SM i have in fact written a paper on the evolution of bacteria, but to steer AWAY from you thinking this is a debate between me and you and back to it being you v the evidence, how about a layman explanation from the journal Nature.
That quote you just added to your last reply (sneaky) does not confirm what you said, once again you have miunderstood the text, see if you can spot the difference now..
You: "If no bacteria is resistant prior to the creation of the antibiotic then all the bacteria would be destroyed"
Your Textbook quote: "antibiotic resistance before exposure to the drug."
Antibiotic Resistance, Mutation Rates and MRSA
By: Leslie Pray, Ph.D. © 2008 Nature Education Citation: Pray, L. (2008) Antibiotic resistance, mutation rates and MRSA.
Suppose another student who had walked into the building just minutes beforehand had left the organism there, after grabbing hold of the same doorknob. Now imagine that you have an open cut on your finger, and some of the bacteria that are on that doorknob get into your wound. Although this seems like a minor event, it could actually have great repercussions for your overall health.
Mutation Rates and Bacterial Growth
Even if only a single S. aureus cell were to make its way into your wound, it would take only 10 generations for that single cell to grow into a colony of more than 1,000 (2 10 = 1,024), and just 10 more generations for it to erupt into a colony of more than 1 million (2 20 = 1,048,576). For a bacterium that divides about every half hour (which is how quickly S. aureus can grow in optimal conditions), that is a lot of bacteria in less than 12 hours. S. aureushas about 2.8 million nucleotide base pairs in its genome. At a rate of, say, 10 -10 mutations per nucleotide base, that amounts to nearly 300 mutations in that population of bacteria within 10 hours!
To better understand the impact of this situation, think of it this way: With a genome size of 2.8 × 10 6 and a mutation rate of 1 mutation per 10 10 base pairs, it would take a single bacterium 30 hours to grow into a population in which every single base pair in the genome will have mutated not once, but 30 times! Thus, any individual mutation that could theoretically occur in the bacteria will have occurred somewhere in that population—in just over a day.
Mutations, Antibiotic Resistance, and Staph Infections
Now, say that a few days after your initial infection with S. aureus, you decide to go to the local health center to have your wound examined. Maybe your finger is not healing as quickly as you had expected. Maybe its red color is a bit worrisome. Maybe the wound is starting to ooze a bit. Maybe you vaguely recall hearing or reading something about some kind of bacterial infection that is popping up on college campuses across the country and landing some students in the hospital. Concerned that your wound might be infected, the physician at the health center decides to prescribe an antibiotic.
Under a best-case scenario, the prescribed antibiotic would kill all of the replicating S. aureus cells in your body, mutant or otherwise, and your wound would quickly heal. After all, the potency of antibiotic treatment is why, when penicillin entered medical care in the 1940s, it was deemed a "miracledrug." Penicillin and other antibiotics have saved countless lives for more than half a century. Under a different scenario, however, any one of those mutations could give your S. aureus infection the ability to resist the particular drug you are being treated with. Luckily, in the real world, usually more than one mutation is required to generate drug resistance, and bacteria cannot double quite so quickly inside a person with a functioning immune system. But the problem still remains: The rapid division of bacterial cells causes them to evolve resistance to most treatments rather quickly.
Thus, although you are on antibiotics and you are otherwise healthy, a total of 600 mutations have accumulated by the time you go to bed that night. Any one of those mutations could give your staph infection the capacity to continue replicating, even in the presence of the antibiotic. All it takes is a single mutated S. aureus—one that, through one of a number of innovative biochemical means, does not die in the presence of whatever antibiotic the physician decided to prescribe—to render that antibiotic useless (at least for this particular infection). Moreover, when that mutant cell replicates, it will pass on its resistant phenotype to its daughter cells, and they to theirs. Thus, a rapidly growing proportion of the replicating bacteria still present in your body will be drug resistant. This is because the drug will kill only those cells that do not have the newly evolved drug-resistance capacity. Thus, the entire bacterial population will eventually become resistant to the prescribed antibiotic. When that happens, your infection will be said to be antibiotic resistant, and your physician will have to prescribe a different drug to combat it.
