Genomic epidemiology of Group B Streptococcus colonization among pregnant women in Japan, 2021–2023

Chizu Nishi; Hirofumi Ohtaki; Masaki Karino; Hiromi Uekita; Ayumi Sano; Tetsuya Kobayashi; Susumu Kaino; Yoshiki Sakamoto; Satoshi Nakano

doi:10.1371/journal.pone.0354799

Abstract

Group B Streptococcus (GBS) colonization in pregnant women is a major risk factor for neonatal diseases; however, molecular epidemiological studies on GBS in Japan remain limited. We characterized 219 GBS isolates recovered from vaginal screening cultures at a general hospital in Osaka Prefecture, Japan between 2021 and 2023. Capsular type, clonal complex/sequence type (CC/ST), virulence factors (pilus islands, Alp family, Srr1/Srr2, and HvgA), and antimicrobial resistance determinants were analyzed using whole-genome sequencing. The predominant lineages were CC19 (27.9%), CC23 (21.9%), and CC1 (21.0%), whereas the hypervirulent CC17 lineage accounted for only 5.5% of isolates. Capsular type Ia, III, and V comprised >60% of the isolates. PI-1/PI-2a (58.0%) was the predominant pilus profile, and rib (35.2%) was the most frequent Alp family gene. The hypervirulence-associated markers hvgA and srr2 were confined to capsular types III/CC17 and IV/CC452. All isolates were susceptible to β-lactams and vancomycin, whereas resistance to macrolides, clindamycin, and levofloxacin was observed at varying frequencies. These findings provide a pre-vaccine molecular baseline for maternal GBS carriage in Japan and highlight srr2-positive CC452 as a potential emerging lineage of concern.

Citation: Nishi C, Ohtaki H, Karino M, Uekita H, Sano A, Kobayashi T, et al. (2026) Genomic epidemiology of Group B Streptococcus colonization among pregnant women in Japan, 2021–2023. PLoS One 21(7): e0354799. https://doi.org/10.1371/journal.pone.0354799

Editor: Baochuan Lin, Defense Threat Reduction Agency, UNITED STATES OF AMERICA　

Received: March 19, 2026; Accepted: July 13, 2026; Published: July 30, 2026

Copyright: © 2026 Nishi et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Data Availability: All relevant data are within the paper and its Supporting information file.

Funding: Satoshi Nakano was supported by the Japan Agency for Medical Research and Development (AMED) under grant numbers JP22fk0108612 and JP22fk0108540. The funder had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.

Competing interests: The authors declare that there are no conflicts of interest regarding the publication of this paper.

Abbreviations: GBS, Group B Streptococcus; CC, clonal complex; ST, sequence type; EOD, early-onset disease; LOD, late-onset disease; Alp, alpha-like protein; HvgA, hypervirulent GBS adhesin; PI, pilus island.

1. Introduction

Group B Streptococcus (GBS; Streptococcus agalactiae) colonizes the gastrointestinal and genital tracts of approximately one in five pregnant women and is a leading cause of neonatal sepsis and meningitis worldwide [1,2]. Neonatal GBS disease is classified by age of onset into early-onset disease (EOD, 0–6 days), late-onset disease (LOD, 7–89 days), and very-late-onset disease (≥90 days) [3]. Intrapartum antibiotic prophylaxis (IAP), implemented on the basis of antenatal screening, substantially reduces EOD by interrupting vertical transmission during labor. However, IAP does not prevent LOD, which typically arises through various postnatal routes of infection [1].

Maternal vaccination is being pursued to close this prevention gap. Hexavalent capsular polysaccharide–conjugate vaccines (GBS6) targeting globally dominant capsular types have shown favorable immunogenicity in phase 1/2 studies in non-pregnant adults and phase 2 studies in pregnant women [4,5]. In addition, protein-based vaccines targeting conserved alpha-like protein (Alp) family surface proteins (e.g., MinervaX GBS-NN/NN2) have progressed through phase 1 trials in healthy adult women [6,7].

