Ebola Fever

Overview

bola fever is a particularly dangerous viral infection caused by the Ebola virus and proceeding with severe hemorrhagic syndrome and manifested by severe headaches and muscle pain, diarrhea and a rash.

Outbreaks of Ebola hemorrhagic fever were first reported in 1976 in rural areas of Sudan (284 cases, 151 of which ended in death) and northern Zaire (318 cases, of which 280 were fatal). In Zaire, diseases were also noted in 1977. In 1979, 34 severe cases of fever were detected in Sudan, 22 patients died. Antibodies to the Ebola hemorrhagic fever virus were found in residents of Cameroon, the Central African Republic, Nigeria, Sierra Leone, Guinea and Senegal, which indicates the possible presence of natural foci of infection in these areas.

Etiology:
The causative agent, the Ebola virus, was isolated in 1976 from the blood of a deceased patient. The virus is pathogenic for newborn white mice and guinea pigs. In transplanted green monkey kidney cells, it actively multiplies, but does not cause clear cytopathic changes. Ebola virus virions are shaped like crimped filaments; their diameter is 80-100 nm, the length varies, reaching 4000 nm. The virion nucleocapsid consists of an axial filament 20–30 nm in diameter surrounded by a capsid helix 40–50 nm in diameter. These formations are enclosed in an outer shell. RNA was found in the virion.

Epidemiology:
The source of the infectious agent is a sick person. The reservoirs of the Ebola virus in nature, despite intensive research, are still unknown. Infection of people with Ebola hemorrhagic fever occurs through contact with the blood of patients, as well as with their feces, urine, vomit, discharge of the nasopharynx containing blood. The most likely transmission of the virus with the blood of patients when it enters the damaged skin or mucous membranes of healthy people. Especially high is the risk of infection of health workers, as well as those caring for patients at home. During outbreaks of Ebola hemorrhagic fever, cases of infection of people with the introduction of medicines with insufficiently sterilized syringes and needles were noted. All observed cases of Ebola hemorrhagic fever occurred in June-November.

Pathogenesis and pathological anatomy:
When it enters the human body, the virus enters the parenchymal organs with the blood stream, where it multiplies, and then again passes into the blood. The development of hemorrhages is promoted by thrombocytopenia and a decrease in the content of factors in the blood that cause its coagulation (see Blood coagulation system ).

In those who died from Ebola hemorrhagic fever, widespread dystrophic and focal necrotic changes in the liver, necrotic changes in the red pulp of the spleen, and proliferation of reticuloendothelial cells are found. Necrotic changes are also observed in the pancreas, adrenal glands, pituitary gland, thyroid gland, testicles and ovaries. Multiple hemorrhages are found in the brain, changes in glial elements are noted, both proliferative (the appearance of glial nodules and rosettes) and degenerative (pyknosis and rhexis nuclei) in nature. A distinctive feature of the pathological process is thrombosis of small vessels and the development of hemorrhages.

Immunity in Ebola hemorrhagic fever is not well understood.
Clinical picture:
The incubation period is from 4 to 16 (usually 7) days. The onset of the disease is acute, there is a rapid rise in temperature to 38-39 °, malaise, severe headaches in the frontal and temporal regions, nausea, and vomiting. At the same time, severe chest pains, dry cough, pains in various muscles and joints develop, especially pronounced in the muscles of the lumbar region. Sometimes there is pain in the eyeballs when pressing on them. 

After 2-3 days, most patients develop diarrhea, often very severe, lasting about a week; stools are watery with an admixture of blood. Diarrhea and vomiting lead to dehydration(cm.)

On the 4-6th day of illness, a maculopapular rash appears, first on the face, then spreading to the trunk and becoming more pronounced on the shoulders and hips. After 4-5 days, peeling begins at the sites of the rash. The mucous membrane of the oral cavity is usually dry, often covered with small ulcers, similar to aphthous (see Aphthae). Dryness in the throat causes severe pain, especially when swallowing. Hemorrhagic phenomena develop - blood in the stool, hematemesis, bleeding from the nose, vagina, skin and subconjunctival hemorrhages. 

With pronounced signs of intoxication and hemorrhagic phenomena, death may occur (more often on the 7-8th day of illness). The acute period of the disease lasts 14-16 days. Recovery of patients is usually slow, the condition improves gradually over several weeks, but exhaustion and weakness persist for a long time. In pregnant women, the disease is often complicated by abortion; men develop orchitis in some cases.



Prevention

Edetection and hospitalization of the sick; observation for 17 days of persons who were in contact with the patient. As a means of specific prevention of Ebola hemorrhagic fever in some cases (an emergency during laboratory work with the virus, accidental injections or cuts during autopsy), immune plasma or blood serum of convalescents is used, which is administered intravenously (250-500 ml).



Treatment

Identified patients (or persons suspected of having a disease) are isolated and hospitalized in a separate ward. If possible, patients are placed in individual isolation cabins with autonomous ventilation and sterilization of the removed air.

As a means of specific therapy for Ebola hemorrhagic fever, immune plasma or blood serum of recovered patients containing specific antibodies is used. They are administered intravenously at a dose of 250-500 ml; if the patient's condition does not improve, immune plasma or blood serum is re-introduced. Prescribe means that help normalize the water-salt balance, eliminate intoxication (see Detoxification therapy ) and hemorrhagic phenomena (water-electrolyte, protein solutions, glucose solution, etc.).


The prognosis is always serious, mortality exceeds 50%.



Tests Required for Diagnosis

Diagnosis is made on the basis of epidemiological history (contact with patients with Ebola hemorrhagic fever), clinical picture, and laboratory results. In the blood, leukopenia and thrombocytopenia are detected; ROE is slow. The diagnosis is confirmed by the detection of a virus in the blood of patients in laboratory tests or by the detection of specific serum antibodies. In the early days of the disease, viral particles in the blood can be detected using electron microscopy (see), and the viral antigen can be detected using an indirect immunofluorescence reaction.(cm.).

 In order to isolate the virus, blood cultures are carried out on a vero cell culture (see Cell and tissue cultures, table). By comparing matched blood serum samples collected at the beginning of the disease and throughout the convalescence phase, an immunofluorescence reaction is used to determine the emergence of particular antibodies in the patient's blood during the course of the disease. In certain cases, antibodies to the hemorrhagic fever-causing Ebola virus can already be found on the fifth or sixth day of sickness.

Ebolas of hemorrhagic fever are differentiated from Lassa fever (see) and cercopithemic hemorrhagic fever (see). Unlike Ebola hemorrhagic fever, Lassa fever develops gradually, accompanied by severe pharyngitis and severe conjunctivitis with periorbital edema; diarrhea in Lassa fever is less pronounced than in Ebola hemorrhagic fever. Ebola hemorrhagic fever is differentiated from cercopithecine hemorrhagic fever based on the results of virological and serological studies.



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