Pathogenesis and stages
The development of Lyme disease is staged. Pathogenetically, three stages are distinguished, reflecting the spread of the infection in the body:
- Early localized period: Lasts 2–3 weeks. The infection is limited to the tick bite site, where a primary affect develops — erythema migrans, followed by scar formation.
- Early disseminated period: Lasts 4–6 weeks. Caused by the entry of borreliae into the bloodstream (spirochetemia) and their circulation. Manifests as the formation of multiple secondary erythemas.
- Late disseminated period: Occurs 1–1.5 months later (after 6 weeks). Characterized by generalization of the infection with the formation of chronic organ lesions.
Interesting fact: The staging of the pathological process in tick-borne borreliosis shares pathogenetic and clinical similarities with syphilis.
Clinical presentation
Symptoms depend on the stage of the disease.
In the first stage (early localized period), the main manifestation is the evolution of the primary affect. A spot appears at the site of tick insertion, which grows centrifugally. Its center gradually pales or turns bluish, forming a characteristic ring — erythema migrans. A crust forms right in the center, followed by a scar. In rare cases, vesicles or phlegmon may occur. The local reaction is accompanied by intoxication: cephalgia, myalgia, and arthralgia. Without etiotropic treatment, the primary erythema regresses within 2–3 weeks.
In the second stage (early disseminated period), multiple annular erythemas appear on various parts of the body, which are always smaller than the primary plaque. Neurological and ophthalmological symptoms may also develop: serous meningitis, cranial nerve neuropathy (especially n. facialis), conjunctivitis.
In the third stage (late dissemination stage), multisystem involvement occurs:
- Musculoskeletal system: Lyme arthritis.
- Cardiovascular system: Lyme carditis.
- Nervous system: lesions of the central and peripheral nervous system.
Diagnostics and treatment
The diagnosis is established comprehensively: epidemiological history is taken into account (visiting endemic areas, fact of tick attachment, for example, in the Tver Oblast), clinical presentation, and laboratory data.
Laboratory diagnostics: The gold standard is enzyme-linked immunosorbent assay (ELISA). A reliable criterion is the detection of IgM antibodies to at least two pathogen polypeptides.
Treatment:
- Etiotropic therapy: Drugs of choice are amoxicillin or doxycycline (the latter is reserved for children over 8 years of age). In case of penicillin allergy, cephalosporins are used.
- Symptomatic therapy: Prescribed individually.
The first stage of therapy must be carried out in a hospital setting, which reduces the risk of chronicity and late complications.
Prevention and follow-up
Convalescents are under medical observation for 2 years with scheduled examinations at 3, 6, 12, and 24 months.
Non-specific prevention: Use of repellents and protective clothing (similar to the prevention of tick-borne encephalitis, with which coinfections are possible).
Emergency prophylaxis (post-exposure): Preventive antibiotic therapy. For adults and children over 8 years old — doxycycline (0.1 g twice daily), for children under 8 years old — amoxicillin.
Class and exam questions
What is the main difference between secondary erythemas and the primary one?
Secondary disseminated elements of the annular rash occurring in the second period are always smaller in size compared to the primary mother erythema.
With which infection is coinfection possible in Lyme disease?
Since ixodid ticks are the vector, coinfection with tick-borne encephalitis is possible.
Which antibiotic is contraindicated in children under 8 years of age for borreliosis?
Doxycycline. For children under 8 years of age, the drug of choice is amoxicillin.
What else to study on this topic
- Features of the pathogenesis of spirochetemia in Lyme disease
- Similarities in the course of tick-borne borreliosis and syphilis
- Clinical presentation of Lyme arthritis and Lyme carditis
- Facial nerve palsy in borreliosis
- Serous meningitis of borrelial etiology
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