Pre-licensure molecular epidemiological studies are essential for anticipating the vaccine impact and detecting potential capsular types or lineage replacements after vaccine introduction. Of particular interest are hypervirulent or emerging clones—most notably clonal complex (CC) 17, a lineage strongly associated with neonatal meningitis and LOD and characterized by hypervirulent GBS adhesin (HvgA) and the serine-rich repeat protein Srr2 [8–10], and CC452, an emerging capsular type IV lineage increasingly reported in carriage and invasive diseases that also harbors srr2 [11–13]. Among the maternal-colonizing isolates, characterization of capsular type, CC/sequence type (ST), virulence factors, and antimicrobial susceptibility profiles is critical for assessing vaccine antigen coverage and interpreting changes following vaccine implementation.

Although several studies have described maternal GBS colonization and related invasive disease in Japan, detailed molecular epidemiological data remain limited [14–18]. To address this gap, we conducted a molecular epidemiological study of 219 GBS isolates recovered from vaginal screening samples of pregnant women receiving antenatal care at a general hospital in Osaka Prefecture, Japan. We characterized capsular type distribution, population structure (CC/ST), major surface-antigen repertoires (pilus islands [PIs], Alp family, Srr1/Srr2, and HvgA), and antimicrobial susceptibility. These findings may complement reports from other regions and provide a pre-vaccine baseline for Japan to inform clinical prevention strategies and future vaccine evaluations.

2. Materials and methods

2.1. Ethics statement

This study was approved by the ethics committee of Mimihara General Hospital (Approval No. 202403-2-1) and the National Institute of Infectious Diseases (Approval No. 1512). Clinical and laboratory data related to maternal GBS screening were accessed for research purposes between 01/05/2024 and 28/06/2024. The study used anonymized clinical and laboratory data. The requirement for written informed consent was waived by the ethics committees, and informed consent was obtained using an opt-out approach.

2.2. Bacterial isolates and identification

Maternal GBS screening samples were collected between 11/09/2021 and 19/09/2023. During this period, GBS screening tests were performed in 1,461 women. The screening test was conducted in accordance with the ASM guideline, Guidelines for the Detection and Identification of Group B Streptococcus [19]. Pregnant women at 35–37 weeks of gestation were screened using vaginal-rectal swabs. Immediately after collection, the swabs were transported to the in-house laboratory and culture was initiated without delay. The swabs were first inoculated into Todd–Hewitt broth supplemented with colistin and nalidixic acid (Nikken Bio, Inc., Kyoto, Japan), a selective enrichment broth for GBS, and incubated aerobically at 35 °C overnight. The enrichment broth was then subcultured onto selective agar for GBS (Vi GBS agar; Eiken Chemical Co., Ltd., Tokyo, Japan) and incubated aerobically at 35 °C overnight according to the manufacturer’s instructions. All isolates were identified as S. agalactiae using matrix-assisted laser desorption/ionization time-of-flight mass spectrometry (MALDI Biotyper; Bruker Daltonics, Bremen, Germany).

2.3. Antimicrobial susceptibility testing and capsular typing

Minimum inhibitory concentrations and inducible clindamycin resistance were determined using the broth microdilution method with commercially prepared Dry Plate Eiken DP44 panels (Eiken Chemical Co., Ltd., Tokyo, Japan), according to the manufacturer’s instructions. Susceptibility breakpoints and interpretation of inducible clindamycin resistance were based on the Clinical and Laboratory Standards Institute document M100, 35th edition [20].

Capsular typing was performed using a GBS latex agglutination test kit, the ImmuLex™ Strep-B Kit (SSI Diagnostica, Hillerød, Denmark), according to the manufacturer’s instructions. The capsular types shown in Tables 1–3 and Fig 1 are based on the latex agglutination results.

