Genomic surveillance of the pneumonia outbreak caused by Mycoplasma pneumoniae among patients in Russia from January 2024 to June 2025.

BACKGROUND

Mycoplasma pneumoniae (MP) is one of the major pathogens that causes respiratory tract infections, including community-acquired pneumonia (CAP). The aim of the current study was to conduct molecular genetic surveillance of an outbreak of pneumonia caused by MP in various regions of the Russian Federation between January 2024 and June 2025.

METHODS

MP, viral and bacterial co-infections were detected in 482 nasopharyngeal swabs from patients with CAP using real-time PCR method. To investigate the mutations associated with resistance to macrolides and quinolones we describe the development and usage of primer panels for the complete mgpA, 23S, parC, parE, gyrA, gyrB genes followed by high-throughput sequencing. To support the results of PCR for MP we applied the ELISA for 75 serum samples.

RESULTS

MP was confirmed in 81.5% samples by real-time PCR and in 69.3% samples by ELISA. Bacterial co-infections were identified in 27.8% samples. H. influenzae was the most prevalent, detected in 19.7% samples, followed by S. pneumoniae (13.1%) and C. pneumoniae (0.8%). The most prevalent viral co-infections were RSV (16.2%), RV (14.7%), and hPIVs (9.5%). The A2063G mutation associated with macrolide resistance was found in 23% samples. Point mutations, A2064G and A2064C, were detected in 6 samples (1,8%). No significant mutations associated with resistance to quinolones were identified according to the sequencing of complete parC, parE, gyrA, gyrB genes. The phylogenetic analysis revealed that the mgpA gene sequences formed two distinct clades, 97.2% were classified as P1 type 1, while the remaining 2.8% were classified as P1 type 2.

CONCLUSION

This study demonstrates a fundamental shift in the epidemiology of MP in the post-COVID-19 era, characterized by a transition from cyclical epidemics to year-round endemic circulation. We document increased disease severity, a dynamic profile of viral and bacterial co-infections, and significant geographic heterogeneity in macrolide resistance rates, which ranged from 0% to 50% across regions. The overall macrolide resistance rate was 23%, which is lower than previously reported. Furthermore, genotyping of the complete P1 adhesin gene revealed divergence, with a majority of sequences clustering within P1 type 1 and a minority within P1 type 2.