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A Fatal Case of Coxsackievirus B4 Meningoencephalitis

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A Fatal Case of Coxsackievirus B4 Meningoencephalitis OBSERVATION A Fatal Case of Coxsackievirus B4 Meningoencephalitis Bruce C. Cree, MD, PhD; Gary L. Bernardini, MD, PhD; Arthur P. Hays, MD; Gina Lowe, MD Background: Coxsackieviruses and echoviruses are nervous system infection and myocarditis. Magnetic reso- common causes of aseptic meningitis, but they rarely cause nance imaging showed focal hyperintense lesions in the life-threatening illness. We report a fatal case of coxsack- substantia nigra that corresponded to the location of ievirus B4 meningoencephalitis in a woman who devel- pathological changes seen at autopsy. oped extrapyramidal symptoms suggestive of encepha- litis lethargica. The exact causative agent of encephalitis Conclusions: This patient had a fulminant coxsackie- lethargica has rarely been found, but most cases of the virus B4 viral meningoencephalitis with a clinical pat- syndrome are assumed to be of viral origin. tern reminiscent of encephalitis lethargica and striking focal abnormalities in the substantia nigra identified on Case Description: A 33-year-old woman previously magnetic resonance imaging. The magnetic resonance im- treated with methylprednisolone and cyclophospha- aging findings correlated with pathological changes iden- mide for Henoch-Scho¨nlein purpura was transferred from tified at autopsy that were similar to the pathological find- a referring hospital because of sore throat, fever, and chills. ings observed in patients with encephalitis lethargica and Her neurologic findings progressed from headache with postencephalitic parkinsonism. It is likely that the pa- mild photophobia to lethargy, cogwheeling, increased tone tient’s immunocompromised state led to an overwhelm- in all 4 limbs, and brisk reflexes. The patient was diag- ing infection from an otherwise relatively innocuous vi- nosed as having coxsackievirus B4 meningoencephali- ral infection. tis and, despite treatment with the experimental antivi- ral agent pleconaril, died of an overwhelming central Arch Neurol. 2003;60:107-112 PPROXIMATELY 20000 cases ticularly in children, but are rarely life of acute encephalitis are threatening.2-6 We report a fatal case of me- reported each year in the ningoencephalitis and inflammatory myo- United States.1 In most carditis caused by coxsackievirus B4 likely cases, the causative infec- owing to susceptibility in an individual Atious agent is viral, including Enteroviri- with a pharmacologically induced state of dae (eg, echovirus or coxsackievirus), ar- immunosuppression. bovirus (eg, West Nile, eastern or western equine, St Louis, Venezuelan equine, Cali- REPORT OF A CASE fornia, or LaCrosse virus), Herpesviridae (eg, herpesvirus type 1 or 2, varicella- A 33-year-old woman was admitted to a zoster virus, Epstein-Barr virus, and cy- community hospital because of 1 week of tomegalovirus), and parvovirus, and can malaise, sore throat, subjective fever, chills, be identified from the cerebrospinal fluid bilateral ear pain, and joint pain in her (CSF) and/or blood.1 However, determi- hands and feet. The patient had a history nation of the exact cause can be difficult, of Henoch-Scho¨nlein purpura, juvenile From the Neurological Institute often requiring repeated CSF sampling and rheumatoid arthritis treated with methyl- of New York, New York– polymerase chain reaction amplification prednisolone and cyclophosphamide, and Presbyterian Hospital, of the CSF. Abnormalities within the brain required hemodialysis for IgA nephropa- Columbia-Presbyterian Medical parenchyma (eg, medial temporal lobes or thy. On presentation, her temperature was Center, New York, NY brainstem) seen on magnetic resonance 39.8°C and a 2/6 systolic murmur was (Drs Cree, Hays, and Lowe), and Division of Stroke and (MR) imaging with T2- or T1-weighted im- heard at the left sternal border. Results of Neurocritical Care, Department ages after gadolinium contrast injection can general physical and neurologic examina- of Neurology, Albany Medical help to establish the diagnosis. tion were normal. Routine complete blood Center, Albany, NY Coxsackievirus and echovirus are fre- cell count showed a white blood cell (Dr Bernardini). quent causes of aseptic meningitis, par- (WBC) count of 1.7 ϫ103/µL, with a dif- (REPRINTED) ARCH NEUROL / VOL 60, JAN 2003 WWW.ARCHNEUROL.COM 107 ©2003 American Medical Association. All rights reserved. Downloaded From: https://jamanetwork.com/ on 10/02/2021 Cerebrospinal Fluid Analysis Day of Hospitalization Variable 4 6 17 22 Opening pressure, cm H2ONDNDND190 WBC count, cellsϫ103/µL 0.079 0.021 0.069 0.010 Differential count, % Neutrophils 86 79 6 ND Lymphocytes 14 21 94 88 Monocytes ND ND ND 12 Eosinophils ND ND ND ND RBC count, cellsϫ106/µL 0.000014 0.000009 0.000005 0.00010 Protein, g/dL 0.128 0.115 0.077 0.032 Glucose, mg/dL 68 68 78 68 Abbreviations: ND, not determined; RBC, red blood cell; WBC, white blood cell. SI conversion factor: To convert glucose to millimoles per liter, multiply by 0.0555. ferential