Correction: Two Streptococcus agalactiae ST283 invasive infections in Portugal raise the possibility of the emergence of this unusual lineage in Europe

Correction on: Martins ER, Forofontov M, Mota Freitas J, Melo-Cristino J, Ramirez M and Portuguese Group for the Study of Streptococcal Infections (2026) Two Streptococcus agalactiae ST283 invasive infections in Portugal raise the possibility of the emergence of this unusual lineage in Europe. Front. Microbiol. 16:1712362. doi: 10.3389/fmicb.2025.1712362 Adding/removing text state the error that was made. In the published article, there was an error in the Discussion section, 3 rd paragraph, regarding the attribution of fluoroquinolone resistance-associated QRDR mutations. The article stated that mutations gyrA S81L and parC S79Y had been previously reported in ST283 isolates by Ouancharee et al. (2025). However, in that study these mutations were identified in other Streptococcus agalactiae lineages and not in ST283 isolates. The paragraph read: The detection of fluoroquinolone resistance-associated QRDR mutations in our isolates is also noteworthy in the context of ST283 epidemiology. Mutations such as gyrA S81L and parC S79Y, previously described in resistant human ST283 isolates (Ouancharee et al., 2025) and in enrofloxacin-resistant fish-derived strains (Lukkana et al., 2016), are known to confer high-level fluoroquinolone resistance. Given the widespread use of enrofloxacin in freshwater aquaculture in SEA and the established role of raw freshwater fish consumption in ST283 transmission, the presence of these mutations highlights the potential for cross-sector selection, particularly as fluoroquinolones are rarely used to treat human GBS infections and underscores the importance of sustained genomic surveillance to detect and monitor resistant ST283 lineages.The sentence has been corrected to clarify that while these substitutions are established fluoroquinolone resistance determinants in S. agalactiae, their presence in ST283 isolates had not been previously documented in that study.A correction has been made to the section Discussion, 3 rd Paragraph: The detection of fluoroquinolone resistance-associated QRDR mutations in our isolates is noteworthy in the context of ST283 epidemiology. Substitutions such as gyrA S81L and parC S79Y are well-established determinants of high-level fluoroquinolone resistance in GBS, having been described in resistant human isolates from multiple lineages (Ouancharee et al., 2025) and in enrofloxacin-resistant fish-derived strains from aquaculture settings (Lukkana et al., 2016). These mutations are present in our isolates as well as other isolates recovered from humans in SEA and The Netherlands (Figure 1). Given the widespread use of enrofloxacin in freshwater aquaculture in SEA and the established role of raw freshwater fish consumption in ST283 transmission, these findings highlight the potential for cross-sector selection, particularly as fluoroquinolones are rarely used to treat human GBS infections and underscore the importance of sustained genomic surveillance to detect and monitor resistant ST283 lineages.for a reason not seen here, please contact the journal's editorial office.