Viral hemorrhagic fever
 | This articleneeds morereliable medical referencesforverificationor relies too heavily onprimary sources.(July 2020) |  |
| Viral hemorrhagic fever | |
|---|---|
| Other names | viral haemorrhagic fever |
 | |
| Two nurses standing nearMayinga N'Seka,a nurse with Ebola virus disease in the1976 outbreak in Zaire.N'Seka died a few days later due to severe internalhemorrhage. | |
| Specialty | Infectious disease |
Viral hemorrhagic fevers(VHFs) are a diverse group of animal and humanillnesses.VHFs may be caused by five distinct families ofRNA viruses:the familiesFiloviridae,Flaviviridae,Rhabdoviridae,and several member families of theBunyaviralesorder such asArenaviridae,andHantaviridae.All types of VHF are characterized by fever and bleeding disorders and all can progress to high fever, shock and death in many cases. Some of the VHF agents cause relatively mild illnesses, such as the Scandinaviannephropathia epidemica(ahantavirus), while others, such asEbola virus,can cause severe, life-threatening disease.
Signs and symptoms
[edit]Signs and symptoms of VHFs include (by definition) fever and bleeding:
- Flushing of the face and chest, small red or purple spots (petechiae), bleeding, swelling caused byedema,low blood pressure (hypotension), and circulatory shock.
- Malaise,muscle pain,headache, vomiting, and diarrhea occur frequently.
The severity of symptoms varies with the type of virus. The "VHF syndrome" (capillary leak,bleeding diathesis,and circulatory compromise leading to shock) appears in a majority of people withfiloviralhemorrhagic fevers (e.g., Ebola andMarburg virus),Crimean–Congo hemorrhagic fever(CCHF), and theSouth American hemorrhagic feverscaused byarenaviruses,but only in a small minority of patients withdengueorRift Valley fever.
Causes
[edit]Five families of RNA viruses have been recognised as being able to cause hemorrhagic fevers.[citation needed]
- The orderBunyaviralesincludes the familiesArenaviridae,Fimoviridae,and all members of the former familyBunyaviridae,especiallyPeribunyaviridae.
- The familyArenaviridaeinclude the viruses responsible forLassa fever(Lassa virus),Lujo virus,Argentine(Junin virus),Bolivian(Machupo virus),Brazilian(Sabiá virus), Chapare hemorrhagic fever (Chapare virus),Venezuelan(Guanarito virus) andWhitewater Arroyo virushemorrhagic fevers.
- The former familyBunyaviridaeincludes
- the causative agents ofHantavirus hemorrhagic fever with renal syndrome(HV-HFRS) (Hantaviridae),
- theCrimean-Congo hemorrhagic fever(CCHF) virus from the genusOrthonairovirus(Nairoviridae),
- Garissa virusandIlesha virusfrom the genusOrthobunyavirus(Peribunyaviridae), and
- theRift Valley fever(RVF) virus from the genusPhlebovirus(Phenuiviridae).
- The familyFiloviridae(orderMononegavirales) includesEbola virusandMarburg virus.
- The familyFlaviviridae(orderAmarillovirales) includesdengue,yellow fever,and two viruses in thetick-borne encephalitisgroup that cause VHF:Omsk hemorrhagic fevervirus andKyasanur Forest diseasevirus.
- The familyTogaviridae(orderMartellivirales) includesChikungunya viruswhich causesChikungunya fever.
- FamilyRhabdoviridae(orderMononegavirales): In September 2012 scientists writing in the journalPLOS Pathogensreported the isolation of a member of theRhabdoviridaeresponsible for two fatal and two non-fatal cases of hemorrhagic fever in the Bas-Congo district of the Democratic Republic of Congo. The virus was namedBas-Congo virus.The non-fatal cases occurred in healthcare workers involved in the treatment of the other two, suggesting the possibility of person-to-person transmission.[1]This virus is related to theEphemerovirusandTibrovirusgenera.
