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.