Nosocomial Bacteremia and Urinary Tract Infections Caused by Extended-Spectrum β-Lactamase-Producing Klebsiella pneumoniae with Plasmids Carrying Both SHV-5 and TLA-1 Genes

• Published in: Clinical infectious diseases Vol. 38; no. 8; pp. 1067 - 1074
• Main Authors: Alcantar-Curiel, Dolores, Tinoco, Juan Carlos, Gayosso, Catalina, Carlos, Angeles, Daza, Carlos, Perez-Prado, Maria C., Salcido, Lorena, Santos, Jose I., Alpuche-Aranda, Celia M.
• Format: Journal Article
• Language: English
• Published: United States The University of Chicago Press 15.04.2004; University of Chicago Press
• Subjects: Antibiotics; Antimicrobials; Bacteremia; Bacteremia - microbiology; beta-Lactam Resistance; beta-Lactamases - genetics; Cross Infection - microbiology; Drug Resistance, Bacterial; Gels; Genotype; Hospital units; Hospitals; Humans; Infections; Klebsiella Infections - microbiology; Klebsiella pneumoniae; Klebsiella pneumoniae - drug effects; Major Articles; Microbial Sensitivity Tests; Phenotypes; Plasmids; Plasmids - genetics; Urinary tract infections; Urinary Tract Infections - microbiology; Mexico
• ISSN: 1058-4838; 1537-6591
• DOI: 10.1086/382354

We describe the prevalence and molecular characteristics of extended-spectrum β-lactamase (ESBL)-producing Klebsiella pneumoniae causing nosocomial bacteremia and urinary tract infections in a Mexican general hospital. We analyzed 82 episodes of bacteremia (∼60% of episodes) and urinary tract infection (∼40% of episodes) due to K. pneumoniae during a 23-month surveillance period. The neonatal intensive care unit accounted for 49% of all episodes. All strains were imipenem susceptible; 62.2% of the strains were resistant to ceftazidime, cefotaxime, and aztreonam; 69.5% were resistant to amikacin; 58.5% were resistant to gentamicin; and 7.3% were resistant to ciprofloxacin. All strains were associated with 28 pulsed-field gel electrophoresis patterns, and dissemination of 2 ceftazidime-resistant clones produced 44% of the cases. The ESBL phenotype in these clones was transferred by identical or highly related megaplasmids. The ESBL activity corresponded to SHV-5 and TLA-1. Cross-transmission of 2 ceftazidime-resistant clones and the horizontal spread of identical or highly related megaplasmids explain the high prevalence of ESBL phenotype in these infections.