Causes and Diagnosis of Lyme Disease

What is Lyme Disease?

Lyme borreliosis (synonyms: Lyme disease, Lyme borreliosis, ixodic tick-borne borreliosis.) Currently, Lyme disease is considered as a natural focal, infectious, polysystemic disease with a complex pathogenesis involving a complex of immune-mediated reactions.

Various clinical manifestations of Lyme disease have long been known and described as independent diseases or as syndromes of unclear etiology: chronic migrating erythema, Erythema Afcelius, tick-borne erythema, acrodermatitis, chronic atrophic acrodermatitis, lymphodenosis of the skin, serous meningitis, radiculoneuroses, and lymphocytes, cytodermatitis, lymphodenosis of the skin, serous meningitis, lymphocytosis, lymphocytes, cytodermatitis, chronic lymphodenosis of the skin, serous meningitis, lymphocytosis, lymphocytes, systroma ), chronic arthritis, etc. In 1981, the spirochetotic etiology of these manifestations was established, after which it was already possible to speak about diseased and how nosological form with different clinical manifestations.

Lyme disease was first described in 1975 as a local outbreak of arthritis in Lyme, Connecticut (USA); develops after a bite of ixodic ticks infected with borrelia. In subsequent years, as a result of research, it turned out that the geographical spectrum of the spread of this infection is much wider. The disease is found not only in North America, but also in many countries in Europe and Asia. Tick-borne Lyme borreliosis is also widespread in Russia. BL in our country was first serologically verified in 1985, in 1991 included in the official list of nosological forms available in Russia. Much work on the study of this infection and the dissemination of accumulated experience was carried out under the direction of EI Korenberg at the Republican Center for the Study of Borreliosis (Research Institute of Microbiology named after NF Gamalei of the Russian Academy of Medical Sciences).

Causes of Lyme Disease

The family Spirochaetaceae, a genus of Borrelia, includes a significant number of pathogens of humans and animals. In 1984, R. Johnson described a new species of borrelia – Borrelia bitrgdorferi, which got its name in honor of the American microbiologist W. Burgdorfer, who first isolated Borrelia from ixodic ticks in 1981. The connection of an outbreak of arthritis in the town of Lyme with isolated borrelia has been proven.

The spirochete Borrelia burgdorferi resembles in its form a corkscrew-twisted spiral consisting of an axial filament around which the cytoplasm is located, its length is from 11 to 25 μm and its width is 0.18-0.25 μm; sizes vary in different hosts and under cultivation. Curls are uneven, with vital observation they make slow rotational movements. Both right-handed and levogyrate forms were found (the pathogenetic significance is unknown so far). In terms of morphology, these spirochetes are more similar to treponemas, but larger than them. They have groups of surface antigens Osp A, Osp B and Osp C, which determine the difference between individual strains. Belong to gram-negative bacteria. Aniline dyes are stained more intensely than treponema, and slightly weaker than other borrelia. Like other Borrelia, they are cultivated in Kelly’s modified medium (BSK-K5 selective medium).

Until very recently, it was believed that the only causative agent of Lyme disease is Borrelia burgdoiferi. However, some differences in the protein composition of isolates of Borrelia from different natural foci allowed initially to suggest that Lyme borreliosis is etiologically heterogeneous.

Currently, more than 10 genomic groups belonging to the Borrelia burgdorferi sensu lato complex, are unevenly distributed around the globe. The groups B. burgdorferi sensu stricto, V. garinii, V. garinii (type NT29), B. afielii, B. valaisiana (group VS116), V. lusitaniae (group PotiB2), B. japonica, B. tanukii and B. turdae, and in America – Borrelia burgdorferi s. s., B. andersonii (group DN127), 21038, CA55 and 25015. As regards the B-japonica found in Japan, it seems to be non-pathogenic for humans. It should be noted that today the pathogenic potential of the group VS116 (V. valaisiana) is also unknown. The results of studies and clinical observations in recent years suggest that the nature of organ lesions in a patient may depend on the type of borrelia. Thus, data on the existence of an association between V. garinii and neurological manifestations, B. burgdorferi s. s. and Lyme arthritis, V. afielii and chronic atrophic dermatitis. Consequently, the observed differences in the clinical picture of the course of Lyme disease in patients at different points of the nosoareal of this infection may be based on the genetic heterogeneity of the B. complex. Burgdorferi sensu lato. Considering all these facts, at present, the term “Lyme disease” is commonly meant to mean a whole group of etiologically independent ixodic tick-borne borreliosis.

Pathogenesis during Lyme Disease

At the stage of accumulation of knowledge about borreliosis, given the generality of epidemiology, the similarity of pathogenesis and clinical manifestations, it is quite acceptable to unite them under the common name “Ixodic tick-borne borreliosis” or “Lyme disease”, paying tribute to the first described tick-borne ixodic borreliosis.

