What causes recurrent typhoid fever?
Last reviewed: 23.04.2024
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The cause of recurrent typhoid fever
Recurrent lice typhus is caused by the spirochete Borrelia recurrentis Obermeieri family Spirochaetaceae, genus Borrelia, in shape resembling a threadlike spiral with 6-8 curls; has active mobility; anaerobe. Propagated by transverse division. It is well colored with aniline dyes, gram-negative. It grows on special nutrient media.
The amount of Borrelia protein antigens reaches several tens, their synthesis is encoded by different genes, some of which are periodically inactive in a "silent" form. During the disease, as a result of rearrangements in the chromosome, the "silent" gene is activated and generates borrelia with a new antigenic composition.
Spirochete Obermeier contains endotoxins. Pathogenic for monkeys, white mice and rats; not pathogenic for guinea pigs.
In the environment , the recurrentis is not very stable, it quickly perishes when it is dried and heated to 50 ° C. It is sensitive to benzylpenicillin, tetracyclines, chloramphenicol, erythromycin.
Pathogenesis of recurrent typhoid fever
Penetrating through the skin into the human body, Borrelia are captured by the cells of the histiophagocytic system and multiply in them - this phase corresponds to the incubation period. Then the pathogen enters the bloodstream - borreliaemia develops, clinically manifested by chills, fever, etc. After a few days, antibodies that inactivate Borrelia are produced. In peripheral blood, microbes are not detected, fever is stopped. Due to the death of spirochetes, endotoxin is released, acting on the endothelial cells of the vessels. Liver, spleen, causing a violation of thermoregulation and microcirculation. The accumulation of Borrelia in small vessels leads to the development of thromboses, hemorrhages, and DIC syndrome. Borrelemia and toxinemia are manifested with the first febrile attack, after which a part of the spirochaete remains in the central nervous system, bone marrow and spleen. They multiply, and a few days after the normalization of the temperature, they again enter the blood, causing a second febrile attack. The new generation of Borrelia in the structure of antigens differs from the previous one, so the causative agent is resistant to the antibodies formed during the first attack, but is destroyed by the action of phagocytes and antibodies produced during the second attack. This process is repeated until the patient has antibodies to all Borrelia generations.
Pathological and anatomical changes in those who died of vesicular recurrent typhus are found primarily in the spleen, liver, brain, kidneys. The spleen can be enlarged 5-8 times, the capsule is strained, easily torn; in the parenchyma, hemorrhages, infarcts, foci of necrosis, in the blood vessels - thromboses, a large number of borrelia. In the liver, foci of necrosis are found. In the brain, vasodilation, hemorrhage, perivascular infiltrates are revealed.
Epidemiology of recurrent typhoid fever
The source of the infection is a sick person. The likelihood of infection increases during the time of fever. The bearer of Borrelia is a louse (mostly a dressing, less often a head louse), which can transmit the infection 6 to 28 days after it is saturated with the blood of a sick person. Spirochetes multiply and accumulate in the hemolymph of lice. Infection of a person occurs when the hemolymph of a crushed louse hits the damaged skin (combs, singing by clothes).
People's susceptibility to this infection is absolute.
Immunity after the transferred vshinogo recurrent typhoid is unstable, repeated diseases are possible.
In the past, typhus recurrent typhus was widespread in many countries of the world, the incidence sharply increased during wars, famine and other socio-economic disasters. In the years of the First and Second World Wars epidemics were noted everywhere. In Ukraine, typhoid return typhus was completely eliminated in the middle of the last century, but it is impossible to exclude the possibility of importing this disease into our country from endemic regions: some countries of Asia, Africa, Central and South America. Typical seasonality with an increase in morbidity in the winter-spring period.
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