Continuing Education Activity

Group B Streptococcus (GBS) colonization affects up to one-third of healthy women, often residing silently in the gastrointestinal or genitourinary tracts. However, during childbirth, GBS can be transmitted to the newborn, leading to life-threatening infections such as sepsis, pneumonia, or meningitis. Despite established screening and prophylaxis protocols, GBS remains a leading cause of neonatal morbidity and mortality worldwide.

This activity provides an in-depth review of the organism’s epidemiology, pathophysiology, modes of transmission, diagnostic methods, and evolving prevention strategies that have reduced early-onset neonatal disease through targeted maternal screening and intrapartum antibiotic prophylaxis. Emerging evidence on antibiotic resistance and vaccine development is also discussed. Participants will also gain evidence-based insights into the clinical presentation, diagnostic approach, and therapeutic management of GBS infections across age groups, including neonatal, obstetric, and adult populations.

The course emphasizes optimal antimicrobial selection, duration of therapy, and strategies to prevent recurrence and colonization, as well as recent updates to prophylactic guidelines and their implications for patient safety and perinatal outcomes. This activity for healthcare professionals is designed to enhance the learner's competence in identifying GBS-related infections, performing the recommended evaluation, and implementing an appropriate interprofessional approach when caring for mothers and infants affected by GBS, ultimately optimizing perinatal care and reducing neonatal infection rates. 

Objectives:

• Identify the clinical manifestations of group B Streptococcus infection across age groups.
• Apply current evidence-based guidelines for the screening of group B Streptococcus infection in perinatal care.
• Differentiate between group B Streptococcus infection subtypes to guide clinical management.
• Collaborate effectively within the interprofessional healthcare team to improve the implementation of timely interventions for patients at risk of group B Streptococcus infection.

Introduction

The pathogen Streptococcus agalactiae represents group B Streptococcus (GBS). The commonly used term for GBS is based on the Lancefield grouping, which takes into account specific cell wall carbohydrate antigens. This pathogen is a common colonizer of the genital and gastrointestinal tracts, and GBS colonization in pregnant women is a significant risk factor for neonatal and infant infection.[1] The widespread screening of pregnant women for this organism in the third trimester and subsequent antibiotic prophylaxis for maternal colonization has dramatically reduced the incidence of early-onset neonatal disease from 1.7 cases per 1000 live births in the early 1990s to 0.22 cases per 1000 live births in 2017. Direct medical costs of neonatal disease before prevention were $294 million annually. This article discusses different aspects of GBS infection in neonates, infants, pregnant women, and older adults.

Edmond Nocard first recognized this pathogen in 1887 as a source of bovine mastitis that resulted in agalactia or lack of milk production. Decades later, S agalactiae gained recognition as a human pathogen responsible for infections, most commonly in pregnant women and newborns. However, the significance of this organism was not discovered until 1938, when Fry described 3 fatal cases of postpartum sepsis. Numerous reports continued to ascribe neonatal infections to this pathogen until the 1970s, when GBS emerged as the predominant organism causing bacteremia and meningitis in newborns and young infants younger than 3 months old.[2] GBS is also an occasional cause of infections in postpartum women (endometritis) and individuals with impaired immune systems, in whom the organism may cause septicemia or pneumonia.[3]

Etiology

Pathogen Characteristics

GBS is a gram-positive, catalase-negative organism that appears as cocci in pairs and chains on Gram stain (see Image. Group B Streptococcus, Gram Stain). When grown on blood agar, they appear as small colorless colonies that cause beta-hemolysis or complete hemolysis (see Image. Comparisons of Hemolytic Activity for Groups A, B, G, and F Streptococci). This is because S agalactiae forms a toxin which causes complete lysis of the hemoglobin in red blood cells.[4]

The group B-specific cell wall carbohydrate antigen is common to all strains of GBS, and a surface capsular polysaccharide allows classification into types Ia, Ib, II, III, IV, V, VI, VII, VIII, and IX (Lancefield classification scheme). A surface protein antigen, C protein, with alpha and beta components, is common to all Ib strains, to 30% of type Ia strains, to 60% of type II strains, and to some type IV, V, and VI strains. Another surface component is a pilus that facilitates attachment to mucosal surfaces. The hypervirulent clonal complex ST-17 of type III has a tropism for meninges and is typically present among invasive but not colonizing neonatal isolates.