Natural foci of Lyme disease are confined mainly to the glued landscapes of the temperate climate zone. In the USA, the main carriers are pasture mites fxodes scapularis (the old species name /. Dammini), and are of less importance. pacificus, in the Eurasian part of its nozareareal, are two common ixodid ticks: taiga (/. persulcatus) and forest (/. ricinus). In Russia, the taiga tick is of paramount epidemiological and epizootological importance; as a carrier, more effective than /. ricinus. Tick ​​larvae more often parasitize on small rodents, nymphs and mature individuals – on many vertebrates, mainly forest animals. A certain epidemiological role belongs to dogs. The natural infection of ticks with borrelia in endemic foci reaches 60%. The possibility of symbiosis of several species of borrelia in one tick has been proved. The simultaneous infection of ixodic ticks with tick-borne encephalitis and Lyme disease causative agents determines the existence of conjugate natural foci of these two infections, which creates prerequisites for the simultaneous infection of people and the development of mixed infection. Human infection occurs in a transmissible manner. The pathogen is inoculated when a tick bites with its saliva. It is not excluded, but a different route of infection, for example, alimentary (like tick-borne encephalitis) has not been definitively proven. Transplacental transfer of borrelia during pregnancy from the mother to the fetus is possible, which can be explained by a rather high percentage of patients of preschool and primary school age. Human susceptibility to borrelia is very high, and possibly absolute. No infection is transmitted from a patient to a healthy person. For primary infections, spring-summer seasonality is characteristic, due to the period of activity of ticks (from April to October). Infection occurs during a visit to the forest, in a number of cities – in forest parks within the city limits. In terms of incidence, this infection is in our country one of the first places among all natural focal zoonoses.

When infected, a complex of inflammatory-allergic skin changes usually develops at the site of tick infestation, manifested as a specific erythema characteristic of Lyme disease. The local persistence of the pathogen for a certain period of time determines the characteristics of the clinical picture — relatively satisfactory state of health, mild general intoxication syndrome, the absence of other manifestations characteristic of Lyme disease, the lateness of the immune response.

With the progression of the disease (or in patients without a local phase immediately) in the pathogenesis of the symptom complexes, the hematogenous, possibly lymphogenous pathway of borrelia from the site of introduction to the internal organs, joints, lymphatic formations matters; perineural, and subsequently rostral, with involvement of the meninges in the inflammatory process. When the pathogen enters the various organs and tissues, an active irritation of the immune system occurs, which leads to a generalized and local humoral and cellular hyperimmune response. At this stage of the disease, the production of IgM antibodies and then IgG occurs in response to the appearance of the flagella flagellate antigen of Borrelia with a mass of 41 kD. An important immuno-genome in pathogenesis is the surface proteins Osp C, which are characteristic mainly for European strains. In the case of disease progression (absence or insufficient treatment), the spectrum of antibodies to spirochete antigens (to polypeptides from 16 to 93 kD) expands, which leads to a long-term production of IgM and IgG. The number of circulating immune complexes increases. Immune complexes can also be formed in the affected tissues, which activate the main factors of inflammation – the generation of leucotactic stimuli and phagocytosis. A characteristic feature is the presence of lymphoplasmic infiltrates found in the skin, subcutaneous tissue, lymph nodes, spleen, brain, peripheral ganglia. The cellular immune response is formed as the disease progresses, with the highest reactivity of mononuclear cells manifested in the tissues of the “targets”. The level of T-helperovi T-suppressors, the index of stimulation of blood lymphocytes increases. It has been established that the degree of change in the cellular element of the immune system depends on the severity of the course of the disease.

The leading role in the pathogenesis of arthritis is borne by liposaccharides that are part of borrelia, which stimulate the secretion of interleukin-1 by monocyte-macrophage cells, some T-lymphocytes, B-lymphocytes, etc. that is, it activates inflammation in the joints, which leads to bone resorption, destruction of cartilage, stimulates the formation of pannus.

The delayed immune response associated with relatively late and mild borrelemia, the development of autoimmune reactions and the possibility of intracellular persistence of the pathogen are among the main causes of chronic infection.

Diagnosing Lyme Disease

The diagnosis of Lyme disease is complicated especially in the late period due to pronounced clinical polymorphism and the frequent absence of typical manifestations of the disease. Diagnosis is based primarily on the clinical picture, epidemiological data and is confirmed by the results of serological research. Clinical diagnosis can be considered reliable only in cases where a history of migrating erythema – a clinical marker of the disease. Borrelia cultures from a sick person stand out with difficulty. Serological methods are widely used to confirm the diagnosis. In our country, indirect immunofluorescence (n-REEF) and enzyme-labeled antibodies (ELISA) are used to detect antibodies to borrelia. However, there are seronegative variants of the disease. Often false-positive results are observed with syphilis. About possible infection can be judged by the detection of Borrelia in preparations of the intestine of a sucking tick using dark-field microscopy. In the affected organs and tissues, borrelia can be detected by electron microscopy, special silver staining, and monoclonal anti-borreliosis antibodies. A promising method is chain polymerization (polimerase chain reaction – PCR), the use of which allows one to confirm the diagnosis with a small number of microbial bodies in the body.

Peripheral blood changes in Lyme disease are non-specific and mainly reflect the degree of inflammatory changes in the organs.

The differential diagnosis is carried out with tick-borne encephalitis, a group of serous meningitis and meningoencephalitis, reactive and rheumatoid arthritis, acute rheumatism, neuritis, radiculo-neuritis, heart diseases with conduction and rhythm disorders, myocarditis, dermatitis of various etiology.

Lyme Disease Prevention

Specific prevention of Lyme disease is currently not developed. Non-specific prophylaxis measures are similar to those in tick-borne encephalitis. A very effective way to prevent infection is to prevent ticks from sticking (use of protective clothing and scaring agents).

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