# 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.

## Key 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.