Marburg hemorrhagic fever is a rare, severe type of hemorrhagic fever that affects both humans and non-human primates. Marburg is the first member of the family Filoviridae (or “thread” viruses), which also includes the Ebola virus. Like Ebola, Marburg is an enveloped, single-stranded, unsegmented, negative-sense RNA virus. It has the same characteristic filamentous (thread-like) structure, can appear shaped like a U, a 6, or spiraled like a snail; and can sometimes be branched.
The Marburg virus is identical to Ebola in form and structure; however, it is genically distinct from Ebola (meaning that it stimulates the production of different antibodies). Marburg virions are 80 nm (nanometers) in diameter and average approximately 800 nm in length, although length can vary up to 14,000 nm. The four species of Ebola virus are the only other known members of the filoviridae family. As with Ebola, the exact procedure of Marburg is unknown. However, virion surface spikes are made solely of large glycoprotein (compound consisting of carbohydrates and protein).
It is assumed that, as with other negative-strand RNA viruses, these surface spikes bind to receptors on the host cell and act as a go-between entry into susceptible cells. Viral replication takes place in the cytoplasm, and envelopment is the result of budding preformed by nucleocapsids (viral protein coat and nucleic acid). Ultimately, the virus involves the liver, lymphoid organs, and kidneys. Marburg virus was first recognized in 1967, when outbreaks of hemorrhagic fever occurred simultaneously in laboratories in Marburg and Frankfurt, Germany and in Belgrade, Yugoslavia (now Serbia).
A total of 37 people became ill; they included laboratory workers as well as several medical personnel and family members who had cared for them. The first people infected had been exposed to African green monkeys or their tissues. In Marburg, the monkeys had been imported for research and to prepare polio vaccine. Recorded cases of the disease are rare, and have appeared in only a few locations. While the 1967 outbreak occurred in Europe, the disease agent had arrived with imported monkeys from Uganda.
No other case was recorded until 1975, when an Australian traveler most likely exposed in Zimbabwe became ill in Johannesburg, South Africa and passed the virus to his traveling companion and a nurse. The year 1980 saw two other cases, one in Western Kenya not far from the Ugandan source of the monkeys implicated in the 1967 outbreak. This patients attending physician in Nairobi became the second case. Another human Marburg infection was recognized in 1987 when a young man who had traveled extensively in Kenya, including western Kenya, became ill and later died. Marburg virus is native to Africa.
While the geographic area to which it is native is unknown, this area appears to include at least parts of Uganda and Western Kenya, and perhaps Zimbabwe. As with Ebola virus, the actual animal host for Marburg virus also remains a mystery, though the imported monkeys are highly suspected. Both of the men infected in 1980 in Western Kenya had traveled extensively, including making a visit to a cave, in that region. The cave was investigated by placing healthy animals inside to see if they would become infected, and by taking samples from numerous animals and arthropods trapped during the investigation.
The investigation yielded no virus: the animals remained healthy and no virus isolations from the samples obtained have been reported. Just how the animal host first transmits Marburg virus to humans is unknown. However, as with some other viruses that cause viral hemorrhagic fever, humans who become ill with Marburg hemorrhagic fever may spread the virus to other people. This may happen in several ways. Persons handling infected monkeys who come into direct contact with them or their fluids or cell cultures, have become infected.
Spread of the virus between humans has occurred in a setting of close contact, often in a hospital. Droplets of body fluids, or direct contact with persons, equipment, or other objects contaminated with infectious blood or tissues are all highly suspected as sources of disease. After an incubation period of 5-10 days, the onset of the disease is sudden and is marked by fever, chills, headache, and myalgia (severe pain in the bodys connective tissues). Around the fifth day after the onset of symptoms, a maculopapular (measles-like) rash, most prominent on the chest, back, or stomach, may occur.
Nausea, vomiting, chest pain, a sore throat, abdominal pain, and diarrhea then may appear. Symptoms become increasingly severe and may include jaundice, inflammation of the pancreas, severe weight loss, delirium, shock, liver failure, massive hemorrhaging, and multi-organ dysfunction. Because many of the signs and symptoms of Marburg hemorrhagic fever are similar to those of other infectious diseases, such as malaria or typhoid fever, diagnosis of the disease can be difficult, especially if only a single case is involved. A specific treatment for this disease is unknown.
However, supportive hospital therapy should be utilized. This includes balancing the patients fluids and electrolytes, maintaining their oxygen status and blood pressure, replacing lost blood and clotting factors and treating them for any complicating infections. Sometimes treatment also has used transfusion of fresh-frozen plasma and other preparations to replace the blood proteins important in clotting. One controversial treatment is the use of heparin (which blocks clotting) to prevent the consumption of clotting factors.
Some researchers believe the consumption of clotting factors is part of the disease process. Recovery from Marburg hemorrhagic fever may be prolonged and accompanied by uveitis (inflammation of the vascular eye coating), recurrent hepatitis, transverse myelitis (inflammation of the spinal cord and/or bone marrow), or orchitis (inflammation of the testes). People who have close contact with a human or non-human primate infected with the virus are at risk. Such persons include laboratory or quarantine facility workers who handle non- uman primates that have been associated with the disease.
In addition, hospital staff and family members who care for patients with the disease are at risk. Due to our limited knowledge of the disease, preventive measures against transmission from the original animal host have not yet been established. Measures for prevention of secondary transmission are similar to those used for other hemorrhagic fevers. If a patient is either suspected or confirmed to have Marburg hemorrhagic fever, barrier-nursing techniques should be used to prevent direct physical contact with the patient.
These precautions include wearing of protective gowns, gloves, and masks; placing the infected individual in strict isolation; and sterilization or proper disposal of needles, equipment, and patient excretions. Marburg hemorrhagic fever is a very rare human disease. However, when it does occur, it has the potential to spread to other people, especially health care staff and family members who care for the patient. Therefore, increasing awareness among health-care providers of clinical symptoms in patients that suggest Marburg hemorrhagic fever is critical.
Better awareness can help lead to taking precautions against the spread of virus infection to family members or health-care providers. Improving the use of diagnostic tools is another priority. A fuller understanding of Marburg hemorrhagic fever will not be possible until the ecology and identity of the virus reservoir are established. In addition, the impact of the disease will remain unknown until the actual incidence of the disease and its endemic areas are determined.
