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CBRNE - Viral Hemorrhagic Fevers

  • Author: David C Pigott, MD; Chief Editor: Zygmunt F Dembek, PhD, MPH, MS, LHD  more...
 
Updated: Mar 30, 2015
 

Background

Viral hemorrhagic fevers (VHFs) are a group of febrile illnesses caused by RNA viruses from several viral families. These highly infectious viruses lead to a potentially lethal disease syndrome characterized by fever, malaise, vomiting, mucosal and gastrointestinal (GI) bleeding, edema, and hypotension. The four viral families known to cause VHF disease in humans include the Arenaviridae, Bunyaviridae, Filoviridae, and Flaviviridae. General characteristics of these viral families can be found in the table below.

The image below depicts palatal petechiae and hemorrhage in a patient with Ebola hemorrhagic fever.

Filovirus disease - Ebola fever. Patient with Ebol Filovirus disease - Ebola fever. Patient with Ebola hemorrhagic fever during 1976 outbreak in Zaire demonstrating palatal petechiae and hemorrhage. Photo courtesy of Joel Breman.

See Ebola: Care, Recommendations, and Protecting Practitioners, a Critical Images slideshow, to review treatment, recommendations, and safeguards for healthcare personnel.

Also, see the 11 Travel Diseases to Consider Before and After the Trip slideshow to help identify and manage infectious travel diseases.

 

Table. Viral Families Causing Viral Hemorrhagic Fever (Open Table in a new window)

Virus Family Disease (Virus) Natural Distribution Usual Source of Human Infection Incubation (Days)
Arenaviridae        
Arenavirus Lassa fever Africa Rodent 5-16
  Argentine HF (Junin) South America Rodent 7-14
  Bolivian HF (Machupo) South America Rodent 9-15
  Brazilian HF (Sabia) South America Rodent 7-14
  Venezuelan HF (Guanarito) South America Rodent 7-14
Bunyaviridae        
Phlebovirus Rift Valley fever Africa Mosquito 2-5
Nairovirus Crimean-Congo HF Europe, Asia, Africa Tick 3-12
Hantavirus Hemorrhagic fever with renal syndrome, hantavirus pulmonary syndrome Asia, Europe, worldwide Rodent 9-35
Filoviridae        
Filovirus Marburg and Ebola Africa Fruit bat 3-16
Flaviviridae        
Flavivirus Yellow fever Tropical Africa, South America Mosquito 3-6
  Dengue HF Asia, Americas, Africa Mosquito Unknown for dengue HF, 3-5 for dengue

Arenaviridae

Arenaviridae are spread to humans by rodent contact and include Lassa virus in Africa and several rare South American hemorrhagic fevers such as Machupo, Junin, Guanarito, and Sabia. Lassa virus is the most clinically significant of the Arenaviridae, accounting for serious morbidity and mortality in West Africa.

Lassa fever first appeared in Lassa, Nigeria, in 1969. It has been found in all countries of West Africa and is a significant public health problem in endemic areas. In populations studied, Lassa fever accounts for 5-14% of hospitalized febrile illnesses. Its natural reservoir is a small rodent whose virus-containing excreta is the source of transmission.


Mastomys natalensis, natural host of Lassa virus. Mastomys natalensis, natural host of Lassa virus. Photo courtesy of BioMed Central, originally published in Kelly JD, Barrie MB, Ross RA, Temple BA, Moses LM, Bausch DG. Housing equityfor health equity: a rights-based approach to the control of Lassa fever inpost-war Sierra Leone. BMC Int Health Hum Rights. 2013 Jan 2;13:2.

Bunyaviridae

This group includes Rift Valley fever (RVF) virus, Crimean-Congo hemorrhagic fever (CCHF) virus, and several hantaviruses. The RVF and CCHF viruses are both arthropod-borne viruses. RVF virus, an important African pathogen, is transmitted to humans and livestock by mosquitos and by the slaughter of infected livestock. CCHF virus is carried by ticks and causes a fulminant, highly pathogenic form of VHF notable for aerosol transmission of infective particles. Outbreaks of CCHF have occurred in Africa, Asia, and Europe.

Bunyavirus infection. Ecchymoses encompassing left Bunyavirus infection. Ecchymoses encompassing left upper extremity one week after onset of CCHF. Ecchymoses often are accompanied by hemorrhage in other locations: epistaxis, puncture sites, hematemesis, melena, and hematuria. Image provided by Robert Swaneopoel, PhD, DTVM, MRCVS, National Institute of Virology, Sandringham, South Africa.