Virulence

Streptococcus agalactiae has several virulence factors that help it attach to the host cells and evade the immune system, including:[5][6]

• This bacterium is encapsulated by a polysaccharide layer rich in sialic acid, which is a substance also found in human cells. Thus, inexperienced immune cells in a newborn may confuse S agalactiae for self-cells, allowing them to survive inside the body. A type-specific capsular polysaccharide is released from cells, and the amount elaborated has been correlated with virulence.

• The capsule also has pili, which are hair-like structures that help the bacteria attach to a host cell.

• S agalactiae makes beta-hemolysin, a pore-forming toxin that destroys the host’s red blood cells, resulting in hemolysis.

• GBS produces several bacterial products. Most strains possess C5a-ase, an enzyme of the serine esterase class that inactivates complement component C5a.[7] This C5a is a potent chemoattractant for neutrophils. This GBS enzyme helps the bacteria evade the host immune system by hindering the accumulation of neutrophils at the infection site.[5][6]

Group B Streptococcus Colonization

GBS can be found colonizing normal gastrointestinal and genitourinary flora in up to one-third of healthy asymptomatic women. Several factors associated with a higher risk of colonization include Black race, obesity, multiple sexual partners, man-to-woman oral sex, frequent sexual intercourse, tampon use, and infrequent hand washing. Pregnant women colonized with GBS can spread the bacteria to their infants before or during childbirth. The acquisition of neonatal GBS presumably occurs either by ascending transmission through ruptured membranes or from contact with the organism in the genital tract during vaginal deliveries.

Research has also described horizontal transmission from mothers or other nosocomial and community contacts.[8] Research studies investigating the causes of late-onset GBS disease propose an acquired fecal-oral route of transmission. Whether late-onset disease results from an exogenous source, eg, breast milk, or established colonization, or both, remains unclear. In addition to newborn infants, GBS can also cause invasive infections in those with a weakened immune system, eg, pregnant women or immunocompromised adults with malignancy, diabetes mellitus, or HIV. Also, patients with either asplenia or functional asplenia, eg, those with sickle cell disease, may be at risk for invasive GBS infection, given the spleen’s important role in neutralizing encapsulated organisms. 

Epidemiology

Colonization and infection in neonates largely correlate with maternal colonization at the time of delivery. Vertical transmission from colonized mothers to their neonates occurs in approximately 41% to 72% of cases (mean, approximately 50%). However, about 1% to 12% of colonized infants (mean, 5%) are born to noncolonized mothers.[9] Furthermore, heavy maternal colonization in the genital tract (>10 colony-forming units/mL) dramatically increases the rates of vertical transmission and heavily colonized infants. Heavily colonized infants are then more likely to have either early- or late-onset GBS disease.

Before the widespread use of intrapartum prophylactic antibiotics, reported attack rates of early-onset neonatal GBS infections ranged from 1.8 to 4.0 per 1000 live births. Early-onset disease (onset within the first 6 days of life) accounted for approximately 80% of cases or about 7600 cases annually. Following the 2002 guidelines for universal screening and administration of prophylactic antibiotics to colonized pregnant women, the incidence of early-onset disease has decreased to approximately 0.25 cases per 1000 live births, a finding representing a decline of nearly 85% from 1990 (see Image. Incidence of Early and Late-Onset Group B Streptococcus Disease).[10]

However, the incidence of late-onset disease (onset from 7 through 89 days of life) did not change with maternal intrapartum antibiotic prophylaxis, remaining at approximately 0.27 per 1000 live births.[11] Late-onset GBS disease occurs in infants older than 3 months of age and accounts for 7% to 13% of childhood GBS infections. Affected infants typically were born before 34 weeks of gestation or have an underlying immunodeficiency or concomitant infection with HIV (see Image. Indications for Intrapartum Antibiotic Prophylaxis). In the past 2 decades, 2-fold to 4-fold increases in the incidence of GBS disease have occurred in nonpregnant adults, mostly those who have underlying medical conditions or are 65 years of age or older. Residents of nursing homes have a markedly higher incidence of invasive group B streptococcal disease than community residents.[12]

