Extended-spectrumβ-lactamase (ESBL)-producing Escherichia coli has emerged worldwide as a significant group of community pathogens.^1,2 This is of clinical importance because E coli is the most common cause of community-acquired urinary tract infections (UTIs), and ESBL-producing isolates are frequently resistant to many of the antimicrobial agents recommended for the treatment of such infections; this is particularly true of oral agents.³ While many studies have reported the microbiological characterization of community-acquired ESBL-producing E coli, published data that are clinically orientated are scarce; the few studies published concerning risk factors or the clinical significance of such infections involved only small samples of cases and were carried out in individual centers.^4-6 As the epidemiologic features of ESBL-producing organisms may show significant local variations, multicenter studies are particularly important to obtain comprehensive knowledge of risk factors for these infections. Likewise, studies that evaluate the efficacy of the few potentially useful oral drugs available for treatment are also needed.

Background. It is necessary to clarify the incidence of and risk factors for tuberculosis (TB) among solid-organ transplant (SOT) recipients as well

We investigated the mechanisms of resistance to carbapenems, aminoglycosides, glycylcyclines, tetracyclines, and quinolones in 90 multiresistant clinical strains of Acinetobacter baumannii isolated from two genetically unrelated A. baumannii clones: clone PFGE-ROC-1 (53 strains producing the OXA-58 β-lactamase enzyme and 18 strains with the OXA-24 β-lactamase) and clone PFGE-HUI-1 (19 strains susceptible to carbapenems). We used real-time reverse transcriptase PCR to correlate antimicrobial resistance (MICs) with expression of genes encoding chromosomal β-lactamases (AmpC and OXA-51), porins (OmpA, CarO, Omp33, Dcap-like, OprB, Omp25, OprC, OprD, and OmpW), and proteins integral to six efflux systems (AdeABC, AdeIJK, AdeFGH, CraA, AbeM, and AmvA). Overexpression of the AdeABC system (level of expression relative to that by A. baumannii ATCC 17978, 30- to 45-fold) was significantly associated with resistance to tigecycline, minocycline, and gentamicin and other biological functions. However, hyperexpression of the AdeIJK efflux pump (level of expression relative to that by A. baumannii ATCC 17978, 8- to 10-fold) was significantly associated only with resistance to tigecycline and minocycline (to which the TetB efflux system also contributed). TetB and TetA(39) efflux pumps were detected in clinical strains and were associated with resistance to tetracyclines and doxycycline. The absence of the AdeABC system and the lack of expression of other mechanisms suggest that tigecycline-resistant strains of the PFGE-HUI-1 clone may be associated with a novel resistance-nodulation-cell efflux pump (decreased MICs in the presence of the inhibitor Phe-Arg β-naphthylamide dihydrochloride) and the TetA(39) system.