Carbapenemase-producing Klebsiella pneumoniae : a key pathogen set for global nosocomial dominance

Abstract

The management of infections due to Klebsiella pneumoniae has been complicated by the emergence of antimicrobial resistance, especially to the carbapenems. Resistance to the carbapenems in K. pneumoniae involves 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 up regulation of efflux systems. The latter two mechanisms are often combined with high levels of other types of β-lactamases (e.g.AmpC). K. pneumonaie ST258 emerged during the early to mid-2000s as important human pathogens and has spread extensively throughout the world. ST258 comprises of 2 distinct lineages namely clade I and clade II and it seems that ST258 is a hybrid clone that was created by a large recombination event between ST11 and ST442. Incompatiblity group F plasmids with blaKPC have contributed significantly to the success of ST258. The optimal treatment of infections due to carbapenemase-producing K. pneumoniae remains unknown. Some newer agents show promise for treating infections due to KPC-producers, however effective options for the treatment of NDM-producers remain elusive.