Viral hemorrhagic fever

Viral hemorrhagic fever
Other names: viral haemorrhagic fever
Two nurses standing near Mayinga N'Seka, a nurse with Ebola virus disease in the 1976 outbreak in Zaire. N'Seka died a few days later due to severe internal hemorrhage.
SpecialtyInfectious disease


Viral hemorrhagic fevers (VHFs) are a diverse group of animal and human illnesses in which fever and hemorrhage are caused by a viral infection.[1] VHFs may be caused by four distinct families of RNA viruses: the families Filoviridae, Flaviviridae, Bunyavirales and Arenaviridae.[2] 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, while others, such as Ebola virus, can cause severe, life-threatening disease.[2]

Signs and symptoms

Signs and symptoms of VHFs include, by definition fever and bleeding:[2][3]

  • Flushing of the face and chest, small red or purple spots (petechiae), bleeding, and circulatory shock.
  • Malaise, muscle pain, headache, vomiting, and diarrhea occur frequently.

The severity of symptoms varies with the type of virus. Capillary leak, bleeding diathesis, and circulatory compromise leading to shock, appears in a majority of people with filoviral hemorrhagic fevers , Crimean–Congo hemorrhagic fever , and the South American hemorrhagic fevers caused by arenaviruses.[2][4]

Causes

Crimean-Congo Hemorrhagic Fever (CCHF) Virus-viral particles (yellow) budding from the surface of cultured epithelial cells

Four families of RNA viruses have been recognised as being able to cause hemorrhagic fevers.[2]

  • Arenaviridae family
Rift valley fever

The pathogen that caused the cocoliztli epidemics in Mexico of 1545 and 1576 is still unknown, and the 1545 epidemic may have been bacterial rather than viral.[5][6]

Pathophysiology

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 , 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. [7][8]

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 by macrophages and dendritic cell. The second mechanism is prevention of antigen specific immune response. The third mechanism is apoptosis of lymphocytes. The fourth mechanism is when infected macrophages interact with toxic cytokines, leading to diapedesis and coagulation deficiency. From the vascular perspective, the virus will infect vascular endothelial cells, leading to the reorganization of the VE-cadherin catenin complex. 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.[9][4][10][11]

The reasons for variation among people 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 of antibody-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.[9][2][12]

Diagnosis

Definitive diagnosis is usually made at a reference laboratory with advanced biocontainment capabilities. The findings of laboratory investigation vary somewhat between the viruses, in some cases, there is a decrease in the total white cell count, a decrease in the platelet count, an increase in the blood serum liver enzymes.[2][13][14] Additionally there is a reduced blood clotting ability measured as an increase in both the prothrombin (PT) and activated partial thromboplastin times (PTT). The serum urea and creatine may be raised but this is dependent on the hydration status of the patient. The bleeding time tends to be prolonged.[15][2][13]

Prevention

Vaccination

With the exception of yellow fever vaccine and Ebola vaccines, vaccines for VHF-associated viruses are generally not available. Post-exposure prophylactic (preventive) ribavirin may be effective for some bunyavirus and arenavirus infections.[16][17]

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 to nosocomial (hospital-based) spread. Airborne precautions should be utilized including, at a minimum, a fit-tested, HEPA filter-equipped respirator (such as an N-95 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) or phenolic disinfectants.[18]

Management

In 2020, the FDA approved Inmazeb a combination of three monoclonal antibodies and Ebanga a single monoclonal antibody for treating Zaire ebolavirus (disease infection)[19] Medical management of VHF patients may require intensive supportive care. Antiviral therapy with intravenous ribavirin may be useful in Bunyaviridae and Arenaviridae infections,[20] specifically, Lassa fever, RVF,and CCHF and can be used only under an experimental protocol as IND approved by the U.S. Food and Drug Administration (FDA).[20][2][21]

Epidemiology

Democratic Republic of the Congo

The epidemiology of viral hemorrhagic fevers have been shown to be as follows:

  • Cocoliztli in Mexico 1545 and 1576.[5]
  • The Great Yellow Fever Epidemic of 1793 in Philadelphia, PA, US. Nearly 10% of the population of 50,000 succumbed to the disease.[22]
  • Mékambo in Gabon is the site of several outbreaks of Ebola virus disease.[23]
  • Orientale Province, Democratic Republic of the Congo villages of Durba and Watsa were the epicenter of the 1998–2000 outbreak of Marburg virus disease.[24]
  • Uíge Province in Angola was the site of another outbreak of Marburg virus disease in 2005, the largest one to date of this disease.[25]
  • A VHF outbreak in the village of Mweka, 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) by Ebola virus.[26]
  • A viral hemorrhagic fever is a possible cause of the Plague of Athens during the Peloponnesian War.[27]
  • The initial, and currently only, outbreak of Lujo virus in September–October 2008 left 4/5 patients dead.[28]
  • The 2014 West Africa Ebola outbreak, which was the biggest outbreak in history.[29]

Society and culture

Biowarfare potential

The VHF viruses are spread in a variety of ways. Some may be transmitted to humans through a respiratory route.[30] The virus is considered by military medical planners to have a potential for aerosol dissemination, weaponization, or likelihood for confusion with similar agents that might be weaponized.[31][32]

See also

  • Dr. Matthew Lukwiya
  • C. J. Peters
  • Biosafety
  • Jordi Casals-Ariet

References

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  31. Woods 2005, p. 145
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