Superbug’s Achilles heel found
Scientists have found a hidden weakness of the superbug MRSA...
If you have ever had an overnight stay in hospital, you may have had a swab taken from your nose or armpit beforehand, to check if you are carrying MRSA: methicillin-resistant staphylococcus aureus. This is an antibiotic-resistant strain of the Staph aureus bacterium that commonly lives on the skin and in the front part of the nose. In these places it is usually harmless, but if it gets into a cut or open wound it can cause a serious - and even lethal - infection.
But in a recent study, a team of researchers in Cambridge were surprised to come across a sample of MRSA that was nevertheless susceptible to two widely-available drugs, penicillin and clavulanic acid, to which MRSA was widely believed to be resistant. Penicillin is one of the oldest antibiotics used in medicine. It works by weakening the bacterial cell wall, causing the bacteria to break apart. Clavulanic acid, on the other hand, works a bit like a decoy, soaking up the molecules bacteria use to attack antibiotics.
When they first spotted their penicillin-sensitive MRSA strain, the researchers thought it was a fluke. But after screening a large number of other MRSA isolates, they found that a large proportion of these were also susceptible to a penicillin-clavulanic acid combination. Intrigued, Ewan Harrison and his colleagues at the Wellcome Sanger Institute went on to decode the genomes of the bacteria to identify which genes had changed to render them susceptible to the antibiotic combo.
To sidestep antibiotics, MRSA produces a protein that deactivates penicillin-like molecules. So the team focused their initial search on the part of the bacterial genome responsible for producing this protein. Compared to strains of MRSA that did not respond, the pencillin-clavulanic acid sensitive bacteria were carrying mutations in this protein. “We found one mutation that lowered the level of this protein,” says Harrison. “And we found another [mutation] that was actually in the protein sequence itself.” The second mutation actually improved the ability of penicillin to bind on.
As well as finding a potential MRSA treatment using widely-available drugs, this study demonstrates a proof-of-principle for the methods used, which could have far wider consequences. Developing new drugs is a lengthy and expensive process. Harrison thinks that the methods of “large-scale surveillance and whole-genome sequencing” that they have employed could in future be used for other drug-resistant bacteria in order to identify possible new treatment options without needing to develop new drugs. The methods could identify new, successful combinations of existing drugs, or Harrison says, “in some cases we may find that bacteria have become resistant to one antibiotic, and that actually makes them susceptible to another.”