ArticleFrontiers in microbiology2026
Genomic characterization of ceftazidime/avibactam-resistant KPC-producing
Article in Frontiers in microbiology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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Who cites it
1 citing paper in PubMed.
- Emerging Cross-Resistance to Cefiderocol and Ceftazidime-Avibactam in KPC-ProducingAntibiotics (Basel, Switzerland) · 2026Article
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Authors and funding
14 authors.
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Abstract
Background: The clinical management of bloodstream infections (BSIs) caused by KPC- Methods: We retrospectively investigated 16 BSIs caused by KPC-Kp isolates resistant to CAZ/AVI collected from January 2022 to July 2025. Antimicrobial susceptibility testing (AST) was performed to assess resistance profiles against last-line agents. Whole Genome Sequencing (WGS) and bioinformatic analyses were employed to identify molecular drivers of resistance and evaluate genetic relatedness. Patients' data were collected to integrate clinical outcomes with the microbiological features of the isolated strains. Results: The BSIs analyzed were characterized by a high degree of severity, with 9/16 patients presenting a Pitt bacteremia score ≥ 4 and 7/16 (44%) a 30-days mortality rate. Intestinal colonization by KPC-Kp was identified in 14/16 patients, and prior CAZ/AVI-based therapy had been administered to 12/16, suggesting the resistance development under selective antimicrobial pressure. AST revealed resistance to last-line agents: imipenem/relebactam (4/16), meropenem/vaborbactam (2/16) and colistin (3/16), alongside reduced susceptibility to cefiderocol (11/16), thereby limiting effective treatment strategies. Besides the predominance of high-risk clones, such as ST101 (8/16) and ST512 (3/16), phylogenetic analysis highlighted a cluster within ST101 group, suggesting a hospital outbreak. Furthermore, two novel sequence types, ST9507 and ST8640 were identified. Multiple KPC variants were detected, including the novel KPC-293 and KPC-296, which were not previously described. All isolates exhibited a truncated OmpK35 in combination or not with a highly mutated OmpK36, with insertion in loop3 being the most prevalent alteration. Given the heterogeneity of the KPC variants found in the isolates, and the consistent loss of porin function, the OmpK35/36 impairment may represent the pivotal driver of the MDR phenotype in these strains. Conclusion: Our findings indicate that the synergy between multiple KPC variants and porin structural alterations may represent a critical determinant underlying the clinical challenge posed by CAZ/AVI resistance in invasive infections.
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