Many hantaviruses are spread worldwide, causing 2 major syndromes: hemorrhagic fever with renal syndrome (HFRS) and hantavirus pulmonary syndrome (HPS). They are divided into Old World hantaviruses (such as the prototypical Hantaan virus of Korea), which generally cause HFRS, and New World hantaviruses, causing HPS. Rodents carry both types. A previously undiscovered Hantavirus, Sin Nombre virus, was the cause of an outbreak of highly lethal HPS in the southwestern US in 1993. More than 450 cases have been identified in the US since 1993 with a 35% mortality rate.[1]

Filoviridae

The most notorious of the VHF viruses, including Ebola and Marburg viruses, belong to the Filoviridae family. Ebola virus first was described in 1976 after outbreaks of a febrile, rapidly fatal hemorrhagic illness were reported along the Ebola River in Zaire (now the Democratic Republic of the Congo) and Sudan. Sporadic outbreaks have continued since that time, usually in isolated areas of central Africa. An outbreak in Kikwit, Zaire, in 1995 led to 317 confirmed cases, with an 81% mortality rate. Two thirds of the patients were among health care workers caring for infected individuals. An outbreak in Uganda in late 2000 resulted in 425 cases and claimed 225 lives. In late 2012, 7 cases of Ebola virus infection were reported, including 4 deaths.

Ebola has 4 distinct subtypes: Ebola-Zaire, Ebola-Sudan, Ebola-Ivory Coast, and Ebola-Reston, a form that causes illness in nonhuman primates, and as has been recently discovered, in pigs.[2] A 2007 Ebola outbreak in Uganda, however, has been attributed to a new form of Ebola. This new Ebola subtype, which appears to be closely related to Ebola-Ivory Coast, has been given the proposed name Bundibugyo Ebola virus (named after the Bundibugyo district in Western Uganda).[3]

Fruit bats have been identified as a reservoir for Ebola-Zaire virus.[4]

Ebola virus. Electron micrograph courtesy of the C Ebola virus. Electron micrograph courtesy of the Centers for Disease Control and Prevention.

Marburg virus, named after the German town where it first was reported in 1967, is another highly pathogenic member of the Filoviridae family that is traced to central Africa. As in Ebola-Zaire, the natural host for the virus is likely the fruit bat. Marburg virus was contracted by a traveler to central Africa in 1987 and has been endemic since 1998 in Durba, Democratic Republic of the Congo, and in persons exposed in caves or mines. Marburg virus was determined to be the causative agent in a 2004-2005 outbreak of hemorrhagic fever in Angola that led to 252 confirmed cases and 227 deaths (90% case-fatality rate). In late 2012, an outbreak in Uganda resulted in 15 confirmed and 8 probable cases of Marburg virus infection, including 15 deaths.

Marburg virus. Negative stain image courtesy of th Marburg virus. Negative stain image courtesy of the Centers for Disease Control and Prevention.

Flaviviridae

Yellow fever and dengue fever are the most well known diseases caused by flaviviruses. Both are mosquito-borne; yellow fever is found in tropical Africa and South America, and dengue fever is found in Asia, Africa, and the Americas. They are notable for their significant effect on prior military campaigns and their continued presence throughout endemic areas.

Due to a resurgence in the last 3 decades, dengue fever is now considered second only to malaria in terms of importance as a tropical disease. Multiple recent large outbreaks have occurred throughout the tropics, with the most severe outbreaks occurring in Southeast Asia and the western Pacific regions. Transmission is via the bite of the infected female Aedes mosquito, although dengue can also be transmitted via transfusion.[5]

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Pathophysiology

The primary defect in patients with viral hemorrhagic fever (VHF) is that of increased vascular permeability. Hemorrhagic fever viruses have an affinity for the vascular system, leading initially to signs such as flushing, conjunctival injection, and petechial hemorrhages, usually associated with fever and myalgias. Later, frank mucous membrane hemorrhage may occur, with accompanying hypotension, shock, and circulatory collapse. The relative severity of the clinical presentation may vary depending on the virus in question, amount, and route of exposure.

In acute disease, patients are extremely viremic, and messenger ribonucleic acid (mRNA) evidence of multiple cytokine activation exists. In vitro studies reveal these cytokines lead to shock and increased vascular permeability, the basic pathophysiologic processes most often seen in viral hemorrhagic fever infection. Another prominent pathologic feature is pronounced macrophage involvement. Inadequate or delayed immune response to these novel viral antigens may lead to rapid development of overwhelming viremia. Extensive infection and necrosis of affected organs also are described. Hemorrhagic complications are multifactorial and are related to hepatic damage, consumptive coagulopathy, and primary marrow injury to megakaryocytes. Aerosol transmission of some viral hemorrhagic fever infections is reported among nonhuman primates and likely is a mode of transmission in patients with severe infection.

