Marburg virus is considered to be a re-emerging pathogen that poses a significant threat to human health. This naturally occurring virus can cause a fulminating hemorrhagic disease with a severe shock syndrome and high mortality in both humans and nonhuman primates – also known as Marburg hemorrhagic fever.
Marburg virus belongs to the family Filoviridae, which contains three genera – Ebolavirus, Marburgvirus and Cuevavirus. The genus Marburgvirus contains only one species: Marburg marburgvirus, more commonly termed Marburg virus. Its genome contains linear, non-segmented, single-stranded RNA molecule that is of a negative polarity.
This hazardous agent was initially recognized in 1967, when outbreaks of hemorrhagic fever occurred synchronously in laboratories in Germany (Marburg and Frankfurt) and former Yugoslavia, now Serbia (Belgrade). 31 patients (25 with primary and 6 with secondary infections) developed severe illness that resulted in death for seven infected individuals.
Marburg virus outbreaks that occur sporadically in Africa are characterized by high mortality and a high incidence of nosocomial transmission. The disease it causes is considered a zoonosis that persists in healthy reservoir host (fruit bats) in the endemic areas of Africa, whereas humans and nonhuman primates enter the cycle as spillover hosts with a high rate of fatal outcomes.
After an initial 1967 outbreak in Europe, the virus was not in the focus for eight years when a young Australian travelling throughout Zimbabwe developed similar symptomatology. The largest Marburg hemorrhagic fever outbreak to date occurred in northeastern Angola in the spring of 2005, with over 90 cases and 90% mortality rate.
Primary specific routes of viral spread between humans (but also between other animals and humans) are direct and indirect contact, as well as droplet transmission. Contact with equipment and other objects contaminated with infectious blood or tissues is also a possible way of transmission.
Marburg hemorrhagic fever is characterized by an abrupt onset presenting with fever, chills and myalgia. Two features of the disease are critical in its pathogenesis: endothelial damage orchestrated by both the virus and the up-regulation of toxic cytokines (with extensive vascular leakage as a consequence), and disseminated intravascular coagulation which leads to serious thrombocytopenia.
As a result, severe hemorrhage can ensue at several body sites within approximately 5 to 7 days after the onset of symptoms. Bleeding from the nose, gums, and eyes is commonly observed, whereas considerable gastrointestinal hemorrhage will often manifest as frank blood in the stool or vomit. Dehydration is a frequent consequence.
The case-fatality ratio for this disease ranges from 23 to 90%. Survivors of Marburg hemorrhagic fever experience a prolonged convalescence characterized by myalgia, muscle weakness, arthralgia, myelitis, hepatitis, ocular disease, hearing loss, and in some instances even psychosis.
In patients presenting with a history of travel to certain African countries, the following clinical criteria should be considered in suspected cases: high fever (more than 38 °C for less than three weeks), muscle pain and at least two hemorrhagic symptoms (rash, nosebleed, vomiting of blood, coughing of blood, or blood in stools).
Nevertheless, the diagnosis is difficult as many of the signs and symptoms mimic those of other more frequent infectious diseases, such as typhoid fever or malaria; hence, microbiological methods (such as antigen-capture ELISA, IgM-capture ELISA and polymerase chain reaction) are employed to confirm a case of Marburg hemorrhagic fever.
Currently there are no options available for the prophylaxis or therapy of individuals with this type of hemorrhagic fever. Treatment is therefore supportive, which includes providing supplemental oxygen, balancing the patient’s fluids and electrolytes, maintaining circulatory volume and blood pressure, and introducing treatment for any complicating infections.
Establishment of strict quarantine measures preventing further virus transmission is still the only way to fight this infection in the field. Albeit multiple anti-viral therapies and candidate vaccines against Marburg virus are currently in development, classical public health surveillance and outbreak control guidelines will undoubtedly remain the cornerstone of disease control.