Case Presentation: A 37 year old Indian male with no significant past medical history presented to the emergency room complaining of fevers, urinary retention and bilateral lower extremity weakness with pain for 4 days. Travel history was significant for a trip to Kenya 4 weeks prior, where he developed non-bloody diarrhea, fevers and night sweats which had been self limited.Upon admission his vitals were stable. Physical exam was significant for 3/5 strength bilaterally in the lower extremities, and diminished patellar reflexes (1+). Given the concern for Guillain-Barre Syndrome (GBS), the patient was started on steroids, and admitted to the intensive care unit. A lumbar puncture was significant for a WBC count of 1524 cells/hpf, 79% lymphocytes, protein of 293mg/dL and glucose of 69mg/dL; suggesting a viral etiology prompting empiric anti-viral therapy. Magnetic Resonance imaging (MRI) showed a longitudinal lesion with gadolinium enhancement, throughout the central thoracic spine and a radiologic diagnosis of longitudinal extensive transverse myelitis was made.
While cultures were negative for bacterial infection, viral titers returned positive for IgM to Echovirus 9 (1:32), with weaker positivity for Coxsackie virus B6 (1:16) and Echovirus 7 (1:8). The patient responded to pulse corticosteroids with 1000 mg methylprednisolone followed by prednisone 60mg daily, and supportive management. He continued to improve and was discharged on a tapering dose of corticosteroids. At a follow up visit 4 weeks post discharge, his motor function had improved by 85% and he had recovered spontaneous micturition, but still reported mild sensory deficits.

Discussion: While ascending paralysis in the setting of a diarrheal infection is classic for GBS, the presence of lymphocytic pleocytosis in the CSF along with radiologic findings argues against this. Longitudinal transverse myelitis raises concerns for Neuromyelitis Optica spectrum disorder (NMOSD), however, antibodies to aquaporin-4 (NMO-IgG/AQP4-Ab) were negative. The presence of viral prodromal symptoms including fevers, diarrhea, and malaise, along with paresis which rapidly improved with supportive therapy, supports a diagnosis of viral AFM.
In diagnosing viral AFM, the CDC has proposed these guidelines; acute onset of symptoms, MRI showing lesions restricted to gray matter or cerebrospinal fluid with pleocytosis and elevated protein. They distinguish probable from confirmed cases based on the presence of radiographic findings.

Conclusions: The incidence of viral induced acute flaccid myelitis (AFM) has been increasing over the past few years. Cases have been predominantly reported in the fall, similar to our patient. While the majority of cases have been documented in children, this case highlights an adult who suffered AFM secondary to a presumed enteroviral infection. Given the prevalence and novelty of these viral sequelae, we believe it’s important to document adult cases as well.