No abstract

Streptococcus agalactiae (Group B Streptococcus, GBS) is a pathogen which causes neonatal sepsis, meningitis, and invasive infections in the elderly and people with medical conditions (1,2). Although β-lactams are prescribed as first line drugs for the treatment and prevention of GBS infections, in case of patients with penicillin-allergies, macrolides and lincosamides are often prescribed for the same (1,2). However, macrolide and lincosamide resistance rates in GBS have been increasing worldwide (3-5). Macrolide resistant Streptococcus spp. has the following 2 major phenotypes: macrolides, lincosamides, streptogramin B (MLSB) and M (6,7). The MLSB phenotype confers a broad resistance to macrolides, lincosamides, and streptogramin B, whereas the M phenotype confers resistance to macrolides, but not to lincosamides and streptogramin B. In addition, an L phenotype also exists, which confers resistance to lincosamides, but not to macrolides (7). A macrolide resistance gene (erm) encoding erythromycin ribosomal methylase, confers typical MLSB phenotype (8). However, in the present study, 3 clinical ermB-PCR-positive isolates of GBS with L phenotype were isolated in Korea and the mechanisms