Highly specific physical findings include erythema migrans, cranial nerve palsy, high-grade or progressive conduction block, and recurrent migratory polyarthritis. 3Įarly disease is further subdivided into “localized” infection (stage 1), characterized by a single erythema migrans lesion and local lymphadenopathy, and “disseminated” infection (stage 2), associated with multiple erythema migrans lesions distant from the bite site, facial nerve palsy, radiculoneuritis, meningitis, carditis, or migratory arthritis or arthralgia. 3Ĭertain host-genetic factors also play a role in the pathogenesis of Lyme disease, such as the HLA-DR4 allele, which has been associated with antibiotic-refractory Lyme-related arthritis. It can decrease its expression of specific immunogenic surface-ex posed proteins, change its antigenic properties through recombination, and bind to the patient’s extracellular matrix proteins to facilitate further dissemination. 5ĭespite the immune system’s robust series of defenses, untreated B burgdorferi infection can persist, as the organism has a bag of tricks to evade destruction. Once a patient is exposed and mounts an antibody-mediated response to the spirochete, the antibody profile may persist for months to years, even after successful antibiotic treatment and cure of the disease. 6īecause IgM can also cross-react with antigens other than those associated with B burgdorferi, the IgM test is less specific than the IgG test for Lyme disease. The IgM antibody response occurs in 1 to 2 weeks, followed by a robust IgG response in 2 to 4 weeks. 3 Both cell-mediated and antibody-mediated immunity swing into action to kill the spirochetes at this stage. If the infection is not treated, the spirochete may disseminate through the blood from the bite site to different tissues. Immunoglobulin M (IgM) antibody titers peak between 8 and 14 days after tick contact, but IgM antibodies may never develop if the patient is started on early appropriate antimicrobial therapy. 5Īntibody levels remain below the detection limits of currently available serologic tests in the first 7 days after exposure. Hence, a rash occurring within the first few hours of tick contact is not erythema migrans and does not indicate infection, but rather an early reaction to tick salivary antigens. A rash develops in only about 85% of patients who are infected and can appear at any time between 3 and 30 days, but most commonly after 7 days. 5 However, once infected, the patient’s innate immune system mounts a response that results in the classic erythema migrans rash at the bite site. It is estimated that only 5% of infected ticks that bite people actually transmit their spirochetes to the human host. The pathogenesis and the different stages of infection should inform laboratory testing in Lyme disease. This review describes the epidemiology and pathogenesis of Lyme disease, the advantages and disadvantages of current diagnostic methods, and diagnostic algorithms. The full spectrum of disease was first recognized and the disease was named in the 1970s during an outbreak of arthritis in children in the town of Lyme, Connecticut. Lyme disease is a complex multisystem bacterial infection affecting the skin, joints, heart, and nervous system. When interpreting the test results, be aware of false-positives and the reasons for them. Interpretation of the bands depends on the duration of infection. ![]() Standard 2-tiered testing is the diagnostic testing method of choice-enzyme-linked immunoassay followed by Western blot. Its diagnosis is mainly clinical and epidemiologic and, when doubtful, is supported by serologic testing. Certain clinical features are diagnostic. Lyme disease preferably affects the skin, joints, and nervous system and presents with typical and atypical features. ![]() Lyme disease, the most common tick-borne infection in North America, is a complex multisystem bacterial disease caused by Borrelia burgdorferi.
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