Abstract
Streptococcus suis (S. suis) has emerged as an important zoonotic pathogen that can cause serious human infections. S. suis sequence type 1 (ST1) is predominant in sporadic human infections. However, few studies have characterized S. suis ST1 isolated directly from human clinical specimens.Streptococcus suis 366 was isolated from the cerebrospinal fluid (CSF) of a patient with purulent meningitis. Antimicrobial susceptibility testing and whole-genome sequencing were performed. Detailed functional annotations (CARD, VFDB, GO, KEGG, and COG), along with pangenome, phylogenetic, and comparative genomic analyses, were conducted using rigorously curated bioinformatics tools. The clinical strain belonged to ST1 and was resistant to erythromycin, clindamycin, and tetracycline. 5 mobile genetic elements were detected but no plasmids were detected. The resistance phenotype was consistent with those associated with 2 resistance genes (tet-(o) and ErmB). The isolate was predicted to be highly pathogenic and harboured 4 virulence genes (hasC, cpsF, neuB, and pavA). However, no resistance genes or virulence genes were identified on 5 mobile genetic elements. In the biological process category, terms related to ‘cellular process’ and ‘metabolic process’ were the most prominently enriched, suggesting that the gene set is primarily involved in cellular adaptation. The most significantly enriched pathway was the ‘ko02010 ABC transporter pathway’. The functions of the genes in the strain are concentrated mainly in categories such as E (amino acid transport and metabolism), G (carbohydrate transport and metabolism), J (translation, ribosomal structure, and biogenesis), and R (general function prediction only). Pangenome analysis revealed that ST1 and ST7 shared a large number of core genes. Phylogenetic and comparative analysis revealed that ST1 and ST7 were closely related and that there was an evolutionary connection. This study provides significant insights into the genomic characteristics associated with S. suis ST1, enhancing the understanding of this zoonotic pathogen from human CSF. Furthermore, the findings enhance the understanding of the evolutionary connection between the ST1 and ST7 strains. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1038/s41598-026-41475-6.