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Antimicrobial Agents and Chemotherapy, March 1998, p. 596-600, Vol. 42, No. 3
0066-4804/98/$04.00+0
Copyright © 1998, American Society for Microbiology. All rights reserved.

Plasmid-Mediated Resistance to Expanded-Spectrum Cephalosporins among Enterobacter aerogenes Strains

Johann D. D. Pitout,1,dagger Kenneth S. Thomson,1,* Nancy D. Hanson,1 Anton F. Ehrhardt,1 Philip Coudron,2 and Christine C. Sanders1

Department of Medical Microbiology and Immunology, Creighton University School of Medicine, Omaha, Nebraska 68178,1 and Department of Pathology, Hunter Holmes McGuire Medical Center, Richmond, Virginia 232492

Received 12 May 1997/Returned for modification 9 September 1997/Accepted 17 December 1997

Resistance to expanded-spectrum cephalosporins commonly develops in Enterobacter aerogenes during therapy due to selection of mutants producing high levels of the chromosomal Bush group beta -lactamase. Recently, resistant strains producing plasmid-mediated extended-spectrum beta -lactamases (ESBLs) have been isolated as well. A study was designed to investigate ESBL production among 31 clinical isolates of E. aerogenes from Richmond, Va., with decreased susceptibility to expanded-spectrum cephalosporins and a positive double-disk potentiation test. Antibiotic susceptibility was determined by standard disk diffusion and agar dilution procedures. beta -Lactamases were investigated by an isoelectric focusing overlay technique which simultaneously determined isoelectric points (pIs) and substrate or inhibitor profiles. Decreased susceptibility to cefotaxime, ceftazidime, and aztreonam (MIC range, 1 to 64 µg/ml) was detected and associated with resistance to gentamicin and trimethoprim-sulfamethoxazole. All strains produced an inducible Bush group 1 beta -lactamase (pI 8.3). Twenty-nine of the 31 isolates also produced an enzyme similar to SHV-4 (pI 7.8), while 1 isolate each produced an enzyme similar to SHV-3 (pI 6.9) and to SHV-5 (pI 8.2). The three different SHV-derived ESBLs were transferred by transconjugation to Escherichia coli C600N and amplified by PCR. Plasmid profiles of the clinical isolates showed a variety of different large plasmids. Because of the linkage of resistance to aminoglycosides and trimethoprim-sulfamethoxazole with ESBL production, it is possible that the usage of these drugs was responsible for selecting plasmid-mediated resistance to extended-spectrum cephalosporins in E. aerogenes. Furthermore, it is important that strains such as these be recognized, because they can be responsible for institutional spread of resistance genes.


* Corresponding author. Mailing address: Department of Medical Microbiology and Immunology, Creighton University School of Medicine, 2500 California Plaza, Omaha, NE 68178. Phone: (402) 280-1881. Fax: (402) 280-1225. E-mail: kstaac{at}creighton.edu.

dagger Present address: Department of Medical Microbiology, University of the Orange Free State, Bloemfontein, South Africa 9300.


Antimicrobial Agents and Chemotherapy, March 1998, p. 596-600, Vol. 42, No. 3
0066-4804/98/$04.00+0
Copyright © 1998, American Society for Microbiology. All rights reserved.



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