Lyme Arthritis: Pathogenesis, Clinical Presentation, and Management
Section snippets
Pathogenesis of acute and chronic arthritis in Lyme disease
After the initial tick bite, B burgdoferi changes the expression of several immunostimulatory outer-surface lipoproteins that probably play a role in dissemination to the synovial tissue and in the pathogenesis of inflammation in the joint itself [6]. The acute arthritis results from the spirochete-induced infiltration of mononuclear cells into the synovial tissue and the accumulation of neutrophils, immune complexes, complement, and cytokines in the synovial fluid. In untreated Lyme arthritis,
Spectrum of clinical presentation
The most complete description of the natural history of Lyme arthritis probably remains the article by Steere and colleagues [22] chronicling the musculoskeletal manifestations of 55 untreated patients who had erythema migrans observed during the years 1976 to 1979, before the treatment of Lyme disease with antibiotics was established. Of these 55 patients, 11 (20%) had no musculoskeletal symptoms after the resolution of erythema migrans. The remaining 44 (80%) had joint involvement of some
Diagnosis of Lyme arthritis
The diagnosis of Lyme arthritis begins with the appropriate determination as to whether a patient suffering from arthritis has an active infection with B burgdorferi. The basis of this determination is the clinical picture as described earlier together with the standard two-tier serologic test—a sensitive ELISA or immunofluorescence assay followed by a Western blot for confirmation of any positive or indeterminate ELISA [23]. In Lyme arthritis, immunoglobulin (Ig)G serologies are almost always
Management of Lyme arthritis
Appropriate antibiotic therapy at the time of early localized or early disseminated infection has been shown to prevent the development of subsequent arthritis. In a study of 140 patients who had early disseminated Lyme disease (mostly erythema migrans) and received early treatment with ceftriaxone or doxycycline [33], only one patient had objective evidence of arthritis after 21 days of doxycycline therapy, which then resolved after a course of ceftriaxone. Initial antibiotic therapy of Lyme
Arthralgias in the initial presentation of Lyme disease
Of the 55 patients who had untreated Lyme disease observed by Steere and colleagues [22] (as previously discussed in an earlier section of this article), 10 (18%) developed arthralgias or pain in periarticular structures without ever developing corresponding objective joint abnormalities. These symptoms had their onset up to 8 weeks after the onset of erythema migrans, tended to affect one or two sites at a time (large or small joints, tendons, bursae, muscles, bones, or entheses), and were
Post-Lyme pain syndromes
A subset of patients may experience an array of chronic symptoms including musculoskeletal symptoms for months to years after Lyme disease. In the absence of an objective abnormality (eg, a joint effusion), however, no evidence of persistent infection has been documented [41]. These more chronic and persistent symptoms should be distinguished from the arthralgias seen in acute or untreated infection, in that they occur after the spirochete has most likely been eliminated by appropriate
Summary
Lyme arthritis is an inflammatory arthritis caused by B burgdorferi infection that is likely mediated by the immune response to the spirochete in the joint. It is easily distinguished from septic arthritis and tends to follow a relapsing/remitting course, affecting large joints (predominantly the knee) more frequently than small joints, usually with an asymmetric distribution. Diagnosis rests on standard serologic and clinical definitions of Lyme disease coupled with a typical mono- or
Acknowledgments
The authors thank Dr. Linden Hu for his insightful comments on this manuscript.
References (43)
- et al.
Chemokines and toll-like receptors in Lyme disease pathogenesis
Trends Mol Med
(2005) - et al.
Autoimmune mechanisms in antibiotic treatment-resistant Lyme arthritis
J Autoimmun
(2001) - et al.
Molecular characterization of the OspA(161-175) T cell epitope associated with treatment-resistant Lyme arthritis: differences among the three pathogenic species of Borrelia burgdorferi sensu lato
J Autoimmun
(2004) Lyme arthritis
Infect Dis Clin North Am
(2005)Mechanism of action of hydroxychloroquine as an antirheumatic drug
Semin Arthritis Rheum
(1993)- et al.
Lyme arthritis: an epidemic of oligoarticular arthritis in children and adults in three Connecticut communities
Arthritis Rheum
(1977) - et al.
Lyme disease—a tick-borne spirochetosis?
Science
(1982) - et al.
Borrelia burgdorferi in joint fluid in chronic Lyme arthritis
Ann Intern Med
(1986) - et al.
Detection of Borrelia burgdorferi DNA by polymerase chain reaction in synovial fluid from patients with Lyme arthritis
N Engl J Med
(1994) - et al.
The clinical assessment, treatment, and prevention of Lyme disease, human granulocytic anaplasmosis, and babesiosis: clinical practice guidelines by the Infectious Diseases Society of America
Clin Infect Dis
(2006)