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Background    Enterococcus faecalis  plays a dual role in human ecology, predominantly existing as a commensal in the alimentary canal, but also as an opportunistic pathogen that frequently causes nosocomial infections like bacteremia. A number of virulence factors that contribute to the pathogenic potential of  E. faecalis  have been established. However, the process in which  E. faecalis  gains access to the bloodstream and establishes a persistent infection is not well understood.    Methodology/Principal Findings  To enhance our understanding of how this commensal bacterium adapts during a bloodstream infection and to examine the interplay between genes we designed an  in vitro  experiment using genome-wide microarrays to investigate what effects the presence of and growth in blood have on the transcriptome of  E. faecalis  strain V583. We showed that growth in both 2xYT supplemented with 10% blood and in 100% blood had a great impact on the transcription of many genes in the V583 genome. We identified several immediate changes signifying cellular processes that might contribute to adaptation and growth in blood. These include modulation of membrane fatty acid composition, oxidative and lytic stress protection, acquisition of new available substrates, transport functions including heme/iron transporters and genes associated with virulence in  E. faecalis .    Conclusions/Significance  The results presented here reveal that cultivation of  E. faecalis  in blood  in vitro  has a profound impact on its transcriptome, which includes a number of virulence traits. Observed regulation of genes and pathways revealed new insight into physiological features and metabolic capacities which enable  E. faecalis  to adapt and grow in blood. A number of the regulated genes might potentially be useful candidates for development of new therapeutic approaches for treatment of  E. faecalis  infections.

The Transcriptome of the Nosocomial Pathogen Enterococcus faecalis V583 Reveals Adaptive Responses to Growth in Blood