Stressors have extensive effects on vertebrate immunity and behavior, but how these effects translate into competence for transmission of new infections remains obscure. In anthropogenically modified habitats or other adverse areas, stress hormones might make some individuals or species particularly prone to alter disease dynamics. Here, we directly investigated the role of corticosterone on the interaction among West Nile virus (WNV), one of its vectors (Culex quinquefaciatus), and a passerine (the zebra finch, Taeniopygia guttata). We were interested to learn how experimental elevation of this hormone would alter host competence, namely mosquito foraging preference, host defensive behavior, mosquito productivity, and resistance and tolerance of WNV.
Corticosterone elevation doubled the likelihood that mosquitoes would forage on birds when treated and control birds were housed together. This outcome was not due to poor defense by experimental birds; birds with corticosterone were more defensive, but unable to protect against mosquito bites. Mosquitoes feeding on stressed birds also laid larger clutches faster than control birds, indicating that feeding choice benefitted vectors. West Nile virus competency was greatly affected by corticosterone too; only stressed birds maintained enough WNV in circulation to transmit it to mosquitoes. This elevated WNV competence persisted for much longer than typical (8 vs. 3 days), with infected, stressed animals performing no differently (flight, body mass maintenance, etc.) than control individuals while infected. Stress hormones elevated host mortality to WNV, but these effects manifested well after peak viremia. Collectively, these data suggest that corticosterone might be a physiological driver of the 20:80 rule, that 20% of individuals cause 80% of many infections.