Over the past decade, strains of the bacteria Staphylococcus have grown increasingly resistant to almost all antibiotics. Most still yield to the "last resort" drug, vancomycin. But cases of related vancomycin-resistant bacteria are on the rise, leading to a growing concern that the ubiquitous S. aureus will develop such resistance and wreak havoc in hospitals and elsewhere. To that end, research appearing in the current issue of the journal Science may offer new hope in the battle against these emerging superbugs. According to the report, researchers have developed a technique that resensitizes vancomycin-resistant bacteria to the antibiotic.

Vancomycin operates by binding to the bacterial cell wall and interfering with cell wall growth. Resistant bacteria, however, have an alteration in the chemical composition of the cell wall that prevents vancomycin from binding to it. To get around that problem, Gabriela Chiosis of Columbia University and Ivo G. Boneca of Rockefeller University designed a small molecule, dubbed SProC5, that cleaves the chemically-altered cell wall component, thereby restoring the bacteria's vulnerability to vancomycin. Exposing resistant Enterococcus faecium (a relative of the staph bacteria) to vancomycin in combination with SProC5 effectively combatted the bacteria in mice, the team found.

Whether the approach will work in humans remains to be seen. But so far, restoring vancomycin sensitivity with molecules that cleave the resistant bacteria's altered cell wall component, the authors conclude, "is a promising strategy."

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