Viral Haemorrhagic Fever


Viral Haemorrhagic Fever (VHF) is a term whose onset is attributed to Russian physicians of the 1940s. VHF represents a class of viral infections that are attributed to similar manifestations such as fever, general malaise, edema, shock and others. However, different infections will present a multitude of similar and unspecific manifestations. Therefore, known VHFs including Ebola, Marburg, Crimea-Congo VHFs, Lassa and others are indistinguishable in their plausible characterisations. The other notable characteristics about VHF is the affinity for the tropics and also animal hosts (zoonotic).

Aetiologic Agents

VHFs are viral infections that are mainly vectored through Arthropods and rodents. CDC identifies that there are five main families of VHF viruses including Arenaviridae, Bunyaviridae, Filoviridae, Flaviviridae, and Paramyxoviridae. While the unifying factor is still a matter of debate, this virus family identifies through a number of common features.

  1. The default identifier is the cellular structure that reveals a characteristic lipid envelope. Furthermore, all the viruses are categorical RNA viruses.
  2.  VHF viruses have their natural reservoir predominantly in rodents, arthropods such as ticks, bats and non-human primates.

    The viruses will not cause disease in their hosts. The virus innocuously infect into their hosts to propagate and survive.

  3. The virus transmission is contact based. Contact with the host rodents’ fluids such as blood, urine, faecal matter can transmit the virus. In arthropods transmission, the virus is transmitted through bites.
  4. Consequently, when a host to human transmission occurs, humans can transmit the virus one to another by any means of contact.
  5. VHF viruses have shown a residence relation that is relative to a geographical area that is also the natural home of the virus’ host.

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    Additionally, outbreaks are not readily predictable.

The five RNA virus families above identified are known to cause one of more VHF disease.

The Filoviridae family is directly implicated with the Marburg and Ebola virus.

The Flaviviridae is known to propagate Yellow fever and Dengue fever.

The Bunyaviridae family is quite extensive with genus or subfamilies such as the Nairovirus, Phlebovirus, Hantavirus, Orthobunyavirus and others. The Crimea-Congo Haemorrhagic fever (CCHF), the Rift Valley Fever (RVF) and the Renal Syndrome Haemorrhagic Fever are attributed to the Bunyaviridae RNA virus family.


VHF infections follow the patterns of their host species such as ticks, mosquitoes, rodents, bats and others. There can be primary and secondary epidemic areas in the disease distribution pattern where infected people travel to other areas and spread the disease through person to person contact. Ebola and Marburg do not have a directly attributable host reservoir. There is age-dependent epidemiology where infants born to VHF immune can be easily severed by the disease. This case has been observed with Dengue fever – Infant DHF.


The pathogenesis of each of the VHF diseases vary. Varying factors are relatively due to the virus vector or a property unique to the virus. For instance, while the endothelial cells are the main facilitator for CCHFV, antibody response and properties such as Antibody Dependent Enhancement (ADE) is the main facilitator for Dengue fever virus (DENV) (Diamond & Pierson, 2015; Karlberg, 2015). Arenaviruses induce through an intricate process of cellular-protein biology. Empirical understanding indicates that New World clade B viruses including CHAPV, GTOV, JUNV, MACV and SABV are known to find cellular entry through transferrin receptor(TfR1) binding (Shao, Liang, & Ly, 2015).

The generic finding is that CCHFV shows an organ decimation pathophysiology, Dengue fever takes advantage of antibody response shortcomings while Arenaviruses seek access into the cytoplasm to enable rapid propagation through DNA replication. It is important to remark that each of the VHF will invoke different pathogenic approaches on the event of overwhelming the host biology.

Clinical Manifestations

It is crucial to identify that clinical manifestations in VHF are innumerably confounding. Though there are persisting distinctions between infections they are neither forthcoming nor a

reliable determination of the prevailing disease. One important aspect in identifying manifestation is the progression or implied intensity of the disease. In critical disease management, it assists clinicians in triage or other management structure that is in place. VHF manifestations can be categorised into incubation, pre-haemorrhagic, haemorrhagic and convalescence phases (Karlberg, 2015).

