key: cord-320583-te8fv3gq
authors: Mergeay, Matthias; Coeckelbergh, Evelien; De Cauwer, Harald; Viaene, Mineke; Van der Mieren, Gerry
title: An adult case of metapneumovirus-induced acute encephalitis
date: 2019-03-30
journal: Acta Neurol Belg
DOI: 10.1007/s13760-019-01128-0
sha: 
doc_id: 320583
cord_uid: te8fv3gq

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Because a (meningo-)encephalitis was suspected a spinal tap was performed and acyclovir, amoxicilline and ceftriaxone were initiated. CSF results, indicative for viral encephalitis, are shown in Table 1 . Due to impaired consciousness and the need of vital parameter monitoring, the patient was transferred to the intensive care unit (ICU). During the first hours on the ICU the patient presented with two episodes of tonic-clonic seizures, successfully treated with intravenous benzodiazepines. After the second episode of seizures, levetiracetam 1 g 3 dd was added to the therapeutic regimen.

The next day the patïent was fully awake, he had a Glasgow Coma Scale of 15/15, with a normal neurological examination.

PCR revealed to be negative for Enterovirus, Cytomegalovirus, Varicella zoster virus, Herpes simplex, Cryptococcus neoformans, Listeria monocytogenes, Haemophilus influenza, Neisseria meningitides, Str. Pneumoniae in CSF and negative for Influenza A/B, Parainfluenzavirus, Rhinovirus, Bocavirus, Adenovirus and Coronavirus in serum. Mycoplasma pneumoniae, Chlamydophila pneumoniae, Bordetella pertussis and Bordetella parapertussis also were excluded. Nasopharyngeal aspirate was negative for Coronavirus, but showed RNA strands of Human Metapneumovirus (HMPV) with a low viral load suggestive for a recent infection.

Control EEG the same day showed a normalization of the basal rhythm to 9 Hz. Viral conjunctivitis was conf ir med by the ophthalmologist.

Cultures of blood and CSF remained sterile. Because HMPV encephalitis was diagnosed, antibiotics were discontinued. MRI of the brain did not reveal cerebral infectious disease nor recent ischemia. Levetiracetam was discontinued after 4 months because of favourable outcome with complete remission.

In adult HMPV encephalitis cases influenza-like symptoms or respiratory infection (bronchiolitis, bronchitis or interstitial pneumonia) were reported in all, though in our and Tan's case the patient was admitted because of other complaints, and respiratory tract infection was only revealed by chest radiography [1, 3, 4] .

Neurological features of HMPV encephalitis include coma, delirious behavior, impaired consciousness, seizures, and refractory status epilepticus [2] . In the previously reported adult cases two presented with altered mental status, one with seizures. In all cases encephalitis was diagnosed on clinical grounds despite lacking laboratory support e.g. despite normal CSF analysis in Tan's and Fok's cases. In Jeannet's and our case, clinical presentation, CSF pleocytosis and elevated protein levels were indicative for viral encephalitis (Table1) [1, 3, 4] .

Antiviral drugs e.g. acyclovir or ribavirin were used in three patients, in two antibiotic regimen was given because of the associated interstitial pneumonia. In our patient acyclovir and antibiotics were initiated and administered until serological testing, PCR and cultures were available [1, 3, 4] .

Extensive testing for viral and bacterial pathogens can help the clinician in getting a much faster diagnosis, initiating proper treatment, and predicting outcome.

Treatment for HMPV essentially remains supportive, although ribavirin was shown to be active against RSV and HMPV [1] .

In Fok's case the patient was treated with a 5 days course of methylprednisolone because of no clinical improvement was noticed and autoimmune encephalitis/cerebral vasculitis was suspected [3] .

In some patients MR imaging does suggest autoimmune pathogenesis [1, 3] . In HMPV-induced encephalitis scattered cortical and subcortical T2w/FLAIR hyper intensities have been described. This is in contrast with the MR findings in Herpes encephalitis or influenza-associated encephalopathy (IAE) [5] .

However, it is unclear whether direct viral cerebral invasion, or nonspecific inflammation/vasculitis, or excessive extracellular release of neurotransmitters is the responsible pathogenic factor [1, 3, 5] .

In our patient MRI was within normal limits: this might be due to the uncomplicated clinical course or because of the time lapse between MRI and the clinical symptoms. In IAE rapid recovery both clinically and radiographically has been reported [5] .

In patients with suspected viral encephalitis, HMPV may be considered as the causative agent, and testing for HMPV in nasopharyngeal aspirate and CSF is then required. 

Conflict of interest All the authors report no disclosure nor conflict of interest relevant to the manuscript. All authors report no financial disclosure.

Ethical approval This manuscript does not contain any studies with human participants or animals performed by any of the authors.

Informed consent Informed consent was obtained from all individual participants included in the study. Additional informed consent was obtained from all individual participants for whom identifying information is included in this article.

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