Fatal enterovirus 71 encephalomyelitis

Lum, Lucy Cs; Wong, Kum Thong; Lam, SK; Chua, Kaw Bing; Goh, Adrian; Lim, WL; Ong, Boon Hoong; Paul, George; AbuBakar, Sazaly; Lambert, M.

doi:10.1016/s0022-3476(98)70155-6

Cited by 301 publications

(312 citation statements)

References 15 publications

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“…However, pulmonary edema or hemorrhage was not reported in Bulgarian epidemic. In contrast, the frequency of pulmonary edema or hemorrhage was considerably high in the fatal cases in Taiwan and Malaysia (3)(4)(5). We report the first such case proved by postmortem studies in an 8-year-old girl during this outbreak.…”

mentioning

confidence: 76%

“…Coagulation profile revealed a prothrombin time of 15.3 seconds and a partial thromboplastin time of 46.9 seconds. Follow-up data showed white blood cell count of 31,800 cells/mm 3 , blood sugar of 254 mg/dL, and aspartate aminotransferase level of 68 U/L. She became hypoxic with severe metabolic acidosis and rapid decline of her consciousness level.…”

Section: Case Reportmentioning

confidence: 99%

“…Her neck was stiff and her urinary bladder was distended. Laboratory studies revealed a white blood cell (white blood cell count) count of 14,300 cells/ mm 3 and hemoglobin of 12.3 g/dL. Blood sugar was 134 mg/dL and the aspartate aminotransferase was 23 U/L.…”

Section: Case Reportmentioning

confidence: 99%

“…Eight sets of primers were used for amplification and sequencing of the entire genome of the viral DNA. They were designed from published sequence data of EV 71 BrCr strain: primer pair I, 5Ј-TTAAAA-CAGCTGTGGGTTG [nucleotide (nt) [1][2][3][4][5][6][7][8][9][10][11][12][13][14][15][16][17][18][19] as the sense strand primer, 5Ј-GAACTTCCAGTACCACCCC (nt 1196 -1178) as the antisense strand primer; primer pair II, 5Ј-TATGGTGAGTGGCCTTCATACTG (nt 1053-75) as the sense strand primer, 5Ј-AGTGAGTGTTAC-TGATCCATGGT (nt 2241-2218) as the antisense strand primer; primer pair III, 5Ј-TACACACCACCAG-GAGGCCCCT (nt 2115-2126) as the sense strand primer, 5Ј-ACCAGCATAATTTGGGTTGGCT (nt 3282-3261) as the antisense strand primer; primer pair IV, 5Ј-TTCCATTCATGT -CACCTGCGA (nt 2964 -2984) as the sense strand primer, 5Ј-GAAATGGGCGAG -GTATGACACA (nt 4291-4269) as the antisense strand primer; primer pair V, 5ЈATTAGTAAGTTTATT-TATTGGCT(nt 4149 -4171) as the sense strand primer, 5Ј-ACAACTGCAACCACAGTTGCTAT(nt 5271-5249) as the antisense strand primer; primer pair VI, 5Ј-TCCATTGCTACTGTGGTAGCAGT (nt 5253-5275) as the sense strand primer, 5Ј-TAGCAGGCTTCTTCC-ATTCTCAT (nt 6241-6219) as the antisense strand primer; primer pair VII, 5Ј-ACTAAGCTGGAA-CCCAGTG (nt 6003-6021) as the sense strand primer, 5Ј-ATAACAAATTTACCCCCACC (nt 7396 -7377) as the antisense strand primer; primer pair VIII, 5Ј-GAGAAATTTGTGAGTACAA (nt 7227-7245) as the sense strand primer, 5Ј-AGCAGTGGTAACAACGC-AGAG-TACT(30)CN (nt 7408 -7342). RT-PCR was carried out by RT-PCR beads (Pharmacia Biotech, Sweden).…”

Section: Reverse Transcriptase-polymerase Chain Reaction (Rt-pcr) Ampmentioning

confidence: 99%

“…The disease is usually self-limited without neurological deficits (6), whereas in HFMD associated with EV 71, serious and lethal complications may develop. There were two such outbreaks of EV 71 with rapid deterioration to death in young children previously (3,7). One was in Bulgaria in 1975 and the other was in Malaysia in 1997.…”

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confidence: 99%

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Acute Encephalomyelitis during an Outbreak of Enterovirus Type 71 Infection in Taiwan: Report of an Autopsy Case with Pathologic, Immunofluorescence, and Molecular Studies

et al. 2000

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We report a fatal case of enterovirus type 71 (EV 71) infection in an 8-year-old girl during a summer outbreak of hand, foot, and mouth disease in 1998 in Taiwan. The clinical course was rapidly progressive, with manifestations of hand, foot, and mouth disease, aseptic meningitis, encephalomyelitis, and pulmonary edema. The patient died 24 hours after admission. Postmortem study revealed extensive inflammation in the meninges and central nervous system and marked pulmonary edema with focal hemorrhage. Brain stem and spinal cord were most severely involved. The inflammatory infiltrates consisted largely of neutrophils involving primarily the gray matter with perivascular lymphocytic cuffing, and neuronophagia. The lungs and heart showed no evidence of inflammation. EV 71 was isolated from the fresh brain tissues and identified by immunofluorescence method with type-specific EV 71 monoclonal antibody. It was also confirmed by neutralization test and reverse-transcriptase polymerase chain reaction with sequence analysis. The present case was the first example in which EV 71 was demonstrated to be the causative agent of fatal encephalomyelitis during its epidemic in Taiwan. Enterovirus type 71 (EV 71), a member of the genus enterovirus within the family picornavirus, was initially isolated from the feces of a 9-month-old infant with fatal encephalitis in California in 1969 (1). Subsequent outbreaks were encountered in New

