A 6-year-old boy presents with recurrent sinopulmonary infections since infancy. Serum immunoglobulins show markedly reduced IgG, IgA, and IgM. Flow cytometry reveals absence of CD19+ B cells but normal CD3+ T cell counts. Genetic testing confirms a mutation in Bruton tyrosine kinase (BTK). Which of the following best describes the underlying mechanism of his susceptibility to encapsulated bacterial infections?
- A Reduced neutrophil oxidative burst secondary to absent B-cell cytokine support
- B Defective opsonization due to absent specific IgG antibodies against polysaccharide capsules ✓
- C Impaired NK cell cytotoxicity against capsulated organisms
- D Defective complement activation via the alternative pathway
Explanation
X-linked agammaglobulinaemia (XLA) due to BTK mutation results in arrest of B-cell development at the pro-B stage, leading to profound panhypogammaglobulinaemia. Encapsulated bacteria (Streptococcus pneumoniae, Haemophilus influenzae) require opsonisation by specific IgG for efficient phagocytosis; without IgG, neutrophil-mediated killing is markedly impaired. Complement alternative pathway and NK cells function independently of B cells, but they provide insufficient protection against polysaccharide-encapsulated pathogens.
Reference: Ananthanarayan & Paniker's Textbook of Microbiology, 11th ed.
High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP
Written and medically reviewed by the StethoPrep medical team.