Replication Data for: Uncoupled shedding and spreading drive transmission heterogeneity

Disease transmission is highly heterogeneous, yet hosts are often classified as high- or low-risk transmitters based on single metrics such as parasite load or shedding. Here, we show that this simplification obscures the biological structure of transmission. Using a natural Caenorhabditis–Leucobacter system, we decompose transmission into sequential steps spanning the infection cycle, including host susceptibility, parasite shedding, infection-induced dispersal (spreading), and infection outcomes in recipient hosts. These components varied largely independently across host genotypes and infection routes, leading to repeated reordering of transmission potential across stages. Notably, high parasite shedding did not reliably predict infectiousness: parasites from different hosts produced divergent infection outcomes in standardized recipient hosts even at comparable exposure doses. This outcome demonstrates that hosts shape not only parasite quantity but also parasite performance after transmission. Transmission was further shaped by ecological context, with the infection route reversing host susceptibility and altering downstream transmission patterns. Together, our results show that transmission heterogeneity emerges from distinct ecological bottlenecks across the infection cycle. By separating transmission quantity from transmission quality, we show that more parasites do not mean more transmission.