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Lyme disease is caused by the spirochete Borrelia burgdorferi. The spirochete is transmitted to humans through the bite of Ixodes species ticks. Endemic areas for Lyme disease in the United States (US) correspond with the distribution of 2 tick species, Ixodes dammini (Northeastern and Upper Midwestern US) and Ixodes pacificus (West Coast US). In Europe, Ixodes ricinus transmits the spirochete.
Lyme disease exhibits a variety of symptoms that may be confused with immune and inflammatory disorders. Any of the following clinical manifestations may be present in patients with Lyme disease: skin lesions, cardiac disease, or neurological disease. In the first stage of disease, inflammation around the tick bite causes skin lesions, erythema chronicum migrans (ECM)-a unique expanding skin lesion with central clearing that results in a ring-like appearance. Culture of skin biopsies obtained near the margins of ECM are frequently positive. Neurologic and cardiac symptoms may appear with stage 2, and arthritic symptoms with stage 3 of Lyme disease. In some cases, a definitive distinction between stages is not always seen. Further, secondary symptoms may occur even though the patient does not recall a tick bite or rash.
The presence of cerebrospinal fluid antibodies to Borrelia burgdorferi is indicative of neurologic Lyme disease (Lyme neuroborreliosis). PCR testing also may be used to confirm late-stage neurologic disease.
Early antibiotic treatment of Lyme disease can resolve clinical symptoms and prevent progression of the disease to later stages. Treatment with beta lactams such as amoxicillin, cefixime or ceftriaxone, or doxycycline are considered the most appropriate therapy.
Aiding in the diagnosis of Lyme neuroborreliosis
Intrathecal synthesis of antibody to Borrelia burgdorferi is indicative of neurological Lyme disease.
A negative result does not rule-out Lyme neuroborreliosis.
According to the manufacturer’s package insert, patients in early stages of infection may not produce detectable levels of antibody. Antibiotic therapy in early disease may prevent antibody production from reaching detectable levels.(1) Patients with clinical history and/or symptoms suggestive of Lyme disease or where early Lyme disease is suspected, but with negative test results should be retested in 2 to 4 weeks.
Results should be interpreted in the context of clinical findings.
False-positive results may be caused by breakdown of the blood-brain barrier, or by the introduction of blood into the cerebrospinal fluid at collection.
Because clinical studies are limited, the advantage of immunoassays over PCR (or vice versa) has not been conclusively demonstrated for diagnosing central nervous system Lyme disease. If the result for the immunoassay is negative and there is a high suspicion of Lyme neuroborreliosis, consider performing PBORR / Lyme Disease (Borrelia burgdorferi), Molecular Detection, PCR.
Reference values apply to all ages.
1. Package insert: Immunetics C6 B burgdorferi (Lyme) ELISA Kit, Immunetics, Inc, Boston, MA, 2006
2. Steere AC: Borrelia burgdorferi (Lyme disease, Lyme borreliosis). In Principles and Practice of Infectious Diseases. Fifth edition. Edited by GL Mandell, JE Bennett, R Dolin. Philadelphia, Churchill Livingstone, 2000, pp 2504-2518