Pathogen persistence in wildlife populations: case studies of plague in prairie dogs and rabies in bats
Date
2009
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Abstract
Disease ecology focuses, in part, on how pathogens persist within host wildlife populations For my dissertation my colleagues and I investigated pathogen persistence mechanisms in two host-pathogen systems: Yersinia pestis (plague) in prairie dogs and rabies virus in bats. Plague, caused by the bacterium Yersinia pestis, recently spread into the range of black-tailed prairie dogs (Cynomys ludovicianus) in North America, and has caused drastic and rapid reduction in local prairie dog populations which have generated a metapopulation dynamic for prairie dogs. We developed a stochastic patch occupancy model to determine if prairie dog populations could persist long-term given the effects of plague. Our model demonstrates that metapopulation dynamics can allow prairie dog persistence. Town extinction in this system is caused by plague. Thus, town extinction and plague colonization are two sides of the same coin, which allows to us to interpret plague dynamics implicit within the prairie dog metapopulation. Long-term metapopulation dynamics indicate plague persists within the system and does not require the involvement of additional reservoir hosts (i.e., other resistant rodent species). Bats are a natural reservoir for rabies, and an increasing number of emerging zoonotic viruses. Little is known about mechanisms that generate unique seasonal patterns and allow enzootic pathogen persistence in bat populations. We propose that life history characteristics unique to many bat species coupled with viral adaptations allow for rabies persistence. First, we developed a statistical model to investigate seasonal patterns of rabies cases in bats. Second, we used data from a five-year study of rabies in big brown bats (Eptesicus fuscus) to parameterize a dynamic disease model that elucidates pathogen persistence mechanisms. We show rabies persists in two distinct ways, (1) through effects on bat population viability, and (2) through effects on viral persistence within a viable bat population. Mortality rates vary across seasons, and low rates during hibernation allow long-term bat population viability. Within a viable bat population, viral persistence occurs because of a lengthy incubation period, enhanced by the metabolic effects of host torpor. The mechanisms we identify may be operating in a similar manner for other bat-borne diseases.
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Subject
bats
pathogen persistence
plague
prairie dogs
rabies
Yersinia pestis
ecology