This study reveals high lincosamide resistance in southern China's GBS, highlighting resistance gene spread and co-transfer mechanisms.
Lincosamides serve as alternative therapeutic agents for penicillin-allergic patients with Streptococcus agalactiae [group B Streptococcus (GBS)] infections, but the escalating antibiotic resistance has severely compromised their clinical efficacy. This study investigated the epidemiological characteristics of antibiotic resistance and the co-transfer mechanisms of lincosamide resistance genes lsa(E) and lnu(B) in 631 clinical GBS isolates from southern China. The results showed that 98.3% of isolates carried at least one antibiotic resistance gene, with lincosamide resistance genes detected in 76.1% of isolates. The lsa(E) and lnu(B) were identified as prevalent lincosamide resistance determinants alongside erm(B), with 18.7% of isolates co-carrying lsa(E) and lnu(B), and double-positive isolates predominantly distributed in high-risk clonal complexes (CCs): CC10 (15.4%), CC17 (21.7%), CC19 (17.9%) and CC103 (35.5%). Genomic analyses revealed that lsa(E)-lnu(B) formed composite resistance modules by integrating into resistance gene clusters within integrative and conjugative elements (ICEs), with insertion sequence-mediated mobilization increasing their dissemination risk. In CC10 and CC17, ICESag37 served as the primary ICE harbouring lsa(E)-lnu(B), while novel genetic contexts for lsa(E)-lnu(B) were identified in CC19, CC23 and CC103. This study highlights the high prevalence of lsa(E)-lnu(B) resistance clusters in GBS clinical isolates from southern China and their ICE-mediated dissemination mechanisms, providing critical molecular epidemiological evidence for resistance surveillance and precision therapeutic strategies.
No takes yet. Share an insight, caveat, or question.
Wu et al. (2025) studied this question.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: