Antibiotics

1. Overview

Antibiotics are chemicals that kill bacteria or stop them growing without damaging human cells. They work because bacterial cells have structures and processes that human cells do not, such as a peptidoglycan cell wall and 70S ribosomes, which the antibiotic can target. Penicillin is a classic example: it stops growing bacteria building their cell walls. Because viruses have no cell wall and carry out no metabolism of their own, antibiotics cannot affect them. The widespread, and often careless, use of antibiotics has applied a selection pressure that favours resistant bacteria, so resistant strains have spread. This topic covers how penicillin acts, why viruses are unaffected, how resistance arises and spreads, and the steps needed to reduce its impact.

Key Definitions

• Antibiotic: a chemical, originally made by a microorganism such as a fungus or bacterium, that kills or inhibits the growth of bacteria without harming human cells.
• Penicillin: an antibiotic that prevents the formation of cross-links in the peptidoglycan (murein) cell wall of growing bacteria.
• Bactericidal antibiotic: an antibiotic that kills bacteria, for example by causing the cell to burst.
• Bacteriostatic antibiotic: an antibiotic that stops bacteria growing and dividing without directly killing them.
• Antibiotic resistance: the ability of bacteria to survive and grow in the presence of an antibiotic that would normally kill them or stop their growth.
• Selection pressure: an environmental factor, such as the presence of an antibiotic, that favours the survival and reproduction of individuals with a particular allele.
• Capsid: the protective protein coat that surrounds the genetic material of a virus particle.
• Plasmid: a small circular piece of DNA, separate from the main chromosome, that can carry resistance genes and pass between bacteria.
• Conjugation: the direct transfer of a plasmid from one bacterium to another through a connecting tube (pilus).

Content

In a nutshell: antibiotics attack features that only bacteria have (cell wall, 70S ribosomes). Penicillin weakens the wall so the cell bursts. Viruses lack these features, so antibiotics do nothing to them. Overuse selects for resistant bacteria, which spread fast via plasmids - so we must use antibiotics carefully.

How penicillin acts on bacteria

A bacterial cell wall is made of peptidoglycan (also called murein), a mesh of sugar chains held together by short cross-links between amino acids. These cross-links give the wall its strength and let it resist the high internal pressure of the cell.

When a bacterium grows and divides it must make new wall material, so enzymes break and re-form the cross-links. Penicillin inhibits the enzyme that forms these cross-links (a transpeptidase). The new wall that is built is therefore weak, because its cross-links are missing.

Water continues to enter the cell by osmosis, raising the internal pressure. With no strong wall to resist it, the weakened wall cannot hold, so the cell swells and bursts (lyses) and dies. Penicillin is therefore bactericidal. Importantly, it only affects bacteria that are actively growing and making new wall; cells that are not dividing keep their existing intact wall and are not destroyed.

Why penicillin does not harm human cells

Penicillin acts on a structure that human cells do not have: a peptidoglycan cell wall. Human cells are bounded only by a cell surface membrane, so there is no target for penicillin and our cells are unaffected. This is why a good antibiotic shows selective toxicity - it harms the pathogen but not the host.

Other antibiotic targets

Not all antibiotics attack the cell wall. Some bind to the bacterial 70S ribosomes and block translation, so the bacterium cannot make the proteins it needs. Human cells use larger 80S ribosomes, so these antibiotics do not interfere with our protein synthesis.

The key skill is to match the mechanism to the target:

If the antibiotic acts on...	Then explain its effect on...	Why human cells are safe
The peptidoglycan cell wall (e.g. penicillin)	Cross-link formation to weakened wall to lysis	Human cells have no cell wall
The 70S ribosomes	Protein synthesis (translation) is blocked	Human cells use 80S ribosomes

If a question describes an antibiotic as acting on ribosomes, write about protein synthesis, not the cell wall.

Why antibiotics do not affect viruses

A virus particle is not a cell. It consists of a genome of either DNA or RNA (never both) surrounded by a protein capsid; many also have a lipid envelope. A virus therefore has:

• no cell wall for penicillin to target;
• no ribosomes of its own - it hijacks the host cell's ribosomes to make its proteins;
• no metabolism of its own outside a host cell.

Because antibiotics work by attacking bacterial structures and processes, and viruses have none of these (and replicate inside human cells), antibiotics have no effect on viruses. Viral infections are instead treated with antiviral drugs that target stages of the viral replication cycle.

How antibiotic resistance arises

Resistance begins with mutation. By chance, a random mutation in a bacterial gene may give a cell an advantage, for example:

• an enzyme that breaks down the antibiotic (such as penicillinase, which destroys penicillin);
• a change in the target so the antibiotic no longer binds;
• a pump that removes the antibiotic from the cell.

When an antibiotic is present it acts as a selection pressure: non-resistant bacteria are killed, but the rare resistant cell survives. It then reproduces (by binary fission), passing the resistance allele to its offspring, so the proportion of resistant bacteria in the population rises. This is natural selection acting on bacteria.

