Author:
Pitout Johann D. D.,Nordmann Patrice,Poirel Laurent
Abstract
ABSTRACTThe management of infections due toKlebsiella pneumoniaehas been complicated by the emergence of antimicrobial resistance, especially to carbapenems. Resistance to carbapenems inK. pneumoniaeinvolves multiple mechanisms, including the production of carbapenemases (e.g., KPC, NDM, VIM, OXA-48-like), as well as alterations in outer membrane permeability mediated by the loss of porins and the upregulation of efflux systems. The latter two mechanisms are often combined with high levels of other types of β-lactamases (e.g., AmpC).K. pneumoniaesequence type 258 (ST258) emerged during the early to mid-2000s as an important human pathogen and has spread extensively throughout the world. ST258 comprises two distinct lineages, namely, clades I and II, and it seems that ST258 is a hybrid clone that was created by a large recombination event between ST11 and ST442. Incompatibility group F plasmids withblaKPChave contributed significantly to the success of ST258. The optimal treatment of infections due to carbapenemase-producingK. pneumoniaeremains unknown. Some newer agents show promise for treating infections due to KPC producers; however, effective options for the treatment of NDM producers remain elusive.
Publisher
American Society for Microbiology
Subject
Infectious Diseases,Pharmacology (medical),Pharmacology
Cited by
629 articles.
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