LAUSR

Abstract A consequence of genetic recombination can be the evolution of highly virulent pathogen strains. Virulence can manifest through various mechanisms of host–pathogen interaction that facilitate transmission. We discovered a highly virulent chimeric ranavirus in Georgia, USA, estimated transmission parameters using controlled experiments, and developed compartmental disease models to examine potential consequences on tadpoles of a susceptible host species (Lithobates sylvaticus). Our models included three transmission pathways: direct transmission via host contact, environmental transmission via shed virions in water, and transmission via necrophagy of morbid individuals. Unlike previous models, we categorized individuals into multiple stages of infection (susceptible, latency, and infectious), where the probability of disease-induced mortality increased throughout the duration of infection following a gamma distribution with an integer shape parameter. Our simulations showed that accounting for pathogen incubation improved model predictions when compared to survival data from controlled experiments. We found that transmission due to direct contact of tadpoles was the dominant transmission pathway; however, environmental transmission played a larger role as tadpole density increased and the epidemic progressed. Estimated R 0 (basic reproduction number) values >570 for all transmission pathways indicate that targeting only one transmission pathway is unlikely to thwart invasion. Additionally, the high invasion potential and diseased-induced mortality associated with this chimeric ranavirus indicate that this pathogen is a substantial threat to amphibian biodiversity in the United States.