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Infant Group B Streptococcal Disease Incidence and Serotypes Worldwide: Systematic Review and Meta-analyses

Lola Madrid, Anna C Seale, Maya Kohli-Lynch and 31 more

Clinical Infectious Diseases · 2017 · Meta-analysis · CC BY

doi:10.1093/cid/cix656

Abstract

Background. Group B Streptococcus (GBS) remains a leading cause of neonatal sepsis in high-income contexts, despite declines due to intrapartum antibiotic prophylaxis (IAP). Recent evidence suggests higher incidence in Africa, where IAP is rare. We investigated the global incidence of infant invasive GBS disease and the associated serotypes, updating previous estimates.

Methods. We conducted systematic literature reviews (PubMed/Medline, Embase, Latin American and Caribbean Health Sciences Literature [LILACS], World Health Organization Library Information System [WHOLIS], and Scopus) and sought unpublished data regarding invasive GBS disease in infants aged 0–89 days. We conducted random-effects meta-analyses of incidence, case fatality risk (CFR), and serotype prevalence.

Results. We identified 135 studies with data on incidence (n = 90), CFR (n = 64), or serotype (n = 45). The pooled incidence of invasive GBS disease in infants was 0.49 per 1000 live births (95% confidence interval [CI],.43–.56), and was highest in Africa (1.12) and lowest in Asia (0.30). Early-onset disease incidence was 0.41 (95% CI,.36–.47); late-onset disease incidence was 0.26 (95% CI,.21–.30). CFR was 8.4% (95% CI, 6.6%–10.2%). Serotype III (61.5%) dominated, with 97% of cases caused by serotypes Ia, Ib, II, III, and V.

Conclusions. The incidence of infant GBS disease remains high in some regions, particularly Africa. We likely underestimated incidence in some contexts, due to limitations in case ascertainment and specimen collection and processing. Burden in Asia requires further investigation.

Full text

From PubMed Central, U.S. National Library of Medicine, as current on Oct 17, 2026. Paragraph numbers are ours, so an answer can point at one.

Group B Streptococcus (GBS; Streptococcus agalactiae) is a leading infectious cause of neonatal morbidity and mortality, well described in high-income contexts (HICs), but less well studied in low- to middle-income contexts (LMICs) and low-income contexts (LICs). A systematic review in 2012, reported an overall incidence of invasive GBS disease among infants of 0.53 per 1000 live births (95% confidence interval [CI],.41–.62), with the highest incidence in Africa (1.21 per 1000 live births), followed by the Americas (0.67 per 1000 live births) and the lowest incidence in the Western Pacific (0.15 per 1000 live births) and Southeast Asia (0.016 per 1000 live births). Although data, especially from LICs, were limited, case fatality risks (CFRs) were higher in Africa (22%) compared with the Americas (11%) or Europe (7%).

Understanding the global burden of GBS disease in young infants (0–89 days), including neonates (0–27 days), is important to guide public health decision making on interventions. Many HICs have implemented intrapartum antibiotic prophylaxis (IAP), aiming to reduce early-onset GBS disease (EOGBS; days 0–6) for women with rectovaginal GBS colonization detected through microbiological screening or with clinical risk factors. However, this strategy will not reduce late-onset infant GBS disease (LOGBS; onset on days 7–89 of life), and in LMICs and LICs, where there are more home deliveries and women present later for delivery, IAP may be less feasible and effective than other potential strategies for prevention, such as a maternal GBS vaccine.

This article therefore aims to examine the incidence of invasive GBS disease among young infants and the associated CFR and serotypes causing GBS invasive disease (Figure 1). It is part of a supplement estimating the burden of GBS disease among pregnant women, stillbirths, and infants. The supplement includes systematic reviews and meta-analyses on GBS colonization, and adverse outcomes associated with GBS around birth, which provide data inputs for estimating the worldwide burden of GBS.

OBJECTIVES

1. To provide a comprehensive, systematic literature review and meta-analyses on the burden of infant invasive GBS disease to include:

a. Incidence of infant GBS disease: overall incidence risk, including stratification by EOGBS and LOGBS.

b. CFR for EOGBS and LOGBS (7–89 days) and neonatal disease (7–27 days).

c. Serotype distribution: prevalence of GBS serotypes causing GBS disease among infants.

2. To generate parameters to be used as data inputs in a compartmental model estimating the burden of GBS in pregnancy for women, stillbirth, and infants; including

a. EOGBS to LOGBS ratio.

b. Clinical syndrome (proportion of neonatal disease that was meningitis or sepsis).

3. To evaluate data gaps and recommend improvements for the data regarding GBS disease in young infants.

METHODS

This article is part of a protocol entitled “Systematic estimates of the global burden of GBS in pregnant women, stillbirths and infants,” submitted for ethical approval to the London School of Hygiene & Tropical Medicine (reference number 11966) and approved on 30 November 2016. The general methods are described elsewhere; here we present details specific to estimates related to the incidence of invasive GBS disease among infants.

We included studies that described incidence risk, deaths, or serotypes of bacterial isolates among infants aged 0–89 days with invasive GBS disease. Eligible studies were those reporting data published or unpublished between 1 January 2000 and 31 January 2017, limited to humans and with no language restrictions. We identified data through systematic review of the published literature and through an investigator group that sought unpublished data from clinicians, researchers, and relevant professional institutions worldwide.

Definitions

Invasive GBS disease was defined as laboratory isolation of S. agalactiae from any normally sterile site using conventional microbiological methods together with any signs of clinical disease. EOGBS was defined as invasive GBS disease in infants aged 0–6 days after birth and LOGBS in infants 7–89 days after birth. Incidence risk was defined as cases per 1000 live births and CFR as number of deaths in GBS cases divided by total GBS cases.

Search Strategy

We undertook systematic literature searches of PubMed/Medline, Embase, Literature in the Health Sciences in Latin America and the Caribbean (LILACS), the World Health Organization Library Information System (WHOLIS), and Scopus databases using the search terms (“Streptococcus agalactiae” [Medical subject headings (MeSH)] OR “Streptococcus Group B” OR “Group B streptococcal”) AND “infant,” “outcome,” “death,” “mortality,” “case AND fatality AND rate.” We limited searches to humans and publications from 1 January 2000 to 31 January 2017 (see Supplementary Table 1 for the full list of search terms). For consistency, we used the same search terms as a previous systematic review. We did not apply date or language restrictions; texts were translated to English when published in other languages. An additional search for reports with serotype data was performed, using the search terms (“Streptococcus agalactiae serotype” [MeSH] OR “Streptococcus Group B serotype” OR “Group B streptococcal serotype”) using the same limits above. We used snowball searches of article reference lists including reviews to identify additional studies

One investigator performed the database search, screened for duplicates, and screened titles and abstracts to assess eligibility for inclusion. Two independent investigators (L. M. and M. K. L.) assessed the full-length articles associated with selected abstracts to confirm eligibility and extract data. Where there was discrepancy between the 2 reviewers, a third investigator (A. S.) made the final decision.

