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Pseudomonas Infections / Beta-lactamase Inhibitors · Journal article
Emerging Microbes & Infections · July 2, 2026
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This ten-year retrospective study of 916 carbapenem-resistant P. aeruginosa isolates identified 50 blaGES-positive strains with five distinct subtypes exhibiting subtype-specific resistance: GES-1, -7, -15, and -69 conferred elevated ceftazidime-avibactam MICs while GES-5 increased imipenem-relebactam MICs. The variants were predominantly associated with high-risk clone ST235 and showed evidence of cross-species distribution, suggesting that GES enzyme subtype variation may differentially shape the activity of β-lactam/β-lactamase inhibitor combinations.
Ten-year retrospective screening with functional cloning experiments and genomic analysis. Carbapenem-resistant Pseudomonas aeruginosa isolates collected from 2016 to 2025, predominantly high-risk clone ST235.
50 of 916 CRPA isolates (5.5%) were blaGES-positive, with GES-1 (68%), GES-5 (24%), GES-15 (4%), GES-7 (2%), and novel GES-69 (2%) GES-1, GES-7, GES-15, and GES-69 showed elevated ceftazidime-avibactam MICs GES-5 was associated with increased imipenem-relebactam MICs
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Clinicians should recognize that GES β-lactamase subtype determines which β-lactam/inhibitor combination is likely to retain activity: GES-5-producing strains may respond to ceftazidime-avibactam while other GES variants may compromise its efficacy. The predominance of these resistance mechanisms in ST235 clones underscores the need for molecular diagnostics to guide therapy in carbapenem-resistant P. aeruginosa infections.
Laboratory and genomic analysis identifies subtype-specific GES variant resistance patterns to novel β-lactam/inhibitor combinations in a retrospective collection, but lacks clinical outcome data.
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Clinicians should recognize that GES β-lactamase subtype determines which β-lactam/inhibitor combination is likely to retain activity: GES-5-producing strains may respond to ceftazidime-avibactam while other GES variants may compromise its efficacy. The predominance of these resistance mechanisms in ST235 clones underscores the need for molecular diagnostics to guide therapy in carbapenem-resistant P. aeruginosa infections.
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Ceftazidime-avibactam (CZA) and imipenem-relebactam (IMR) are β-lactam/β-lactamase inhibitor combinations active against carbapenem-resistant Pseudomonas aeruginosa (CRPA), yet resistance to these agents is increasingly reported. In this study, 916 CRPA isolates collected from 2016 to 2025 were screened for blaGES by PCR, and fifty isolates were identified as blaGES-positive. Five subtypes were detected, including GES-1 (68%), GES-5 (24%), GES-7 (2%), GES-15 (4%), and a novel variant, GES-69 (2%). Antimicrobial susceptibility testing by broth microdilution revealed distinct resistance patterns. Isolates carrying blaGES-1, blaGES-7, blaGES-15, and blaGES-69 showed elevated CZA MICs, whereas blaGES-5 was associated with increased IMR MICs. Cloning experiments and structural modelling suggested that substitutions at position 170, Ω-loop conformational changes, and alterations in residues such as E104 may affect substrate binding and inhibitor interactions. Whole-genome sequencing showed that blaGES variants were located on the chromosome within class 1 integrons embedded in Tn6584-like transposons. Analysis of publicly available genomes further indicated that blaGES-positive isolates were mainly associated with the high-risk clone ST235, were distributed across multiple Gram-negative species with P. aeruginosa as the predominant host and exhibited an expanding cross-species distribution. In summary, these findings demonstrate that subtype-specific variation in GES enzymes is likely to shape the activity of β-lactam/β-lactamase inhibitor combinations within a conserved ST235 background.
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