A Decade-Long Nationwide Surveillance of Antimicrobial Resistance in Coagulase-Negative Staphylococci in China (2014-2023) and Characterization of a Rare Teicoplanin-Resistant Staphylococcus haemolyticus.

INTRODUCTION: Coagulase-negative staphylococci (CoNS) have emerged as important clinical pathogens. In this study, CoNS isolates were continuously collected across 21 provinces in China between 2014 and 2023 to characterize distribution, antimicrobial susceptibility profiles, and temporal trends. METHODS: A total of 11,277 CoNS isolates were subjected to minimum inhibitory concentration determination for commonly used antibiotics using the microdilution method. In addition, a teicoplanin-resistant Staphylococcus haemolyticus(S. haemolyticus) strain was further characterized by transmission electron microscopy, biofilm formation assays, and evaluation of cell wall synthesis. RESULTS: Staphylococcus epidermidis (S. epidermidis) and Staphylococcus hominis predominated in bloodstream infections (BSIs), whereas S. epidermidis and Staphylococcus capitis (S. capitis) were most common in cerebrospinal fluid (CSF) infections. Over time, S. epidermidis and Staphylococcus lugdunensis increased in BSIs, while S. capitis increased in CSF infections. Bloodstream isolates and CSF isolates exhibited high resistance rates. From 2014 to 2023, the proportion of methicillin-resistant CoNS decreased significantly in both BSIs and CSF isolates. Vancomycin susceptibility remained stable throughout the study period. Notably, a rare teicoplanin-resistant S. haemolyticus isolate was identified, exhibiting significant cell wall thickening and enhanced biofilm formation, without detectable glycopeptide resistance genes. CONCLUSION: A decade-long nationwide multicenter surveillance revealed the epidemiological patterns and temporal trends of CoNS infections in China. Despite high resistance to multiple antibiotic classes, CoNS remained consistently susceptible to glycopeptides. A teicoplanin-resistant isolate highlighted a non-classical resistance mechanism involving cell wall thickening and enhanced biofilm formation.