Stressor type modulates host fitness and infectivity in
different ways
Our meta-analysis documented the dominant effects of stressors on host
fitness and pathogen infectivity. Interestingly, we found that infected
and uninfected hosts had proportionally similar sensitivity to stressors
regarding survival and fecundity. Furthermore, stressor type determined
host fitness and pathogen infectivity outcomes. Although we found that
resource limitation decreased host fecundity and pathogen intensity,
other authors have described positive, negative, and unimodal
relationships across animal taxa. For example, Cressler et al.(2014) found that as invertebrates increased their resource uptake, they
increased their pathogen intensity, whereas increased resource
consumption decreased pathogen intensity in vertebrates. They argued
that this differential response could be due to their distinct immune
systems and body sizes (Cressler et al. 2014). Contrary to their
results, we found that both vertebrate and invertebrate hosts (which
represented most of our data) reproduced less and carried a lower
pathogen burden when facing limiting resources. One possible explanation
is that hosts are investing resources in their immune defense mechanism
at the cost of reproduction. In support of this hypothesis, it has been
proposed that illness-mediated anorexia may enhance immune function by
acting as a “master switch” that reduces the investment in other
physiological processes (Hite et al. 2020). For example, Cumnocket al. (2018) showed that malaria-infected mice strongly reduced
their food intake and switched their metabolism from burning sugar
(glycolysis) to burning fats (ketosis), which influenced host tolerance
to infections. Alternatively, resource limitations could negatively
affect pathogens, decreasing their capacity to reproduce within hosts. A
third explanation could be that hosts under limited resources could be
smaller, and small hosts may carry fewer pathogens, therefore decreasing
pathogen intensity within host. This has been reported in the
snail-Schistosome system, where smaller snails carry fewer parasites
(Civitello et al. 2022). Moreover, in Daphnia populations,
food shortage reduced body size with subsequent reductions in spore
loads of a microsporidian parasite (Pulkkinen & Ebert 2004).
Regarding endogenous environmental stressors, we found that when hosts
are stressed, they survive less but have higher pathogen intensity.
Coping with fluctuating abiotic environments can be energetically
demanding for hosts, and human activities may exacerbate the frequency
and severity of naturally occurring fluctuations. For example,
temperature variation occurs naturally, but climate change makes it
unpredictable or more drastic (Harvell et al. 2002; Marcogliese
2008). It is likely that hosts barely persisting in an environment are
not able to resist infections (increasing pathogen proliferation) and/or
compensate for the damage done by the pathogen (tolerating infection).
One of the most documented examples of this possible scenario is given
by the amphibian-chytrid fungus system under the pressure of climate
change, increasing their susceptibility to pathogen infections (Alfordet al. 2007; Rollins-Smith et al. 2011).
Finally, we found that hosts exposed to pollutants increased their
mortality but decreased pathogen prevalence. However, we note that these
results must be interpreted cautiously, given that the experimental
studies included in our meta-analysis intentionally use sub-lethal doses
of toxins. Low prevalence may be due to hosts dying before replicating
and transmitting the pathogen. This result is consistent with
mechanistic models of how toxicants influence pathogen transmission
showing that infection prevalence was lower in more contaminated
landscapes due to high host mortality (Sánchez et al. 2020).
Although pollution can decrease parasitism if infected hosts suffer more
than uninfected hosts from pollutant exposure, our analysis showed that
hosts are equally sensitive to toxins regardless of infection status.
Alternatively, parasites could also be negatively affected by pollution.
For example, Gheorgiu et al. (2006) studied the effects of zinc
concentration on a fish-parasite system and showed that while mortality
increases in infected hosts as zinc concentration increased, parasite
burden peaked at intermediate zinc concentrations. A follow-up study
revealed that both parasite lifespan and fecundity were also negatively
affected by zinc (Gheorgiu et al. 2007).