Ebola Virus–Related Encephalitis: Table 1.

Greslan, T. De; Billhot, M.; Rousseau, Claire; Nab, Christine Mac; Karkowski, L.; Cournac, J.M.; Bordes, Julien; Gagnon, Nicolas; Dubrous, P.; Duron, Sandrine; Moroge, Sophie; Quentin, Benoit; Koulibaly, Fassou; Bompaire, Flavie; Renard, Jean-Luc; Cellarier, Gilles

doi:10.1093/cid/ciw469

Cited by 28 publications

(23 citation statements)

References 15 publications

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“…Complications collectively referred to as 'post-Ebola syndrome' , including musculoskeletal pain, headache and ocular problems, have been noted in a number of survivors of filovirus infection [24][25][26][27][28][29] . In rare cases, encephalitis has also been noted [30][31][32][33] . Filoviruses have also been detected by PCR and/or virus isolation in the breast milk 34,35 and semen [36][37][38][39] of survivors.…”

Section: Clinical Manifestationsmentioning

confidence: 99%

Post-exposure treatments for Ebola and Marburg virus infections

Cross

Mire

Feldmann

et al. 2018

Nat Rev Drug Discov

107

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| The filoviruses -Ebola virus and Marburg virus -cause lethal haemorrhagic fever in humans and non-human primates (NHPs). Filoviruses present a global health threat both as naturally acquired diseases and as potential agents of bioterrorism. In the recent 2013-2016 outbreak of Ebola virus, the most promising therapies for post-exposure use with demonstrated efficacy in the gold-standard NHP models of filovirus disease were unable to show statistically significant protection in patients infected with Ebola virus. This Review briefly discusses these failures and what has been learned from these experiences, and summarizes the current status of post-exposure medical countermeasures in development, including antibodies, small interfering RNA and small molecules. We outline how our current knowledge could be applied to the identification of novel interventions and ways to use interventions more effectively. R E V I E W SNATURE REVIEWS | DRUG DISCOVERY VOLUME 17 | JUNE 2018 | 413 © 2 0 1 8 M a c m i l l a n P u b l i s h e r s L i m i t e d , p a r t o f S p r i n g e r N a t u r e . A l l r i g h t s r e s e r v e d . AstheniaMuscular weakness. MyalgiaMuscular pain. ArthralgiaJoint pain. LeukopeniaA condition of having a low number of circulating leukocytes, including neutrophils, eosinophils, basophils, lymphocytes and monocytes. LymphocytopeniaA condition of having a low number of circulating leukocytes, including natural killer cells, T cells and B cells. ThrombocytopeniaA condition of having a low number of circulating thrombocytes, also known as platelets.and Ebolavirus. The Marburgvirus genus contains a single species, Marburg marburgvirus, which contains two members, Marburg virus (MARV) and Ravn virus (RAVV). The Ebolavirus genus consists of five distinct species: Bundibugyo ebolavirus (BDBV), Reston ebolavirus (RESTV), Sudan ebolavirus (SUDV), Tai Forest ebolavirus (TAFV; previously termed 'Côte d'Ivoire ebolavirus' but more commonly known as 'Ivory Coast ebolavirus') and Zaire ebolavirus (EBOV). MARV, RAVV, BDBV, SUDV and EBOV are important human pathogens, with case fatality rates often up to 90% for MARV, RAVV and EBOV, and around 55% for SUDV 8,10 . On the basis of two small outbreaks in 2007 and 2012, BDBV seems to be the least pathogenic, with a case fatality rate of about 40-48% 11,12 . In 1994, TAFV was associated with a number of deaths in chimpanzees and a single symptomatic but non-lethal human infection in the Republic of Côte d'Ivoire 13,14 . RESTV is lethal for macaques but is not thought to cause disease in humans 15 . An outbreak of RESTV was reported in pigs in the Philippines in 2008; however, it remains uncertain whether the disease observed in the pigs was caused by RESTV or other agents reported to have co-infected the animals 16 . Clinical manifestationsClinical and laboratory signs of disease caused by filovirus infection are nonspecific and usually associated with an incubation period of 2-21 days (mean 4-10 days) 8,17 . Illness begins with an abrupt onset of fever, astheni...

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Section: Clinical Manifestationsmentioning

confidence: 99%

Post-exposure treatments for Ebola and Marburg virus infections

Cross

Mire

Feldmann

et al. 2018

Nat Rev Drug Discov

107

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“…A subset of patients develop central nervous system manifestations and encephalopathy. Although several underlying causes could be involved, EBOV RNA has been detected in the cerebrospinal fluid of patients with EVD, suggesting that meningoencephalitis may be directly mediated by the virus 149,150 .…”

Section: Diagnosis Screening and Prevention Clinical Manifestations mentioning

confidence: 99%

“…Although poorly understood, viral encephalitis or encephalopathy has been circumstantially implicated in a patient with seizures after recovery from EVD and MRI findings of encephalomalacia (softening or loss of brain tissue from injury to the brain including infarction or ischaemia) and haemorrhagic encephalitis (I.C., unpublished observations). In Guinea, EBOV RNA has been detected in the cerebrospinal fluid of four patients with clinical signs of meningoencephalitis during acute illness 149,150 . Delirium or agitation can be a challenging feature of EVD.…”

