We studied 138 glycopeptide-resistant enterococci (GRE) strains, consisting of 131 glycopeptide-resistant Enterococcus faecium (GREfm) and 7 glycopeptide-resistant Enterococcus faecalis (GREfs). The GREfm strains were resistant to penicillin, ampicillin, vancomycin, and teicoplanin, while the GREfs strains were only resistant to vancomycin and teicoplanin. The van A gene was the only glycopeptide determinant present in all GRE isolates investigated. Genes coding for Hyl and Hyl+ Esp were detected in 39 (29.8%) and 92 (70.2%) of the 131 GREfm isolates, respectively. Three of the 7 GREfs were positive for gelE+asa 1 genes, 3 for gel E gene, and 1 for asa 1 gene. The genetic relationship between the 138 GRE was analyzed by pulsed-field gel electrophoresis (PFGE) and multilocus sequence typing (MLST). GREfm isolates were clustered in a single genogroup (pulsotype A), and GREfs were clustered in six genogroups (pulsotypes B-G). Among the isolates investigated by MLST, only 18 PCR products were sequenced (12 E. faecium and 6 E. faecalis), and 9 sequence types (STs) were identified.

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This first large national study indicates the need for thorough epidemiological monitoring and a stewardship programme to prevent and detect mupirocin resistance in staphylococci.

Home nursing care appears to be an independent risk factor for MRSA acquisition in the community. The reservoir probably consists of MRSA carriers discharged from the hospital. Community nurses seem to be a potential vector.

Sixty-two clinical isolates of Enterobacter aerogenes resistant to expanded-spectrum cephalosporins were collected between July 2003 and May 2005. Among these isolates, 23 (37.1%) were imipenem (IPM) susceptible, and 39 (62.9%) were IPM insusceptible, of which 89.7% (35/39) were resistant and 10.3% (4/39) were intermediate. Isolate genotypes were compared by pulsed-field gel electrophoresis. Of 62 isolates, 48 belonged to epidemic pulsotype A (77.4%). This pulsotype included 37.5% and 58.4% of ␤-lactam phenotypes b and a, respectively. Nine isolates (14.5%) belonged to pulsotype E, which included 22.3% and 77.7% of phenotypes b and a, respectively. The ␤-lactamases with pIs of 5.4, 6.5, 8.2, and 8.2 corresponded to extended-spectrum ␤-lactamases (ESBLs) TEM-20, TEM-24, SHV-5, and SHV-12, respectively. Of 39 IPM-insusceptible E. aerogenes isolates, 26 (66.6%) were determined to be metallo-␤-lactamase producers, by using a phenotypic method. Of these isolates, 24 harbored a bla IMP-1 gene encoding a protein with a pI of >9.5, and two carried the bla VIM-2 gene encoding a protein with a pI of 5.3, corresponding to ␤-lactamases IMP-1 and VIM-2, respectively. The remaining 13 (33.4%) isolates were negative for the bla IMP-1 and bla VIM-2 genes but showed an alteration of their outer membrane proteins (OMPs). Ten of these isolates produced the two possible OMPs (32 and 42 kDa), with IPM MICs between 8 and 32 g/ml, and three others produced only a 32-kDa OMP with IPM MICs >32 g/ml. This work demonstrates that, in addition to resistance to expanded-spectrum cephalosporins, IPM resistance can occur in ESBL-producing E. aerogenes isolates by carbapenemase production or by the loss of porin in the outer membrane.Enterobacter aerogenes has recently emerged as an important hospital pathogen (13). The prevalence of this bacterial species has increased considerably since the introduction of extendedspectrum cephalosporins into clinical practice (18). Various resistance mechanisms have been described in this species, such as extended-spectrum ␤-lactamases (ESBLs), plasmidmediated production (21), and hyperproduction of the Bush group 1 chromosomally mediated cephalosporinases (32). Although these enzymes are specifically characteristic of some Enterobacter spp., the appearance of similar plasmid-mediated ␤-lactamases in Klebsiella pneumoniae and Escherichia coli raises concerns about the spread of resistance (21, 32). For both ESBL-producing and AmpC-producing isolates, carbapenems are the only ␤-lactam agents active against both resistance mechanisms. Data from previous studies have shown that both ESBL and AmpC ␤-lactamase producers had reduced susceptibility to imipenem (IPM) due to either carbapenemhydrolyzing enzymes (carbapenemase) (30), decreased membrane permeability due to loss of porin in the outer membrane (14, 39), or active efflux (27).The IPM resistance of ESBL-producing E. aerogenes strains was observed for the first time at Amiens University Hospital (A.U.H.) in 2002. To determine whether the strains were epidem...

From June to November 1994 (period 1) and from February to June 1995 (period 2), multiresistant Acinetobacter baumanniistrains were isolated in intensive care units and surgical wards of the Amiens Teaching Hospital Center (Amiens, France). Eighteen isolates were obtained from 17 (1%) of 1,706 patients admitted during both of these periods, giving an incidence rate of nosocomial infection per 1,000 patient days of 0.6%. Of 17 infected patients, 9 had pneumonia, 3 had urinary tract infection, 2 had peritonitis, 1 had septicemia, 1 had a catheter infection, and 1 had pneumonia and urinary tract infection. According to typing results, four antibiotic resistance profiles were detected: a, b, c, and d; seven ribotypes were distinguished by both restriction enzymes EcoRI andSalI (A, B, C, D, E, F, and G). By combining antibiotyping and ribotyping, we obtained eight groups of strains (groups I to VIII). Group I contained five strains (strains 4, 5, 7, 8, and 9) which had antibiogram pattern a and ribopattern A and constituted the outbreak strains. The strains of group II (strains 3, 10, 11, 13, and 14) were closely related to outbreak strain A and appeared to be variants of ribotype A (A2 [strain 3]; A4 [strain 10]; A5 [strains 11, 13, and 14]). Groups III, IV, V, VI, VII, and VIII included strains which were epidemiologically unrelated to the strains of group I and were considered nonoutbreak strains.

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Between February 1997 and December 2002, 3340 hospitalised patients yielded samples positive for Proteus mirabilis, of whom 45 (1.3%) were colonised/infected by P. mirabilis producing extended-spectrum beta-lactamases (ESBLs). The gross incidence of patients colonised/infected by ESBL-producing P. mirabilis was 1.61/10(5) days of hospitalisation, with 20% of isolates being collected from patients in urology wards, most frequently (53.3%) from urine samples. Seventeen (37.7%) of the 43 isolates were obtained from samples collected within 48 h of hospitalisation, indicating that they were community-acquired. Isoelectric focusing assays and sequencing identified the TEM-24, TEM-92 and TEM-52 ESBLs. Pulsed-field gel electrophoresis revealed eight pulsotypes (I-VIII), with the two most common pulsotypes, IV and VI, comprising ten (23.3%) and 12 (26.6%) isolates, respectively. These pulsotypes were considered to represent epidemic strains and spread in various wards of the hospital.