Bloodstream infections caused by Staphylococcus epidermidis are among the most frequent and serious infections in neonatal intensive care units (NICU), being responsible for high rates of morbidity and mortality. However, how S. epidermidis prevails, disseminates and evolves to cause outbreaks in NICU is poorly understood. We aimed to understand what is the genomic basis of S. epidermidis outbreaks in NICU to provide guidelines for a better infection control. We collected all S. epidermidis isolated from newborn blood cultures admitted to a hospital NICU in Brazil over one-year and compared their genomes. The S. epidermidis infection incidence rate was 1.17 per baby-year. 83,64% of S. epidermidis were resistant to methicillin (MRSE) and 84,5% belonged to sequence type 2 (ST2) or related, carrying the staphylococcal cassette chromosome mec (SCCmec) type III or IVa. Single nucleotide polymorphisms (SNPs) analysis showed that S. epidermidis infections resulted from the co-existence of three ST2 transmission chains originating from distinct endemic sources (<50 SNPs). Each transmission chain was characterized by specific antibiotic resistance and virulence profile and content in staphylococcal cassette chromosome elements (SCCmec, SCC non-mec and ACME). During transmission, other mobile genetic elements were acquired/lost and mutations emerged in genes involved in adhesion, signal transduction, general metabolism, replication, recombination and repair. Tracking S. epidermidis transmission chains in the NICU will require a deep genomic analysis, combining bacterial genetic background and accessory genome. This study highlighted the need for the integration of whole genome sequencing as a key surveillance tool for infection control in NICUs.
Keywords: Antibiotic resistance; Genomic surveillance; Molecular epidemiology; Neonatal intensive care units (NICU); Nosocomial infections.
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