antimicrobial resistance
Antimicrobial resistance is when microbes that a drug used to kill or stop now survive and grow despite it. It is evolution in fast-forward: expose a huge bacterial population to a drug, and the rare individuals that happen to withstand it survive, multiply, and pass on their advantage, until the once-reliable drug stops working.
Microbes resist in several ways. They can produce enzymes that destroy the drug, such as beta-lactamases that cleave penicillins; alter the drug's target so it no longer binds; pump the drug out using efflux transporters; or reduce uptake so the drug never gets in. These traits can arise by mutation or, more alarmingly, be shared between bacteria on mobile genetic elements like plasmids, spreading resistance even across species.
Resistance is driven by selection pressure, which means every unnecessary or incomplete course of antibiotics, in humans or in agriculture, accelerates it. The countermeasure is antimicrobial stewardship: prescribing the right drug only when needed, at the right dose and duration, and preserving last-line agents. Resistance is one of the foremost public-health threats of the era, with some infections already approaching the point of being untreatable.
Methicillin-resistant Staphylococcus aureus, MRSA, has altered its penicillin-binding protein so that most beta-lactams no longer bind it.
Altering the drug target is one of the principal routes to resistance.
Resistance is a property of the microbe, not the patient; saying a person is resistant to an antibiotic is a common but misleading shorthand for an infection caused by a resistant organism.