The role of epidemic resistance plasmids and international high-risk clones in the spread of multidrug-resistant Enterobacteriaceae

Abstract

Escherichia coli ST131and Klebsiella pneumoniae ST258 emerged in the 2000s as important human pathogens; have spread extensively throughout the world and are responsible for the rapid increase in antimicrobial resistance among E. coli and K. pneumoniae respectively. E. coli ST131 causes extra-intestinal infections, is often fluoroquinolone resistant and associated with Extend-spectrum β-lactamase production especially CTX-M-15. K. pneumoniae ST258 causes urinary and respiratory tract infections and is associated with carbapenemases most often KPC-2 and KPC-3. The most prevalent lineage within ST131 is named fimH30 because it contains the 2 H30 variant of the type 1 fimbrial adhesin gene and recent molecular studies have demonstrated that this lineage emerged in early 2000‟s and was then followed by the rapid expansion of its sublineages H30-R and H30-Rx. K. pneumoniae ST258 comprises of 2 distinct lineages namely clade I and clade II. Moreover, it seems that ST258 is a hybrid clone that was created by a large recombination event between ST11 and ST442. Epidemic plasmids with blaCTX-M and blaKPC belonging to the incompatiblity group F have contributed significantly to the success of these clones. E. coli ST131 and K. pneumoniae ST258 are the quintessential examples of international multidrug-resistant high risk clones.