Pathophysiology

In pregnant women colonized with S agalactiae, bacteria can ascend from the genitourinary tract towards the uterus or bladder. In the uterus, the bacteria can affect the fetal membranes, causing chorioamnionitis, potentially leading to premature labor, miscarriage, or intrauterine fetal demise if the bacterium invades the neonate. Alternatively, the bacterium may invade the newborn’s respiratory tract through amniotic fluid or contact with maternal colonization during vaginal delivery, causing inflammation of the lung tissue or GBS pneumonia. Occasionally, S agalactiae can destroy the baby’s alveolar lining with beta-hemolysin and reach the bloodstream, causing bacteremia and concomitant neonatal sepsis. Furthermore, bacteria from the bloodstream may cross the blood-brain barrier and migrate to the cerebrospinal fluid (CSF), causing neonatal meningitis. Finally, although less common, the bacteria may also travel via the bloodstream to joints, causing septic arthritis.

History and Physical

Group B Streptococcus Neonatal Infection

GBS has remained the primary cause of neonatal sepsis since the 1970s. Based on the age of presentation, GBS is divided into the following early-onset, late-onset, and late-late onset types:

• Early-onset disease

  • Defined as the onset of infection in the first 6 days of life, but most neonates (61% to 95%) become ill within the first 24 hours (median, 1 hour). 
  • Infants typically present with respiratory distress, eg, apnea or tachypnea, grunting respirations, and cyanosis. Other signs include lethargy, poor feeding, abdominal distention, pallor, jaundice, tachycardia, and hypotension.
  • Fever is usually present in term neonates, but preterm infants are often nonfebrile or hypothermic. 
  • Bacteremia is the most common form of early-onset GBS disease, accounting for approximately 80% of cases. Pneumonia and meningitis, although not uncommon, are less likely presentations in early-onset disease, accounting for 15% and 5% to 10%, respectively.

• Late-onset disease

  • Defined as GBS infection from day 7 to day 89 of life (median 37 days), late-onset GBS has a similar clinical presentation to early-onset disease.[13]
  • Although bloodstream infections remain the most common presentation of late-onset disease, meningitis occurs in about 30% of cases, as opposed to 5% in early-onset disease.
  • Late-onset GBS has no known effective prevention measures.
  • Late-onset disease may also present with other less common foci of infections (eg, osteomyelitis, pyogenic arthritis, and cellulitis-adenitis syndrome).[14] 
  • The proximal humerus is the most frequently affected site in infants with osteomyelitis, whereas pyogenic arthritis typically affects the hip and knee joints.
  • GBS cellulitis-adenitis syndrome is generally unilateral, involving facial or submandibular sites, although the literature describes it in inguinal, scrotal, and prepatellar regions. This syndrome presents with swelling of the affected soft tissue area and enlarged adjacent lymph nodes. Aspiration of the affected area of cellulitis often yields GBS, and concomitant bacteremia is very often present.

• Late, late-onset GBS disease (ie, very late-onset GBS)

  • Defined as GBS infection in infants 3 months of age or older.
  • Most cases of late, late-onset GBS disease occur in premature infants or those with very low birth weights whose corrected postmature age is younger than 3 months.
  • In full-term infants, late, late-onset GBS disease can be associated with HIV infection or immunodeficiency. The clinical manifestations in these older infants are similar to those in patients with typical late-onset infection; bacteremia without a focus and meningitis are the most common clinical features.

Adult Group B Streptococcus Infection

Invasive GBS disease contributes significantly to morbidity and mortality among adults older than 65, Black individuals, and those with diabetes. Most adults affected by invasive GBS infection have underlying medical conditions, with diabetes present in 41% of cases, heart disease in 36%, and malignancy in 17%. These comorbidities increase susceptibility and complicate the clinical course of infection.

