WASHINGTON: Scientists have cracked the genetic code of superbugs such as MRSA, figuring out why they have become so resistant to anti-bioitics in mixed infections.

Since 2005, superbugs, which included methicillin resistant Staph aureus (MRSA), have killed more than 18,000 people every year in the US alone.

In 2002, a new MRSA with resistance to even the last-line drug vancomycin (VRSA) surfaced. Since the first case in Michigan, there have been other well-documented cases in parts of the US.

Michael Gilmore, professor of ophthalmology at Harvard, who led the study with Veronica Kos, said: "The genome sequence gave us unprecedented insight into what makes these highly resistant bacteria tick. Several things were remarkable.

"Vancomycin resistance repeatedly went into just one tribe of MRSA, so the question became 'what makes that group special -- why did they start getting vancomycin resistance,'" he added.

Scientists at the Centres for Disease Control, Harvard University and elsewhere have been working to determine the origin of these VRSA to understand why they have turned up, and to understand the risk of spread, according to a Harvard University statement.

Most VRSA occurred in foot and limb infections of diabetics who are often in and out of health care facilities.
Each of these infections is believed to have had multiple bacteria, an MRSA plus a vancomycin resistant bacterium called Enterococcus (or VRE).

VRE has caused vancomycin resistant hospital-acquired infections since the 1980s.

"What we found was that this group of MRSA has properties that appear to make it more social, so they can live with other bacteria like Enterococcus. This would allow those MRSA to more easily pick up new resistance," added Kos.

"The good news is that some of these properties weaken the strain's ability to colonize, and may be limiting their spread," said Kos.