The pathogen that caused thecocoliztliepidemics in Mexico of 1545 and 1576 is still unknown, and the 1545 epidemic may have been bacterial rather than viral.[2][3]
Pathophysiology
[edit]Different hemorrhagic fever viruses act on the body in different ways, resulting in different symptoms. In most VHFs, it is likely that several mechanisms contribute to symptoms, including liver damage,disseminated intravascular coagulation(DIC), and bone marrow dysfunction. In DIC, small blood clots form in blood vessels throughout the body, removing platelets necessary for clotting from the bloodstream and reducing clotting ability. DIC is thought to cause bleeding in Rift Valley, Marburg, and Ebola fevers. For filoviral hemorrhagic fevers, there are four general mechanisms of pathogenesis. The first mechanism is dissemination of virus due to suppressed responses bymacrophagesanddendritic cell(antigen presenting cells). The second mechanism is prevention ofantigenspecific immune response. The third mechanism isapoptosisof lymphocytes. The fourth mechanism is when infected macrophages interact with toxiccytokines,leading todiapedesisand coagulation deficiency. From the vascular perspective, the virus will infect vascular endothelial cells, leading to the reorganization of theVE-cadherincatenin complex (a protein important in cell adhesion). This reorganization creates intercellular gaps in endothelial cells. The gaps lead to increased endothelial permeability and allow blood to escape from the vascular circulatory system.[citation needed]
The reasons for variation among patients infected with the same virus are unknown but stem from a complex system of virus-host interactions. Dengue fever becomes more virulent during a second infection by means ofantibody-dependent enhancement.After the first infection,macrophagesdisplay antibodies on their cell membranes specific to the dengue virus. By attaching to these antibodies, dengue viruses from a second infection are better able to infect the macrophages, thus reducing the immune system's ability to fight off infection.[citation needed]
Diagnosis
[edit]Definitive diagnosis is usually made at a reference laboratory with advancedbiocontainmentcapabilities. The findings of laboratory investigation vary somewhat between the viruses but in general, there is a decrease in the total white cell count (particularly thelymphocytes), a decrease in theplateletcount, an increase in the blood serumliver enzymes,and reduced blood clotting ability measured as an increase in both theprothrombin(PT) and activatedpartial thromboplastin times(PTT). Thehematocritmay be elevated. The serum urea and creatine may be raised but this is dependent on the hydration status of the patient. Thebleeding timetends to be prolonged.[citation needed]
Prevention
[edit]With the exception ofyellow fever vaccineandEbola vaccines,vaccines for VHF-associated viruses are generally not available. Post-exposure prophylactic (preventive)ribavirinmay be effective for some bunyavirus and arenavirus infections.[4][5]
VHF isolation guidelines dictate that all VHF patients (with the exception of dengue patients) should be cared for using strict contact precautions, including hand hygiene, double gloves, gowns, shoe and leg coverings, and face shield or goggles. Lassa, CCHF, Ebola, and Marburg viruses may be particularly prone tonosocomial(hospital-based) spread. Airborne precautions should be utilized including, at a minimum, afit-tested,HEPA filter-equipped respirator (such as anN95 mask), a battery-powered, air-purifying respirator, or a positive pressure supplied air respirator to be worn by personnel coming within 1.8 meter (six feet) of a VHF patient. Groups of patients should be cohorted (sequestered) to a separate building or a ward with an isolated air-handling system. Environmental decontamination is typically accomplished with hypochlorite (e.g. bleach) orphenolic disinfectants.[6]
Management
[edit]Medical management of VHF patients may require intensive supportive care. Antiviral therapy with intravenousribavirinmay be useful in Bunyaviridae and Arenaviridae infections (specifically Lassa fever, RVF, CCHF, and HFRS due to Old World Hantavirus infection) and can be used only under an experimental protocol as IND approved by theU.S. Food and Drug Administration(FDA). Interferon may be effective in Argentine or Bolivian hemorrhagic fevers (also available only as IND).[citation needed]
Epidemiology
[edit]- Cocoliztliin Mexico 1545 and 1576 (suspected)[2][7][8][9][10]
- The GreatYellow Fever Epidemic of 1793in Philadelphia, PA, US. Nearly 10% of the population of 50,000 died from the disease.
- MékamboinGabonis the site of several outbreaks ofEbola virusdisease.
- Orientale Province,Democratic Republic of the Congovillages ofDurbaandWatsawere the epicenter of the 1998–2000 outbreak ofMarburg virusdisease.
- Uíge ProvinceinAngolawas the site of another outbreak of Marburg virus disease in 2005, the largest one to date of this disease.[11]
- A VHF outbreak in the village ofMweka, Democratic Republic of the Congo(DRC) that started in August 2007, and that has killed 103 people (100 adults and three children), has been shown to be caused (at least partially) byEbola virus.
- A viral hemorrhagic fever is a possible cause of thePlague of Athensduring thePeloponnesian War.[12]
- A viral hemorrhagic fever is an alternatetheoryof the cause of theBlack Deathand thePlague of Justinian[13]
- The initial, and currently only, outbreak ofLujo virusin September–October 2008 left four of five patients dead.[14]
- The2014 West Africa Ebola outbreak,which was the biggest outbreak in history.
Biowarfare potential
[edit]The VHF viruses are spread in a variety of ways. Some may be transmitted to humans through a respiratory route.[citation needed]The viruses are considered by military medical planners to have a potential for aerosol dissemination, weaponization, or likelihood for confusion with similar agents that might be weaponized.[15][16]
See also
[edit]
- Biosafety
- Jordi Casals-Ariet
- Dr.Matthew Lukwiya(1957–2000)
- C. J. Peters
References
[edit]- ^Grard G, Fair JN, Lee D, et al. (September 2012)."A novel rhabdovirus associated with acute hemorrhagic fever in central Africa".PLOS Pathog.8(9): e1002924.doi:10.1371/journal.ppat.1002924.PMC3460624.PMID23028323.
