Background Invasive group B streptococcus (GBS) infections in adults are increasing, particularly in the elderly with underlying diseases. The clinical manifestations and serotype distribution differ with neonatal infections, however the molecular characteristics of the bacteria are not well described in adults. This study aimed to investigate the molecular characteristics and antimicrobial resistance of GBS in adults with invasive bacterial infection over a 10-year period in Korea. Methods GBS isolates previously obtained from adults with invasive GBS disease at Seoul National University Bundang Hospital (2006-2015) were analyzed for capsular serotype, multilocus sequence type (ST), antimicrobial susceptibility and resistance genes. Antibiotic susceptibility testing was done by E-test and macrolide resistance genes were detected using PCR amplification. Results A total of 74 isolates were included in the analysis. The most common serotype was Ib (31.1%), followed by III (21.6%), V (20.3%), Ia (12.2%) and VI (12.2%). Thirteen STs were found; ST1 (32.4%), ST10 (14.9%), ST19 (12.2%) and ST23 (8.1%) were most prevalent. The dominant serotype capsule expressed by ST1 was serotype V, ST 10 were all serotype Ib, ST19 were all serotype III, and ST23 were all serotype Ia. Erythromycin resistance was found in 35.1% and levofloxacin resistance was found in 31.1%. Dominant strains in erythromycin resistance were ermB-positive ST1 serotype V (n=13/15, 86.7%) and ermA-positive ST335 serotype III (n=4/4, 100%). Dominant strains in levofloxacin resistance were ST10 serotype Ib (n=11/11, 100%) and ST654 serotype Ib (n=3/3, 100%). Conclusions Serotype Ib, III and V were most common in adults, which shows discrepancy with recent reports of serotype distribution among young infants in Korea where serotype III, V and Ia predominated. All ST10 serotype Ib strains and ST654 serotype Ib strains had levofloxacin resistance. The difference in serotype distribution compared with children may be associated with the selective pressure of antibiotic resistant clones.