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Influenza a Virus and Reye's Syndrome in Adults

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Influenza a Virus and Reye's Syndrome in Adults J Neurol Neurosurg Psychiatry: first published as 10.1136/jnnp.43.6.516 on 1 June 1980. Downloaded from Journal of Neurology, Neurosurgery, and Psychiatry, 1980, 43, 516-521 Influenza A virus and Reye's syndrome in adults LARRY E DAVIS AND MARIO KORNFELD From the Neurology Service, Veterans Administration Medical Center and Department of Neurology and Pathology, University of New Mexico School of Medicine, Albuquerque, New Mexico S U M M A R Y We report fatal Reye's syndrome in two adults following proven influenza A viral infections. Reye's syndrome is, therefore, not confined to children but may also occur in adults. Many reported cases of postinfluenza A encephalopathy have clinical and pathological features of Reye's syndrome suggesting that they are not due to postinfectious perivenous demyelination. In 1963, Reye, Morgan, and Baral described 21 died. No one in his family had ever had illnesses children who, following a prodromal illness, suggesting abnormalities of the urea cycle. developed vomiting, seizures, coma and death.' Laboratory tests included a normal brain com- Noninflammatory cerebral oedema and fatty meta- puterised tomogram (CT), blood count, and serum morphosis of the liver was found at necropsy. An electrolytes. A traumatic lumbar puncture done Protected by copyright. increasing number of similar cases have since on admission had a normal opening pressure. The been reported worldwide. Reye's syndrome is gen- cerebrospinal fluid (CSF) contained 900 fresh red erally thought to occur only in children. The blood cells per mm3, 5 lymphocytes per mm3, 250 aetiology is unknown, but the syndrome has been mg per dl protein, 150 mg per dl glucose, and associated with epidemics of influenza B virus2 sterile bacterial and fungal cultures. The SGOT and varicella zoster virus.3 level was 114 milli-International Units per ml We describe two adults with mild influenza virus (mIU/ml) (normal 9 to 41) and lactic dehydro- illness followed by clinical, biochemical and genase (LDH) level was 800 mIU/ml (normal pathologic features of Reye's syndrome. We sug- 60 to 100). Total serum bilirubin was normal. gest that this syndrome can occur in adults in Toxicology studies demonstrated moderate sali- association with influenza A virus infections. cylate levels in the blood, but no toxins. Case 2 An 18 year old waitress with no previous Case reports health problems became ill with influenza. Two days later, she developed nausea and vomiting. Case 1 A 57 year old, previously healthy, white The next day confusion and seizures developed. http://jnnp.bmj.com/ male developed fever, cough and myalgia on Initial neurological examination was normal ex- 6 March 1978, during an epidemic of influenza cept for confusion. Five hours after admission, A/Victoria/3/75. The patient was mildly ill and she became comatose without localising signs. was recovering. Three days later vomiting, con- Three hours later the patient had fixed dilated fusion and seizures developed. He was hospitalised pupils, absent reflexes, and no spontaneous respir- with a temperature of 38 90C, stuporous with bi- ations. An EEG showed electrocerebral silence. lateral Babinski signs. No papilloedema or focal She was maintained on a respirator for four days neurological signs were present. The liver was before death. She had had no previous episodes of on September 29, 2021 by guest. not enlarged and no other abnormalities were encephalopathy or liver disease and there was no present. The patient rapidly progressed into a family history of individuals with abnormalities coma with fixed, dilated pupils and absent reflexes. of the urea cycle. The next day the electroencephalogram (EEG) Laboratory tests included a normal blood count, showed electrocerebral silence and the patient serum electrolytes, drug and toxin screen, skull x-ray and isotope brain scan. Lumbar puncture Address for reprint requests: Dr Davis, Department of Neurology, University of New Mexico School of Medicine, Albuquerque, NM showed a normal opening pressure. The CSF con- 87131 USA. tained 95 RBC per mm3, no WBCs, 23 mg per dl Accepted 1 December 1979 protein, 105 mg per dl glucose, nonreactive 516 J Neurol Neurosurg Psychiatry: first published as 10.1136/jnnp.43.6.516 on 1 June 1980. Downloaded from Influenza A virus and Reye's syndrome in adults 517 Venereal Disease Research Laboratory results, and present in most of the hepatocytes which did not sterile bacterial and fungal cultures. On admission displace the nucleus (fig 2). Numerous fine lipid the SGOT was 198 mIU per ml, LDH was 250 droplets in hepatocytes were seen on the oil red mIU per ml, and serum total bilirubin was nor- 0 stain (fig 2 inset). These lipid droplets were mal; these tests remained abnormal thereafter. often present in higher concentrations at the per- iphery of the lobules and were typical of fatty Necropsy findings of cases 1 and 2 metamorphosis found in