Bacterial antigens in synovial biopsy specimens in yersinia triggered reactive arthritis

Article Abstract:

Reactive arthritis causes inflammation of the joints and occurs following an infection elsewhere in the body. The initial infection is commonly caused by Yersinia, Salmonella, Chlamydia, Shigella or Campylobacter bacteria. It is thought that the organism causing the infection persists in the body after the infection is gone and even after stool samples become negative (do not contain the organism). In patients who develop arthritis after having an infection with Yersinia (Yersinia-triggered reactive arthritis), specific Yersinia proteins (antigens) can be found in the blood and in the fluid within the affected joints (synovial fluid). To evaluate further the presence of Yersinia antigens in patients with reactive arthritis, fluid samples from the knees of 23 patients with inflammatory joint disease were examined. Ten of the patients had reactive arthritis caused by Yersinia, four had reactive arthritis caused by microbes other than Yersinia, two had arthritis affecting the spine (ankylosing spondylitis), and seven had inflammation of the joints caused by diseases other than reactive arthritis. Nonviable (dead) particles from Yersinia enterocolitica bacteria were found in the joint fluid samples and joint cells in 8 out of the 10 patients with Yersinia-reactive arthritis. All 13 of the samples from the patients who did not have Yersinia-reactive arthritis tested negative for (did not contain) Yersinia. These findings indicate that foreign material (particles or pieces of dead bacteria) may be important in causing reactive arthritis. (Consumer Summary produced by Reliance Medical Information, Inc.)

Analysis, Measurement, Causes of, Inflammation, Arthritis, Infectious, Infectious arthritis, Synovial fluid, Synovial membranes, Synovial membrane, Yersinia enterocolitica, Bacterial antigens, O antigens

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Pathogenesis of square bodies in ankylosing spondylitis

Article Abstract:

Ankylosing spondylitis is a chronic, progressive disease involving the vertebrae, the bony segments of the spine. Sclerosis or thickening of the sacroiliac joint located at the base of the spine is a diagnostic sign of ankylosing spondylitis, and changes in joint structure resemble those seen in rheumatoid arthritis, an inflammatory joint disease. Studies have shown that the vertebrae in ankylosing spondylitis undergo abnormal transformations resulting in a square-shaped structure. One study suggested that the mechanism that causes squaring of the vertebrae involves loss of bone tissue. A case is described of a 25-year-old man with ankylosing spondylitis of five years duration; he committed suicide and was found to have squaring of the vertebrae at autopsy. The findings indicate that the disease process was associated with osteitis, or inflammation of the bone, resulting in damage to the vertebrae. The inflammatory bone disintegration was followed by formation of new bone, resulting in the squaring of the vertebrae. Thus, the development of square vertebral bodies results from destructive osteitis and subsequent repair. (Consumer Summary produced by Reliance Medical Information, Inc.)

Abnormalities, Vertebrae, Osteitis

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IgA1 and IgA2 subclass antibodies against Klebsiella pneumoniae in the sera of patients with peripheral and axial types of ankylosing spondylitis

Article Abstract:

The antibodies immunoglobulin A1 (IgA1) and A2 (IgA2) specific for the commonly found intestinal bacteria, Klebsiella, may interact in the development of ankylosing spondylitis (AS). AS is an inflammatory and deteriorating joint disease that may lead to fusion of affected joints either in the trunk of the body (axial AS) or in the limbs (peripheral AS). Researchers compared the IgA1 and IgA2 blood levels of 171 patients with either axial or peripheral AS against 100 healthy volunteers. They also tested the IgA antibody response in the AS patients during a 26-week treatment with sulphasalazine. The IgA1 and IgA2 Klebsiella specific antibody levels were higher in the AS patients as compared to the healthy volunteers. IgA1 antibody levels decreased in the patients with axial AS after sulphasalazine treatment. IgA2 antibody levels in both classes of AS patients did not change significantly with sulphasalazine treatment.

Immunoglobulin A

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