The tendency, under selective pressures, is for organisms to become more fit over time. By applying constant antibiotic-induced generalised selective pressure, you're greatly increasing those odds
"More fit" only makes sense with regards to the pressure. I.e. the bacteria may survive antibiotics, but that may come at the expense of general pathogenicity.
The fact that the gene is not already widespread suggests that in the absence of the selective pressure of the antibiotic it has other effects that decrease fitness in a typical environment.
I agree with your statement if it was a single (or a limited number of) species of antibiotic resistance bacteria.
But, the problem seems to be that they'll be acting more like a gang (where each gang member is a species of bacteria) by multiplying and transferring their weapons (in this case, antibiotic resistant MCR-1 gene) among different bacteria species by means of horizontal gene transfer[1].
Here, horizontal gene transfer means bacteria don't need to carry the "general pathogenicity" as parts of its genome and transfer to future generations (by sexual/asexual re-production)[2]. They only have to be good (and will be damn good by MCR-1 gene) at whatever pathogen they carry. "Horizontal gene transfer" will take care of the rest.
I think we'll get a better idea of the problem I'm trying to explain if we look at it from "Unix philosophy" perspective which "favors composability as opposed to monolithic design"[3]. I hope that I'm decidedly proven wrong in this regard. But, it's just a hope.
Note:
I don't have any formal education/background in medical sciences.
The fact that the gene is not already widespread suggests that in the absence of the selective pressure of the antibiotic it has other effects that decrease fitness in a typical environment.