Fig. 5
From: Disease-associated genotypes of the commensal skin bacterium Staphylococcus epidermidis
Contrasting models of S. epidermidis infection and associated variation in conceptual genomic data. Each panel summarises scenarios for subcutaneous colonization from the primary commensal skin environment to the blood (left), and the impact on an S. epidermidis population of two clones (blue and red circles) and their genomes (internal circles) which may be enriched for putative pathogenicity-associated genes (red) or not (blue). Genealogical reconstructions of isolates sampled from infected blood are shown in the middle column. The prevalence of disease determinants in the genome of isolates from skin and blood are shown on the right. a Proliferation of pathogenic clones: clones with genomes enriched for pathogenicity determinants proliferate in the blood and other strains do not, observed as a discrete pathogen lineage on the tree. b True opportunistic pathogenicity: multiple genetically divergent clones proliferate in the blood and disease determinants are equally distributed among the genomes of isolates from the skin and the blood (or would be undetectable). c Divided genomes: horizontal gene transfer (R) spreads pathogenicity determinants into multiple genomic backgrounds allowing divergent clones to colonize the blood successfully
