Skip to content

AHow resistance appears and spreads

Antibiotic resistance ? A shared drug budget under selection in hospitals, farms and wastewater — stewardship, not a lab manual.

A cell can alter a target, destroy a drug, pump it out, or block entry. Those are categories, not instructions.

Spread is often social: conjugation and other gene transfer move cassettes faster than waiting for a new mutation in every lineage.

Parts

Drug target

Ribosomes, wall-building enzymes and gyrases are classic aims; a changed target may bind the drug less well.

Inactivating enzymes

Beta-lactamases cut penicillins and related drugs. Extended-spectrum and carbapenemase families widened the problem.

Efflux pumps

Membrane pumps lower the internal dose. They often move several chemical classes at once.

Porin change

Gram-negative outer membranes can admit less drug when porin patterns shift.

Plasmids and integrons

Mobile DNA files resistance genes in stacks that can hop between cells.

Persisters vs resistance

Some cells survive a pulse without heritable resistance. That is a different, still conceptual, problem.

Life cycle

1Exposure

A drug reaches a community in a patient, animal or pipe.

2Unequal survival

Susceptible cells fall; already resistant or lucky mutants remain.

3Gene traffic

Plasmids and phages can move successful cassettes to new species.

4Clinical failure

A treatment that used to work fails more often; labs and policies notice.

No protocol for inducing resistance belongs on an encyclopedia page for the public.

Keep exploring

More in Change & defence