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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
-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)
Gln (CAG), at the position of amino acid
70. None of the isolates, however, expressed the MexEF-OprN efflux
system. For the characterization of
-lactamases, at least 13 isolates were the depressed mutants, and 12 strains produced secondary
-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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