evolution in action23 May 2007
Last weekend, right before I went out to mill around and take pictures at the Luis Palau festival, I entertained myself by drinking a few beers and watching the whole of the debate between evolutionists and Kirk Cameron, who claimed he could prove (without faith; with SCIENCE!!) the existence of god. (Hey, we all have our hobbies.). You can watch the first part here, but be warned. There are 18 of them. It’s excruciating at times, and hilarious at others. The best parts are the expressions on the evolutionist girl’s face as she tries alternately not to laugh or to explode in frustration. The evo-guy, on the other hand, had a pretty good poker face up until about halfway through, at which point he had obviously given up the pretense of having a rational debate. So, in light of that, it’s interesting to encounter this:
The spread of multidrug-resistant Staphylococcus aureus (MRSA) strains in the clinical environment has begun to pose serious limits to treatment options. Yet virtually nothing is known about how resistance traits are acquired in vivo. Here, we apply the power of whole-genome sequencing to identify steps in the evolution of multidrug resistance in isogenic S. aureus isolates recovered periodically from the bloodstream of a patient undergoing chemotherapy with vancomycin and other antibiotics. After extensive therapy, the bacterium developed resistance, and treatment failed. Sequencing the first vancomycin susceptible isolate and the last vancomycin nonsusceptible isolate identified genome wide only 35 point mutations in 31 loci. These mutations appeared in a sequential order in isolates that were recovered at intermittent times during chemotherapy in parallel with increasing levels of resistance.
I’ve always wanted to write a blog post with “Staphylococcus aureus” as tag.