Acute disseminated encephalomyelitis as a concomitant presentation of anti-mog, covid and hiv: case report

Case presentation: A 21-year-old male patient, a student from Itabaiana-PB, presented with thoracic/lumbar dorsalgia that began 5 days before admission. His condition progressively worsened to paraparesis, and subsequently paraplegia with urinary and fecal retention, with a sensory level at T10, along with drowsiness. He denied any trauma, infectious symptoms, or exposure to river or lake water. Cranial MRI revealed subtle ovoid lesions affecting the deep periventricular white matter of the cerebral hemispheres at the callosal-septal interface of the frontoparietal regions. Cervical spine MRI showed extensive signal alteration affecting the cervical and thoracic spinal cord, associated with mild medullary expansion. Cerebrospinal fluid (CSF) culture was negative, with 14.3 leukocytes (10% polymorphonuclear, 90% mononuclear), glucose 82, protein 68.8, and a negative viral panel. HIV and COVID tests were not performed in the CSF due to lack of availability. Anti-aquaporin-4 antibody was negative, Herpes IgG/IgM was reactive. HIV was reactive with CD4 298 / CD8 692 / VL 102,000 copies/ml, COVID positive. He received 1g of methylprednisolone for 7 days and immunoglobulin for 5 days. The patient showed improved upper limb strength, sensory level improvement, remaining hypoesthesia in the thigh root, and significant radiological improvement. He was discharged on oral corticosteroids and regular antiretroviral therapy (ART). One month after discharge, anti-MOG results were positive. A new cycle of immunoglobulin was administered, and anti-MOG was repeated 3 months post-discharge, remaining positive. Discussion: When anti-MOG antibody disease involves the brain, the phenotype resembles acute disseminated encephalomyelitis (ADEM), with mental status changes and good outcomes following treatment with corticosteroids and intravenous immunoglobulins. Unlike ADEM, which is classically monophasic, MOG antibody seropositivity indicates a high probability of relapse. Transverse myelitis is a known manifestation of primary HIV infection. Speculated factors in the formation and infiltration of post-infectious MOG antibodies into the CNS include molecular mimicry and the breakdown of the blood-brain barrier due to prior viral inflammation, although the precise mechanisms of post-infectious demyelinating disease remain to be elucidated. Final comments: The presentation of anti-MOG-associated encephalomyelitis in a patient with asymptomatic COVID co-infection, along with a recent HIV diagnosis, sparked significant discussion regarding the possibility of a false-positive anti-MOG result and the appropriate long-term therapeutic approach. Given the severity of the clinical condition, cycles of immunoglobulin were chosen, and anti-MOG antibody levels are being monitored. This case report is highly relevant for academic discussion due to its uniqueness and therapeutic evolution.