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Introduction Staphylococcus aureus sequence type (ST) 672 is a pathogenic clone first identified in Asia, associated with invasive infections in healthy individuals and outbreaks in hospitals and the community. In Mexico, this clone was reported in 2022 as a cause of osteoarticular infections in children; however, its virulence and resistance profiles remain unknown. Therefore, the aim of this study was to phenotypically and genomically characterize S. aureus ST672 isolates obtained from invasive paediatric infections at a tertiary-care hospital in Mexico. Methods Eight S. aureus ST672 isolates from patients at the National Institute of Paediatrics (INP) were included. Antimicrobial susceptibility testing and the induction of small colony variants (SCV) phenotype were performed. Whole-genome sequencing was carried out using Illumina technology. Bioinformatics tools were used to identify resistance and virulence genes, as well as mutations in their regulatory regions and mobile genetic elements. Twenty-five genomes from public databases were included for phylogenetic comparison. The clinical course of patients was described. Results All S. aureus ST672 isolates were methicillin-susceptible and showed a reversible SCV phenotype; the bla Z gene was detected in six isolates. Adhesins atl, efb, ebp, fnb A/B , sdr C/D/E, ica A/B/C/R were identified in all isolates, as well as agr operon type I. The pvl gene was detected in six isolates. Additionally, five carried a mobilizable plasmid, pN315-like. All strains harboured an intact ϕSa6-like prophage. The luk SF-PV operon was found in the ϕSa2/ϕSa2-like prophage. Mexican strains formed a single clade and, unlike other genomes, carried the luk SF-PV. Seven infections were community-acquired and showed no evidence of a local outbreak. Conclusions The methicillin-susceptible S. aureus (MSSA) ST672 clone represents a community lineage with genomic features associated with invasion and emergent persistence in Mexico and shows the capacity to adapt to the hospital environment. These findings support the need for genomic surveillance of MSSA clones.
Juárez-Hinojos et al. (Fri,) studied this question.