Study Selection

We included studies with original data on GBS disease in infants who were aged 0–89 days at onset of infection episode, with clinical specimens obtained from a sterile site, which had a population denominator (total live births). We excluded studies focusing on very high-risk groups (such as only human immunodeficiency virus [HIV]–infected infants or only preterm infants), where data were not representative of live births in the population. Where countries had multiple or duplicated publications or systematically collected surveillance data, we included the most recent data. Studies reporting GBS disease in infants aged 0–90 days that did not specify age at onset for the individual cases were included with the 0–89 day studies as the probability of a case on day 90 is negligible. For full details of inclusion and exclusion criteria, see Supplementary Table 2.

Data Abstraction

We used a standardized data abstraction tool to capture information on the study design (prospective or retrospective), setting (health facility or not), use of IAP, timing of clinical disease (onset in the first 24–48 hours, EOGBS, and LOGBS), outcomes (survived or died), sample type (cerebrospinal fluid, blood, or other sterile site) and GBS serotype. For facility-based studies limited to babies born at the facility, facility live births was used as denominator. Where studies included inborn and outborn babies, a population denominator of all live births in the catchment area of the health facility was used. Data on study location were also abstracted including country and town. These data were imported into Stata version 14 software.

Analysis

We used random-effects meta-analyses to estimate overall infant disease incidence, EOGBS and LOGBS incidence, the EOGBS to LOGBS incidence ratio, and CFRs using the DerSimonian and Laird method. In addition to worldwide estimates, estimates by United Nations regions and/or subregions were obtained when sufficient data were available.

To assess bias, we performed the following sensitivity analyses:

1. Invasive disease:

a. Infant invasive disease limited to facility-based studies where denominator was facility births.

b. EOGBS estimates limited to studies including data for days 0–6 after birth.

c. LOGBS estimates limited to studies including data for days 7–89 after birth.

d. Late-onset neonatal incidence limited to studies with data for days 7–27 after birth.

2. The ratio of early-onset disease to late-onset disease, including only studies considered to be less subject to case finding bias resulting from low access to care, nonsystematic sampling, or suboptimal laboratory detection methods as considered by the expert advisory group.

Literature Search and Study Selection

We identified 7535 articles for consideration from database searches, 318 additional records from expert groups in neonatal care and reference lists, and 7 datasets from an investigator group (Araujo da Silva et al. unpublished, Dhaded et al. unpublished, Saha et al. unpublished, Sigaúque et al. unpublished). One hundred thirty-five articles (reporting data from 57 countries) met our inclusion criteria (search strategy of study selection in Figure 2). Of these, 90 reported incidence, (EOGBS: 74 studies; LOGBS: 33 studies), 64 reported CFR, and 45 reported serotype data. (The full list of articles included in this review is available in Supplementary Table 3.) Articles excluded because more recent data from the same population were available are shown in Supplementary Table 4 and Supplementary Figure 1. Compared to the previously published global GBS invasive disease estimates, we included 61 additional studies: 34 reporting incidence, 35 CFR, and 26 serotype (Supplementary Figure 2).

Study Characteristics

There were more data from HICs (77 studies) compared to LMICs (18 studies), of which 12 were from Africa (11 in sub-Saharan Africa, 1 in North Africa). Data inputs are illustrated in Figure 3A and 3B. Data inputs of the previous systematic review are shown in Supplementary Figures 3A and 3B. Most studies (109/135) were facility based and information about IAP use was available from 116 of 135 studies (Table 1). Seventy-six studies reported any use of IAP: 27 of 76 (35.5%) were based on screening, 14 of 76 (18.4%) were based on a risk factor algorithm, and 35 of 76 (46.1%) did not specify a strategy. Of those studies reporting incidence, 58 of 90 (64.4%) reported use of any IAP; this was highest in developed countries (46/58 [79.3%]) and lowest in sub-Saharan Africa (3/11 [27.3%]) (Supplementary Figure 4). Of 74 studies that reported EOGBS, 49 (67.1%) reported IAP use and approximately one-third of articles (24/74 [32.4%], including 6 studies from LICs and LMICs) reported information about age at onset of EOGBS. Serotype was available in studies from 25 countries (developed countries, 16; Central and South America, 4; Southern and Eastern Africa, 3; Eastern Asia, 2). We were unable to abstract data on laboratory methods used, maternal risk factors, and weight or gestational age at birth of neonates.

Incidence Risk of Group B Streptococcus Disease

There were 6199 infants with invasive GBS disease among 13300000 live births in 53 countries. The incidence risk (per 1000 live births) for infant GBS disease was 0.49 (95% CI,.43–.56) overall, being 1.12 in Africa, 0.49 in Latin America and the Caribbean, 0.46 in developed countries, and the lowest in Asia, 0.30. Incidence was highest in Southern Africa (2.00 [95% CI,.74–3.26]) and lowest in Southeast Asia (0.21 [95% CI,.09–.32]; meta-analysis in Figure 4). There were 3664 cases of EOGBS from 9866793 live births. Incidence risk (per 1000 live births) of EOGBS worldwide was 0.41 (95% CI,.36–.47) and ranged from 0.32 (95% CI,.22–.41) in Asia to 0.71 (95% CI,.24–1.18) in Africa. The Caribbean had the highest incidence risk of EOGBS (1.47), followed by Southern Africa (1.07) and South Asia the lowest (0.20) (Supplementary Figure 5). Among EOGBS cases, 68% (95% CI, 57%–79%) developed symptoms in the 24 hours after birth, being higher in HIC (74% [95% CI, 58%–89%]) compared with LICs (31% [95% CI, –20% and 82%]); meta-analysis included as Supplementary Figure 6). There were 2003 cases of LOGBS among 8975899 live births. Incidence risk of LOGBS worldwide was 0.26 (95% CI,.21–.30), ranging from 0.04 (95% CI, –.02 to.09) in Asia to 0.65 (95% CI,.25–1.05) in Africa. Southern Africa had the highest incidence risk of LOGBS (0.93), and South America, Western Africa, and Southeastern Asia had the lowest (0.0, 0.0, and 0.03, respectively, based on the single study captured from each of these regions; Supplementary Figure 7).

