ArticleScientific reports2025
Multicenter analysis of the Mycoplasma pneumoniae resurgence in China 2023-2024.
Article in Scientific reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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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.
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Who cites it
6 citing papers in PubMed.
- Reporting macrolide-resistantJournal of clinical microbiology · 2026Review
- Multi-Omics Profiling Identifies Immune-Metabolic Signatures and Gut Microbial Biomarkers in a Murine Model ofBiology · 2026Article
- Beyond Ribosomal Mutations: Identification ofMicroorganisms · 2026Article
- Comparing differences in onset and clinical manifestations between children and adults withFrontiers in public health · 2026Article
- Clinical correlation of A2063G gene mutation in mycoplasma pneumoniae pneumonia in children: a retrospective analysis.Frontiers in pediatrics · 2026Article
- Macrolide Resistance ofInfection and drug resistance · 2026Article
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Authors and funding
11 authors.
Funding
Abstract
Mycoplasma pneumoniae is a significant cause of community-acquired pneumonia, with epidemic peaks occurring every 3–7 years. This multicenter, retrospective study analyzed 421 M. pneumoniae strains from four regions in China (Liaoning, Zhejiang, Wuhan, Guizhou) collected between November 2023 and January 2024, alongside 147 publicly available genomes, to investigate genotypic diversity and macrolide resistance during a recent resurgence. Infection rates in 2023 ranged from 19.4 to 35.9%, reflecting a significant increase compared to the reduced incidence (1.69%) during the COVID-19 pandemic (2020–2021). Genomic sequencing revealed that the P1-1 genotype predominated (87.3–94.9%), with P1-2c and a rare P1-2 g variant also detected. Macrolide resistance was observed in 97.1% of samples, primarily driven by the A2063G mutation in the 23 S rRNA gene, though 80% of P1-2 strains lacked resistance mutations. Phylogenetic analysis, including sequences from Beijing, Shenzhen, Suzhou, and Taiwan, indicated widespread circulation of macrolide-resistant P1-1 strains since 2016. No significant differences in bacterial load or blood parameters were observed between genotypes or resistance profiles. The resurgence aligns with global trends, with P1-1 dominance and high macrolide resistance complicating treatment, particularly in children. These findings highlight the need for ongoing surveillance, updated treatment guidelines, and alternative therapeutic strategies to address the challenges posed by macrolide-resistant M. pneumoniae. Continuous monitoring of genotypic variations and resistance patterns is essential to inform public health strategies and improve clinical outcomes.
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