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Table 1. Distribution of sequence types and capsular types by clonal complexes.

https://doi.org/10.1371/journal.pone.0354799.t001

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Table 2. Distribution of pilus island types and major surface protein-associated virulence genes.

https://doi.org/10.1371/journal.pone.0354799.t002

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Table 3. Distribution of antimicrobial susceptibility results for macrolides, clindamycin, minocycline, and levofloxacin by sequence type and capsular type.

https://doi.org/10.1371/journal.pone.0354799.t003

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Fig 1. Distribution of sequence types and capsular types on the goeBURST Full MST.

https://doi.org/10.1371/journal.pone.0354799.g001

2.4. Whole genome sequencing analysis

Genomic DNA was extracted using the QIAamp® DNA Mini Kit (QIAGEN, Hilden, Germany) according to the manufacturer’s instructions. Short-read DNA libraries for Illumina sequencing were prepared using the Enzymatic 5X Whole genome sequencing (WGS) Fragmentation Mix and 5X WGS Ligase Mix (BioStream Corp, Tokyo, Japan) together with an automated library preparation system Biomek i7 Workstation (Beckman Coulter Inc., Brea, CA, USA).

Paired-end 150-bp short-reads were generated using the NovaSeq X Plus platform (Illumina, San Diego, CA, USA). In silico multilocus sequence typing, antimicrobial resistance gene detection, and surface protein detection, including candidate vaccine targets, were performed using an in-house pipeline [21]. This pipeline included in silico capsular typing with GBS-SBG [22]. CCs were identified using the S. agalactiae database on the PubMLST.org website [23]. Genetic relationships among the identified STs were analyzed using the goeBURST Full MST algorithm implemented in PHYLOViZ 2.0 [24].

3. Results

3.1. Distribution of CCs, STs, and capsular types

Among the 1,461 study participants, GBS was detected in 273 women (18.7%). Of these, 219 isolates were preserved and subjected to subsequent analysis.

The distribution of CCs, STs, and capsular types among the 219 GBS isolates is summarized in Fig 1, and detailed data are presented in Table 1. The isolates were assigned to 31 STs, including seven novel STs, and grouped into nine CCs. CC19 was the most frequent lineage (n = 61, 27.9%), followed by CC23 (n = 48, 21.9%) and CC1 (n = 46, 21.0%). The hypervirulent lineage CC17 accounted for 12 isolates (5.5%) and ranked fifth overall.

The capsular type distribution was as follows: Ia, 50 (22.8%); Ib, 24 (11.0%); II, 25 (11.4%); III, 38 (17.4%); IV, 12 (5.5%); V, 51 (23.3%); VI, 6 (2.7%); VIII, 2 (0.9%); IX, 6 (2.7%); and non-typeable, 5 (2.3%). Among the 219 isolates, 14 (6.4%) showed discordant capsular typing results between latex agglutination and WGS-based analysis. These included six isolates identified as capsular type IX and five non-typeable isolates by latex agglutination, all of which were assigned to other capsular types by WGS-based analysis (S1 Table). The dominant CCs within each capsular type were CC23 for Ia, CC12 for Ib, CC19 and CC1 for II, CC17 and CC19 for III, CC452 for IV, and CC1 and CC19 for V. CC1 was represented across all capsular types except Ia, III, and IV.

Multilocus sequence typing identified 31 sequence types (STs) represented by nodes. The size of each node was proportional to the number of isolates on a logarithmic scale. The goeBURST Full MST algorithm was used to visualize the genetic relationships among STs based on their allelic profiles. Node colors distinguish sub-group founders (dark green) from other nodes (light blue). Colored sectors within each ST node indicate the distribution of capsular types (Ia, Ib, II, III, IV, V, VI, VIII, IX, and non-typeable [NT]). Links between nodes represent single-locus variants. Dashed lines delineate the nine identified clonal complexes (CCs).

3.2. Distribution of PI types and major surface protein-associated virulence genes

Sequencing statistics are shown in S1 Table. The average coverage (±standard deviation) was 412 (±135). Draft genome data are available under accession number PRJDB39678.

PI profiles were distributed as follows; PI-1/PI-2A (n = 127, 58.0%), PI-2A alone (n = 68, 31.1%), PI-2B alone (n = 16, 7.3%), and PI-1/PI-2B (n = 8, 3.7%). Within the Alp family genes, rib was the most common (n = 77, 35.2%), followed by bca (n = 53, 24.2%), alp1 (n = 46, 21.0%), and alp2/3 (n = 28, 12.8%); 15 isolates (6.8%) lacked all four of these Alp genes (Table 2).