Reye's syndrome. Kidney Case 1 had normal kidneys. Case 2 had Brain The brains were swollen with flattened fine lipid droplets in the cells of the collecting gyri, narrow sulci, and compressed ventricles. tubules. They weighed 1580 grams in case 1 and 1330 Lungs There were foci of bronchopneumonia grams in case 2. Histological findings in both and disseminated zones of atelectasis in both cases. brains were similar. There were numerous empty pericellular, perivascular, and interfibrillary spaces Virology and serological studies in sections from all parts of the cerebrum. Within the convolutional white matter, there was astro- Viral cultures were obtained in case 1 from car- cytosis with swollen, often lobulated nuclei and diac blood, trachea, frontal, temporal and occipital pale, eosinophilic, ill-defined cell bodies. Micro- cortex, and thoracic and lumbar spinal cord. No gliosis was also present. Blood vessels within the virus isolation studies were attempted on the other brain were dilated and rare foci of recent haemor- case. Influenza virus was isolated from ten-day rhage could be seen. No inflammatory cells were embryonated eggs following intra-amniotic inocu- seen in meninges, brain parenchyma, or spinal lation with 10% suspension of trachea and cord. There were no defects of myelin in the thoracic spinal cord. The other tissue samples Protected by copyright. brain or spinal cord. Many cells in the choroid contained no virus. Both influenza isolates were plexus contained cytoplasmic vacuoles (fig 1). identified as influenza A/Victoria/75 at the World These vacuoles were similar to those described in Health Organization Influenza Reference Lab- Reye's syndrome by Brown and Madge.4 oratory at the Center for Disease Control, Liver The livers of both patients were normal in Atlanta, GA. size and shape. Histologically, fine vacuoles were Serological studies on blood obtained at nec- http://jnnp.bmj.com/ on September 29, 2021 by guest. Fig 2 Fatty metamorphosis of liver; A (case 1), B (case 2), H & E. Insets show fine lipid eosin (original magnification X64). J Neurol Neurosurg Psychiatry: first published as 10.1136/jnnp.43.6.516 on 1 June 1980. Downloaded from 518 Larry E Davis and Mario Kornfeld 4~~~~~~~~~~~~~~~~~ iF~~~~~~~~~~~~~~~~~~~~~~~~~~~~~- 40~~~~~~~~~~~ t,i+Q....R: j v 2 "i b Q 4 | . 'S t i 6,,AN, X: < * 8 ;s F X^ vS,<~~~~~~~~~~~~~~.A S >z>. k:O.< *;:~~~~~~...1. i-b,\d*''';':: droplets within h y o r 0 Protected by copyright. Rk -.4~~~~~~~~~ Ai>%6W 4 t< w x 4 i9!.e 401. avn a**t a r 4~~~~~~~~~~~~~~~~~~~M ~~4 *4 V~~~~ %~~~~~~~~~~~~~ A~~~~~~~~~~~ .K'h. 4... .. Fig Fat meaopois; of lier; A (cs 1), ';(cae 2) H & E. Insets sho finlpi ...~~~~...~ ~ ....'~ ~ ~ ~ ~ ~ ~~~ ~ .. http://jnnp.bmj.com/ ;.. ... ....A.. .s B~~~~~~ W f X ... f ivr;A cae ),B cae ),H E Ises ho fnelii dropletsFi2Fatymeamrposswithinhepatocytes,oil red 0 (original magnifications X130).~~~~~~~~~~~~~~~~~ ~~~~~~~~~~~~... on September 29, 2021 by guest. J Neurol Neurosurg Psychiatry: first published as 10.1136/jnnp.43.6.516 on 1 June 1980. Downloaded from Influenza A virus and Reye's syndrome in adults 519 ropsy of case 2 showed a complement fixation (CF) changes were present. Thus, the clinical and titre of 1: 1024 against influenza A virus antigen pathologic criteria for the diagnosis of Reye's and a titre of 1: 16 against influenza B viral syndrome were met in both cases.5 Virological or antigen. The influenza A antibody titre was con- serological evidence of an acute influenza A virus sidered by the WHO Influenza Reference Lab- infection was present. This suggests the associ- oratory to demonstrate concomitant or recent in- ation of Reye's syndrome with influenza A virus fection with influenza A virus. No CF antibodies in these patients. to western equine encephalitis. Venezuelan en- Although Reye's syndrome has been associated cephalitis and Saint Louis encephalitis viruses with prior influenza B2 and varicella viruss infec- were present. tions, a virus has only rarely been recovered from the liver or brain.6 The isolation of influenza A Discussion and review of literature virus from the spinal cord of case 1 is difficult to interpret as it was recovered in only one of seven In both cases, the diagnosis was not made before brain and spinal cord samples and histological death. Prothrombin times, ammonia levels, and examination of the spinal cord did not suggest a ultrastructure of the liver were, therefore, not myelitis. available. In retrospect, both cases presented with Central nervous system complications of influ- typical features of Reye's syndrome. There was a enza A virus infection are often called influenza mild influenza illness followed by an abrupt onset encephalomyelitis. This term is used to describe of vomiting, seizures and an encephalopathy ter- patients of all ages who developed stupor, coma, minating in death. Biochemical evidence of and seizures following influenza. The pathology is hepatocellular damage and severe fatty metamor- often described in textbooks as a postinfectious phosis of the liver were found.
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