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Editorial
February 10, 1999

Extended-Spectrum β-LactamasesA Plague of Plasmids

Author Affiliations

Author Affiliations: Veterans Affairs Healthcare System San Diego (Dr Fierer) and the School of Medicine, University of California, San Diego (Drs Fierer and Guiney).

JAMA. 1999;281(6):563-564. doi:10.1001/jama.281.6.563

Broad-spectrum (third-generation) cephalosporins were designed to be highly active against gram-negative bacteria, in part because these antimicrobial agents initially were resistant to all known plasmid-encoded β-lactamase enzymes. It was, perhaps, to be expected that bacteria would find a way to overcome these drugs because their survival was at stake. In 1983, Knothe et al1 reported the first extended-spectrum β-lactamase (ESBL) with isolation of strains of Klebsiella and Serratia that had transferable plasmids encoding a mutated enzyme that made the bacteria resistant to cefotaxime sodium. Since then, these enzymes have been described in isolates of Escherichia coli and, more recently, Salmonella species.2 Resistance plasmids are the major source of ESBLs, which appear to have evolved in recent years by the mutation of β-lactamases that previously had poor activity against newer cephalosporins, such as ceftazidime sodium.3

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