Regarding serine-rich repeat adhesins, srr1 was detected in 170 isolates (77.6%) and srr2 in 21 isolates (9.6%). srr2-positive isolates were almost exclusively confined to CC17/capsular type III and CC452/ capsular type IV. The hypervirulence-associated adhesin gene hvgA was present in 11 isolates (5.0%), all belonging to CC17/ capsular type III (Table 2).

3.3. Antimicrobial susceptibility and resistance determinants

Antimicrobial susceptibility results and detailed resistance profiles are presented in Table 3 and S1 Table. All isolates were susceptible to β-lactams. In contrast, macrolide resistance was common: 123 isolates (56.2%) were resistant to erythromycin, and all erythromycin resistant isolates were also resistant to azithromycin. Among these isolates, the most frequently detected macrolide resistance determinant was ermB (64 isolates, 52.9%), followed by co-detection of mefA and msrD (32 isolates, 26.4%) and ermA (27 isolates, 22.3%). Macrolide resistance was frequent in ST1, ST10, ST17, ST23, CC19 and CC327.

Clindamycin resistance was observed in 82 isolates (37.4%), including 13 isolates exhibiting inducible resistance. Among isolates characterized as clindamycin-susceptible or clindamycin-intermediate, 8.7% displayed inducible resistance on confirmatory testing.

Minocycline resistance was observed in 156 isolates (71.2%). Among these isolates, tetM was the most frequently detected tetracycline resistance gene (122 isolates, 78.2%), followed by tetO (34 isolates, 21.8%). Among the ten capsular type III/ST17 isolates, six exhibited a characteristic profile comprising: ermB positivity, tetO positivity, PI-2B positivity, and absence of PI-1. Minocycline was included for epidemiological purposes to characterize tetracycline-class resistance phenotypes associated with resistance determinants such as tetM and tetO, rather than as a therapeutic option during pregnancy.

Levofloxacin resistance was observed in 50 isolates (22.8%) and was enriched in ST3, ST10, and ST19, as well as in capsular types Ib and V. Most levofloxacin-resistant isolates harbored two quinolone resistance-associated amino acid substitutions; GyrA S81L together with either ParC S79F or ParC S79Y.

4. Discussion

In this study, we characterized 219 colonizing GBS isolates from pregnant women in Osaka Prefecture with respect to CC/ST and capsular type distribution, virulence factors, and antimicrobial susceptibility. Detailed assessment of virulence factors provided insights into the characteristics of maternal colonizing strains and their potential to cause invasive diseases.

The CC lineage distribution observed in our isolates, predominantly CC19, CC23, and CC1, was consistent with findings from other maternal carriage studies in Japan. For example, Kawaguchiya et al. reported that CC19 (29%), CC23 (25%), and CC1 (17%) were the major lineages among pregnant women in Hokkaido [16]. Hypervirulent CC17 accounted for 5.5% of the isolates in our study, which is lower than the carriage rate of approximately 10% reported in previous studies [16,25]. Capsular type III accounted for 17.4% of all isolates, despite the relatively low frequency of CC17. This discrepancy is largely explained by the high prevalence of capsular type III/CC19 (ST335) isolates in our collection, a distribution pattern consistent with a previous report [16]. In contrast, invasive disease surveillance studies have consistently shown that CC17 predominates among isolates causing neonatal meningitis and LOD. For example, Takeuchi et al. identified CC17 as the leading clone among invasive cases in Chiba Prefecture [15]. In Japan, a recent nationwide surveillance study reported that 21.5% of infants with GBS meningitis develop neurodevelopmental sequelae [14]. Because capsular type III/CC17 accounts for the majority of neonatal GBS meningitis cases worldwide, these findings suggest that the hypervirulent CC17 clone is a major contributor to meningitis-associated neurological sequelae. Taken together, these observations indicate that although CC17 is carried by only a small proportion of pregnant women, it contributes disproportionately to neonatal diseases.

