Infectious disease within outmigrant juvenile salmon in the Columbia River Basin is modulated, in part, by abiotic stressors that influence host-susceptibility. Through the application of a dose-structured population dynamic model, we show that chemical (both in the river and in the estuary) and in-river (e.g., dams and/or predation) stressors influence host-susceptibility, increasing the mean force of infection (defined as the per capita acquisition rate of infection) by a factor of 2.2 and 1.6, respectively. Using Listonella anguillarum as a model pathogen, nonchemical in-river and chemical stressors contribute equally to a cumulative incidence of delayed disease-induced mortalities in Chinook salmon that range from 3% to 18% for estuary residence times of 30-120 days, respectively. Mitigation of environmental stressors that increase host-susceptibility could represent a significant component in future management strategies to recover listed stocks.