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Africa
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Diagnostic Approach to Fulminant Hepatitis in the Critical Care Unit
Published in Cheston B. Cunha, Burke A. Cunha, Infectious Diseases and Antimicrobial Stewardship in Critical Care Medicine, 2020
Ebola, also called Ebola hemorrhagic fever, is a viral hemorrhagic fever of humans caused by the Ebola virus, a member of the Filoviridae family. It is spread by direct contact with body fluids, such as blood, stool, and vomitus of an infected human. Ebola is characterized by fever, fatigue, vomiting, diarrhea, rash, kidney, liver failure, and occasionally bleeding. It is associated with a high case fatality rate of 54.7%, with fatality rates reported to increase with age and high viral load [28]. Patients with Ebola virus disease were found to have AST/ALT levels of more than five times the upper limit of normal and, in severe cases, levels of more than 15 times the upper limit of normal [29]. Diagnosis of Ebola can be made by serum PCR on blood drawn within 3 days of the onset of symptoms. A rapid chromatographic immunoassay (ReEBOV) that detects Ebola virus antigen can provide results within 15 minutes; however, this has been associated with false-positive results in 10% of patients who tested negative by PCR [30]. On postmortem liver biopsy, hepatocellular necrosis with minimal inflammation is the primary histological finding. There is no specific therapy for Ebola, and treatment includes fluids and supportive care.
Viral and Rickettsial Hemorrhagic Fevers: Laboratory Investigation of the Hemorrhagic State
Published in James H. S. Gear, CRC Handbook of Viral and Rickettsial Hemorrhagic Fevers, 2019
In summary, there appears to be no shortage of documented lesions capable of contributing towards the bleeding state in viral hemorrhagic fevers. If there is any degree of pathogenetic similarity among the various hemorrhagic fevers, functional damage to the endothelium with its subsequent effects could account for many of the observations made in human subjects and in experimental animals. However, other mechanisms may also play a role, the relative importance of which probably varies, depending on the pathogen involved and the stage of the disease. A summary of literature dealing with different mechanisms of bleeding in the various viral hemorrhagic fevers is presented in Table 3.
Infectious diseases (and tropical medicine and sexually transmitted diseases)
Published in Shibley Rahman, Avinash Sharma, A Complete MRCP(UK) Parts 1 and 2 Written Examination Revision Guide, 2018
Shibley Rahman, Avinash Sharma
Not all viruses in these families cause viral haemorrhagic fever. Viral haemorrhagic fevers share certain clinical manifestations, regardless of the virus that causes the disease. Common clinical manifestations of viral haemorrhagic fever are increased capillary permeability, leucopenia and thrombocytopaenia. Viral haemorrhagic fever is manifested by sudden onset, fever, headache, generalised myalgia, backache, petechiae and conjunctivitis.
Managing thrombosis and cardiovascular complications of COVID-19: answering the questions in COVID-19-associated coagulopathy
Published in Expert Review of Respiratory Medicine, 2021
Toshiaki Iba, Jerrold H. Levy, Jean Marie Connors, Theodore E. Warkentin, Jecko Thachil, Marcel Levi
Virus infection is known to induce viral hemorrhagic fevers. COVID-19 is a mysterious virus infectious disease which is frequently associated with hypercoagulability and a high incidence of thromboembolic complications. The accumulated evidences have revealed besides localized proinflammatory consequences of severe lung damage, multiple other factors are involved in the pathophysiology of CAC, including cytokine storm, perturbed autoimmune system, platelet activation, fibrinolytic shutdown, and endothelial damage. Although the above pathophysiology is considerably overlapped with that seen in sepsis-associated DIC, the risk of VTE is higher, and the complications of arterial thrombosis and vascular diseases are unique feature of CAC. Perhaps, other than the host immune responses, unknown mechanisms still exist in CAC and further research is necessary.
Defibrotide: potential for treating endothelial dysfunction related to viral and post-infectious syndromes
Published in Expert Opinion on Therapeutic Targets, 2021
Edward Richardson, David García-Bernal, Eleonora Calabretta, Rubén Jara, Marta Palomo, Rebecca M. Baron, Gregory Yanik, Jawed Fareed, Israel Vlodavsky, Massimo Iacobelli, Maribel Díaz-Ricart, Paul G. Richardson, Carmelo Carlo-Stella, Jose M. Moraleda
Viral hemorrhagic fevers are caused by four families of RNA viruses: arenaviruses, bunyaviruses, filoviruses, and flaviviruses. These viruses have diverse pathogenic mechanisms, resulting in varying disease severity and presentation [62]. The Ebola virus, a filovirus, accounts for few infections annually but stands among the most lethal viruses known, with reported fatality rates ranging from 24% to 100% in different outbreaks [63]. Dengue virus, a flavivirus, accounts for an estimated 390 million infections per year, of which only 96 million manifests with disease symptoms [64]. Hantavirus, a bunyavirus, manifests itself as two hemorrhagic febrile diseases: hemorrhagic fever with renal syndrome (HFRS) and hantavirus cardiopulmonary syndrome (HCPS) [65]. While these diseases differ in severity, incidence, and presentation, their severe manifestations share features of vascular instability, hemorrhage, and cytokine storm [62]. These viruses are noteworthy, furthermore, for their interaction with ECs, such as Ebola virus, dengue virus, and Hantavirus each directly infect ECs in the course of disease pathogenesis [66–68].
Recent advances in the development and evaluation of molecular diagnostics for Ebola virus disease
Published in Expert Review of Molecular Diagnostics, 2019
John Tembo, Edgar Simulundu, Katendi Changula, Dale Handley, Matthew Gilbert, Moses Chilufya, Danny Asogun, Rashid Ansumana, Nathan Kapata, Francine Ntoumi, Giuseppe Ippolito, Alimuddin Zumla, Matthew Bates
Viruses from the family Filoviridae can cause viral hemorrhagic fevers (VHFs), including Ebola virus disease (EVD) and Marburg virus disease (MVD) [1]. There are five known Ebolavirus species, namely Zaire ebolavirus, Sudan ebolavirus, Taï Forest ebolavirus, Bundibugyo ebolavirus, and Reston ebolavirus, represented by the following viruses, respectively, Ebola virus (EBOV), Sudan virus (SUDV), Taï Forest virus (TAFV), Bundibugyo virus (BDBV) and Reston virus (RESTV) [2]. There is also one newly proposed ebolavirus isolated from insectivorous bats, Bombali virus (BOMV), as yet not known to cause human disease [3]. There is only one known marburgvirus species, Marburg marburgvirus, with two known viruses, Marburg virus (MARV) and Ravn virus (RAVV) [2]. There is a third genus within the Filoviridae called Cuevavirus that is not linked to VHF in humans.