ABSTRACT
BACKGROUND: Yersinia pestis, the causative agent of plague, is responsible for some of the greatest epidemic scourges of mankind. It is widespread in the western United States, although it has only been present there for just over 100 years. As a result, there has been very little time for diversity to accumulate in this region. Much of the diversity that has been detected among North American isolates is at loci that mutate too quickly to accurately reconstruct large-scale phylogenetic patterns. Slowly-evolving but stable markers such as SNPs could be useful for this purpose, but are difficult to identify due to the monomorphic nature of North American isolates. METHODOLOGY/PRINCIPAL FINDINGS: To identify SNPs that are polymorphic among North American populations of Y. pestis, a gapped genome sequence of Y. pestis strain FV-1 was generated. Sequence comparison of FV-1 with another North American strain, CO92, identified 19 new SNP loci that differ among North American isolates. CONCLUSIONS/SIGNIFICANCE: The 19 SNP loci identified in this study should facilitate additional studies of the genetic population structure of Y. pestis across North America.
Subject(s)
Genome, Bacterial , Phylogeny , Polymorphism, Single Nucleotide , Yersinia pestis/genetics , Animals , Arizona/epidemiology , Base Sequence , DNA, Bacterial/genetics , Disease Outbreaks/veterinary , Disease Reservoirs , Evolution, Molecular , Humans , Molecular Sequence Data , North America , Plague/epidemiology , Plague/microbiology , Rodent Diseases/epidemiology , Rodent Diseases/microbiology , Rodentia , Sciuridae , Yersinia pestis/isolation & purification , Yersinia pseudotuberculosis/geneticsABSTRACT
Plague, the disease caused by the bacterium Yersinia pestis, has greatly impacted human civilization. Y. pestis is a successful global pathogen, with active foci on all continents except Australia and Antarctica. Because the Y. pestis genome is highly monomorphic, previous attempts to characterize the population genetic structure within a single focus have been largely unsuccessful. Here we report that highly mutable marker loci allow determination of Y. pestis population genetic structure and tracking of transmission patterns at two spatial scales within a single focus. In addition, we found that in vitro mutation rates for these loci are similar to those observed in vivo, which allowed us to develop a mutation-rate-based model to examine transmission mechanisms. Our model suggests there are two primary components of plague ecology: a rapid expansion phase for population growth and dispersal followed by a slower persistence phase. This pattern seems consistent across local, regional, and even global scales.
