Nosocomial Bacteremia and Urinary Tract Infections Caused by Extended‐Spectrum β‐Lactamase–ProducingKlebsiella pneumoniaewith Plasmids Carrying Both SHV‐5 and TLA‐1 Genes
Author(s) -
Marı́a Dolores Alcántar-Curiel,
Juan Carlos Tinoco,
Catalina Gayosso,
Ángeles CarlosReyes,
Carlos Daza,
Maria C. PerezPrado,
Lorena Salcido,
José Ignacio Santos,
Celia AlpucheAranda
Publication year - 2004
Publication title -
clinical infectious diseases
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.44
H-Index - 336
eISSN - 1537-6591
pISSN - 1058-4838
DOI - 10.1086/382354
Subject(s) - ceftazidime , klebsiella pneumoniae , aztreonam , amikacin , bacteremia , microbiology and biotechnology , cefotaxime , ciprofloxacin , imipenem , medicine , gentamicin , klebsiella , antibiotics , biology , antibiotic resistance , pseudomonas aeruginosa , bacteria , escherichia coli , gene , genetics
We describe the prevalence and molecular characteristics of extended-spectrum beta -lactamase (ESBL)-producing Klebsiella pneumoniae causing nosocomial bacteremia and urinary tract infections in a Mexican general hospital. We analyzed 82 episodes of bacteremia (approximately 60% of episodes) and urinary tract infection (approximately 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.
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