Case Fatality Risk

There were 570 deaths among 6501 infant cases. The overall CFR was 8.4% (95% CI, 6.6%–10.2%). CFR in Africa (18.9% [95% CI, 13.7%–24.0%]) was 4 times higher than in developed countries (4.7% [95% CI, 3.3%–6.1%]) (meta-analysis in Supplementary Figure 8). EOGBS CFR was 10.0% (95% CI, 7.0%–12.0%) ranging from 5.0% (95% CI, 4.0%–7.0%) in developed countries to 27.0% (95% CI, 17.0%–37.0%) in Africa. LOGBS CFR was 7.0% (95% CI, 4.0%–9.0%) and, consistently with overall and EOGBS CFR, was lowest in developed countries (4.0% [95% CI, 3.0%–6.0%]) and highest in Africa (12.0% [95% CI, 5.0%–19.0%]) (meta-analysis in Supplementary Figures 9 and 10, respectively).

Serotype Distribution

A total of 6500 bacterial isolates were included in the meta-analysis of serotype prevalence (data inputs are illustrated in Supplementary Figure 11). Five serotypes (Ia, Ib, II, III, and V) accounted for 97% of invasive isolates in all regions with serotype data (Figure 5). Serotype III was the most prevalent serotype across the United Nations subregions, although it was lower in South America (34%) compared with other subregions. Nearly half (47%) of EOGBS cases and 73.0% of LOGBS cases were caused by serotype III. Serotype Ia, Ib, and V were frequently isolated in EOGBS (22.8%, 8.0%, and 10.6%, respectively) and LOGBS (14.2%, 5.3%, and 4.0%) (Supplementary Figure 12).

Early-Onset to Late-Onset Group B Streptococcus Disease Ratio

The overall ratio of EOGBS to LOGBS disease was 1.72 (95% CI, 1.35–2.21). The highest ratio was in Asia (5.99 [95% CI, 2.40–14.92]) and lowest in Africa (1.02 [95% CI,.82–1.28]). The ratio in developed countries was similar to the overall ratio, at 1.82 (95% CI, 1.29–2.57) (meta-analysis as Supplementary Figure 13).

Clinical Syndrome (Sepsis or Meningitis)

Twenty-three percent of all GBS invasive cases (95% CI, 14%–32%) were meningitis. Among EOGBS cases, 78% (95% CI, 67%–88%) had sepsis and 16% (95% CI, 8%–25%) had meningitis (meta-analysis of meningitis cases among EOGBS cases in Supplementary Figure 14). The meningitis/sepsis ratio was 0.18 (95% CI,.13–.25). Among LOGBS cases, there was a lower percentage of sepsis; 53% (95% CI, 43%–62%) had sepsis and 43% (95% CI, 34%–51%) had meningitis (meta-analysis of meningitis cases among LOGBS cases in Supplementary Figure 15). The meningitis:sepsis ratio was 0.78 (95% CI,.55–1.10).

Sensitivity Analyses to Assess Bias

Among facility-based studies with facility births denominator (n = 71), the incidence among infants 0–89 days of age was slightly higher than the main analysis (0.53 [95% CI,.44–.61]). The highest incidence was in Southern Africa (2.00 [95% CI,.73–3.26]) and the lowest in Southeastern Asia (0.21 [95% CI,.09–.32]) (Supplementary Figure 16). EOGBS incidence was 0.43 (95% CI,.35–.50) per 1000 live births (Supplementary Figure 17) and LOGBS incidence was 0.31 (95% CI,.24–.38) per 1000 live births (Supplementary Figure 18).

When we limited estimates of EOGBS to studies with reported data for days 0–6 of life (42/74 studies with EOGBS data reported), EOGBS incidence (0.42 [95% CI,.35–.49]) was similar to the main analysis (meta-analyses in Supplementary Figure 19).

When we limited LOGBS estimates to studies with complete data for days 7–89 after birth (11/33 studies), the incidence estimate was 0.40 per 1000 live births (95% CI,.27–.53), higher than the main analysis (meta-analysis in Supplementary Figure 20). Including only studies with data for days 7–27 after birth (3/32 studies), the incidence was 0.16 per 1000 live births (95% CI,.08–.24) (meta-analysis in Supplementary Figure 21).

When we limited estimates of the EOGBS to LOGBS ratio to studies considered to be less subject to bias (14 studies), the estimated ratio was 1.11 (95% CI,.96–1.30) and, unlike the main analysis, was similar across geographic regions (meta-analysis in Supplementary Figure 13).

DISCUSSION

Our comprehensive review and meta-analyses represent an important update to the previous global invasive infant GBS disease burden estimates, and most notably include new data from LMICs (18 new studies from 10 LICs and LMICs). Infant invasive GBS disease incidence and case fatality is high in every world region, yet likely considerably underestimated in settings with limited access to care and diagnostics as <10% of neonates with suspected serious infection have a positive blood culture. The overall estimated incidence of infant GBS disease, 0.49 per 1000 live births, is slightly lower than the previous estimate of 0.53 per 1000 live births (95% CI,.41–.62). While fewer studies in this review reported IAP use compared to the previous review (66% vs 77.0%), more weight (>50%) was applied to the data from Europe and the Americas where IAP is in use. The reduction in overall incidence is likely driven by lower incidence of invasive infant GBS disease in the Americas (0.43/1000 live births here vs 0.67/1000 live births in the previous review), and Europe (0.53 vs 0.57/1000 live births). This difference, especially in the United States where infant GBS rates declined notably during the study period, reflects the use of more recent data in our analysis.

Similarly, the incidence of invasive infant GBS disease in Africa (1.12/1000 live births) was also slightly lower than previously reported, although >2 times higher than in developed countries (0.46/1000 live births). This is the result of broader incidence data from Africa, including large studies in South Africa Mozambique ”(Sigaúque et al, Unpublished data)”, and Gambia reporting a high incidence of invasive GBS disease, in contrast to studies in Nigeria and Zambia reporting a very low incidence. Our point estimate for EOGBS incidence for Africa was higher compared to that reported in the most recent worldwide review, although LOGBS incidence for the same region was similar in both reviews. There are many possible reasons for the increase in EOGBS incidence in Africa, which could be due to true emergence, increases in comorbidities such as HIV, or improved data collection to detect early disease. This high incidence is important in terms of total burden, as CFRs in Africa were also 4 times higher than in developed countries (18.9% and 4.7%, respectively); thus the greatest burden of cases, and deaths, is in Africa. However, our data are limited to few African studies mostly in Southern and Eastern Africa.

