Marburg Virus Disease: Clinical Features, Diagnosis, Management and Prevention

Clinical Medicine Year 3 • a severe filovirus infection linked to bats, caves, body fluids and high-consequence outbreaks

Learning outcomes

• Describe Marburg virus classification, morphology, reservoir and routes of transmission.
• Explain the incubation period, phases of illness and mechanisms of shock and coagulopathy.
• Recognise early, gastrointestinal, haemorrhagic, neurologic, ocular and genital complications.
• Plan safe diagnostic testing and differential diagnosis.
• Describe supportive care, infection prevention, contact monitoring and survivor counselling.

Definition and virology

Marburg virus and Ravn virus are enveloped, filamentous, non-segmented, negative-sense RNA viruses in the family Filoviridae and genus Marburgvirus (often called Orthomarburgvirus in current taxonomy). The virion contains nucleoprotein and polymerase-associated proteins surrounded by a lipid envelope with glycoprotein spikes. The virus replicates in macrophages, dendritic cells, endothelial cells, hepatocytes and other tissues.

Marburg disease was first recognised in 1967 after laboratory-associated outbreaks in Marburg and Frankfurt and Belgrade linked to imported African green monkeys from Uganda. Later outbreaks in Africa have been associated with cave or mine exposure and human-to-human transmission.

Reservoir and transmission

The Egyptian fruit bat, Rousettus aegyptiacus, is the principal natural reservoir identified for Marburg virus. People may become infected while entering caves/mines or handling bats, then transmit virus to others through body fluids after symptoms begin.

• Blood, vomit, stool, urine, saliva, sweat, breast milk, semen and other body fluids.
• Direct contact with a symptomatic patient’s mucous membranes or broken skin.
• Unsafe injections, contaminated instruments or blood products.
• Contact with a body during funeral preparation or burial.
• Sexual exposure to survivors because virus may persist in semen.

Patients are not generally infectious before symptoms. Casual contact without body-fluid exposure is not the usual route, but every suspected patient should be assessed conservatively until testing and an exposure history are clear.

Incubation and infectious period

The incubation period is usually 2–21 days. Early illness may resemble malaria or influenza. Infectivity increases as viral load rises and as vomiting, diarrhoea, bleeding and other wet symptoms develop. In fatal cases, deterioration commonly occurs during the second week, but course and fatality vary by outbreak, viral strain, timing of care and access to intensive support.

Pathophysiology

1. Virus enters through mucosa, broken skin, injection or contaminated body-fluid exposure.
2. It replicates in antigen-presenting cells and macrophages and spreads through lymphatics and blood.
3. Immune dysregulation causes high cytokine activity while adaptive immune responses are delayed or ineffective.
4. Endothelial injury and inflammatory mediators increase vascular permeability and promote capillary leak.
5. Hepatocellular injury reduces clotting-factor synthesis; platelet and coagulation abnormalities amplify bleeding.
6. Vomiting and diarrhoea cause severe volume and electrolyte loss, while shock leads to kidney, liver, brain and cardiac dysfunction.

Clinical presentation

1. Early dry phase

• Abrupt high fever and severe frontal or temporal headache.
• Severe malaise, profound weakness, chills and myalgia/arthralgia.
• Photophobia, conjunctival injection, sore throat and anorexia.
• Nausea and early abdominal discomfort.

2. Gastrointestinal/wet phase

From approximately day 3–5, many patients develop watery diarrhoea, repeated vomiting, abdominal pain, chest pain, cough, hiccups, dehydration and rapid weight loss. The combination of high stool/vomit volume and capillary leak can produce shock even before bleeding appears.

3. Rash and bleeding

A non-itchy maculopapular rash may appear around days 5–7. Severe disease may cause petechiae, ecchymoses, bleeding from gums and nose, haematemesis, melaena, haematuria, vaginal bleeding or oozing from venepuncture sites. Bleeding is a late and serious sign, but is neither necessary nor sufficient to diagnose MVD.

