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You are reporting one side of a three-sided coin. You can find instances of phage resistance linked to increased antibiotic susceptibility, decreased antibiotic susceptibility, and in most cases no change in antibiotic susceptibility. Studies linking phage resistance to increased antibiotic susceptibility are based on in vitro selections resulting in genetic disruptions that would never arise in a host, and are likely due to the relaxation of selective pressures when bacteria are grown in rich broth. For example, phage that use LPS as a receptor cannot infect cells with LPS defects, but those cells are so sick and mucoid that they become susceptible to just about any other stress, including antibiotics. We never isolate bacteria with LPS defects in the wild because they would go extinct in any competitive environment.

The real lessons we need to learn from phages and other antibacterial systems is that resistance is inevitable. These systems have built in flexibility and modularity to accommodate changes and mutate rapidly. Almost all of these systems follow a similar pattern: bind to target cell, get inside target cell, destroy target cell. There are many ways to accomplish each of those steps, and these systems are set up to rapidly evolve new ways accomplish each. This evolution is not limited to the slow single mutations we often associate with evolution. We often observe recombination where another target cell binding domain can be swapped in to generate a new functional system.

Modern phage therapy advocates suggest combination therapies, where multiple antibacterial agents are deployed to substantially lower the rate of resistance. But we will never get that number to zero. Also phage therapy is limited in efficacy based on the site of infection (phage do not penetrate tissues like small molecule antibiotics do) Instead of evolution being a brick wall for therapy, we need to play the game. We need to get off of broad-spectrum antibiotics, focus on functional modules (like cell entry, cell toxicity, etc), and reform our regulatory structure to enable mixing and matching of these modules in regimented phases in response to the resistance that we know will arise. Phage therapy is not the answer; the phage evolutionary cycle is the answer.

I understand what you're saying about drift, but I'm not sure that feels sufficient to explain the prevalence of anti-biotic resistance. You're right to highlight that the genes for antibiotic resistance already exist and it's just a question of how prevalent they are in different populations/generations, but I don't think this excludes it from being evolution. I would consider the human use of antibiotics in medicine and agriculture to be a selective pressure that is increasing the prevalence of antibiotic resistant genes in bacteria, especially in combination with human activities that facilitate the global spread of antimicrobial resistance.

I agree that "evolution" is a pretty muddy term though, which is made trickier by the fact that with how language evolves, some people use it in a different sense than what is probably strictly "correct". I'm a biochemist, for example, and I don't know if I could give a strictly correct definition for evolution. Along those lines, I realise I may be misinterpreting your point.

Separate to all that, it sounds like you're well versed on the bacteriophage stuff, are there any articles that you think cover the topic well? I'm more of a protein structure gal myself, so I only have patchy, undergrad level knowledge of microbiology stuff.

Your comment is confusing. Yes, genetic drift is evolution, so saying "people cite evolution" and then dismissing it is not a good approach.

Perhaps you mean it isn't natural selection, but then the trait being under balancing selection (a tradeoff between phage resistance and antibiotic resistance) is still under selection. And the presence of antibiotics shifts the balance heavily in favor of resistance even if that means decreasing resilience in the absence of antibiotics.

You say the traits are already there and just need to be expressed, so perhaps it's mutation you think is not happening. That's often the case, but it still took mutation to create the means of resistance to begin with. Some of it is passed around on plasmids, but they the traits had to evolve in the first place. In addition, once resistance becomes dominant, there is enough diversity to select for compensatory mutations that increase the fitness of the resistant bacteria. Things like compensating for cell wall weaknesses or pumps that were initially favored despite their drawbacks.