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

TL;DR

A study in China found that a specific strain of Mycoplasma pneumoniae became dominant in children with pneumonia after a decline during the pandemic, and this strain is resistant to certain antibiotics.

Contribution

The study identifies a clonal replacement event by the P1-1/ST3 lineage in pediatric Mycoplasma pneumoniae cases in China, highlighting its association with increased disease severity and macrolide resistance.

Findings

The P1-1/ST3 lineage increased from 41.9% to 84.0% of cases between 2021 and 2024.

The lineage is associated with higher severity of disease and carries macrolide resistance.

Genomic analysis revealed reduced diversity and enrichment of replication/recombination/repair functions in the dominant clade.

Abstract

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.

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.

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 susceptibility to tetracycline and levofloxacin was retained.

The 2023–2024 resurgence coincided with clonal replacement by P1-1/ST3 in a setting of fixed macrolide resistance and an increase in severe pediatric disease. Given the retrospective, culture-based design, this should be interpreted as a temporal association rather than evidence that ST3 intrinsically caused more severe disease. These findings support consideration of non-macrolide agents in similar high-resistance settings and motivate prospective genomic-clinical surveillance.

Figures