Lyme disease is a vector–borne infection, the causative agent of which is the Borrelia spirochete, which enters the body when an ixod mite bites. The clinical course includes local cutaneous (chronic migrating erythema) and systemic (fever, myalgia, lymphadenopathy, neuritis of peripheral and cranial nerves, meningitis, encephalitis, myelitis, myocarditis, pericarditis, oligoarthritis, etc.) manifestations. Confirmation of the diagnosis is facilitated by clinical and epidemiological data, the detection of antibodies to borrelia by the RIF method and the DNA of the pathogen by PCR. Etiotropic therapy is carried out with tetracycline antibiotics.
A69.2 Lyme Disease
Lyme disease – (lymborreliosis, tick–borne borreliosis) is a natural focal infectious disease, the carrier of which is an ixodic tick. Lyme disease is characterized by a complex of skin and systemic manifestations, prone to chronic course. According to statistics, every third tick studied is infected.
Lyme disease is widespread in North America, Europe and Asia. The disease was named after the town of Lyme (Connecticut, USA), where in 1975 there was an outbreak of infection, which included such manifestations as arthritis, carditis, meningitis. Lyme disease can occur at any age, but it is more often diagnosed in children and adolescents under 15 years of age, as well as adults aged 25-44 years. Due to the wide range of clinical manifestations, tick-borne borreliosis is of clinical interest not only for infectious diseases, but also for dermatology, neurology, cardiology, rheumatology, etc.
Lyme disease is caused by gram-negative spirochaetes of the genus Borrelia of three species: B. burgdorferi (predominant in the USA), Borrelia garinii and Borrelia afzelii. Borrelia enter the human body mainly by transmission, with the bites of infected ticks (pasture, forest, taiga) belonging to the genus Ixodes. The pathogen penetrates into the blood with tick saliva or its feces (when scratching bite sites). Less often, an alimentary pathway of infection is possible (for example, when using raw cow’s and goat’s milk) or transplacental transmission of borrelia.
Domestic and wild animals serve as a reservoir and source of the spread of Lyme disease. The risk of contracting Lyme disease increases in the spring and summer period (the season of tick activity lasts from April to October). Risk factors are visits to forests and forest park areas, as well as the prolonged (more than 12-24 hours) presence of an infected tick on the skin. After Lyme disease, unstable immunity is developed; after a few years, repeated infection with tick-borne borreliosis is possible.
Shortly after a tick bite, a complex of inflammatory and allergic reactions develops in the form of migrating ring-shaped erythema at the site of its introduction into the epidermis. From the primary focus with lymph and blood flow, borrelia spread throughout the body, causing a cascade of immunopathological reactions in various organs, mainly the central nervous system, joints, and heart.
In the clinical course of Lyme disease, there is an early period (stages I-II) and a late period (stage III):
- I – stage of local infection (erythemic and non-erythemic forms)
- II – stage of dissemination (variants of the course – febrile, neuritic, meningeal, cardiac, mixed)
- III – stage of persistence (chronic Lyme arthritis, chronic atrophic acrodermatitis, etc.).
According to the severity of pathological reactions, Lyme disease can occur in mild, moderate, severe and extremely severe forms.
Lyme disease symptoms
The stage of local infection
After the end of the incubation period (about 7-14 days), a stage of local infection occurs, characterized by skin manifestations and intoxication syndrome. At the site of the tick bite, an itchy, slightly painful red papule appears, prone to peripheral growth (migrating tick-borne erythema). As the redness zone expands, the migrating erythema takes the form of a ring with a diameter of 10-20 cm, having a bright red corolla at the edges and a paler central part. In most cases, erythema migrans in Lyme disease spontaneously resolves within 1-2 months, and weak pigmentation and peeling remain in its place. Local manifestations of Lyme disease are accompanied by a general infectious syndrome: fever with chills, headache, arthralgia, pain in bones and muscles, pronounced weakness. Other symptoms in stage I may include urticaria, conjunctivitis, regional lymphadenitis, runny nose, pharyngitis.
Stage of dissemination
Over the next 3-5 months, the disseminated stage of Lyme disease develops. In the case of an anerythemic form of infection, tick-borne borreliosis can immediately manifest with systemic manifestations. Most often, damage to the nervous and cardiovascular system develops at this stage. Among the neurological syndromes for Lyme disease, serous meningitis, encephalitis, peripheral radiculoneuritis, facial nerve neuritis, myelitis, cerebral ataxia, etc. are the most typical. During this period, manifestations of Lyme disease may include throbbing headache, photophobia, myalgia, neuralgia, significant fatigue, sleep and memory disorders, skin sensitivity and hearing disorders, lacrimation, peripheral paralysis and paresis, etc.
