ArticleScientific reports2026
Mechanistic and clinical insights into a PmrB mutation driving colistin resistance and virulence in Acinetobacter baumannii.
Article in Scientific reports, 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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1 citing paper in PubMed.
- Convergent Architecture of thePathogens (Basel, Switzerland) · 2026Article
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5 authors.
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Abstract
The global rise of colistin-resistant Acinetobacter baumannii (CRAB) is a critical health threat, particularly in the Middle East. The pmrB c.235T > A (p.Leu79Ile) mutation is frequently observed in clinical isolates, but its comprehensive characterization is lacking. In this multicenter study, 465 clinical A. baumannii isolates were collected from Iran (n = 378) and Iraq (n = 87) between January 2023 and June 2024. Colistin susceptibility was determined by broth microdilution, and the pmrCAB operon was sequenced. The structural impact of p.Leu79Ile was assessed via 200-ns molecular dynamics simulations. Functional consequences were evaluated using lipid A profiling, biofilm assays, serum resistance, and a murine pneumonia model. Phylogeographic analysis and a LASSO-regularized logistic regression model for 30-day mortality prediction were performed. Colistin resistance was detected in 47.8% of isolates, with 94.2% of resistant isolates harboring pmrCAB mutations; c.235T > A was predominant (76.8%). Simulations indicated that Leu79Ile stabilizes the active conformation of PmrB (ΔΔG = -3.8 kcal/mol), increasing the root mean square deviation (RMSD; 4.7 Å vs. 2.3 Å) and altering protein dynamics. This correlated with a 1.93-fold increase in pEtN-modified lipid A and a strong inverse correlation with colistin MIC (ρ = -0.89). Mutant isolates exhibited enhanced biofilm formation (2.3-fold), serum survival (47.6% increase), and murine mortality (70% vs. 30%). Phylogenetics identified a dominant ST848-bla ~ OXA-23~^+^ clone emerging around 2016 (95% HPD: 2015-2017), with evidence of Iran-Iraq cross-border transmission. The mortality prediction model (predictors: age > 65, CCI > 3, ventilation, shock, c.235T > A, ST848) achieved an AUC = 0.87 in validation. This study suggests the pmrB c.235T > A mutation confers a dual phenotype of colistin resistance and hypervirulence, driven by structural stabilization of PmrB within an expanding regional clone.
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