Why antibiotics don’t work

Bacteria exist in our bodies by the billions. Some 1,000 different species live in the human gut alone. With such a large and thriving population, it’s easy to understand how a few bacteria might randomly acquire traits that make them more resistant to ‘killer’ drugs like antibiotics. Through Darwinian evolution the strongest, most resistant bacteria survive. Bacteria acquire these resistant traits through two mechanisms: genetic mutations or by genetic transfer from other organisms. These new traits effectively block antibiotic particles from reaching their target enzymes inside the bacterial cell wall.

1 Target site

In a normal bacterium the antibacterial treatment attaches to targeted bacterial enzymes, stopping DNA replication.

2 Mutation

Random gene mutations cause the enzymes to change shape or chemical make-up, so the antibacterial agent can’t attach.

3 Efflux pump

Some bacteria have evolved a valve in the cell wall that can actively pump out antibacterial agents as they enter the cytoplasm.

4 Solid cell walls

Antibacterial agents enter via porin, tiny holes in the cell wall. Some mutated bacteria lack sufficient porin to allow a lethal amount in.

5 Inactivation

Some bacteria have evolved destructive enzymes that swim through the cytoplasm, zapping antibiotic agents before they can reach the target site.