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Clonal replacement by a P1-1/ST3 lineage in pediatric Mycoplasma pneumoniae, Jinan, China, 2021-2024

M. Fang, Xiao Wang, Xiao-long Yu, Jianmei Yu, Luo Yuan, Shuang-Yin Wang, Haijian Zhou, Ti Liu et al.

Frontiers in Cellular and Infection Microbiology, 2026

1 citation

Abstract

INTRODUCTION: After a prolonged lull during COVID-19 non-pharmaceutical interventions, Mycoplasma pneumoniae activity re-emerged in 2023 in multiple regions; in China this occurred against a backdrop of very high macrolide resistance. We conducted a retrospective single-center study of pediatric M. pneumoniae pneumonia in Jinan, comparing a pre-resurgence period (2021) with 2023-2024.

METHODS: Clinical data were linked to whole-genome sequencing of 227 cultured isolates. We assessed lineage composition and relatedness using core-genome phylogenetics and SNP-threshold networks, and compared diversity and pan-genome functional profiles across major clades. Phenotypic antimicrobial susceptibility testing was performed.

RESULTS: The proportion of severe cases increased from 7.4% (2021) to 19.9% (2024). Over the same interval, the P1-1/ST3 lineage rose from 41.9% to 84.0%, displacing previously co-circulating lineages. Core-genome analyses indicated reduced diversity and a compact ST3 cluster within the T1-3R subclade of the P1-type 1 lineage (EC1 clone), alongside a smaller P1-type 2/T2-2 (EC2/ST14) clade. Using a ≤11-SNP threshold, 74% of isolates fell within the largest connected component. Pan-genome comparisons suggested enrichment of replication/recombination/repair functions in T1-3R, whereas canonical adhesion factors and the CARDS toxin were conserved. All isolates carried the 23S rRNA A2063G substitution with phenotypic macrolide resistance, while in vitro…

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