Common presenting manifestations of GBS infection in adults include fever, chills, and altered mental status. A considerable proportion of adult infections occur in association with pregnancy, with GBS responsible for 15% of peripartum endometritis cases, 15% of pregnancy-associated bacteremia, and 15% of postcesarean wound infections. Beyond pregnancy-related illness, GBS frequently causes focal infections, eg, pneumonia, endocarditis, skin and soft tissue infections, and osteomyelitis. Approximately 4% of nonpregnant adults who recover from an initial episode of GBS bacteremia experience a second recurrence within 1 year, underscoring the need for vigilant monitoring and appropriate follow-up care.

Evaluation

Meningitis in early-onset GBS disease presents clinical features indistinguishable from bacteremia without a focus, and up to 30% of neonates with meningitis demonstrate negative blood cultures. A lumbar puncture remains essential to confirm or exclude meningeal involvement, even when a focal GBS infection exists. Rapid antigen detection methods fail to provide reliable alternatives to cultures obtained from blood or other normally sterile body fluids, and repeating antigen tests during therapy offers no clinical benefit.

A limited study utilizing real-time polymerase chain reaction to detect deoxyribonucleic acid in the blood of 8 neonates with culture-proven GBS sepsis produced corresponding positive findings. However, additional prospective studies are required to determine the sensitivity and specificity of this diagnostic approach. Definitive diagnosis of GBS infection depends on culturing the organism from a sterile body site, which confirms the presence of invasive disease and guides appropriate antimicrobial management.

Treatment / Management

Empiric Treatment

The initial therapy for suspected neonatal sepsis is ampicillin and an aminoglycoside, typically gentamicin. Both ampicillin and gentamicin have activity against GBS, which is the most common cause of neonatal sepsis. Additionally, this combination has a synergistic effect and is more effective than either ampicillin or penicillin G alone in killing most GBS strains in vitro and in vivo. Following confirmation of GBS as the causative pathogen, sterility of the bloodstream and CSF is documented, and clinical improvement is observed; penicillin G alone should be used to complete therapy. The focus and severity of the infection should dictate recommendations concerning the optimal dose and duration of treatment.[15]

Specific Treatment

Infants with GBS meningitis should undergo a second lumbar puncture 1 to 2 days after initiating therapy to confirm CSF sterility. When CSF culture results are negative, treatment may continue with penicillin G alone for a minimum of 14 days. Persistent positive CSF cultures warrant an extended treatment course and further diagnostic evaluation. Contrast-enhanced neuroimaging assists in detecting unresolved cerebritis or ventriculitis and may reveal rare complications, eg, subdural empyema or intracranial abscess. Imaging also aids in identifying cerebrovascular complications, including septic thrombophlebitis, which can significantly influence prognosis.

A repeat lumbar puncture following therapy helps assess CSF cell count and protein levels. Polymorphonuclear cells exceeding 30% or protein levels above 200 mg/dL indicate cerebritis or parenchymal destruction and justify prolonged therapy. All infants recovering from GBS meningitis should undergo a diagnostic auditory brainstem response (ABR) test to evaluate potential hearing impairment.

Infants with bacteremia without a focal infection require a complete 10-day course of intravenous antibiotics. Although uncommon, relapse has been reported with shorter regimens. Oral therapy lacks sufficient efficacy and remains inappropriate for managing invasive GBS disease (see Image. Therapeutic Management for Group B Streptococcus Disease in Infants).

Recurrent Infections

The recurrence rate for early-onset GBS disease is approximately 1%. Although rare, recurrence can be due to inadequate dose or duration of therapy, reinfection with a second strain or type, supportive foci, HIV infection, or a humoral immune deficiency. Humoral immune deficiency may be too early to diagnose definitively; however, total IgG levels are usually significantly lower than expected for the patient’s age.

