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JAC Advance Access first published online on May 20, 2009
This version published online on May 21, 2009
Journal of Antimicrobial Chemotherapy, doi:10.1093/jac/dkp186
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© The Author 2009. Published by Oxford University Press on behalf of the British Society for Antimicrobial Chemotherapy. All rights reserved. For Permissions, please e-mail: journals.permissions@oxfordjournals.org

Original research

Correlation of the expression of acrB and the regulatory genes marA, soxS and ramA with antimicrobial resistance in clinical isolates of Klebsiella pneumoniae endemic to New York City

Simona Bratu, David Landman, Avrille George, Jerome Salvani and John Quale*

Department of Medicine, SUNY Downstate Medical Center, Brooklyn, NY, USA

Received 13 February 2009; returned 26 March 2009; revised 22 April 2009; accepted 27 April 2009

* Corresponding author. Division of Infectious Diseases Box 77, SUNY Downstate Medical Center, 450 Clarkson Avenue, Brooklyn, NY 11203, USA. Tel: +1-718-270-2148; Fax: +1-718-270-2465; E-mail: jquale{at}downstate.edu

Objectives: Nosocomial isolates of Klebsiella pneumoniae resistant to all commonly used antimicrobial agents have emerged in many regions of the world. It is unknown if efflux systems contribute to the multidrug resistance phenotype.

Methods: The expression of genes encoding the efflux pump AcrAB and the global regulators MarA, SoxS and RamA were examined and correlated with antimicrobial resistance.

Results: Twenty isolates belonged to the two important clones representing KPC-possessing strains endemic to our region. Virtually all of these isolates had negligible or absent expression of the genes, and resistance to fluoroquinolones and aminoglycosides could be explained by alternative mechanisms. All of these isolates were susceptible to tigecycline. A group of 14 heterogeneous isolates was also examined. There was a correlation between expression of marA with expression of soxS. Only expression of soxS was significantly correlated with expression of acrB. With a background substitution in GyrA, increased expression of acrB and marA appeared to contribute to fluoroquinolone resistance in some isolates. A correlation was noted between expression of soxS and ramA (but not marA and acrB) and tigecycline MICs. Following in vitro exposure to tigecycline, resistance occurred in association with a marked increase in marA and acrB expression in isolates lacking expression of soxS and ramA.

Conclusions: While laboratory-derived tigecycline resistance was associated with increased acrB expression, the variation in tigecycline MICs in clinical isolates was associated only with selected regulator genes. It appears that other mechanisms beyond activation of the acrAB system mediate tigecycline resistance.

Key Words: efflux , tigecycline , multidrug-resistant

The original version was incorrect. Page 5 of the proof, line 7 of the Discussion: ‘suggest’ should have read ‘suggests’.


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