There are other important regional differences. The incidence of infant GBS disease was strikingly low in Asia at 0.31 per 1000 live births, with the lowest incidence in Southeast Asia (0.21/1000 live births). This may reflect a true regional difference, which could be related to differences in lower overall prevalence of maternal colonization and/or lower prevalence of serotype III, which is more commonly associated with the most virulent clone, clonal complex 17. Some of the difference may also be due to incomplete case ascertainment, being in Asia more challenging as they have more home births than Africa. For the earliest-onset cases (<24 hours of birth), differences in access to care and rapid and high case fatality can reduce case ascertainment. Cerebrospinal fluid sampling is infrequently performed in many parts of this region and that would reduce the apparent incidence of LOGBS disease, which is more frequently associated with meningitis. However, the lack of late-onset cases in this region does not fully align with those reasons and also suggests there may be more at play, potentially related to strain differences, level of natural acquired protective maternal antibody, or other host, environmental, or behavioral factors that may affect disease burden.

Difficulties in case ascertainment in LICs likely contribute to the higher incidences observed when the analysis was limited to facility-based studies, particularly in Africa. Studies in contexts where access to care, particularly for home deliveries, is difficult are likely to underestimate EOGBS disease incidence, due to the preponderance of cases with onset on day zero, which can be as high as 90% in studies with high-quality ascertainment but was 68% among the studies we included where this information could be extracted. Late-onset disease is likely underestimated too, due to studies that did not capture cases for the full 7–89 days; the sensitivity analysis showed the incidence of late onset disease to be almost twice as high (0.40 vs 0.26) when only studies with data for days 7–89 were included. This may result in an underestimation of the burden of GBS meningitis in particular, a significant concern given the morbidity associated with this condition.

Differences in the early- to late-onset disease ratios in different regions in the main analysis may also reflect (and reveal) biases in the data. Asia had the highest ratio of EOGBS disease to LOGBS disease, with the lowest in Africa (5.99 vs 1.02). It is possible that Asia has less LOGBS disease, consistent with the lower prevalence of maternal colonization with serotype III, a serotype commonly associated with LOGBS disease. Interestingly, when limiting the EOGBS:LOGBS ratio to high-quality studies, the estimate was similar across regions and lower than the overall EOGBS:LOGBS ratio. This is likely to be influenced by those countries with widespread IAP as well as South Africa, which may have a uniquely low ratio due to the high prevalence of maternal HIV infection, which predisposes to late-onset disease. However, no study from Asia was included in this analysis.

In terms of serotypes causing invasive disease, serotype III accounted for over half of all disease-causing isolates followed by serotypes Ia, V, and II, consistent with previous work. Disease-causing serotypes were similar in prevalence across different regions, with some slight variations. The lowest prevalence of serotype III (where data were available) was found in South America and Southeast Asia, 2 of the regions with the lowest prevalence of serotype III among colonized pregnant women. Serotype distribution was similar to that reported in the previous review, suggesting stability over time.

Our findings suggest GBS disease is an important cause of infant disease, despite the limitations in the data and uncertainties about the low incidence in Asia. In Africa, where the incidence is highest, the CFR is also highest, suggesting this is the region where prevention strategies are most critical to introduce. Existing preventive strategies using IAP are not usually available in low-income contexts and, with a higher number of home deliveries and late presentation to health facilities for delivery, IAP may be more difficult to implement. Maternal vaccination offers an alternative strategy, and the data we have suggest that a pentavalent conjugate vaccine (including Ia/Ib/II/III/V) would cover almost all disease-causing serotypes (96%) in young infants worldwide (Table 2).

Supplementary Data

Supplementary materials are available at Clinical Infectious Diseases online. Consisting of data provided by the authors to benefit the reader, the posted materials are not copyedited and are the sole responsibility of the authors, so questions or comments should be addressed to the corresponding author.

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    Andersen J, Christensen R, Hertel J Clinical features and epidemiology of septicaemia and meningitis in neonates due to Streptococcus agalactiae in Copenhagen County, Denmark: a 10 year survey from 1992 to 2001. Acta Paediatr2004; 93:1334–9.

    Not in our library10.1080/08035250410023016

  34. 34.

    Barbosa NG, Dos Reis H, Mantese OC, Mussi-Pinhata MM, Abdallah VO, Gontijo Filho PP Early-onset neonatal sepsis by group B Streptococcus in a Brazilian public hospital. Braz J Infect Dis2016; 20:647–8.

    Not in our library10.1016/j.bjid.2016.07.013

  35. 35.

    Bell Y, Barton M, Thame M, Nicholson A, Trotman H Neonatal sepsis in Jamaican neonates. Ann Trop Paediatr2005; 25:293–6.

    Not in our library10.1179/146532805x72449

  36. 36.

    Ben Hamida Nouaili E, Harouni M, Chaouachi S, Sfar R, Marrakchi Z [Early-onset neonatal bacterial infections: a retrospective series of 144 cases [in French]. Tunis Med2008; 86:136–9.

    Not in our library

  37. 37.

    Berardi A, Baroni L, Bacchi Reggiani ML; GBS Prevention Working Group Emilia-Romagna The burden of early-onset sepsis in Emilia-Romagna (Italy): a 4-year, population-based study. J Matern Fetal Neonatal Med2016; 29:3126–31.

    Not in our library10.3109/14767058.2015.1114093

  38. 38.

    Berardi A, Rossi C, Lugli L Group B Streptococcus late-onset disease: 2003–2010. Pediatrics2013; 131:e361–8.

    Not in our library10.1542/peds.2012-1231

  39. 39.

    Bromiker R, Ernest N, Meir MB Correlation of bacterial type and antibiotic sensitivity with maternal antibiotic exposure in early-onset neonatal sepsis. Neonatology2013; 103:48–53.

    Not in our library10.1159/000342215

  40. 40.

    Bulkowstein S, Ben-Shimol S, Givon-Lavi N, Melamed R, Shany E, Greenberg D Comparison of early onset sepsis and community-acquired late onset sepsis in infants less than 3 months of age. BMC Pediatr2016; 16:82.

    Not in our library10.1186/s12887-016-0618-6

  41. 41.

    Carbonell-Estrany X, Figueras-Aloy J, Salcedo-Abizanda S, de la Rosa-Fraile M Probable early-onset group B streptococcal neonatal sepsis: a serious clinical condition related to intrauterine infection. Arch Dis Child Fetal Neonatal Ed2008; 93:F85–9.

    Not in our library10.1136/adc.2007.119958

  42. 42.
    Increased Risk for Group B Streptococcus Sepsis in Young Infants Exposed to HIV, Soweto, South Africa, 2004–2008 · 2015
    Not checked
  43. 43.

