JAC Advance Access originally published online on February 28, 2007
Journal of Antimicrobial Chemotherapy 2007 59(4):806-807; doi:10.1093/jac/dkm022
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Correspondence |
Hospital dissemination of a clonal complex 17 vanB2-containing Enterococcus faecium
1 Microbiology Department, Hospital General de Soria, Soria, Spain 2 Antibiotic Laboratory, Bacteriology Service, Centro Nacional de Microbiología, Instituto de Salud Carlos III, Carretera Pozuelo a Majadahonda, 28220 Majadahonda, Madrid, Spain 3 Preventive Medicine Department, Hospital General de Soria, Soria, Spain 4 Consejo Superior de Investigaciones Científicas, Madrid, Spain
* Corresponding author. Tel: +91 822 3650; Fax: +91 509 7966; E-mail: jesus.oteo{at}isciii.es
Keywords: vancomycin , outbreaks , multiresistance
Since the first report in 1988, vancomycin-resistant enterococci (VRE) have emerged as an important cause of hospital-acquired infections, particularly in the United States. However, infections with VRE are still relatively uncommon in many European hospitals. The aim of this study was to characterize isolates from a prolonged outbreak of vancomycin-resistant and teicoplanin-susceptible (VanB phenotype) Enterococcus faecium that occurred in a Spanish hospital.
Between January 2004 and July 2006, 107 E. faecium isolates were isolated from clinical samples in the Hospital General de Soria (HGS), Spain (estimated catchment population of 92 700): 30 were isolated in 2004, 44 in 2005 and 33 in 2006. Of these, 34 (31.8%) isolates from separate patients showed VanB phenotypes, for which the annual distribution was 23.2% (7 isolates) in 2004, 29.5% (13 isolates) in 2005 and 42.4% (14 isolates) in 2006. The remaining 73 E. faecium isolates were susceptible to both vancomycin and teicoplanin. From March 2004 to October 2005, only sporadic cases appeared; however, in November 2005 three cases were detected, peaking in March and April 2006 with five and four cases, respectively.
Most VanB isolates were from males (58.8%), age >65 years (84.4%), admitted to ICU (32.4%) and were isolated from wounds (35.3%) or the urinary tract (23.6%). Twenty-eight patients (82.4%) had predisposing underlying conditions, principally respiratory/cardiac diseases (27.3%), neurological diseases (27.3%), tumoral pathologies (27.3%) and urinary tract pathologies (21.2%). Thirty-two patients were treated with antibiotics within the month prior to infection; the most frequent agents were cephalosporins (47.1%) and vancomycin (23.5%). Statistical comparisons of demographic data, clinical characteristics, microbiological features and clinical outcomes of the 34 patients infected by VanB E. faecium with 50 patients infected by vancomycin-susceptible E. faecium showed that only previous treatment with cephalosporins and/or vancomycin was associated with the emergence of VanB E. faecium (P < 0.05).
All 34 VanB isolates were also resistant to ampicillin (MICs > 8 mg/L), erythromycin (MICs > 4 mg/L) and levofloxacin (MICs > 2 mg/L), but were susceptible to high concentrations of gentamicin (MICs 4–8 mg/L). Seventeen of these isolates were randomly selected and subjected to further molecular and epidemiological studies.
A vanB gene was detected by PCR in all 17 isolates, and sequencing confirmed that this was identical to the vanB2 allele.1 In addition, the intergenic region vanSB–vanYB, sequenced in four isolates, showed previously reported point mutations and a 5 bp deletion in vanB2.1 Amplification and posterior sequencing of vanXB–ORFC amplicons demonstrated genetic linkage of the vanB2 operon to a Tn5382-like element.2 The pbp5 gene was detected by PCR in the four isolates, but we did not find genetic linkage of pbp5 and the vanB2-containing Tn5382.3 This latter finding is in accordance with the high rate of ampicillin resistance (82.6%; 60/73 isolates) among our vancomycin-susceptible E. faecium isolates.
The 17 VanB isolates harboured the enterococcal surface protein gene, esp, but not the hyl, gelE, cylA or asa1 virulence genes.
By PFGE, the VanB2 isolates exhibited a genetic relatedness of 92–100%, and 12 were indistinguishable (Figure 1) indicating an outbreak strain. Five VanB isolates from other hospitals and one vancomycin-susceptible strain from HGS were used as controls, showed <70% similarity (Figure 1) and were considered unrelated. Multilocus sequence typing (MLST) analysis showed that isolates of the outbreak strain had an identical allelic profile, ST17 belonging to the clonal complex 17 (CC-17). Four E. faecium isolates were used as controls in the MLST analysis, two vancomycin-susceptible isolates from HGS had the ddl2 allele, instead of the ddl1 of the vanB2 isolates, and belonged to ST16; and two other vanB producers from other hospitals were ST18 and ST132.
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Infections caused by VanB vancomycin-resistant E. faecium belonging to CC-17 are still relatively uncommon in Europe. In two hospitals in Zaragoza (Spain), a clonal relationship was demonstrated between seven vanB2-containing E. faecium isolates.4 The first VanB E. faecium isolated in a Spanish hospital was described in 2004.5 In Sweden, a nosocomial outbreak of VanB2 E. faecium with the purK allele 1 has been reported.6
An enhanced infection control programme was introduced in the HGS during 2006. Patients infected by VanB enterococci were isolated in single rooms whenever possible, and these rooms were mechanically cleaned each day. The outbreak of VanB E. faecium finished in August 2006, with no further cases detected.
In conclusion, to the best of our knowledge, we describe the first outbreak in Spain of a vanB2 E. faecium strain belonging to CC-17 and which was multiply resistant to vancomycin, ampicillin and fluorquinolones.
None to declare.
Acknowledgements
This study was supported by research grant from Instituto de Salud Carlos III, Fondo de Investigaciones Sanitarias, Ministry of Health, Spain (Red Española de Investigación en Patología Infecciosa, REIPI; reference RD06/0008/0023), and by the Dirección General de Salud Pública, Ministry of Health, Spain (reference 1429/05-11).
Silvia García-Cobos is a recipient of a fellowship of the ISCIII (reference 05/0033).
References
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Dahl KH, Lundblad EW, Rokenes TP, et al. (2000) Genetic linkage of the vanB2 gene cluster to Tn5382 in vancomycin-resistant enterococci and characterization of two novel insertion sequences. Microbiol 146:1469–79.
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Carias LL, Rudin SD, Donskey CJ, et al. (1998) Genetic linkage and cotransfer of a novel, vanB-containing transposon (Tn5382) and a low-affinity penicillin-binding protein 5 gene in a clinical vancomycin-resistant Enterococcus faecium isolate. J Bacteriol 180:4426–34.
4
Torres C, Escobar S, Portillo A, et al. (2006) Detection of clonally related vanB2-containing Enterococus faecium strains in two Spanish hospitals. J Med Microbiol 55:1237–43.
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