Temporal flux in β-lactam resistance among Klebsiella pneumoniae in Western Australia

J Med Microbiol. 2016 May;65(5):429-437. doi: 10.1099/jmm.0.000242. Epub 2016 Mar 4.

Abstract

Our aim was to identify long-term β-lactam resistance trends in local Klebsiella pneumoniae isolates, which are a common cause of sepsis in Western Australia. We studied three collections of K. pneumoniae isolates from Western Australia between 1977 and 2015 comprising contemporary blood culture (n = 98), multiresistant (n = 21) and historical (n = 50) isolates. Antimicrobial resistance was determined by Clinical and Laboratory Standards Institute agar dilution methods. PCR DNA sequencing identified β-lactamase variants and porin mutations contributing to β-lactam resistance. Isolates were genotyped by PFGE, multilocus sequence typing and a variable number tandem repeat method. From 1989 onwards, we detected the SHV-2a extended-spectrum β-lactamase (ESBL) in ceftriaxone-resistant isolates, and in ceftazidime- and aztreonam-resistant isolates from 1993. Ceftriaxone, ceftazidime and aztreonam resistance persisted, with blaCTX-M types becoming the dominant ESBLs by 2010. CTX-M-15 was encountered in both multiresistant and blood culture isolates. Meropenem resistance was detected for the first time in 2011 in a locally isolated blaIMP-4-positive K. pneumoniae. We found sequence types ST23 and ST86 that occurred in multiple isolates from invasive infections. ST86 was the most common and maintained a high degree (90 %) of similarity by PFGE since 1977. Ceftazidime-resistant K. pneumoniae sequence types have caused invasive infections in Western Australia since 1993. Invasive isolates producing CTX-M-14 and CTX-M-15 appeared in Western Australia during the last decade, before the appearance of carbapenemases. The diversity of β-lactam resistance and β-lactamase resistance mechanisms in Western Australian K. pneumoniae has increased since ESBLs were first described locally.