LAUSR

A 36-year-old healthy man presented with headache, neck stiffness, photophobia, confusion, and flaccid paraplegia 10 days after a developing fever, sore throat, and rhinorrhea. A MRI of the spine demonstrated a non-enhancing central cord lesion extending from C6-T12 (Fig. 1). Gadolinium-enhanced MRI of the brain was normal. Cerebrospinal fluid (CSF) evaluation revealed 203 red blood cells (RBCs)/lL, 214 white blood cells (WBCs)/lL (95% lymphocytes), 143 mg/dL protein, and 46 mg/dL glucose (95 mg/dL serum glucose). Extensive serum and CSF evaluation for infection, inflammation, and malignancy were negative including testing for HIV-1/2, herpes simplex virus, varicella-zoster virus, Epstein–Barr virus, cytomegalovirus, West Nile virus, syphilis, enterovirus polymerase chain reaction (PCR), Lyme, neuromyelitis optica (NMO) antibody, angiotensin converting enzyme (ACE), paraneoplastic antibodies cytology, cryptococcus, and CSF bacterial and fungal cultures. Transbronchial lymph node biopsy was negative for sarcoid and malignancy. Increases in acute and convalescent serum Coxsackie B3 (1:160 to C1:640) and B4 (1:320 to C1:640) antibody titers over 27 days indicated recent Coxsackie infection. The patient was treated with 1 g of methylprednisolone for 5 days, followed by five sessions of plasmapheresis with clinical and radiographic improvement. At 3-month follow-up, he was ambulatory with 4+/5 lower extremity strength. Coxsackie virus (amember of the enterovirus (EV) genus) is a common cause of meningitis and encephalitis, but few cases of Coxsackie (B3/B4)-related transverse myelitis have been reported [1]. Acute flaccid myelitis is a subtype of transverse myelitis with predominantly gray matter and motor neuron involvement. Other enteroviruses such as poliovirus, EV-D68, and EV-71 are associated with acute flaccid myelitis, theoretically due to virally-induced IgG that cross-react with spinal cord gray matter [2]. Alternately, direct viral neurotropism is possible since Coxsackie B can utilize the coxsackie and adenovirus receptor (CAR) expressed onmotor neurons to trigger internalization of viral particles [3]. Additionally, Coxsackie B4 virus viral particles have been reported to persist up to 10 days inmice brains [4]. Since our patient was PCR negative and responded to immune-modulating treatment, we suspect a post-infectious immune-mediated disease mechanism.