A preterm neonate at 32 weeks develops temperature instability, feed intolerance, and apneic episodes on day 3 of life. Blood culture grows Group B Streptococcus. Which of the following best describes the mechanism of GBS virulence in neonates?
- A Capsular polysaccharide sialic acid residues inhibit complement activation by masking from phagocytes ✓
- B Production of beta-lactamase making it intrinsically penicillin-resistant
- C Endotoxin-mediated DIC through lipopolysaccharide
- D Biofilm formation on vascular catheters as primary pathogenesis
Correct answer: A. Capsular polysaccharide sialic acid residues inhibit complement activation by masking from phagocytes
Explanation
Group B Streptococcus (Streptococcus agalactiae) expresses a capsular polysaccharide whose terminal sialic acid residues bind factor H and inhibit the alternative complement pathway, preventing opsonization. Neonates have physiologically low levels of maternal IgG antibodies (especially in premature infants) and immature complement function, rendering them particularly susceptible. GBS remains sensitive to penicillin (option B is wrong). GBS is gram-positive and lacks LPS. Biofilm on catheters is a feature of coagulase-negative Staphylococci.
Reference: Ghai Essential Pediatrics, 10th ed.
High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP
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