The occurrence of extended-spectrum ␤-lactamase (ESBL)-producing isolates has increased worldwide. Fecal carriage of ESBL-producing isolates has mainly been detected in nosocomial outbreaks, and few studies have evaluated fecal carriage during nonoutbreak situations and among patients in the community. We have studied the prevalence of ESBLs in 1,239 fecal samples from 849 patients (64.1% of whom were ambulatory) in 1991 and have compared the prevalence data with those obtained in 2003 for 400 fecal samples from 386 patients (75.9% of whom were ambulatory) and 108 samples from independent healthy volunteers. Samples were diluted in saline and cultured in two MacConkey agar plates supplemented with ceftazidime (1 g/ml) and cefotaxime (1 g/ml), respectively. Colonies were screened (by the double-disk synergy test) for ESBL production. The clonal relatedness of all ESBL-producing isolates was determined by pulsed-field gel electrophoresis with XbaI digestion; and the ESBLs of all ESBL-producing isolates were characterized by isoelectric focusing, PCR, and sequencing. The rates of fecal carriage of ESBL-producing isolates increased significantly (P < 0.001) in both hospitalized patients and outpatients, from 0.3 and 0.7%, respectively, in 1991, to 11.

Susceptibility patterns to 15 different antibiotics and the presence of resistance genes were evaluated in recent fecal Enterococcus isolates recovered from 42 healthy volunteers (HV) and 43 food-handlers (FH). A total of 142 Enterococcus faecalis, 74 Enterococcus faecium, and 23 Enterococcus spp. with different antibiotic susceptibility patterns were studied. A higher percentage of resistance for moxifloxacin, erythromycin, glycopeptides and high-level resistance (HLR) to gentamicin were observed in the FH group. Ampicillin- or linezolid-resistant isolates were not recovered in any of the groups. The tet(M) gene was found in 96% and in 85% of tetracycline-resistant isolates from HV and FH, respectively. HLR-kanamycin was mediated by aph(3')-IIIa, or aac(6')-aph(2"), or both genes in all isolates from HV group and in 86% from FH group. The aac(6')-aph(2") gene was found in all HLR-gentamicin isolates. Ninety-one percent of HV and 71% of FH erythromycin-resistant isolates harbored the erm(B) gene (erythromycin MIC range of 8-128 microg/ml), whereas erm(A), erm(C), or mef(A) genes were not detected. Coexistence of erm(B), aph(3')-IIIa, and tet(M) genes was observed in 17% of the isolates of both groups. The HLR-gentamicin isolates presented unrelated PFGE patterns while 2 out of 3 vanA E. faecium isolates showed an indistinguishable SmaI-pulsed-field gel electrophoresis (PFGE) pattern. This study shows that despite 4 years of official banning of antibiotic growth promoters in animals, enterococci isolated from FH are more resistant than those from HV. This suggests the permanence of resistant clones or transferable resistance elements in farms and a possible exchange between food products and humans, or eventually the long-term permanence of certain clones in the FH intestinal tract.

Proteus penneri, formerly P. vulgaris biogroup 1, was recognized as a new species in 1982. This species is associated with clinical processes similar to those involving P. mirabilis and P. vulgaris and expresses similar pathogenic determinants. In clinical samples, P. penneri is mainly isolated from urine (50%), wound and soft tissue exudates (25%), and blood cultures (15%), mostly of nosocomial origin. Although P. penneri is easy to identify, it can be misidentified as P. vulgaris by automatic systems that do not include the indol test result in the identification process. This species has a characteristic susceptibility profile, essentially due to the production of the chromosomal inducible beta-lactamase HugA, which presents a high homology (86%) with CumA from P. vulgaris. HugA is inhibited by clavulanic acid and determines resistance to aminopenicillins and first- and second-generation cephalosporins, including cefuroxime, but does not affect cephamycins or carbapenems, and is inhibited by clavulanic acid. HugA is derepressed due to mutational processes in gene regulators, affecting the activity of cefotaxime and, to a much lesser extent, that of ceftazidime and aztreonam. This phenotype resembles the production of an extended spectrum beta-lactamase. Like other Proteus species, P. penneri is resistant to tetracyclines and should be considered resistant to nitrofurantoin.

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