count of 34% polymorphonuclear leukocytes equivocal Babinski signs. Follow-up CSF examination on (PMNs), 4% bands, 38% lymphocytes, and 24% mono- the 17th hospital day yielded a protein level of 0.077 g/dL, cytes; a hemoglobin level of 11.9 g/dL; and a platelet count glucose level of 78 mg/dL (4.3 mmol/L), RBC count of of 262ϫ103/µL. Results of serum chemistry studies were 0.000005 ϫ106/µL, and WBC count of 0.069 ϫ103/µL, normal except for an elevated serum urea nitrogen level but now a lymphocytic predominance was observed: 6% of 71 mg/dL (25.3 mmol/L) and creatinine level of 4.6 mg/dL PMNs and 94% lymphocytes (Table). Serologic studies (407 µmol/L), consistent with her chronic renal failure. She sent for antibodies to Rickettsia, parvovirus B19, and Bru- was treated with intravenous antibiotics, stress-dosed cor- cella were negative; toxoplasmosis and Epstein-Barr vi- ticosteroids, and granulocyte colony-stimulating factor for rus antibody testing was positive for IgG but negative for empirical coverage of presumed bacterial infection in a set- IgM antibodies. Malaria organisms were not seen on ting of cyclophosphamide-induced leukopenia. blood smear, and multiple blood cultures yielded no On the fourth hospital day, the patient developed a growth. Polymerase chain reaction examination of CSF headache, mild photophobia, nuchal rigidity, and tem- did not amplify DNA for herpesvirus 1 or 2, cytomega- perature of 40.0°C but was otherwise neurologically in- lovirus, Mycobacterium tuberculosis,orBorrelia burgdor- tact. A lumbar puncture was performed, yielding clear, col- feri. Cytologic examination of the CSF was negative. Thy- orless CSF with a protein level of 0.128 g/dL, glucose level roid function test results and complement levels were of 68 mg/dL (3.8 mmol/L), red blood cell (RBC) count of normal. Other imaging studies including single-photon 0.00014 ϫ106/µL, and WBC count of 0.079 ϫ103/µL, with emission computed tomography of the brain, cerebral a differential count of 86% PMNs and 14% lymphocytes MR angiography, and total-body indium scan were (Table). An opening pressure was not recorded. The gram negative. stain and cultures did not show any organisms, but anti- The patient was transferred to New York– biotic therapy was broadened for empirical treatment of Presbyterian Hospital, New York, NY, on the 22nd day af- suspected bacterial meningitis. The patient’s neurologic ter the initial hospitalization. She was afebrile and her neck findings worsened 2 days later when she became stupor- was supple but she remained stuporous, responding only ous, responding only to painful stimuli. Brainstem re- to noxious stimulation with withdrawal of the limbs. Brain- flexes remained intact, with semipurposeful withdrawal stem reflexes were intact and deep tendon reflexes were of all 4 limbs and symmetrically brisk reflexes. A noncon- brisk, with bilateral ankle clonus and equivocal plantar re- trast computed tomographic scan of the head was nor- sponses. Laboratory studies at our institution showed a mal, and an electroencephalogram (EEG) showed diffuse serum WBC count elevated to 14.0 ϫ103/µL with a dif- slowing but no epileptiform activity. Repeated CSF sam- ferential count of 92% PMNs, 6% lymphocytes, and 2% pling yielded a protein level of 0.115 g/dL, glucose level monocytes. The elevated WBC count was presumed to be of 68 mg/dL (3.8 mmol/L), RBC count of 0.000009 ϫ106/ partly a consequence of treatment with granulocyte colony- µL, and WBC count of 0.021 ϫ103/µL, with continued poly- stimulating factor. The CSF examination showed an op- morphonuclear pleocytosis: 79% PMNs and 21% lympho- ening pressure of 190 cm H2O, protein level of 0.032 g/dL, cytes (Table). Cryptococcal antigen was not detected, and glucose level of 68 mg/dL (3.8 mmol/L), RBC count of no organisms were seen on gram stain. 0.0001 ϫ106/µL, and WBC count of 0.010 ϫ103/µL, with During the next 2 weeks the patient’s level of arousal a differential count of 88% lymphocytes and 12% mono- fluctuated between coma and lethargy. Periods of inter- cytes (Table). Repeat polymerase chain reaction studies mittent tachypnea were observed. She had marked dys- of the CSF did not amplify DNA for herpesvirus 1 or 2, arthria and roving eye movements in the horizontal plane Epstein-Barr virus, or cytomegalovirus, and CSF cultures and could occasionally follow some commands with hand did not grow bacteria or acid-fast bacilli; the VDRL test squeezing. There was marked increase in tone with cog- was nonreactive. An MR image of the brain showed focal, wheel rigidity in upper extremities and hyperactive deep linear, nonenhancing hyperintense lesions on T1- and T2- tendon reflexes; bilateral ankle clonus was noted but with weighted images in the region of the substantia nigra (REPRINTED) ARCH NEUROL / VOL 60, JAN 2003 WWW.ARCHNEUROL.COM 108 ©2003 American Medical Association. All rights reserved. Downloaded From: https://jamanetwork.com/ on 10/02/2021 A B RLRL C D 350 µm 35 µm A and B, Axial magnetic resonance images demonstrating bilateral, symmetric increased signal intensity within the substantia nigra.
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