What counts as a drug?

The IGCSE Biology definition is precise: a drug is any substance taken into the body that modifies or affects chemical reactions in the body. That single sentence is worth memorising word-for-word, because examiners penalise vague alternatives such as "a substance that changes how the body works." The key phrase is chemical reactions.

Notice that the definition says nothing about whether the effect is helpful or harmful. Paracetamol is a drug. Caffeine is a drug. Alcohol is a drug. An antibiotic prescribed by a doctor is a drug. The classification depends on how the substance interacts with the body's chemistry, not on whether it arrives in a blister pack or a coffee cup.

Categories worth knowing

The syllabus does not demand a full taxonomy of drug types, but understanding the broad categories helps you answer discussion questions confidently:

  • Therapeutic drugs - prescribed or used to treat disease or relieve symptoms (antibiotics, painkillers, antivirals)
  • Recreational drugs - taken for their effect on the mind or body rather than to treat illness (alcohol, nicotine, caffeine)
  • Performance-enhancing drugs - used to improve physical ability (anabolic steroids, stimulants)

For your Cambridge IGCSE exam, the syllabus zeroes in on one therapeutic category above all others: antibiotics.

Antibiotics: the logic of how they work

An antibiotic is a drug that kills bacteria or prevents them from reproducing. The reasoning behind this is structural. Bacteria are living cells with their own metabolic machinery: they have cell walls, ribosomes that synthesise proteins, and enzymes that copy DNA. Antibiotics target one or more of these bacterial structures.

Penicillin, for example, interferes with the construction of the bacterial cell wall. Without a functional wall, the bacterium absorbs water by osmosis, swells and bursts. Other antibiotics block bacterial ribosomes so the bacterium cannot make the proteins it needs to survive.

Exam strategy: When a question asks why antibiotics are effective against bacteria, frame your answer around the target: antibiotics attack structures or processes specific to bacterial cells, such as cell wall synthesis or protein production on bacterial ribosomes.

Why antibiotics do not work on viruses

This is one of the most frequently tested distinctions in the entire IGCSE Biology course. The reasoning is straightforward once you follow the logic:

  1. Viruses are not cells. They have no cell wall, no ribosomes and no independent metabolism.
  2. A virus reproduces by injecting its genetic material into a host cell and hijacking the host's own machinery to make copies of itself.
  3. Antibiotics target bacterial cell structures. Since viruses lack those structures, there is nothing for the antibiotic to act on.
  4. To destroy the virus you would need to destroy the host cell it occupies, which is exactly what the body's own immune system attempts to do.
FeatureBacteriaViruses
Cell structureComplete cell with cell wall, membrane, cytoplasm, ribosomes, DNANot a cell; protein coat surrounding genetic material (DNA or RNA)
ReproductionBinary fission (independent)Must hijack a host cell
MetabolismOwn metabolic reactionsNo independent metabolism
Affected by antibiotics?YesNo
Treated byAntibioticsThe immune system (antivirals may slow replication but do not "cure")

Antibiotic resistance: a natural selection problem

The syllabus states that some bacteria are resistant to antibiotics, which reduces the effectiveness of antibiotics. The Supplement objective goes further: you need to explain how resistance develops and why limiting antibiotic use helps.

The mechanism is a textbook case of natural selection. Follow it step by step:

  1. Variation exists. In any large population of bacteria, random mutations mean that a few individuals carry a gene that makes them resistant to a particular antibiotic.
  2. Selection pressure is applied. When a patient takes the antibiotic, the non-resistant bacteria are killed. The resistant ones survive.
  3. Survival and reproduction. With competition removed, the resistant bacteria multiply rapidly.
  4. Inheritance. The offspring inherit the resistance gene. Within a short time the entire population is resistant.
  5. Spread. Resistant bacteria can transfer to other people through direct contact or contaminated surfaces.
Key reasoning point: The antibiotic does not cause the mutation. The mutation already existed. The antibiotic simply removes non-resistant individuals, giving the resistant ones a selective advantage. This distinction trips up many students.

MRSA: a worked example

MRSA stands for methicillin-resistant Staphylococcus aureus. It is the exam board's go-to example of antibiotic resistance, so treat the following as required knowledge.

Staphylococcus aureus is a common bacterium found on human skin and in the nose. Most strains are harmless or cause minor skin infections treatable with standard antibiotics. However, through the natural selection process described above, some strains acquired resistance to methicillin and related antibiotics.

MRSA infections are difficult to treat because the usual first-line antibiotics fail. Doctors must use alternative, often more expensive and less convenient antibiotics. In hospitals, where patients already have weakened immune systems, MRSA can cause serious wound infections, bloodstream infections and pneumonia.

