Description

Viral hemorrhagic fever (VHF) is caused by a distinct group of viruses. The initial phase resembles influenza-like illness, while later stages (the hemorrhagic stage and convalescence) comprise a significant minority of critically ill patients. Later stages evolve into multisystem organ dysfunction, shock, and death. Most VHFs are not endemic in most of the U.S. There are no rapid diagnostic assays; diagnosis requires a high index of suspicion and a targeted/detailed history

Etiology

• Important VHF vectors:
  • Hantaviridae (HV): Rodent reservoir, aerosolized rodent excreta (Southwest U.S.):
    • Hemorrhagic fever with renal syndrome
    • Hantavirus pulmonary syndrome
  • Filoviruses: Fruit bat reservoir, unclear mode of transmission (sub-Saharan Africa):
    • Ebola
    • Marburg
  • Arenaviruses: Rodent reservoir, aerosolized rodent excreta (sub-Saharan Africa):
    • Lassa
    • South American hemorrhagic fevers
  • Flaviviruses: Human reservoir, via mosquito (tropics, increasingly worldwide):
    • Dengue (most common cause of VHF)
    • Yellow fever
  • Bunyaviridae: Rodent reservoir, via tick or mosquito (Europe, South Asia, Africa):
    • Rift Valley fever
    • Crimean–Congo hemorrhagic fever (CCHF)
• RNA viruses that have zoonotic life cycles in specific geographic areas

Pathophysiology

• VHFs generally cause cytokine storm similar to septic shock, wherein later stages of the disease display multisystem organ dysfunction, derangement microvasculature function, and membrane/capillary permeability
• VHF shock state is both hypovolemic and distributive; often difficult to reverse. Hypotension can progress swiftly and is associated with high mortality
• DIC appears to be a regular feature of Marburg and CCHF but is less frequent with Arenavirus infections
• Dengue hemorrhagic fever is immune-complex mediated and is usually the result of secondary infection. It is among the most common causes for VHF
• Short incubation period (2–21 d)