Therefore, one finds at least two categories of manifestations, the non-specific symptoms and relatively isolated symptoms. The profile of non-specific symptoms is long but elusive of distinctive characterisations. The illness offsets with a strong fever that is accompanied by constitutional symptoms including anorexia, dizziness lumbosacral pain, myalgia, sore throat, headache, malaise, athralgia, chest pains, hypotension, gastrointestinal manifestations such as diarrhea, vomiting, nausea, abdominal tenderness, abdominal pain and others (Cecil, Goldman, & Schafer, 2012).

Vascular instability is endemic in VHF manifestations. At the core rather advanced stage and never in the first few days of illness, conjuctival haemorrhage, edema, rashes in fair skinned people, venipuncture, gum bleeding, melaena, haematemesis, metrorrhagia will manifest. Specific to CCHF is the development of large ecchymoses. At this stage, there are also Central Nervous System (CNS) related manifestations including, convulsions, disorientation, gait anomalies and tremors. Most shocking is the spontaneous abortions that account for close to 100% of fetal and maternal mortality in third trimester (Cecil, Goldman, & Schafer, 2012).

Hantavirus pulmonary syndrome and Haemorrhagic fever with renal syndrome can be detected immediately after the initial stages due to their pathophysiological patterns.

Management and Prognosis

The first step into the management of VHF is identifying the frequency of reported early indicators relative to a locality. The second step is the monitoring of progress in the earlier cases as well as the continued report of new cases. The objective is to determine whether the cases fit into

the conventional VHF progression phases viz. incubation, pre-haemorrhagic, haemorrhagic and Convalescence. Blood samples should also be obtained and sent to the nearest laboratory that is equipped for a reliable response via the determination of coagulopathy. In case the patterns of an outbreak are evident, the third step is the use of media as a means of alerting and informing the public on the disease implications. In the clinical aspect, nurses and the health vocation involved should consult WHO for requirements such as the Biosafety Levels (BSL) and other containment and contingent approaches at the control stages.

Prevention and Treatment

Prevention and treatment go hand in hand with the prior management and prognosis. In both instances, the process is required to contain the escalation of new infections. The main method that is applied in this case is quarantine. The treatment approach can vary. However, it has been established that the early administration of haemodynamic and haemostasis management including fluid replacement therapy increase the chance of survival. Supportive care is paramount in any form of treatment. Drug treatment is a contentious issue since VHF or RNA viruses are far from effective control. Due to the rapid occurrence of these diseases, WHO has found it ethical to treat with experimental drugs. Ribavirin is one of the approved drugs that is effective in some infections. Zmapp is a cocktail of antibodies that though not approved, it has shown a great promise in Ebola cases (Goeijenbier et al. 2014). Supplements could also be used to assist the patient’s metabolism.


VHFs are a family of viral infections that occur in rapid unpredictable patterns. The control of these infections has been elusive. In the least, it is a clear challenge to modern day medicine. The manifestations though confounding can be supported by pathogenic analysis. VHFs are still without a cure or clear treatment approach.


  1. Cecil, R. L. F., Goldman, L., & Schafer, A. I. (2012). Goldman’s Cecil Medicine, Expert Consult Premium Edition–Enhanced Online Features and Print, Single Volume, 24: Goldman’s Cecil Medicine (Vol. 1). Elsevier Health Sciences.
  2. Diamond, M. S., & Pierson, T. C. (2015). Molecular insight into dengue virus pathogenesis and its implications for disease control. Cell, 162(3), 488-492.
  3. Goeijenbier, M., Van Kampen, J. J., Reusken, C. B., Koopmans, M. P., & Van Gorp, E. C. (2014). Ebola virus disease: a review on epidemiology, symptoms, treatment and pathogenesis. Neth J Med, 72(9), 442-8.
  4. Junghanss, T., Johnson, R. C., Pluschke, G., & White, J. F. J. H. J. K. L. J. (2014). Manson’s Tropical Infectious Diseases.
  5. Karlberg, H. (2015). Crimean-Congo hemorragic fever virus: studies on molecular pathogenesis and host-cell interactions. Inst för mikrobiologi, tumör-och cellbiologi/Dept of Microbiology, Tumor and Cell Biology.
  6. Shao, J., Liang, Y., & Ly, H. (2015). Human hemorrhagic fever causing arenaviruses: molecular mechanisms contributing to virus virulence and disease pathogenesis. Pathogens, 4(2), 283-306.

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Viral Haemorrhagic Fever. (2022, Feb 11). Retrieved from

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