Abstract Details

Title West Nile Virus Meningoencephalitis Exacerbating Ocular Myasthenia Gravis and Facial Nerve Palsy

Topic Infectious Disease

Presentation(s) P11 - Poster Session 11 (11:45 AM-12:45 PM)

Poster/Presentation
Number 3-014

Objective

To describe a rare case of West Nile virus (WNV) meningoencephalitis unmasking latent ocular Myasthenia Gravis (MG) and causing sequential contralateral facial nerve palsy.

Background A 49-year-old man with a history of hyperlipidemia, diabetes, obesity, and prior left-sided Bell’s palsy presented with fever, neck pain, headache, diarrhea, and confusion. CSF studies showed elevated protein (76 mg/dL) and normal glucose (59 mg/dL). MRI brain revealed ventriculitis of the left occipital horn. CSF and serum were positive for WNV IgM/IgG, consistent with WNV meningoencephalitis. EEG showed no seizures. During hospitalization, he developed left eye ptosis, diplopia, and saccadic eye movements concerning for ocular MG. Acetylcholine receptor antibody returned positive, and symptoms improved on pyridostigmine. While recovering in inpatient rehabilitation, he developed acute right facial droop. Stroke workup including CT/CTA/CTP and MRI was negative. Examination confirmed right lower motor neuron facial weakness with intact limb and bulbar strength, consistent with new contralateral facial nerve palsy.

Design/Methods

Results This case illustrates a rare overlap between viral neuroinvasive disease and autoimmune neuromuscular pathology. Prior reports have shown delayed MG onset after WNV infection, suggesting a postinfectious immune mechanism. In this case, ocular MG became clinically apparent during active infection, implying direct immune activation and loss of tolerance triggered by WNV. The subsequent contralateral Bell’s palsy likely represents an immune-mediated cranial neuropathy within the same inflammatory spectrum. The clinical course underscores the potential for viral infections to unmask latent autoimmune processes and to affect multiple cranial nerves through parainfectious mechanisms.

Conclusions WNV meningoencephalitis can trigger or worsen autoimmune disorders such as ocular MG and produce multifocal cranial neuropathies. Awareness of this interaction is crucial, as treatment choices like corticosteroids may carry dual risks in the setting of active infection and MG. Recognizing atypical or sequential cranial neuropathies in viral encephalitis should prompt evaluation for overlapping autoimmune etiologies.

Authors/Disclosures
Ayla Barakat, MD PRESENTER	Dr. Barakat has nothing to disclose.
Shayan Marsia, MBBS	Dr. Marsia has nothing to disclose.
Farah Barakat, MD, MBBS	Ms. Barakat has nothing to disclose.
Samantha R. Cencer, DO (Spectrum Health)	Dr. Cencer has nothing to disclose.

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