Erythema migrans is a cutaneous manifestation of the first stage of borreliosis infection. It occurs at the bite site of a tick infected with borreliosis when the pathogen of the disease penetrates into the skin with insect saliva. A distinctive feature of erythema is its constant increase in size with simultaneous resolution of hyperemia in the center. Pathology is diagnosed after consultation with an infectious disease specialist, taking into account the data of enzyme immunoassay of venous blood for antibodies to the pathogen. Treatment – antibiotic therapy, sometimes glucocorticoids and antihistamines.
Erythema migrans is an infectious dermatosis that occurs when a tick is bitten, which is the transmitter of borreliosis. It is characterized by a high rate of spread and a rapid change in the boundaries of the pathological focus, which causes the use of the word “migrating” in the name of the disease. Pathology has no age, racial or gender characteristics. Natural foci of borreliosis are constantly expanding. More recently, the USA, Australia, insular Europe, Primorye and Siberia were considered endemic territories, currently the tick is found almost everywhere. 80% of cases are registered in summer.
For the first time, “migrating dermatitis” of unclear etiology was described by A. Afzelius in 1908. The disease was called erythema migrans by B. Lipschutz in 1913. Dermatologists have been considering erythema migrans as an allergic skin reaction in Lyme disease since the 70s-80s of the last century, after the discovery of borrelia and the compilation of a description of borreliosis. Currently, the relationship between erythema migrans and borreliosis is practically not debated, dermatosis is considered an early cutaneous marker of Lyme disease. The urgency of the problem is associated with the migration of ticks, a large number of individuals infected with borreliosis in the population, a long period of their active existence (from May to September), living in forests, urban gardens, parks and squares.
The causative agent of erythema migrans is borrelia, the carrier of which is an infected ixod mite. There are natural foci of its habitat, the tick is found in forests, coastal zones and parks, where the insect lives on the stems of flowers and grasses. Infection of a person occurs at the moment of a bite, when a tick injects borrelia into the blood with saliva. The duration of the carrier’s stay on the skin does not matter, the infectious-allergic process begins to develop immediately after the penetration of saliva with the pathogen into the patient’s blood. The hosts of borrelia are domestic or wild animals, the tick acts only as a lifelong carrier, becoming a carrier of infection after the bite of an infected animal.
A tick bite violates the integrity of the skin. Part of the borrelia remains at the site of insertion, the rest with the flow of blood and lymph are carried to all organs and tissues, settle in the lymph nodes. Infectious-allergic erythema is a pathognomonic manifestation of the onset of Lyme disease and forms on the skin in the first hours after infection. Following it, a month later, multiple organ symptoms appear. It should be noted that in 25% of cases, erythema migrans does not develop. This is probably due to the peculiarities of the functioning of the body’s immune system, the strength of the response, the amount of pathogen that has penetrated the skin and its virulence.
Borrelia penetrates into the skin, penetrates through the lymphatic vessels into the deep layers and causes inflammation, while sensitizing the dermis. Cells of the immune and histiocytic system of the skin, lymphocytes and macrophages participate in the process of alteration, exudation and proliferation. They bind borrelia, perceiving them as foreign antigens. At the same time, cell proliferation is stimulated with the replacement of a tissue defect at the site of a tick bite.
Erythema itself occurs as a result of a perverse reaction of vasodilation of the skin, slowing blood flow and increasing plasma pressure on the walls of capillaries. As a result of these processes, the “squeezed out” part of the plasma from the vessels permeates the dermis, which swells, lifting the spot above the surrounding skin. Following the plasma, vascular T-lymphocytes migrate into the dermis, which control the foreign introduction, eliminating the remaining borrelia. Erythema begins to resolve from the center. In the area of primary damage, the inflammation subsides, and an erythematous shaft of T-lymphocytes and dermal cells continues to grow along the edges. This is how, centrifugal, the size of the erythema increases.
Erythema migrans is a key sign that allows you to establish the presence of borreliosis, so early diagnosis of this disease is extremely important. The pathological process in the occurrence of erythema migrans has an incubation period of 32 days and includes 3 clinical stages of development: early, disseminated and late.