Multisystem organ failure affecting the hematopoietic, neurologic, and pulmonary systems often accompanies the vascular involvement. Hepatic involvement varies with the infecting organism and is at times seen with Ebola, Marburg, RVF, CCHF, and yellow fever. Renal failure with oliguria is a prominent feature of HFRS seen in Hantavirus infection and may be seen in other VHFs as intravascular volume depletion becomes more pronounced. Bleeding complications are particularly prominent with Ebola, Marburg, CCHF, and the South American arenaviruses.

Although the pathophysiology of dengue infection is complex and incompletely understood, severe dengue infection can be differentiated from milder forms by the presence of increased vascular permeability. The greatest risk factor for severe dengue infection is secondary infection with a dengue serotype different from the initial dengue infection. This increased vascular permeability is thought to be secondary to widespread T-cell activation and apoptosis and is also thought to be related to a process known as antibody-dependent enhancement, best described as the balance between neutralizing versus enhancing antibodies after an initial dengue infection, which can contribute to the severity of secondary dengue infection.

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Epidemiology

Frequency

United States

Cases of viral hemorrhagic fever in the United States are extremely rare and usually are found in patients who recently have visited endemic areas or among those with potential occupational exposure to hemorrhagic fever viruses. Lassa fever has been reported in the United States in travelers from West Africa and was most recently reported in the United States in August 2004. In 1994, a virologist working with Sabia, a Brazilian HF virus, accidentally contracted the disease. Sporadic cases of HPS due to Sin Nombre virus continue to be reported throughout the southwestern United States.[6]

No human cases of Ebola or Marburg virus disease have been reported in the United States. In 1989, an outbreak of hemorrhagic fever among imported macaque monkeys in Reston, Virginia, led to the discovery of Ebola-Reston, a variant of Ebola virus that originated in the Philippines and does not cause disease in humans.

An estimated 100-200 cases of imported dengue fever are reported in the United States each year. Occasional dengue outbreaks have occurred in the United States, and well-documented local transmission of dengue continues to occur in south Florida, specifically in Key West.[7]

International

Lassa fever is responsible for an estimated 100,000-300,000 infections per year, with 5,000 deaths. Cases have been reported throughout West Africa, particularly in Nigeria, Sierra Leone, Guinea, and Liberia. Other arenaviruses are responsible for sporadic VHF outbreaks throughout South America.

Rift Valley fever (RVF) virus and Crimean-Congo hemorrhagic fever (CCHF) are responsible for intermittent epidemics in Africa (for RVF) and in areas of Africa, Asia, and Europe (for CCHF). HFRS due to Hantavirus infection continues to be an ongoing health concern, particularly in Asia, affecting up to 200,000 patients annually.

Ebola virus appears sporadically in endemic areas of the former Zaire and Sudan. Ebola virus also has been reported in Gabon, the Ivory Coast, and Uganda. Outbreaks appear to propagate in hospital settings, often involving health care providers.

Yellow fever continues to be a serious problem in tropical areas of South America and Africa, where vaccination is not widespread. The World Health Organization estimates that approximately 200,000 cases per year occur in Africa.

Dengue HF is endemic in Southeast Asia, Africa, Central America, and South America, and the WHO estimates that 50-100 million cases occur annually. In 2012, Rio de Janeiro recorded more than 180,000 cases of dengue infection.[8]

Dengue Virus Notice posted outside Maracanã Stadiu Dengue Virus Notice posted outside Maracanã Stadium, Rio de Janeiro, Brazil, 2012. Translation: This site is a strategic point for controlling Dengue.

Mortality/Morbidity

Case-fatality rates of patients with VHF vary from less than 10% (eg, in dengue HF) to approximately 90%, as has been reported in patients with Ebola-Zaire and the recent Angola Marburg outbreak. The most recent outbreak of Ebola-Sudan in Uganda had a 50% case-fatality rate.

Complications from VHF infection include retinitis, orchitis, hepatitis, transverse myelitis, and uveitis. In patients who recover from Lassa fever infection, deafness is the most common complication. Spontaneous abortion also is common. Renal insufficiency is associated with HFRS infection.

Race

No racial predilection has been identified, although cases have originated in African areas.

Sex

No predilection for either sex has been identified.

Age

VHF affects all ages according to exposure and local demographics.

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Contributor Information and Disclosures
Author

David C Pigott, MD RDMS, FACEP, Professor of Emergency Medicine, Co-Director of Emergency Ultrasound, Vice Chair for Academic Development, Department of Emergency Medicine, University of Alabama at Birmingham School of Medicine

David C Pigott, MD is a member of the following medical societies: American College of Emergency Physicians, Emergency Medicine Residents' Association, Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Specialty Editor Board

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.

