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The bacterium Pseudomonasae ruginosa is a significant cause of acute nosocomial infections as well as chronic respiratory infections inpatients with cystic fibrosis (CF). Recent reports of the intercontinentals pread of a CF-specific epidemics train, combined with high intrinsic levels of antibiotic resistance, have made this opportunistic pathogen an important public health concern. Strain-specific differences correlate with variation in clinical out comes of infected CF patients, increasing the urgency to understand the evolutionary origin of genetic factors conferring important phenotypes that enable infection, virulence, or resistance. Here, we describe the genome-wide patterns of homologous and nonhomologous recombination in P. aeruginosa, and the extent to which the genomes are affected by these diversity-generating processes. Based on whole-genome sequence data from 32 clinical isolates of P. aeruginosa, we examined the rate and distribution of recombination along the genome, and its effect on there construction of phylogenetic relationships. Multiple lines of evidence suggested that recombination was common and usually involves short stretches of DNA (200–300bp). Although mutation was the main source of nucleotide diversity, the import of polymorphisms by homologous recombination contributed nearly as much. We also identified the genomic regions with frequent recombination, and the specific sequences of recombinant origin within epidemic strains. The functional characteristics of the genes contained therein were examined for potential associations with a pathogenic life style or adaptation to the CF lung environment. A common link between many of the high-recombination genes was their functional affiliation with the cell wall, suggesting that the products of recombination maybe maintained by selection for variation in cell-surface molecules that allows for evasion of the host immune system.
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