Our understanding of the ecological and evolutionary context of novel infections is largely based on viral diseases, even though bacterial pathogens may display key differences in the processes underlying their emergence. For instance, host-shift speciation, in which the jump of a pathogen into a novel host species is followed by the specialization on that host and the loss of infectivity of previous host(s), is commonly observed in viruses, but less often in bacteria. Here, we suggest that the extent to which pathogens evolve host generalism or specialism following a jump into a novel host will depend on their level of adaptation to dealing with different environments, their rates of molecular evolution and their ability to recombine. We then explore these hypotheses using a formal model and show that the high levels of phenotypic plasticity, low rates of evolution and the ability to recombine typical of bacterial pathogens should reduce their propensity to specialize on novel hosts. Novel bacterial infections may therefore be more likely to result in transient spillovers or increased host ranges than in host shifts. Finally, consistent with our predictions, we show that, in two unusual cases of contemporary bacterial host shifts, the bacterial pathogens both have small genomes and rapid rates of substitution. Further tests are required across a greater number of emerging pathogens to assess the validity of our hypotheses. This article is part of the theme issue 'Dynamic and integrative approaches to understanding pathogen spillover'.
Keywords: emerging infectious disease; host range; host shift; phenotypic plasticity; specialization; spillover.