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Viral Haemorrhagic fevers
Ross Calcroft
Overview
- endemic on almost every continent except Australia
- characterised by abrupt onset of high fever and in some cases, high
mortality
- 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
- Bunyaviridae
- Crimean Congo haemorrhagic fever (CCHF): ticks; Africa, SE Europe, Middle
East, and Asia
- Hantavirus: everywhere; natural silent infections of rodents.
- Arenaviridae
- natural infections of rodents; Lassa fever is most important-W Africa
- Filoviridae
- Flaviviridae
- yellow fever virus and dengue virus
(mosquitos).
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
bleeding ensue.
- 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.
Laboratory diagnosis
- 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.
Management
- 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
recommended
- early accurate diagnosis and intensive therapy are the cornerstones of good
management
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
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