Lyme disease (tick borreliosis) is the most common tick-borne disease in the northern hemisphere. The name of the disease comes from the town of Old Lyme (USA) where in the mid-1970s a number of cases of arthritis following tick bites were described. The causative agent of Lyme disease, a spirochete from the group Borrelia burgdorferi, was first identified in 1982 by the American microbiologist Willy Burgdorfer.
Signs and symptoms of Lyme borreliosis, as well as other spirochaetoses, are classified into stages and are characterized by lesions of various tissues and organs, including skin, joints, heart and nervous system. Early disease (stage 1) is characterized by primary migrating erythema, a ringlike skin rash (diameter 10-20 cm) which develops few days or weeks after tick bite. Migrating erythema occurs in 60-80% of patients. Other symptoms of the disease (fever, headache, myalgia, severe weakness and fatigue) are nonspecific. Stage 2 disease develops few weeks or months after localized stage. It is caused by dissemination of spirochetes via blood and presents itself as multiple skin lesions (secondary erythema migrans), meningitis, neuritis, arthritis and myocarditis. Chronic infection (stage 3) can develop from several months to several years after primary lesion, and is characterized by acrodermatitis chronica atrophicans (ACA), varying degrees of encephalopathy and encephalomyelitis, and persistent arthritis.
Thus, Lyme disease is characterized by very diverse clinical symptoms, which may complicate its timely diagnosis. Early diagnosis is based on clinical and epidemiological data. The diagnosis is confirmed by laboratory methods, mainly serological ones, such as detection of specific antibodies to B. burgdorferi in blood. Serological methods are highly sensitive and specific comparing to pathogen isolation, B. burgdorferi antigen detection and histological examination of the skin, which is additionally is an invasive method.
The specific IgM antibodies appear within the first few weeks after infection, and they are usually remains on a high level in the patients with early symptoms. IgG antibodies begin to appear 4-6 weeks after infection and reach maximum level 2-3 months after disease onset. The level of IgG antibodies may decrease 2-4 months after the successful antimicrobial therapy but these antibodies can be detected and circulate in the blood for a long time (from several months to several years). However, IgG antibodies often are not detectable at early stage or after successful antimicrobial therapy. Due to inability to induce long-lived immune responses patients who had Lyme disease and recovered could be later reinfected by B. burgdorferi.
hide »
