Literature DB >> 28674059

In Vivo Emergence of Resistance to Novel Cephalosporin-β-Lactamase Inhibitor Combinations through the Duplication of Amino Acid D149 from OXA-2 β-Lactamase (OXA-539) in Sequence Type 235 Pseudomonas aeruginosa.

Pablo A Fraile-Ribot1, Xavier Mulet1, Gabriel Cabot1, Ester Del Barrio-Tofiño1, Carlos Juan1, José L Pérez1, Antonio Oliver2.   

Abstract

Resistance development to novel cephalosporin-β-lactamase inhibitor combinations during ceftazidime treatment of a surgical infection by Pseudomonas aeruginosa was investigated. Both initial (97C2) and final (98G1) isolates belonged to the high-risk clone sequence type (ST) 235 and were resistant to carbapenems (oprD), fluoroquinolones (GyrA-T83I, ParC-S87L), and aminoglycosides (aacA7/aacA8/aadA6). 98G1 also showed resistance to ceftazidime, ceftazidime-avibactam, and ceftolozane-tazobactam. Sequencing identified blaOXA-2 in 97C2, but 98G1 contained a 3-bp insertion leading to the duplication of the key residue D149 (designated OXA-539). Evaluation of PAO1 transformants producing cloned OXA-2 or OXA-539 confirmed that D149 duplication was the cause of resistance. Active surveillance of the emergence of resistance to these new valuable agents is warranted.
Copyright © 2017 American Society for Microbiology.

Entities:  

Keywords:  Pseudomonas aeruginosa; ceftazidime-avibactam; ceftolozane-tazobactam; extended-spectrum OXA; multidrug resistance

Mesh：

Substances：

Year:  2017        PMID： 28674059      PMCID： PMC5571340          DOI： 10.1128/AAC.01117-17

Source DB:  PubMed          Journal:  Antimicrob Agents Chemother        ISSN： 0066-4804            Impact factor:   5.191


  30 in total

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10.  Mechanisms of Resistance to Ceftolozane/Tazobactam in Pseudomonas aeruginosa: Results of the GERPA Multicenter Study.

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