Can Germs Prevent Arthritis?
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Genes and Infection
Since the late 1930s, when a researcher at the Rockefeller Institute in New York named Thomas McPherson Brown, MD, found infectious organisms now called mycoplasms in the synovial fluid of people with RA, scientists have suspected that infection could be a catalyst for some forms of arthritis and related conditions.
For several conditions, an infectious cause has already been identified. Lyme disease is caused by infection with a bacterium called Borrelia burgdorferi. When a tick infected with the bacterium bites a person, the bacterium enters and travels through the bloodstream, attaching to body tissues, including the skin and joints, where it causes inflammation and pain. Rheumatic fever follows infection with the streptococcus bacterium, such as the common strep throat or less common scarlet fever.
In people with certain genetic patterns, proteins in some tissues (including the joints and heart valves) share some similarities with strep proteins. If the immune system mistakes the body’s own proteins for the proteins in the infection it is supposed to fight, it may mistakenly attack the body’s tissues. Reactive arthritis, which occurs as a reaction to infection elsewhere in the body, has been associated with several types of bacteria including Chlamydia trachomatis of the genitals and urinary tract and intestinal infection with Salmonella, Shigella, Yersinia or Campylobacter.
Although it is not clear how these infections trigger arthritis, genetics appears to play a role. Approximately 80 percent of people with reactive arthritis test positive for the genetic type HLA-B127, which is also seen in high percentages of people with at least two other forms of arthritis – psoriatic arthritis and anklylosing spondylitis. Research has shown that the arthritis associated with Lyme disease is more likely to become chronic in people with the genetic types HLA-DR4 and HLA-DR2.
Scientists believe that a similar interplay between infection and genetics may be responsible for diseases such as RA and lupus. “If you look at RA, research shows that about half of the risk is genetic,” says David Pisetsky, MD, PhD, professor of medicine and chief of rheumatology, allergy and clinical immunology at Duke University Medical Center in Durham, N.C. “That means the other half is something in the environment or just bad luck.”
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