Marburg hemorrhagic fever pathophysiology

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]Associate Editor(s)-in-Chief:

Pathophysiology

Pathogen

Electron micrograph (TEM) of the Marburg Hemorrhagic Virus (MHV) . Image provided by the CDC Centers for Disease Control and Prevention

• Marburg virus is the causative agent of Marburg haemorrhagic fever (MHF). Marburg and Ebola viruses are the two members of the Filoviridae family (filovirus). Though caused by different viruses, the two diseases are clinically similar.
• The viral structure is typical of filoviruses, with long threadlike particles which have a consistent diameter but vary greatly in length from an average of 800 nanometers up to 14,000 nm. Peak infectious activity is at approximately 790 nm.
• Virions contain seven known structural proteins. Four proteins form the nucelocapsid of the Marburg virus: NP, VP35, VP30, and L. While nearly identical to Ebola virus in structure, Marburg virus is antigenically distinct from Ebola virus.
• Marburg virus was the first filovirus to be identified.

Transmission

• Initial human infection results from prolonged exposure to mines or caves inhabited by Rousettus bat colonies. The reservoir host of Marburg virus is the African fruit bat, Rousettus aegyptiacus. Primates (including humans) can become infected with Marburg virus, and may develop serious disease with high mortality.
• Transmission is mainly human-to-human, resulting from close contact with the blood, secretions, organs or other bodily fluids of infected persons.
• Transmission via infected semen can occur up to seven weeks after clinical recovery.
• Transmission to health-care workers has been reported while treating Marburg patients, mainly due to incorrect or inadequate use of personal protective equipment.

Pathogenesis

Marburg virus

Dendritic cells

Adrenal Cortical cells

Hepatocytes

Macropohages

Paralysis of cellular antiviral response

Dysregulated costimulation

Tissue factor

TNF-α IL-6

TNF-α

Endothelial cells

T lymphocytes(CD4+/CD8+ and Natural killer cells

Coagulation dysregulation (DIC)

Increased vascular permeability

TNF-related apoptosis-inducing ligand(TRAIL)

Liver dysfunction Inhibition of coagulation factor synthesisF02=Apoptosis of lymphocytes leading to lymphopenia

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Immunosupression

Hypotension Metabolic disorder

Hemorrhagic syndrome

Shock Multiorgan failure