Staph causes a wide range of maladies, from local infections of the skin, lungs, bones and heart valves, to toxic shock syndrome and death, and it is a leading cause of hospital-acquired infections, striking some 500,000 patients each year. The bug can infect surgical wounds and has a great affinity for implanted foreign objects, such as catheters. It can also be completely benign the bacterium regularly inhabits our nasal passages without causing disease.
What accounts for the organism's ability to cause such widely different effects in the body? The new study, published in this week's issue of the Proceedings of the National Academy of Sciences, advances the understanding of how this bacterium goes about its unsavory business, says Richard Novick, M.D., Professor of Microbiology and Medicine at NYU School of Medicine, who led the new study.
In the new study, Dr. Novick and co-workers Nikola Vojtov and Hope Ross, Ph.D., demonstrate toxic shock toxin inhibits the genes that encode most of the other toxic proteins produced by Staph. This finding explains why Staph strains causing toxic shock syndrome produce few of the other staphylococcal proteins involved in the causation of disease.
"Our study essentially adds a new dimension to the way we understand bacterial pathogenesis," says Dr. Novick. Understanding how this dangerous bug operates is an important field of research, especially because in recent years Staph increasingly has become resistant to the most commonly used antibiotics. The develop
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Contact: Pamela McDonnell
Pamela.McDonnell@med.nyu.edu
212-404-3555
New York University Medical Center and School of Medicine
8-Jul-2002