ArticleFrontiers in cellular and infection microbiology2026
Adaptive microevolution in CC17
Article in Frontiers in cellular and infection microbiology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Background: The hypervirulent CC17 GBS is a major cause of neonatal invasive disease. Although this lineage can acquire mutations during host adaptation, the functional significance of such microvariations for bacterial pathogenesis remains unclear. Methods: The GBS strains were isolated from a mother-neonate pair, with clinical data obtained from electronic medical record. MALDI-TOF MS was used for species identification. Antimicrobial susceptibility testing was performed using K-B method and interpreted by CLSI criteria. Serotyping and MLST were used for molecular epidemiological analysis. Growth curve, hemolysin activity, serum inhibition and hyaluronic acid survival assays were performed to evaluate phenotypic differences between strains. Cell invasion assays and Results: A total of 5 GBS strains were collected and identified, and all were susceptible to penicillin, but resistant to clindamycin and erythromycin. The strains could be classified into ST17 and ST2247. The two types of strains showed no significant differences in growth curve, hemolysis activity, or serum inhibition. In hyaluronic acid solution, the ST2247 strain exhibited higher viability compared to the ST17 ( Conclusion: ST17 GBS can experience microevolution within maternal and infant hosts, evolving through minor genomic mutations into new strains. Variations in
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