Retrospective analysis of the transmission of difficult-to-treat resistant Pseudomonas aeruginosa - genotype beats phenotype
- Journal
- Antimicrobial resistance and infection control (Q1)
- Published
- 30 October 2026
- Study design
- Unclassified
- Evidence level
- Level 5, Expert Opinion (CEBM 5)
- Authors
- Jasmin Kaur Jasuja, Philipp Maximilian Maurer, Laura Carlsen, Eva-Maria Theresia Klupp, Cristina Elena Belmar Campos, Holger Rohde, et al.
- PMID
- 42963799
- DOI
- 10.1186/s13756-026-01851-3
Why clinicians should know about it
- Picked for Microbiology (medical) (paper of the day, 4 November 2026): WGS and epidemiology assess resistant Pseudomonas transmission and IPC
Abstract
BACKGROUND: Difficult-to-treat resistant Pseudomonas aeruginosa (DTRPA) represents a challenging resistance phenotype with carbapenem-resistant P. aeruginosa playing a major role. However, carbapenemase-negative DTRPA (CN-DTRPA) are more susceptible to reserve antibiotics and rarely reported in outbreaks, differing from frequently outbreak-associated carbapenemase-producing DTRPA (CP-DTRPA) with limited therapeutic options. Despite, international guidelines recommend equal infection prevention and control (IPC) measures. Here, we analysed the transmission of CP-DTRPA and CN-DTRPA using epidemiology and whole-genome sequencing (WGS). METHODS: Clinical DTRPA isolates collected between 2019 and 2024 were subjected to WGS. Genetic clusters were defined using cgMLST thresholds of ≤ 11 and ≤ 3 allelic differences. Epidemiological relatedness was estimated on hospital stay, interpatient contact and environmental exposures. For possibly epidemiologically linked cases, precolonisation with carbapenem-susceptible P. aeruginosa (CSPA) and antibiotic exposure during hospitalisation were assessed. RESULTS: Among 190 DTRPA isolates, CN-DTRPA (79.5%) was predominant compared to 20.5% CP-DTRPA, mainly carrying blaVIM-2. Twelve genetic clusters involving 39 patients were identified. Seven clusters (CP-DTRPA n = 4; CN-DTRPA n = 2, CP-DTRPA/CN-DTRPA-mixed n = 1) showed possible epidemiological relatedness. CP-DTRPA isolates were frequently associated with clusters (OR 17.47, 95% CI 7.43-41.08) and environmental transmission. Diverse CN-DTRPA were rather linked to interpatient CSPA-transmission following CN-DTRPA emergence after prolonged antibiotic exposure. CONCLUSION: CN-DTRPA predominated and displayed high diversity, consistent with possible antibiotic-driven resistance development in precolonised patients. In contrast, less frequent and less diverse CP-DTRPA were associated to outbreaks. These findings highlight the need to evaluate differentiated IPC strategies, including targeted screening and environmental interventions for CP-DTRPA, while further investigating the potential role of antimicrobial stewardship in preventing the emergence of CN-DTRPA. Multicentre studies are required for evidence-based IPC strategies.
Abstract as published, via PubMed.
For healthcare professionals. The summary is generated by AI from the published abstract, and the evidence level is assigned automatically from the study design on the Oxford CEBM hierarchy. Neither is medical advice. Read the full paper before changing practice.