Marburg Virus Disease (MVD)

Marburg virus disease (MVD, previously known as Marburg hemorrhagic fever) is a viral hemorrhagic fever caused by one of two Marburg Viruses namely Marburg virus (MARV) and Ravn virus (RAVV). Its clinical signs resemble that of the Ebola virus disease (EVD). Egyptian fruit bats are thought to be the natural carriers of the Marburg virus, and RNA from them has been isolated.

Marburg Virus Disease Latest Updates

The World Health Organization (WHO) confirmed the first-ever outbreak of Marburg disease in Equatorial Guinea.

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Causes of Marburg Virus Disease

MVD is caused by two viruses from the Filoviridae family, Marburg virus (MARV) and Ravn virus (RAVV). Marburgviruses are endemic in equatorial Africa’s dry woods. The majority of marburgvirus infections have been linked to individuals accessing natural caves or working in mines. In 2009, the effective isolation of infectious MARV and RAVV from healthy Egyptian fruit bats collected in caves was reported. This finding strongly shows that Old World fruit bats play a role in the natural management of marburgviruses and also that entering bat-infested caves is a potential risk factor for contracting marburgviruses. More research is needed to determine whether Egyptian rousettes are the original hosts of MARV and RAVV, or if they become infected by contact with another species and hence function only as intermediate hosts. Interaction with nonhuman primates is yet another risk factor, albeit just one outbreak of MVD (in 1967) was caused by contact with infected monkeys. In contrast to the Ebola viral disease (EVD), which has been linked to heavy rains following extended periods of dry weather, triggering mechanisms for the Marburg virus’s spread into the human population have yet to be identified.

Signs and Symptoms of Marburg Virus Disease

Hemorrhagic symptoms include a maculopapular rash, petechiae, purpura, ecchymoses, and hematomas (particularly around needle injection sites). Contrary to popular assumption, bleeding does not produce hypovolemia and does not cause mortality (total blood loss is minimal except during labour). Instead, mortality occurs as a result of fluid redistribution, hypotension, disseminated intravascular coagulation, and focal tissue necroses caused by multiple organ dysfunction syndromes (MODS).

The clinical stages of Marburg Hemorrhagic Fever are as follows:

• Incubation period: 2-21 days, with an average of 5-9 days.
• The generalisation phase lasts from the first day of clinical symptoms to the fifth day. Marburg hemorrhagic fever (MHF) is characterised by a high temperature of 104 °F (40 °C) and a severe headache, as well as chills, exhaustion, nausea, vomiting, diarrhoea, pharyngitis, maculopapular rash, abdominal discomfort, conjunctivitis, and malaise.
• Day 5 to Day 13: Early Organ Phase Prostration, dyspnea, oedema, conjunctival injection, viral exanthema, and CNS symptoms such as encephalitis, disorientation, psychosis, apathy, and aggressiveness are among the symptoms. Hemorrhagic symptoms usually appear late and signal the end of the early organ phase, which can result in either eventual recovery or deterioration and death. Bloody stools, ecchymoses, blood flow from venipuncture sites, mucosal and visceral haemorrhaging, and perhaps hematemesis are all symptoms.
• Day 13 through Day 21+: Late Organ Phase Symptoms divide into two groups for surviving and fatal instances. Survivors will experience myalgia, fibromyalgia, hepatitis, asthenia, ophthalmic problems, and psychosis as they recover. Fatal cases continue to deteriorate, with symptoms such as fever, obtundation, stupor, convulsions, generalised coagulopathy, metabolic abnormalities, shock, and death occurring between days 8 and 16.

Diagnosis of Marburg Virus Disease

MVD is clinically indistinguishable from Ebola virus disease (EVD), and it is easily confused with a variety of other diseases common in Equatorial Africa, such as:

• Other Viral Hemorrhagic Fevers
• Falciparum Malaria
• Typhoid Fever
• Shigellosis
• Typhus
• Cholera
• Gram-negative Sepsis
• Relapsing Fever or Acute Promyelocytic Leukaemia
• Hemolytic Uremic Syndrome
• Snake Envenomation
• Clotting Factor Deficiencies/Platelet Disorders
• Thrombotic Thrombocytopenic Purpura
• Hereditary Hemorrhagic Telangiectasia
• Kawasaki disease
• Warfarin Intoxication

The patient’s medical history, particularly the travel and occupational history (countries and caverns visited) and the patient’s exposure to animals, is the most crucial indicator that may lead to the suspicion of MVD during a clinical examination (e.g. bats).

Filovirions can be easily detected and identified in cell culture using electron microscopy due to their unusual filamentous morphologies, however, despite some overall length differences, electron microscopy cannot distinguish the numerous filoviruses. Immunofluorescence assays are employed to confirm the presence of marburgvirus in cell cultures. Virus isolation and electron microscopy are rarely viable choices during an outbreak. RT-PCR in conjunction with antigen-capture ELISA is thus the most commonly used diagnostic procedure, which can be conducted in the field or in mobile hospitals and laboratories. In the field, indirect immunofluorescence assays (IFAs) are no longer utilised to diagnose MVD.

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Classification of Marburg Virus Disease

Marburg viral disease (MVD) is the official nomenclature in the World Health Organization’s International Statistical Classification of Diseases and Related Health Problems 10 (ICD-10) for either of the two marburgviruses, Marburg virus (MARV) as well as Ravn virus (RAVV). Marburg hemorrhagic fever (MHF) is frequently used as an unauthorised alternate name for the same disease in the scientific literature. Both disease names are taken from Marburg, Germany, where MARV was first identified.

Transmission of Marburg Virus Disease

The specifics of the initial transmission of MVD to humans are still unclear. Transmission is most likely by Egyptian fruit bats or some other natural host, like non-human primates, or through bush meat intake, but the particular methods and body fluids involved are unknown. MVD is transmitted from person to person by direct contact with contaminated bodily fluids such as blood.

Prevention of Marburg Virus Disease

There is presently no vaccines licenced by the FDA for the prevention of MVD. Many vaccination candidates have been produced and tested in animal models. The most viable are DNA vaccines or vaccines based on Venezuelan equine encephalitis virus replicons, vesicular stomatitis Indiana virus (VSIV), or filovirus-like particles (VLPs), as all of these candidates have the potential to protect nonhuman primates from marburgvirus-induced illness. Clinical trials for DNA vaccinations have begun. Marburgviruses are highly contagious but not particularly infectious. During natural MVD outbreaks, they are not transferred via aerosol. Because there is no licenced vaccine, MVD prevention is mostly based on quarantine of confirmed or high likelihood cases, adequate personal protective equipment, and sterilisation and disinfection.

Because Marburg viruses can not transmit by aerosol, the most simple way to avoid MVD outbreaks is to prevent direct (skin-to-skin) contact with the infected individual, their excretions and bodily fluids, and any potentially contaminated items and utensils. Patients should be secluded but may be visited by family members. Medical personnel must be trained in and use stringent barrier nursing procedures (disposable face masks, gloves, goggles, and a gown at all times). Traditional burial procedures, particularly those requiring body embalming, should be discouraged or modified, preferably with the assistance of local traditional healers.

Treatment of Marburg Virus Disease

Currently, there is no effective marburgvirus-specific therapy for MVD. Treatment is primarily supportive in nature, consisting of minimising invasive procedures, balancing fluids and electrolytes to prevent dehydration, administering anticoagulants early in infection to avoid or control disseminated intravascular coagulation, administering procoagulants late in infection to control haemorrhaging, maintaining oxygen levels, pain management, and administering antibiotics or antifungals to treat secondary infections.

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