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Last Updated: Saturday, 28 July 2007, 23:54 GMT 00:54 UK
Gene clues from dying MRSA victim
MRSA - Pfizer
MRSA can be deadly
Scientists have built a compelling genetic picture of how lethal superbug MRSA changed day-by-day to overwhelm a heart patient.

It shows how it mutated to beat even the most powerful antibiotics used by doctors fighting to save his life.

The plight of the unnamed man, tracked by New York's Rockefeller University, features in Proceedings of the National Academy of Sciences.

They hope it will improve understanding of how bacteria adapt and survive.

The research shows a very clear chain of events, and will hopefully help us come up with new targets for future antibiotics
Dr Mark Enright, Imperial College London

MRSA (Methicillin resistant Staphylococcus aureus) poses a serious problem for all hospitals.

Patients left weakened by serious illness or surgery are particularly vulnerable to strains of the bacteria which are much harder to kill using conventional antibiotics.

Winning formula

Recent years have seen the emergence of bacteria which have developed some resistance even to very powerful drugs such as vancomycin, traditionally held back to use as a last resort.

The precise mechanisms by which bacteria adapt to survive antibiotic attack are not completely clear, although the more often that bacteria are exposed to a particular drug, the more likely it is that it will, by chance, come up with a winning genetic formula.

This is why the overuse of antibiotics in human and animal medicine is partly blamed for the rise of MRSA.

The Rockefeller team looked closely at six blood samples taken over the final three months in the life of the man, who had picked up an MRSA infection in his heart valve.

They broke down the entire genetic structure of the bacteria found in the samples, and recorded how the genetic code changed during the 12 week period.

During this time, doctors unsuccessfully tried a number of different types of antibiotic, including vancomycin.

Real time results

The results from virtually every blood sample showed small genetic shifts, including several known to be linked to bacteria increasing their resistance against antibiotics.

In particular, bacteria from the first sample showed no genetic signs of vancomycin resistance - but a few samples later, they were far better equipped genetically to survive the drug.

Writing in the journal, the team predicted that as the cost and speed of this type of genome analysis fell in future, then doctors would be able to track the progress of infections in 'real-time', adjusting a patient's medication as drug resistance emerged.

Dr Mark Enright, a researcher on antibiotic resistance from Imperial College London, said that the paper represented a 'smoking gun' on the methods used by the bacteria as they became resistant to vancomycin.

He said: "Fortunately this type of infection is very rare, and, as this case shows, it becomes very difficult to treat when it is this deep seated.

"The research shows a very clear chain of events, and will hopefully help us come up with new targets for future antibiotics."

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