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A 25-year-old man with no relevant medical history presented with bilateral lower limb weakness, pain, and paresthesia. Magnetic resonance imaging showed bilateral T2 hyperintense and FLAIR hyperintense myelitis of the spinal cord. The patient’s symptoms became worse, with fever and tachycardia and he also developed thoracic back pain. The patient received intravenous corticosteroid therapy. The symptoms gradually resolved. Three weeks later, he was reevaluated because of recurrence of the symptoms. He had acute pain with reduced spinal mobility in his chest area. The skin overlying the spine was tender and warm. The patient also complained of constipation, but a physical examination of other organs was unremarkable. The patient underwent spinal MRI with and without contrast. It showed no gadolinium enhancement and T2-weighted hyperintense lesions in the spinal cord. On signal abnormality review, it showed hypointensity on T1-weighted images, and hyperintense on FLAIR sequences. The images were read as acute T2 hyperintense cord lesions. These lesions were not enhanced with gadolinium. The chest X-ray demonstrated abdominal calcifications compatible with falciparum malaria. The D-dimer level was elevated. It was measured twice on admission and then twice again 10 days after onset. Immunological and serologic tests did not show any abnormalities. The patient’s symptoms resolved.

Brain imaging was performed to look for an infectious etiology. Magnetic resonance imaging of the brain showed new right frontal cortical and subcortical T2 hyperintense lesions with gadolinium enhancement. A proton density-weighted and T2-weighted magnetic resonance imaging and diffusion-weighted imaging with ADC maps showed a hyperintense lesion in the right cerebral peduncle and a hypointense lesion in the right splenium ([Figure 1](#F1){ref-type=»fig»}). A viral/parasitic etiology was suspected. There was no history of travel or any known source of infection, and a serum and cerebrospinal fluid antibody

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