Homeostatic mechanisms optimise our cellular chemistry. #antibiotics treatments are developed specifically to work in our narrow-band homeostatic chemical milieu to be delivered through blood to #infection sites for intimate combat with #bacterial invaders.
With #cystitis, the bacteria are planktonic in urine and attached to urothelial cell membranes, so are too far away to be influenced by that approach. For #antibiotic tablets to have any chance to be effective against cystitis uropathogens, they enter the system, but must exit via the kidneys (offering nothing good during that part of their journey), in order to enter the #bladder cavity to confront the enemies. The drugs being only dripped into an infected #urinary pool, of sometimes hundreds of millilitres, that constraint could offer #bacteria sufficient time to develop #AMR before the #urinary drug concentration reaches a therapeutic level. Furthermore, there are no homeostatic controls to ensure a drug would work as developed for the completely different environment.
Although some bacteria would die even in the sub-therapeutically toxic urine milieu, to produce symptom relief enough of them could survive the course to produce plenty of descendants to resume aggressive battle. We call that “recurrent infection.”
In military terms, it’s allowing your enemies to blow up your own ammunition depots. But we’d only know about it retrospectively, when patients present with recurrent infections, when we might see “Resistant” next to antibiotic sensitivity results. Drip-feed, dilution and no homeostasis; that’s three strikes against the treatment. If that isn’t bad enough, consider the likely side effects and gut microbiome damage the drugs could cause along the circuitous journey from mouth to battlefield.
Given oral antibiotics are deployed so commonly in battles with cystitis, can anyone suggest how much AMR might have emerged this way in accordance with the most rigorous antibiotic stewardship?