Key result
During a 2016 pediatric outbreak, enterovirus infection caused neurological disease primarily presenting as brainstem encephalitis (67.3%, mostly EV-A71) and acute flaccid myelitis (5.5%, EV-D68).
Why the study?
The study was conducted to describe cases of neurological disease associated with an enterovirus outbreak across three regions in Northern Spain during 2016.
Observational (n=55)
Yes
In a 2016 Northern Spain pediatric outbreak of enterovirus neurological disease, EV-A71 primarily caused brainstem encephalitis with good prognosis, whereas EV-D68 caused acute flaccid myelitis with severe persistent sequelae.
Alerts clinicians to EV-A71 encephalitis predominance in pediatric outbreaks; leaves open serotype-specific prevention strategies.
OBJECTIVE: The study aimed to describe the cases of neurological disease related to the outbreak of enterovirus (EV) in three regions in Northern Spain during 2016. MATERIALS AND METHODS: Multicenter retrospective observational study. Clinical, radiological, and microbiological data were analyzed from patients younger than 15 years with confirmed EV-associated neurological disease admitted to 10 hospitals of Asturias, Cantabria, and Castile and Leon between January 1 and December 31, 2016. RESULTS: Fifty-five patients were included. Median age was 24 months (interquartile range = 18.5 months). Fifteen patients were classified as aseptic meningitis (27.3%). In total, 37 cases presented brainstem encephalitis (67.3%), 25 of them due to EV-A71 with excellent prognosis (84.6% asymptomatic 2 months following the onset). Three cases of acute flaccid myelitis (5.5%) by EV-D68 were reported and presented persistent paresis 2 months following the onset. Microbiological diagnosis by reverse transcriptase polymerase chain reaction was performed in all cases, finding EV in cerebrospinal fluid in meningitis, but not in brainstem encephalitis and acute flaccid myelitis, where EV was found in respiratory or rectal samples. Step therapy was administrated with intravenous immunoglobulin (IVIG; 32.7%), methylprednisolone (10%), and plasmapheresis (3.6%). Four patients received fluoxetine (7.3%). Twenty patients needed to be admitted to pediatric intensive care unit (36.4%). CONCLUSION: Clinical, microbiological, and radiological diagnosis is essential in outbreaks of EV neurological disease, taking into account that it can be difficult to identify EV-A71 and EV-D68 in CSF, requiring throat or rectal samples. There is not specific treatment to these conditions and the efficacy and understanding of the mechanism of action of immune-modulatory treatment (IVIG, corticosteroids, and plasmapheresis) is limited.
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Hedrera-Fernández et al. (2021) conducted an observational in Enterovirus-associated neurological disease (n=55). Enterovirus infection (EV-A71 and EV-D68) was evaluated. During a 2016 pediatric outbreak, enterovirus infection caused neurological disease primarily presenting as brainstem encephalitis (67.3%, mostly EV-A71) and acute flaccid myelitis (5.5%, EV-D68).
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