When dose matters: Linking exposure, environment, and epidemic persistence in wildlife systems

Understanding how infectious disease spreads through exposure is key to predicting outbreaks and effective control measures. This is important for wildlife, where outbreaks often lead to devastating ecological consequences. Traditional epidemiological models often assume equal infection risk regardless of exposure dose and focus on a single infection stage. This assumption eventually overlook variations in initial dose and the role of environmental pathogen reservoirs. We hypothesized that higher exposure dose accelerate disease progression, increase mortality, and elevate pathogen shedding but reduce infectious periods. To evaluate this, we estimated key disease parameters – including latency rate, disease-induced mortality, zoospore shedding rates, and transmission probability – from datasets of eastern newt ( Notophthalmus viridescens ) exposed to varying zoospore concentrations of fungal pathogen Batrachochytrium salamandrivorans (Bsal) . Guided by the empirical evidence, we developed a novel mathematical model capturing dose-dependent transmission, multiple exposure stages, and environmental pathogen accumulation. This empirically driven modeling framework reveals how exposure levels shape disease trajectory, host outcomes and pathogen persistence. Our findings indicate that high initial dose lead to faster disease progression and higher mortality. On the other hand, environmental transmission can sustain outbreaks even under low direct contact rates. By integrating dose dependence with environmental transmission, our framework advances epidemiological modeling of pathogen persistence.