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| Viral hemorrhagic fever | |
|---|---|
| Other names | viral haemorrhagic fever |
 | |
| Two nurses standing nearMayinga N'Seka, a nurse withEbola 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 ofdiseases. "Viral" means a health problem caused byinfection from avirus, "hemorrhagic" means to bleed, and "fever" means an unusually high body temperature. Bleeding and fever are common signs of VHFs, which is how the group of infections got its common name.
There are five known families ofRNA viruses which cause VHFs:Arenaviridae,Filoviridae,Flaviviridae,Hantaviridae, andRhabdoviridae. Some VHFs are usually mild, such asnephropathia epidemica (within the familyHantaviridae), but some are usually severe and have a high death rate, such asEbola virus (within the familyFiloviridae). All VHFs can potentially cause severe blood loss, high fever, and death.
Bothhumans and non humananimals can be infected.
The following aresigns and symptoms of most or all VHFs.
The severity of symptoms varies with the type of virus. The "VHF syndrome" causes bleeding diathesis, capillary leak, and circulatory shock. It happens to most people who haveFiloviridae infections (such as Ebola virus orMarburg virus),Crimean–Congo hemorrhagic fever (CCHF), or the South American hemorrhagic fevers (which are caused byArenaviridae). VHF syndrome only happens to a small minority of people who havedengue fever orRift Valley fever.
Five families of RNA viruses have been recognized as being able to cause hemorrhagic fevers.[citation needed]
The pathogen that caused thecocoliztli epidemics in Mexico of 1545 and 1576 is still unknown, and the 1545 epidemic may have been bacterial rather than viral.[2][3]
Different hemorrhagic fever viruses act on the body differently, resulting in variable symptoms. In most VHFs, several mechanisms likely 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 the dissemination of the virus due to suppressed responses bymacrophages anddendritic cell (antigen-presenting cells). The second mechanism is prevention ofantigen specific immune response. The third mechanism isapoptosis of lymphocytes. The fourth mechanism is when infected macrophages interact with toxiccytokines, leading todiapedesis and coagulation deficiency. From the vascular perspective, the virus will infect vascular endothelial cells, leading to the reorganization of theVE-cadherin catenin 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,macrophages display 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]
Definitive diagnosis is usually made at a reference laboratory with advancedbiocontainment capabilities. 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 theplatelet count, 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). Thehematocrit may be elevated. The serum urea and creatine may be raised but this is dependent on the hydration status of the patient. Thebleeding time tends to be prolonged.[citation needed]
With the exception ofyellow fever vaccine andEbola vaccines, vaccines for VHFs are generally not available. For someone exposed to CCHF,ribavirin is available aspost-exposure prophylaxis (PEP).[4] Ribavirin may also help in exposure to Lassa fever.[5]
Any person who is taking care of a patient with any VHF (except dengue fever) should take multiple precautions against exposure and infection. The precautions include hand hygiene, double gloves, gowns, shoe and leg coverings, and face shields 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 meters (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]
Medical management of VHF patients may require intensive supportive care. Antiviral therapy with intravenousribavirin may 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]
A potential novel treatment, theNMT inhibitor, has been shown to completely inhibitLassa (LAS) andJunín (JUN) viral infections in cells based assays.[7] Another host-directed antiviral acts onEPRS1 which in turn acts, in human cells, as a proviral factor in mammarenaviruses infection, includingLCMV,JUNV, andLASV, and its inhibition usinghalofuginon compound, a prolyl domain inhibitor ofEPRS1, completely abolishes the viral infection by interrupting viral assembly and budding.[8] PKR has been shown to act as a proviral factor[9] while the inhibition of its kinase activity restricted the virus replication and infectivity.[10]
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.[19][20]
Scientific Research Institute of Medicine of the Ministry of Defense in Sergiyev Posad was researching the military use potential of hemorrhagic fever viruses.
