Breaking the chain
Infection control aims to interrupt the chain of transmission. Hand hygiene removes or kills microbes on skin. Standard precautions treat blood and body fluids as potentially infectious and use barriers such as gloves and masks. Aseptic technique keeps unwanted microbes out of a sample or wound: in the lab, flaming an inoculating loop before and after use destroys contaminants. Cleaning, disinfecting surfaces and sterilising instruments reduce the number of microbes in the environment.
How antimicrobials work
This section describes ideas only and is not guidance on treatment or on choosing a drug. The key concept is selective toxicity: a useful antimicrobial harms the microbe far more than the host. It works best where microbes have a structure or pathway that human cells lack. Common targets include:
- Cell wall synthesis. Beta-lactam drugs interfere with the cross-linking of peptidoglycan; human cells have no peptidoglycan.
- Protein synthesis. Some drugs bind the bacterial 30S or 50S ribosomal subunit; human cytoplasmic ribosomes are 80S.
- Nucleic acid synthesis and folate pathways.
- Cell membrane integrity.
Drugs can be bacteriostatic (stop growth) or bactericidal (kill). A narrow-spectrum drug acts on few groups; a broad-spectrum drug on many. Antibacterials do not act on viruses, which have no cell wall or ribosomes of their own. The minimum inhibitory concentration (MIC) is the lowest concentration that prevents visible growth in a test culture.
Resistance
Resistance means a microbe survives a drug that once stopped it. Main mechanisms: an enzyme destroys the drug (for example beta-lactamase breaks the beta-lactam ring); the target changes so the drug no longer binds; efflux pumps push the drug out; or permeability falls. Resistance arises by random mutation or by gaining genes, often on plasmids passed through conjugation.
Worked example: selection pressure
Imagine a flask of 1,000,000 bacteria in which 1 cell in 1,000,000 carries a resistance mutation, so 1 resistant cell.
- Add a drug that kills susceptible cells. About 999,999 die. The resistant cell survives.
- With competitors gone, the resistant cell divides. After 20 generations, 2 to the power 20 is 1,048,576 descendants, all resistant.
- The drug did not cause the mutation; it selected for a trait already present.
- If the resistance gene sits on a plasmid, conjugation can pass it to other species, spreading resistance sideways.
This is why using drugs more than necessary increases the chance that resistant strains become common.