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Background  The bacterium  Listeria monocytogenes  is a saprotroph as well as an opportunistic human foodborne pathogen, which has previously been shown to consist of at least two widespread lineages (termed lineages I and II) and an uncommon lineage (lineage III). While some  L. monocytogenes  strains show evidence for considerable diversification by homologous recombination, our understanding of the contribution of recombination to  L. monocytogenes  evolution is still limited. We therefore used STRUCTURE and ClonalFrame, two programs that model the effect of recombination, to make inferences about the population structure and different aspects of the recombination process in  L. monocytogenes . Analyses were performed using sequences for seven loci (including the house-keeping genes  gap ,  prs ,  purM  and  ribC , the stress response gene  sigB , and the virulence genes  actA  and  inlA ) for 195  L. monocytogenes  isolates.    Results  Sequence analyses with ClonalFrame and the Sawyer's test showed that recombination is more prevalent in lineage II than lineage I and is most frequent in two house-keeping genes ( ribC  and  purM ) and the two virulence genes ( actA  and  inlA ). The relative occurrence of recombination versus point mutation is about six times higher in lineage II than in lineage I, which causes a higher genetic variability in lineage II. Unlike lineage I, lineage II represents a genetically heterogeneous population with a relatively high proportion (30% average) of genetic material imported from external sources. Phylograms, constructed with correcting for recombination, as well as Tajima's D data suggest that both lineages I and II have suffered a population bottleneck.    Conclusion  Our study shows that evolutionary lineages within a single bacterial species can differ considerably in the relative contributions of recombination to genetic diversification. Accounting for recombination in phylogenetic studies is critical, and new evolutionary models that account for the possibility of changes in the rate of recombination would be required. While previous studies suggested that only  L. monocytogenes  lineage I has experienced a recent bottleneck, our analyses clearly show that lineage II experienced a bottleneck at about the same time, which was subsequently obscured by abundant homologous recombination after the lineage II bottleneck. While lineage I and lineage II should be considered separate species from an evolutionary viewpoint, maintaining single species name may be warranted since both lineages cause the same type of human disease.

Lineage specific recombination rates and microevolution in Listeria monocytogenes