scholarly journals Bacterial and Host Determinants of Group B Streptococcal Vaginal Colonization and Ascending Infection in Pregnancy

2021 ◽  
Vol 11 ◽  
Author(s):  
Alyssa Brokaw ◽  
Anna Furuta ◽  
Matthew Dacanay ◽  
Lakshmi Rajagopal ◽  
Kristina M. Adams Waldorf
Keyword(s):  
Group B Streptococcus ◽  
Neonatal Infection ◽  
Adverse Outcomes ◽  
Effective Vaccine ◽  
Host Determinants ◽  
Vaginal Colonization ◽  
Ascending Infection ◽  
Wide Range ◽  
Group B ◽  
Maternal Fetal Interface

Group B streptococcus (GBS) is a gram-positive bacteria that asymptomatically colonizes the vaginal tract. However, during pregnancy maternal GBS colonization greatly predisposes the mother and baby to a wide range of adverse outcomes, including preterm birth (PTB), stillbirth, and neonatal infection. Although many mechanisms involved in GBS pathogenesis are partially elucidated, there is currently no approved GBS vaccine. The development of a safe and effective vaccine that can be administered during or prior to pregnancy remains a principal objective in the field, because current antibiotic-based therapeutic strategies do not eliminate all cases of invasive GBS infections. Herein, we review our understanding of GBS disease pathogenesis at the maternal-fetal interface with a focus on the bacterial virulence factors and host defenses that modulate the outcome of infection. We follow GBS along its path from an asymptomatic colonizer of the vagina to an invasive pathogen at the maternal-fetal interface, noting factors critical for vaginal colonization, ascending infection, and vertical transmission to the fetus. Finally, at each stage of infection we emphasize important host-pathogen interactions, which, if targeted therapeutically, may help to reduce the global burden of GBS.

scholarly journals Streptococcus salivarius K12 Limits Group B Streptococcus Vaginal Colonization

2015 ◽  
Vol 83 (9) ◽  
pp. 3438-3444 ◽  
Author(s):  
Kathryn A. Patras ◽  
Philip A. Wescombe ◽  
Berenice Rösler ◽  
John D. Hale ◽  
John R. Tagg ◽  
...  
Keyword(s):  
Group B Streptococcus ◽  
Neonatal Infection ◽  
Antibacterial Activities ◽  
Invasive Disease ◽  
Oral Microbiota ◽  
Streptococcus Salivarius ◽  
Content Type ◽  
Vaginal Colonization ◽  
Group B

Streptococcus agalactiae(group B streptococcus [GBS]) colonizes the rectovaginal tract in 20% to 30% of women and during pregnancy can be transmitted to the newborn, causing severe invasive disease. Current routine screening and antibiotic prophylaxis have fallen short of complete prevention of GBS transmission, and GBS remains a leading cause of neonatal infection. We have investigated the ability ofStreptococcus salivarius, a predominant member of the native human oral microbiota, to control GBS colonization. Comparison of the antibacterial activities of multipleS. salivariusstrains by use of a deferred-antagonism test showed thatS. salivariusstrain K12 exhibited the broadest spectrum of activity against GBS. K12 effectively inhibited all GBS strains tested, including disease-implicated isolates from newborns and colonizing isolates from the vaginal tract of pregnant women. Inhibition was dependent on the presence of megaplasmid pSsal-K12, which encodes the bacteriocins salivaricin A and salivaricin B; however, in coculture experiments, GBS growth was impeded by K12 independently of the megaplasmid. We also demonstrated that K12 adheres to and invades human vaginal epithelial cells at levels comparable to GBS. Inhibitory activity of K12 was examinedin vivousing a mouse model of GBS vaginal colonization. Mice colonized with GBS were treated vaginally with K12. K12 administration significantly reduced GBS vaginal colonization in comparison to nontreated controls, and this effect was partially dependent on the K12 megaplasmid. Our results suggest that K12 may have potential as a preventative therapy to control GBS vaginal colonization and thereby prevent its transmission to the neonate during pregnancy.

scholarly journals Biomarkers for a histological chorioamnionitis diagnosis in pregnant women with or without group B streptococcus infection: a case-control study

