[Resistance to the latest beta-lactams: mechanisms of acquisition and spread of resistance in Enterobacteriaceae].
Resistance to antibiotics may drastically diminish the efficacy of therapy in some clinical circumstances. The emergence of Enterobacteriaceae (Klebsiella pneumoniae, Aerobacter aerogenes, Escherichia coli) resistant to the more recent beta-lactam agents (cefepime, cefpirome, azthreonam and carbapenems) generally results from misuse of antibiotics, leading to the selection of preexisting resistant mutants. Resistance is usually due to beta-lactamase expression, through: -- mutations involving the beta-lactamase structure (TEM, SHV, OXA, CTX-M beta-lactamase families) and/or mutations of beta-lactamase synthesis regulators (AmpC beta-lactamases); or -- the appearance of new enzymes (PER, VEB, CMY, DHA-1, ACC-1, etc.). The level of resistance (particularly to carbapenems) is increased when porin mutations are associated with beta-lactamase expression. The spread of these new resistance mechanisms is amplified by mobilisation of resistance genes from the chromosome to a plasmid (SHV, CTX-M, CMY DHA-1 beta-lactamases genes) and by the location of these genes in mobile elements (integrons and transposons). The recent appearance of these mechanisms (particularly CTX-M beta-lactamases) in strains circulating in the community is a matter of concern.
Michel-Briand
Yvon
Y
y.michelbriand@wanadoo.fr
D000900:Anti-Bacterial Agents / Q000494:pharmacology; D004755:Enterobacteriaceae; D004756:Enterobacteriaceae Infections / Q000188:drug therapy*; D006801:Humans; D009154:Mutation; D018440:beta-Lactam Resistance / Q000235:genetics*; D001618:beta-Lactamases / Q000235:genetics*
D000900:Anti-Bacterial Agents; D001618:beta-Lactamases