A 30-minute old, 39 2/7 week gestation female was admitted to the newborn nursery. The past medical history showed she was born to a G2P1 now 2, 28 year old mother who had received appropriate prenatal care. Her pregnancy had been complicated by group B streptococcus (GBS) positive vaginal colonization, but negative for GBS bacturia. She had rupture of membranes 7 hours prior to vaginal delivery and had received 2 doses of ampicillin at 6.5 and 3 hours prior to delivery. She had no intrapartum fever. Apgars were 8 and 9. The family history showed some diabetes and heart disease. The 2.5 year old sibling had a normal birth and delivery.
The pertinent physical exam showed a healthy female who was 3.163 kg (50%), head circumference of 35 cm (65%) and length 49 cm (50%) and the Ballard assessment was 39 weeks gestation. Her vital signs were normal without tachypnea or temperature instability. Her examination was normal. The diagnosis of a healthy female with a mother who was GBS positive was made. The infant was admitted to the newborn nursery and had a screening laboratory evaluation that showed normal complete blood count, C-reactive protein of < 0.5 mg/dl and erythrocyte sedimentation rate of 5 mm/hr. The infant was not started on antibiotics as the mother had been treated within 4 hours of delivery with antibiotics and the screening labs were normal as was her physical examination and vital signs. The infant’s clinical course over the next 2 days was normal with a mildly increased bilirubin of 6.8 mg/dl at discharge. Her repeat screening laboratory testing at 24 hours was also normal and she was discharged home. At followup on day of life 4 the infant was doing well. Her transcutaneous bilirubin was 9.6 mg/dl and her weight was only decreased by 7% from her birthweight. Her mother’s breast milk had come in and the infant was feeding vigorously.
Streptococcus agalactiae or Lancefield Group B streptococcus (GBS) was first described in 1887 and the first neonatal cases were described in the early 1960s. GBS can cause infections in all age groups but pregnant women and infants share most of the burden of the disease. GBS asymptomatically colonizes the genital and gastrointestinal tracts of pregnant women (15-40%). GBS is then transmitted vertically to infants generally after the rupture of fetal membranes or onset of labor. It is estimated that 50% of infants born to GBS+ mothers become colonized and 1% have invasive disease. Recurrent infections do occur in about 1-6% of patients.
For infants, the GBS disease is classified by age of onset:
- Early onset (EOGBS)
- Occurs from day 0-day 6 of life
- 60-70% of cases of disease
- Greatest risk in first 24 hours of life, especially the first 12 hours of life
- Caused by vertical transmission
- Risk factors include: maternal GBS colonization (most important factor), maternal GBS bacturia, male gender, black race, prolonged rupture of membranes, prematurity, intrapartum fever, low maternal GBS antibodies, previous infant with EOGBS
- Usually presents with sepsis, pneumonia, or meningitis. Death occurs in 2-20% depending on risk factors.
- Late onset (LOGBS)
- Occurs from 7 -89 days of life
- Cause is vertical transmission most often but also nosocomial or community contacts
- Risk factors include maternal GBS colonization, male sex, black race, twin with LOBGBS, prematurity and infants born to HIV+ mothers.
- Usually presents with bactermia, meningitis, bone/joint infections, or cellulitis/adenitis. Death occurs in 1-6% depending on risk factors.
- Late, late onset
- > 90 days of life
- More common in < 28 week premature infants or those with an immunodeficiency
- Cause is from maternal, familial or community contact, usually not vertical transmission.
- Usually presents with fever without a source, bone/joint infections, skin and soft tissue infections.
Intrapartum antibiotics (IAP) have been shown to reduce the risk of delivering an infant with GBS disease. Guidelines from the American Academy of Pediatrics and other organizations help clinicians to evaluate an individual infant’s risk factors to determine if and when screening laboratories should be obtained and repeated, when and if prophylactic antibiotics should be started and which antibiotics to use, evaluation of an infant suspected to have sepsis, and duration of antibiotic therapy for those suspected or proven to have GBS disease. See To Learn More below.
GBS has a capsular polysaccharide antigen which is the major virulence factor and which helps the organism to counteract host defense mechanisms. The serotypes of GBS are divided into 10 different types based on this capsular polysaccharide antigen. They are Ia, Ib, II, III, IV, V, VI, VII, VIII and IX.
- While all serotypes can cause neonatal disease, in the US and Europe the invasive serotypes are mainly Ia, IB, II, III and V.
- Most frequent serotypes from all data sources are III(48.9%), Ia, (22.9%), V (9.1%), Ib (7%) and II (6.2%).
- LOGBS and neonatal meningitis are associated most often with III.
- EOGBS is associated most often with Ia, II, III, and V.
Maternal GBS vaccines are being developed. A recent cost-effectiveness analysis of using maternal vaccination (trivalent with serotypes Ia, Ib and III) along with IAP found that while vaccination would cost ~$362.7 million the cost savings would be $43.5 million. This $43.5 million may be comparable to other recently approved vaccines for children and adolescents in the US.
Questions for Further Discussion
1. How are practices for maternal intrapartum screening and antibiotics different in middle or low income countries?
2. What are GBS disease manifestations for postpartum women?
3. What prophylactic antibiotics are usually given for infants exposed to GBS?
- Symptom/Presentation: Health Maintenance and Disease Prevention
To Learn More
To view pediatric review articles on this topic from the past year check PubMed.
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Le Doare K, Heath PT. An overview of global GBS epidemiology. Vaccine. 2013 Aug 28;31 Suppl 4:D7-12.
Ohlsson A1, Shah VS. Intrapartum antibiotics for known maternal Group B streptococcal colonization.Cochrane Database Syst Rev. 2014 Jun 10;6:CD007467. doi: 10.1002/14651858.CD007467.pub4.
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Puopolo KM, Baker CJ. Group B Streptococcal Infection in Neonates and Young Infants. Up To Date.
(rev. 8/10/15, cited 11/19/2015).
Nuccitelli A, Rinaudo CD, Maione D. Group B Streptococcus vaccine: state of the art. Ther Adv Vaccines. 2015 May;3(3):76-90.
Donna M. D’Alessandro, MD
Professor of Pediatrics, University of Iowa Children’s Hospital