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Jie Ren ◽  
Zhe Qiang ◽  
Yuan-yuan Li ◽  
Jun-na Zhang
Keyword(s):  
Cord Blood ◽  
Pregnant Women ◽  
Peripheral Blood ◽  
Group B Streptococcus ◽  
Diagnostic Value ◽  
Adverse Outcomes ◽  
Intercellular Adhesion Molecule ◽  
Tnf Α ◽  
Group B ◽  
The Impact

Abstract Background Chorioamnionitis may cause serious perinatal and neonatal adverse outcomes, and group B streptococcus (GBS) is one of the most common bacteria isolated from human chorioamnionitis. The present study analyzed the impact of GBS infection and histological chorioamnionitis (HCA) on pregnancy outcomes and the diagnostic value of various biomarkers. Methods Pregnant women were grouped according to GBS infection and HCA detection. Perinatal and neonatal adverse outcomes were recorded with a follow-up period of 6 weeks. The white blood cell count (WBC), neutrophil ratio, and C-reactive protein (CRP) level from peripheral blood and soluble intercellular adhesion molecule-1 (sICAM-1), interleukin 8 (IL-8), and tumor necrosis factor α (TNF-α) levels from cord blood were assessed. Results A total of 371 pregnant women were included. Pregnant women with GBS infection or HCA had a higher risk of pathological jaundice and premature rupture of membranes and higher levels of sICAM-1, IL-8, and TNF-α in umbilical cord blood. Univariate and multivariate regression analysis revealed that sICMA-1, IL-8, TNF-α, WBC, and CRP were significantly related to an increased HCA risk. For all included pregnant women, TNF-α had the largest receiver operating characteristic (ROC) area (area: 0.841; 95% CI: 0.778–0.904) of the biomarkers analyzed. TNF-α still had the largest area under the ROC curve (area: 0.898; 95% CI: 0.814–0.982) for non-GBS-infected pregnant women, who also exhibited a higher neutrophil ratio (area: 0.815; 95% CI: 0.645–0.985) and WBC (area: 0.849; 95% CI: 0.72–0.978), but all biomarkers had lower value in the diagnosis of HCA in GBS-infected pregnant women. Conclusion GBS infection and HCA correlated with several perinatal and neonatal adverse outcomes. TNF-α in cord blood and WBCs in peripheral blood had diagnostic value for HCA in non-GBS-infected pregnant women but not GBS-infected pregnant women.

Group B Streptococcal Infections in Neonates

1979 ◽  
Vol 1 (1) ◽  
pp. 5-15
Author(s):  
Carol J. Baker
Keyword(s):  
Group B Streptococcus ◽  
Newborn Infants ◽  
Neonatal Infection ◽  
Etiologic Agent ◽  
Diagnostic Methods ◽  
Bacterial Disease ◽  
Absolute Increase ◽  
Mortality And Morbidity ◽  
The Past ◽  
Group B

β-Hemolytic streptococci of Lancefield group B have been causally linked to neonatal disease since 1938, but only in the last decade has the group B Streptococcus become the leading etiologic agent for bacteremia and/or meningitis occurring during the first two months of life. Neither the reasons for the emergence of this organism nor the shifts over the past 40 years in the prevalence of various bacteria responsible for neonatal infection has been adequately explained. However, the importance of the group B Streptococcus as a frequent cause of neonatal mortality and morbidity demands a thorough understanding of the epidemiology and pathogenesis, clinical features, diagnostic methods, and management of these infections by physicians caring for newborn infants. INCIDENCE The common occurrence of neonatal group B streptococcal septicemia and meningitis in several geographically distant centers since 1970 has allowed the relatively precise determination of attack rates for early onset type (≤5 days) infection. Reported attack rates have been surprisingly uniform, varying from 1.3/1,000 to 4.0/1,000 live births (Table 1). Because the attack rates for serious neonatal infections associated with Escherichia coli and other maternally acquired coliform organisms have been constant since 1960, the appearance of the group B Streptococcus resulted in an absolute increase in the incidence of neonatal bacterial disease during the past decade in many hospitals in this country.

scholarly journals Serum Procalcitonin Concentrations in Term Delivering Mothers and Their Healthy Offspring: A Longitudinal Study

