Group B Streptococcus infections in Pediatric Age

Introduction to Group B Streptococcus (GBS) Infections in Pediatrics

Group B Streptococcus (GBS), also known as Streptococcus agalactiae, is a gram-positive, beta-hemolytic bacterium that can cause serious infections in neonates and young infants. It is a leading cause of neonatal sepsis, meningitis, and pneumonia worldwide. Understanding GBS infections is crucial for pediatricians and neonatologists to effectively prevent, diagnose, and treat these potentially life-threatening conditions.

Epidemiology of GBS Infections

GBS colonizes the gastrointestinal and genitourinary tracts of 10-30% of pregnant women. Vertical transmission from mother to infant can occur in utero, during delivery, or in the postpartum period. The incidence of early-onset GBS disease (occurring within the first week of life) has decreased significantly with the implementation of intrapartum antibiotic prophylaxis, from 1.7 cases per 1,000 live births in the 1990s to approximately 0.23 cases per 1,000 live births in recent years. Late-onset disease (occurring between 1 week and 3 months of age) has an incidence of about 0.3-0.4 cases per 1,000 live births.

Risk factors for early-onset GBS disease include:

  • Maternal GBS colonization
  • Preterm birth (<37 weeks gestation)
  • Prolonged rupture of membranes (>18 hours)
  • Maternal intrapartum fever (>38°C)
  • Previous infant with GBS disease

Pathogenesis of GBS Infections

GBS possesses several virulence factors that contribute to its pathogenicity:

  1. Capsular polysaccharide: Helps the bacterium evade host immune responses.
  2. Pili: Facilitate adherence to host cells and promote biofilm formation.
  3. Beta-hemolysin/cytolysin: A pore-forming toxin that damages host cells.
  4. C5a peptidase: Cleaves complement component C5a, impairing neutrophil recruitment.
  5. Serine protease: Inactivates chemokines and impairs neutrophil function.

GBS can invade the bloodstream through the respiratory or gastrointestinal tract, leading to sepsis. It can also cross the blood-brain barrier, causing meningitis. The immature immune system of neonates and young infants contributes to their susceptibility to invasive GBS infections.

Clinical Manifestations of GBS Infections

GBS infections in pediatric patients can be categorized into early-onset disease (EOD) and late-onset disease (LOD):

Early-Onset Disease (0-6 days of life)

  • Sepsis (85-90% of cases)
  • Pneumonia (10-15% of cases)
  • Meningitis (5-10% of cases)

Symptoms typically appear within the first 24-48 hours of life and may include:

  • Respiratory distress
  • Temperature instability
  • Poor feeding
  • Lethargy or irritability
  • Hypotension

Late-Onset Disease (7-90 days of life)

  • Bacteremia without focus (65% of cases)
  • Meningitis (25-30% of cases)
  • Osteoarticular infections (5-10% of cases)
  • Cellulitis or adenitis (rare)

Symptoms of LOD may be more subtle and include:

  • Fever
  • Poor feeding
  • Lethargy
  • Irritability
  • Seizures (in cases of meningitis)

Diagnosis of GBS Infections

Prompt diagnosis is crucial for effective management of GBS infections. Diagnostic approaches include:

  1. Blood culture: The gold standard for diagnosis of GBS sepsis.
  2. Cerebrospinal fluid (CSF) analysis: Performed when meningitis is suspected, including culture, cell count, glucose, and protein levels.
  3. Complete blood count (CBC): May show leukocytosis or leukopenia, thrombocytopenia.
  4. C-reactive protein (CRP) and Procalcitonin: Elevated in bacterial infections, but not specific to GBS.
  5. Chest X-ray: To evaluate for pneumonia in cases of respiratory distress.
  6. Polymerase Chain Reaction (PCR): Rapid detection of GBS in blood or CSF, but not routinely used in all settings.

It's important to note that empiric treatment should be initiated in suspected cases while awaiting culture results, as delays in treatment can lead to poor outcomes.

Treatment of GBS Infections

Treatment of GBS infections in pediatric patients involves prompt antimicrobial therapy and supportive care:

Antimicrobial Therapy

  • First-line therapy: Ampicillin plus Gentamicin
    • Ampicillin: 100-200 mg/kg/day divided every 6-8 hours (dose varies by age and condition)
    • Gentamicin: 4-5 mg/kg/day divided every 24 hours for neonates
  • Alternative therapy: Penicillin G monotherapy
    • 200,000-250,000 units/kg/day divided every 8-12 hours
  • For meningitis: Higher doses of ampicillin (300-400 mg/kg/day) or penicillin G (450,000-500,000 units/kg/day)
  • Duration of therapy:
    • Bacteremia without focus: 10 days
    • Meningitis: 14-21 days
    • Osteomyelitis or septic arthritis: 3-4 weeks

