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Volume 35, Issue 6, Pages 519-523 (June 2010)


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Resistance to rifampicin: at the crossroads between ecological, genomic and medical concerns

Audrey TupinabCorresponding Author Informationemail address, Maxime Gualtieriab, Françoise Roquet-Banèresab, Zakia Morichaudab, Konstantin Brodolinab, Jean-Paul Leonettiab

published online 25 February 2010.

Abstract 

The first antibiotic of the ansamycin family, rifampicin (RIF), was isolated in 1959 and was introduced into therapy in 1962; it is still a first-line agent in the treatment of diseases such as tuberculosis, leprosy and various biofilm-related infections. The antimicrobial activity of RIF is due to its inhibition of bacterial RNA polymerase (RNAP). Most frequently, bacteria become resistant to RIF through mutation of the target; however, this mechanism is not unique. Other mechanisms of resistance have been reported, such as duplication of the target, action of RNAP-binding proteins, modification of RIF and modification of cell permeability. We suggest that several of these alternative resistance strategies could reflect the ecological function of RIF, such as autoregulation and/or signalling to surrounding microorganisms. Very often, resistance mechanisms found in the clinic have an environmental origin. One may ask whether the introduction of the RIF analogues rifaximin, rifalazil, rifapentine and rifabutin in the therapeutic arsenal, together with the diversification of the pathologies treated by these molecules, will diversify the resistance mechanisms of human pathogens against ansamycins.

a Université Montpellier 1, Centre d’études d’agents Pathogènes et Biotechnologies pour la Santé (CPBS), CNRS, UMR 5236, 4 Bd Henri IV, CS 69033, F-34965 Montpellier, Cedex 2, France

b Université Montpellier 2, CPBS, F-34095 Montpellier, France

Corresponding Author InformationCorresponding author. Tel.: +33 4 67 54 86 07; fax: +33 4 67 54 86 04.

PII: S0924-8579(10)00017-8

doi:10.1016/j.ijantimicag.2009.12.017


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