Marburg virus disease (MVD) is a rare but serious illness caused by the Marburg virus, which belongs to the same virus family as Ebola. The disease was first identified in 1967 during outbreaks in Germany and what is now Serbia, after laboratory workers were exposed to African green monkeys brought from Uganda. In nature, the virus is carried by fruit bats of the Rousettus genus, which act as the main source of infection. People can become infected through long-term contact with bat colonies, often in caves or mines, and the virus can then spread between humans through contact with blood, vomit, saliva, or other body fluids of an infected person. It can also spread indirectly through contaminated surfaces, equipment, or materials.
The disease has a very high death rate, which can range from about one-quarter to nearly all infected individuals, depending on the outbreak and available medical care. Symptoms usually start suddenly with fever, headache, chills, and muscle pain. These are often followed by stomach problems such as nausea, vomiting, and diarrhea. In severe cases, patients may experience bleeding, organ failure, and shock. People who survive the illness may continue to have health problems such as tiredness, joint pain, or vision difficulties.
Outbreaks of Marburg virus disease have occurred from time to time in sub-Saharan Africa, including in Angola, the Democratic Republic of the Congo, Uganda, Kenya, Ghana, and Equatorial Guinea. These outbreaks often occur in regions where fruit bats are common.
There is currently no approved treatment or vaccine for the disease, although experimental options are being studied. The best chance of survival comes from early medical support, which includes replacing lost fluids, maintaining salt and mineral balance in the body, and treating complications. Preventing the disease focuses on avoiding contact with bats, practicing safe burial procedures, improving infection control in hospitals, and spreading public awareness to reduce person-to-person transmission.
Historical Background
Marburg virus disease (MVD) was first identified in 1967 during simultaneous outbreaks in Marburg and Frankfurt, Germany, and Belgrade, Yugoslavia (now Serbia). These outbreaks were linked to laboratory workers exposed to African green monkeys (Chlorocebus aethiops) imported from Uganda for research. A total of 31 people were infected, resulting in 7 deaths, and the event marked the discovery of the Marburg virus as a new human pathogen.
Following its identification, sporadic cases and outbreaks continued to emerge, mainly in East and Central Africa. In 1975, a traveler returning to South Africa from Zimbabwe developed the disease, and secondary cases were reported in his close contacts. Larger outbreaks were later recorded in Kenya (1980 and 1987), the Democratic Republic of the Congo (1998–2000), and Uganda (2007, 2012, and 2014). The most severe outbreak occurred in Angola between 2004 and 2005, resulting in more than 250 cases with a case fatality rate of approximately 90%.
More recently, isolated cases and outbreaks have been reported in Uganda, Ghana (2022), and Equatorial Guinea and Tanzania (2023).
Across all outbreaks, case fatality rates have varied widely, ranging between 24% and 88%, influenced by factors such as the quality of healthcare, speed of outbreak detection, and the viral strain involved.
Comparison With Related Viral Hemorrhagic Fevers
Marburg virus is a member of the Filoviridae family, which also includes the Ebola virus. Both viruses are classified as filoviruses and are among the most virulent pathogens known to infect humans. They cause viral hemorrhagic fevers, a group of illnesses characterized by fever, vascular damage, and, in severe cases, hemorrhaging, multi-organ dysfunction, and high case fatality rates.
The clinical presentation of Marburg virus disease (MVD) and Ebola virus disease (EVD) is strikingly similar. Both begin with a sudden onset of fever, headache, muscle aches, and gastrointestinal symptoms, followed in severe cases by bleeding, organ failure, and shock. Long-term complications in survivors, such as fatigue, joint pain, and vision problems, have been reported in both diseases. Because of the similarity in symptoms, laboratory testing is required to distinguish between Marburg and Ebola infections.
