Emergence of cefiderocol resistance during ceftazidime/avibactam treatment caused by a large genomic deletion, including ampD and piuCD genes, in Pseudomonas aeruginosa

Antimicrob Agents Chemother. 2024 Jan 10;68(1):e0119223. doi: 10.1128/aac.01192-23. Epub 2023 Dec 8.

Abstract

We report the emergence of cefiderocol resistance during the treatment of a ST312 Pseudomonas aeruginosa respiratory infection with ceftazidime/avibactam. whole genome sequencing (WGS) revealed that resistance was caused by a large genomic deletion, including PiuDC (iron transport system) and AmpD (ampC negative regulator), driven by the integration of phage DNA. Thus, our findings alert that this type of deletion could be an efficient (two mechanisms in one step) specific cefiderocol resistance mechanism that might occur nonspecifically upon treatment with β-lactams that select for AmpC overexpression.

Keywords: Pseudomonas aeruginosa; cefiderocol; ceftazidime-avibactam; drug resistance evolution; iron transport.

MeSH terms

  • Anti-Bacterial Agents / pharmacology
  • Anti-Bacterial Agents / therapeutic use
  • Azabicyclo Compounds / pharmacology
  • Azabicyclo Compounds / therapeutic use
  • Bacterial Proteins / genetics
  • Cefiderocol
  • Ceftazidime* / pharmacology
  • Ceftazidime* / therapeutic use
  • Drug Combinations
  • Genomics
  • Humans
  • Microbial Sensitivity Tests
  • Pseudomonas Infections* / drug therapy
  • Pseudomonas aeruginosa / genetics
  • beta-Lactamases / genetics

Substances

  • Ceftazidime
  • Cefiderocol
  • Anti-Bacterial Agents
  • avibactam
  • Bacterial Proteins
  • Azabicyclo Compounds
  • Drug Combinations
  • beta-Lactamases