
Extended-spectrum beta-lactamases (ESBLs) are enzymes which hydrolyze broad-spectrum beta-lactam antibiotics by expanding the substrate spectra into the so-called anti-beta-lactamase beta-lactams such as oxyimino-cephalosporins, cephamycins, oxacephems, carbapenems and monobactams, conferring resistance to many kinds of beta-lactams on pathogenic bacteria. Recently, ESBLs have been demonstrated from various types of beta-lactamases phylogenetically belonging to the molecular class, A, B, C, or D. The genes coding for ESBLs are chromosome- or plasmid-mediated and some of them have developed by point or insertion mutations in the parental genes coding for the narrow-spectrum beta-lactamase. If the genes are plasmid-mediated, the dissemination among various species of pathogenic bacteria would cause hospital-acquired infections by ESBL-producing bacteria.
Bacteria, beta-Lactams, beta-Lactam Resistance, beta-Lactamases, Anti-Bacterial Agents, Mutagenesis, Insertional, Genes, Bacterial, Humans, Point Mutation, Plasmids
Bacteria, beta-Lactams, beta-Lactam Resistance, beta-Lactamases, Anti-Bacterial Agents, Mutagenesis, Insertional, Genes, Bacterial, Humans, Point Mutation, Plasmids
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