Despite these parallels, several distinctions exist. The geographical distribution of outbreaks differs: Ebola virus has a broader endemic range, with outbreaks recorded across West, Central, and East Africa, while Marburg virus outbreaks have primarily occurred in East and Central Africa. Historically, Ebola outbreaks have tended to involve larger numbers of cases, such as the 2014–2016 West African epidemic, which affected tens of thousands of people. By contrast, Marburg virus outbreaks have been smaller in scale but remain highly lethal, with case fatality rates ranging between 24% and 88%. Ebola outbreaks have shown similarly high mortality, but case fatality rates have varied depending on the viral species involved, ranging from approximately 25% to 90%.
Both viruses share the same primary routes of transmission: human-to-human spread occurs through direct contact with the blood, secretions, or other bodily fluids of infected individuals, as well as through contaminated surfaces and materials. Healthcare settings have often played a central role in amplification during outbreaks, particularly in the absence of strict infection prevention and control measures. Protective clothing, safe burial practices, and rapid isolation of cases are critical in controlling the spread of both diseases.
Research into vaccines and treatments has advanced more rapidly for Ebola than for Marburg virus. Several Ebola vaccines and therapeutic options have been developed and, in some cases, deployed during outbreaks. For Marburg virus, however, no licensed vaccines or specific antiviral therapies currently exist, though multiple experimental candidates are under development. This disparity reflects differences in the scale of outbreaks and the urgency of the public health response, with Ebola historically attracting greater international attention due to its larger and more frequent epidemics.
Causes and Transmission
Marburg virus disease arises from a virus linked to specific natural hosts and spreads through direct contact with infected bodily fluids.
Marburg Virus Origin
The Marburg virus was first identified in 1967 following simultaneous outbreaks in Marburg and Frankfurt, Germany, and in Belgrade, Yugoslavia (now Serbia). These outbreaks were linked to laboratory workers who had been exposed to tissues and blood from African green monkeys (Chlorocebus aethiops) imported from Uganda. While monkeys were the source of the first recognized human infections, they are not the natural host of the virus.
Extensive ecological studies have identified the Egyptian fruit bat (Rousettus aegyptiacus) as the natural reservoir of the Marburg virus. These bats carry the virus without developing illness, allowing it to persist in nature. Transmission from bats to humans typically occurs when people enter bat-inhabited environments, such as caves or mines, or handle bats directly. The presence of Marburg virus RNA and antibodies in wild bat populations across Africa supports their role in maintaining the virus in the wild.
Modes of Transmission
The virus spreads to humans through direct contact with the blood, secretions, organs, or other bodily fluids of infected individuals or animals. Contaminated surfaces, medical equipment, and materials such as bedding and clothing can also serve as indirect sources of infection. Once introduced into human populations, the virus can spread rapidly, especially in healthcare and household settings where close physical contact occurs.
Human-to-human transmission is a defining feature of Marburg virus disease outbreaks. It often affects family members caring for sick relatives and healthcare workers treating patients without adequate infection prevention measures. Transmission via airborne particles has been demonstrated under experimental laboratory conditions but is not considered a significant route of spread during natural outbreaks.
Risk Factors for Infection
Several factors contribute to the risk of Marburg virus infection. Individuals who work or travel in bat-inhabited caves and mines in endemic regions face heightened exposure. Handling of infected wildlife, including fruit bats and nonhuman primates, is another recognized risk.
Healthcare workers are particularly vulnerable during outbreaks when personal protective equipment (PPE) is insufficient or infection control measures are inadequate. Traditional burial practices, which often involve direct contact with the body of the deceased, have been associated with numerous chains of transmission in African outbreaks. In addition, delayed diagnosis, lack of public awareness, and weak health infrastructure can amplify the spread of the virus in affected regions.
Symptoms and Clinical Manifestations
Marburg virus disease (MVD) presents with a wide range of clinical features that typically progress through distinct phases, beginning with nonspecific symptoms that resemble common viral illnesses and advancing to severe, often life-threatening complications. The disease has an incubation period of 2 to 21 days, during which individuals do not show symptoms but remain capable of suddenly developing illness once the virus has multiplied within the body.
