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Antimicrobial Agents and Chemotherapy, February 2001, p. 480-484, Vol. 45, No. 2
0066-4804/01/$04.00+0   DOI: 10.1128/AAC.45.2.480-484.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.

Carbapenem Resistance Mechanisms in Pseudomonas aeruginosa Clinical Isolates

Hyunjoo Pai,1,* Jong-Won Kim,2 Jungmin Kim,3 Ji Hyang Lee,1 Kang Won Choe,4 and Naomasa Gotoh5

Division of Infectious Disease, Department of Internal Medicine,1 and Department of Microbiology,3 College of Medicine, University of Dankook, Chonan, Department of Clinical Pathology, Sungkyunkwan University College of Medicine,2 and Department of Internal Medicine, Seoul National University College of Medicine,4 Seoul, Korea, and Department of Microbiology, Kyoto Pharmaceutical University, Kyoto, Japan5

Received 31 March 2000/Returned for modification 8 August 2000/Accepted 10 November 2000

In order to define the contributions of the mechanisms for carbapenem resistance in clinical strains of Pseudomonas aeruginosa, we investigated the presence of OprD, the expressions of the MexAB-OprM and MexEF-OprN systems, and the production of the beta -lactamases for 44 clinical strains. All of the carbapenem-resistant isolates showed the loss of or decreased levels of OprD. Three strains overexpressed the MexAB-OprM efflux system by carrying mutations in mexR. These three strains had the amino acid substitution in MexR protein, Arg (CGG) right-arrow Gln (CAG), at the position of amino acid 70. None of the isolates, however, expressed the MexEF-OprN efflux system. For the characterization of beta -lactamases, at least 13 isolates were the depressed mutants, and 12 strains produced secondary beta -lactamases. Based on the above resistance mechanisms, the MICs of carbapenem for the isolates were analyzed. The MICs of carbapenem were mostly determined by the expression of OprD. The MICs of meropenem were two- to four-fold increased for the isolates which overexpressed MexAB-OprM in the background of OprD loss. However, the elevated MICs of meropenem for some individual isolates could not be explained. These findings suggested that other resistance mechanisms would play a role in meropenem resistance in clinical isolates of P. aeruginosa.

* Corresponding author. Mailing address: Division of Infectious Disease, Department of Internal Medicine, College of Medicine, University of Dankook, San 29, Anseo-dong, Chonan, Chungnam, 330-715, Korea. Phone: 82-41-550-3918. Fax: 82-41-556-3256. E-mail: paihj{at}unitel.co.kr.

Antimicrobial Agents and Chemotherapy, February 2001, p. 480-484, Vol. 45, No. 2
0066-4804/01/$04.00+0   DOI: 10.1128/AAC.45.2.480-484.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.


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