Chief Editor

Zygmunt F Dembek, PhD, MPH, MS, LHD Associate Professor, Department of Military and Emergency Medicine, Adjunct Assistant Professor, Department of Preventive Medicine and Biometrics, Uniformed Services University of the Health Sciences, F Edward Hebert School of Medicine

Zygmunt F Dembek, PhD, MPH, MS, LHD is a member of the following medical societies: American Chemical Society, New York Academy of Sciences

Disclosure: Nothing to disclose.

Additional Contributors

Jerry L Mothershead, MD Medical Readiness Consultant, Medical Readiness and Response Group, Battelle Memorial Institute; Advisor, Technical Advisory Committee, Emergency Management Strategic Healthcare Group, Veteran's Health Administration; Adjunct Associate Professor, Department of Military and Emergency Medicine, Uniformed Services University of the Health Sciences

Jerry L Mothershead, MD is a member of the following medical societies: American College of Emergency Physicians, National Association of EMS Physicians

Disclosure: Nothing to disclose.

Acknowledgements

The authors and editors of Medscape Drugs & Diseases gratefully acknowledge the contributions of previous author, Thomas W McGovern, MD, to the development and writing of this article.

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Ebola virus. Electron micrograph courtesy of the Centers for Disease Control and Prevention.
Marburg virus. Negative stain image courtesy of the Centers for Disease Control and Prevention.
Mastomys rodent, natural host of Lassa virus. Image courtesy of the Centers for Disease Control and Prevention.
Bunyavirus infection. Ecchymoses encompassing left upper extremity one week after onset of CCHF. Ecchymoses often are accompanied by hemorrhage in other locations: epistaxis, puncture sites, hematemesis, melena, and hematuria. Image provided by Robert Swaneopoel, PhD, DTVM, MRCVS, National Institute of Virology, Sandringham, South Africa.
Apodemus agrarius, the vector of Korean hemorrhagic fever caused by a hantavirus. Photo courtesy of David McClain, MD.
Bunyavirus infection - Hantaan virus. Patient with Korean hemorrhagic fever caused by Hantaan virus demonstrating typical 'sunburn flush' of cheeks, chin, and base of neck. Photo courtesy of John Huggins, PhD.
Bunyavirus infection. A patient with Korean hemorrhagic fever demonstrating conjunctival hemorrhages, facial petechiae, and "sunburn flush" of the cheeks. Photo courtesy of John Huggins, PhD.
Filovirus disease - Ebola fever. Patient with Ebola hemorrhagic fever during 1976 outbreak in Zaire demonstrating palatal petechiae and hemorrhage. Photo courtesy of Joel Breman.
Patient with morbilliform exanthem of dengue fever. Note islands of sparing characteristics for dengue. Photo courtesy Duane Gubler, PhD.
Patient with dengue hemorrhagic fever complicated by ecchymoses. Photo courtesy of Duane Gubler, PhD.
Dengue Virus Notice posted outside Maracanã Stadium, Rio de Janeiro, Brazil, 2012. Translation: This site is a strategic point for controlling Dengue.
Mastomys natalensis, natural host of Lassa virus. Photo courtesy of BioMed Central, originally published in Kelly JD, Barrie MB, Ross RA, Temple BA, Moses LM, Bausch DG. Housing equityfor health equity: a rights-based approach to the control of Lassa fever inpost-war Sierra Leone. BMC Int Health Hum Rights. 2013 Jan 2;13:2.
Table. Viral Families Causing Viral Hemorrhagic Fever
Virus Family Disease (Virus) Natural Distribution Usual Source of Human Infection Incubation (Days)
Arenaviridae        
Arenavirus Lassa fever Africa Rodent 5-16
  Argentine HF (Junin) South America Rodent 7-14
  Bolivian HF (Machupo) South America Rodent 9-15
  Brazilian HF (Sabia) South America Rodent 7-14
  Venezuelan HF (Guanarito) South America Rodent 7-14
Bunyaviridae        
Phlebovirus Rift Valley fever Africa Mosquito 2-5
Nairovirus Crimean-Congo HF Europe, Asia, Africa Tick 3-12
Hantavirus Hemorrhagic fever with renal syndrome, hantavirus pulmonary syndrome Asia, Europe, worldwide Rodent 9-35
Filoviridae        
Filovirus Marburg and Ebola Africa Fruit bat 3-16
Flaviviridae        
Flavivirus Yellow fever Tropical Africa, South America Mosquito 3-6
  Dengue HF Asia, Americas, Africa Mosquito Unknown for dengue HF, 3-5 for dengue
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