ArticleBiofilm2024
Collateral susceptibility-guided alternation of ceftolozane/tazobactam with imipenem prevents resistance development in XDR
Article in Biofilm, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
3 citing papers in PubMed.
- Phenotypic convergence and collateral susceptibility development in Pseudomonas aeruginosa under antibiotic exposure in ICU patients.npj antimicrobials and resistance · 2026Article
- Robust antibiotic sensitization of pathogenic Pseudomonas aeruginosa via negative hysteresis in the cell envelope.Nature communications · 2026Article
- Current and future options for the treatment of serious infections due to carbapenem-resistantClinical microbiology reviews · 2025Review
Corrections and comments
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Authors and funding
10 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Objectives: New combinations of β-lactams and β-lactamase inhibitors, such as ceftolozane/tazobactam could be useful to combat biofilm-driven chronic infections by extensively resistant (XDR) Methods: A carbapenem-resistant XDR Results: Ceftolozane/tazobactam monotherapy failed to reduce the biofilms of the 104-B7 XDR strain and led to the selection of resistant mutants that showed AmpC Ω-loop mutations (T96I, L244R or aa236Δ7). On the contrary, alternation with imipenem enhanced activity (3 Logs reduction at day 6) and prevented the emergence of ceftolozane/tazobactam-resistant mutants. Likewise, treatment with ceftolozane/tazobactam dramatically amplified the resistant strain 104-I9 in mixed biofilms (>90 % of the population), while the alternation regimen counterselected it. Conclusions: Collateral susceptibility-guided alternation of ceftolozane/tazobactam with imipenem effectively prevented the selection of resistant mutants and thus could be a potential therapeutic strategy for the treatment of
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