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mentioning

confidence: 76%

Section: Case Reportmentioning

confidence: 99%

Section: Case Reportmentioning

confidence: 99%

Section: Reverse Transcriptase-polymerase Chain Reaction (Rt-pcr) Ampmentioning

confidence: 99%

mentioning

confidence: 99%

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Acute Encephalomyelitis during an Outbreak of Enterovirus Type 71 Infection in Taiwan: Report of an Autopsy Case with Pathologic, Immunofluorescence, and Molecular Studies

et al. 2000

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Clinical Characteristics and Functional Motor Outcomes of Enterovirus 71 Neurological Disease in Children

et al. 2016

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IMPORTANCE Enterovirus 71 (EV71) causes a spectrum of neurological complications with significant morbidity and mortality. Further understanding of the characteristics of EV71-related neurological disease, factors related to outcome, and potential responsiveness to treatments is important in developing therapeutic guidelines. OBJECTIVE To further characterize EV71-related neurological disease and neurological outcome in children. DESIGN, SETTING, AND PARTICIPANTS Prospective 2-hospital (The Sydney Children's Hospitals Network) inpatient study of 61 children with enterovirus-related neurological disease during a 2013 outbreak of EV71 in Sydney, Australia. The dates of our analysis were January 1, to June 30, 2013. MAIN OUTCOMES AND MEASURES Clinical, neuroimaging, laboratory, and pathological characteristics, together with treatment administered and functional motor outcomes, were assessed. RESULTS Among 61 patients, there were 4 precipitous deaths (7%), despite resuscitation at presentation. Among 57 surviving patients, the age range was 0.3 to 5.2 years (median age, 1.5 years), and 36 (63%) were male. Fever (100% [57 of 57]), myoclonic jerks (86% [49 of 57]), ataxia (54% [29 of 54]), and vomiting (54% [29 of 54]) were common initial clinical manifestations. In 57 surviving patients, EV71 neurological disease included encephalomyelitis in 23 (40%), brainstem encephalitis in 20 (35%), encephalitis in 6 (11%), acute flaccid paralysis in 4 (7%), and autonomic dysregulation with pulmonary edema in 4 (7%). Enterovirus RNA was more commonly identified in feces (42 of 44 [95%]), rectal swabs (35 of 37 [95%]), and throat swabs (33 of 39 [85%]) rather than in cerebrospinal fluid (10 of 41 [24%]). Magnetic resonance imaging revealed characteristic increased T2-weighted signal in the dorsal pons and spinal cord. All 4 patients with pulmonary edema (severe disease) demonstrated dorsal brainstem restricted diffusion (odds ratio, 2; 95% CI, 1-4; P = .001). Brainstem or motor dysfunction had resolved in 44 of 57 (77%) at 2 months and in 51 of 57 (90%) at 12 months. Focal paresis was evident in 23 of 57 (40%) at presentation and was the most common persisting clinical and functional problem at 12 months (observed in 5 of 6 patients), with 1 patient also requiring invasive ventilation. Patients initially seen with acute flaccid paralysis or pulmonary edema had significantly greater frequencies of motor dysfunction at follow-up compared with patients initially seen with other syndromes (odds ratio, 15; 95% CI, 3-79; P < .001). CONCLUSIONS AND RELEVANCE Enterovirus 71 may cause serious neurological disease in young patients. The distinct clinicoradiological syndromes, predominantly within the spinal cord and brainstem, enable rapid recognition within evolving outbreaks. Long-term functional neurological morbidity is associated with paresis linked to involvement of gray matter in the brainstem or spinal cord.

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Immunohistochemical detection of infected neurons as a rapid diagnosis of enterovirus 71 encephalomyelitis

1999

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Fatal enterovirus 71 encephalomyelitis

Cited by 301 publications

References 15 publications

Acute Encephalomyelitis during an Outbreak of Enterovirus Type 71 Infection in Taiwan: Report of an Autopsy Case with Pathologic, Immunofluorescence, and Molecular Studies

Acute Encephalomyelitis during an Outbreak of Enterovirus Type 71 Infection in Taiwan: Report of an Autopsy Case with Pathologic, Immunofluorescence, and Molecular Studies

Clinical Characteristics and Functional Motor Outcomes of Enterovirus 71 Neurological Disease in Children

Immunohistochemical detection of infected neurons as a rapid diagnosis of enterovirus 71 encephalomyelitis

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