London, Apr 12 (ANI): For the first time, researchers at Michael G. DeGroote Institute for Infectious Disease Research, have uncovered how bacteria recognize and develop resistance to a powerful antibiotic used to treat superbug infections.
Led by Gerry Wright, a professor in the Department of Biochemistry and Biomedical Sciences at McMaster University, the researchers have identified the specific mechanism that triggers resistance to vancomycin.
The discovery reveals new understanding about what is happening at the molecular level in vancomycin resistance.
It also represents an essential first step in developing new antibiotics that can evade the sensing mechanism of bacteria and overcome resistance.
"Vancomycin is the antibiotic of last resort and is only given when all other treatments fail," said Wright.
"For years it was thought that resistance would be slow to emerge since vancomycin works in an unusual way. But with the widespread use of the drug to treat infections caused by the hospital superbug MRSA, it has become a serious clinical problem," he added.
MRSA is the short-form for methicillin-resistant staphylococcus aureus, a bacterial infection that is highly resistant to some antibiotics.
MRSA bacteria are responsible for a large percentage of hospital-acquired staph infections, but may also be acquired in the community.
Vancomycin is used to treat enterococcal infections that develop in patients following abdominal surgery.
For 20 years, scientists around the world have debated whether bacteria sense the drug itself to trigger resistance or whether they sense the impact it has on the cell wall of bacteria.
Most antibiotics work by inhibiting an enzyme but vancomycin binds to cell wall building blocks, causing a weakness in the structure of the cell wall so the cell bursts and dies.
The researchers studied the vancomycin-resistance mechanism in the harmless soil bacteria Streptomyces coelicolor.
The scientists showed that bacteria detect vancomycin itself.
They also conducted preliminary experiments that suggest the same mechanism exists in disease causing bacteria.
"We have finally cracked the alarm system used by bacteria, and hopefully new antibiotics can be developed that don't set it off," said Mark Buttner, a study collaborator and senior scientist at the John Innes Centre.
The study has been published online in the high-impact journal Nature Chemical Biology. (ANI)