At the early (local, localized) stage of erythema migrans, a bright pink or red spot with a papule or macula in the center (at the bite site) appears on the skin. The spot is slightly convex, hot to the touch, has clear borders and grows rapidly. After increasing to 5 centimeters, the resolution of the element in the central part begins, the spot acquires a ring-shaped shape. Unpleasant sensations are possible, less often itching, burning and pain in the affected area. Sometimes there are prodromal phenomena, jaundice-free hepatitis and signs of damage to the meninges. The spots persist for 3-30 days, and then begin to peel off and “dissolve”, leaving a slight hyperpigmentation along the contour. When antibacterial therapy is connected, the pathological process stops there. In the absence of treatment or insufficient therapy, the second stage occurs.
In the disseminated stage of erythema migrans, borrelia enter the blood in large quantities from lymph nodes. Erythema increases in size. There is an additional sensitization of the body, there is a decrease in immunity. New multiple urticary rashes and secondary ring-shaped elements appear, benign lymphocytoma cutis is possible. Fever and headache are added, weakness and insomnia are increasing, neurological and cardiac symptoms are revealed. The second stage lasts from 6 months to 2 years. With an insufficient immune response, an incorrectly calculated dose of the drug, high virulence and a large number of borrelia, the disease enters the third stage.
The chronic (late) stage of erythema migrans is characterized by the development of acrodermatitis and chronic Lyme arthritis. There is a symmetrical lesion of the joints, accompanied by edema, restriction of movements, local hyperemia and hyperthermia. Erythema migrans acquires a purple hue, becomes thinner and atrophies in the center, vessels and underlying tissues begin to shine through the skin. At the same time, the spot is still growing, increasing in size, but it is no longer localized in the place of the tick bite, but next to the joints or on the extensor surface of the limbs. The stage lasts for years.
The speed and accuracy of diagnosis in erythema migrans are important for timely relief of the process. The diagnosis is made collectively by a dermatologist and an infectious disease doctor based on the clinical picture and anamnesis data. To confirm, an enzyme immunoassay of venous blood taken 21 days after a tick bite (previously, antibodies were not distinguishable) is carried out for antibodies to borrelia. The method of indirect immunofluorescence, immunoblotting (a combination of electrophoresis and ELISA or RIA) is used. Immunofluorometry and indirect agglutination reaction are used less often.
To exclude meningitis and concomitant infection, a lumbar puncture is performed with a study of cerebrospinal fluid by PCR and ELISA. The pathomorphological picture is nonspecific. Erythema migrans is differentiated with bee stings and other insects, dermatitis, trichophytia, syphilitic roseola, scleroderma, Darya’s erythema, migrating miasis.
Self-medication is excluded. The treatment of erythema migrans is pathogenetic, carried out by an infectious disease specialist. There is no need for local therapy. During the incubation period, cephalosporins, tetracycline and penicillin antibiotics are prescribed prophylactically on an outpatient basis. Similar therapy is continued at an early stage of the disease. An individual regimen of taking antibacterial drugs is calculated for each patient per kilogram of weight. In case of complications or resistance to the therapy, antibiotics are injected in combination with antihistamines. In severe cases, glucocorticoids are used.
After the relief of erythema migrans, the patient must be monitored by an infectious disease doctor for 1.5-3 years (depending on the severity of the pathological process), periodically passing a blood test for the titer of antibodies to borrelia.
Prevention and prgnosis
There is no specific prevention of borreliosis. In summer, during the phase of active activity of ticks, it is necessary to minimize the risk of insects getting on the skin: remember that ticks live in the grass, use repellents when going out into nature, dress in light clothes that maximally cover the skin from insects (long sleeves, trousers with elastic bands, high boots, hats), inspect the skin on return home.
When a tick is bitten, you should not wait for the development of erythema migrans. It is necessary to remove the insect from the skin, place it in a sealed vessel and take it for analysis to the SES. You need to contact an infectious disease specialist who can inject interferon or (less often) prescribe a preventive course of antibacterial therapy. After receiving the results of the analysis, the decision on the further management of the patient is made by a specialist. The prognosis with timely diagnosis and treatment is favorable.