Antibiotics are the bedrock of modern healthcare. Whilst they obviously treat patients infected with life threatening microorganisms, they are also absolutely required in many other areas of medicine to prevent infection; from diabetes to cancer, from emergency surgery to joint replacement in later life. Without them, what we understand and expect from modern medicine would shrink to pre-WW2 levels. Whilst these wonder drugs have changed modern medicine, successive generations have not used them wisely. This has lead to the spread of resistance genes and development of resistance mechanisms in bacteria leading to increasing instances of infections that are difficult to treat in the clinic and community. We call this Antimicrobial resistance: AMR. Simply put, the adaptation of microorganisms to environmental stress, evolution in action.

So how do we address this and what is going on at Warwick in this area? The scientific community is in general agreement that there are certain areas of bacterial metabolism that are their “Achilles heel” and still good areas for antimicrobial drug action and discovery. One of these is the way in which bacteria make their cell walls, the target for lots of existing drugs like penicillin and vancomycin for example. The drugs based on penicillin are successful as they target multiple different versions of the same vital protein activity in the same bacterium simultaneously. As a result the bacteria cannot compensate for this loss of multiple protein function by simple mutation. Whilst some bacteria have developed the ability to degrade the penicillin drug before it reaches its target for example, the target itself still remains vulnerable.

At Warwick we have developed tools and technology to understand these protein targets in a totally new way. Using these tools, we are developing the knowledge base that will help develop the next generation of antimicrobial drugs that hit these old targets in new ways. In addition, we are also conducting research on the ways in which bacteria become resistance to existing antimicrobial drugs. By understanding these processes at a molecular level we will learn how to target these resistance mechanism themselves, so that the old drugs can still be used.

In doing so, we learn how the bacteria adapt in the first place so that future antimicrobial drugs may be used more efficaciously in the future. This is a particularly important point, since in one sense drug resistance is inevitable, but if we learn the lessons of the past we may use old and new drugs more sensibly and effectively, leading to a more healthy and long lived future.