We characterized 100 Escherichia coli urosepsis isolates from adult patients according to host compromise status by means of ribotyping, PCR phylogenetic grouping, and PCR detection of papG alleles and the virulence-related genes sfa/foc, fyuA, irp-2, aer, hly, cnf-1 and hra. We also tested these strains for copies of pap and hly and their direct physical linkage with other virulence genes in an attempt to look for pathogenicity islands (PAIs) described for the archetypal uropathogenic strains J96, CFT073, and 536. Most of the isolates belonged to E. coli phylogenetic groups B2 and D and bore papG allele II, aer, and fyuA/irp-2. papG allele II-bearing strains were more common in noncompromised patients, while papG allele-negative strains were significantly more frequent in compromised patients. Fifteen ribotypes were identified. The three archetypal strains harbored different ribotypes, and only one-third of our urosepsis strains were genetically related to one of the archetypal strains. Three and 18 strains harbored three and two copies of pap, respectively, and 5 strains harbored two copies of hly. papGIII was physically linked to hly, cnf-1, and hra (reported to be PAI II J96 -like genetic elements) in 14% of the strains. The PAI II J96 -like domain was inserted within pheR tRNA in 11 strains and near leuX tRNA in 3 strains. Moreover, the colocalized genes cnf-1, hra, and hly were physically linked to papGII in four strains and to no pap gene in three strains. Escherichia coli is the most frequent cause of gram-negative bacterial extraintestinal infections, such as cystitis, prostatitis, pyelonephritis, bacteremia, and neonatal meningitis, in humans. Several virulence factors enhance the capacity of E. coli to cause systemic infections; unlike most commensal E. coli strains, extraintestinal isolates possess genes encoding various combinations of adhesins (P and S fimbriae), iron acquisition systems (e.g., aerobactin and yersiniabactin), host defense avoidance mechanisms (capsule or O-specific antigen), and toxins (e.g., hemolysin and cytonecrotizing factor) (13,14,17,42). Genes coding for multiple virulence factors are located together on large blocks of chromosomal DNA known as pathogenicity islands (PAIs) (18).Recent studies suggest that extraintestinal pathogenic E. coli strains belong mostly to phylogenetic group B2 and, to a lesser extent, group D (5, 8, 39). In contrast, commensal E. coli strains generally belong to phylogenetic groups A and B1 (12).In this study, we determined the phylogenetic group, genetic diversity, and virulence gene distribution of 100 well-characterized E. coli blood isolates from adults with communityacquired urosepsis, according to host compromise status. We also sought copies of pap and hly and their direct physical linkage with certain virulence genes, consistent with their colocalization on PAIs described for archetypal uropathogenic E. coli strains. MATERIALS AND METHODSBacterial strains. One hundred E. coli strains were recovered by blood culture from 100 consecutive adult...

A total of 1,500 recent throat isolates of Streptococcus pyogenes collected between 1996 and 1999 from children throughout France were tested for their susceptibility to erythromycin, azithromycin, josamycin, clindamycin, and streptogramin B. The erythromycin-resistant isolates were further studied for their genetic mechanism of resistance, by means of PCR. The clonality of these strains was also investigated by means of serotyping and ribotyping. In all, 6.2% of the strains were erythromycin resistant, and 3.4 and 2.8% expressed the constitutive MLS B and M resistance phenotypes and harbored the ermB and mefA genes, respectively; ermTR was recovered from one isolate which also harbored the ermB gene. Ten serotypes and 8 ribotypes were identified, but we identified 17 strains by combining serotyping with ribotyping. Among the eight ribotypes, the mefA gene was recovered from six clusters, one being predominant, while the ermB gene was recovered from four clusters, of which two were predominant.Penicillin is the drug of choice for the treatment of Streptococcus pyogenes infection. However, for patients sensitive to ␤-lactam antibiotics, and when these drugs fail, macrolides are often the recommended substitute. Penicillin resistance has not yet been described in S. pyogenes, but resistance to erythromycin and related antibiotics has been widely reported (2,3,5,8,10,11,17,20,29,33,43,46). The mechanism of acquired resistance to erythromycin involves a target site modification mediated by a methylase which modifies the 50S ribosomal subunit, leading to the MLS B resistance phenotype encoded by erm genes (25,36,47). Erythromycin resistance due to an efflux mechanism (M phenotype), encoded by mef genes, has recently been described (6,45). While the prevalence of the S. pyogenes resistance to macrolides has been reported worldwide, very few recent data deal with the French situation (1,8). The aims of this study were to assess the macrolide sensitivity of recent throat isolates of S. pyogenes collected from French children, to determine the genetic mechanisms of resistance, and to explore clonality by means of serotyping and molecular methods. MATERIALS AND METHODSBacterial isolates. A total of 1,500 consecutive S. pyogenes isolates were collected between 1996 and 1999 throughout France. They were isolated by swabbing the throats of children, 4 to 17 years old (mean age, 11 years), with pharyngitis. The isolates were identified as S. pyogenes by colony morphology, beta-hemolysis on blood agar, and a commercial agglutination technique (Murex Diagnostics UK).Susceptibility testing. The procedures for susceptibility testing were those recommended by the National Committee for Clinical Laboratory Standards (NCCLS) (30).(i) Detection of erythromycin resistance and determination of resistance phenotypes. Erythromycin-resistant strains were initially identified by the disk diffusion method on Mueller-Hinton agar supplemented with 5% defibrinated horse blood (Diagnostic Pasteur, Marnes la Coquette, France) using 15-g erythrom...

Macrolide susceptibility was investigated in clinical group B streptococci obtained from neonates or pregnant women in 2000 in France. Of 490 consecutive isolates, 18% were resistant to erythromycin. The erm(B), erm(A) subclass erm(TR), and mef(A) genes were harbored by 47, 45, and 6% of these strains, respectively. Two isolates did not harbor erm or mef genes.

We describe a 7-month outbreak of nosocomial Burkholderia cepacia bacteremia involving eight children in a pediatric hospital and the results of epidemiological investigations. A B. cepacia strain genotypically identical to the blood isolates was recovered from the upper surface of capped rubber stoppers of bottles of a commercial lipid emulsion used for parenteral nutrition.

The genetic relatedness of French isolates of Streptococcus pneumoniae highly resistant to amoxicillin (MIC, ≥4 μg/ml, equal to or exceeding those of penicillin) was investigated by molecular fingerprinting. The results suggest that high-level resistance to amoxicillin has emerged within preexisting penicillin-resistant clones.