Broad Resistance Due to Plasmid‐Mediated AmpC β‐Lactamases in Clinical Isolates ofEscherichia coli
Author(s) -
Ruba Odeh,
Sujata Kelkar,
Andrea M. Hujer,
Robert A. Bonomo,
Paul C. Schreckenberger,
John P. Quinn
Publication year - 2002
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 - 10.1086/340742
Subject(s) - ertapenem , meropenem , cefepime , microbiology and biotechnology , imipenem , plasmid , escherichia coli , ceftazidime , cephalosporin , medicine , biology , virology , antibiotic resistance , antibiotics , bacteria , dna , gene , pseudomonas aeruginosa , genetics
Escherichia coli that produce plasmid-mediated AmpC beta-lactamases are rare in the United States. The clinical features associated with infection with these organisms have not been well described. We identified 2 clinical isolates of E. coli that produced the plasmid-mediated AmpC enzyme beta-lactamase CMY-2. These organisms were recovered from urine specimens and were resistant to ceftazidime, ceftriaxone, and cefepime. One isolate was resistant to ertapenem but susceptible to imipenem and meropenem; the other was susceptible to imipenem, meropenem, and ertapenem. One of the 2 infected patients did not require specific therapy; the other required imipenem for cure. The presence of the CMY-2 beta-lactamase was confirmed by DNA sequencing. Hybridization studies confirmed that the bla(CMY-2) gene was on a plasmid in both isolates; in one of them, the probe also hybridized with chromosomal DNA. Infection with plasmid-mediated AmpC beta-lactamases in E. coli in the United States may be associated with treatment failure, and these strains may become a serious nosocomial threat.
Accelerating Research
Robert Robinson Avenue,
Oxford Science Park, Oxford
OX4 4GP, United Kingdom
Address
John Eccles HouseRobert Robinson Avenue,
Oxford Science Park, Oxford
OX4 4GP, United Kingdom