Marburg fever

An acute viral disease characterized by a severe course, high mortality, hemorrhagic syndrome, damage to the liver, gastrointestinal tract and central nervous system.

Etiology, pathogenesis. The disease was first observed in 1967 in Marburg and Frankfurt am Main (Marburg fever), and later similar diseases were observed in Sudan, in the village of Maridi (Maridi fever) and in Zaire near the Ebola River (Ebola fever). The Marburg, Ebola, and Maridi viruses are similar in their morphology and properties; only slight antigenic differences have been established. The source of infection in Europe (Germany, Yugoslavia) was tissue from African green monkeys, and there were also secondary diseases.

Infection of people can occur through airborne droplets and contact. For medical workers, contact with the blood of patients is especially dangerous. Contact with the skin due to microtrauma leads to infection.

The mucous membranes (oral cavity, eyes) can also serve as a gateway to infection. Hematogenous dissemination of the virus is characteristic. Its reproduction can occur in various organs and tissues.

The virus is detected in blood and semen for a long time (up to 1-2 weeks). Morphological changes are noted in the liver, kidneys, spleen, myocardium, and lungs.

Symptoms, course. The incubation period is 2-16 days. Clinical symptoms, severity, and outcomes do not differ between diseases described as Marburg fever and Maridi fever. There is no prodromal period.

The disease begins acutely, with a rapid increase in body temperature to 39-40 ° C, severe intoxication (headache, weakness, muscle and joint pain). After a few days, hemorrhagic syndrome and damage to the gastrointestinal tract appear; Dehydration develops and consciousness is impaired.

In the initial period, patients complain of headache, stabbing pain in the chest, cough, dry throat. There is hyperemia of the mucous membrane of the pharynx, the tip and edges of the tongue are red; vesicles appear on the hard and soft palate and tongue, and when opened, surface erosions are formed; unlike Lassa fever, no pronounced necrosis is observed. The tone of the muscles, especially the muscles of the back, neck, and masticatory muscles, is increased, and their palpation is painful.

From the 3-4th day, cramping pain in the abdomen begins. The stool is loose, watery, and half of the patients have blood in the stool (sometimes in clots) or signs of gastrointestinal bleeding (melena). Diarrhea appears in almost all patients and lasts about a week, vomiting is less common (6-8%), lasting for 4-5 days.

In half of the patients, on the 4th-5th day of illness a rash appears, most often measles-like, which affects the torso and limbs, and there may be skin itching. At the end of the 1st week, sometimes at the 2nd week, signs of toxicosis reach their maximum severity. Symptoms of dehydration and infectious-toxic shock appear.

During this period, patients often die.

The diagnosis is based on epidemiological data (staying in areas with natural foci of Marburg fever, working with tissues of African marmosets) and characteristic clinical symptoms. Specific laboratory research methods can detect the virus or antibodies to it.

Treatment. Causal therapy has not been developed. Pathogenetic therapy is of primary importance.

A set of measures is being carried out aimed at combating dehydration and infectious-toxic shock. Oxygen inhalation is prescribed through the nasal passages. 70-90 mg of prednisolone, 10,000 units of heparin, 10% glucose solution, hemodez (up to 300 ml) are administered intravenously.

The disease occurs with leukopenia and a decrease in immunological reactivity, so it is necessary to administer human immunoglobulin 10-15 ml intramuscularly every 10 days in the acute period and 6 ml in the convalescence period.

The prognosis is always serious, mortality 25%, cm