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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,
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 1
-lactamase. Recently, resistant strains producing plasmid-mediated extended-spectrum
-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.
-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
-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.

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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