Abstract
Environmental sources of infection can play a primary role in shaping epidemiological dynamics; however, the relative impact of environmental transmission on host-pathogen systems is rarely estimated. We developed and fit a spatially explicit model of African swine fever virus (ASFV) in wild boar to estimate what proportion of carcass-based transmission is contributing to the low-level persistence of ASFV in Eastern European wild boar. Our model was developed based on ecological insight and data from field studies of ASFV and wild boar in Eastern Poland. We predicted that carcass-based transmission would play a substantial role in persistence, especially in low-density host populations where contact rates are low. By fitting the model to outbreak data using approximate Bayesian computation, we inferred that between 53% and 66% of transmission events were carcass-based that is, transmitted through contact of a live host with a contaminated carcass. Model fitting and sensitivity analyses showed that the frequency of carcass-based transmission increased with decreasing host density, suggesting that management policies should emphasize the removal of carcasses and consider how reductions in host densities may drive carcass-based transmission. Sensitivity analyses also demonstrated that carcass-based transmission is necessary for the autonomous persistence of ASFV under realistic parameters. Autonomous persistence through direct transmission alone required high host densities; otherwise re-introduction of virus periodically was required for persistence when direct transmission probabilities were moderately high. We quantify the relative role of different persistence mechanisms for a low-prevalence disease using readily collected ecological data and viral surveillance data. Understanding how the frequency of different transmission mechanisms vary across host densities can help identify optimal management strategies across changing ecological conditions.