selective toxicity
Selective toxicity is the founding idea of all antimicrobial therapy: harm the invading microbe while leaving the patient's own cells largely untouched. It is the equivalent of a smart bomb that recognises the enemy's uniform; the drug exploits something the pathogen has and we do not, or something it relies on far more heavily than we do.
The cleanest selective targets are features unique to the microbe. Bacteria have a peptidoglycan cell wall that human cells lack, so cell-wall-active drugs like penicillins are extremely safe; bacterial ribosomes and folate-making enzymes differ enough from ours to be attacked with relatively little host harm. The wider the biochemical gap between pathogen and host, the wider the safety margin tends to be.
Selective toxicity is a spectrum, not an absolute. It is easiest for bacteria, harder for fungi (whose cells resemble ours more closely), and hardest of all for viruses, which hijack our own cellular machinery, and for cancer cells, which are our own cells gone wrong. This explains why many antifungal, antiviral and anticancer drugs are more toxic to the patient than antibacterials, and why finding selective targets remains the central challenge of drug design.
Penicillin epitomises selective toxicity: it cripples the bacterial cell wall, a structure human cells simply do not possess.
The bigger the difference between microbe and host, the safer the drug can be.
Paul Ehrlich's early-twentieth-century search for a magic bullet that would strike the pathogen alone is the historical origin of the selective-toxicity concept and of chemotherapy itself.