Post Infectious Triggered Anti-Myelin Oligodendrocyte Glycoprotein Antibody-Associated Disease (MOGAD) via CMV in an Immunocompetent Host (P10-5.030)

Abstract

<h3>Objective:</h3> N/A <h3>Background:</h3> A previously healthy, immunocompetent 38-year-old female presented with initial complaints of subacute, waxing and waning high grade fevers, general malaise, and muscle aches for two weeks. Acutely she developed severe lumbar radiculopathy with significant urinary retention and bilateral lower extremity weakness leading to ED presentation. The patient was subsequently admitted with rapidly progressive lower extremity paraplegia and brisk reflexes over a 24-hour span. MRI imaging was notable for longitudinally extensive transverse myelitis (LETM) over continuous cervical and thoracic segments with significant gray matter involvement and left parahippocampal FLAIR hyperintensities Serum subsequently demonstrated positive anti-CMV IgM/IgG antibodies with a PCR load of 61 copies/mL indicative of a CMV infection with low viremia. LP CSF was CMV PCR negative with mildly elevated opening pressures and trace neurotrophic pleocytosis. Given stagnant clinical changes after five days of IV steroids, plasmapheresis was initiated with marked improvements in functional lower extremity strength. Soon afterwards, initial presenting lab work resulted, demonstrating high serum titers (1:2560) of anti-MOG antibodies. <h3>Design/Methods:</h3> N/A <h3>Results:</h3> N/A <h3>Conclusions:</h3> In immunocompetent hosts, CMV infection itself is a rarely described cause of inflammatory myelopathy with only 14 prescribed cases. With both deep gray matter FLAIR hyperintensities and cervical and thoracic LETM, a concomitant para-infectious CMV and new MOGAD is unlikely in our clinical setting. Additionally, systemic findings typically indicative of severe CMV infections such as retinitis, pericarditis/myocarditis, transaminitis, thrombocytopenia, and leukopenia were absent. Given prior reports of sequence similarities between MOG T-cell epitopes and a major capsid protein of CMV, molecular mimicry between antigen presenting cells has been hypothesized. Here we detail a first described case report of a possible post-infectious MOG antibody transverse myelitis triggered presumptively via CMV infection. Furthermore, presenting in an immunocompetent host, our case report highlights a further wrinkle into the pathophysiology and presence of post infectious triggered autoimmunity for MOGAD. <b>Disclosure:</b> Dr. Chen has nothing to disclose. Dr. Kwon has nothing to disclose.