Recent epidemiological and genomic studies from other regions have highlighted both shared and region-specific features of GBS epidemiology. In Argentina, a national multicenter genomic study of human GBS isolates collected during 2014–2015 from invasive disease, urinary tract infections, and maternal colonization showed that capsular type Ia/CC23 and capsular type Ib/CC12 were the most prevalent lineages regardless of isolation source, whereas capsular type III/CC19 exhibited a high density of prophages, virulence factors, and antimicrobial resistance determinants [26]. In Brazil, recent genomic epidemiological analysis of GBS isolates from colonized pregnant women identified the neonatal disease-associated CC23 lineage as the predominant lineage [27]. In coastal Kenya, WGS analysis of maternal colonizing and neonatal disease isolates demonstrated a maternal colonization prevalence of approximately 12% and a substantial contribution of CC17 to both maternal colonization and neonatal disease [28]. In Western Australia, WGS of perinatal isolates collected from pregnant women during 2015–2017 and neonatal invasive isolates collected during 2012–2014 showed that the major clonal complexes were CC1, CC12, CC17, CC19, and CC23 [29]. These findings suggest that the major colonizing lineages observed in Japan partially overlap with global GBS populations, although their relative prevalence differs substantially among regions.

The detection of ST452, although limited in number, warrants special attention. This lineage, associated with capsular type IV and srr2 positivity, is internationally recognized as an emerging invasive clone. Campisi et al. demonstrated that capsular type IV/ST452 likely arose through large genomic recombination events between CC23 and the hypervirulent CC17 lineage [30]. Teatero et al. also identified ST452 among invasive capsular type IV GBS isolates in Toronto, Canada [31]. In Japan, Kasai et al. demonstrated that most capsular type IV pediatric invasive isolates detected since 2019 belonged to CC452, including ST452 and single-locus variants of ST452 [13]. Recent genomic data from Argentina further identified capsular type Ia/CC452 among human-associated GBS lineages, indicating that CC452-related lineages are also present in South America [26]. Together with the identification of srr2-positive CC452 isolates in the present study, these observations support the inclusion of ST452/CC452-related lineages in ongoing maternal carriage and invasive disease surveillance.

Regarding PI distribution, PI-1/PI-2A was the predominant profile among our isolates. This finding is consistent with previous studies showing that PI-1/PI-2A is commonly observed among maternal colonizing isolates, whereas PI-2B is closely associated with capsular type III/ST17 invasive isolates [32,33]. The low frequency of PI-1/PI-2B (3.7%) in our study likely reflects the limited representation of hypervirulent CC17 lineages in maternal carriage. Notably, 60% of the capsular type III/ST17 isolates identified in this study were ermB- and tetO-positive and carried PI-2B alone. Isolates with these characteristics have been reported globally [34–36] and this clone has also been detected at high frequencies among pediatric invasive GBS isolates in Japan [13]. These findings suggest that maternal carriage may contribute to the maintenance and dissemination of this GBS clone.

Among the Alp family genes, rib was the most prevalent, consistent with findings from international studies showing that rib predominates in capsular type III and CC17 isolates [1]. However, in our collection, rib was also frequently observed in CC19 and CC23, indicating that this antigen is not restricted to invasive clones in Japan. Conversely, alp2/3 was less frequent (12.8%), consistent with its limited distribution among CC1 lineages reported in other regions [37]. These observations suggest that colonizing GBS strains in Japan share conserved surface protein repertoires with strains reported globally, thereby providing useful information for vaccine antigen selection.

The distribution of Srr adhesins also provides insight into potential virulence. The predominance of srr1 (77.6%) and the limited presence of srr2 (9.6%) were consistent with global observations that srr1 is widespread among colonizing isolates, whereas srr2 is strongly associated with hypervirulent CC17 lineages [9]. Mechanistic studies have shown that Srr2 mediates stronger binding to fibrinogen than Srr1 and also interacts with fibronectin, thereby enhancing adhesion to host ligands and cervicovaginal epithelial cells [38,39]. In our study, srr2 was confined to CC17 and CC452, suggesting that CC452 may share adhesive or invasive potential with the prototypical hypervirulent CC17 lineage. The detection of srr2-positive capsular type IV/CC452 colonizing isolates, which has rarely been reported in Japan, further supports the need for continued monitoring of this lineage.

