“…However, we captured some variation in pathogen loads in our model because (i) pathogen loads and Bd ‐induced mortality in the field are often greatest in the winter (Grogan et al., ; Phillott et al., ), simulated with Bd ‐induced winter mortality in our model and (ii) newly infected individuals only transmitted Bd after they had been infected for a year, which would be expected if pathogen loads must accumulate before transmission. We chose to model transmission in a density‐dependent manner rather than through the environment because (i) previous studies have found evidence for density‐dependent transmission of Bd (Rachowicz & Briggs, ) and that altering the amount of Bd in the environment has little to no impact on host population outcomes (Drawert et al., ), (ii) in most conditions, Bd zoospores remain motile for only short periods of time outside the host (Piotrowski, Annis, & Longcore, ; Voyles et al., ; Woodhams, Alford, Briggs, Johnson, & Rollins‐Smith, ) and are unlikely to survive long periods of freezing temperatures in the winter (Boyle et al., ), and (iii) transmission and mortality are decoupled in this system, such that allowing for build‐up of zoospores within the environment would only influence the number of infected individuals within a given year, which we modelled by changing the transmission rate (see below). Once infected with Bd , individuals remained infected through metamorphosis and across years.…”