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A brief summary and explanation of lyme disease and lyme arthritis

Rosenberg, in Diagnostic Pathology of Infectious Disease Second Edition2018 Lyme Arthritis Borreliosis Lyme borreliosis was first described in 1975 in the United States, after the perplexing outbreak of juvenile rheumatoid arthritis in the vicinity of Lyme, Connecticut. The causative agent, the spirochete Borrelia burgdorferi, was not identified until 1982.

Lyme disease is now recognized as the most common vector-borne disease in North America and Europe, with annual incidence rates as high as 31. In the United States it is localized to three endemic areas: However, these regions continue to enlarge as the geographic range of the vector ticks infected with B. Three members of the Borrelia genus are known to cause Lyme disease in humans: Borreliosis is a vector-borne disease, with pathogens transmitted by the bite of infected Ixodes ricinus ticks.

In the larval and nymph stages of the tick life cycle, ticks feed primarily on small rodents—predominantly the white-footed mouse in the United States and the vole in Europe and Asia.

These animals then serve as a disease reservoir for horizontal transmission between nymphs and larval ticks. In contrast, larger mammals, such as deer or humans, preferred as a food source for adult ticks, are dead-end hosts for Borrelia.

For Borrelia transmission to occur, the tick must be attached to its host for at least 24 hours; this allows the bacteria to migrate from the tick midgut into the salivary gland, a process mediated by cell surface adhesion molecules, including OspA and Ospc.

A number of factors have been implicated in disease transmission.

  • Chronic Lyme disease is considered to be a controversial diagnosis, and theories on its pathogenesis range from autoimmunity, to lingering B;
  • In most patients, arthritis occurs in flares, which resolve over a period of years;
  • The predominant infectious disease, pediatric, and neurology organizations discount chronic Lyme disease as a distinct clinical entity, while other academic, professional, and advocacy organizations argue the contrary;
  • Some attribute chronic Lyme disease symptoms to drug-resistant reservoirs of B.

Tick saliva is thought to contain vasodilators, anticoagulants, and immunomodulators, which may facilitate Borrelia transmission to the host. Additional factors assist in immune evasion, by modulating host response or downregulation of immunogenic cell surface markers. The pathognomonic lesion of early acute Lyme disease is the erythema migrans rash, which appears at the site of tick bite within 5 to 14 days, then spontaneously resolves after several days to weeks.

The rash is erythematous, often with a central clearing, or bull's-eye, and is usually painless and nonpruritic. Within a few weeks of infection, untreated patients develop symptoms of early disseminated disease, including fever, malaise, aseptic meningitis, facial palsy, radiculoneuropathy, or carditis, as well as migratory arthralgias and myalgias.

True arthritis typically develops weeks or months after the initial infection. Lyme arthritis is usually a monoarticular or oligoarticular arthritis that typically affects the knee or other large joints.

Related terms:

Joints of the digits are occasionally involved, and tendonitis and bursitis may also occur. In most patients, arthritis occurs in flares, which resolve over a period of years.

  • Rarely, degenerative changes, such as subarticular sclerosis and osteophyte formation, may be seen;
  • Early disseminated Lyme disease may manifest as multiple erythema migrans, usually appearing 3—5 weeks following the tick bite;
  • Tick saliva is thought to contain vasodilators, anticoagulants, and immunomodulators, which may facilitate Borrelia transmission to the host.

In a minority of patients, chronic synovitis may develop despite appropriate antibiotic treatment. Chronic Lyme disease is considered to be a controversial diagnosis, and theories on its pathogenesis range from autoimmunity, to lingering B. The crux of this controversy is the persistence of arthritis despite eradication of spirochetes in the affected joint.

Lyme borreliosis

Evidence for persistent disease has been controversial at best, with the majority of studies finding no serologic or culture evidence of B. The argument for an autoimmune response leading to arthritis is more convincing. Mechanistically this immune response is thought to be caused by focal homology between the B. T cells are thought to be an important mediator of subsequent inflammatory changes, along with secreted proinflammatory cytokines. On imaging, acute Lyme arthritis shows effusion of the knee joint.

Intraarticular edema can be seen, along with a spectrum of soft tissue changes involving the infrapatellar fat pad, periarticular soft tissues, and entheses.

  • Suffering is often exacerbated by a self- or provider-validated cycle that attributes common somatic complaints to serious conditions;
  • The argument for an autoimmune response leading to arthritis is more convincing;
  • Mechanistically this immune response is thought to be caused by focal homology between the B;
  • Fibrin deposition is seen, along with synovial hypertrophy, neovascularization, and infiltration by histiocytes, plasma cells, and a subsynovial mixed lymphocyte population Fig;
  • A number of factors have been implicated in disease transmission;
  • For Borrelia transmission to occur, the tick must be attached to its host for at least 24 hours; this allows the bacteria to migrate from the tick midgut into the salivary gland, a process mediated by cell surface adhesion molecules, including OspA and Ospc.

In chronic Lyme arthritis, an inflammatory arthritis is seen, with juxtaarticular osteoporosis, loss of cartilage, and bony erosions. Rarely, degenerative changes, such as subarticular sclerosis and osteophyte formation, may be seen. The histologic features of acute Lyme synovitis are similar to those observed in other septic arthritides, with edema and abundant neutrophilic infiltration of synovium and adjacent soft tissues.

Organisms have been demonstrated in synovial tissues in the early stages of infection by Warthin-Starry silver stain Fig.

Lyme Disease

Histologic examination of synovial tissue from chronic Lyme arthritis demonstrates nonspecific features of chronic inflammatory or rheumatoid arthritis. Fibrin deposition is seen, along with synovial hypertrophy, neovascularization, and infiltration by histiocytes, plasma cells, and a subsynovial mixed lymphocyte population Fig.

In this setting the morphologic changes overlap with those of other, noninfectious inflammatory arthropathies. Diagnosis of Lyme arthritis should be considered in patients who have recently been in areas endemic for B.

Lyme Disease and the Orthopaedic Implications of Lyme Arthritis

A history of erythema migrans is helpful, but not required, to proceed to serologic or synovial fluid testing. Treatment of acute Lyme arthritis involves oral or intravenous antibiotic therapy. If arthritis does not resolve with two courses of an appropriate antibiotic regimen and PCR testing of synovial fluid is negative for B.