More on MRSA

Given the number of comments related to the MRSA article, I thought that I would provide a few thoughts.

MRSA refers to methicillin resistant staphylococcus aureus. For the non-physicians, that means that the old penicillin variants that we once use for staph infections (oxacillin, dicloxacillin, nafcillin) do no work to kill these staph. Staph infections commonly cause skin infections, like boils, but may cause even more serious infections.

Where did MRSA come from? Bacteria develop resistance by natural selection and mutation (the purest form of evolution). Bacteria naturally mutate. When we use antibiotics, we always have a probability that a mutant strain (starting with only 1 bacteria) will occur. If that mutant has resistance to the antibiotic, then it will multiply and become the prodominant infecting bacterial strain.

This process fits our understanding of natural selection perfectly. Unfortunately, staph infections spread easily between patients. Thus, once a mutant is selected and grows, it becomes capable of infecting other patients.

Some bacteria more often develop resistant strains (i.e., they mutate more often). Staph does mutate often.

Even with appropriate antibiotic use, the biology almost insures that resistance will develop. Over the past decade MRSA first became a problem in intensive care units, then hospital wards, and now the general community.

The cow is out of the barn. We now assume that staph are resistant (unless we prove otherwise with cultures and sensitivity testing).

Understanding how staph became methicillin resistant reemphasizes our need to use antibiotics prudently. They are great and powerful aids to treating serious infections. Whenever possible we need to use the most specific antibiotics possible. However, even with perfect antibiotic usage, we will still develop resistance organisms – genetics and evolution drive the development.

Continued research into the mechanisms of resistance will enable us to “defeat” the resistance – at least for a period of time. We can blame the emergence of resistance on many people and antibiotic uses. Our obligation though is to use antibiotics intelligently for clear indications. This will slow the emergence (not stop the emergence) of resistance and give research the opportunity to develop the next generations of antibiotics. We have an ongoing struggle against bacterial, viral and fungal infections. We can win battles, but will always lose some battles also.