Abstract
Many Enterococcus faecalis strains display tolerance or resistance to many antibiotics, but genes that contribute to the resistance cannot be specified. The multiresistant E. faecalis V583, for which the complete genome sequence is available, survives and grows in media containing relatively high levels of chloramphenicol. No specific genes coding for chloramphenicol resistance has been recognized in V583. We used microarrays to identify genes and mechanisms behind the tolerance to chloramphenicol in V583, by comparison of cells treated with subinhibitory concentrations of chloramphenicol and untreated V583 cells. During a time course experiment, more than 600 genes were significantly differentially transcribed. Since chloramphenicol affects protein synthesis in bacteria, many genes involved in protein synthesis, for example, genes for ribosomal proteins, were induced. Genes involved in amino acid biosynthesis, for example, genes for tRNA synthetases and energy metabolism were downregulated, mainly. Among the upregulated genes were EF1732 and EF1733, which code for potential chloramphenicol transporters. Efflux of drug out of the cells may be one mechanism used by V583 to overcome the effect of chloramphenicol.
Highlights
Chloramphenicol (Cm) has been used as an broad-spectrum antibiotic in human and veterinary medicine since the 1950s, but the use of chloramphenicol in humans is rather limited [1]
In this paper we present the transcriptional profile of Enterococcus faecalis V583 (V583) treated with chloramphenicol
We report the transcriptional patterns of E. faecalis V583 treated with chloramphenicol
Summary
Chloramphenicol (Cm) has been used as an broad-spectrum antibiotic in human and veterinary medicine since the 1950s, but the use of chloramphenicol in humans is rather limited [1]. The structure of chloramphenicol is relatively simple, and it was the first chemically synthesized antibiotic on the market [1].Chloramphenicol inhibits translation in bacteria, by inhibition of the peptidyl transferase reaction of the large subunit of the ribosome. A number of resistance mechanisms to chloramphenicol in bacteria has been described, of which the most common is enzymatic inactivation by acetylation of chloramphenicol via chloramphenicol transferases (CATs) [1]; Chloramphenicol acetyltransferases (CATs) have been described in both. The inactivation of chloramphenicol can be performed by xenobiotic acetyltransferases [1, 3]. Several examples of chloramphenicol resistance or lowered sensitivity to chloramphenicol due to efflux pumps (specific or multidrug transporters) have been described, mainly in Gram-negative bacteria [1]. Chloramphenicol resistance may be due to mutations in 23S rRNA, thereby changing the binding site of chloramphenicol in the cells [1]
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
