Influenza-associated acute encephalopathy in Japanese children in 1994–2002

Togashi, Takehiro; Matsuzono, Yoshihiro; Narita, Mitsuo; Morishima, Tsuneo

doi:10.1016/j.virusres.2004.02.016

Cited by 169 publications

(134 citation statements)

References 5 publications

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“…1 As accepted in the literature, we used the term infection-associated encephalopathy rather than encephalitis to denote encephalitis related to influenza virus or rotavirus. [17][18][19] In cases with multiple etiologies (Supplemental Table 4), the agent with the strongest hierarchical association (confirmed . probable .…”

Section: Etiologic Causationmentioning

confidence: 75%

Infectious and Autoantibody-Associated Encephalitis: Clinical Features and Long-term Outcome

et al. 2015

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BACKGROUND AND OBJECTIVES: Pediatric encephalitis has a wide range of etiologies, clinical presentations, and outcomes. This study seeks to classify and characterize infectious, immunemediated/autoantibody-associated and unknown forms of encephalitis, including relative frequencies, clinical and radiologic phenotypes, and long-term outcome.METHODS: By using consensus definitions and a retrospective single-center cohort of 164 Australian children, we performed clinical and radiologic phenotyping blinded to etiology and outcomes, and we tested archived acute sera for autoantibodies to N-methyl-D-aspartate receptor, voltage-gated potassium channel complex, and other neuronal antigens. Through telephone interviews, we defined outcomes by using the Liverpool Outcome Score (for encephalitis).RESULTS: An infectious encephalitis occurred in 30%, infection-associated encephalopathy in 8%, immune-mediated/autoantibody-associated encephalitis in 34%, and unknown encephalitis in 28%. In descending order of frequency, the larger subgroups were acute disseminated encephalomyelitis (21%), enterovirus (12%), Mycoplasma pneumoniae (7%), N-methyl-D-aspartate receptor antibody (6%), herpes simplex virus (5%), and voltage-gated potassium channel complex antibody (4%). Movement disorders, psychiatric symptoms, agitation, speech dysfunction, cerebrospinal fluid oligoclonal bands, MRI limbic encephalitis, and clinical relapse were more common in patients with autoantibodies. An abnormal outcome occurred in 49% of patients after a median follow-up of 5.8 years. Herpes simplex virus and unknown forms had the worst outcomes. According to our multivariate analysis, an abnormal outcome was more common in patients with status epilepticus, magnetic resonance diffusion restriction, and ICU admission. CONCLUSIONS:We have defined clinical and radiologic phenotypes of infectious and immunemediated/autoantibody-associated encephalitis. In this resource-rich cohort, immune-mediated/ autoantibody-associated etiologies are common, and the recognition and treatment of these entities should be a clinical priority. WHAT'S KNOWN ON THIS SUBJECT:Encephalitis is a serious and disabling condition. There are infectious and immune-mediated causes of encephalitis, but many cases remain undiagnosed. WHAT THIS STUDY ADDS:This large single-center study on childhood encephalitis provides insight into the relative frequency and clinicoradiologic phenotypes of infectious, autoantibody-associated, and unknown encephalitis. Risk factors for an abnormal outcome are also defined. 4 and a prospective study of adults (n = 134) and children (n = 69) with encephalitis found that infectious encephalitis and immunemediated forms were identified in 42% and 21% of the cohort, respectively. 5 However, most of the previous larger studies of encephalitis in children were undertaken before the advent of neuronal autoantibody testing. [6][7][8] We studied clinical and radiologic features, serum autoantibodies in acute archived samples, and longterm outcomes in a large ret...

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Section: Etiologic Causationmentioning

confidence: 75%

Infectious and Autoantibody-Associated Encephalitis: Clinical Features and Long-term Outcome

et al. 2015

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“…In most cases, it caused subclinical infections or mild-to-moderate upper respiratory tract diseases. However, in some patients, it caused severe respiratory diseases, neurological complications, [2][3][4] and myocardial symptoms. 5,6 The 2009 H1N1 virus caused viral pneumonia with acute respiratory distress syndrome, 7 which is not generally caused by seasonal influenza strains.…”

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confidence: 99%

Histopathological and immunohistochemical findings of 20 autopsy cases with 2009 H1N1 virus infection

et al. 2012

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, were histopathologically analyzed. Hematoxylin-eosin staining, immunohistochemistry for type A influenza nucleoprotein antigen, and real-time reverse transcription-PCR assay for viral RNA were performed on formalin-fixed and paraffin-embedded specimens. In addition, the D222G amino acid substitution in influenza virus hemagglutinin, which binds to specific cell receptors, was analyzed in formalinfixed and paraffin-embedded trachea and lung sections by direct sequencing of PCR-amplified products. There were several histopathological patterns in the lung according to the most remarkable findings in each case: acute diffuse alveolar damage (DAD) with a hyaline membrane (four cases), organized DAD (one case), acute massive intra-alveolar edema with variable degrees of hemorrhage (three cases), neutrophilic bronchopneumonia (five cases) and tracheobronchitis with limited histopathological changes in alveoli (four cases). In two cases, the main findings were due to preexisting disease. Influenza virus antigen was only detected in the respiratory tract in 10 cases by immunohistochemistry. The antigen was detected in type II pneumocytes (three cases) in the epithelial cells of the trachea, bronchi and glands (six cases), and in the epithelial cells in both of the above (one case). The four cases with acute DAD presented with antigen-positive type II pneumocytes. In one case, the D222G substitution was detected in the lung as a major sequence, although 222D was prominent in the trachea, suggesting that selection of the viral clones occurred in the respiratory tract. In five

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“…For example, influenza virus or viral antigens are rarely demonstrated in the cerebrospinal fluid or brain of patients suffering from influenza encephalopathy [7,14,19]. In addition, Guillain Barré, Kleine-Levin and Reye's syndrome all are associated with infections not necessarily involving influenza virus, and, in the case of Reye's syndrome, the role of viral infection, if there is any, may be limited [3,17].…”

Section: Discussionmentioning

confidence: 99%

“…It appears that invasion and replication of influenza virus in the central nervous system (CNS) is not the primary cause of influenza-associated neurological disease but that infection with viruses may occasionally induce excessive immunological and physiological responses leading to neurological disorders. Indeed, hypercytokinemia has been suggested to be involved in the pathogenesis of influenza encephalopathy [11,14,19]. The fact that influenza-associated encephalopathy was observed in Japan, but not elsewhere, during an H3N2 epidemic may be explained by a genetic component that predisposes an individual for hypercytokinemia [14].…”

Section: Discussionmentioning

confidence: 99%

Master donor viruses A/Leningrad/134/17/57 (H2N2) and B/USSR/60/69 and derived reassortants used in live attenuated influenza vaccine (LAIV) do not display neurovirulent properties in a mouse model

Voeten¹,

Kiseleva

Glansbeek³

et al. 2010

Arch Virol

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Influenza-associated acute encephalopathy in Japanese children in 1994–2002

Cited by 169 publications

References 5 publications

Infectious and Autoantibody-Associated Encephalitis: Clinical Features and Long-term Outcome

Infectious and Autoantibody-Associated Encephalitis: Clinical Features and Long-term Outcome

Histopathological and immunohistochemical findings of 20 autopsy cases with 2009 H1N1 virus infection

Master donor viruses A/Leningrad/134/17/57 (H2N2) and B/USSR/60/69 and derived reassortants used in live attenuated influenza vaccine (LAIV) do not display neurovirulent properties in a mouse model

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