Document Detail


Plasmid-mediated resistance to expanded-spectrum cephalosporins among Enterobacter aerogenes strains.
MedLine Citation:
PMID:  9517938     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
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 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 microg/ml) was detected and associated with resistance to gentamicin and trimethoprim-sulfamethoxazole. All strains produced an inducible Bush group 1 beta-lactamase (pI 83). 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.
Authors:
J D Pitout; K S Thomson; N D Hanson; A F Ehrhardt; P Coudron; C C Sanders
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Publication Detail:
Type:  Journal Article    
Journal Detail:
Title:  Antimicrobial agents and chemotherapy     Volume:  42     ISSN:  0066-4804     ISO Abbreviation:  Antimicrob. Agents Chemother.     Publication Date:  1998 Mar 
Date Detail:
Created Date:  1998-05-12     Completed Date:  1998-05-12     Revised Date:  2013-04-18    
Medline Journal Info:
Nlm Unique ID:  0315061     Medline TA:  Antimicrob Agents Chemother     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  596-600     Citation Subset:  IM    
Affiliation:
Department of Medical Microbiology and Immunology, Creighton University School of Medicine, Omaha, Nebraska 68178, USA.
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MeSH Terms
Descriptor/Qualifier:
Cephalosporins / pharmacology*
Conjugation, Genetic / drug effects*
DNA, Bacterial / analysis
Drug Resistance, Microbial / genetics
Enterobacter / classification,  drug effects*,  enzymology
Humans
Microbial Sensitivity Tests
Plasmids / genetics*
Polymerase Chain Reaction
beta-Lactamases / genetics,  metabolism*
Chemical
Reg. No./Substance:
0/Cephalosporins; 0/DNA, Bacterial; EC 3.5.2.-/beta-lactamase CAZ-5; EC 3.5.2.6/beta-Lactamases
Comments/Corrections

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