Marburg Virus Disease

Marburg virus disease, commonly but incorrectly named 'green monkey' disease, is a severe distinctive haemorrhagic febrile illness of humans, first described in 1967, when 31 cases with seven deaths in Germany and Yugo slavia were traced to direct contact with blood, organs or tissue cell cultures from a batch of African green monkeys (Cercopithicus aethiops) that had been trapped in Uganda. Several secondary cases occurred in hospital personnel by contact with the blood of patients. One further case was apparently transmitted by sexual intercourse 83 days after the initial illness, and virus was isolated from the semen. The case fatality rate was 29% for the primary cases, but no deaths occurred in the six secondary cases. This previously unrecognised disease was caused by an infectious agent probably new to medical science. Three more cases were reported in Johannesburg in 1975, in two young Australians who crossed central Africa, and a nurse treating them. One of the primary cases died. There have been two other detected recurrences of Marburg virus disease in 1980 and in 1987, all in travellers in rural Africa, and none has led to extensive transmission.

Nature of the Infectious Agent

Marburg virus is classified as a filovirus with two genotypes, Marburg and Ebola. Marburg virus has no known subtypes and is antigenically distinct from Ebola virus, which has four subtypes. The morphology of these two viruses is unique with a long, but variable, filamentous shape of particles (Figure 6.11). Particles may be branched, circular, U-shaped or resemble a torus (Figure 6.12)

Torus Medicine

Figure 6.12 (a) Surface spikes on Marburg virus. Negative stain, x 200 000. (b) A torus form of Marburg virus showing the RNA core. Negative stain, x 200 000. (c) A filamentous form of Marburg virus curling up into a torus. The final infective particle is believed to be the torus form. x 200 000. (Courtesy of Dr David Ellis, reproduced from Principles and Practice of Clinical Virology, 1st edition, 1987)

Figure 6.12 (a) Surface spikes on Marburg virus. Negative stain, x 200 000. (b) A torus form of Marburg virus showing the RNA core. Negative stain, x 200 000. (c) A filamentous form of Marburg virus curling up into a torus. The final infective particle is believed to be the torus form. x 200 000. (Courtesy of Dr David Ellis, reproduced from Principles and Practice of Clinical Virology, 1st edition, 1987)

and have a diameter of 85 nm. Spikes are present on the surface (Figure 6.12a) and there is an axial channel within the ribonucleoprotein (Figure 6.12c). The genome consists of a single negative-stranded RNA. Molecular analysis of the genome indicates that the filoviruses are the closest relatives to rhabdoviruses and paramyxoviruses.

primary infection appears to be limited to Central Africa.

The incubation period is 4-16 days. Transmission is by contact with infected blood or tissue and transmission by the sexual route has been described.

Reservoir of the Infection

Epidemiology and Geographical Distribution

The reservoir of the infection remains unknown despite intensive investigation of a host of vertebrates and an-thropods. In the case of the Australian traveller who acquired the disease in Zimbabwe, he had often slept outdoors, and once in a house occupied with bats in the attic. He was also stung on the leg while resting at a roadside 6 days before the onset of illness.

The original outbreak resulting from exposure to the blood and tissues of African green monkeys remains unexplained, and since experimental infection of these monkeys invariably results in death, African green monkeys are not the natural host of the virus.

Seroprevalence studies indicate that Marburg virus disease is very rare, and the geographical distribution of

Not known.

Pathology

There is extensive involvement of the liver, severe renal damage, changes in vascular permeability and activation of the clotting cascade, and disseminated intravascular coagulation with involvement of complex immunological mediators and cytokine release.

Clinical Features and Diagnosis

The illness begins characteristically with sudden onset of fever, malaise, headache and myalgia, followed by nausea, vomiting and watery diarrhoea. A maculopapular rash appears between 5 and 7 days after the onset of illness and is most marked on the buttocks, trunk and lateral aspects of the upper arms. Conjunctivitis is common. A tendency to bleed develops, particularly from the gums and from needle punctures, and severe bleeding into the gastrointestinal tract and elsewhere may occur. There is functional evidence of liver damage but clinical jaundice has not been reported. Renal damage occurs and is manifested by proteinuria, oliguria and viruria.

Laboratory diagnosis includes electron microscopy, indirect immunofluorescence, ELISA and immunoblot techniques. Antigen can be localised in tissues by im-munocytochemistry and immunofluorescence, and viral RNA by PCR.

Management and Treatment

Management is essentially supportive. Isolation in a Trexler tent, strict barrier nursing techniques with protective clothing by trained personnel, and careful disposal of patient material and of the deceased are absolutely essential. Laboratory procedures must be carried out in high security level 4 containment facilities.

Protective Measures and Prevention

Epidemiological information, surveillance and health education are important. The natural reservoir of infection remains unknown and vectors have not been identified.

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