Viral Haemorrhagic Fevers
Ebola, Marburg, Lassa fever, Rift Valley fever, and Crimean-Congo haemorrhagic fever are best understood together as a clinical and biosafety group because they share important pathogenic and infection-prevention principles despite belonging to different viral families.
| Virus | Family | Genome |
|---|---|---|
| Ebola | Filovirus | Negative-sense ssRNA |
| Marburg | Filovirus | Negative-sense ssRNA |
| Lassa fever | Arenavirus | Ambisense ssRNA |
| Rift Valley fever | Bunyavirus group | Segmented negative-sense/ambisense ssRNA |
| Crimean-Congo haemorrhagic fever | Bunyavirus group | Segmented negative-sense ssRNA |
Despite spanning three distinct virus families, all five share enveloped structure and, more importantly, a shared final common pathway of severe vascular and multiorgan pathology.
| Virus | Reservoir | Transmission |
|---|---|---|
| Ebola/Marburg | Bats (suspected), nonhuman primates as intermediate amplifying hosts | Direct contact with infected body fluids from a symptomatic patient or animal |
| Lassa fever | Multimammate rat | Contact with rodent excreta; person-to-person via infected body fluids |
| Rift Valley fever | Livestock (sheep, cattle) | Mosquito bite; direct contact with infected livestock blood/tissue |
| Crimean-Congo haemorrhagic fever | Wild and domestic animals (tick-maintained cycle) | Hyalomma tick bite; direct contact with infected animal or human blood/tissue |
A recurring theme runs across this group: zoonotic origin (bats, rodents, livestock, or a wider wild and domestic animal cycle). Several members can also spread from human to human via direct body fluid contact. A single zoonotic spillover event can therefore seed a sustained human outbreak chain even without any further animal exposure. This is the central epidemiological concern driving rigorous infection prevention measures.
Despite differing in specific viral family and molecular detail, the viruses in this group converge on a broadly shared pathogenic endpoint: infection and dysfunction of vascular endothelium and of key immune cells, monocytes, macrophages, dendritic cells.
This produces increased vascular permeability and impaired coagulation, via a combination of direct endothelial damage, consumption of clotting factors, and dysregulated cytokine release.
In some cases it progresses to frank disseminated intravascular coagulation and, in the most severe presentations, multiorgan failure.
This shared endothelial and immune cell tropism, rather than any single shared genome feature, is the true unifying biological thread connecting an otherwise taxonomically diverse group of viruses under the single clinical umbrella term viral haemorrhagic fever.
The balance of haemorrhagic manifestation versus other organ-specific involvement varies by organism. Examples are hepatic involvement in yellow fever, a related but distinct flavivirus example of this same broader haemorrhagic fever concept, renal involvement in some hantavirus presentations, and neurological involvement in Rift Valley fever's encephalitic presentation. The underlying vascular and coagulation disturbance is the shared mechanistic core.
A generally shared clinical arc runs across this group. It begins with an abrupt febrile prodrome, often with headache, myalgia and gastrointestinal symptoms.
In the more severe presentations specifically, this progresses to haemorrhagic manifestations (petechiae, mucosal bleeding) and, in the most severe cases, overt haemorrhage and multiorgan involvement.
Case fatality rates vary substantially by specific virus and by outbreak, reflecting both intrinsic viral virulence differences and the quality of available supportive care. For several members of this group they reach some of the highest rates of any human viral infection, particularly Ebola and Marburg in their more virulent species and strains.
Not every virus in this group produces uniformly severe disease in every infected individual. Lassa fever in particular produces asymptomatic or mild illness in the majority of infections. This is a genuine point of clinical heterogeneity within the viral haemorrhagic fever category and should not be flattened into an assumption of uniform severity across the whole group.
PCR is the standard confirmatory test across this entire group, offering rapid, sensitive direct detection during the acute, viraemic phase of illness.
Testing for suspected viral haemorrhagic fever must be performed under strict biosafety precautions, reflecting both the severity of disease these organisms can cause and their capacity for person-to-person transmission via body fluid contact. Specimens require specific handling, packaging, and transport protocols, and testing is frequently centralised to reference laboratories with appropriate high-containment, biosafety level 4 for the filoviruses specifically, capability rather than performed in a standard clinical laboratory.
Serology, IgM and IgG, provides supportive or retrospective diagnostic information but is generally secondary to PCR for acute clinical diagnosis in this specific organism group, given the clinical urgency of rapid, sensitive direct detection during an active outbreak or individual case investigation.
Personal protective equipment with full barrier precautions (gown, gloves, eye and face protection) is required for any healthcare worker in direct contact with a suspected or confirmed case, given the demonstrated risk of body-fluid-contact transmission.
Depending on the clinical scenario and local protocol, high-risk direct patient care activities need additional enhanced PPE such as impermeable coveralls and powered air-purifying respirators.
Isolation is required for suspected and confirmed cases. The precaution category, contact alongside droplet precautions in some protocols, is determined by local, national, or WHO guidance for the specific organism and clinical scenario.
Contact tracing and symptom monitoring is the standard outbreak containment strategy, given that transmission generally requires direct contact with body fluids from a symptomatic individual. Structured symptom and temperature monitoring of exposed but currently asymptomatic contacts, rather than presumptive isolation of all contacts indefinitely, allows exposed individuals to continue normal activity unless and until they develop symptoms themselves.
Safe burial practice is a specific and important point for the filoviruses in particular, given the recognised risk of transmission from an infected deceased patient's body.
Viral load can remain high at the time of death, and traditional burial practices involving direct contact with the body have been documented as a significant source of outbreak amplification in several historical Ebola outbreaks specifically.
Safe, dignified burial practice minimising direct body contact is a core, culturally sensitive component of outbreak response for this organism group.
Healthcare-associated transmission risk is specifically recognised for several viruses in this group: filoviruses, Lassa fever and Crimean-Congo haemorrhagic fever. They were historically responsible for significant healthcare worker morbidity and mortality during outbreaks before modern PPE protocols were consistently applied. This directly underlies the emphasis on rigorous PPE and isolation practice.













