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What causes Lyme disease (lyme borreliosis)?
Medical expert of the article
Last reviewed: 04.07.2025
Causes of Lyme Disease
Lyme disease is caused by a gram-negative spirochete of the Borrelia burgdorferi complex: nsu lato of the Spirochaetaceae family of the Borreliae genus. B. burgdorferi is the largest of the Borrelia: its length is 10-30 μm, its diameter is about 0.2-0.25 μm. It is capable of active movement with the help of flagella. The microbial cell consists of a protoplasmic cylinder, which is surrounded by a three-layer cell membrane containing heat-stable LPS with endotoxin properties. There are three groups of Borrelia antigens: surface (OspA, OspB, OspD, OspE and OspF), flagellar and cytoplasmic.
Borrelia are grown in a specially created liquid nutrient medium enriched with amino acids, vitamins, bovine and rabbit serum albumin and other substances (BSK medium).
More than ten genomic groups of Borrelia belonging to the Borrelia burgdorferi sensu lato complex have been isolated using molecular genetics methods. B. burgdorferi sensu stricto, B. garinii, and B. afzelii are pathogenic for humans. The division of the pathogen into genomic groups has clinical significance. Thus, B. burgdorferi sensu stricto is associated with predominant joint damage, B. garinii with the development of venous radiculitis, and B. afzelii with skin lesions.
Borrelia are unstable in the environment: they die when dried out; they survive well at low temperatures; at a temperature of 50 °C they die within 10 minutes; they die under the influence of ultraviolet radiation.
[ Pathogenesis of Lyme disease (Lyme borreliosis)
From the site of the bite, borrelia penetrate the skin with the tick's saliva, causing the development of migratory annular erythema. After the pathogen multiplies in the area of the entry gate, hematogenous and lymphogenous dissemination into the lymph nodes, internal organs, joints, and the central nervous system occurs. In this case, partial death of borrelia is observed with the release of endotoxin, which causes intoxication (malaise, headache, loss of appetite, fever).
B. burgdorferi stimulate the production of various inflammatory mediators (IL-1, IL-6, TNF-a) involved in the development of Lyme arthritis. Autoimmune reactions are assumed to be involved in the pathogenesis of neuroborreliosis. Of significant importance are the processes associated with the accumulation of specific immune complexes containing spirochete antigens in the synovial membrane of the joints, dermis, kidneys, and myocardium. The immune response in patients is relatively weak. In the early stages of the disease, IgM begins to be produced, the content of which reaches a maximum level in the 3rd-6th week of the disease. IgG are detected later; their concentration increases 1.5-3 months after the onset of the disease.
Epidemiology of Lyme disease
The geographic distribution of Lyme disease is similar to that of tick-borne encephalitis, which can lead to simultaneous infection with two pathogens and the development of mixed infection.
The reservoir of the pathogen is mouse-like rodents, wild and domestic animals: birds, spreading infected ticks during migratory flights. Borrelia is transmitted to humans through the bites of ixodid ticks: I. nanus, I. persukatus - in Europe and Asia; I. scapularis, I. pacificus - in North America.
Ticks can attack humans at all stages of their life cycle: larva → nymph → imago. The possibility of transovarial and transphase transmission of the pathogen in ticks has been established.
The spring-summer seasonality of the disease is due to the period of tick activity (May-September). The natural susceptibility of people is close to absolute. Cases of the disease are registered among all age groups. The adult working-age population gets sick more often.
Post-infection immunity is non-sterile; reinfection is possible.