Supportive Care

  • Respiratory support (oxygen, mechanical ventilation if needed)
  • Fluid and electrolyte management
  • Vasopressor support for hypotension
  • Seizure management in cases of meningitis
  • Close monitoring of vital signs and laboratory parameters

Prevention of GBS Infections

Prevention strategies focus primarily on reducing the risk of early-onset GBS disease:

Intrapartum Antibiotic Prophylaxis (IAP)

IAP is recommended for women who:

  • Have a positive GBS screening culture at 36-37 weeks gestation
  • Have GBS bacteriuria during the current pregnancy
  • Have a history of a previous infant with invasive GBS disease
  • Have unknown GBS status and develop risk factors during labor

Recommended IAP regimen:

  • Penicillin G: 5 million units IV initial dose, then 2.5-3 million units every 4 hours until delivery
  • Alternative: Ampicillin 2g IV initial dose, then 1g every 4 hours until delivery
  • For penicillin-allergic patients: Cefazolin, Clindamycin, or Vancomycin (based on susceptibility testing)

Vaccine Development

GBS vaccines are currently under development and show promise for future prevention strategies. These vaccines target the capsular polysaccharides of GBS and could potentially prevent both early- and late-onset disease.



Group B Streptococcus infections in Pediatric Age
  1. What is the scientific name for Group B Streptococcus?
    Streptococcus agalactiae
  2. Which age group is most at risk for invasive Group B Streptococcus (GBS) infection?
    Neonates (0-90 days old)
  3. What is the primary source of GBS infection in neonates?
    Maternal genital tract colonization
  4. What percentage of pregnant women are colonized with GBS?
    10-30%
  5. What are the two main types of neonatal GBS disease based on age of onset?
    Early-onset disease (0-6 days) and late-onset disease (7-90 days)
  6. What is the most common clinical presentation of early-onset GBS disease?
    Sepsis and pneumonia
  7. What is the most common clinical presentation of late-onset GBS disease?
    Meningitis
  8. When is maternal GBS screening typically performed during pregnancy?
    Between 35-37 weeks of gestation
  9. What is the recommended method for maternal GBS screening?
    Rectovaginal swab culture
  10. What is the primary prevention strategy for early-onset GBS disease?
    Intrapartum antibiotic prophylaxis
  11. Which antibiotic is the first choice for intrapartum GBS prophylaxis?
    Penicillin G
  12. What is the alternative antibiotic for penicillin-allergic women in GBS prophylaxis?
    Clindamycin or vancomycin (if GBS is resistant to clindamycin)
  13. How long before delivery should intrapartum antibiotic prophylaxis be administered?
    At least 4 hours before delivery
  14. What is the mortality rate for early-onset GBS disease in developed countries?
    2-3%
  15. Which serotype of GBS is most commonly associated with invasive disease in neonates?
    Serotype III
  16. What is the recommended first-line treatment for confirmed GBS infection in neonates?
    Ampicillin and gentamicin
  17. How long is the typical duration of antibiotic treatment for GBS sepsis without meningitis?
    10 days
  18. What is the recommended duration of antibiotic treatment for GBS meningitis?
    14-21 days
  19. Which diagnostic test is used to confirm GBS infection in neonates?
    Blood culture or cerebrospinal fluid culture
  20. What is the role of C-reactive protein (CRP) in managing neonatal GBS infection?
    Monitoring response to treatment
  21. What long-term complication can occur in survivors of GBS meningitis?
    Neurological sequelae (e.g., hearing loss, developmental delays)
  22. Which maternal factor increases the risk of early-onset GBS disease in neonates?
    Prolonged rupture of membranes (>18 hours)
  23. What is the recommended management for a neonate born to a GBS-positive mother who did not receive adequate intrapartum prophylaxis?
    Close observation for at least 48 hours
  24. What is the role of lumbar puncture in evaluating neonates with suspected GBS infection?
    To diagnose or rule out meningitis
  25. Which vaccine is currently under development to prevent GBS infections?
    GBS conjugate vaccine
  26. What is the significance of GBS bacteriuria during pregnancy?
    It indicates heavy colonization and increased risk of neonatal infection
  27. How does GBS evade the host immune system?
    Through its polysaccharide capsule
  28. What is the role of CAMP factor in GBS pathogenesis?
    It acts as a pore-forming toxin
  29. Which body system, other than respiratory and central nervous system, can be affected by late-onset GBS disease?
    Osteoarticular system (septic arthritis, osteomyelitis)
  30. What is the recommended follow-up for infants who have recovered from GBS meningitis?
    Regular neurodevelopmental assessments and hearing tests


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