Early Symptoms
The onset of MVD is abrupt. Patients usually experience a sudden high fever accompanied by severe headache, chills, and pronounced fatigue. Muscle aches and body pains are common during the initial stage. Within a few days, gastrointestinal symptoms such as nausea, vomiting, abdominal cramps, and profuse watery diarrhea often develop, contributing to rapid weight loss and dehydration. These digestive disturbances can persist for several days and are frequently reported as one of the most debilitating aspects of early infection.
Other early manifestations may include conjunctivitis (inflammation and redness of the eyes) and, in some cases, a non-itchy maculopapular rash, typically appearing between days 2 and 7 after symptom onset. The nonspecific nature of these early signs makes diagnosis difficult, as they overlap with malaria, typhoid fever, and other endemic infectious diseases.
Progression of Disease
As MVD advances, the illness typically enters a more severe phase characterized by multi-organ involvement. Hemorrhagic symptoms become prominent, including bleeding from the gums, nose, gastrointestinal tract, and puncture or injection sites. Patients may also experience blood in vomit or stool. Subcutaneous bleeding can cause bruising and petechiae (small red or purple spots on the skin).
Neurological complications often emerge during this stage, with confusion, irritability, agitation, and seizures reported in some patients. As liver and kidney functions deteriorate, patients may develop jaundice, abdominal swelling, and reduced urine output, signaling acute organ failure. Respiratory distress, low blood pressure, and circulatory collapse (shock) are also common features of advanced disease.
Complications and Severe Outcomes
Severe MVD frequently results in widespread internal bleeding, profound metabolic imbalance, and multi-organ failure. In fatal cases, death usually occurs between 8 and 16 days after the onset of symptoms, most often due to shock, severe blood loss, or organ dysfunction.
Survivors of MVD often experience prolonged recovery periods. Post-infection complications may include persistent muscle and joint pain, chronic fatigue, vision and hearing problems, and in some cases, psychological effects such as depression or memory impairment. Because the immune system is weakened during and after the illness, secondary bacterial infections can also occur.
Diagnosis and Detection
Accurate diagnosis of Marburg Virus Disease relies on specific laboratory tests and careful clinical evaluation. Identifying the virus early through proper testing is essential for effective patient management and outbreak control.
Laboratory Testing Methods
Laboratory confirmation of MVD relies on molecular and serological techniques conducted in facilities with high-level biosafety precautions. The most widely used method is reverse transcription-polymerase chain reaction (RT-PCR), which detects viral RNA in blood or tissue samples. RT-PCR is highly sensitive and can confirm infection during the acute stage of illness, often within days of symptom onset. This method is critical in identifying cases rapidly and initiating control measures.
Virus isolation in cell culture remains the definitive diagnostic technique, but it is rarely performed outside research settings due to the extreme biosafety risks involved. Culturing live Marburg virus requires a Biosafety Level 4 (BSL-4) laboratory, of which only a limited number exist worldwide. Serological assays, such as enzyme-linked immunosorbent assay (ELISA), are used to detect virus-specific antibodies. IgM antibodies indicate recent infection, while IgG antibodies suggest past exposure or recovery. These tests are particularly useful for retrospective diagnosis or for confirming cases during the later stages of illness.
Other methods include immunohistochemistry, which detects viral antigens in tissue specimens and is valuable for postmortem analysis. Antigen-capture ELISA tests can also be employed during acute infection. Because of the biosafety risks associated with handling specimens, all laboratory testing for Marburg virus must be performed in specialized facilities equipped to handle highly infectious pathogens.
Clinical Diagnosis Criteria
Clinical diagnosis of MVD relies on recognition of symptoms consistent with the disease in patients with relevant epidemiological exposure. The illness typically begins with sudden fever, severe headache, malaise, and muscle pain.
As the disease progresses, gastrointestinal symptoms such as diarrhea and vomiting become prominent, followed by hemorrhagic signs including bleeding from gums, the gastrointestinal tract, or injection sites. Additional features may include jaundice, rash, confusion, and signs of multi-organ dysfunction.
