HUMAN PLAGUE OUTBREAKS occur after fleas infected with Yersinia pestis can find no other preferred hosts. Thus, plague is similar to the vector-borne infectious diseases that have been described as “spillovers,” because humans are not directly involved in the primary ecological processes that govern pathogen persistence (McMichael 2010; Ostfeld 2011; Quammen 2012). Plague persists via transmissions within a population of reservoir hosts, such as Eurasian great gerbils and marmots. This hidden, silent stage of plague transmission is now called “maintenance phase” plague, and involves only burrowing rodents and their fleas. Burrows provide protected microenvironments for temporary survival of both bacteria and flea larvae (Anisimov, Lindler, and Pier 2014; Wimsatt and Biggens 2009). The precise mechanisms and ecological triggers that cause a wider, explosive “amplification phase” of plague, when highly susceptible animals begin to die, are not yet fully understood (Gage 2012). Intensive laboratory and field research projects focus on events early in a “transmission shift”: from ongoing flea-borne transmission within a maintenance host population to rapidly widening rodent die-offs, spread by many flea species (Buhnerkempe et al. 2011).

Today, several low-tech, early-alert surveillance systems teach people living near plague hotspots how to notice deaths among the rodents involved in plague amplification. Should the warning signs escape notice, laboratory and/or autopsy investigation of sudden human deaths in a plague-endemic region become the next-best alert that it is time to inter rupt plague's spread. The remedy in both cases is the same: using pesticides to kill the fleas and flea larvae in areas near human habitation or worksites (Dennis and Staples 2009; Duplantier 2012; Stenseth et al. 2008). Yersinia pestis persists because it can infect a wide range of fleas, many of which do not feed on humans (Hinnebusch 2010).

Environmental conditions that favor flea activity and replication are linked to plague amplification (Wimsatt and Biggins 2009; Adjemian et al. 2007; Davis, Calvet, and Leirs 2005; Keeling and Gilligan 2000). Indeed, Yersinia pestis evolved from its ancestor, Yersinia pseudotuberculosis, through the acquisition of DNA permitting the infection of fleas. Because Y. pseudotuberculosis is able to live and replicate freely, typically in water, it needs genes that allow it to utilize environmental resources as nutrients. The new species Yersinia pestis lacks such capacity: it is an obligate pathogen.