Anti-MOG antibody-positive ADEM following infectious mononucleosis due to a primary EBV infection: a case report

Abstract

BackgroundAnti-Myelin oligodendrocyte glycoprotein (MOG) antibodies are detected in various demyelinating diseases, such as pediatric acute disseminated encephalomyelitis (ADEM), recurrent optic neuritis, and aquaporin-4 antibody-seronegative neuromyelitis optica spectrum disorder. We present a patient who developed anti-MOG antibody-positive ADEM following infectious mononucleosis (IM) due to Epstein–Barr virus (EBV) infection.Case presentationA 36-year-old healthy man developed paresthesia of bilateral lower extremities and urinary retention 8 days after the onset of IM due to primary EBV infection. The MRI revealed the lesions in the cervical spinal cord, the conus medullaris, and the internal capsule. An examination of the cerebrospinal fluid revealed pleocytosis. Cell-based immunoassays revealed positivity for anti-MOG antibody with a titer of 1:1024 and negativity for anti-aquaporin-4 antibody. His symptoms quickly improved after steroid pulse therapy followed by oral betamethasone. Anti-MOG antibody titer at the 6-month follow-up was negative.ConclusionsThis case suggests that primary EBV infection would trigger anti-MOG antibody-positive ADEM. Adult ADEM patients can be positive for anti-MOG antibody, the titers of which correlate well with the neurological symptoms.

Unfavorable Structural and Functional Outcomes in Myelin Oligodendrocyte Glycoprotein Antibody–Associated Optic Neuritis

“…To the best of our knowledge, this is only the third case with vaccination-related MOG-seropositive disease (9). Other MOG-seropositive cases have been associated with viral or bacterial infection including influenza virus infection, Epstein-Barr virus-induced infectious mononucleosis and Chlamydia pneumoniae infection (20)(21)(22). In these cases, autoreactive MOG antibodyproducing B cells may be activated by both the simultaneous uptake of the cognate autoantigen (MOG) and the "bystander" viral antigen (e.g., influenza hemagglutinin) into B cells from infected parenchymal cells and by T cells specific for the respective antigen (23).…”

Autoimmune and Paraneoplastic Myelopathies

“…67 Presumed parainfectious/postinfectious inflammatory myelopathies have been reported in association with a variety of viral and bacterial triggers, but a definitive inflammatory etiology and correlation with infection is often difficult to prove, and infections are also well-established triggers of other definable inflammatory myelopathies such as MS, 15 AQP4-IgG seropositive NMOSD, 68 and MOG-IgG CNS demyelinating disease. [69][70][71] Fig . 2 Imaging findings in mimickers of inflammatory myelopathies.…”

Clinical Characteristics of Epstein–Barrvirus Infection in the Pediatric Nervous System

“…(2) Immune-mediated infection: compared with other herpesviruses, EBV can cause immune-mediated symptoms in the NS, which may be related to the age and immune status of the host. EBV may share a common antigen with neurological myelin oligodendrocyte glycoprotein [3], which make the immune system produce autoimmune T lymphocytes and anti-neuronal antibodies to autoantigens [4]. 3Reactivation of latent infection: when the ratio of EBV antibody titer in the CSF and serum is larger than the ratio of serum gamma globulin concentration, suggesting that the speci c EBV antibody is produced in the sheath, EBV infe-ction in the NS is reactivated after primary infection.…”