1 - Unidade de Infecciologia
2 - Serviço de Neurologia Pediátrica
3 – Departamento de Neurorradiologia, Hospital de Dona Estefânia, Centro Hospitalar de Lisboa Central, EPE, Lisboa
–31st Annual Meeting of the European Society for Paediatric Infeccious Diseases (ESPID 2013). Milão, Itália 28 Mai-1 Jun 2013
Background: The pathogenesis of influenza-associated encephalopathy is not clear. It is controversial whether the influenza virus invades the brain parenchyma. An association with human herpes virus 7 (HVV7) co-infection has been suggested previously.
Aims: We describe a case of influenza-associated encephalopathy and HHV7.
Methods: We used data collected from our patient´s hospital file on December 2012, during epidemic seasonal influenza in Portugal (H3N2 virus)
Results: We report a 12-year-old male patient who presented severe acute behavioral disturbance, characterized by agitation, mental confusion, incoherent speech, sexual disinhibition and hetero-aggressiveness alternating with apathy, three days after fever, frontal headaches and vomiting. He had been vaccinated with Pandemrix® in 2010. Toxic screen was negative. CSF analysis showed 21 cells/µL, 100% lymphocytes with IgGoligoclonal bands. Brain MRI showed multifocal parenchymal lesions in cerebral cortex and subcortical white matter, thalami, brainstem and cerebellar peduncles The EEG revealed diffuse intermittent delta activity, more evident on frontal leads. Viral RNA by real time PCR in CSF was positive to HHV7 and negative to influenza virus but blood serologic tests for Influenza A ELISA IgG +, IgM+ were positive. Antipsychotics drugs and oseltamivir were administered. The outcome was excellent with no neurologic sequelae.
Conclusion: These findings suggest that influenza-induced inflammatory response and HHV7 co-infection may participate in the pathogenesis of meningoencephalitis. We can speculate that the encephalitis could result either from a dual infection of influenza virus and HHV-7 or a latent infection withHHV-7 in central nervous system could be reactivated by influenza virus infection.
Key-words: influenza, encephalopathy, human herper virus 7