    Darlow BA, Voss L, Lennon DR, Grimwood K Early-onset neonatal group B Streptococcus sepsis following national risk-based prevention guidelines. Aust N Z J Obstet Gynaecol2016; 56:69–74.

    Not in our library10.1111/ajo.12378

  44. 44.

    Darmstadt GL, Saha SK, Choi Y; Bangladesh Projahnmo-2 (Mirzapur) Study Group Population-based incidence and etiology of community-acquired neonatal bacteremia in Mirzapur, Bangladesh: an observational study. J Infect Dis2009; 200:906–15.

    Not in our library10.1086/605473

  45. 45.

    Delgado Picado E; Saenz-Sanchez C, Calderon Zumiga A Rate of colonization of streptococcus agalactiae in pregnant women and neonates, Women’s Hospital Dr Adolfo Carit Eva. Rev Costarric Cienc Méd2004; 25:25–32.

    Not in our library

  46. 46.

    Didier C, Streicher MP, Chognot D Late-onset neonatal infections: incidences and pathogens in the era of antenatal antibiotics. Eur J Pediatr2012; 171:681–7.

    Not in our library10.1007/s00431-011-1639-7

  47. 47.

    Ekelund K, Konradsen HB Invasive group B streptococcal disease in infants: a 19-year nationwide study. Serotype distribution, incidence and recurrent infection. Epidemiol Infect2004; 132:1083–90.

    Not in our library10.1017/s0950268804002808

  48. 48.

    El-Said MF, Bessisso MS, Janahi MA, Habob LH, El-Shafie SS Epidemiology of neonatal meningitis in Qatar. Saudi Med J2002; 23:789–92.

    Not in our library

  49. 49.
    Group B streptococcus neonatal infection in an intensive care unit in Brazil: high fatality and missed opportunities for antibiotic prophylaxis · 2015
    Not checked
  50. 50.

    Fiolo K, Zanardi CE, Salvadego M Infection rate and Streptococcus agalactiae serotypes in samples of infected neonates in the city of Campinas (São Paulo), Brazil. Rev Bras Ginecol Obstet2012; 34:544–9.

    Not in our library10.1590/s0100-72032012001200003

  51. 51.

    Fjalstad JW, Stensvold HJ, Bergseng H Early-onset sepsis and antibiotic exposure in term infants: a nationwide population-based study in Norway. Pediatr Infect Dis J2016; 35:1–6.

    Not in our library10.1097/inf.0000000000000906

  52. 52.

    Fluegge K, Siedler A, Heinrich B; German Pediatric Surveillance Unit Study Group Incidence and clinical presentation of invasive neonatal group B streptococcal infections in Germany. Pediatrics2006; 117:e1139–45.

    Not in our library10.1542/peds.2005-2481

  53. 53.

    Freitas FT, Romero GA Early-onset neonatal sepsis and the implementation of group B Streptococcus prophylaxis in a Brazilian maternity hospital: a descriptive study. Braz J Infect Dis2017; 21:92–7.

    Not in our library10.1016/j.bjid.2016.09.013

  54. 54.

    Giannoni E, Berger C, Stocker M; Swiss Pediatric Sepsis Study Group Incidence and outcome of group B streptococcal sepsis in infants in Switzerland. Pediatr Infect Dis J2016; 35:222–4.

    Not in our library10.1097/inf.0000000000000974

  55. 55.

    Gimenez M, Sanfeliu I, Sierra M Group B streptococcal early-onset neonatal sepsis in the area of Barcelona (2004–2010). Analysis of missed opportunities for prevention [in Spanish]. Enferm Infecc Microbiol Clin2015; 33:446–50.

    Not in our library10.1016/j.eimc.2014.10.015

  56. 56.

    Gray KJ, Bennett SL, French N, Phiri AJ, Graham SM Invasive group B streptococcal infection in infants, Malawi. Emerg Infect Dis2007; 13:223–9.

    Not in our library10.3201/eid1302.060680

  57. 57.

    Hajdu A, Blystad H, Høiby EA, Klouman E, Schimmer B, Nygård K Unexpected increase in case fatality of invasive group B streptococcal infections in infants in Norway, January-July 2006. Euro Surveill2006; 11:E060727.2.

    Not in our library10.2807/esw.11.30.03010-en

  58. 58.

    Hammoud MS, Al-Taiar A, Al-Abdi SY Culture-proven early-onset neonatal sepsis in Arab states in the Gulf region: two-year prospective study. Int J Infect Dis2017; 55:11–5.

    Not in our library10.1016/j.ijid.2016.12.006

  59. 59.

    Hasseltvedt V Systemic streptococcal group B disease in Norway—an increasing health problem. Euro Surveill2001; 5:2086.

    Not in our library

  60. 60.

    Lea J Screening of hemolytical Streptococcus of group B in pregnancy and prevention of infection in newborns. Ceska Gynekologie2004; 69:91–4.

    Not in our library

  61. 61.

    Juncosa-Morros T, Guardia-Llobet C, Bosch-Mestres J Streptococcus agalactiae late-onset neonatal infections in Barcelona (1996–2010) [in Spanish]. Enferm Infecc Microbiol Clin2014; 32:574–8.

    Not in our library10.1016/j.eimc.2013.09.012

  62. 62.

    Kabwe M, Tembo J, Chilukutu L Etiology, antibiotic resistance and risk factors for neonatal sepsis in a large referral center in Zambia. Pediatr Infect Dis J2016; 35:e191–8.

    Not in our library10.1097/inf.0000000000001154

  63. 63.

    Ko DW, Zurynski Y, Gilbert GL; GBS Study Group Group B streptococcal disease and genotypes in Australian infants. J Paediatr Child Health2015; 51:808–14.

    Not in our library10.1111/jpc.12830

  64. 64.

    Kim JS, Jang YT, Kim JD Incidence of Haemophilus influenzae type B and other invasive diseases in South Korean children. Vaccine2004; 22:3952–62.

    Not in our library10.1016/j.vaccine.2004.04.003

  65. 65.

    Kruse AY, Thieu Chuong do H, Phuong CN Neonatal bloodstream infections in a pediatric hospital in Vietnam: a cohort study. J Trop Pediatr2013; 59:483–8.

    Not in our library10.1093/tropej/fmt056

  66. 66.

    Kuhn P, Dheu C, Bolender C Incidence and distribution of pathogens in early-onset neonatal sepsis in the era of antenatal antibiotics. Paediatr Perinat Epidemiol2010; 24:479–87.

    Not in our library10.1111/j.1365-3016.2010.01132.x

  67. 67.

    Larcher JS, Capellino F, De Giusto R Group B streptococcus colonization during pregnancy and prevention of early onset of disease [in Spanish]. Medicina (B Aires)2005; 65:201–6.

