Biology and cultural properties
Morphologically, the pathogens are thin spirochetes measuring $0.3–0.6 \times 2–20$ µm. They have three to ten large coils, and motility is ensured by a special fibrillar apparatus (with 15–20 fibrils). When stained with Romanowsky-Giemsa, the bacteria turn blue-purple, readily taking up aniline dyes.
The genetic apparatus is unique among bacteria: it is represented by a small linear chromosome and numerous circular and linear plasmids. Cultivating these microorganisms is difficult because they are fastidious regarding nutrient media. Cultivation requires complex compositions supplemented with serum, ascitic fluid, or tissue extracts. Optimal conditions include a temperature of 28–35 °C and an atmosphere enriched with carbon dioxide (5–10% $CO_2$). An alternative route is the inoculation of chicken embryos into the yolk sac.
The microorganisms are unstable in the environment. They die rapidly upon heating (a temperature of 45–48 °C kills them in 30 minutes) and drying. However, the bacteria tolerate low temperatures and freezing processes very well.
History of discovery and etiology of Lyme disease
The first clinical description of erythema migrans was made by Afzelius in 1909. Later, in 1975, an outbreak of specific arthritis occurred among children in the American town of Lyme, which attracted researchers' attention. The pathogen itself was isolated from a tick only in 1982 by the scientist W. Burgdorfer.
Depending on the geographical region, the disease is caused by various species of the Borrelia burgdorferi complex. The classical species B. burgdorferi predominates in North America, whereas B. garinii and B. afzelii play a leading role in Eurasia (including the territory of Russia). These species differ markedly in their antigenic structure.
Small mammals, primarily deer mice, serve as the natural reservoir of infection. Transmission is vector-borne, via the bites of ixodid ticks during the summer period. Susceptibility to the infection is high, but human-to-human transmission is impossible (an infected patient is epidemiologically safe).
Antigenic structure and pathogenicity factors
The antigenic system is complex and variable. It includes:
- Internal antigens: These are fibrillar proteins (p41, flagellin) and cytoplasmic cylinder proteins (p93). Antibodies against them are synthesized at early stages, but they are unable to protect the body from developing the infection.
- Surface antigens (Osp): Lipid-modified outer membrane proteins (types A, B, C, D, E, F). They are encoded by plasmids and provide protection for the pathogen.
A unique feature is antigenic phase variation. The OspC protein is expressed in the tick body and during early stages of human infection. The OspA protein (which has 7 serovars) dominates in the late stages of the disease, as well as during in vitro cultivation.
Pathogenesis is associated with the penetration of the bacterium into host cells via lipid-modified proteins. Next, the pathogen interacts with macrophages, which release interleukin-1, triggering systemic inflammation. Arthritis occurs due to autoimmune processes: at body temperature (37 °C), the bacterium begins to synthesize a heat shock protein that is structurally identical to human protein (molecular mimicry phenomenon).
Clinical presentation and diagnostic principles
The disease runs a chronic course with three sequential phases. After an incubation period (3–32 days), a red papule appears at the bite site.
- Local stage: Characterized by migrating annular erythema, rapid growth of the red spot, lymphadenopathy, and a flu-like syndrome.
- Organ stage (dissemination): Develops at weeks 4–5. The pathogen is carried by the bloodstream to target organs. Benign disorders of the heart (myocarditis) and central nervous system (aseptic meningitis) appear.
- Late stage: Occurs 6 weeks or more later. The main manifestation is involvement of large joints (arthritis).
Isolating the culture from the patient's blood or cerebrospinal fluid is extremely difficult. Therefore, diagnostics follow an algorithm. At the first stage, biopsy specimens from the erythema zone are examined by microscopy. From the second stage onwards, serological methods (ELISA, IFA) are used to detect IgM or rising IgG titers. PCR is used for cerebrospinal fluid and synovial fluid.
Treatment is etiotropic, employing tetracycline antibiotics. There is no specific vaccine; prevention comes down to wearing protective clothing and acaricidal treatments.
Briefly: answers to topical questions
Which groups of antibiotics, in addition to tetracyclines, are used for the etiotropic therapy of Lyme disease?
For the etiotropic therapy of Lyme disease, in addition to tetracyclines, the following groups of antibacterial drugs are used:
- Penicillins — benzylpenicillin.
- Semi-synthetic penicillins — amoxicillin, ampicillin, amoxicillin/clavulanic acid.
- Second- and third-generation cephalosporins — cefuroxime, ceftriaxone, cefotaxime.
- Macrolides — azithromycin, roxithromycin, clarithromycin, erythromycin.
What specific neurological syndromes (e.g., Bannwarth syndrome) develop during the dissemination stage of Lyme disease?
During the dissemination stage of Lyme disease, involvement of the central and peripheral nervous system is possible. Specific neurological manifestations include:
- Bannwarth syndrome — a triad including serous meningitis, facial nerve palsy, and radiculoneuritis.
- Bell's palsy — sudden weakness or paralysis of the muscles on one side of the face due to facial nerve involvement.
- Polyradiculoneuritis, serous or lymphocytic meningitis, cranial neuritis, and peripheral nerve monoparesis.
Which specific species of Borrelia causes louse-borne relapsing fever?
Louse-borne relapsing fever is caused by a specific species of pathogenic spirochetes — Borrelia recurrentis (also known as Obermeier's spirochetes). This microorganism belongs to the genus Borrelia, which morphologically differs from Treponema by the presence of 3–8 large coils. The specific vector of this pathogen is the body louse (Pediculus humanus humanus).
To remember antigenic phase variation: OspC works First (in the tick body and at the onset of the disease), and OspA comes in Later (in humans during later stages).
Class and exam questions
Why are joints affected upon infection?
This is due to autoimmune reactions. At 37 °C, the bacterium produces a heat shock protein identical to a human one, causing the immune system to attack its own tissues (molecular mimicry).
Do early antibodies protect against the progression of the infection?
No. Antibodies to internal antigens (e.g., p41/flagellin) appear early, but they lack protective activity.
Can you catch Lyme disease from an infected person?
The infection is not transmitted from person to person. Transmission occurs exclusively via a vector-borne route — through the bite of an ixodid tick.
What else to study on this topic
- Characteristics of the pathogen of louse-borne relapsing fever
- Specifics of the antigenic structure of B. garinii and B. afzelii
- Mechanisms of hematogenous dissemination of spirochetes
- Interpretation of false-positive reactions in serological diagnostics (ELISA, IFA)
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