Slowly but surely, modern medicine is losing the battle to infectious bacteria. Blame the overprescription of antibiotics if you want for the rapid development of resistant strains of bacteria – have a sniffle? have some penicillin! – but regardless of the timetable, evolution would eventually win out. Every time somebody gets a bacterial infection and takes antibiotics, there’s a chance that some of those little buggers are going to have some random mutation that allows a few of them to survive. And a few hundred generations later, you end up with a population that has evolved a defense to our treatments.
Naturally, the microscopic arms race continues. When resistant bacteria are found, we hit it with even stronger antibiotics. But I’m sure you can see where this is going. Eventually we run out of stronger drugs to throw at the diseases. This inevitability is why doctors are so loathe prescribing our strongest defenses.
Nonetheless, strings of “super bugs” have sprung up. The most notorious of the bunch is methicillin-resistant Staphylococcus aureus, better known as MRSA. This badass bacteria can be found lurking in hospitals across the country and is responsible for more deaths in this country every year than HIV/AIDS. So as bacteria get stronger and stronger, researchers across the world are looking for new ways to fight back.
And they’re looking in some pretty wild places. For instance, enzymes with antibiotic properties have been found in the blood of animals like pandas. As science writer extraordinaire Ed Yong reminded us recently, however, such discoveries don’t really mean shit until they are at least proven to fight infections in mice.
Well, researchers at the University of Illinois recently crossed that barrier of news-worthyness. In a recent study, a new compound was shown to cure mice infected with MRSA by attacking a new link in the chain of events giving rise to new baby bacteria.
The enzyme known as Farnesyl pyrophosphate synthase (FPPS for short), is a catalyst for other reactions essential for building cell walls. Researchers used computer simulations to look for potential chinks in the armor of the enzyme, but came up empty. Undeterred, they took the most promising compound and tested it against the next enzyme essential to the biological process of building a cell wall, Undecaprenyl pyrophosphate synthase (UPPS this time). This time, they found that the test drug was 1,000 times more active than the first hit they had against the FPPS.
With a promising compound in hand, the team administered the potential drug to 20 mice that were infected with MRSA. All 20 survived.
Of course, years of more studies will be needed to determine if the compound or others like it are effective in humans. However, while other antibiotics also disrupt the building of cell walls, this compound attacks the process from a new angle. And developing drugs that work on different aspects of a disease’s reproduction process is crucial to staying ahead of the evolution of resistance. After all, it’s difficult to simultaneously evolve multiple mutations on a host of genetic stretches that will at the same time protect bacteria from new drugs but also not disrupt their natural functions.
The paper, “Antibacterial Drug Leads Targeting Isoprenoid Biosynthesis,” was published in the Proceedings of the National Academy of Sciences by University of Illinois chemistry professor Eric Oldfield and UC San Diego professor Andrew McCammon.