Ebola viral encephalitis and myelitis

Abstract

Ebola Virus Disease (EVD), formerly known as Ebola Haemorrhagic Fever, is a severe, often fatal illness in humans. To the best of our knowledge there is no link between Ebola and Encephalitis.Recent evidence suggests converging pathways through which viral infection, and its associated immune surveillance processes, may alter integrity of the BBB, and lead to inflammation, swelling of the brain parenchyma and associated neurological syndromes.Classical presentation is as a triad of fever, headache and altered mental state. There may be other findings either on examination or on imaging which, together with a travel history, may give clues as to the aetiology. It is important to note that in high- and middle-income countries the commonest cause of viral encephalitis is herpes simplex and Ebola.The organs of monkeys infected with Ebola haemorrhagic fever were examined by light and electron microscopy during the acute stage of disease. The virus caused focal coagulative necrosis in liver, spleen, kidney, lung and testis and widespread mild vascular damage. In brain there was intense congestion, with erythrocyte 'sludging', but no inflammatory reaction, significant injury to microvasculature in all organs. Virus replicated in endothelial cytoplasm causing focal necrosis, separation of tight junctions and detachment from basement membranes. These changes were associated with oedema and haemorrhage, contributing to hypovolaemic shock were not sufficiently extensive to account for severity of vascular collapse.Therefore, alongside with chest and abdominal pain, cough, conjunctivitis, jaundice, pancreatitis, lymphadenopathy, delirium, and coma, other complications after second week of infection include transverse myelitis and encepalitis. Ebola Virus Disease (EVD), formerly known as Ebola Haemorrhagic Fever, is a severe, often fatal illness in humans. To the best of our knowledge there is no link between Ebola and Encephalitis. Recent evidence suggests converging pathways through which viral infection, and its associated immune surveillance processes, may alter integrity of the BBB, and lead to inflammation, swelling of the brain parenchyma and associated neurological syndromes. Classical presentation is as a triad of fever, headache and altered mental state. There may be other findings either on examination or on imaging which, together with a travel history, may give clues as to the aetiology. It is important to note that in high- and middle-income countries the commonest cause of viral encephalitis is herpes simplex and Ebola. The organs of monkeys infected with Ebola haemorrhagic fever were examined by light and electron microscopy during the acute stage of disease. The virus caused focal coagulative necrosis in liver, spleen, kidney, lung and testis and widespread mild vascular damage. In brain there was intense congestion, with erythrocyte 'sludging', but no inflammatory reaction, significant injury to microvasculature in all organs. Virus replicated in endothelial cytoplasm causing focal necrosis, separation of tight junctions and detachment from basement membranes. These changes were associated with oedema and haemorrhage, contributing to hypovolaemic shock were not sufficiently extensive to account for severity of vascular collapse. Therefore, alongside with chest and abdominal pain, cough, conjunctivitis, jaundice, pancreatitis, lymphadenopathy, delirium, and coma, other complications after second week of infection include transverse myelitis and encepalitis.