Streptococcus agalactiae (Group B Streptococcus) causing neonatal meningitis. The primary virulence factor enabling GBS to colonise neonatal meninges and evade complement killing is:

• A Streptolysin O forming pores in membranes
• B Protein A binding IgG Fc region
• C Pyrogenic exotoxin B degrading complement proteins
• D Polysialic acid capsule mimicking host 'self' antigen ✓

Explanation

S. agalactiae (GBS) capsular polysaccharides are rich in sialic acid (N-acetylneuraminic acid). Sialic acid is a 'self'-mimic that engages inhibitory Siglec receptors on phagocytes and activates factor H binding, thereby downregulating complement deposition and opsonisation — a major immune evasion mechanism. This is particularly important in neonates who have limited functional antibody against GBS serotypes. The capsule type III is most associated with neonatal meningitis. Protein A is a S. aureus virulence factor. Streptolysin O is a GAS toxin. Pyrogenic exotoxin B (SPE-B) is a cysteine protease of GAS.

Reference: Ananthanarayan & Paniker's Textbook of Microbiology, 11th ed.

High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP

Written and medically reviewed by the StethoPrep medical team.