What causes Lyme disease (lime-borreliosis)?

Causes of Lyme Disease

The cause of Lyme disease is the gram-negative spirochete of the Borrelia burgdorferi complex: nsu lato of the family Spirochaetaceae of the genus Borreliae. B. Burgdorferi is the largest of Borrelia: its length is 10-30 microns, its diameter is about 0.2-0.25 microns. It is capable of actively moving with the help of flagella. The microbial cell consists of a protoplasmic cylinder surrounded by a three-layered cell membrane containing a thermostable LPS with endotoxin properties. There are three groups of Borrelia antigens: surface (OspA, OspB, OspD, OspE and OspF), flagellate and cytoplasmic.

Borrelia are grown on a specially created liquid nutrient medium enriched with amino acids, vitamins, bovine and rabbit serum albumin and other substances (BSK medium).

Based on the methods of molecular genetics, more than ten genomic groups of borrelia, belonging to the complex Borrelia burgdorferi sensu lato, have been isolated. For human pathogens B. Burgdorferi sensu stricto, V. Garinii and V. Afzelii. Separation of the causative agent into genomic groups is of clinical importance. So, V. Burgdorferi sensu stricto is associated with the primary lesion of the joints, V. Garinii - with the development of ueningoradiculitis, V. Afzelii - with skin lesions.

Borrelia are poorly resistant in the environment: they perish when dry; well retained at low temperatures; at a temperature of 50 ° C perished for 10 minutes; die under the influence of ultraviolet irradiation.

[1], [2], [3], [4], [5],

Pathogenesis of Lyme disease (lime-borreliosis)

From the bite site with the tick saliva, borrelia penetrate the skin, causing the development of migratory annular erythema. After the propagation of the pathogen in the entrance gate area, hematogenous and lymphogenous dissemination occurs in the lymph nodes, internal organs, joints, CNS. In this case, partial death of Borrelia with the release of endotoxin, causing the phenomenon of intoxication (malaise, headache, lack of appetite, fever) is observed.

B. Burgdorferi stimulate the production of various mediators of inflammation (IL-1, IL-6, TNF-a) involved in the development of lime arthritis. The pathogenesis of neuroborreliosis involves the involvement of autoimmune reactions. Essential are the processes associated with the accumulation of specific immune complexes containing spirochete antigens in the synovial membrane of the joints, dermis, kidneys, myocardium. The immune response in patients is relatively mild. In the early stages of the disease, IgM begins to be produced, the content of which reaches a maximum level at the 3rd-6th week of the disease. IgG are detected later; their concentration increases after 1.5-3 months after the onset of the disease.

Epidemiology of Lyme disease

The geographical distribution of Lyme disease is similar to that of tick-borne encephalitis, which can lead to simultaneous infection of two pathogens and the development of mixed infection.

The reservoir of the causative agent is mice, rodents, wild and domestic animals: birds that spread infected ticks during migratory flights. The transfer of borrelia to humans is carried out through the bites of ixodids: I. Nanus, I. Persukatus - in Europe and Asia; I. Scapularis, I. Pacificus - in North America.

Ticks can attack a person in all stages of the life cycle: larva → nymph → imago. The possibility of transovarial and transphasic transmission of the pathogen in ticks is established.

Spring-summer seasonality of the disease is due to a period of activity of ticks (May-September). The natural susceptibility of people is close to absolute. Cases of the disease are recorded among all age groups. The adult able-bodied population is more often ill.

Post-infectious immunity is non-sterile; possibly re-infection.

[6], [7], [8], [9], [10]