Stressors constrain host defenses
Hosts invest resources to defend themselves from pathogens via behavioral or physiological mechanisms. While avoidance behavior is less understood (Buck et al. 2018), physiological mechanisms, such as infection resistance or disease tolerance, are well documented (Råberget al. 2007, 2009; Svensson & Råberg 2010). Resistance mechanisms control parasite growth and reproduction, reducing infection intensity, while tolerance reduces or compensates for infection-induced pathology without reducing pathogen burden (Boots 2008; Medzhitovet al. 2012). Although resistance limits pathogen replication while tolerance does not, leading to different disease implications (Schneider & Ayres 2008), both strategies have high energetic requirements, and hosts should only elicit them if parasite infections reduce their fitness (Ayres & Schneider 2009; Cumnock et al.2018). Consequently, trade-offs exist between immune response and other energetically costly physiological processes, such as reproduction and growth (Lochmiller & Deerenberg 2000), in both vertebrates (Gustafssonet al. 1994) and invertebrates (Schwenke et al. 2016). Furthermore, there is recent evidence that trade-offs between reproduction and immune function exist at the transcriptomic level and may be conserved across animals (Rodrigues et al. 2021). Given these trade-offs, host defense may be compromised under stressful conditions (Sheldon & Verhulst 1996; Gervasi et al. 2015).
Stressors may modulate host defensive mechanisms against infections. Malnutrition can impair immune function by reducing T-cell-mediated immune response (Alonso-Alvarez & Tella 2001), toxicants can immunocompromise a host (Caren 1981) or upregulate host immunity (Pölkkiet al. 2012), and extreme temperature variation can impair immunity leading to species declines (Rohr & Raffel 2010). Owenet al . (2021) showed that food-deprived robins (Turdus migratorius ) developed higher West Nile Virus titers and were infectious longer than robins fed normally. Similarly, amphibians exposed to pesticides have experienced eosinophil recusation (a resistance mechanism) and associated increases in trematode infections and subsequent limb malformations (Kiesecker 2002). Conversely, infection tolerance in Galapagos mockingbirds (Mimus parvulus ) has been impaired by climatically-induced food stress, exhibiting lower fledging success in dry years (when resources were scarce) compared to wet years, due to inability to compensate for costs of parasitic fly nest infestations (McNew et al. 2019). These examples show that host susceptibility to infections and/or pathogen transmission may increase under stressful conditions.