Antibiotics work by targeting specific bacterial structures or biological processes that differ meaningfully enough from the corresponding structures or processes in human cells that a drug can damage or disable the bacteria without also seriously harming the patient. This principle, called selective toxicity, shapes which specific bacterial targets antibiotic classes actually go after: the bacterial cell wall, bacterial-specific ribosomes, and enzymes involved in bacterial DNA replication are among the most heavily exploited, precisely because they're different enough from their human equivalents to allow this kind of selective attack.
The bacterial cell wall is a target human cells simply don't have
One major antibiotic class, which includes penicillin and related drugs, targets the synthesis of the bacterial cell wall, a rigid structural layer many bacteria depend on that human cells don't possess at all, since human cells are instead bounded only by a flexible membrane. By interfering specifically with the enzymes bacteria use to build and maintain this cell wall, these antibiotics can severely weaken or destroy susceptible bacteria while having essentially no equivalent target to act on in the patient's own wall-free cells, making this an especially clean example of selective toxicity in practice.
Bacterial ribosomes differ from human ribosomes just enough to be targeted separately
Other major antibiotic classes target bacterial protein synthesis by binding to bacterial ribosomes, the cellular machinery that translates genetic instructions into proteins. Bacterial ribosomes are structurally distinct enough from human ribosomes that certain antibiotics can bind selectively to the bacterial version while leaving human ribosomes largely unaffected, disrupting the bacteria's ability to produce the proteins it needs to survive and reproduce without seriously impairing the patient's own cellular protein production in the process. This structural difference, while real, isn't always perfectly clean, which is part of why some antibiotics in this class carry a greater risk of side effects than cell-wall-targeting drugs do.
What we're still unsure about
The basic principle of selective toxicity, and the specific bacterial targets exploited by major antibiotic classes, are well established, extensively documented pharmacology. What remains a genuinely urgent, actively worked-on area is developing effective new antibiotics faster than bacteria can evolve resistance to existing ones, since discovering a genuinely new antibiotic class with a novel bacterial target has become considerably harder and less commercially incentivised over recent decades than refining existing drug classes — researchers and public health bodies continue to treat this slowing pipeline of new antibiotic discovery as a serious, unresolved problem rather than one already on a clear path to being solved.
This sits inside Antimicrobial Agents & Antibiotic Resistance, one of seven topics in Pharmacology, one of four domains in Medicine, one of seventeen subjects the app can quiz you on.