From Los Angeles, at the annual meeting of the American Society for Microbiology
When it infects the cervix or urethra, Neisseria gonorrhoeae, the bacterium behind gonorrhea, fails to produce symptoms in many women. That’s not necessarily good. Women with such silent infections never get treatment, permitting N. gonorrhoeae to spread to the fallopian tubes and elsewhere in the upper genital tract. There the bacteria cause pelvic inflammatory disease (PID), a condition that strikes an estimated 1 million U.S. women every year and leaves 10 percent of them infertile.
Stella Nowicki of the University of Texas Medical Branch in Galveston and her colleagues have now identified a gene that the bacterium may use to colonize the upper genital tract. Previously, they showed that strains of N. gonorrhoeae isolated from women with PID are more virulent than bacteria from women with gonorrhea. PID strains, for example, aren’t killed by human blood serum and thrive in the blood of infant rats.
Further work by Nowicki’s group suggested how PID strains are distinct from ones producing gonorrhea. The investigators slowly homed in on a DNA region that differs between the strains and have now found a gene there that’s present much more often in the PID strains. It doesn’t match any previously discovered bacterial genes, reports Khoa Nguyen, a member of Nowicki’s research team. The gene encodes a protein that may reside on the surface of N. gonorrhoeae, he adds.
The investigators are now conducting tests to determine the protein’s role and whether it contributes to the bacterium’s virulence. If it does, physicians may want to add a test for the gene’s presence to their screening for gonorrhea infections. Such an assay could help predict which infections pose the highest risk of leading to PID and therefore merit the most aggressive treatment, says Nguyen.