Because these manifestations overlap with those of other infectious diseases, clinical diagnosis alone cannot establish certainty. However, during outbreaks or in patients with known exposure to caves inhabited by fruit bats (Rousettus aegyptiacus) or direct contact with confirmed cases, a strong clinical suspicion may prompt immediate isolation and initiation of supportive treatment while laboratory confirmation is pursued. Contact tracing and detailed exposure histories play a critical role in clinical evaluation.
Differential Diagnosis
The symptoms of MVD are similar to those of other viral hemorrhagic fevers, making differential diagnosis essential. Ebola virus disease is the closest clinical mimic, as both viruses belong to the Filoviridae family and present with nearly identical progression. Other hemorrhagic fevers such as Lassa fever, Rift Valley fever, and Crimean-Congo hemorrhagic fever also overlap in clinical presentation.
Beyond viral causes, several non-viral illnesses can resemble early MVD. Malaria, typhoid fever, bacterial sepsis, and leptospirosis are common in endemic regions and can cause fever, gastrointestinal disturbances, and systemic illness similar to early Marburg virus infection. Laboratory confirmation is therefore indispensable to avoid mismanagement and to ensure that patients receive appropriate care.
A precise differential diagnosis prevents mismanagement, unnecessary use of resources, and supports targeted infection control measures to limit transmission.
Treatment and Medical Management
The treatment and medical management of Marburg Virus Disease (MVD) primarily rely on supportive care, as no antiviral drug or vaccine has yet been licensed for widespread clinical use. The primary objectives are to alleviate symptoms, prevent secondary complications, and maintain essential organ function until the patient’s immune system can mount a sufficient response.
Supportive Care Interventions
Supportive care remains the cornerstone of MVD treatment. Patients often present with severe dehydration due to vomiting, diarrhea, and profuse sweating, making fluid and electrolyte replacement critical. Intravenous fluid therapy helps restore hydration and correct electrolyte imbalances, which can otherwise lead to life-threatening complications such as hypovolemic shock.
Oxygen supplementation is employed when respiratory distress develops, while careful monitoring of blood oxygen levels guides clinical decisions. Hemodynamic support, including vasopressors, may be necessary for patients progressing toward septic or hypovolemic shock.
Because hemorrhagic manifestations are common, blood transfusions and clotting factor replacement may be indicated to manage anemia or coagulopathies. Patients are also closely monitored for signs of multi-organ failure, with interventions tailored to renal, hepatic, or cardiovascular dysfunction as needed.
Symptom-directed management plays an important role: antipyretics reduce high fever, analgesics relieve pain, and antiemetic medications control nausea and vomiting. Nutritional support, ideally through safe enteral feeding, is recommended to strengthen immune responses and assist in recovery.
Strict infection prevention and control protocols are vital to minimize nosocomial transmission. Healthcare workers employ personal protective equipment (PPE), enforce isolation of confirmed cases, and adhere to rigorous decontamination procedures for medical equipment and facilities.
Experimental Therapies
Although no specific antiviral treatment has been officially approved for MVD, several investigational approaches are under study. Monoclonal antibody therapies, designed to neutralize Marburg virus glycoproteins, have shown protective effects in non-human primate studies and are undergoing further evaluation in early-phase clinical trials.
Broad-spectrum antivirals, such as remdesivir and favipiravir, have demonstrated some activity against filoviruses in laboratory settings, though definitive clinical evidence in MVD patients is lacking. Small interfering RNA (siRNA)-based therapies and other nucleic acid–directed approaches are also being investigated as potential strategies to disrupt viral replication.
Vaccine development is advancing, with several candidates, particularly viral vector–based vaccines, demonstrating protective efficacy in preclinical models. Some vaccines are currently in early-stage human trials, though widespread availability is limited. Emergency compassionate use of investigational vaccines has been considered during outbreaks, but none are yet licensed for routine use.