    Not in our library

  68. 68.

    Le Doare K, Jarju S, Darboe S Risk factors for group B Streptococcus colonisation and disease in Gambian women and their infants. J Infect2016; 72:283–94.

    Not in our library10.1016/j.jinf.2015.12.014

  69. 69.

    Li YP, Kuok CM, Lin SY, Hsieh WS, Shyu MK Group B Streptococcus antimicrobial resistance in neonates born to group B Streptococcus-colonized mothers: single-center survey. J Obstet Gynaecol Res2016; 42:1471–5.

    Not in our library10.1111/jog.13082

  70. 70.

    Liu H, Zeng H, Wang W Estimating the burden of invasive group B streptococcal disease in young infants in southern mainland China: an observational study. Int J Clin Exp Med2015; 8:13699–707.

    Not in our library

  71. 71.

    Lomuto C, Queiruga M, Nigri C, Fatur D, Messina A, Santos N Approach to the epidemiologic situation in Argentina of the perinatal infection by beta hemolytic streptococcus of the B group (EGB). Rev Hosp Matern Infant Ramon Sarda2006; 25:13–9.

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  72. 72.

    Martin TC, Adamson J, Dickson T, DiGiantomasso E, Nesbitt C Does group B streptococcal infection contribute significantly to neonatal sepsis in Antigua and Barbuda?West Indian Med J2007; 56:498–501.

    Not in our library

  73. 73.

    Matsubara K, Hoshina K, Suzuki Y, Matsubara K, Hoshina K, Suzuki Y Early-onset and late-onset group B streptococcal disease in Japan: a nationwide surveillance study, 2004–2010. Int J Infect Dis2013; 17:e379–84.

    Not in our library10.1016/j.ijid.2012.11.027

  74. 74.

    Miyata A, Takahashi H, Kubo T Early-onset group B streptococcal disease following culture-based screening in Japan: a single center study. J Obstet Gynaecol Res2012; 38:1052–6.

    Not in our library10.1111/j.1447-0756.2011.01830.x

  75. 75.

    Neto MT Group B streptococcal disease in Portuguese infants younger than 90 days. Arch Dis Child Fetal Neonatal Ed2008; 93:F90–3.

    Not in our library10.1136/adc.2007.127464

  76. 76.

    Niduvaje K, Amutha C, Roy J Early neonatal streptococcal infection. Indian J Pediatr2006; 73:573–6.

    Not in our library10.1007/bf02759920

  77. 77.

    Ojukwu JU, Abonyi LE, Ugwu J, Neonatal septicemia in high risk babies in south-eastern Nigeria. J Perinat Med2005; 34:166–72.

    Not in our library10.1515/jpm.2006.030

  78. 78.

    Persson E, Berg S, Trollfors B Serotypes and clinical manifestations of invasive group B streptococcal infections in western Sweden 1998–2001. Clin Microbiol Infect2004; 10:791–6.

    Not in our library10.1111/j.1469-0691.2004.00931.x

  79. 79.

    Petersen KB, Johansen HK, Rosthøj S, Krebs L, Pinborg A, Hedegaard M Increasing prevalence of group B streptococcal infection among pregnant women. Dan Med J2014; 61:A4908.

    Not in our library

  80. 80.

    Poliquin V, Cohen E, Poliquin PG, Schneider C, Menticoglou S Ongoing cases of early-onset group B streptococcal disease in the era of screening and prophylaxis. J Obstet Gynaecol Can2016; 38:926–9.

    Not in our library10.1016/j.jogc.2016.05.006

  81. 81.

    Rivera L, Sáez-Llorens X, Feris-Iglesias J Incidence and serotype distribution of invasive group B streptococcal disease in young infants: a multi-country observational study. BMC Pediatr2015; 15:143.

    Not in our library10.1186/s12887-015-0460-2

  82. 82.

    Sakata H Evaluation of intrapartum antibiotic prophylaxis for the prevention of early-onset group B streptococcal infection. J Infect Chemother2012; 18:853–7.

    Not in our library10.1007/s10156-012-0426-3

  83. 83.

    Sridhar S, Grace R, Nithya PJ Group B streptococcal infection in a tertiary hospital in India—1998–2010. Pediatr Infect Dis2014; 33:1091–2.

    Not in our library10.1097/inf.0000000000000377

  84. 84.

    Straková L, Motlová J Active surveillance of early onset disease due to group B streptococci in newborns. Indian J Med Res2004; 119(suppl):205–7.

    Not in our library

  85. 85.

    Sundaram V, Kumar P, Dutta S Blood culture confirmed bacterial sepsis in neonates in a North Indian tertiary care center: changes over the last decade. Jpn J Infect Dis2009; 62:46–50.

    Not in our library

  86. 86.

    Tapia IJ, Reichhard TC, Saldias RM Neonatal sepsis in the era of antenatal antibiotic prophylaxis. Rev Chilena Infectol2007; 24:111–6.

    Not in our library10.4067/s0716-10182007000200004

  87. 87.

    Thatrimontrichai A, Chanvitan P, Janjindamai W, Dissaneevate S, Jefferies A, Shah V Trends in neonatal sepsis in a neonatal intensive care unit in Thailand before and after construction of a new facility. Asian Biomedicine2014; 8:771–8.

    Not in our library

  88. 88.

    Tiskumara R, Fakharee SH, Liu CQ Neonatal infections in Asia. Arch Dis Child Fetal Neonatal Ed2009; 94:F144–8.

    Not in our library10.1136/adc.2008.139865

  89. 89.

    Trijbels-Smeulders M, de Jonge GA, Pasker-de Jong PC Epidemiology of neonatal group B streptococcal disease in the Netherlands before and after introduction of guidelines for prevention. Arch Dis Child Fetal Neonatal Ed2007; 92:F271–6.

    Not in our library10.1136/adc.2005.088799

  90. 90.

    Trotman H, Bell Y Neonatal group B streptococcal infection at the University Hospital of the West Indies, Jamaica: a 10-year experience. Ann Trop Paediatr2006; 26:53–7.

    Not in our library10.1179/146532806x90619

  91. 91.
    A survey of the incidence of neonatal sepsis by group B Streptococcus during a decade in a Brazilian maternity hospital
    Not checked
  92. 92.

    Villanueva-Uy ME, Wongsiridej P, Sangtawesin V The burden of invasive neonatal group B streptococcal (GBS) disease in Thailand and the Philippines. Southeast Asian J Trop Med Public Health2015; 46:728–37.

    Not in our library

  93. 93.

