Assistant Research Scientist
University of Michigan
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.
We use a transmission modeling framework to develop an infectious disease model with biphasic pathogen decay. We take a differential algebra approach to assessing model identifiability, calculate basic reproduction numbers by the next generation method, and use simulation to explore model dynamics.
For both long and short time-scales, we demonstrate that epidemic-potential-preserving trade-offs have implications for epidemic dynamics: 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 when combined with basic environmental monitoring data. However, risk could be indirectly ascertained by developing methods to separately monitor labile and persistent subpopulations. Alternatively, 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.
A better understanding of persistence-infectivity trade-offs and associated dynamics can improve our ecological understanding of environmentally transmitted pathogens, as well as our risk assessment and disease control strategies.