Outcomes and Prognosis
The prognosis of Marburg virus disease varies considerably depending on viral strain, the speed of diagnosis, and the quality of supportive medical care available. Case fatality rates have historically ranged from 24% to 88%, with the highest mortality observed in outbreaks where healthcare resources were limited. Patients who receive early and aggressive supportive care have significantly higher chances of survival.
Survivors often face a prolonged convalescence, during which they may experience post-viral sequelae such as chronic fatigue, arthralgia, ocular complications (including uveitis), and psychological distress. Long-term organ damage, particularly involving the liver and kidneys, has been documented in some cases.
Prevention and Control Measures
Effective prevention and control of Marburg Virus Disease require targeted actions in healthcare environments, community practices, and ongoing vaccine research. Measures focus on minimizing virus transmission, protecting healthcare workers, and raising public awareness.
Infection Prevention in Healthcare Settings
Hospitals and clinics play a central role in both the treatment of patients and the containment of MVD outbreaks. Infection prevention relies on strict adherence to standard precautions and barrier nursing techniques. Healthcare workers are required to use personal protective equipment (PPE), such as gloves, gowns, masks, face shields, and eye protection, to minimize direct exposure to blood, secretions, and other bodily fluids of infected individuals.
Isolation of patients is an established principle in managing filovirus outbreaks. Suspected and confirmed cases should be placed in dedicated treatment units or negative-pressure isolation wards when available. This segregation prevents cross-infection with uninfected patients and reduces the risk of transmission to visitors or hospital staff.
Sterilization and disinfection protocols are critical. Reusable medical instruments must undergo appropriate decontamination, while disposable items, including syringes and gloves, should be destroyed using incineration or safe burial. Contaminated linens and surfaces require treatment with effective disinfectants such as chlorine solutions.
Healthcare workers must also receive specialized training in the recognition of early clinical signs, the correct donning and doffing of PPE, and the management of accidental exposures. Surveillance measures, including contact tracing and active monitoring of healthcare staff who have been in close proximity to confirmed patients, further assist in preventing nosocomial outbreaks.
Community-Level Prevention Strategies
At the community level, prevention is focused on minimizing contact with the virus’s natural reservoirs and reducing risky human behaviors that facilitate spread. Fruit bats of the Rousettus genus are considered the principal reservoir of the virus. Activities such as hunting, trapping, or consuming bats and other bushmeat are discouraged in endemic areas. In addition, communities living near caves or mines inhabited by bats are advised to limit exposure or use protective measures.
Public health education campaigns form the backbone of community-level control. Messaging emphasizes the importance of regular hand hygiene, avoiding direct contact with symptomatic individuals, and implementing safe burial practices. Traditional funeral rites, which often involve washing or touching the deceased, have been linked to Marburg transmission; therefore, culturally sensitive modifications are promoted to reduce infection risk while respecting local customs.
Vaccine Development Efforts
As of August 2025, there is no licensed vaccine available for Marburg virus. Research efforts have accelerated in recent years, building upon knowledge gained from vaccine development for Ebola virus, a closely related filovirus. Candidate vaccines under investigation employ diverse technological platforms, including viral vectors (such as adenovirus-based vaccines), recombinant protein subunits, and virus-like particles (VLPs).
The primary objectives of vaccine research are to elicit a rapid and durable immune response capable of providing protection in outbreak conditions. However, progress is complicated by several factors: the sporadic and geographically limited occurrence of outbreaks makes it difficult to conduct large-scale efficacy trials; the high biosafety requirements for handling the virus limit research opportunities; and the urgency of response often outpaces traditional vaccine development timelines.
Epidemiology and Global Impact
Marburg virus is endemic to parts of Africa, especially in Uganda, Kenya, Angola, the Democratic Republic of Congo, and South Africa. Cases usually arise near caves or mines inhabited by the Egyptian fruit bat (Rousettus aegyptiacus), the natural reservoir of the virus. These bats spread the virus through their excretions, creating a risk to humans entering these environments.
