Dermatologic Manifestations of Viral Hemorrhagic Fevers 

Viral hemorrhagic fevers (VHFs) are a group of etiologically diverse viral diseases unified by common underlying pathophysiology. These febrile diseases result from infection by viruses from 4 viral families: Arenaviridae, Bunyaviridae, Filoviridae, and Flaviviridae.

The viruses in the 4 families are all RNA viruses. All share the feature of having a lipid envelope. Survival and perpetuation of the viruses is dependent on an animal host known as a natural reservoir; humans are not the natural reservoir. With the exception of a vaccine for yellow fever and ribavirin, which is used as a drug treatment for some arenaviral infections, no cures or drug treatments for viral hemorrhagic fever exist. Only supportive treatment is possible.

Not all viruses in these families cause viral hemorrhagic fever. Viral hemorrhagic fevers share certain clinical manifestations, regardless of the virus that causes the disease. However, different viruses can cause a range of various clinical problems in addition to viral hemorrhagic fever. Common clinical manifestations of viral hemorrhagic fever are increased capillary permeability, leukopenia, and thrombocytopenia. Viral hemorrhagic fever is manifested by sudden onset, fever, headache, generalized myalgia, backache, petechiae, conjunctivitis, and severe prostration. Various hemorrhagic symptoms follow, ultimately resulting in focal inflammatory reaction and necrosis with leukocytosis.

Although the viruses are distributed all over the world, they have a higher occurrence in tropical areas, such as South America, Africa, and the Pacific Islands. They have a higher likelihood of importation because of increased travel and scientific research involving the use of imported tropical animals, which often serve as intermediate hosts. The viruses are transmitted by 2 main categories of natural reservoirs: arthropods and rodents. Arenaviruses and Hantavirus (a Bunyavirus) are primarily rodent-borne, whereas flaviviruses, as well as nairoviruses and phleboviruses (both bunyaviruses), are arthropod-borne.

Transmission occurs mainly by means of contact with the following: natural reservoirs (eg, mosquito bites, rodent bites); reservoir excretions, secretions, or blood; aerosolized particles contaminated by reservoir secretions, excretions, or blood; or intermediate hosts (eg, monkeys, livestock) or their excretions, secretions, or blood. Person-to-person transmission and nosocomial transmission also occur. Nosocomial outbreaks are not uncommon in developing countries, where safe infectious disease practices have not been implemented and supplies are in shortage.

Also see the Medscape Reference articles CBRNE - Viral Hemorrhagic Fevers and Viral Hemorrhagic Fevers (Pediatrics version).

The main common underlying pathophysiologic feature of viral hemorrhagic fevers is that the vascular bed is attacked, with resultant microvascular damage and changes in vascular permeability. However, specific pathophysiologic findings can vary depending on the virus family and the species involved.

In general, an initial febrile illness is followed by hemorrhaging into the skin and the mucous membranes; hemorrhagic rashes; and hemorrhages from body orifices, especially gastrointestinal and genitourinary bleeding. Lassa fever, although fatal, is not characterized by significant bleeding. Other clinical findings include thrombocytopenia and leukocytopenia.

Frequency

United States

Most of the natural reservoirs of these viruses live in tropical areas. Hence, the virus does not typically infect persons in the United States. Random cases of infection occur as a result of the importation of viruses by travelers or the importation of scientific research animal subjects. Several cases of infection resulting in Hantavirus pulmonary syndrome (HPS), however, have been reported across the United States.^[1]

International

Table 1. Geographic Distribution of Viral Hemorrhagic Fevers (Open Table in a new window)

Mortality/Morbidity

Children can develop dengue hemorrhagic shock syndrome (DHSS), a complication with a mortality rate of 4-12%.

Table 2. Viral Hemorrhagic Fever Mortality Rates (Open Table in a new window)

Race

No race is known to be more vulnerable than another to RNA viral infection. Geography is a determining factor.

Sex

Neither sex is known to be more or less vulnerable to RNA viral infection.

Age

Age plays a role in increasing the vulnerability to infection in only 2 circumstances, as follows:

• First, young and elderly persons are more susceptible because of their weaker immune systems.
• Second, adults are more susceptible if they work in settings in which the exposure risk is increased (eg, clinics or hospitals, agrarian settings).