A sustained hospital outbreak of VRE bacteraemia due to the emergence of Enterococcus faecium ST203
Abstract number: P1019
Johnson P.D., Ballard S.A., Grabsch E.A., Stinear T.P., Seeman T., Young H., Grayson M.L., Howden B.P.
Objectives: Improved infection control at our health service has been associated with a progressive reduction in MRSA bacteraemia but a paradoxical rise in vancomycin resistant Enterococcus faecium bacteraemia. We hypothesised that a new hospital-adapted strain of Enterococcus faecium (Efm) was responsible for this paradox.
Methods: We reviewed all patient episodes of Efm bacteraemia (both vancomycin-sensitive [VSEfm] and vancomycin-resistant [VREfm]) over an 11.5-year period (19982009). The first available isolate from each patient with confirmed VSEfm or VREfm bacteraemia was typed using multi-locus sequence typing (MLST). We also performed optical mapping and whole genome sequencing on representative isolates from the two most common sequence types (STs), one from early in the study period (October 1998, AUS0004, ST 17) and the other more recent (February 2009, AUS0085, ST 203).
Results: 85 isolates (51 VSEfm, 33 VREfm vanB genotype and 1 VREfm vanA genotype) obtained from patients with Efm bacteraemia were typed by MLST. Seventeen different STs were identified. From 1998 to 2006, bacteraemia rates remained stable and the most common blood culture isolate was Efm ST 17 (21/45 [47%]). Efm ST 203 was not isolated. In late November 2005 Efm ST 203 was detected for the first time as VSEfm in a patient's blood culture. The first VREfm ST 203 was isolated in a blood culture obtained in March 2007. Since 2007, coinciding with the emergence of VREfm ST 203, the rate of VREfm bacteraemia has increased exponentially with ST 203 accounting for 19/25 (76%) of VREfm blood culture isolates, while ST 17 only accounted for 4/25 (16%) in the same period. During 2009, 10/14, (71.4%) of all Efm bacteraemia isolates were ST 203. Although Efm ST 203 is only a double locus variant of Efm ST 17, comparative genomics revealed more than 500 kb of sequence difference between AUS0004 (ST 17) and AUS0085 (ST 203), suggesting Efm ST 203 was introduced recently from outside our hospital rather than developing locally from an endemic ST 17 strain.
Conclusions: The initial detection of VSEfm ST 203 was followed within 15 months by the emergence of VREfm vanB ST 203 that is now causing a sustained outbreak of VRE bacteraemia. The dominance of Efm ST 203, compared with other Efm-STs, suggests enhanced survival and/or virulence under hospital conditions, but the determinants of this adaptation/virulence are not yet known.
|Session name:||Abstracts 20th European Congress of Clinical Microbiology and Infectious Diseases|
|Location:||Vienna, Austria, 10 - 13 April 2010|
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