Abstract
The resistance mechanism of extended-spectrum cephalosporins in clinical isolates of Citrobacter freundii , Enterobacter spp., and Serratia marcescens was studied. Of 152 isolates, 45 isolates (29.6%) were derepressed AmpC mutants and 39 isolates (25.7%) produced extended-spectrum β-lactamase (ESBLs). The most prevalent ESBLs were CTX-M enzymes, followed by TEM-52 and SHV-12.
Keywords

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