ArticleNature microbiology2019
The high prevalence of antibiotic heteroresistance in pathogenic bacteria is mainly caused by gene amplification.
Article in Nature microbiology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 257 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
257 citing papers in PubMed, 1 synthesis or guideline pooled it, 400 citations in OpenAlex.
- Global trends and research profile of antibiotic heteroresistance: a bibliometric and visual analysis.Frontiers in microbiology · 2026Pooled it
- Dual population-level processes contribute to polyclonal ceftiofur heteroresistance in swine-derivedVirulence · 2026Article
- Within-patient carbapenem heteroresistance inCurrent research in microbial sciences · 2026Article
- Genomic and Clinical Features Associated With Reduced Susceptibility to Cefiderocol and Cross-Resistance to β-Lactam/β-Lactamase Inhibitors in a Global Cohort of Pseudomonas aeruginosa.The Journal of infectious diseases · 2026Observational
- Bacterial strategies for surviving antibiotics during urinary tract infection: could uropathogenic Escherichia coli be persisters?Nature reviews. Urology · 2026Review
- Heteroresistance tolerance and persistence in antibiotic treatment failure.Folia microbiologica · 2026Review
- Population size modulates the transition from gene amplification-mediated heteroresistance to stable resistance.npj antimicrobials and resistance · 2026Article
- Transcriptional regulation drives heteroresistance inmSystems · 2026Article
- ISmLife · 2026Article
- Combinatorial action of regulatory systems generates colistin heteroresistance.Science advances · 2026Article
- Heterogeneity in the response to the metabolic environment drives fosfomycin heteroresistance.Nature communications · 2026Article
- Non-uniform susceptibility profiles observed inMicrobiology spectrum · 2026Article
- Non-canonical gene amplifications facilitate adaptive evolution in bacteria.Nature microbiology · 2026Article
- A lab-on-a-silicon-chip platform for all-electrical antibiotic susceptibility tests with a sample-to-results time within 20 minutes.Science advances · 2026Article
- Bacterial heteroresistance mechanisms, dynamics, and emerging diagnostic approaches.Bioscience reports · 2026Review
- Biofilm Formation and the Pore ProteinsAntibiotics (Basel, Switzerland) · 2026Article
- Beyond susceptibility results: understanding the clinical and diagnostic burden of bacterial heteroresistance.Molecular biology reports · 2026Review
- Resistance potentiators: Evolutionary catalysts of antibiotic resistance.PLoS biology · 2026Article
- Beyond resistance and tolerance: rethinking evolutionary responses to antibiotics from the perspective of individual bacterial cells.Nature communications · 2026Review
- Clinical characteristics and temporal trends of meropenem and piperacillin/tazobactam heteroresistance in Pseudomonas aeruginosa isolates.Annals of clinical microbiology and antimicrobials · 2026Article
197 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
When choosing antibiotics to treat bacterial infections, it is assumed that the susceptibility of the target bacteria to an antibiotic is reflected by laboratory estimates of the minimum inhibitory concentration (MIC) needed to prevent bacterial growth. A caveat of using MIC data for this purpose is heteroresistance, the presence of a resistant subpopulation in a main population of susceptible cells. We investigated the prevalence and mechanisms of heteroresistance in 41 clinical isolates of the pathogens Escherichia coli, Salmonella enterica, Klebsiella pneumoniae and Acinetobacter baumannii against 28 different antibiotics. For the 766 bacteria-antibiotic combinations tested, as much as 27.4% of the total was heteroresistant. Genetic analysis demonstrated that a majority of heteroresistance cases were unstable, with an increased resistance of the subpopulations resulting from spontaneous tandem amplifications, typically including known resistance genes. Using mathematical modelling, we show how heteroresistance in the parameter range estimated in this study can result in the failure of antibiotic treatment of infections with bacteria that are classified as antibiotic susceptible. The high prevalence of heteroresistance with the potential for treatment failure highlights the limitations of MIC as the sole criterion for susceptibility determinations. These results call for the development of facile and rapid protocols to identify heteroresistance in pathogens.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.