Cardiac syndrome in Lyme disease in most cases is represented by atrioventricular blockades of varying degrees, rhythm disturbances, myocarditis, pericarditis, dilated cardiomyopathy. The joints are characterized by migrating myalgia and arthralgia, bursitis, tendinitis, arthritis (usually in the form of monoarthritis of a large joint, less often – symmetrical polyarthritis). In addition, the course of the disseminated stage of Lyme disease may include skin lesions (multiple migrating erythema, lymphocytoma), genitourinary system (proteinuria, microhematuria, orchitis), eyes (conjunctivitis, iritis, chorioretinitis), respiratory tract (sore throat, bronchitis), digestive system (hepatitis, hepatolienal syndrome), etc.
Lyme disease becomes chronic in 6 months – 2 years after the acute stage. In the late period of Lyme disease, skin lesions most often occur in the form of atrophic acrodermatitis or benign lymphoplasia or joint damage (chronic arthritis). Atrophic acrodermatitis is characterized by the appearance of edematous erythematous foci on the skin of the extremities, in place of which atrophic changes develop over time. The skin becomes thin, wrinkled, telangiectasia and scleroderm-like changes appear on it. A benign lymphocytoma has the appearance of a reddish cyanotic node or plaque with rounded outlines. It is usually localized on the skin of the face, auricles, axillary or inguinal area; in rare cases, it can transform into malignant lymphoma.
Chronic Lyme arthritis is characterized not only by damage to the synovial membrane of the joints, but also periarticular tissues, leading to the development of bursitis, tendinitis, ligamentitis, enthesopathy. In its clinical course, arthritis in the late stage of Lyme disease resembles rheumatoid arthritis, Reiter’s disease, Bekhterev’s disease, etc. In the late stages of chronic arthritis, thinning of cartilage, osteoporosis, and marginal usures are radiologically detected.
In addition to skin-joint syndromes, neurological syndromes can develop at the chronic stage of Lyme disease: encephalopathy, chronic encephalomyelitis, polyneuropathy, ataxia, chronic fatigue syndrome, dementia. With transplacental infection, pregnancy can end in stillbirth and miscarriage. In live-born children, intrauterine infection leads to prematurity, causes the formation of congenital heart defects (aortic stenosis, aortic coarctation, endocardial fibroelastosis), delayed psychomotor development.
During the diagnosis of Lyme disease, the epidemiological history (visits to forests, park areas, the fact of tick bite) and early clinical manifestations (migrating erythema, flu-like syndrome) should not be underestimated.
Depending on the stage of tick-borne borreliosis, microscopy, serological reactions (ELISA or RIF) and PCR examination are used to detect the pathogen in biological media (blood serum, synovial fluid, cerebrospinal fluid, skin biopsies). In order to assess the severity of organ-specific lesions, joint radiography, ECG, EEG, diagnostic puncture of joints, lumbar puncture, skin biopsy, etc. can be performed.
Differential diagnosis of Lyme disease is carried out with a wide range of diseases: serous meningitis, tick-borne encephalitis, rheumatoid and reactive arthritis, Reiter’s disease, neuritis, rheumatism, dermatitis, erysipelas. It should be borne in mind that false-positive serological reactions can be observed in patients with syphilis, infectious mononucleosis, recurrent typhus, rheumatic diseases.
Lyme disease treatment
Patients with Lyme disease are subject to hospitalization in an infectious hospital. Drug therapy is carried out taking into account the stage of the disease. At an early stage, tetracycline antibiotics (tetracycline, doxycycline) are usually prescribed for 14 days, amoxicillin can be taken. During the transition of Lyme disease to stage II or III and the development of articular, neurological and cardiac lesions, it is advisable to use penicillins or cephalosporins for a course of 21-28 days. Against the background of antibiotic therapy, a Yarish-Herksheimer reaction may occur, characterized by an exacerbation of the symptoms of spirochetosis due to the death of borrelia and the release of endotoxins into the blood. In this case, antibiotic therapy is stopped for a short time, and then resumed in a lower dosage.
Pathogenetic treatment for Lyme disease depends on the clinical manifestations and their severity. Thus, detoxification therapy is indicated for general infectious symptoms; for arthritis – NSAIDs, analgesics, physiotherapy; for meningitis – dehydration therapy. In severe systemic Lyme disease, glucocorticoids are prescribed orally or in the form of intra-articular injections (with synovitis).
Early or preventive antibiotic therapy can prevent the transition of Lyme disease to a disseminated or chronic stage. With delayed diagnosis or the development of severe lesions of the central nervous system, persistent residual phenomena occur, leading to disability; a fatal outcome is possible. Within a year after the end of treatment, patients with Lyme disease should be registered with an infectious disease specialist, neurologist, cardiologist, arthrologist to exclude the chronization of infection.
In order to prevent infection with tick-borne borreliosis, when visiting forests, it is necessary to wear protective clothing; use repellents that repel ticks; after walking through the forest, carefully examine the skin for possible introduction of a blood-sucking insect. If a tick is detected, it must be removed independently with tweezers or contact the nearest emergency room for appropriate manipulation by a surgeon. The extracted tick must be delivered to the sanitary and epidemiological laboratory for an express test for borrelia by dark-field microscopy. Preventive anti-tick treatment of forests and forest park areas has not lost its relevance.