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About the Authors:
Karoun H. Bagamian
* E-mail: [email protected]
Affiliations Population Biology, Ecology, and Evolution Program, Emory University, Atlanta, Georgia, United States of America, Medical Ecology Unit, Viral Special Pathogens Branch, U.S. Centers for Disease Control and Prevention, Atlanta, Georgia, United States of America, Department of Biology, Montana Tech, University of Montana, Butte, Montana, United States of America
Richard J. Douglass
Affiliation: Department of Biology, Montana Tech, University of Montana, Butte, Montana, United States of America
Arlene Alvarado
Affiliation: Cfwep.Org, Institute for Educational Opportunities, Montana Tech, University of Montana, Butte, Montana, United States of America
Amy J. Kuenzi
Affiliation: Department of Biology, Montana Tech, University of Montana, Butte, Montana, United States of America
Brian R. Amman
Affiliation: Medical Ecology Unit, Viral Special Pathogens Branch, U.S. Centers for Disease Control and Prevention, Atlanta, Georgia, United States of America
Lance A. Waller
Affiliation: Department of Biostatistics and Bioinformatics, Rollins School of Public Health, Emory University, Atlanta, Georgia, United States of America
James N. Mills
Affiliations Population Biology, Ecology, and Evolution Program, Emory University, Atlanta, Georgia, United States of America, Medical Ecology Unit, Viral Special Pathogens Branch, U.S. Centers for Disease Control and Prevention, Atlanta, Georgia, United States of America
Introduction
In the past 30 years, numerous theoretical models have been proposed to explain how pathogens become established and spread in host populations. Early models assumed that the driving force behind directly transmitted parasites was population density (density-dependent transmission) and, because these models were useful to understanding many human diseases, they were applied to wildlife populations [1], [2]. For a horizontally transmitted pathogen, higher host population density may lead to higher prevalence of infection, because there is an increased number of potential hosts and because more susceptible hosts provide more opportunities for direct transmission through contact [3]. Additionally, higher densities of infective donors and susceptible hosts may amplify indirect transmission by increasing the amount of infectious pathogen in the environment [4]. Higher host abundance may also result in increased competition for limited resources and mates, increasing stress and leading to decreased immunological capacity [5]. However, the relationship between wildlife host population density and disease prevalence is complex, as reviewed by Adler et al. [3]. While some mark-recapture studies of hantaviruses and arenaviruses in rodent populations in the United...