Ebola Virus 4 Essay, Research Paper
EBOLA VIRUS
Ebola virus, a member of the Filoviridae, burst from obscurity with spectacular outbreaks of severe, haemorrhagic fever. It was first associated with an outbreak of 318 cases and a case-fatality rate of 90% in Zaire and caused 150 deaths among 250 cases in Sudan. Smaller outbreaks continue to appear periodically, particularly in East, Central and southern Africa. In 1989, a haemorrhagic disease was recognized among cynomolgus macaques imported into the United States from the Philippines. Strains of Ebola virus were isolated from these monkeys. Serologic studies in the Philippines and elsewhere in Southeast Asia indicated that Ebola virus is a prevalent cause of infection among macaques (Manson 1989).
These threadlike polymorphic viruses are highly variable in length apparently owing to concatemerization. However, the average length of an infectious virion appears to be 920 nm. The virions are 80 nm in diameter with a helical nucleocapsid, a membrane made of 10 nm projections, and host cell membrane. They contain a unique single-stranded molecule of noninfectious (negative sense ) RNA. The virus is composed of 7 polypeptides, a nucleoprotein, a glycoprotein, a polymerase and 4 other undesignated proteins. Proteins are produced from polyadenylated monocistronic mRNA species transcribed from virus RNA. The replication in and destruction of the host cell is rapid and produces a large number of viruses budding from the cell membrane.
Epidemics have resulted from person to person transmission, nosocomial spread or laboratory infections. The mode of primary infection and the natural ecology of these viruses are unknown. Association with bats has been implicated directly in at least 2 episodes when individuals entered the same bat-filled cave in Eastern Kenya. Ebola infections in Sudan in 1976 and 1979 occurred in workers of a cotton factory containing thousands of bats in the roof. However, in all instances, study of antibody in bats failed to detect evidence of infection, and no virus was isolated form bat tissue.
The index case in 1976 was never identified, but this large outbreak resulted in 280 deaths of 318 infections. The outbreak was primarily the result of person to person spread and transmission by contaminated needles in outpatient and inpatient departments of a hospital and subsequent person to person spread in surrounding villages. In serosurveys in Zaire, antibody prevalence to Ebola virus has been 3 to 7%. The incubation period for needle- transmitted Ebola virus is 5 to 7 days and that for person to person transmitted disease is 6 to 12 days.
The virus spreads through the blood and is replicated in many organs. The histopathologic change is focal necrosis in these organs, including the liver, lymphatic organs, kidneys, ovaries and testes. The central lesions appear to be those affecting the vascular endothelium and the platelets. The resulting manifestations are bleeding, especially in the mucosa, abdomen, pericardium and vagina. Capillary leakage appears to lead to loss of intravascular volume, bleeding, shock and the acute respiratory disorder seen in fatal cases. Patients die of intractable shock. Those with severe illness often have sustained high fevers and are delirious, combative and difficult to control.
EBOLA SEROLOGY
The serologic method used in the discovery of Ebola was the direct immunofluorescent assay. The test is performed on a monolayer of infected and uninfected cells fixed on a microscopic slide. IgG- or IgM-specific immunoglobulin assays are performed. These tests may then be confirmed by using western blot or radioimmunoprecipitation. Virus isolation is also a highly useful diagnostic method, and is performed on suitably preserved serum, blood or tissue specimens stored at -70oC or freshly collected.
TREATMENT OF EBOLA
No specific antiviral therapy presently exists against Ebola virus, nor does interferon have any effect. Past recommendations for isolation of the patient in a plastic isolator have given way to the more moderate recommendation of strict barrier isolation with body fluid precautions. This presents no excess risk to the hospital personnel and allows substantially better patient care, as shown in Table 2. The major factor in nosocomial transmission is the combination of the unawareness of the possibility of the disease by a worker who is also inattentive to the requirements of effective barrier nursing. after diagnosis, the risk of nosocomial transmission is small.
PREVENTION AND CONTROL OF EBOLA
The basic method of prevention and control is the interruption of person to person spread of the virus. However, in rural areas, this may be difficult because families are often reluctant to admit members to the hospital because of limited resources and the culturally unacceptable separation of sick or dying patients from the care of their family. Experience with human disease and primate infection suggests that a vaccine inducing a strong cell- mediated response will be necessary for virus clearance and adequate protection. Neutralizing antibodies are not observed in convalescent patients nor do they occur in primates inoculated with killed vaccine. A vaccine expressing the glycoprotein in vaccinia is being prepared for laboratory evaluation.
SELECTIVE PRESSURES AND CONSTRAINTS
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