Filoviruses of Viral Haemorrhagic Fever Infections
Filoviruses
In 1967, a unique viral haemorrhagic fever appeared in laboratory workers in Marburg in West Germany, which was traced to contact with the blood and tissues of a group of African Green or vervet monkeys imported from Uganda. In 1976, 2 epidemics of severe haemorrhagic fever were reported from northern Zaire and southern Sudan. The virus, which was similar to Marburg virus, was named after the Ebola river which separates Zaire and Sudan. Clinically, they cause the most severe form of viral haemorrhagic fever known, with 60 to 90% mortality.
A. Properties
Enveloped RNA virus of unique morphology, forms tubular structures of 80nm in diameter and up to 10,000nm in length.
Infectious particles are 800-900nm in length.
helical nucleocapsids surrounded by an envelope bearing 5 to 10nm projections.
Marburg and Ebola viruses are clearly different viruses in that their peptides have different molecular weights and in that they differ antigenically.
Electronmicrograph of Marburg virus particles (Source: CDC)
B. Epidemiology
Marburg virus has been identified in restricted regions of
eastern and southern Africa. Ebola virus has been isolated from
Zaire and Sudan. However, serological surveys suggests that
Marburg and Ebola viruses had been active in numerous African
countries (10 to 50% of sera showed initial reactivity, although
studies using western blots showed that the vast majority of the
sera were non- specifically reactive). What is not resolved is
why areas of high antibody prevalence do not correlate with
reported disease. Recognized disease has occurred in sporadic
cases, case clusters or epidemics. The usual pattern seen with
large outbreaks begins with a focus that disseminates infection
to a nucleus of patients, for example, to workers in a laboratory
processing African monkey tissue, or a hospital outbreak where
patients were infected by contaminated syringes. Secondary and
subsequent generations of disease occur as close members or
medical personnel are infected. It appears that the major route
of interhuman transmission requires direct contact with infective
blood or body fluids, although droplet and aerosol infections may
occur.
C. Clinical Manifestations
The onset of illness is sudden and marked by fever, chills,
headache, myalgia, and anorexia. Abdominal pain, sore throat,
N+V, cough, and arthralgia and diarrhoea are also common. A
maculopapular rash may be seen. Haemorrhagic phenomena develop at
the height of the illness, with GI bleeding being most commonly
recognized, but petechiae and mucosal haemorrhages are also seen.
Suggestive evidence of DIC is often present. The mortality is
extremely high, being in the order of 60 to 90%.
D. Diagnosis, Treatment and Prevention
Virological diagnosis is readily achieved by virus isolation from serum during the febrile phase of the illness. Vero cells are the most widely used laboratory system for isolation. Blood and tissue specimens may also be inoculated into guinea pigs. In practice, viral isolation is rarely carried out because of the need for Class IV containment and dangers involved. Diagnosis is usually made by the direct detection of viral antigen by ELISA or viral-RNA by PCR, and serology. A serological diagnosis can be made by the detection of virus- specific IgM antibodies by ELISA and IF techniques. There is no proven virus-specific treatment. Supportive therapy should be directed toward the maintenance of the effective blood volume. Once cases are identified, person to person spread must be prevented. Ordinary sterilization techniques and barrier nursing will suffice to prevent continued transmission. No vaccine is available and the need for one remains to be established.
