Tuesday, January 16, 2007

Modes and Modulations of Antibiotic Resistance Gene Expression.

Modes and Modulations of Antibiotic Resistance Gene Expression.

Clin Microbiol Rev. 2007 Jan;20

Depardieu F,
Podglajen I,
Leclercq R,
Collatz E,
Courvalin P.

Unite des Agents Antibacteriens, Institut Pasteur, 75724 Paris Cedex 15, France.

Since antibiotic resistance usually affords a gain of function, there is an associated biological cost resulting in a loss of fitness of the bacterial host. Considering that antibiotic resistance is most often only transiently advantageous to bacteria, an efficient and elegant way for them to escape the lethal action of drugs is the alteration of resistance gene expression. It appears that expression of bacterial resistance to antibiotics is frequently regulated, which indicates that modulation of gene expression probably reflects a good compromise between energy saving and adjustment to a rapidly evolving environment.

Modulation of gene expression can occur at the transcriptional or translational level following mutations or the movement of mobile genetic elements and may involve induction by the antibiotic. In the latter case, the antibiotic can have a triple activity: as an antibacterial agent, as an inducer of resistance to itself, and as an inducer of the dissemination of resistance determinants. We will review certain mechanisms, all reversible, that bacteria have elaborated to achieve antibiotic resistance by the fine-tuning of the expression of genetic information.

PMID: 17223624 [PubMed - as supplied by publisher]

Related Article:

Genetic linkage and horizontal gene transfer, the roots of the antibiotic multi-resistance problem.

Anim Biotechnol. 2006

Summers AO.

Department of Microbiology, University of Georgia, Athens, Georgia 30602, USA. summers@uga.edu

Bacteria carrying resistance genes for many antibiotics are moving beyond the clinic into the community, infecting otherwise healthy people with untreatable and frequently fatal infections. This state of affairs makes it increasingly important that we understand the sources of this problem in terms of bacterial biology and ecology and also that we find some new targets for drugs that will help control this growing epidemic.

This brief and eclectic review takes the perspective that we have too long thought about the problem in terms of treatment with or resistance to a single antibiotic at a time, assuming that dissemination of the resistance gene was affected by simple vertical inheritance. In reality antibiotic resistance genes are readily transferred horizontally, even to and from distantly related bacteria.

The common agents of bacterial gene transfer are described and also one of the processes whereby nonantibiotic chemicals, specifically toxic metals, in the environment can select for and enrich bacteria with antibiotic multiresistance. Lastly, some speculation is offered on broadening our perspective on this problem to include drugs directed at compromising the ability of the mobile elements themselves to replicate, transfer, and recombine, that is, the three "infrastructure" processes central to the movement of genes among bacteria.


Bacteriophage, Evolution, Integron, Plasmid, Toxic metal resistance, Transposon