We evaluated the effect of macrolide-resistant mutations in the Mycoplasma pneumoniae 23S rRNA gene on the severity of lower respiratory tract infections in immunocompetent young adults treated at the Smolensk Military Hospital between 25 October 2017, and 17 November 2021. All analyzed cases represented a non-severe infection of the lower respiratory tract: 44 case histories with community-acquired pneumonia and 20 cases with acute bronchitis. The presence of mutations in the gene 23S rRNA of M. pneumoniae was determined with standard Sanger sequencing. The macrolide-resistant genotype was found in 4/44 (9.1%) of the samples of the patients with pneumonia and in 3/20 (15%) of the samples of the patients with acute bronchitis. The analyzed cases with identified M. pneumoniae carrying a mutation in the 23S rRNA gene did not show any differences in the clinical presentation in terms of disease severity caused by M. pneumoniae with the wild-type (WT) phenotype.

Objective. To evaluate effect of 23S rRNA gene mutations in Mycoplasma pneumoniae on severity of community-acquired pneumonia (CAP) in young adult patients. Materials and Methods. A total of 42 case histories of young adult patients with CAP treated at the Smolensk military hospital over the period of 25 October 2017 to 25 December 2019 were reviewed. «AmpliSens® Mycoplasma pneumoniae/Chlamydophila pneumoniae-FL» real-time PCR kit was used to detect M. pneumoniae from nasopharyngeal swabs collected prior to antimicrobial therapy. Testing for 23S rRNA gene mutations conferring macrolide resistance was performed by real-time PCR melt curve analysis (patent no. 2646123) and confirmed by DNA sequencing. Results. All patients had a clinical picture of non-severe CAP on hospital admission. All patients were treated with standard doses of azithromycin or clarithromycin. No respiratory failure or any other complications were observed. Macrolide-resistant genotype of M. pneumoniae was detected in 4 (9.5%) patients. Clinical, laboratory and radiological resolution of pneumonia in all cases occurred on day 10– 16, regardless of the presence of macrolide-resistant genotype. Conclusions. There were no differences in clinical course of severity between CAP caused by M. pneumoniae with 23S rRNA gene mutation and CAP caused by wild-type M. pneumoniae The presence of mutations in the 23S rRNA gene of M. pneumoniae did not worsen the clinical course of CAP.