Molecular characterization of clinical and environmental isolates of vancomycin-resistant Enterococcus faecium and Enterococcus faecalis from a teaching hospital in Wales

Abstract

The present study describes the first molecular characterization of environmental and clinical isolates of vancomycin-resistant enterococci (VRE) in Wales. Over a 3-month period (May-July 2000), 134 isolates of VRE (89 Enterococcus faecium and 45 Enterococcus faecalis) were isolated from the patient environment of the University Hospital of Wales (UHW) in Cardiff, Wales, UK. In addition, over the same time-period, 24 clinical isolates of VRE (20 isolates of E. faecium and four isolates of E. faecalis) were obtained from 14 patients. All study isolates were subjected to PFGE typing and their van genotypes were determined by using multiplex PCR. The vanA PCR product (231 bp) was evident in 146 (92 %) of 158 VRE isolates; the remaining 12 isolates (8 %) were positive for the vanB gene. All isolates of E. faecalis were found to be vanA-positive. In total, 16 PFGE banding profiles (pulsotypes) were observed for environmental isolates of E. faecium, whilst eight pulsotypes were found for isolates of E. faecalis. Some of these pulsotypes were isolated from multiple sites, whereas others were more restricted in their distribution. Eleven pulsotypes were evident for clinical isolates and eight of these (representing 11 isolates) were also encountered in environmental isolates. Eleven clinical isolates of E. faecium (55 %) shared an identical pulsotype that was not detected in environmental isolates. These results demonstrate a heterogeneous environmental population of VRE and an association of certain strains with clinical isolates. Predominance of a single pulsotype (not detected in the environment) amongst clinical isolates suggests non-environmental transmission between patients.

Impact of the reduction of environmental and equipment contamination on vancomycin-resistant enterococcus rates

“…Few studies, however, have used molecular typing to evaluate the environment as a source of VRE [28][29][30]. These studies only investigated the environment as a source of VRE outbreaks [28][29][30]. In the present study, the most frequent environmental sites and equipment contaminated by VRE were those near to the patients and frequently touched by the HCW, such as bedside shelves, sphygmomanometers, bed edge, and stethoscopes, as previously reported.…”

“…Studies using multivariate analysis showed that placement in a contaminated room was associated with VRE acquisition (p = 0.020) [26], and that VRE-colonized room occupants within the previous 2 weeks and previous positive room culture remained independent predictors of VRE acquisition, after being adjusted for colonization pressure and antibiotic exposure [4]. Few studies, however, have used molecular typing to evaluate the environment as a source of VRE [28][29][30]. These studies only investigated the environment as a source of VRE outbreaks [28][29][30].…”

Linezolid vancomycin resistantEnterococcusisolated from clinical samples in Tehran hospitals

“…[13,14] Although we found 8.5%, 3% and 2% of isolates were resistant to vancomycin, teicoplanin and linezolid, respectively, diverse patterns of enterococci resistance have been reported from many countries. [13][14][15] In vitro resistance to linezolid is mediated via mutations in the central region of domain V of 23SrRNA and/ or by as yet unknown mechanisms. [7,6] However, resistance in wild-type isolates of Enterococcus and Staphylococcus is conferred by a single nucleotide transvertion at position 2576 in 23SrRNA.…”

The in vitro Activity of Pentane-1,5-diol against Aerobic Bacteria. A New Antimicrobial Agent for Topical Usage?

“…Such problems are particularly evident in hospitals, where they frequently present as nosocomial outbreaks. The most important nosocomial resistance today is caused by methicillin-resistant Staphylococcus aureus (MRSA) (1,2), vancomycinresistant enterococci (VRE) (3,4) and Enterobacteriaceae with extended-spectrum beta-lactamases (5,6). In addition, MRSA can also be resistant to aminoglycosides, often also to fluoroquinolones, and most other antibiotics (7,8).…”

“…These multiresistant clones of S. aureus often occur as epidemic strains. Moreover, the VRE are also appearing as multiresistant strains which are often resistant to almost all antibiotics (3,4). These bacteria are mainly spread by person-to-person contact (9,10).…”