Furthermore, susceptibility testing from both the initial infection and any recurrent episode should be reviewed to confirm in vitro sensitivity to penicillin. When the cause of recurrence cannot be determined, persistent mucous membrane colonization with GBS often represents the most probable source. Beta-lactam antibiotics, even when administered parenterally, fail to eradicate GBS colonization consistently. Some investigations have demonstrated potential benefits of rifampin at a dosage of 20 mg/kg per day, administered orally during the final 4 days of parenteral therapy, in eliminating mucosal GBS colonization. However, more recent research has shown inconsistent results, with rifampin failing to eradicate GBS colonization in infants reliably.[16]

Intrapartum Antibiotic Prophylaxis

Intrapartum antibiotic prophylaxis (IAP) is indicated for all mothers with a positive GBS screening culture routinely obtained between 36 0/7 to 37 6/7 weeks of gestation.[17] Revised guidelines from 2019 also recommend IAP for pregnant women who have a history of GBS bacteriuria at any point during the current pregnancy or have a history of a previous infant with invasive GBS disease. In pregnant women with unknown GBS status, IAP is indicated if any of the following risk factors are present:

• Preterm delivery less than 37 weeks of gestation
• Membrane rupture for 18 hours or greater
• An intrapartum temperature of 100.4 °F or higher
• The intrapartum nucleic acid amplification test (NAAT) is positive

Prophylaxis with a beta-lactam antibiotic, preferably penicillin, administered 4 or more hours before delivery, provides highly effective protection against early-onset GBS disease. The initial penicillin G dose equals 5 million units, followed by 2.5 to 3 million units every 4 hours until delivery. As an alternative, ampicillin may be used, starting with a 2 g intravenous (IV) loading dose, followed by 1 g IV every 4 hours until delivery.

Women allergic to penicillin who lack a history of anaphylaxis, angioedema, respiratory distress, or urticaria following penicillin or cephalosporin administration should receive cefazolin, starting with 2 g initially and continuing with 1 g every 8 hours until delivery. For women with a severe penicillin allergy, susceptibility testing of the GBS isolate should guide therapy. Based on susceptibility results, clindamycin at 900 mg IV every 8 hours or vancomycin at 1 g IV every 12 hours until delivery may be administered. However, the efficacy of either clindamycin or vancomycin IAP in preventing early-onset GBS neonatal disease has not been validated. Adequate IAP requires administration of penicillin, ampicillin, or cefazolin at least 4 hours before delivery.[18] Any alternative medication, dose, or duration remains inadequate for neonatal management.

Differential Diagnosis

The signs and symptoms of early-onset GBS disease are clinically indistinguishable from neonatal sepsis caused by other bacterial pathogens, including:

• Enterobacteriaceae
• Listeria

The prominence of respiratory signs in early-onset disease may lead to confusion with noninfectious causes of respiratory distress, including:

• Respiratory distress syndrome
• Transient tachypnea of the newborn
• Meconium aspiration

The differential diagnosis of late-onset disease depends on the focus of the infection. For example, meningitis in infants of this age may rarely result from Streptococcus pneumoniae, Neisseria meningitidis, Listeria monocytogenes, Haemophilus influenzae (type b and nontypeable), and more commonly from viruses. The findings of osteomyelitis may be subtle; a patient's inability to move their arm might be attributed to neuromuscular disease or Erb palsy.

Pertinent Studies and Ongoing Trials

A GBS vaccine for maternal immunization is in advanced clinical development. This immunization, which has a hexavalent glycoconjugate vaccine (GBS6), has shown promising safety and immunogenicity in phase 2 trials but is not yet licensed for clinical use as of 2025. Recent studies demonstrate that GBS6, which targets the 6 most prevalent serotypes responsible for nearly all invasive neonatal GBS disease, elicits robust maternal antibody responses. These responses are efficiently transferred to infants, reaching levels associated with a reduced risk of both early- and late-onset GBS disease.[19][20] The vaccine has shown no significant safety concerns in mothers or infants, and the majority of infants achieved antibody concentrations above putative protective thresholds. 

Current prevention relies on IAP, which is highly effective for early-onset disease, but does not prevent late-onset disease, stillbirth, or preterm birth associated with GBS, and is limited in resource-poor settings.[21] A maternal vaccine could address these gaps, reduce antibiotic use, and provide protection in settings where IAP is not feasible.

Prognosis

The outcome of GBS disease is related to the severity and site of infection. The overall mortality rate remains substantial at 3% to 10% for early-onset disease and 1% to 6% for late-onset disease. Premature infants born before 37 weeks of gestation with early-onset disease have the highest mortality rate, approximately 20%. Information on the long-term outcome of patients with GBS sepsis without meningitis is limited. In infants with septic shock, the development of periventricular leukomalacia correlated with neurodevelopmental sequelae. 

