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Hidden toxin gene in chlamydia linked to chronic illnesses

After more than 50 years of searching, scientists have discovered a key gene that enables certain bacteria to cause blindness and debilitating genital tract infections.

Using the recently completed genetic blueprint of the bacterium Chlamydia trachomatis, researchers from the National Institute of Allergy and Infectious Diseases (NIAID) have found a gene that encodes a cell-destroying toxin.

Long suspected but never identified, the toxin helps explain why only some chlamydial strains cause chronic illness. The discovery, described in the Proceedings of the National Academy of Sciences November 13 online early edition, opens potential new avenues for treating or preventing chlamydial diseases.

It also highlights how DNA sequencing can help scientists identify new ways to combat disabling or deadly infections.

Unlike most bacteria, C. trachomatis lives inside cells. Chronic infections of the eyelids can scar the eyes and lead to trachoma, the most common cause of preventable blindness worldwide.

In the United States, C. trachomatis infection is the most common sexually transmitted disease (STD) and can lead to pelvic inflammatory disease, tubal pregnancies and infertility in women.

All of these diseases are caused by chronic inflammation at the site of infection, but not all C. trachomatis strains produce this effect. Since the late 1940s, researchers have believed a toxin might cause the inflammation, but no such toxin had ever been found.

"These bacteria cause debilitating illnesses in hundreds of millions of people throughout the world," says Harlan Caldwell, Ph.D., a leading chlamydia researcher at NIAID's Rocky Mountain Laboratories in Hamilton, Mont. "If we could find a toxin that helps the bacteria attack and destroy cells, we would have a major new target for diagnostic tests, vaccines and drugs."

Dr. Caldwell joined Robert Belland, Ph.D., and their colleagues to look for the toxin using a new to
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Contact: Sam Perdue
sp189u@nih.gov
301-402-1663
NIH/National Institute of Allergy and Infectious Diseases
12-Nov-2001


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