Campylobacter jejuni infection is the most common bacterial cause of diarrhoea in developed countries. Which post-infectious complication occurring 2–4 weeks after gastroenteritis is associated with Campylobacter, and what is the immunological mechanism?
- A Reactive arthritis (Reiter's syndrome) due to persistence of bacterial antigen in synovium
- B Guillain-Barré syndrome due to molecular mimicry between Campylobacter lipooligosaccharide ganglioside-like epitopes and peripheral nerve gangliosides ✓
- C IgA nephropathy due to deposition of Campylobacter-IgA complexes in the mesangium
- D Haemolytic uraemic syndrome due to Shiga-like toxin production by certain strains
Explanation
Campylobacter jejuni is the most common antecedent infection (~30% of GBS cases) preceding Guillain-Barré syndrome (GBS), particularly the acute motor axonal neuropathy (AMAN) variant. The mechanism is molecular mimicry: certain C. jejuni strains (particularly Penner serotypes O:19, O:41) express lipooligosaccharide (LOS) with ganglioside-like structures (GM1, GD1a, GD1b) on their outer core. Antibodies generated against these LOS epitopes cross-react with identical or similar gangliosides on peripheral nerve axolemma, causing axonal injury. Anti-GM1 and anti-GD1a antibodies are detected in AMAN-GBS.
Reference: Ananthanarayan & Paniker's Textbook of Microbiology, 11th ed.
High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP
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