  Human pathogens transmitted through environmental pathways are subject to
stress and pressures outside of the host. These pressures may cause pathogen
pathovars to diverge in their environmental persistence and their infectivity
on an evolutionary time-scale. On a shorter time-scale, a single-genotype
pathogen population may display wide variation in persistence times and exhibit
biphasic decay. Using an infectious disease transmission modeling framework, we
demonstrate in both cases that fitness-preserving trade-offs have implications
for the dynamics of associated epidemics: less infectious, more persistent
pathogens cause epidemics to progress more slowly than more infectious, less
persistent (labile) pathogens, even when the overall risk is the same. Using
identifiability analysis, we show that the usual disease surveillance data does
not sufficiently inform these underlying pathogen population dynamics, even
with basic environmental monitoring. These results suggest directions for
future microbial research and environmental monitoring. In particular,
determining the relative infectivity of persistent pathogen subpopulations and
the rates of phenotypic conversion will help ascertain how much disease risk is
associated with the long tails of biphasic decay. Alternatively, risk can be
indirectly ascertained by developing methods to separately monitor labile and
persistent subpopulations. A better understanding of persistence--infectivity
trade-offs and associated dynamics can improve risk assessment and disease
control strategies.