    Yossuck P, Preedisripipat K Neonatal group B streptococcal infection: incidence and clinical manifestation in Siriraj Hospital. J Med Assoc Thai2002; 85(suppl 2):S479–87.

    Not in our library

  94. 94.

    van den Hoogen A, Gerards LJ, Verboon-Maciolek MA, Fleer A, Krediet TG Long-term trends in the epidemiology of neonatal sepsis and antibiotic susceptibility of causative agents. Neonatology2010; 97:22–8.

    Not in our library10.1159/000226604

  95. 95.

    Yu HW, Lin HC, Yang PH Group B streptococcal infection in Taiwan: maternal colonization and neonatal infection. Pediatr Neonatol2011; 52:190–5.

    Not in our library10.1016/j.pedneo.2011.05.008

  96. 96.

    Frigati L, van der Merwe JL, Harvey J, Rabie H, Theron G, Cotton MF A retrospective review of group B streptococcal infection in the Metro East area of the Western Cape province: 2010 to 2011. S Afr J Infect Dis2014; 29:33–6.

    Not in our library

  97. 97.

    Bartlett AW, Smith B, George CR Epidemiology of late and very late onset group B streptococcal disease: fifteen-year experience from two Australian tertiary pediatric facilities. Pediatr Infect Dis J2017; 36:20–4.

    Not in our library10.1097/inf.0000000000001345

  98. 98.

    Cantoni L, Ronfani L, Da Riol R Physical examination instead of laboratory tests for most infants born to mothers colonized with group B Streptococcus: support for the Centers for Disease Control and Prevention’s 2010 recommendations. J Pediatr2013; 163: 568–73.

    Not in our library10.1016/j.jpeds.2013.01.034

  99. 99.

    Chang CJ, Chang WN, Huang LT Neonatal bacterial meningitis in southern Taiwan. Pediatr Neurol2003; 29:288–94.

    Not in our library10.1016/s0887-8994(03)00273-x

  100. 100.

    Cho HK, Lee H, Kang JH The causative organisms of bacterial meningitis in Korean children in 1996–2005. J Korean Med Sci2010; 25:895–9.

    Not in our library10.3346/jkms.2010.25.6.895

  101. 101.

    Costa N, Carvalho M, Moura S; Júnior SC Beta-hemolytic streptococcus in pregnant women and their newborn infants: a critical analysis of the protocol used at Fernandes Figueira Institute, Oswaldo Cruz Foundation, in Brazil. Rev Paul Pediatr2010; 28.

    Not in our library

  102. 102.

    Díaz-Álvarez M, Claver Isás D, Pérez-Amarillo J Infections due to Streptococcus agalactiae at an open neonatology service. Rev Cubana Pediatr2008; 80.

    Not in our library

  103. 103.

    Hashavya S, Benenson S, Ergaz-Shaltiel Z, Bar-Oz B, Averbuch D, Eventov-Friedman S The use of blood counts and blood cultures to screen neonates born to partially treated group B Streptococcus-carrier mothers for early-onset sepsis: is it justified?Pediatr Infect Dis J2011; 30:840–3.

    Not in our library10.1097/inf.0b013e3182223586

  104. 104.

    Jiang JH, Chiu NC, Huang FY Neonatal sepsis in the neonatal intensive care unit: characteristics of early versus late onset. J Microbiol Immunol Infect2004; 37:301–6.

    Not in our library

  105. 105.

    Mendoza OM, Arias M, Mendoza L Sepsis neonatal Group B Streptococcus and gram negative bacteria: prevalence and risk of meningitis. Rev Chil Pediatr2013; 84.

    Not in our library

  106. 106.

    Milledge J, Calis JC, Graham SM Aetiology of neonatal sepsis in Blantyre, Malawi: 1996–2001. Ann Trop Paediatr2005; 25:101–10.

    Not in our library10.1179/146532805x45692

  107. 107.

    Ovalle A, Levancini M Urinary tract infections in pregnancy. Curr Opin Urol2001; 11:55–9.

    Not in our library10.1097/00042307-200101000-00008

  108. 108.

    Park KH, Kim KH, Kang JH Current status and clinical presentations of invasive neonatal group B streptococcal infections in Korea. Pediatr Int2010; 53:236–9.

    Not in our library10.1111/j.1442-200x.2010.03165.x

  109. 109.

    Reinheimer C, Kempf VA, Wittekindt BE Group B Streptococcus infections in neonates admitted to a German NICU: emphasis on screening and adherence to pre-analytical recommendations. Early Hum Dev2016; 103:37–41.

    Not in our library10.1016/j.earlhumdev.2016.07.007

  110. 110.

    Sakata H, Sakata H Pediatric invasive streptococcal infection in northern and eastern regions of Hokkaido, Japan from 2010 to 2012. Pediatr Int2014; 56:360–3.

    Not in our library10.1111/ped.12250

  111. 111.

    Zeng SJ, Tang XS, Zhao WL, Qiu HX, Wang H, Feng ZC Clinical analysis of cases of neonatal Streptococcus agalactiae sepsis. Genet Mol Res2016; 15.

    Not in our library10.4238/gmr.15027962

  112. 112.

    Almeida A, Villain A, Joubrel C Whole-genome comparison uncovers genomic mutations between group B streptococci sampled from infected newborns and their mothers. J Bacteriol2015; 197:3354–66.

    Not in our library10.1128/jb.00429-15

  113. 113.

    Matsubara K, Yamamoto G Invasive group B streptococcal infections in a tertiary care hospital between 1998 and 2007 in Japan. Int J Infect Dis2009; 13:679–84.

    Not in our library10.1016/j.ijid.2008.10.007

  114. 114.

    Bekker V, Bijlsma MW, van de Beek D, Kuijpers TW, van der Ende A Incidence of invasive group B streptococcal disease and pathogen genotype distribution in newborn babies in the Netherlands over 25 years: a nationwide surveillance study. Lancet Infect Dis2014; 14:1083–9.

    Not in our library10.1016/s1473-3099(14)70919-3

  115. 115.

    Bidet P, Brahimi N, Chalas C, Aujard Y, Bingen E Molecular characterization of serotype III group B-Streptococcus isolates causing neonatal meningitis. J Infect Dis2003; 188:1132–7.

    Not in our library10.1086/378517

  116. 116.

    Brzychczy-Wloch M, Gosiewski T, Bulanda M Multilocus sequence types of invasive and colonizing neonatal group B streptococci in Poland. Med Princ Pract2014; 23:323–30.

    Not in our library10.1159/000362368

  117. 117.
    Genomic analysis reveals multi-drug resistance clusters in Group B Streptococcus CC17 hypervirulent isolates causing neonatal invasive disease in southern mainland China · 2016
    Not checked
  118. 118.