Despite advances in prevention, detection, and care for patients with GBS meningitis, the neurologic outcome of patients remains the same. Approximately 20% to 30% of infants with early- or late-onset meningitis will have permanent severe neurologic impairments, eg, cortical blindness, bilateral sensorineural hearing loss, cerebral palsy, or severe motor deficits. Another 25% of patients will have mild to moderate impairments, eg, hydrocephalus requiring a ventriculoperitoneal shunt, seizures, or mild developmental and learning delays. Only 51% of patients demonstrated normal age-appropriate development. 

Complications

As previously noted, GBS infection can lead to serious complications across neonates, pregnant women, and adults with underlying conditions. In neonates, early-onset disease often presents as sepsis, pneumonia, or meningitis, with potential for cerebritis, ventriculitis, subdural empyema, intracranial abscess, and cerebrovascular complications, eg, septic thrombophlebitis. Late-onset and very late-onset infections can additionally result in osteomyelitis, septic arthritis, and cellulitis-adenitis syndrome.

Infants recovering from GBS meningitis are at risk for long-term sequelae, including hearing impairment, necessitating auditory brainstem response testing. In adults, GBS may cause bacteremia, pneumonia, endocarditis, skin and soft tissue infections, and osteomyelitis, with increased morbidity in older adults, individuals with diabetes, heart disease, or malignancy, and pregnant women. Recurrent infections can occur due to persistent mucosal colonization, highlighting the need for careful monitoring, susceptibility testing, and targeted antimicrobial therapy.

Deterrence and Patient Education

GBS is a bacterium commonly present in the lower gastrointestinal and genital tracts of up to 35% of healthy women. Although most women colonized with GBS are healthy and have no symptoms, a few develop GBS disease when the bacterium invades the body. In pregnant women, this can be critical and life-threatening to both the infant and mother. In expecting mothers, GBS disease may cause urinary tract infections, infection of the amniotic fluid surrounding the baby, or infection of the uterus after delivery. GBS infections may even lead to preterm labor or stillbirth.

Pregnant women who carry GBS can also pass on the bacteria to their newborns, and some of those babies may then develop early-onset disease. Although most infants infected with GBS typically present with symptoms immediately after birth, some will develop an infection months following birth. Symptoms include, but are not limited to, difficulty breathing, grunting sounds, fussiness, sleepiness, poor feeding, low blood pressure, low or high temperatures, or even seizures.

To prevent transmission of GBS from mother to infant, all pregnant women should be screened for GBS colonization as part of their routine prenatal care late in their third trimester (usually between 36 0/7 and 37 6/7 weeks of gestation). Those who test positive for GBS will receive IV antibiotics during labor to lower the risk of transmission to the baby. Penicillin is the most common and most effective antibiotic given for GBS. However, if a patient is allergic to penicillin, other antibiotics are also available and effective. If the GBS status is unknown at delivery, certain risk factors will determine whether to use antibiotic prophylaxis. Clinicians should also keep in mind that some infants may still develop GBS disease even with testing and prophylactic treatment.

Enhancing Healthcare Team Outcomes

GBS remains a leading cause of neonatal sepsis and a significant contributor to maternal and adult infections, particularly among high-risk populations. Colonization in pregnant women poses a substantial risk for early-onset neonatal disease, while late-onset infections continue to challenge clinicians due to limited preventive strategies. Effective prevention and management require comprehensive screening, timely intrapartum antibiotic prophylaxis, accurate diagnosis, and evidence-based antimicrobial therapy, all supported by ongoing research into vaccine development and novel interventions.

Optimal patient-centered care depends on coordinated, interprofessional collaboration. Obstetricians and midwives lead maternal screening and prophylaxis, while neonatologists and pediatricians evaluate and manage at-risk infants. Nurses monitor patients, educate families, and facilitate rapid communication of clinical changes, and pharmacists guide appropriate antibiotic selection, dosing, and monitoring for interactions. Laboratory personnel ensure accurate identification of GBS. Strong interprofessional communication, shared responsibility, and adherence to evidence-based protocols enhance patient safety, improve maternal and neonatal outcomes, and support continuity of care. This integrated approach fosters teamwork, reduces early-onset infections, and advances strategies to prevent late-onset disease. Ultimately, effective teamwork improves safety, continuity of care, and outcomes for both mother and infant.

