Giuseppe
Emeritus
Abstract. The Role of Environmental Transmission in Recurrent Avian Influenza Epidemics.
The Role of Environmental Transmission in Recurrent Avian Influenza Epidemics
Romulus Breban1 *, John M. Drake1, David E. Stallknecht 2, Pejman Rohani 1,3,4
1 Odum School of Ecology, University of Georgia, Athens, Georgia, United States of America,
2 Southeastern Cooperative Wildlife Disease Study, University of Georgia, Athens, Georgia, United States of America,
3 Center for Tropical and Emerging Global Diseases, University of Georgia, Athens, Georgia, United States of America,
4 Fogarty International Center, National Institutes of Health, Bethesda, Maryland, United States of America
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.
Citation: Breban R, Drake JM, Stallknecht DE, Rohani P (2009) The Role of Environmental Transmission in Recurrent Avian Influenza Epidemics. PLoS Comput Biol 5(4): e1000346. doi:10.1371/journal.pcbi.1000346
Editor: Christophe Fraser, Imperial College London, United Kingdom
Received: November 3, 2008; Accepted: March 2, 2009; Published: April 10, 2009
Copyright: ? 2009 Breban et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Funding: RB, DES, and PR were supported by a grant from the Centers for Disease Control and Prevention (5U19Cl000401). JMD was supported by the National Science Foundation (EF-0723601) and the James S. McDonnell Foundation. The authors declare that they do not have any financial interest. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.
Competing interests: The authors have declared that no competing interests exist.
* E-mail: breban@gmail.com
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<cite cite="http://www.ploscompbiol.org/article/info:doi/10.1371/journal.pcbi.1000346#abstract0">PLoS Computational Biology: The Role of Environmental Transmission in Recurrent Avian Influenza Epidemics</cite>Romulus Breban1 *, John M. Drake1, David E. Stallknecht 2, Pejman Rohani 1,3,4
1 Odum School of Ecology, University of Georgia, Athens, Georgia, United States of America,
2 Southeastern Cooperative Wildlife Disease Study, University of Georgia, Athens, Georgia, United States of America,
3 Center for Tropical and Emerging Global Diseases, University of Georgia, Athens, Georgia, United States of America,
4 Fogarty International Center, National Institutes of Health, Bethesda, Maryland, United States of America
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.
Citation: Breban R, Drake JM, Stallknecht DE, Rohani P (2009) The Role of Environmental Transmission in Recurrent Avian Influenza Epidemics. PLoS Comput Biol 5(4): e1000346. doi:10.1371/journal.pcbi.1000346
Editor: Christophe Fraser, Imperial College London, United Kingdom
Received: November 3, 2008; Accepted: March 2, 2009; Published: April 10, 2009
Copyright: ? 2009 Breban et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Funding: RB, DES, and PR were supported by a grant from the Centers for Disease Control and Prevention (5U19Cl000401). JMD was supported by the National Science Foundation (EF-0723601) and the James S. McDonnell Foundation. The authors declare that they do not have any financial interest. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.
Competing interests: The authors have declared that no competing interests exist.
* E-mail: breban@gmail.com
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