(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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