Group B Streptococcal Infections

Edwards, Morven S.; Nizet, Victor; Baker, Carol J.

doi:10.1016/b978-1-4160-6400-8.00012-2

Cited by 118 publications

(66 citation statements)

References 680 publications

(595 reference statements)

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“…Positive GBS culture in tracheal secretions (collected within 30 min after admission, prior to antibiotic use by endotracheal intubation), blood, or cerebrospinal fluid collected from infants aged 1–6 days with symptoms, and diagnosis of pneumonia (regardless of GBS colonization, shortness of breath, exudative shadow in X-ray images, positive GBS culture in tracheal secretions), sepsis, and meningitis [6]. GBS-EOD was diagnosed according to Practical Neonatology (4th ed.)…”

Section: Methodsmentioning

confidence: 99%

Group B Streptococcus Colonization in Late Pregnancy and Invasive Infection in Neonates in China: A Population-Based 3-Year Study

et al. 2019

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Background: As no population-based studies of group B Streptococcus (GBS) colonization rates in late pregnancy (at 35–37 weeks of gestation) have been conducted in China, the incidence of and risk factors for neonatal early-onset GBS disease (GBS-EOD) in China remains poorly understood. Objectives: To determine the GBS colonization rate in late pregnancy and neonatal GBS infection in Xiamen, China, and to assess the effectiveness of intrapartum antibiotic prophylaxis (IAP) for the prevention of neonatal GBS-EOD. Methods: A total of 49,908 pregnant women were enrolled between April 1, 2014 and March 31, 2017. Bacterial culture was used to diagnose GBS infection in both pregnant women and neonates. Women with GBS colonization received IAP during parturition or rupture of fetal membranes. Results: The GBS colonization rate was 13.89% (6,933/49,908); 50,772 neonates were born to 49,908 pregnant women, of whom 75 (1.48 per 1,000) were diagnosed with GBS-EOD. The incidence of GBS-EOD among neonates born to GBS-positive mothers (8.77‰; 62/7,068) was 29 times higher than that of neonates born to GBS-negative mothers (0.30‰; 13/43,704). Logistic regression analysis indicated that gestational bacteriuria, GBS disease in infants from previous pregnancies, and chorioamnionitis were risk factors for GBS-EOD (p = 0.007, p = 0.000, and p = 0.018, respectively). IAP effectively protected against neonatal GBS-EOD (p = 0.011). Conclusions: GBS colonization was detected in nearly 14% of late pregnant women. The IAP for reducing GBS-EOD was effective. Therefore, universal screening of maternal GBS and subsequent IAP for those with GBS colonization should be implemented in China.

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Section: Methodsmentioning

confidence: 99%

Group B Streptococcus Colonization in Late Pregnancy and Invasive Infection in Neonates in China: A Population-Based 3-Year Study

et al. 2019

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“…colonizes the lower gastrointestinal and vaginal mucosae of about one third of women and can cause neonatal pneumonia, sepsis, and meningitis (1,2). It is also an important etiological agent of morbidity in immunocompromised adults and of bovine mastitis (3).…”

Section: S Treptococcus Agalactiae (Group B Streptococcus [Gbs])mentioning

confidence: 99%

The Group B Streptococcus–Secreted Protein CIP Interacts with C4, Preventing C3b Deposition via the Lectin and Classical Complement Pathways

Pietrocola

Rindi

Rosini³

et al. 2016

The Journal of Immunology

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The group B Streptococcus (GBS) is a leading cause of neonatal invasive disease. GBS bacteria are surrounded by a thick capsular polysaccharide that is a potent inhibitor of complement deposition via the alternative pathway. Several of its surface molecules can however activate the classical and lectin complement pathways, rendering this species still vulnerable to phagocytic killing. In this study we have identified a novel secreted protein named complement interfering protein (CIP) that downregulates complement activation via the classical and lectin pathways, but not the alternative pathway. The CIP protein showed high affinity toward C4b and inhibited its interaction with C2, presumably preventing the formation of the C4bC2a convertase. Addition of recombinant CIP to GBS cip-negative bacteria resulted in decreased deposition of C3b on their surface and in diminished phagocytic killing in a whole-blood assay. Our data reveal a novel strategy exploited by GBS to counteract innate immunity and could be valuable for the development of anti-infective agents against this important pathogen.

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“…While it remains a major cause of morbidity and mortality in infants, S. agalactiae is a human commensal that colonizes the rectal and the vaginal mucosa of 15–30% of women [3], [5]. Rebecca Lancefield originally defined two cell wall carbohydrate antigens in S. agalactiae : the group B-specific antigen (GBC) common to all strains and the capsular antigen which currently defines 10 different serotypes (Ia, Ib, II to IX) [6].…”

Section: Introductionmentioning

confidence: 99%

Role of the Group B Antigen of Streptococcus agalactiae: A Peptidoglycan-Anchored Polysaccharide Involved in Cell Wall Biogenesis

et al. 2012

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Streptococcus agalactiae (Group B streptococcus, GBS) is a leading cause of infections in neonates and an emerging pathogen in adults. The Lancefield Group B carbohydrate (GBC) is a peptidoglycan-anchored antigen that defines this species as a Group B Streptococcus. Despite earlier immunological and biochemical characterizations, the function of this abundant glycopolymer has never been addressed experimentally. Here, we inactivated the gene gbcO encoding a putative UDP-N-acetylglucosamine-1-phosphate:lipid phosphate transferase thought to catalyze the first step of GBC synthesis. Indeed, the gbcO mutant was unable to synthesize the GBC polymer, and displayed an important growth defect in vitro . Electron microscopy study of the GBC-depleted strain of S. agalactiae revealed a series of growth-related abnormalities: random placement of septa, defective cell division and separation processes, and aberrant cell morphology. Furthermore, vancomycin labeling and peptidoglycan structure analysis demonstrated that, in the absence of GBC, cells failed to initiate normal PG synthesis and cannot complete polymerization of the murein sacculus. Finally, the subcellular localization of the PG hydrolase PcsB, which has a critical role in cell division of streptococci, was altered in the gbcO mutant. Collectively, these findings show that GBC is an essential component of the cell wall of S. agalactiae whose function is reminiscent of that of conventional wall teichoic acids found in Staphylococcus aureus or Bacillus subtilis . Furthermore, our findings raise the possibility that GBC-like molecules play a major role in the growth of most if not all beta –hemolytic streptococci.

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Group B Streptococcal Infections

Cited by 118 publications

References 680 publications

Group B Streptococcus Colonization in Late Pregnancy and Invasive Infection in Neonates in China: A Population-Based 3-Year Study

Group B Streptococcus Colonization in Late Pregnancy and Invasive Infection in Neonates in China: A Population-Based 3-Year Study

The Group B Streptococcus–Secreted Protein CIP Interacts with C4, Preventing C3b Deposition via the Lectin and Classical Complement Pathways

Role of the Group B Antigen of Streptococcus agalactiae: A Peptidoglycan-Anchored Polysaccharide Involved in Cell Wall Biogenesis

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