What causes relapsing louse typhus?

Cause of relapsing fever

Relapsing louse typhus is caused by the spirochete Borrelia recurrentis Obermeieri of the Spirochaetaceae family , genus Borrelia, which is shaped like a thread-like spiral with 6-8 turns; has active mobility; is anaerobic. It reproduces by transverse division. It stains well with aniline dyes, is gram-negative. It grows on special nutrient media.

The number of protein antigens of Borrelia reaches several dozen, their synthesis is encoded by different genes, some of which are periodically in an inactive "silent" form. During the disease, due to rearrangements in the chromosome, the "silent" gene is activated and a generation of Borrelia with a new antigen composition appears.

Obermeyer's spirochete contains endotoxins. Pathogenic for monkeys, white mice and rats; nonpathogenic for guinea pigs.

In the environment, B. recurrentis is unstable and quickly dies when dried and heated to 50 °C. It is sensitive to benzylpenicillin, tetracyclines, chloramphenicol, and erythromycin.

Pathogenesis of relapsing fever

Borrelia that penetrate the skin into the human body 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 blood - borrelia develops, clinically manifested by chills, fever, etc. After a few days, antibodies are produced that inactivate borrelia. Microbes are not detected in the peripheral blood, the fever stops. As a result of the death of spirochetes, endotoxin is released, which acts on the cells of the vascular endothelium. liver, spleen, causing a violation of thermoregulation and microcirculation. The accumulation of borrelia in small vessels leads to the development of thrombosis, hemorrhage, DIC syndrome. Borrelia and toxinemia manifest with the first febrile attack, after which some spirochetes remain in the central nervous system, bone marrow and spleen. They multiply and after a few days after the temperature has returned to normal, they enter the bloodstream again, causing a second febrile attack. The new generation of Borrelia differs from the previous one in the structure of its antigens, so the pathogen is resistant to the antibodies formed during the first attack, but is destroyed by phagocytes and antibodies produced during the second attack. This process is repeated until the patient has antibodies to all generations of Borrelia.

Pathological and anatomical changes in those who died from louse-borne relapsing fever are found primarily in the spleen, liver, brain, and kidneys. The spleen can be enlarged 5-8 times, its capsule is tense and easily ruptured; hemorrhages, infarctions, and foci of necrosis are found in the parenchyma, and thromboses and a large number of borrelia are found in the vessels. Foci of necrosis are found in the liver. Vascular dilation, hemorrhages, and perivascular infiltrates are found in the brain.

Epidemiology of relapsing fever

The source of infection is a sick person. The probability of infection increases during fever attacks. Borrelia is carried by lice (mainly clothes lice, less often head lice), which can transmit the infection 6-28 days after feeding on the blood of a sick person. Spirochetes multiply and accumulate in the hemolymph of the louse. Human infection occurs when the hemolymph of a crushed louse gets on damaged skin (scratches, contact with clothing).

Human susceptibility to this infection is absolute.

Immunity after louse-borne relapsing fever is unstable, and repeated illnesses are possible.

In the past, louse-borne relapsing fever was widespread in many countries of the world, the incidence sharply increased during wars, famines and other socio-economic disasters. During the First and Second World Wars, epidemics were observed everywhere. In Ukraine, louse-borne relapsing fever was completely eliminated in the middle of the last century, but the possibility of this disease being imported to our country from endemic regions cannot be ruled out: some countries in Asia, Africa, Central and South America. Seasonality is characteristic with an increase in the incidence in the winter-spring period.

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