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About the Authors:
Michael G. Buhnerkempe
* E-mail: [email protected]
Affiliations Department of Biology, Colorado State University, Fort Collins, Colorado, United States of America, Division of Vector-Borne Infectious Diseases, Centers for Disease Control, Fort Collins, Colorado, United States of America
Rebecca J. Eisen
Affiliation: Division of Vector-Borne Infectious Diseases, Centers for Disease Control, Fort Collins, Colorado, United States of America
Brandon Goodell
Current address: Department of Mathematics, North Dakota State University, Fargo, North Dakota, United States of America
Affiliation: Department of Biology, Colorado State University, Fort Collins, Colorado, United States of America
Kenneth L. Gage
Affiliation: Division of Vector-Borne Infectious Diseases, Centers for Disease Control, Fort Collins, Colorado, United States of America
Michael F. Antolin
Affiliation: Department of Biology, Colorado State University, Fort Collins, Colorado, United States of America
Colleen T. Webb
Affiliation: Department of Biology, Colorado State University, Fort Collins, Colorado, United States of America
Introduction
Plague, caused by the bacterium Yersinia pestis, remains a public health concern because of its high virulence in multiple mammal species, including humans, and its role in past pandemics in humans. Despite its historical importance and the continued threat of human cases, plague is primarily a disease of rodents and their fleas. Consequently, humans are at greatest risk of exposure to Y. pestis during plague epizootics when rodent hosts die in large numbers increasing potential exposures to sick or dead animals and infectious fleas [1]. Thus, understanding outbreaks in rodents may aid in prediction, control and prevention of human cases.
However, rodent species show high variability in their population-level response to plague infection, and the mechanisms that determine outbreak conditions are not fully understood. The variability in host response can be compartmentalized into two classes: either enzootic (i.e., low probability of extinction despite persistent infection in a population) or epizootic (i.e., high probability of extinction due to plague). This classification enables predictions that can be based on observable intra-population dynamics rather than invoking landscape-level maintenance mechanisms involving the interaction of plague dynamics in multiple species [2]–[4].
Previous research on plague dynamics depended on observation of host characteristics to differentiate between epizootic and enzootic populations. For example, enzootic hosts, such as great gerbils (Rhombomys opimus) in Kazakhstan, show high levels of prolonged resistance (40–60% of hosts; [4]) while epizootic hosts,...