ArticleBMC infectious diseases2025
Genomic insights into the spread of methicillin-resistant Staphylococcus aureus involved in ear infections.
Article in BMC infectious diseases, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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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
2 citing papers in PubMed.
- Phylogenomic analysis of a methicillin-resistantMicrobial genomics · 2026Article
- Fluoroquinolone resistance without fluoroquinolone use; the genie is truly out of the bottle.Frontiers in microbiology · 2026Review
Corrections and comments
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Authors and funding
10 authors.
Funding
Abstract
backgroundMethicillin-resistant Staphylococcus aureus (MRSA) is a major pathogen causing ear infections. However, genomic epidemiology and determinants influencing transmission of ear infections associated MRSA (EIA-MRSA) in community remain unknown.
methodsIn 2020-2021, 105 EIA-MRSA isolates were collected and sequenced from outpatients across different households in Shanghai, China. Antimicrobial susceptibility testing, core genome MLST, and phylodynamic analyses were conducted to characterize EIA-MRSA dissemination.
resultsQuinolone resistance was identified as a risk factor for EIA-MRSA spread (OR 9, [95% CI 3-31]). The ST764 clone and two subclones of ST22-PT hypervirulent clone have developed an extensive quinolone-resistant (eQR) phenotype, conferring additional resistance to advanced quinolones due to the accumulation of four mutations in gyrA (S84L and either S85P, E88K, or E88G) and parC (S80F and either E84K or E84G). These ST764- and ST22-PT-eQR isolates were highly transmissible and showed increased resistance to other commonly used antimicrobials, posing potential high-risk clones. The eQR phenotype may be inherent to the ST764 lineage, which emerged in the late 1980s, coinciding with the widespread fluoroquinolone usage. The ST22-PT-eQR subclones emerged in around 2017 and are accumulating resistance genes.
conclusionVigilance is crucial for eQR high-risk clones, particularly the convergent ST22-PT-eQR subclones that accumulate resistance and virulence traits, posing risks for ear infections. CLINICAL TRIAL NUMBER: Not applicable.
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