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
in relation to 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
this differential response could be due to 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
invest resources in immune defense 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 investment in other physiological processes (Hite et
al. 2020). For example, Cumnock et al. (2018) showed that
malaria-infected mice reduced their food intake and switched from
burning sugar (glycolysis) to fats (ketosis), which influenced host
tolerance to infections. Alternatively, resource limitation could
negatively affect pathogens, decreasing their capacity to reproduce
within hosts. Lastly, resource-limited hosts are often smaller and may
carry fewer pathogens, reducing pathogen intensity. This has been
reported in the snail-Schistosome system, where smaller snails carry
fewer parasites (Civitello et al. 2022). Moreover, inDaphnia 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 stressed
hosts 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). When stressed,
hosts may not resist infections (increasing pathogen proliferation)
and/or compensate for damage done by the pathogen (tolerating
infection), as seen when higher temperatures increase coral
(Gorgonia ventalina ) susceptibility to fungus (Aspergillus
sydowii ), while also increasing fungal growth and virulence (Wardet al. 2007).
Finally, we found hosts exposed to pollutants had higher mortality but
lower pathogen prevalence. However, we note that these results must be
interpreted cautiously, given that the experimental studies included in
our meta-analysis intentionally used sub-lethal toxin doses. 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, mortality
increased in infected hosts as zinc concentration increased, but
parasite burden peaked at intermediate zinc concentrations in a
fish-parasite system (Gheorgiu et al. 2006). A follow-up study
revealed that both parasite lifespan and fecundity were also negatively
affected by zinc (Gheorgiu et al. 2007).