Pathogens are affected by stressors as well
Pathogens can be affected by stressors directly or indirectly through their hosts. It is critical to distinguish these mechanisms, as each may affect host populations differently. By definition, pathogens rely on host resources to grow and reproduce (Casadevall & Pirofski 2002); therefore, pathogens compete for resources with host physiological processes that mediate disease outcome (i.e., reproduction, growth, immune defense; Cressler et al. 2014). Direct manipulation of immune response by pathogens has been documented (Maizels & Yazdanbakhsh 2003; Schmid-Hempel 2008), but pathogens may also outcompete host immune response by direct resource consumption (Cressleret al. 2014). For example, in a Daphnia -fungal parasite system, more resources equate to greater epidemics due to both higherDaphnia reproductive rates (i.e., host density driven) and higher infection intensity (Civitello et al. 2015), suggesting that food stress lowers parasitism in the Daphnia­ -fungal parasite system.
On the other hand, a common sickness behavior, reduced food consumption, may be an adaptive host response (Murray & Murray 1979; Exton 1997; Ayres & Schneider 2009). Parasite-mediated anorexia can improve host health and recovery (Wang et al. 2016), much like fever (Klugeret al. 1996). Anorexia appears to intensify with higher levels of parasite exposure or intensity (as reviewed by Hite et al. (2020)); however, the advantages or disadvantages of anorexia depend on nutrient stores and quality, and ambient conditions (McKenzie & Townsend 2007; Johnson et al. 2010; Becker et al. 2015; Hite et al. 2020). Sometimes a low-quality resource may be inadequate for the host while sufficient for the pathogen (Dallas & Drake 2014) or lead to fewer resources for the parasite (Kyriazakia et al. 1998; Hallet al. 2009a, b). Conversely, hosts may increase food intake to compensate for energy lost fighting infections (i.e., resource compensation hypothesis (Christe et al. 1996)). As a result, high-resource diets may increase host tolerance to infections by reducing resource competition between hosts and parasites without negatively affecting parasite fitness (Knutie et al. 2017), with possible implications for the evolution of pathogen virulence (Hiteet al. 2020).
Environmental stressors may also directly impact pathogens with environmental stages (Riggs et al. 1987). Fluctuating environmental conditions and pollutants can negatively affect pathogens (Pietrock & Marcogliese 2003). For instance, deviations from temperature and salinity optima can reduce survival and lifespan in free-living helminths (Pechenik & Fried 1995; Measures 1996), and reduced longevity decreases infective periods. Similarly, elevated nitrate concentrations can reduce free-living spore survival, which may counteract the effects of increased intensity within Daphnia(Dallas and Drake 2014). Even when pathogens survive stressors, their capacity to infect hosts could be affected. For instance, metals can impact sensory receptors of environmental stages of parasites, such as cercariae, impairing their ability to locate, recognize and infect hosts (Ghandour & Webbe 1975; King & Higashi 1992; Morley et al.2002).
Finally, differential effects of stressors on directly vs. indirectly transmitted pathogens (i.e., vector-borne or intermediate hosts) may lead to divergent outcomes (Hopkins et al. 2020). For instance, Studer et al. (2010) showed that although increased temperatures favored the development of the trematode Maritrema novaezealandensis within their intermediate amphipod host,Paracalliope novizealandiae , warmer temperatures increased amphipod mortality, creating a bottleneck for pathogen transmission. Similarly, qualitative differences between aquatic and terrestrial systems, due to life history differences and the greater taxonomic diversity of aquatic parasites and hosts (Harvell et al. 2002; McCallum et al. 2004; Byers 2021), may result in divergent disease outcomes. For example, environmental transmission dominates aquatic systems (Lafferty 2017), making pathogens more susceptible to direct effects of stressors.