Genotypic and Phenotypic Characterization of Some psms Hypervirulent Clinical Isolates of Staphylococcus aureus in a Tertiary Hospital in Hefei, Anhui

Abstract

Background Staphylococcus aureus is a highly successful pathogen that can cause various infectious diseases, from relatively mild skin infections to life-threatening severe systemic diseases. The widespread pathogenicity of S. aureus is mainly due to its ability to produce many virulence factors that help destroy various host cells, causing disease. Our primary goal in this study was to explore the genes of highly virulent strains, to identify genes closely associated with high virulence, and to provide ideas for the treatment of infection by highly virulent clinical strains. Results This study collected 221 clinical strains from The First Affiliated Hospital Of The University of Science and Technology of China (USTC); their hemolytic abilities were tested. Eight isolates were selected based on their highly hemolytic ability and tested their hemolytic activity again; their phenotypes and gene sequences were also explored. Whole-genome sequencing (WGS) showed six plasmids (pN315, pNE131, pSJH901, pSJH101, SAP106B, and MSSA476), eight antibiotic resistance genes [ blaR1, blaI, blaZ, mecA, erm(C), erm(T), tet(38 ), and fosB-Saur ] and seventy-two virulence related genes. Three highly virulent strains, namely X21111206, 21092239, and 21112607, were found according the Galleria mellonella infection model. Therefore, we selected 10 representative virulence genes for qRT-PCR: psmα, psmβ, hlgA, hlgB, hlgC, hla, clfA, clfB, spa , and sak . Among them, the expression levels of psmα and psmβ , the three isolates, were significantly higher than the positive control NCTC8325. Conclusion Significant differences appear in the expression of virulence genes in the highly virulent strains, particularly the psmα and psmβ , It may be that the high expression of psm gene is the cause of the high virulence of Staphylococcus aureus . We can reduce the pathogenicity of Staphylococcus aureus by inhibiting the expression of psm gene, which may provide a strong basis for psm as a new target for clinical treatment of S. aureus infection.