Literature survey and study selection
To identify studies that evaluated the effects of environmental
stressors on infectivity and host fitness traits in host-parasite
systems, we conducted a systematic literature search in Web of Science
using the search terms: (parasit* OR pathogen* OR disease) AND
(environment* OR temperature OR pollution OR resource OR provision* OR
toxi* OR contamination) AND (infection OR load OR yield OR resistance)
AND (”birth rate” OR ”death rate” OR surviv* OR mortality OR reproduct*
OR fecundity). We limited our search to journal articles published in
English between 2010 and 2020 and scanned titles and, if relevant,
abstracts of all 20,684 hits. This initial screening was carried out by
two experienced reviewers working independently. In addition, we
identified ten more studies from the references of the selected studies.
One experienced reviewer or two student reviewers further examined
articles documenting effects of environmental stressors on infectivity
and host fitness.
We classified stressors into three groups: 1) environmental factors,
which can vary naturally but are also subject to human-induced
perturbation (hereafter “endogenous environment”); 2) presence or
quantity of chemical pollutants (hereafter “chemical pollution”), that
lead to negative expected outcomes for hosts; and 3) resource
availability for hosts (hereafter “resource limitation”). We excluded
studies in which stressful and control environments differed by the
presence of additional antagonistic biotic interactions (e.g., the
presence of predators or competitors) or by the presence of substances
purposely used as therapeutic interventions on infected hosts (e.g.,
chlorine added to water as a treatment against ectoparasites).
Furthermore, we limited our search to studies with animal hosts and
excluded studies on parasitoid infections (Fig. 1).
We included only experimental studies with hosts exposed to or infected
by parasites under laboratory conditions. Infected hosts were either
exposed to pathogens or infected in laboratory settings. Yet, they could
have cleared the infection during the experiment and had undetectable
pathogen loads by the time fitness traits were quantified. We included
studies only if infected hosts were exposed to stressful and control
treatments and if the authors reported data of both host fitness
(fecundity and/or survivorship) and pathogen infectivity (prevalence
and/or intensity) from the same experiment (i.e., for the same pool of
individuals divided between stressful and control treatments) at matched
timepoint(s) (Fig. 1). For example, if a study reported infection
intensity at 24 h and 72 h post-infection (hpi), but survivorship was
only recorded at 72 hpi, we used the 72h data exclusively. If a study
recorded both fitness and infectivity at multiple time intervals, we
included all matched intervals in data collection. We accounted for the
non-independence of these effects and their sampling errors in the
random structure of our statistical models (see below). We excluded
studies in which parasite shedding was recorded as a proxy for infection
intensity. Studies were further excluded for pseudoreplication, missing
sample size information, or when estimates were reported without
associated errors (Fig. 1).