Clinical Information

Lyme disease is a multisystem and multistage infection caused by 3 species of tick-borne spirochetes in the Borrelia burgdorferi sensu lato genogroup. These spirochetes include Borrelia burgdorferi sensu stricto (North America and Western Europe), Borrelia afzelii (Central and Western Europe and Russia), and Borrelia garinii (Europe, Russia, and northern Asia). Endemic areas for Lyme disease in the United States 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. Inflammation around the tick bite causes skin lesions. Erythema chronicum migrans (ECM), a unique expanding skin lesion with central clearing resulting in a ring-like appearance, is the first stage of the disease. Any of the following clinical manifestations may be present in patients with Lyme disease: arthritis, neurological disease, cardiac disease, or skin lesions. 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 a rash.

Early antibiotic treatment of Lyme disease can resolve clinical symptoms and prevent progression of the disease to later stages. Treatment with penicillin, tetracycline, erythromycin, chloramphenicol, or ceftriaxone is considered appropriate therapy.

Serology is currently the diagnostic method of choice for Lyme disease. The Second National Conference on the Serologic Diagnosis of Lyme Disease (1994) recommended that laboratories use a 2-test approach for the serologic diagnosis of Lyme disease. Accordingly, specimens are first tested by the more sensitive EIA or enzyme-linked immunosorbent assay (ELISA). A Western blot (WB) assay is used to confirm positive Lyme EIA or ELISA results due to the presence of IgG- or IgM-class antibodies. WB identifies the specific proteins to which the patient's antibodies bind. Although there are no proteins that specifically diagnose Borrelia burgdorferi infection, the number of proteins recognized in the WB assay is correlated with diagnosis.

Since serology may not be positive until 2 to 4 weeks after onset of ECM, direct detection of Borrelia burgdorferi-specific target DNA sequences using PCR is a promising adjunct to existing diagnostic tests. PCR has shown utility for detection of Borrelia burgdorferi DNA from skin biopsies of ECM lesions, and from synovial and cerebrospinal fluid in late-stage disease. Borrelia burgdorferi DNA can also, rarely, be detected from blood, but is not the test of choice from this source.