Classification and Transmission Routes
Relapsing fevers are divided into two fundamentally different epidemiological groups:
- Epidemic (louse-borne) relapsing fever. This is a strict anthroponosis caused by Borrelia recurrentis (the pathogen was discovered by O. Obermeier in 1868). The source of infection is a febrile patient. The bacteria are transmitted by lice (primarily body lice, less commonly head and pubic lice), which become infectious 6 to 28 days after taking a blood meal. Transmission occurs via contamination: when scratching the skin, a person rubs in the hemolymph of a crushed insect. The disease is associated with periods of social disruption.
- Endemic (tick-borne) relapsing fever. A vector-borne zoonosis of subtropical and tropical regions, caused by more than 20 species of borreliae (e.g., B. duttoni, B. persica). Reservoirs include rodents and soft ticks of the family Argasidae (transovarial transmission to progeny is possible). Humans are infected directly through the bite of an Ornithodoros tick.
Pathogenesis and Mechanism of Relapses
Upon entering the body, borreliae are engulfed by cells of the mononuclear phagocyte system, where they actively multiply. This is followed by a massive release into the bloodstream, causing bacteremia. This triggers a sharp rise in temperature, chills, and headache.
In response to the infection, the immune system produces antibodies that bind and destroy the majority of the pathogens. Massive aggregates of bacteria and antibodies form in the bloodstream, upon which platelets deposit. These complexes occlude small capillaries, disrupting microcirculation in internal organs.
Why does the disease relapse? The borrelial genome contains dozens of genes encoding various surface antigens. Initially, most of these genes are in a "silent" state. During the disease, chromosomal rearrangements occur: one of the inactive genes becomes activated, generating a new antigenic variant of the microbe. Previous antibodies are ineffective against it, and the new population enters the bloodstream, triggering another fever spike.
Clinical Presentation and Immunity
The latent incubation period averages 7–8 days. The disease presents as a series of febrile attacks with temperatures reaching 39–40 °C. Due to the constant changes in the pathogen's antigenic structure, relapses can recur from 3 to 20 times.
The prognosis for the endemic variant is favorable. In epidemic relapsing fever, the case-fatality rate does not exceed 1%. Humoral immunity develops after the infection, but it is short-lived. However, indigenous populations in endemic regions often acquire resistance to locally circulating borrelia strains.
Laboratory Diagnostics and Treatment
The primary method for pathogen detection is microscopy. At the peak of the febrile attack, a blood sample is taken to prepare a thick blood smear, which is then stained using the Romanowsky-Giemsa method. To observe live borreliae, dark-field microscopy of a hanging drop, Burri's negative method (with India ink), and silver impregnation are used.
Of particular note is the biological assay, which allows precise differentiation of fever types in laboratory animals:
- Borrelia recurrentis is pathogenic to white mice and rats.
- Endemic relapsing fever agents are pathogenic to guinea pigs.
Complement fixation test (CFT) is used as an auxiliary serological method.
Prevention and Treatment: No specific vaccine is available. Treatment is etiotropic, utilizing antibiotics (tetracyclines, chloramphenicol, ampicillin). Non-specific prevention focuses on breaking transmission routes: vector control of lice for the epidemic form, and the eradication of ticks and rodents in natural foci.