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Title: | Genomics And Susceptibility Profiles Of Extensively Drug-resistant Pseudomonas Aeruginosa Isolates From Spain |
Author: | Barrio Tofiño, Ester López Causapé, Carla Cabot, Gabriel Rivera, Alba Benito Hernández, M. Natividad de Segura, Concepción Montero, María Milagro Sorli, Luisa Tubau, Fe Gómez-Zorrilla Martín, Silvia Tormo, Nuria Durá Navarro, Raquel Viedma, Esther Resino Foz, Elena Fernández Martínez, Marta González Rico, Claudia Alejo-Cancho, Izaskun Martínez, José Antonio (Martínez Martínez) Labayru Echverria, Cristina Dueñas, Carlos J. Ayestaran, Ignacio Zamorano, Laura Martínez Martínez, Luis Horcajada Gallego, Juan Pablo Oliver, Antonio |
Keywords: | Epidemiologia molecular Pseudomonas Molecular epidemiology |
Issue Date: | 1-Nov-2017 |
Publisher: | American Society for Microbiology |
Abstract: | This study assessed the molecular epidemiology, resistance mechanisms, and susceptibility profiles of a collection of 150 extensively drug-resistant (XDR) Pseudomonas aeruginosa clinical isolates obtained from a 2015 Spanish multicenter study, with a particular focus on resistome analysis in relation to ceftolozane-tazobactam susceptibility. Broth microdilution MICs revealed that nearly all (> 95%) of the isolates were nonsusceptible to piperacillin-tazobactam, ceftazidime, cefepime, aztreonam, imipenem, meropenem, and ciprofloxacin. Most of them were also resistant to tobramycin (77%), whereas nonsusceptibility rates were lower for ceftolozane-tazobactam (31%), amikacin (7%), and colistin (2%). Pulsed-field gel electrophoresis-multilocus sequence typing (PFGE-MLST) analysis revealed that nearly all of the isolates belonged to previously described high-risk clones. Sequence type 175 (ST175) was detected in all 9 participating hospitals and accounted for 68% (n = 101) of the XDR isolates, distantly followed by ST244 (n = 16), ST253 (n = 12), ST235 (n = 8), and ST111 (n = 2), which were detected only in 1 to 2 hospitals. Through phenotypic and molecular methods, the presence of horizontally acquired carbapenemases was detected in 21% of the isolates, mostly VIM (17%) and GES enzymes (4%). At least two representative isolates from each clone and hospital (n = 44) were fully sequenced on an illumina MiSeq. Classical mutational mechanisms, such as those leading to the overexpression of the beta-lactamase AmpC or efflux pumps, OprD inactivation, and/or quinolone resistance-determining regions (QRDR) mutations, were confirmed in most isolates and correlated well with the resistance phenotypes in the absence of horizontally acquired determinants. Ceftolozane-tazobactam resistance was not detected in carbapenemase-negative isolates, in agreement with sequencing data showing the absence of ampC mutations. The unique set of mutations responsible for the XDR phenotype of ST175 clone documented 7 years earlier were found to be conserved, denoting the long-term persistence of this specific XDR lineage in Spanish hospitals. Finally, other potentially relevant mutations were evidenced, including those in penicillin-binding protein 3 (PBP3), which is involved in beta-lactam (including ceftolozane-tazobactam) resistance, and FusA1, which is linked to aminoglycoside resistance. |
Note: | Reproducció del document publicat a: https://doi.org/10.1128/AAC.01589-17 |
It is part of: | Antimicrobial Agents And Chemotherapy, 2017, vol. 61, num. 11 |
URI: | http://hdl.handle.net/2445/124235 |
Related resource: | https://doi.org/10.1128/AAC.01589-17 |
Appears in Collections: | Articles publicats en revistes (Institut d'lnvestigació Biomèdica de Bellvitge (IDIBELL)) |
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File | Description | Size | Format | |
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del Barrio-TofinoE.pdf | 1.38 MB | Adobe PDF | View/Open |
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