The antimicrobial resistance patterns observed in our isolates were broadly consistent with those reported in a recent Japanese study of GBS isolates from pregnant women, in which susceptibility to β-lactams was preserved, whereas resistance to macrolides, tetracycline-class agents, and levofloxacin was observed [16]. All isolates in our study remained susceptible to β-lactams and vancomycin. In contrast, resistance to macrolides and tetracycline-class agents was common. Macrolide resistance was mainly associated with ermB, co-detection of mefA and msrD, and ermA, whereas tetracycline-class resistance among minocycline-resistant isolates was predominantly associated with tetM and tetO. This pattern is broadly consistent with recent genomic studies of GBS resistance determinants, including studies of maternal colonizing isolates from Brazil and pediatric invasive isolates from Japan [13,27]. Although minocycline is not used therapeutically during pregnancy, its susceptibility profile was useful for epidemiological characterization of resistant clones. Levofloxacin resistance was enriched in ST3, ST10, and ST19 and was mainly associated with canonical quinolone resistance-determining region (QRDR) mutations, similar to findings reported among pediatric invasive GBS isolates in Japan [13]. Taken together, the coexistence of colonization-associated virulence profiles, such as PI-1/PI-2A and srr1, with multiple antimicrobial resistance traits suggests that even non-hypervirulent maternal carriage strains may serve as reservoirs of antimicrobial-resistant GBS.

In our isolate collection, the predicted vaccine coverage exceeded 90% for both the hexavalent capsular polysaccharide conjugate vaccine targeting capsular types Ia, Ib, II, III, IV, and V (GBS6) and protein-based vaccines directed against Alp family antigens (GBS-NN/NN2). These findings suggest that current vaccine designs broadly target the major features of typical invasive lineages from a clinical perspective [7]. Nevertheless, a subset of maternal colonizing strains may remain outside the expected coverage spectrum, and shifts in the distribution of epidemic clones following vaccine implementation are possible. Continued epidemiological surveillance is therefore warranted to identify potential gaps in coverage and detect clonal replacement.

This study has several limitations. First, it was restricted to isolates collected in Osaka Prefecture, and the sample size may not fully represent nationwide carriage patterns. Second, functional assays to confirm gene expression were not performed, and the associations between virulence factors and invasiveness therefore remain inferential. Nevertheless, the detailed mapping of virulence loci in maternal carriage isolates provides a valuable pre-vaccine baseline and a molecular framework for ongoing national surveillance.

In conclusion, our analysis demonstrated that GBS colonizing pregnant women in Osaka was predominantly composed of CC19, CC23, and CC1, which are typical colonization-associated lineages. Although CC17 remained infrequent, it carried all canonical hypervirulence markers (hvgA, srr2, PI-1/PI-2B). The identification of srr2-positive CC452 (capsular type IV) suggests the emergence of a potentially important lineage. As vaccine introduction approaches, continued monitoring of CC/ST distribution, capsular types, virulence factors, and antimicrobial susceptibility will be essential to anticipate epidemiological shifts and sustain progress in the prevention of early- and late-onset GBS disease.

Supporting information

S1 Table. Molecular epidemiological characteristics of Group B Streptococcus carried by pregnant women at a general hospital in Osaka prefecture, Japan.

https://doi.org/10.1371/journal.pone.0354799.s001

(XLSX)

Acknowledgments

We would like to thank Editage for English language editing.

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Figures

Abstract

1. Introduction

2. Materials and methods

2.1. Ethics statement

2.2. Bacterial isolates and identification

2.3. Antimicrobial susceptibility testing and capsular typing

2.4. Whole genome sequencing analysis

3. Results

3.1. Distribution of CCs, STs, and capsular types

3.2. Distribution of PI types and major surface protein-associated virulence genes

3.3. Antimicrobial susceptibility and resistance determinants

4. Discussion

Supporting information

S1 Table. Molecular epidemiological characteristics of Group B Streptococcus carried by pregnant women at a general hospital in Osaka prefecture, Japan.

Acknowledgments

References