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.
