Viral hemorrhagic fevers

Viral hemorrhagic fevers are a diverse group of infectious diseases caused by RNA viruses, distinguished by the clinical triad of fever, bleeding diathesis, and capillary permeability abnormalities. The term 'viral' indicates the etiologic agent, 'hemorrhagic' refers to bleeding-associated pathology, and 'fever' denotes the characteristic hyperthermic response. Five virus families are recognized as causative agents: Arenaviridae, Filoviridae, Flaviviridae, Hantaviridae, and Rhabdoviridae. These infections share common laboratory findings including leukopenia and thrombocytopenia alongside increased capillary permeability.

The clinical presentation of VHFs varies considerably by causative virus, ranging from mild illness to rapidly progressive fatal disease. The 'VHF syndrome' encompasses bleeding diathesis, capillary leak, and circulatory shock, occurring in most infections with Filoviridae such as Ebola and Marburg viruses, Crimean-Congo hemorrhagic fever, and South American hemorrhagic fevers, but only in a minority of dengue or Rift Valley fever cases. Pathophysiologic mechanisms include liver damage, disseminated intravascular coagulation, and bone marrow dysfunction, with DIC particularly implicated in Rift Valley, Marburg, and Ebola hemorrhagic fevers. All VHFs carry potential for hypotension, high fever, and mortality.

Viral hemorrhagic fevers exhibit global distribution with distinct geographic associations for specific agents. The infections are predominantly zoonotic, transmitting from wild animal reservoirs to human populations; for example, Lassa arenavirus is maintained in rodent populations and spills over to humans. Both humans and non-human animals serve as susceptible hosts. The disease burden varies widely by virus type, with some VHFs such as nephropathia epidemica causing relatively mild illness while others, particularly Ebola and Marburg infections, produce high case fatality rates. Surveillance complexity arises from the diversity of causative agents and their varied ecologies.

Transmission of viral hemorrhagic fevers occurs through multiple routes depending on the specific virus. Zoonotic transmission from wild animal reservoirs represents the primary exposure mechanism for initial human infections, with rodents serving as reservoirs for arenaviruses including Lassa virus. Human-to-human transmission occurs through direct contact with infected bodily fluids, with Lassa, Crimean-Congo hemorrhagic fever, Ebola, and Marburg viruses demonstrating particular propensity for nosocomial spread. Airborne precautions are recommended as a minimum standard when caring for VHF patients.

Source-backed detail is not yet available.

Prevention strategies for VHFs depend on the specific virus and available medical countermeasures. Vaccines exist only for yellow fever and Ebola viruses among the VHF agents; vaccines for other VHFs are generally unavailable. Post-exposure prophylaxis with ribavirin is available for Crimean-Congo hemorrhagic fever exposure and may provide benefit following Lassa fever exposure. Infection prevention for healthcare workers caring for VHF patients requires multiple precautions including hand hygiene, double gloving, protective gowns, shoe and leg coverings, and face shields or goggles, with airborne precautions implemented at minimum.

Surveillance for viral hemorrhagic fevers must account for the syndrome's diverse etiologic spectrum and variable clinical severity. Laboratory confirmation requires reference facilities with appropriate biocontainment capabilities due to the biosafety level requirements of VHF agents. Characteristic laboratory findings include leukopenia, thrombocytopenia, elevated liver enzymes, and prolonged clotting times, though these findings vary by specific virus. Given the potential for rapid progression and nosocomial transmission, early recognition and implementation of infection control measures are critical surveillance priorities.

1. 1 Wikidata. viral hemorrhagic fever.
2. 2 Wikipedia. Viral hemorrhagic fever - Wikipedia.

ICD-10

ICD-11

Total cases

0

Peak month

2012-09

Coverage

1 reporting countries · 2012-09-14 → 2026-05-02