I guess I'll repost and slightly edit my stuff from the other thread:
that experiment does not address the origin of the resistant bacteria, it simply proves that resistant strains exist and are in the wild.
actually, what it does address is the fact that exposure to a treatment has nothing to do with whether resistance develops or not. It just happens that way at random.
It's kinda like how Lamarck and Darwin had differing opinions on how giraffes got longer necks. Darwin's idea, which is currently the one accepted today, is that Giraffes did not develop longer necks specifically because they needed to get to that higher foliage, it just happened that giraffes with longer necks had a better chance of survival. Those giraffes had little long necked babies and they flourished, having spread their advantageous phenotype to the next generation.
Just the same with bacteria. Bacteria did not suddenly adapt to antibiotics specifically because they were exposed to them, it just happened that bacteria existed that were resistant, having been born with a random mutation that makes them different, and had a better chance of survival. Those bacteria flourished through dividing or transferring their genetic info "horizontally*" and flourished, having spread their advantageous phenotype to generations in both their own and subsequent levels of the phylogenetic tree.
so to reiterate, in answering the question, "how do resistant strains exist?" Current evidence points to "it just happened at random." Given that gazillions of any one species of bacteria are created at any moment, it's not hard to believe. Selective pressure (such as antibiotic use or misuse) just accelerates the process by making the environment favorable to certain bacterial types, forcing them to adapt, by (again) random mutation.
*basically, one bacteria shares genetic information (which can include resistance) to another without creating offspring, which helps a bacteria evolve.
that's pretty much all I have to say about it.