Human-to-human transmission is mainly reported in rural and hospital settings within these countries. The virus has not established sustained transmission outside Africa, limiting its geographic spread.
The first recognized outbreak of Marburg virus disease occurred in 1967 in the cities of Marburg and Frankfurt in Germany, as well as in Belgrade, then part of Yugoslavia. The outbreak was traced to laboratory workers who had been exposed to African green monkeys (Chlorocebus aethiops) imported from Uganda for polio vaccine research. In total, 32 cases were documented, resulting in 7 deaths. Transmission occurred primarily through direct contact with infected tissues and fluids, with several cases linked to needle-stick injuries sustained during laboratory procedures. Notably, no evidence of airborne transmission was recorded, which helped shape early understanding of the virus’s transmission dynamics. This event marked the discovery of the Marburg virus and spurred international recognition of filoviruses as a new category of highly pathogenic agents.
Following the initial recognition of Marburg virus disease in Europe, subsequent major outbreaks were reported across Africa, often linked to contact with infected bats or human-to-human transmission in healthcare settings.
- Angola (2004–2005): Angola experienced the largest documented outbreak of Marburg virus disease to date. Beginning in Uíge Province, the outbreak resulted in 374 reported cases and 329 deaths, representing a case fatality rate (CFR) of approximately 88%.
- Democratic Republic of Congo (1998–2000): An outbreak in the Watsa region of northeastern Democratic Republic of Congo resulted in 154 reported cases and 128 deaths, corresponding to an estimated CFR of 83%. The outbreak was closely associated with gold mining activity, where individuals were believed to have been exposed to the virus in bat-inhabited caves and tunnels.
- Uganda (2007–2017): Uganda has reported multiple outbreaks of Marburg virus disease of varying scale and severity. In 2007, an outbreak in Kamwenge District resulted in 4 cases, including 2 deaths. A larger outbreak in 2012 led to 15 reported cases and 4 deaths (27% CFR). Subsequent smaller outbreaks occurred in 2014, with 1 confirmed case that was fatal, and in 2017, when 2 confirmed and 1 probable case were identified, all of whom died. Uganda’s recurrent outbreaks have been linked to its population of Egyptian fruit bats (Rousettus aegyptiacus), recognized as the natural reservoir of the virus.
- South Africa (1975, 1980): South Africa reported two small clusters of Marburg virus disease. In 1975, three cases were identified, including one fatality, following exposure in Zimbabwe. A second, isolated case occurred in 1980, also imported from Zimbabwe.
Recent and Emerging Outbreaks
In the 21st century, Marburg virus disease has continued to emerge in new geographic regions, reflecting both the virus’s ecological range and improvements in diagnostic capacity.
- Guinea (2021): Guinea reported its first confirmed case of Marburg virus disease in August 2021. The patient died, resulting in a CFR of 100%. This event was significant as it marked the first detection of the virus in West Africa, raising concern for wider geographic spread.
- Ghana (2022): In 2022, Ghana experienced a family cluster of Marburg virus disease in the Ashanti region. Three cases were reported, including two deaths, yielding a CFR of 67%. This represented the country’s first encounter with the virus.
- Equatorial Guinea (2023): Equatorial Guinea declared its first outbreak in 2023, which involved 17 confirmed cases, 12 deaths, and 23 probable deaths. With an overall fatality rate of approximately 71%.
- Tanzania (2023): Tanzania reported its first outbreak in 2023, with 9 confirmed cases and 6 deaths (67% CFR). The outbreak occurred in the Kagera region, and swift containment measures limited further spread.
- Rwanda (2024): Rwanda experienced its first outbreak of Marburg virus disease in 2024, centered in the capital, Kigali. A total of 66 confirmed cases were documented, with 15 deaths, representing a CFR of 23%. Uniquely, a large proportion of cases occurred among healthcare workers. More than 700 contacts were traced and monitored, and the outbreak was declared over in December 2024 after 42 consecutive days without new cases.