Seropositive Myasthenia Gravis Triggered by Lyme Disease: A Case Study of Molecular Mimicry

TL;DR

A man with Lyme disease developed myasthenia gravis, possibly due to molecular mimicry between Borrelia antigens and acetylcholine receptors.

Contribution

This case highlights a rare link between Lyme disease and myasthenia gravis through molecular mimicry.

Findings

A patient with Lyme disease developed seropositive myasthenia gravis.

Molecular mimicry between Borrelia antigens and acetylcholine receptor epitopes is suggested.

Treatment with plasma exchange and antibiotics led to significant improvement.

Abstract

Lyme disease, caused by Borrelia burgdorferi, is a multisystem infection that rarely produces neuromuscular complications beyond classic neuroborreliosis. Myasthenia gravis (MG) is an autoimmune disorder characterized by fatigable weakness due to acetylcholine receptor (AChR) antibodies. We describe a 74-year-old man with coronary artery disease, chronic kidney disease, and prostate cancer who developed progressive dysphagia, dysphonia, ptosis, and neck weakness. Initial attribution to medication-related angioedema delayed recognition. Neurological examination revealed bulbar weakness and fatigable ptosis. Electrodiagnostic testing confirmed post-synaptic neuromuscular junction dysfunction, and AChR antibody assays were strongly positive across binding, blocking, and modulating subtypes. Concurrent Lyme serologies were positive for immunoglobulin G and immunoglobulin M. The patient required intensive care monitoring and was treated with plasma exchange, intravenous ceftriaxone, prednisone, and pyridostigmine, with marked improvement. This case illustrates a rare coexistence of neuroborreliosis and seropositive MG, highlighting potential molecular mimicry between Borrelia antigens and AChR epitopes.

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