Journal
ANTIMICROBIAL AGENTS AND CHEMOTHERAPY
Volume 53, Issue 9, Pages 3908-3913Publisher
AMER SOC MICROBIOLOGY
DOI: 10.1128/AAC.00453-09
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Funding
- Ministere de l'Education Nationale et de la Recherche [UPRES-EA3539]
- Universite Paris XI, France
- European Community [LSHM-CT-2005-018705, TROCAR HEALTH-F3-2008-223031]
- INSERM
- Coordenacao de Aperfeicoamento de Pessoal de Nivel Superior ( CAPES) [3682/07-2]
- Conselho Nacional de Desenvolvimento Cientifico e Tecnologico (CNPq) [307714/2006-3]
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A retrospective survey was conducted to characterize beta-lactamases in a collection of 43 ceftazidime-resistant Pseudomonas aeruginosa isolates recovered from patients with bloodstream infections hospitalized at a Brazilian teaching hospital between January and December 2005. Resistance rates for carbapenems, aminoglycosides, and quinolones were over 80%, with only colistin remaining active against all isolates. Pulsed-field gel electrophoresis analysis identified seven different genotypes. AmpC overproduction was found to be the sole beta-lactamase-mediated mechanism responsible for ceftazidime resistance in four isolates (9.3%). Nine isolates (20.9%) produced an extended-spectrum beta-lactamase (ESBL), either GES-1 (n = 7, 16.3%) or CTX-M-2 (n = 2, 4.6%). Carbapenemase activity was detected in 30 (70%) additional isolates. Among those isolates, two isolates (4.6%) produced the ESBL GES-5, possessing the ability to hydrolyze imipenem; a single isolate (2.3%) produced the metallo-beta-lactamase (MBL) IMP-1; and 27 isolates produced the MBL SPM-1 (62.8%). None of the isolates coproduced both ESBL and MBL. Insertion sequence elements ISCR4 and ISCR1 were associated with bla(SPM-1) and bla(CTX-M-2) genes, respectively, whereas the bla(GES-1) and bla(GES-5) genes were part of class 1 integron structures. This study underlines the spread of MBL- and ESBL-producing P. aeruginosa isolates as an important source of ceftazidime resistance in Brazil.
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