2000 ◽  
Vol 46 (10) ◽  
pp. 1583-1587 ◽  
Author(s):  
Marcello Assumma ◽  
Fabrizio Signore ◽  
Lucia Pacifico ◽  
Naila Rossi ◽  
John F Osborn ◽  
...  
Keyword(s):  
Risk Factors ◽  
Longitudinal Study ◽  
Group B Streptococcus ◽  
Neonatal Infection ◽  
Postnatal Period ◽  
Perinatal Factors ◽  
Healthy Neonate ◽  
Term Newborns ◽  
Group B ◽  
Endogenous Synthesis

Abstract Background: The reported sensitivities and specificities of procalcitonin (PCT) concentrations for the diagnosis of neonatal infection vary widely. A postnatal increase of PCT has been observed in healthy term newborns with a peak at ≈24 h of age, and many questions remain regarding maternal and perinatal factors that may influence the normal PCT kinetics during the immediate postnatal period. Methods: We prospectively investigated the association between the serum PCT values obtained from 121 mothers at delivery and serum PCT in their healthy, term offspring at birth as well as at 24 and 48 h of age. We also analyzed whether obstetric and perinatal factors would alter maternal and neonatal PCT response. Results: PCT concentrations in the babies at birth were significantly higher than in the mothers (P <0.0001), with even larger differences at 24 and 48 h of age. None of the variables identified from maternal and perinatal histories had a significant effect on maternal PCT response. In the healthy neonate, the variables that significantly affected the concentration of PCT at birth were the mothers’ PCT (P <0.01), maternal group B streptococcus colonization (P <0.05), and rupture of membranes ≥18 h (P <0.01). The coefficient of linear correlation between the mother’s PCT concentration and that of the baby at birth was 0.32 (P <0.01). The only variable that significantly altered the PCT concentration at both 24 (P <0.01) and 48 (P <0.01) h of age was rupture of membranes ≥18 h. Nonetheless, the PCT response observed during the 48-h period after birth among healthy babies born to mothers with risk factors for infection was well below that reported previously among age-matched neonates with sepsis. Conclusions: The postnatal increase of PCT observed in the healthy neonate with peak values at 24 h of age most likely represents endogenous synthesis. In estimating the sensitivities and specificities of PCT for diagnosis of sepsis throughout the initial 48 h of life, it is important to consider the normal PCT kinetics and the pattern(s) of PCT response in the healthy neonate.

scholarly journals A hemolytic pigment of Group B Streptococcus allows bacterial penetration of human placenta

2013 ◽  
Vol 210 (6) ◽  
pp. 1265-1281 ◽  
Author(s):  
Christopher Whidbey ◽  
Maria Isabel Harrell ◽  
Kellie Burnside ◽  
Lisa Ngo ◽  
Alexis K. Becraft ◽  
...  
Keyword(s):  
Preterm Birth ◽  
Amniotic Fluid ◽  
Preterm Labor ◽  
Group B Streptococcus ◽  
Dependent Manner ◽  
Microbial Infection ◽  
Amniotic Cavity ◽  
Protein Toxin ◽  
Ascending Infection ◽  
Group B

Microbial infection of the amniotic fluid is a significant cause of fetal injury, preterm birth, and newborn infections. Group B Streptococcus (GBS) is an important human bacterial pathogen associated with preterm birth, fetal injury, and neonatal mortality. Although GBS has been isolated from amniotic fluid of women in preterm labor, mechanisms of in utero infection remain unknown. Previous studies indicated that GBS are unable to invade human amniotic epithelial cells (hAECs), which represent the last barrier to the amniotic cavity and fetus. We show that GBS invades hAECs and strains lacking the hemolysin repressor CovR/S accelerate amniotic barrier failure and penetrate chorioamniotic membranes in a hemolysin-dependent manner. Clinical GBS isolates obtained from women in preterm labor are hyperhemolytic and some are associated with covR/S mutations. We demonstrate for the first time that hemolytic and cytolytic activity of GBS is due to the ornithine rhamnolipid pigment and not due to a pore-forming protein toxin. Our studies emphasize the importance of the hemolytic GBS pigment in ascending infection and fetal injury.

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