ArticleAnnals of clinical microbiology and antimicrobials2025
Heteroresistance is associated with mutations during low concentration of tigecycline therapy in multiple-resistant Klebsiella pneumoniae.
Article in Annals of clinical microbiology and antimicrobials, 2025. 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.
- Phage and endolysin-based inhibition ofFrontiers in cellular and infection microbiology · 2026Review
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6 authors.
Funding
Abstract
backgroundHeteroresistance can lead to treatment failure and has brought a rigorous challenge to clinical laboratories for detecting them. The aim of this study was to investigate the potential for tigecycline-susceptible Klebsiella pneumoniae (K. pneumoniae) clinical isolates to develop heteroresistance under antibiotic pressure.
methodIn this study, inducing experiment in vitro was used to acquire tigecycline heteroresistance phenotype. Population analysis profiling was used to confirm heteroresistance. Potential tigecycline heteroresistance mechanism through whole-genome sequencing and quantitative reverse-transcription PCR (qRT-PCR) were explored. Time-kill assay was used to explore the effect of tigecycline monotherapy or combination with other antibiotics.
resultTwo clinically isolated K. pneumonia strains were found to change from tigecycline susceptible to resistance during treatment of tigecycline in vivo. Experimental-evolved tigecycline heteroresistant colonies were successfully obtained by exposing to concentration of tigecycline at usual therapy of tigecycline (serum concentration of 0.1 mg/L). Heteroresistant phenotypes were stable, and the minimal inhibitory concentration sustained at resistant after 7 days serially passed in tigecycline-free medium. Frequency of heteroresistant subpopulation ranged from 7.0 × 10
conclusionThe findings reveal the phenomenon where tigecycline may induce resistance in initially susceptible strains during clinical treatment, associated with several mutations of ramR, acrR and rpsJ, resulting in treatment failure. The heteroresistant strains induced by low concentrations of tigecycline in vitro provide a perspective for exploring the molecular mechanisms of tigecycline resistance in K. pneumoniae. Combination with other antibiotics like polymyxin B and amikacin would show synergistic effects in evading regrowth of resistant subpopulations.
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