Abstract
Staphylococcus epidermidis (S. epidermidis), usually a harmless skin bacterium, can become an opportunistic pathogen in newborns, particularly those with risk factors like premature membrane rupture. Although it commonly causes late-onset sepsis, its association with neonatal acute respiratory distress syndrome (NARDS) is rare. This report describes a unique case of NARDS in a full-term newborn caused by S. epidermidis. The infant, born via cesarean at 40 2/7 weeks with a 30.5-hour membrane rupture, developed severe respiratory failure shortly after birth, necessitating mechanical ventilation. Initial treatment with penicillin and cefotaxime was ineffective, and by day 3, the infant's condition worsened, showing respiratory distress, petechial rashes, and high inflammatory markers. Treatment was changed to vancomycin and meropenem, with the addition of intravenous immunoglobulin and two doses of pulmonary surfactant. Metagenomic next-generation sequencing (mNGS) confirmed S. epidermidis in the airway secretions. The patient was discharged after 19 days with a diagnosis of NARDS, intrauterine infectious pneumonia, neonatal air leak syndrome, type II respiratory failure, neonatal sepsis, and congenital heart defects. In conclusion, S. epidermidis is a novel pathogen capable of causing NARDS in high-risk infants with prolonged membrane rupture. The proposed mechanisms-including surfactant dysfunction and biofilm-associated virulence-are supported by experimental literature and are consistent with the clinical phenotype observed in our patient, though direct confirmation requires further study. Notably, skin symptoms like erythematous rash and petechiae may indicate invasive S. epidermidis infection, especially in cases of respiratory distress with skin symptoms following premature rupture of membranes. Moreover, mNGS is vital for pathogen identification when traditional cultures fail.