Molecular mimicry between the host proteins and microbial antigens is the harbinger for development of autoimmune disorders. A young girl with multi-drug resistant (MDR) pulmonary tuberculosis (TB) on bedaquiline based MDR anti-tubercular therapy (ATT), developed acute onset paraparesis with sensory loss below the abdomen and neuro-vesical dysfunction. Magnetic resonance imaging (MRI) was consistent with myelitis extending from T6 to T10 levels with cerebrospinal fluid analysis showing pleocytosis and negative Xpert TB PCR. Serology tests showed strong positivity to myelin oligodendrocyte glycoprotein (MOG) antibodies. She had a good clinico-radiological response to steroids, continuing ATT. MOG antibody disease (MOGAD) combined with tuberculosis reiterates the association between mycobacterial antigens with host proteins. This in turn, results in a higher prevalence of autoimmune inflammatory diseases in TB endemic regions. Concomitant auto-immunity therefore needs to be excluded among patients with active TB with new onset neurological deficits.
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