4. Neurologic, ocular and genital complications

• Confusion, agitation, drowsiness, seizures, encephalitis or coma.
• Eye pain, photophobia, uveitis, visual loss or other post-acute ocular disease.
• Orchitis, testicular pain and possible viral persistence in semen.
• Pregnancy complications, fetal loss and infection of placental/reproductive tissues.

History and examination

Investigations

Safety first

Before collecting blood or swabs, notify the reference laboratory and infection-prevention team. Use trained personnel, appropriate PPE, leak-proof triple packaging and approved transport. Never send a suspected high-risk specimen through an ordinary uncoordinated route.

Specific tests

• RT-PCR: detects viral RNA during acute disease and is the principal confirmatory method.
• Antigen detection: can support early diagnosis in approved reference or field systems.
• IgM/IgG serology: helps distinguish recent infection or later immune response but may be negative early.
• Virus isolation/electron microscopy: specialised high-containment methods; electron microscopy identifies filovirus morphology but does not reliably distinguish Marburg from Ebola.

Severity assessment

• Full blood count, platelets, glucose, electrolytes, urea, creatinine and bicarbonate.
• AST/ALT, bilirubin, albumin, coagulation tests, fibrinogen and lactate.
• Malaria test, blood cultures and other targeted tests where safe and clinically indicated.
• Chest imaging, ECG, neurologic assessment and eye examination according to symptoms and available expertise.

Differential diagnosis

Management

• Admit to a designated isolation/treatment unit and minimise unnecessary movement.
• Assess airway, breathing, circulation, mental state, glucose, urine output and bleeding frequently.
• Give oral rehydration when alert and able to drink; use IV/IO isotonic fluids for shock or severe dehydration with close reassessment.
• Correct glucose, potassium, sodium, bicarbonate, hypoxaemia and acidosis.
• Treat vomiting and diarrhoea, provide nutrition and pain/fever control that does not worsen renal, hepatic or bleeding risk.
• Use oxygen, vasopressors, renal replacement therapy, blood products and ventilatory support according to clinical need and specialist guidance.
• Treat malaria, bacterial sepsis and other proven infections using safe protocols; do not let a suspected VHF diagnosis prevent treatment of life-threatening differentials.
• Avoid unnecessary IM injections, lumbar puncture, endoscopy or surgery while coagulopathy/high exposure risk is present.

Infection prevention and outbreak control

• Standard precautions plus contact/droplet precautions and risk-based respiratory protection for aerosol-generating procedures.
• Dedicated equipment, safe injection practices, environmental cleaning, controlled waste and a monitored PPE donning/doffing process.
• Safe and dignified burial; no washing, touching or transporting bodies outside the trained burial system.
• List and monitor contacts for 21 days after the last exposure; rapidly isolate anyone who develops symptoms.
• Trace healthcare-worker exposures and provide immediate occupational-health advice after any PPE breach or needlestick.
• Engage cave workers, miners, faith leaders, funeral teams, communities and survivors to reduce fear and unsafe practices.

Survivor and reproductive-health care

• Assess fatigue, joint pain, eye disease, hearing, mental health, stigma and social reintegration.
• Provide condoms and semen-testing/clearance counselling according to national survivor guidance.
• Discuss breastfeeding and pregnancy with specialist teams because virus can persist in reproductive tissues and breast milk.
• Survivors should receive respectful follow-up; ordinary social contact after recovery is not a reason for discrimination.

Exam-focused pearls

• Marburg is a filovirus; its clinical syndrome closely resembles Ebola.
• Rousettus aegyptiacus fruit bats are the principal recognised reservoir.
• Cave or mine exposure is a classic epidemiologic clue.
• Incubation is 2–21 days; watery diarrhoea and vomiting may precede bleeding.
• No approved vaccine or specific antiviral currently exists; early supportive care improves survival.
• Do not diagnose or exclude MVD from bleeding alone—test safely and protect staff from the beginning.

References and further reading

• SlideShare: Marburg disease
• WHO: Marburg virus disease fact sheet
• WHO: Marburg virus disease overview
• CDC: Clinical overview of Marburg virus disease
• WHO: Ebola and Marburg infection-prevention guideline