    Chang B, Wada A, Hosoya M; Japanese Invasive Disease Study Group Characteristics of group B Streptococcus isolated from infants with invasive infections: a population-based study in Japan. Jpn J Infect Dis2014; 67:356–60.

    Not in our library10.7883/yoken.67.356

  119. 119.

    Davies HD, Raj S, Adair C, Robinson J, McGeer A; Alberta GBS Study Group Population-based active surveillance for neonatal group B streptococcal infections in Alberta, Canada: implications for vaccine formulation. Pediatr Infect Dis J2001; 20:879–84.

    Not in our library10.1097/00006454-200109000-00011

  120. 120.

    Davies HD, Jones N, Whittam TS, Elsayed S, Bisharat N, Baker CJ Multilocus sequence typing of serotype III group B Streptococcus and correlation with pathogenic potential. J Infect Dis2004; 189:1097–102.

    Not in our library10.1086/382087

  121. 121.

    Figueira-Coelho J, Ramirez M, Salgado MJ, Melo-Cristino J Streptococcus agalactiae in a large Portuguese teaching hospital: antimicrobial susceptibility, serotype distribution, and clonal analysis of macrolide-resistant isolates. Microb Drug Resist2004; 10:31–6.

    Not in our library10.1089/107662904323047772

  122. 122.

    Fluegge K, Supper S, Siedler A, Berner R Serotype distribution of invasive group B streptococcal isolates in infants: results from a nationwide active laboratory surveillance study over 2 years in Germany. Clin Infect Dis2005; 40:760–3.

    Not in our library10.1086/427942

  123. 123.

    Fluegge K, Wons J, Spellerberg B Genetic differences between invasive and noninvasive neonatal group B streptococcal isolates. Pediatr Infect Dis J2011; 30:1027–31.

    Not in our library10.1097/inf.0b013e31822a2a1f

  124. 124.

    Hoshina K, Suzuki Y, Nishida H Trend of neonatal group B streptococcal infection during the last 15 years. Pediatr Int2002; 44:641–6.

    Not in our library10.1046/j.1442-200x.2002.01638.x

  125. 125.

    Imperi M, Gherardi G, Berardi A Invasive neonatal GBS infections from an area-based surveillance study in Italy. Clin Microbiol Infect2011; 17:1834–9.

    Not in our library10.1111/j.1469-0691.2011.03479.x

  126. 126.
    Hypervirulent Clone of Group B Streptococcus Serotype III Sequence Type 283, Hong Kong, 1993–2012 · 2016
    Not checked
  127. 127.

    Joubrel C, Tazi A, Six A Group B Streptococcus neonatal invasive infections, France 2007–2012. Clin Microbiol Infect2015; 21:910–6.

    Not in our library10.1016/j.cmi.2015.05.039

  128. 128.

    Martínez MA, Ovalle A, Durán C Serotypes and antimicrobial susceptibility of Streptococcus agalactiae [in Spanish]. Rev Med Chil2004; 132:549–55.

    Not in our library10.4067/s0034-98872004000500003

  129. 129.

    Martins ER, Pessanha MA, Ramirez M, Melo-Cristino J; Portuguese Group for the Study of Streptococcal Infections Analysis of group B streptococcal isolates from infants and pregnant women in Portugal revealing two lineages with enhanced invasiveness. J Clin Microbiol2007; 45:3224–9.

    Not in our library10.1128/jcm.01182-07

  130. 130.

    Morozumi M, Wajima T, Kuwata Y Associations between capsular serotype, multilocus sequence type, and macrolide resistance in Streptococcus agalactiae isolates from Japanese infants with invasive infections. Epidemiol Infect2014; 142:812–9.

    Not in our library10.1017/s0950268813001647

  131. 131.

    Óladóttir GL, Erlendsdóttir H, Pálsson G, Björnsdóttir ES, Kristinsson KG, Haraldsson Á Increasing incidence of late-onset neonatal invasive group B streptococcal infections in Iceland. Pediatr Infect Dis J2011; 30:661–3.

    Not in our library10.1097/inf.0b013e3182184fe4

  132. 132.

    Six A, Firon A, Plainvert C Molecular characterization of nonhemolytic and nonpigmented group B streptococci responsible for human invasive infections. J Clin Microbiol2016; 54:75–82.

    Not in our library10.1128/jcm.02177-15

  133. 133.

    Souza VC, Kegele FC, Souza SR, Neves FP, de Paula GR, Barros RR Antimicrobial susceptibility and genetic diversity of Streptococcus agalactiae recovered from newborns and pregnant women in Brazil. Scand J Infect Dis2013; 45:780–5.

    Not in our library10.3109/00365548.2013.810814

  134. 134.

    Teatero S, McGeer A, Low DE Characterization of invasive group B Streptococcus strains from the greater Toronto area, Canada. J Clin Microbiol2014; 52:1441–7.

    Not in our library10.1128/jcm.03554-13

  135. 135.

    Trijbels-Smeulders MA, Kimpen JL, Kollée LA Serotypes, genotypes, and antibiotic susceptibility profiles of group B streptococci causing neonatal sepsis and meningitis before and after introduction of antibiotic prophylaxis. Pediatr Infect Dis J2006; 25:945–8.

    Not in our library10.1097/01.inf.0000237821.65559.08

  136. 136.

    Wang P, Ma Z, Tong J Serotype distribution, antimicrobial resistance, and molecular characterization of invasive group B Streptococcus isolates recovered from Chinese neonates. Int J Infect Dis2015; 37:e115–e8.

    Not in our library10.1016/j.ijid.2015.06.019

  137. 137.

    Yoon IA, Jo DS, Cho EY, Choi EH, Lee HJ, Lee H Clinical significance of serotype V among infants with invasive group B streptococcal infections in South Korea. Int J Infect Dis2015; 38:136–40.

    Not in our library10.1016/j.ijid.2015.05.017

  138. 138.

    Zhao Z, Kong F, Zeng X, Gidding HF, Morgan J, Gilbert GL Distribution of genotypes and antibiotic resistance genes among invasive Streptococcus agalactiae (group B Streptococcus) isolates from Australasian patients belonging to different age groups. Clin Microbiol Infect2008; 14:260–7.

    Not in our library10.1111/j.1469-0691.2007.01914.x

  139. 139.

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    Sinha A, Russell LB, Tomczyk S; GBS Vaccine Cost-Effectiveness Analysis in Sub-Saharan Africa Working Group Disease burden of group B Streptococcus among infants in sub-Saharan Africa: a systematic literature review and meta-analysis. Pediatr Infect Dis J2016; 35:933–42.

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