Abstract
Avian influenza virus (AIV) persists in North American wild waterfowl, exhibiting major outbreaks every 2–4 years. Attempts to explain the patterns of periodicity and persistence using simple direct transmission models are unsuccessful. Motivated by empirical evidence, we examine the contribution of an overlooked AIV transmission mode: environmental transmission. It is known that infectious birds shed large concentrations of virions in the environment, where virions may persist for a long time. We thus propose that, in addition to direct fecal/oral transmission, birds may become infected by ingesting virions that have long persisted in the environment. We design a new host–pathogen model that combines within-season transmission dynamics, between-season migration and reproduction, and environmental variation. Analysis of the model yields three major results. First, environmental transmission provides a persistence mechanism within small communities where epidemics cannot be sustained by direct transmission only (i.e., communities smaller than the critical community size). Second, environmental transmission offers a parsimonious explanation of the 2–4 year periodicity of avian influenza epidemics. Third, very low levels of environmental transmission (i.e., few cases per year) are sufficient for avian influenza to persist in populations where it would otherwise vanish.
Highlights
Many important infectious diseases persist on a knife-edge: rapid rates of transmission coupled with brief infectious periods generate boom-and-bust epidemics that court extinction
Avian influenza viruses in wild waterfowl constitute the historic source of human influenza viruses [11], with a rich pool of genetic and antigenic diversity [11,12] that often leads to cross-species transmission
Avian influenza viruses (AIVs) in wild waterfowl constitute the historic source of human influenza viruses, having a rich pool of genetic and antigenic diversity that often leads to cross-species transmission
Summary
Many important infectious diseases persist on a knife-edge: rapid rates of transmission coupled with brief infectious periods generate boom-and-bust epidemics that court extinction. Such violent epidemic behavior has been observed in measles [1,2,3,4], plague [5], cholera [6], meningitis [7,8], and pertussis [9], among others. Rich strain polymorphism allows echoviruses –responsible for aseptic meningitis– to circumvent host immunity and reinvade the population [7,8] These examples illustrate the need for understanding alternate persistence/re-invasion mechanisms of infectious diseases for effective management and control
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