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Human pathogens transmitted through environmental pathways are subject tostress and pressures outside of the host. These pressures may cause pathogenpathovars to diverge in their environmental persistence and their infectivityon an evolutionary time-scale. On a shorter time-scale, a single-genotypepathogen population may display wide variation in persistence times and exhibitbiphasic decay. Using an infectious disease transmission modeling framework, wedemonstrate in both cases that fitness-preserving trade-offs have implicationsfor the dynamics of associated epidemics: less infectious, more persistentpathogens cause epidemics to progress more slowly than more infectious, lesspersistent (labile) pathogens, even when the overall risk is the same. Usingidentifiability analysis, we show that the usual disease surveillance data doesnot sufficiently inform these underlying pathogen population dynamics, evenwith basic environmental monitoring. These results suggest directions forfuture microbial research and environmental monitoring. In particular,determining the relative infectivity of persistent pathogen subpopulations andthe rates of phenotypic conversion will help ascertain how much disease risk isassociated with the long tails of biphasic decay. Alternatively, risk can beindirectly ascertained by developing methods to separately monitor labile andpersistent subpopulations. A better understanding of persistence--infectivitytrade-offs and associated dynamics can improve risk assessment and diseasecontrol strategies.

Persistence-infectivity trade-offs in environmentally transmitted pathogens change population-level disease dynamics