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Extended-Spectrum -Lactamases

A Plague of Plasmids

Joshua Fierer, MD; Donald Guiney, MD

JAMA. 1999;281:563-564.

	Since this article does not have an abstract, we have provided the first 150 words of the full text and any section headings.

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 -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 -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 -lactamases that previously had poor activity against newer cephalosporins, such as ceftazidime sodium.³

As so often happens with antibiotic resistance, what initially appears . . . [Full Text of this Article]

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

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