An additional step in the transmission of Yersinia pestis?

Abstract

Plague, caused by the bacterium Yersinia pestis, is a mammalian vector-borne disease, transmitted by fleas that serve as the vector between rodent hosts. For many pathogens, including Y. pestis, there are strong evolutionary pressures that lead to a reduction in 'useless genes', with only those retained that reflect function in the specific environment inhabited by the pathogen. Genetic traits critical for survival and transmission between two environments, the rodent and the flea, are conserved in epizootic/epidemic plague strains. However, there are genes that remain conserved for which no function in the flea-rodent cycle has yet been observed, indicating an additional environment may exist in the transmission cycle of plague. Here, we present evidence for highly conserved genes that suggests a role in the persistence of Y. pestis after death of its host. Furthermore, maintenance of these genes points to Y. pestis traversing a post-mortem path between, and possibly within, epizootic periods and offering insight into mechanisms that may allow Y. pestis an alternative route of transmission in the natural environment.

Evolution with a seed bank: The population genetic consequences of microbial dormancy

“…For example, Yersinia pestis, the causative agent of the plague, often enters a dormant stage that allows it to persist between infections (Pawlowski et al, 2011). In addition, Y. pestis contains several highly conserved genes that can contribute toward its ability to survive in a dormant state long after the host has expired (Easterday et al, 2012). Because the pathogen is capable of infecting a new host, any trade-off between virulence and transmission could potentially be reduced.…”

Deletion of Braun Lipoprotein and Plasminogen-Activating Protease-Encoding Genes Attenuates Yersinia pestis in Mouse Models of Bubonic and Pneumonic Plague

“…Promising recombinant subunit plague vaccines, which are under clinical investigation, consist of a low-calcium-response V (LcrV [V]) antigen, a component of the type 3 secretion system (T3SS), as well as an effector and the capsular antigen F1. These vaccines elicit high antibody titers in rodents; however, their potential as efficacious vaccines has been debated because of varied responses in nonhuman primates (NHPs) (12)(13)(14)(15)(16). Specifically, African green monkeys (AGMs), in which the symptoms of plague mimic those in humans and represent an ideal model with which to study Y. pestis infection (17)(18)(19)(20)(21), exhibit highly varied protective responses to pneumonic plague (despite similar antibody titers).…”

“…The organism is endemic in a wide variety of rodents and their fleas, thus making eradication impractical (11). Y. pestis has also been known to naturally reestablish itself (possibly due to a third life cycle), which enables the bacterium to persist in a dormant state in dead hosts (5,12). For example, outbreaks occurred in Algeria (2003) after 48 years of silence and in India (1994) after 28 years of silence, and each outbreak had an extremely high number of plague-associated deaths, as the public health sector was unprepared for an outbreak (5,12).…”

“…Y. pestis has also been known to naturally reestablish itself (possibly due to a third life cycle), which enables the bacterium to persist in a dormant state in dead hosts (5,12). For example, outbreaks occurred in Algeria (2003) after 48 years of silence and in India (1994) after 28 years of silence, and each outbreak had an extremely high number of plague-associated deaths, as the public health sector was unprepared for an outbreak (5,12). The availability of a vaccine as a prophylaxis would negate possible plague threats, either natural or intentional.…”

Persistence of plague outbreaks among great gerbils in Kazakhstan: effects of host population dynamics

“…The disease may skip a peak of gerbil abundance, which in turn may lead to a reduced amount of infective agent in the environment. Survival of the bacterium in the soil or in dead hosts are two of several hypotheses on how it persists during interepizootic periods (Gage and Kosoy 2005;Easterday et al 2012;Schmid et al 2012).…”