Review Questions

• Access free multiple choice questions on this topic.
• Click here for a simplified version.
• Comment on this article.

References

1.

Neubauer-Bruckner C, Sommer I, Nußbaumer-Streit B. [WHO recommendation on screening of pregnant women for intrapartum antibiotic prophylaxis for the prevention of early onset Group B streptococcus disease in newborns]. Gesundheitswesen. 2025 Aug;87(8-09):560-563. [PubMed: 40789292]

2.

Cheng L, Xu FL, Niu M, Li WL, Xia L, Zhang YH, Xing JY. [Pathogens and clinical features of preterm infants with sepsis]. Zhongguo Dang Dai Er Ke Za Zhi. 2019 Sep;21(9):881-885. [PMC free article: PMC7390238] [PubMed: 31506146]

3.

Tevdorashvili G, Tevdorashvili D, Andghuladze M, Tevdorashvili M. Prevention and treatment strategy in pregnant women with group B streptococcal infection. Georgian Med News. 2015 Apr;(241):15-23. [PubMed: 25953932]

4.

Six A, Firon A, Plainvert C, Caplain C, Bouaboud A, Touak G, Dmytruk N, Longo M, Letourneur F, Fouet A, Trieu-Cuot P, Poyart C. Molecular Characterization of Nonhemolytic and Nonpigmented Group B Streptococci Responsible for Human Invasive Infections. J Clin Microbiol. 2016 Jan;54(1):75-82. [PMC free article: PMC4702713] [PubMed: 26491182]

5.

Burcham LR, Spencer BL, Keeler LR, Runft DL, Patras KA, Neely MN, Doran KS. Determinants of Group B streptococcal virulence potential amongst vaginal clinical isolates from pregnant women. PLoS One. 2019;14(12):e0226699. [PMC free article: PMC6919605] [PubMed: 31851721]

6.

Paoletti LC, Kasper DL. Surface Structures of Group B Streptococcus Important in Human Immunity. Microbiol Spectr. 2019 Mar;7(2) [PMC free article: PMC11590616] [PubMed: 30873933]

7.

Takahashi S, Aoyagi Y, Adderson EE, Okuwaki Y, Bohnsack JF. Capsular sialic acid limits C5a production on type III group B streptococci. Infect Immun. 1999 Apr;67(4):1866-70. [PMC free article: PMC96539] [PubMed: 10085029]

8.

Morinis J, Shah J, Murthy P, Fulford M. Horizontal transmission of group B streptococcus in a neonatal intensive care unit. Paediatr Child Health. 2011 Jun;16(6):e48-50. [PMC free article: PMC3328229] [PubMed: 22654550]

9.

Berardi A, Rossi C, Creti R, China M, Gherardi G, Venturelli C, Rumpianesi F, Ferrari F. Group B streptococcal colonization in 160 mother-baby pairs: a prospective cohort study. J Pediatr. 2013 Oct;163(4):1099-104.e1. [PubMed: 23866714]

10.

Berardi A, Spada C, Vaccina E, Boncompagni A, Bedetti L, Lucaccioni L. Intrapartum beta-lactam antibiotics for preventing group B streptococcal early-onset disease: can we abandon the concept of 'inadequate' intrapartum antibiotic prophylaxis? Expert Rev Anti Infect Ther. 2020 Jan;18(1):37-46. [PubMed: 31762370]

11.

Kristeva M, Tillman C, Goordeen A. Immunization Against Group B Streptococci vs. Intrapartum Antibiotic Prophylaxis in Peripartum Pregnant Women and their Neonates: A Review. Cureus. 2017 Oct 13;9(10):e1775. [PMC free article: PMC6017184] [PubMed: 29946507]

12.