- ^abAcuna-Soto R, Stahle DW, Cleaveland MK, Therrell MD (April 2002)."Megadrought and megadeath in 16th century Mexico".Emerging Infect. Dis.8(4): 360–62.doi:10.3201/eid0804.010175.PMC2730237.PMID11971767.
- ^"500 years later, scientists discover what probably killed the Aztecs".The Guardian.Agence France-Presse.2018-01-16.
- ^Ergönül Ö, Keske Ş, Çeldir MG, Kara İA, Pshenichnaya N, Abuova G, et al. (2018)."Systematic Review and Meta-analysis of Postexposure Prophylaxis for Crimean-Congo Hemorrhagic Fever Virus among Healthcare Workers".Emerg Infect Dis.24(9): 1642–1648.doi:10.3201/eid2409.171709.PMC6106438.PMID30124196.
{{cite journal}}:CS1 maint: multiple names: authors list (link) - ^Hadi CM, Goba A, Khan SH, Bangura J, Sankoh M, Koroma S, et al. (2010)."Ribavirin for Lassa fever postexposure prophylaxis".Emerg Infect Dis.16(12): 2009–11.doi:10.3201/eid1612.100994.PMC3294560.PMID21122249.
{{cite journal}}:CS1 maint: multiple names: authors list (link) - ^Woods LC, ed. (2005).USAMRIID's Medical Management of Biological Casualties Handbook(PDF)(6th ed.). Fort Detrick MA:U.S. Army Medical Institute of Infectious Diseases.pp. 143–44. Archived fromthe original(PDF)on 2007-06-09.Retrieved2007-06-09.
- ^"Was the Huey Cocoliztli a Haemorrhagic Fever?"(PDF).Archived fromthe original(PDF)on 2010-06-17.Retrieved2010-07-25.
- ^Indigenous Hemorrhagic Fever and The Spanish Conquest
- ^Acuna-Soto R, Romero LC, Maguire JH (June 2000)."Large Epidemics of Hemorrhagic Fevers in Mexico 1545–1815"(PDF).Am J Trop Med Hyg.62(6): 733–39.doi:10.4269/ajtmh.2000.62.733.PMID11304065.Archived fromthe original(PDF)on 2007-03-20.Retrieved2006-12-04.
- ^"Epidemics in New Spain".Archived fromthe originalon 2010-06-14.Retrieved2010-07-25.
- ^Towner JS, Khristova ML, Sealy TK, Vincent MJ, Erickson BR, Bawiec DA, Hartman AL, Comer JA, Zaki SR, Ströher U, Gomes Da Silva F, Del Castillo F, Rollin PE, Ksiazek TG, Nichol ST (2006)."Marburgvirus Genomics and Association with a Large Hemorrhagic Fever Outbreak in Angola".Journal of Virology.80(13): 6497–516.doi:10.1128/JVI.00069-06.PMC1488971.PMID16775337.
- ^Olson PE, Hames CS, Benenson AS, Genovese EN (1996)."The Thucydides syndrome: Ebola déjà vu? (or Ebola reemergent?)".Emerging Infect. Dis.2(2): 155–56.doi:10.3201/eid0202.960220.PMC2639821.PMID8964060.
- ^Scott, Susan and Duncan, Christopher. (2004).Return of the Black Death: The World's Greatest Serial KillerWest Sussex; John Wiley and Sons.ISBN0-470-09000-6.
- ^Briese T, Paweska J, McMullan L, Hutchison S, Street C, Palacios G, Khristova M, Weyer J, Swanepoel R, Engholm M, Nichol S, Lipkin W (2009)."Genetic Detection and Characterization of Lujo Virus, a New Hemorrhagic Fever–Associated Arenavirus from Southern Africa".PLOS Pathog.5(5): e1000455.doi:10.1371/journal.ppat.1000455.PMC2680969.PMID19478873.
- ^Woods 2005,p. 145
- ^Peters C (2000)."Are Hemorrhagic Fever Viruses Practical Agents for Biological Terrorism?".In Scheld WM, Craig WA, Hughes JM (eds.).Emerging Infections.Vol. 4. Washington, D.C.: ASM Press. pp.201–09.ISBN978-1555811976.
External links
[edit]- "Viral Haemorrhagic Fever".The National Archives of United Kingdom.Public Health England (PHE). Archived fromthe originalon 2014-07-14.
- "Viral Haemorrhagic Fevers".World Health Organization (WHO).United Nations (UN). Archived fromthe originalon August 23, 2004.
- "Viral Hemorrhagic Fevers (VHFs) Virus Families".National Center for Emerging and Zoonotic Infectious Diseases (NCEZID).U.S. Centers for Disease Control and Prevention (CDC). 2019-09-24.
