PANCE Infectious Disease Practice Test

Campylobacter jejuni infection commonly precedes Guillain-Barré syndrome, an autoimmune attack on the peripheral nerves triggered by molecular mimicry between the bacteria’s components and neuronal gangliosides. The immune response, aimed at the infection, cross-reacts with nerve components, causing demyelination or axonal damage that leads to progressive, symmetric weakness with absent reflexes. Clinically, patients often have an ascending pattern of weakness and may develop facial weakness or autonomic instability. Lumbar puncture typically shows high protein with normal cell count (albuminocytologic dissociation), and nerve studies reveal demyelination or axonal damage depending on the variant. Treatment with IVIG or plasmapheresis improves outcomes, and many patients recover, though some may have residual deficits. The other conditions listed are not classically linked as post-infectious complications of Campylobacter jejuni: Bell palsy is facial nerve palsy from various causes; multiple sclerosis involves central nervous system demyelination; myasthenia gravis affects the neuromuscular junction.