Francois Watkins LK, McGee L, Schrag SJ, Beall B, Jain JH, Pondo T, Farley MM, Harrison LH, Zansky SM, Baumbach J, Lynfield R, Snippes Vagnone P, Miller LA, Schaffner W, Thomas AR, Watt JP, Petit S, Langley GE. Epidemiology of Invasive Group B Streptococcal Infections Among Nonpregnant Adults in the United States, 2008-2016. JAMA Intern Med. 2019 Apr 01;179(4):479-488. [PMC free article: PMC6450309] [PubMed: 30776079]

13.

Nanduri SA, Petit S, Smelser C, Apostol M, Alden NB, Harrison LH, Lynfield R, Vagnone PS, Burzlaff K, Spina NL, Dufort EM, Schaffner W, Thomas AR, Farley MM, Jain JH, Pondo T, McGee L, Beall BW, Schrag SJ. Epidemiology of Invasive Early-Onset and Late-Onset Group B Streptococcal Disease in the United States, 2006 to 2015: Multistate Laboratory and Population-Based Surveillance. JAMA Pediatr. 2019 Mar 01;173(3):224-233. [PMC free article: PMC6439883] [PubMed: 30640366]

14.

Ong SW, Barkham T, Kyaw WM, Ho HJ, Chan M. Characterisation of bone and joint infections due to Group B Streptococcus serotype III sequence type 283. Eur J Clin Microbiol Infect Dis. 2018 Jul;37(7):1313-1317. [PubMed: 29671175]

15.

Procianoy RS, Silveira RC. The challenges of neonatal sepsis management. J Pediatr (Rio J). 2020 Mar-Apr;96 Suppl 1(Suppl 1):80-86. [PMC free article: PMC9432313] [PubMed: 31747556]

16.

Fernandez M, Rench MA, Albanyan EA, Edwards MS, Baker CJ. Failure of rifampin to eradicate group B streptococcal colonization in infants. Pediatr Infect Dis J. 2001 Apr;20(4):371-6. [PubMed: 11332660]

17.

Zhu Y, Lin XZ. Updates in prevention policies of early-onset group B streptococcal infection in newborns. Pediatr Neonatol. 2021 Sep;62(5):465-475. [PubMed: 34099416]

18.

Prevention of Group B Streptococcal Early-Onset Disease in Newborns: ACOG Committee Opinion Summary, Number 782. Obstet Gynecol. 2019 Jul;134(1):1. [PubMed: 31241596]

19.

Smith WB, Seger W, Chawana R, Skogeby Z, Silmon de Monerri NC, Feng Y, Gaylord M, Jongihlati B, Beeslaar J, Skinner JM, Bickham K, Anderson AS. A Phase 2b Trial Evaluating the Safety, Tolerability, and Immunogenicity of a 6-Valent Group B Streptococcus Vaccine Administered Concomitantly With Tetanus, Diphtheria, and Acellular Pertussis Vaccine in Healthy Nonpregnant Female Individuals. J Infect Dis. 2025 Jul 11;231(6):e1065-e1074. [PMC free article: PMC12247796] [PubMed: 40036340]

20.

Madhi SA, Anderson AS, Absalon J, Radley D, Simon R, Jongihlati B, Strehlau R, van Niekerk AM, Izu A, Naidoo N, Kwatra G, Ramsamy Y, Said M, Jones S, Jose L, Fairlie L, Barnabas SL, Newton R, Munson S, Jefferies Z, Pavliakova D, Silmon de Monerri NC, Gomme E, Perez JL, Scott DA, Gruber WC, Jansen KU. Potential for Maternally Administered Vaccine for Infant Group B Streptococcus. N Engl J Med. 2023 Jul 20;389(3):215-227. [PubMed: 37467497]

21.

Manuel G, Twentyman J, Noble K, Eastman AJ, Aronoff DM, Seepersaud R, Rajagopal L, Adams Waldorf KM. Group B streptococcal infections in pregnancy and early life. Clin Microbiol Rev. 2025 Mar 13;38(1):e0015422. [PMC free article: PMC11905376] [PubMed: 39584819]

Disclosure: Morcos Hanna declares no relevant financial relationships with ineligible companies.

Disclosure: Manan Shah declares no relevant financial relationships with ineligible companies.