Fighting "superbugs" -- strains of pathogenic bacteria that are impervious to the antibiotics that subdued their predecessor generations -- has required physicians to seek new and more powerful drugs for their arsenals. Unfortunately, in time, these treatments also can fall prey to the same microbial ability to become drug resistant. Now, a research team at the University of North Carolina at Chapel Hill (UNC) may have found a way to break the cycle that doesn't demand the deployment of a next-generation medical therapy: preventing "superbugs" from genetically propagating drug resistance.
The team will present their findings at the annual meeting of the American Crystallographic Association (ACA), held July 28 -- Aug. 1 in Boston, Mass.
For years, the drug vancomycin has been the last-stand treatment for life-threatening cases of methicilin-resistant Staphylococcus aureus, or MRSA. A powerful antibiotic first isolated in 1953 from soil collected in the jungles of Borneo, vancomycin works by inhibiting formation of the S. aureus cell wall so that it cannot provide structural support and protection. In 2002, however, a strain of S. aureus was isolated from a diabetic kidney dialysis patient. This particular strain would not succumb to vancomycin. This was the first recorded instance in the United States of vancomycin-resistant Staphylococcus aureus, or VRSA, a deadly variant that many now consider one of the most dangerous bacteria in the world.