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Investigates how CRISPR1 and virulence genes influence dominance of ST10 in neonatal infections in China, suggesting implications for treatments.
Introduction Streptococcus agalactiae (Group B Streptococcus, GBS) is a major pathogen of neonatal infections worldwide, with significant geographical variation in its prevalent sequence types (STs). In Shanxi, China, ST10 has emerged as the dominant lineage in perinatal infections, yet the mechanisms underlying its regional dominance remain unclear. This study aimed to investigate the molecular epidemiological basis for the predominance of ST10 in this region. Methods We analyzed 55 clinical Streptococcus agalactiae isolates (21 invasive, 34 colonizing) collected from a hospital in Shanxi, China. Multilocus sequence typing (MLST) was performed to determine sequence types. Virulence genes and the CRISPR1 (clustered regularly interspaced short palindromic repeats, CRISPR) system were detected by polymerase chain reaction (PCR). Statistical analyses were conducted to assess associations between ST10, CRISPR1, and virulence gene carriage. Results ST10 accounted for 50.9% (28/55) of all isolates, predominating in both invasive (13/21, 61.9%) and colonizing (15/34, 44.1%) groups. Invasive ST10 strains universally carried the virulence genes cylE , hylB , scpB , and bca (100%) and exhibited complete erythromycin resistance mediated by ermB (100%). The CRISPR1 system was highly prevalent in ST10 isolates (26/28, 92.9%), and its presence was significantly associated with the virulence genes cylE (69.8% vs 25.0%; P=0.014) and hylB (62.8% vs 16.7%; P=0.012). Discussion The findings delineate a "high-virulence/controlled-resistance" phenotype in the locally dominant ST10, characterized by a conserved virulence gene, stable chromosomal ermB resistance, and a high prevalence of CRISPR1. This suggests CRISPR1 may contribute to the fitness of the ST10 lineage by stabilizing chromosomal virulence and resistance determinants while potentially restricting plasmid acquisition. This study establishes CRISPR1 as a potential key driver of ST10 adaptation and a possible predictive marker for monitoring high-risk clones, providing a rationale for regionally tailored prophylaxis strategies.
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Qiao et al. (2026) studied this question.
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