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Lyme disease was originally identified in
Lyme, Connecticut, based upon an unusual cluster of what appeared to be patients with juvenile rheumatoid arthritis. It was subsequently identified as a new clinical entity originally called
Lyme arthritis based on the observation that arthritis was a major clinical feature. However,
Lyme arthritis is now called
Lyme disease based upon the understanding that the clinical features include not only arthritis, but also potential cardiac, dermatologic and neurologic findings.
Lyme disease typically begins with an erythematous rash called erythema migrans (EM). Approximately 4-8% of patients develop cardiac, 11% develop neurologic and 45-60% of patients manifest arthritis. The
disease is transmitted following exposure to a tick bite containing a spirochete in a genetically susceptible host. There is considerable data on spirochetes, including Borrelia burgdorferi (Bb), the original bacteria identified in this
Lyme disease, if an organism had not been identified, would be considered as a classic autoimmune
disease and indeed the effector mechanisms are similar to many human diseases manifest as loss of tolerance. The clinical diagnosis is highly likely based upon appropriate serology and clinical manifestations. However, the serologic features are often misinterpreted and may have false positives if confirmatory laboratory testing is not performed. Antibiotics are routinely and typically used to treat patients with
Lyme disease, but there is no evidence that prolonged or recurrent treatment with antibiotics change the natural history of
Lyme disease. Although there are animal models of
Lyme disease, there is no system that faithfully recapitulates the human
disease. Further research on the effector mechanisms that lead to pathology in some individuals should be further explored to develop more specific therapy.
Copyright © 2014 Elsevier Ltd. All rights reserved.