Section: Supportive Care For Acute Evdmentioning

confidence: 99%

Ebola virus disease

Jacob

Crozier

Fischer

et al. 2020

Nat Rev Dis Primers

421

345

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To date, 12 distinct filoviruses have been described 1. The seven filoviruses that have been found in humans belong either to the genus Ebolavirus (Bundibugyo virus (BDBV), Ebola virus (EBOV), Reston virus (RESTV), Sudan virus (SUDV) and Taï Forest virus (TAFV); Fig. 1) or to the genus Marburgvirus (Marburg virus (MARV) and Ravn virus (RAVV)) 2. The WHO International Classification of Diseases Revision 11 (ICD-11) of 2018 recognizes two major subcategories of filovirus disease (FVD): Ebola disease caused by BDBV, EBOV, SUDV or TAFV, and Marburg disease caused by MARV or RAVV. Ebola virus disease (EVD) is defined as a disease only caused by EBOV. This subcategorization of FVD is largely based on the increasing evidence of molecular differences between ebolaviruses and marburgviruses, differences that may influence virus-host reservoir tropism, pathogenesis and disease phenotype in accidental primate hosts 2. Since the discovery of filoviruses in 1967 (reF. 3), 43 FVD outbreaks (excluding at least five laboratoryacquired infections) have been recorded in or exported from Africa 4. The epidemiological definition of outbreak is one or more cases above the known endemic prevalence. For example, the single case of TAFV infection recorded in a setting in which FVD had never been reported before (Côte d'Ivoire) 5 is still considered an outbreak. All FVD outbreaks, with the exception of that caused by TAFV, were characterized by extremely high case-fatality rates (CFRs, also known as lethality). Until 2013, the most extensive outbreak, caused by SUDV, involved 425 cases and 224 deaths (CFR 52.7%) 6. The overall limited numbers of FVD cases (1967-2013: 2,886 cases including 1,982 deaths 4), the typical remote and rural locations of outbreaks and the often delayed announcement of new outbreaks to the international community 7 have prevented the systematic study of clinical FVD in humans. Thus, the commonly used description of FVD was derived either from observation of small groups of patients in care settings that were not well-equipped for diagnosis, treatment and disease characterization, or from observations of even smaller samples, such as individuals who were transferred from Equatorial Africa to Europe and the USA or who fell sick in Europe or the USA after contracting the virus elsewhere. Pathological characterization of FVD via autopsies has been rare 7,8. In the absence of extensive human clinical data, FVD could only be defined further via the use of experimental animal infections 9,10 .

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“…Central nervous system (CNS) viral invasion by EVD had been suspected but unproven until the West Africa EVD epidemic. In this outbreak, individual case-patient reports describe clinical features of meningoencephalitis or meningitis during and after acute Ebola virus (EBOV) infection, accompanied by EBOV PCR results in nonbloodstained cerebrospinal fluid samples (CSF) ( 2 – 6 ). Cranial imaging of 3 encephalitic patients documented changes consistent with cerebral atrophy ( 3 ), meningoencephalitis ( 4 ), and areas of diffusion restriction suggesting ischemia ( 4 , 5 ).…”

mentioning

confidence: 99%

Case Series of Severe Neurologic Sequelae of Ebola Virus Disease during Epidemic, Sierra Leone

Howlett¹,

Walder²,

Lisk³

et al. 2018

Emerg. Infect. Dis.

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We describe a case series of 35 Ebola virus disease (EVD) survivors during the epidemic in West Africa who had neurologic and accompanying psychiatric sequelae. Survivors meeting neurologic criteria were invited from a cohort of 361 EVD survivors to attend a preliminary clinic. Those whose severe neurologic features were documented in the preliminary clinic were referred for specialist neurologic evaluation, ophthalmologic examination, and psychiatric assessment. Of 35 survivors with neurologic sequelae, 13 had migraine headache, 2 stroke, 2 peripheral sensory neuropathy, and 2 peripheral nerve lesions. Of brain computed tomography scans of 17 patients, 3 showed cerebral and/or cerebellar atrophy and 2 confirmed strokes. Sixteen patients required mental health followup; psychiatric disorders were diagnosed in 5. The 10 patients who experienced greatest disability had co-existing physical and mental health conditions. EVD survivors may have ongoing central and peripheral nervous system disorders, including previously unrecognized migraine headaches and stroke.

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Ebola Virus–Related Encephalitis: Table 1.

Cited by 28 publications

References 15 publications

Post-exposure treatments for Ebola and Marburg virus infections

Post-exposure treatments for Ebola and Marburg virus infections

Ebola virus disease

Case Series of Severe Neurologic Sequelae of Ebola Virus Disease during Epidemic, Sierra Leone

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