Australian Group on Antimicrobial Resistance (AGAR) Australian Enterococcal Sepsis Outcome Programme (AESOP) Annual Report 2016

Abstract

From 1st January to 31st December 2016, 32 institutions around Australia participated in the Australian Enterococcal Sepsis Outcome Programme (AESOP). The aim of AESOP 2016 was to determine the proportion of enterococcal bacteraemia isolates in Australia that were antimicrobial resistant, and to characterise the molecular epidemiology of the E. faecium isolates. Of the 1,058 unique episodes of bacteraemia investigated, 95.2% were caused by either E. faecalis (56.2%) or E. faecium (39.0%) Ampicillin resistance was detected in 0.2% of E. faecalis and in 91.5% of E. faecium. Vancomycin non-susceptibility was reported in 0.3% and 47.7% of E. faecalis and E. faecium respectively. Overall, 49.3% of E. faecium harboured vanA or vanB genes. For the vanA/B positive E. faecium isolates, 55.2% harboured vanB genes and 42.8% vanA genes, 2% harboured vanA and vanB genes. The percentage of E. faecium bacteraemia isolates resistant to vancomycin in Australia is significantly higher than that seen in most European countries. E. faecium consisted of 48 multilocus sequence types (STs) of which 90.2% of isolates were classified into 13 major STs containing 5 or more isolates. All major STs belong to clonal cluster (C) 17, a major hospital-adapted polyclonal E. faecium cluster. Four of the 6 predominant STs (ST17, ST796, ST80 and ST203) were found across most regions of Australia. The most predominant clone ST1421 (previously known as M-type 1) does not have a pstS housekeeping gene and was found in NSW, the ACT and Victoria. This clone was first described in ASSOP 2015. Overall, 74% of isolates belonging to the 6 predominant STs harboured vanA or vanB genes. The AESOP 2016 has shown enterococcal bacteraemias in Australia are frequently caused by polyclonal ampicillin-resistant high-level gentamicin resistant vanA or vanB E. faecium which have limited treatment options.