At the very heart of the growing MRSA crisis in North America is the concept of bacterial resistance to antibiotic therapies. MRSA has found its way into the popular media, and people are becoming accustomed to reading stories about bacterial infections that can’t be treated with standard antibiotics. These stories, however, often gloss over or completely skip one important part – how did these bacteria become impervious to our best medicines in the first place? I’m not talking now about why or how antibiotic overuse and improper use has increased the number of resistant bacterial strains in recent years. Not that that isn’t important, but it’s something I’ve addressed in previous posts. No, I’m talking about how, down at the nitty-grittiest level, one little bacterial cell decides one day that it will no longer be affected by the very poison that was designed specifically to kill it?
I’m going to try not to get too technical in discussing a subject that is inherently technical and scientific in nature. Many clinicians and researchers dedicate entire careers to studying mechanisms of antibiotic resistance, and the detail of understanding now goes right down to the molecular level. Firstly, it must be understood that in many ways a bacterial cell looks and works differently than a cell from our bodies. Bacteria still have a genetic code contained within DNA, but in bacteria some of this DNA floats freely inside the cell, often in circular structures called plasmids. The interesting thing about bacteria is that they can pass plasmids (and thus, genetic code information) amongst each other through a process called plasmid transfer. This process allows certain traits that a single bacterial cell might possess to be shared with nearby bacteria quickly. A second key difference is that a single bacterium can divide into two new cells on its own, without the need for sexual reproduction between two parent cells.