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 ...
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 specialisation 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 adaptation to dealing with different environments, rates of
molecular evolution and recombination may influence the extent to which pathogens evolve
host generalism or specialism following a jump into a novel host. We then test 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 specialise on novel host. 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 predictions.