ESBL-producing E. coli may arise from interactions between ESBL type, strain genetic background, and selective pressures in various ecologic niches.

Background: Owing to its low incidence, the management of Mycobacterium xenopi pulmonary infections is not clearly defined. A multicentre retrospective study was performed to describe the features of the disease and to evaluate its prognosis. Methods: All patients with M xenopi satisfying the 1997 ATS/IDSA criteria from 13 hospitals in north-east France (1983France ( -2003 were included in the study. Clinical, radiological and bacteriological characteristics and data on the management and outcome were collected. Results: 136 patients were included in the analysis, only 12 of whom presented with no co-morbidity. Three types of the disease were identified: (1) a classical cavitary form in patients with pre-existing pulmonary disease (n = 39, 31%); (2) a solitary nodular form in immunocompetent patients (n = 41, 33%) and (3) an acute infiltrate form in immunosuppressed patients (n = 45, 36%). 56 patients did not receive any treatment; the other 80 patients received first-line treatment containing rifamycin (87.5%), ethambutol (75%), isoniazid (66.2%), clarithromycin (30%) or fluoroquinolones (21%). After a follow-up of 36 months, 80 patients (69.1%) had died; the median survival was 16 months (range 10-22). Two independent prognostic factors were found: the acute infiltrate form was associated with a bad prognosis (hazard ratio 2.6, p = 0.001) and rifamycin-containing regimens provided protection (hazard ratio 0.325, p = 0.006). Clarithromycin-containing regimens did not improve the prognosis. Conclusions: In contrast to recent guidelines, this study showed three different types of the disease (cavitary, nodular or diffuse infiltrate forms) with a different prognosis. In order to improve survival, all patients with M xenopi infection should be treated with a rifamycincontaining regimen. The usefulness of clarithromycin remains to be evaluated.Mycobacterium xenopi is a non-tuberculous mycobacterium responsible for lung disease, 1 especially in north-east France, south-east UK and in Ontario, Canada. 2 3 According to the recent ATS/ IDSA statement, its usual feature is an apical cavitary process in patients with obstructive pulmonary disease. 4 However, other features have been described. 5 M xenopi infections are difficult to treat and there is no standard treatment. 2 3 5 Rifampin, ethambutol and sometimes isoniazid or fluoroquinolones are usually recommended in combination with clarithromycin. 4 Two randomised clinical trials have been conducted by Jenkins et al. 6 7 In the first study, 42 patients were treated with rifampin and ethambutol with or without isoniazid, without any difference in the clinical response. 6 The overall mortality rate at 5 years was 69%. In the second study, Jenkins et al compared clarithromycin with a ciprofloxacin-containing regimen in 371 patients infected with non-tuberculous mycobacteria and found no difference in the 34 patients infected with M xenopi. 7 As M xenopi infection could present with different clinical and radiological patterns depending on the patient's immuno...

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In 1996, a monitoring program was initiated at the teaching hospital of Amiens, France, and carried out for 3 years. All extended-spectrum ␤-lactamase (ESBL)-producing Enterobacter aerogenes isolates recovered from clinical specimens were collected for investigation of their epidemiological relatedness by pulsed-field gel electrophoresis and enterobacterial repetitive intergenic consensus PCR (ERIC-PCR) and determination of the type of ESBL harbored by isoelectric focusing and DNA sequencing. Molecular typing revealed the endemic coexistence, during the first 2 years, of two clones expressing, respectively, SHV-4 and TEM-24 ESBLs, while an outbreak of the TEM-24-producing strain raged in the hospital during the third year, causing the infection or colonization of 165 patients. Furthermore, this strain was identified as the prevalent clone responsible for outbreaks in many French hospitals since 1996. This study shows that TEM-24-producing E. aerogenes is an epidemic clone that is well established in the hospital's ecology and able to spread throughout wards. The management of the outbreak at the teaching hospital of Amiens, which included the reinforcement of infection control measures, failed to obtain complete eradication of the clone, which has become an endemic pathogen.

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...

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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.

Among cases of bacteremia, 27% were caused by PNSP, but this level varies according to the counties and the age of the patients. Infection-related mortality was high, but there was no increase related to penicillin G non-susceptibility of the infecting strain.