Data for: Can pharmaceutical pollution alter the spread of infectious disease? A case study using fluoxetine.

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, as well as the
genotype of the pathogen. In contrast, the characteristics of unexposed
animals, and thus the growth and density of susceptible hosts, were robust
to fluoxetine. Using our data to parameterise an epidemiology 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 two-fold 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 on disease dynamics,
with repercussions on pathogen genetic diversity and evolution.