antimicrobial resistance
Antimicrobial resistance is when microbes that a drug used to kill evolve the ability to survive it. Picture a lock-picking war: every time we deploy a drug, the few microbes that happen to carry a workaround multiply, and soon the whole population shrugs the drug off.
Resistance arises through Darwinian selection acting on mutation and gene exchange. Bacteria gain it by several mechanisms — making enzymes that destroy the drug, mutating the target so the drug no longer binds, pumping the drug out with efflux pumps, or thickening barriers to keep it out. Crucially, resistance genes can leap between species on plasmids, so a trait that arose in one bug can spread across many.
Every use of an antimicrobial, appropriate or not, applies selective pressure, which is why overuse and incomplete courses accelerate the problem. The honest reality is that resistance is inevitable in the long run; the goal of stewardship and of medicinal chemistry is to slow it, preserve effective drugs, and keep inventing new ones faster than microbes can adapt.
MRSA — methicillin-resistant Staphylococcus aureus — carries an altered penicillin-binding protein that beta-lactams bind poorly, defeating most penicillins and cephalosporins.
A single altered target protein can defeat a whole drug class.
Resistance is a property of the microbe, not the patient: it is the bacterial population that becomes resistant, even though people sometimes loosely say a person is resistant to an antibiotic.