A total of 151 Escherichia coli strains resistant to cefotaxime and ceftazidime were isolated during a prospective surveillance study. These strains were characterized by clinical, microbiological, and molecular analyses and were distributed into four clusters of 103, 11, 6, and 5 isolates, along with 25 unrelated strains. The principal cluster was isolated from urine, wound, blood, and other samples in three hospitals, eight nursing homes, and a community healthcare center. This cluster was associated with both nosocomial (65%) and community-acquired (35%) infections. Most strains were resistant to ciprofloxacin, gentamicin, tobramycin, cefepime, amoxicillin-clavulanic acid, and trimethoprim-sulfamethoxazole but were susceptible to imipenem. All isolates from the four clusters expressed the extended-spectrum ␤-lactamase (ESBL) CTX-M-15. This enzyme was also present in 8 (30.8%) of the 26 unrelated isolates. The other ESBLs, CTX-M-14 and CTX-M-32, were detected in five and seven cases, respectively, but they were detected in individual E. coli isolates only. In three clusters, bla CTX-M-15 alleles were linked to an ISEcp1-like element, while in eight strains of cluster II an IS26 element preceded the bla CTX-M-15 allele. An additional pool of resistance genes included tetA, drfA14 or dfrA17, sul1 or sul2, aac(6)Ib, and aac(3)IIb. All except one of the 27 isolates tested for genetic virulence markers harbored the same three virulence genes: iutA and fyuA (siderophores), and traT (serum survival factor). Epidemic or occasional isolates of cefotaxime-and ceftazidime-resistant E. coli can spread between distinct health facilities including hospitals, community health centers, and long-term care centers.

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The aim of this study was to describe the genetic characteristics of Streptococcus pyogenes showing the MLS B phenotype of macrolide resistance from 1999 to 2005 in Spain and to highlight the substantial increase in these isolates in the last few years. The antimicrobial susceptibilities of 17,232 group A streptococci isolated from Madrid and Gipuzkoa from 1999 to 2005 were studied. The presence of the resistance genes ermA, ermB, mef, tetM, and tetO and the presence of the intTn and xis genes of the Tn916-Tn1545 transposon family were studied in a sample of 739 MLS B -resistant isolates. The epidemiological relationships among these isolates were analyzed by emm typing, T typing, and multilocus sequence typing. Erythromycin resistance was found in 21.3% of the isolates analyzed (annual variation of 14.3% to 28.9%). Until 2003, most erythromycin-resistant isolates showed the M phenotype, but in 2004 and 2005, about 50% of isolates showed the MLS B phenotype. Among the MLS B -resistant isolates studied, 16 clones were identified. The most prevalent clone was a strange emm11/ T11/ST403 clone with a null yqiL allele. All but one of the 463 emm11/T11/ST403 isolates carried the ermB, tetM, intTn, and xis genes. The second most prevalent MLS B -resistant clone was emm28/T28/ST52, which comprised two subclones: one bacitracin-resistant, tetracycline-susceptible subclone carrying the ermB gene (n ‫؍‬ 115) and another bacitracin-susceptible, tetracycline-resistant subclone carrying the ermB and tetM genes (n ‫؍‬ 33). The rapid diffusion of these two clones, and especially of emm11/T11/ST403, caused the large increase in MLS Bresistant S. pyogenes isolates in Spain, suggesting a potential ability for international dissemination.Streptococcus pyogenes is a pathogen with worldwide distribution that causes a broad spectrum of infections, from uncomplicated pharyngitis to severe life-threatening infections (6). In the absence of a ␤-lactam allergy, the treatment of choice is penicillin, while the first-line alternative treatments are macrolides or lincosamides. There are two main phenotypes of macrolide resistance: the M phenotype, mediated by the mef genes (8), which confer low-level resistance to 14-and 15-membered macrolides but not to 16-membered macrolides, lincosamides, or streptogramin B, and the MLS B phenotype, mediated by the erm genes (20, 34), which confer resistance to macrolides, lincosamides, and streptogramin B antimicrobial agents. This latter phenotype can be constitutive, generally mediated by the ermB gene, or inducible, generally mediated by the ermA subclass TR (ermA) gene (31). Other mechanisms of resistance to macrolides or lincosamides in S. pyogenes (e.g., mutations in ribosomal proteins) are infrequently involved and currently have little clinical impact (4, 17).The factor most directly associated with the increase in antimicrobial resistance is the high level of antibiotic consumption among the population (2, 15). Nonetheless, the final cause of a higher or lower prevalence of antimicrobial resista...

Objectives: To determine the mechanisms of resistance to b-lactam antibiotics in clinical isolates of Haemophilus parainfluenzae.Methods: Twenty clinical isolates of H. parainfluenzae with decreased susceptibility to aminopenicillins were examined and compared with a control group of 20 fully susceptible isolates. In this collection, the presence of amino acid substitutions in the transpeptidase domain of penicillin-binding protein 3 (PBP3), b-lactamase production and the surrounding genetic regions of bla TEM genes in selected isolates were analysed.Results: Of the 20 non-susceptible isolates, 8 produced TEM b-lactamase (gBLPAR), 7 had mutations in the transpeptidase domain of the ftsI gene related to decreased susceptibility to b-lactams (gBLNAR) and 5 had both resistance mechanisms (gBLPACR). No resistance mechanisms were identified in the susceptible control group (gBLNAS). gBLNAR isolates had MIC 90 values 4-to 16-fold higher than gBLNAS isolates for ampicillin, amoxicillin/clavulanic acid, cefuroxime, cefotaxime and cefixime, and the most common PBP3 mutation was Asn526Ser. The additional Ser385Thr substitution (III-like group) may confer decreased susceptibility to cefotaxime, cefixime and aztreonam, as in Haemophilus influenzae. In two b-lactamase-positive isolates without PBP3 mutations, the inhibitor-resistant TEM (IRT) b-lactamases TEM-34 and the novel TEM-182 were detected and carried by a TnA transposon of the Tn2 type; both isolates had an amoxicillin/clavulanic acid MIC of ≥8 mg/L. The TnA transposons of two b-lactamase-positive isolates were inserted between the tfc20 and tfc21 genes, typically associated with integrative and conjugative elements in Haemophilus spp.; the TEM-34 IRT b-lactamase was harboured in a 5.5 kb plasmid. Conclusions:Clinical isolates of H. parainfluenzae express a variety of aminopenicillin resistance mechanisms, either alone or in combination, including PBP3 modifications, bla TEM-1 and IRT b-lactamase production.

Paediatric inflammatory vulvovaginitis is mainly caused by pathogens of the upper respiratory tract and the most common risk factor for this infection is to have suffered an upper respiratory tract infection in the previous month.