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International Journal of Microbiology
Volume 2010, Article ID 483048, 7 pages
http://dx.doi.org/10.1155/2010/483048
Research Article

The Response of Enterococcus faecalis V583 to Chloramphenicol Treatment

1Department of Chemistry, Biotechnology and Food Science, The Norwegian University of Life Sciences, P.O. Box 5003, 1432 Ås, Norway
2Department of Mathematical Sciences and Technology, The Norwegian University of Life Sciences, P.O. Box 5003, 1432 Ås, Norway
3Lerum Konserves AS, P.O. Box 159, 6851 Sogndal, Norway

Received 9 July 2009; Revised 21 April 2010; Accepted 22 April 2010

Academic Editor: Paula J. Fedorka-Cray

Copyright © 2010 Ågot Aakra et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

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.