During the 30 months of surveillance period, 85 pAmpC-producing isolates were detected (prevalence 0.56% overall): blaCMY-2 gene in 70 E. coli, 2 K. pneumoniae and 6 P. mirabilis isolates; and the blaDHA-1 gene in 4 E. coli and 3 K. pneumoniae. In 8.23% of them, other β-lactamases (predominantly OXA-1) were identified. All pAmpC-producing isolates were susceptible to carbapenems, whereas high resistance to nalidixic acid, ciprofloxacin and trimethoprim-sulfamethoxazole was observed among pAmpC-producing isolates (80%, 60%, and 44.7%, respectively). In hospital patients, predisposing factors such as prior antibiotic use, previous hospitalization, presence of an indwelling device, invasive urinary tract procedures and mechanical ventilation were observed. In the community setting, urinary tract infection was the most common type of infection related to pAmpC-producing isolates. A wide heterogeneity of clones was found among our E. coli isolates by PFGE, suggesting that this mechanism of resistance is not due to the dissemination of a clonal strain. Surveillance of these resistance mechanisms in the community is thus needed. Awareness of pAmpC dynamic is required to prevent introduction into hospitals and to control the spread of this emerging resistance within the community.
Keywords: CMY-2; Clinical features; Molecular epidemiology; PFGE; Plasmid-mediated AmpC; Prevalence.
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