Ceftazidime-Resistant Klebsiella pneumoniae and Escherichia coli Bloodstream Infection: A Case-Control and Molecular Epidemiologic Investigation
Author(s) -
Deborah A. Schiappa,
Mary K. Hayden,
Marian Matushek,
Farzane Hashemi,
Jacqueline Sullivan,
Kimberly Y. Smith,
D Miyashiro,
John P. Quinn,
Robert A. Weinstein,
Gordon M. Trenholme
Publication year - 1996
Publication title -
the journal of infectious diseases
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.69
H-Index - 252
eISSN - 1537-6613
pISSN - 0022-1899
DOI - 10.1093/infdis/174.3.529
Subject(s) - ceftazidime , klebsiella pneumoniae , microbiology and biotechnology , bacteremia , molecular epidemiology , escherichia coli , outbreak , ciprofloxacin , biology , enterobacteriaceae , infection control , medicine , antibiotics , virology , genotype , bacteria , pseudomonas aeruginosa , intensive care medicine , gene , genetics
In a molecular, microbiologic, and case-control study to describe the epidemiology of ceftazidime-resistant Klebsiella pneumoniae and Escherichia coli bloodstream infection, 32 unique isolates were recovered over 31 months from the blood of patients hospitalized in a 900-bed hospital in Chicago. Multivariate analysis revealed cases occurred more frequently in debilitated nursing home patients with central venous catheters than in younger, healthier patients. Mortality rates were similar for cases and controls. Case-patients were less likely to die if they received appropriate antibiotic treatment within 3 days of bacteremia onset (P = .02). Pulsed-field gel electrophoresis analysis indicated a polyclonal outbreak, with strain-specific temporal and geographic clustering. Isoelectric focusing results suggested that a predominant enzyme, TEM-10, was responsible for the ceftazidime resistance. The resistance gene was usually carried on a large conjugative plasmid. The polyclonality of the resistant strains suggests that ceftazidime resistance due to TEM-10 is now endemic in Chicago.
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