Note the precise language: the bacteria become resistant - humans do not become "immune to antibiotics". These two words describe completely different things:

Term	What it applies to	What it means
Immunity	A host organism (e.g. a human)	The body's defence against a particular pathogen
Resistance	A pathogen (e.g. bacteria)	The pathogen's ability to survive a drug that would normally kill it

How resistance spreads

Resistance genes are often carried on plasmids. Bacteria can pass plasmids from one cell to another by conjugation, so a resistance allele can spread between different bacteria, even of different species, not only to offspring. Combined with the very short generation times of bacteria, this allows resistance to spread through populations remarkably quickly. Resistant strains can then spread between people through poor hygiene, especially in places such as hospitals (for example MRSA, methicillin-resistant Staphylococcus aureus - note the capital genus and lowercase species).

Consequences of resistance

• Common infections become harder or impossible to treat with first-choice antibiotics.
• Doctors must use stronger or last-resort antibiotics, which may cause more side effects and cost more.
• The risk of untreatable infections rises, increasing illness and deaths.
• Routine medicine is threatened: surgery and cancer treatment rely on antibiotics to prevent infection, so they become far riskier.
• Strains resistant to several antibiotics ("multidrug-resistant") are especially dangerous.

Steps to reduce the impact of resistance

• Prescribe antibiotics only when needed - not for viral infections such as colds and flu, against which they do nothing.
• Complete the full course so that all the target bacteria are killed and partly resistant survivors are not left to reproduce.
• Use narrow-spectrum antibiotics where possible, targeting the specific pathogen and disturbing fewer harmless bacteria.
• Rotate the antibiotics used and avoid relying on one drug.
• Reduce use in farming, where antibiotics have been added to animal feed to promote growth.
• Maintain good hygiene, such as handwashing and isolating infected patients, to limit spread.
• Develop new antibiotics and alternative treatments to stay ahead of resistant strains.

Worked example

Exam-style question: A patient with a sore throat is found to have a viral infection. The doctor refuses to prescribe an antibiotic and explains that overusing antibiotics increases resistance. Using your knowledge of biology, explain (a) why an antibiotic would not help this patient, and (b) how unnecessary antibiotic use leads to resistant bacteria. [5]

Model answer:

• (a) Antibiotics act on bacterial structures such as the cell wall and 70S ribosomes; a virus has no cell wall, no ribosomes and no metabolism of its own, so there is no target for the antibiotic and it cannot affect the virus. [2]
• (b) A random mutation arises by chance in some bacteria before any antibiotic is used, producing resistance, for example an enzyme that breaks down the antibiotic. [1]
• The antibiotic does not cause this mutation; it acts as a selection pressure that kills non-resistant bacteria but allows the resistant ones to survive. [1]
• The surviving resistant bacteria reproduce and pass on the resistance allele (and can spread it via plasmids), so the proportion of resistant bacteria increases. [1]

Key Equations

This topic is qualitative: it is assessed through explanation and biological reasoning rather than calculation, so there are no equations to learn.

Common Mistakes to Avoid

• Saying humans become "immune to antibiotics". Antibiotics target bacteria, not human cells, so only bacteria can become resistant. Reserve "immunity" for an organism's defence against a pathogen.
• Confusing "immunity" with "resistance". Immunity is the host's defence against infection; resistance is a pathogen surviving a drug. Use the right term for the right thing.
• Describing a virus as having both DNA and RNA, or a carbohydrate coat. A virus particle has a genome of either DNA or RNA and a protective protein coat called a capsid.
• Using penicillin's cell-wall mechanism to explain a different antibiotic. If you are told an antibiotic binds to ribosomes, explain its effect on protein synthesis (translation), not on the cell wall.
• Saying the antibiotic "causes" or "triggers" the mutation. The resistance mutation arises by chance, before the antibiotic is present; the antibiotic only selects for bacteria that already carry it.
• Saying penicillin "kills all bacteria instantly". It only affects bacteria that are actively growing and building new wall; the weakened wall then bursts by osmosis.
• Writing scientific names incorrectly. Capitalise the Genus and use lowercase for the species, and italicise or underline, e.g. Staphylococcus aureus.
• Saying water or food is "infected" with a pathogen. Abiotic things like water and food are contaminated; living hosts are infected.

Exam Tips

• For "how penicillin works", build a clear chain: inhibits cross-link formation in peptidoglycan to weakened wall to water enters by osmosis to cell bursts (lyses).
• For "why viruses are unaffected", give specific reasons: no cell wall, no ribosomes, no own metabolism, and they replicate inside host cells.
• When explaining resistance, always include the full sequence: mutation to selection pressure to survival of resistant bacteria to reproduction/spread of the allele.
• For "steps to reduce resistance", give distinct measures (prescribing, completing the course, hygiene, farming, new drugs) rather than rewording the same point.
• The word "discuss" is a high-tariff command word that wants a balanced range: set out several distinct consequences and several distinct measures, and then add a limitation - for example that completing the course depends on patient behaviour, or that developing new antibiotics is slow and costly - rather than a one-line list.
• Watch your wording: resistant bacteria, not "immune" bacteria; contaminated/infected used correctly will earn marks.
• If the question gives you information about an antibiotic's target, use that information to shape your answer rather than defaulting to the penicillin mechanism.