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Acquisition of Extended-Spectrum β-Lactamase GES-6 Leading to Resistance to Ceftolozane-Tazobactam Combination in Pseudomonas aeruginosa
Author(s) -
Laurent Poirel,
José Manuel Ortiz de la Rosa,
Nicolas Kieffer,
Véronique Dubois,
Aurélie Jayol,
Patrice Nordmann
Publication year - 2018
Publication title -
antimicrobial agents and chemotherapy
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.07
H-Index - 259
eISSN - 1070-6283
pISSN - 0066-4804
DOI - 10.1128/aac.01809-18
Subject(s) - pseudomonas aeruginosa , tazobactam , microbiology and biotechnology , broad spectrum , biology , chemistry , bacteria , imipenem , genetics , combinatorial chemistry
A clinical Pseudomonas aeruginosa isolate resistant to all β-lactams, including ceftolozane-tazobactam and carbapenems, was recovered. It belonged to sequence type 235 and produced the extended-spectrum β-lactamase (ESBL) GES-6 differing from GES-1 by two amino acid substitutions (E104K and G170S). GES-6 possessed an increased hydrolytic activity toward carbapenems and to ceftolozane and a decreased susceptibility to β-lactamase inhibitors compared to GES-1, except for avibactam. We show here that resistance to ceftolozane-tazobactam may occur through acquisition of a specific ESBL in P. aeruginosa but that ceftazidime-avibactam combination remains an effective alternative.

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