10.2 Antibiotics

Penicillin stops new peptidoglycan molecules from forming the cross-links that strengthen a growing bacterial cell wall.

• A growing bacterium makes small holes in its wall so the wall can stretch; enzymes called autolysins continue to create these holes.
• Normally, new peptidoglycan is added and cross-linked to reinforce the wall. Penicillin prevents the cross-linking step.
• The holes therefore accumulate while reinforcement is reduced, so the wall becomes progressively weaker.
• Bacteria take up water by osmosis. A weakened wall cannot withstand the pressure from inside indefinitely, so a growing susceptible bacterium can burst.

The effect depends on growth: once bacterial growth is complete, autolysins no longer create new holes and no further cross-links form, so this penicillin mechanism is most effective while the bacterium is growing.

Penicillin weakens a bacterial wall by interrupting its reinforcement; it does not dissolve every bacterium immediately. This card stops at the cell-wall mechanism: the distinction between bacterial and viral targets and the development of antibiotic resistance belong to the neighbouring cards.

Antibiotics work against bacterial structures or processes, but a virus is not a bacterial cell. A virus therefore does not provide the bacterial targets that an antibiotic such as penicillin is designed to affect.

• Bacterial target exists: an antibiotic can interfere with a bacterial cell-wall process, membrane protein, enzyme, DNA process or protein-synthesis process. Penicillin, for example, acts on strengthening a growing bacterial cell wall.
• Viral target is absent: viruses have no bacterial-style cell wall and do not carry out growth and reproduction as independent bacterial cells. During replication they use the host cell’s transcription and translation machinery.
• Treatment consequence: blocking a bacterial target cannot stop the virus from using host-cell machinery, so an antibiotic does not treat the viral infection.

This is a target-matching rule, not a diagnosis from symptoms alone. Cholera and TB are bacterial diseases for which antibiotics may be relevant, whereas HIV is viral and is not treated by antibiotics.

“Antibiotics do not affect viruses” means that antibacterial targets are absent from viruses; it does not mean that no medicine can ever act against a virus. Resistance and other reasons for treatment failure are separate topics, not part of this target distinction.

Antibiotic resistance is a population change: a chance mutation can produce a resistance allele, and antibiotic treatment selects bacteria that survive, allowing resistance to become more common.

• Variation first: random mutation creates genetic variation; the antibiotic does not direct a bacterium to mutate.
• Selection: treatment kills susceptible bacteria, while a bacterium with a resistance allele survives with less competition.
• Frequency increases: the resistant survivor reproduces, so its allele is passed to more offspring and becomes more frequent in the population. Short generation times, clonal offspring and horizontal gene transfer can speed spread.
• Clinical consequence: commonly used antibiotics can become less effective; multidrug-resistant strains can make infections difficult to treat and require complicated, expensive treatments that may not be available to everyone.

• Reduce selection: prescribe antibiotics only when needed, do not use them for viral infections, avoid unnecessary wide-spectrum use, complete the prescribed course and tighten control of antibiotic use in agriculture.
• Limit spread: maintain good hygiene, especially handwashing or sanitiser use in clinical settings, and isolate infected patients when resistant strains could spread.
• Maintain options: develop new antibiotics and alternatives, recognising that this is expensive and time-consuming.

Antibiotics select pre-existing resistant variants; they do not train every bacterium or create a targeted mutation. Resistance is a change in allele frequency in a bacterial population, not immunity of the patient. The penicillin wall mechanism and the virus target boundary are covered by the neighbouring cards.