(706) From Pneumonia to Paralysis: A Rare Guillain-Barré Syndrome Case Linked to Meningococcal Disease

Introduction: Guillain-Barré Syndrome (GBS) is a debilitating neurological disorder characterized by acute progressive inflammatory neuropathy. Acute Motor Axonal Neuropathy (AMAN) is a particularly rare variant of GBS, distinguished by axolemma injury. Acute polyneuropathy in GBS is triggered by an immune response to an antecedent infection/immunization, which cross-reacts with shared epitopes on nerves (molecular mimicry). We report a case of GBS as an atypical complication of meningococcal pneumonia, supported by clinical presentation, nerve conduction studies, and diagnostic findings.

Description: A healthy 28-year-old male presented with rapidly progressing distal weakness spreading to truncal and bulbar muscles requiring intubation. No preceding gastrointestinal, viral, or upper respiratory infections. Exam showed 0/5 strength in extremities and mute deep tendon reflex, with intact sensations. Neuroimaging was unrevealing. Lumbar puncture showed elevated IgG with no evidence of infection, and an elevated ganglioside panel (specifically GM1, Gd1a, Gd1b, Gq1b). Admission chest imaging showed lobar pneumonia, and sputum culture grew Neisseria meningitidis, treated with tailored antibiotics. Viral and enteric PCR was negative for Campylobacter, EBV, VZV, and Mycoplasma pneumoniae. Electromyography showed acute severe, generalised motor axonal polyneuropathy, consistent with AMAN. He underwent plasma exchange followed by IVIG therapy and required a tracheostomy for gradual weaning. With aggressive physical therapy patient slowly recovered and was discharged to rehabilitation facility.

Discussion: The temporal relationship between meningococcal pneumonia and the onset of neuropathy suggests that N. meningitidis infection, was the trigger for autoimmune-mediated nerve damage. Documented cases reports of GBS following meningococcal meningitis, highlights the underlying molecular mimicry with meningococcal infection. Our case is the first reported case of GBS following meningococcal pneumonia and we postulate it occurred via the similar mimicry as when triggered by mentioned meningitis. This case contributes to the limited literature on GBS induced by N. meningitidis and underscores the importance of high clinical suspicion and tailored therapeutic approaches in managing this challenging condition.