Moderators
Our first analysis aimed to determine whether pathogen exposure in
selected studies led to reduced host fitness without environmental
stressors. For this analysis, we used the response trait category
(fecundity or survivorship) as the only moderator and included only data
from hosts in control (i.e., no environmental stress) conditions. We
then focused on effects of environmental stressors on host-pathogen
dynamics and examined three factors that could moderate the magnitude of
these effects. For Q1, we considered infection status (infected and
uninfected), stressor type, and response trait (fecundity and
survivorship) as moderators. We were specifically interested in whether
infection status amplified any negative fitness consequences of
stressors. As mentioned above, stressors were of three types: 1)
endogenous environmental factors (e.g., temperature, humidity, salinity,
dissolved oxygen, and habitat structural complexity), 2) chemical
pollution by toxins or synthetic compounds typically derived from
pesticides or herbicides, and 3) resource limitation (restricted access
to food or specific nutrients, like nitrogen and phosphorus). For
response traits, fecundity was typically recorded as total number of
offspring, whereas survivorship was reported as proportion alive, number
alive, and sometimes, time to death.
In Q2, we focused exclusively on infected individuals under the
abovementioned criteria. We investigated stressor type and response
trait as moderators. We aimed to contrast effects of stress on fitness
vs. infectivity responses. We, therefore, included two additional
response traits as infectivity proxies: infection intensity and
prevalence. Prevalence was always reported as number or percentage of
infected individuals. Infection intensity was often quantified in
different ways for different types of pathogens, for example, (log) copy
number for viruses, colony-forming units for bacteria, mean number of
cercaria for helminths, and spore counts for fungi. To compare relative
sensitivity of fitness and infectivity, and because prevalence and
infection intensity represent the opposite of host defense, signs of
unbiased standardized mean differences were flipped. By doing so, a
positive effect size reflects greater defense and a beneficial outcome
for hosts, whereas, for fitness traits, a positive sign indicates higher
survivorship or fecundity.
We complemented these main models for Q2 with two additional moderators
in separate analyses. We investigated whether transmission environment
(terrestrial or aquatic) or transmission mode (direct or indirect)
modulates effects of environmental stressors on infectivity and host
fitness responses. For hosts that occupy different environments across
life stages, we categorized transmission environment based on life stage
of hosts exposed or infected in each study, which was typically the most
susceptible life stage to the target pathogen. We classified pathogen
transmission as ‘indirect’ if it met one of three conditions: 1)
pathogen required an ecologically distinct intermediate host to complete
its life cycle, 2) pathogen was transmitted between ecologically similar
hosts via vectors, or 3) pathogen could survive independently of host
during free-living stage. Otherwise, pathogens were considered as having
‘direct’ transmission between ecologically similar hosts.