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Antimicrobial Agents and Chemotherapy, October 2007, p. 3531-3536, Vol. 51, No. 10
0066-4804/07/$08.00+0     doi:10.1128/AAC.00503-07
Copyright © 2007, American Society for Microbiology. All Rights Reserved.

Pseudomonas aeruginosa May Accumulate Drug Resistance Mechanisms without Losing Its Ability To Cause Bloodstream Infections{triangledown}

Didier Hocquet,1* Philippe Berthelot,2 Micheline Roussel-Delvallez,3 Roger Favre,4 Katy Jeannot,1 Odile Bajolet,5 Nicole Marty,6 Florence Grattard,2 Patricia Mariani-Kurkdjian,7 Edouard Bingen,7 Marie-Odile Husson,3 Gérard Couetdic,1 and Patrick Plésiat1

Centre National de Référence Résistance aux Antibiotiques: Pseudomonas aeruginosa, Hôpital Jean Minjoz, Besançon,1 Laboratoire de Bactériologie-Virologie, Hôpital Nord, Saint Etienne,2 Laboratoire de Bactériologie, Hôpital Calmette, Lille,3 Laboratoire de Microbiologie Clinique, Hôpital d'Instruction des Armées Bégin, Saint-Mandé,4 Laboratoire de Bactériologie-Hygiène, Hôpital Robert Debré, Reims,5 Laboratoire de Bactériologie-Hygiène, Hôpital Rangueil, Toulouse,6 Laboratoire de Microbiologie, Hôpital Robert Debré, Paris, France7

Received 13 April 2007/ Returned for modification 4 May 2007/ Accepted 25 July 2007

In this study, we systematically investigated the resistance mechanisms to ß-lactams, aminoglycosides, and fluoroquinolones of 120 bacteremic strains of Pseudomonas aeruginosa. Pulsed-field gel electrophoresis genotyping showed that 97 of these strains were represented by a single isolate, 10 by 2 and 1 by 3 clonally related isolates, respectively. Seventy-five percent (90 out of 120) of the bacteremic P. aeruginosa strains displayed a significant resistance to one or more of the tested antimicrobials (up to 11 for 1 strain). These strains were found to harbor a great diversity of resistance mechanisms (up to 7 in 1 strain), leading to various levels of drug resistance. Interestingly, 11 and 36% of the isolates appeared to overproduce the MexAB-OprM and MexXY-OprM efflux systems, respectively. Altogether, our results show that P. aeruginosa may accumulate intrinsic (overproduction of cephalosporinase AmpC, increased drug efflux, fluoroquinolone target mutations, and deficient production of porin OprD) and exogenous (production of secondary ß-lactamases and aminoglycoside-modifying enzymes) resistance mechanisms without losing its ability to generate severe bloodstream infections. Consequently, clinicians should be aware that multidrug-resistant P. aeruginosa may remain fully pathogenic.

* Corresponding author. Mailing address: Centre National de Référence Résistance aux antibiotiques: Pseudomonas aeruginosa, Hôpital Jean Minjoz, 25030 Besançon, Cedex, France. Phone: (33) 3 81 66 82 86. Fax: (33) 3 81 66 89 14. E-mail: dhocquet{at}chu-besancon.fr

{triangledown} Published ahead of print on 6 August 2007.

Antimicrobial Agents and Chemotherapy, October 2007, p. 3531-3536, Vol. 51, No. 10
0066-4804/07/$08.00+0     doi:10.1128/AAC.00503-07
Copyright © 2007, American Society for Microbiology. All Rights Reserved.



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