Viral Haemorrhagic fevers
- endemic on almost every continent except Australia
- characterised by abrupt onset of high fever and in some cases, high
- the bleeding is a complication only of severe disease but the pathology is
of widespread leakage form the capillaries with prominent pulmonary oedema
- clinical syndrome is mainly caused by endothelial dysfunction
- death is usually due to hypovolaemic shock, with or without ARDS
- in survivors recovery is rapid and complete
- caused by many different RNA viruses; almost all are zoonoses, and
infection of humans is an accident.
- There are four main families
- Crimean Congo haemorrhagic fever (CCHF): ticks; Africa, SE Europe, Middle
East, and Asia
- Hantavirus: everywhere; natural silent infections of rodents.
- natural infections of rodents; Lassa fever is most important-W Africa
- yellow fever virus and dengue virus
History and clinical diagnosis:
- incubation period is a maximum of four weeks prior to the onset of fever
- questions must include a recent travel history, information on any possible
contact with ticks, fresh animal blood, rodent urine or blood, wild animals, and
mosquitos and other insects; recent camping in exotic areas; possible entry into
bat caves; attendance at ceremonial funerals; all these usually in remote areas.
- essential element is a short history of fever, usually high and abrupt.
- severe body pains, and headache and may be excruciating
- other features may include sore throat, nausea and vomiting, petechiae,
oozing from the gums, and bradycardia.
- investigations: proteinuria is frequent; peripheral WCC are unhelpful, and
neutrophilia may mislead.
- thrombocytopaenia is usual, and platelet function is impaired; appt may be
prolonged, but PT are usually normal.
- DIC is not a feature except in the terminal phase
- as disease progresses, hypovolaemic shock, pulmonary oedema, and frank
- AST is usually disproportionately raised compared to ALT; ratio of up to
11:1, and the level of the AST also reflects prognosis
- patients are rarely jaundiced, except in yellow fever.
- CNS is relatively spared, but encephalopathy and neurologic sequelae such
as ataxia and deafness occur.
- care with specimens
- diagnosis is by virus isolation; demonstration of a fourfold rise in Ab
titre; or high titre IgG antibody with virus specific IgM antibody in
association with compatible clinical disease.
- techniques include immunofluorescence and ELISA for detection of both
antibody and antigen.
- recently molecular techniques such as polymerase chain reactions (PCR) for
detection of viral RNA have been found to be rapid, reliable, an safe to perform
directly on serum or tissues.
- VHFs are self-limiting and providing the acute crises can be managed,
recovery is rapid and complete
- main challenge is careful management of fluid balance; pulmonary oedema is
a real risk
- blood and platelet infusions may be necessary
- some viruses are highly treatable using the antiviral agent ribavarin,
provided therapy is started as soon as possible
- exchange transfusion and steroids are controversial and are not currently
- early accurate diagnosis and intensive therapy are the cornerstones of good
Prevention of spread
- strict isolation of febrile patients at risk of VHF and rigorous use of
gloves and disinfection
- high risk of infection is associated with direct percutaneous or mucosal
contact with blood or body fluids, and post-exposure prophylaxis with ribavarin
for CCHF and for arenaviruses, especially Lassa fever, should be offered to
contacts with such exposures.
© Ross Calcroft November 1999