AS13. COVID 19 and MIS-C



Title of Case:

SARS-CoV-2 associated meningoencephalitis in a child


Neurological complications of SARS-CoV-2 infection are rarely reported and not well characterized.

Case Presentation Summary:

We report a 6-year old healthy Indian girl with 3 days of mild febrile upper respiratory tract infection due to coronavirus disease-2019 (COVID-19) confirmed by positive nasopharyngeal PCR swab; cycle threshold (Ct) 21.4. On day 7 of infection, she developed saddleback fever with gastrointestinal symptoms, lethargy and reduced oral intake, then subsequent meningoencephalitis on day 14 with irritability, neck stiffness, and altered mental state. Examination showed upper motor neuron signs, globally reduced power, and positive Kernig’s/Brudzinski’s signs. There were no features suggestive of Multisystem Inflammatory Syndrome in Children (MIS-C). Investigations revealed mildly elevated blood inflammatory markers and significant cerebrospinal fluid (CSF) lymphocytic pleocytosis. SARS-CoV-2 PCR Ct 36.6; anti-spike and anti-N capsid antibody positive. Extensive investigations for bacterial and viral pathogens including CSF SARS-CoV-2, blood and CSF autoimmune encephalopathy panels, and serum anti-NMDA-R antibody were negative. Magnetic resonance imaging of the brain showed slightly hyperintense bulky thalami with subtle deep grey matter involvement. She received 5 days of intravenous immunoglobulin (IVIG) on day 18 of infection; fever and meningism resolved. She required ongoing rehabilitation for significant speech, motor, coordination, cognitive, and attention deficits.

Learning Points/Discussion:

Meningoencephalitis in COVID-19 is rare, mostly occurs in severe COVID-19/MIS-C, and is associated with poorer outcomes and higher mortality. Proposed mechanisms are 1) direct viral invasion of the nervous system, 2) molecular mimicry causing a post-infectious immune-mediated response, or 3) indirect cytokine-driven injury due to systemic inflammation. Risk factors, CSF/neuroimaging findings, optimal management and prognosis, are poorly understood. Our patient's clinical course suggests an immune-mediated meningoencephalitis triggered by SARS-CoV-2, which responded well to IVIG although long-term sequelae are still unknown.