these effects on reproduction and suggest future directions that may enable us to better understand and address the effects of environmental pollution.