(Extended/Supplement) The spread of MRSA is directly linked to overuse and misuse of antibiotics. Every unnecessary prescription creates another round of selection pressure, favouring resistant strains. This is why public health campaigns urge patients to complete their full course of antibiotics (to kill all bacteria, not just the susceptible majority) and why doctors are encouraged to prescribe antibiotics only when a bacterial infection is confirmed.

Limiting resistance: the prescription logic

(Extended/Supplement) The Supplement objective asks you to explain how using antibiotics only when essential can limit the development of resistant bacteria. The reasoning chain is:

  • Fewer prescriptions mean fewer selection events where resistant bacteria gain an advantage.
  • Completing the full course ensures that even partially resistant bacteria are killed, reducing the chance of a resistant population surviving.
  • Not using antibiotics for viral infections (where they have no effect) removes pointless selection pressure on bacteria that happen to be present in the body.
  • Agricultural use of antibiotics in animal feed accelerates resistance because it exposes vast bacterial populations to sub-therapeutic doses, the perfect conditions for resistance to evolve.

The effects of specific drug types on the body

While the syllabus focuses on antibiotics, understanding how other drug categories affect the body strengthens your exam answers, particularly in discussion-style questions.

Drug typeExampleEffect on the bodyRisk
DepressantAlcoholSlows nerve impulse transmission, reduces reaction time, impairs judgementLiver damage, addiction, impaired coordination
StimulantCaffeine, nicotineSpeeds up nerve impulse transmission, increases heart rate and alertnessRaised blood pressure, dependency, sleep disruption
PainkillerParacetamol, aspirinBlocks pain signals or reduces inflammationOverdose risk, stomach damage (aspirin)
AntibioticPenicillinKills bacteria or prevents bacterial reproductionAllergic reactions, antibiotic resistance if misused

The common thread is that every drug on this list modifies chemical reactions in the body. Depressants alter the chemistry of synaptic transmission. Stimulants increase the release of neurotransmitters. Painkillers block the enzymes that produce pain-signalling chemicals. Each one fits the IGCSE definition precisely.

Drug testing and clinical trials

Although the Cambridge IGCSE syllabus does not go into great depth on clinical trials, examiners occasionally set questions on why new drugs must be tested before they can be prescribed. The core reasoning is safety and efficacy:

  • Laboratory testing - the drug is tested on cells and tissues to check for toxicity.
  • Animal testing - used to check for side effects in a living organism (this stage raises ethical questions that examiners sometimes ask about).
  • Clinical trials on human volunteers - conducted in phases, starting with small groups to check safety, then larger groups to confirm effectiveness.
  • Peer review and approval - results are reviewed by independent scientists before the drug is licensed.

The process is lengthy because a drug that modifies chemical reactions in the body could have unpredictable effects. Rushing it risks releasing a substance that causes more harm than the disease it treats.

Exam strategy: If asked to "discuss" or "evaluate" drug testing, present both sides. Animal testing provides safety data that protects human volunteers, but raises ethical concerns about animal welfare. A balanced answer that acknowledges both points will score higher than one that takes only a single position.

Common exam mistakes

  1. Confusing antibiotics with antibodies. Antibiotics are drugs. Antibodies are proteins produced by white blood cells (lymphocytes) as part of the immune response. They sound similar, but they are completely different concepts. An antibiotic is something you swallow or inject. An antibody is something your body manufactures.
  2. Saying antibiotics "cure" viral infections. They do not. Antibiotics have zero effect on viruses. If a question describes a patient with the flu being given antibiotics, the correct response is that this is inappropriate because influenza is caused by a virus.
  3. Claiming the antibiotic causes the mutation. The mutation arises randomly before the antibiotic is introduced. The antibiotic selects for pre-existing resistant individuals.
  4. Writing that resistant bacteria are "immune" to antibiotics. The correct term is resistant, not immune. Immunity is a property of organisms with immune systems. Bacteria do not have immune systems.
  5. Forgetting to mention reproduction. When explaining resistance, students often stop at "the resistant bacteria survive." You must add that they reproduce rapidly, passing the resistance gene to offspring, so the resistant population grows.

Self-check questions

  1. Define the term "drug" using the precise IGCSE Biology wording.
  2. Explain why antibiotics are effective against bacteria but not against viruses. Your answer should refer to cell structure.
  3. A doctor prescribes antibiotics for a patient with a bacterial throat infection. The patient feels better after three days and stops taking the tablets, even though the full course is seven days. Explain why stopping early increases the risk of antibiotic resistance developing.
  4. Describe the steps by which a population of bacteria can become resistant to an antibiotic. Use the term "natural selection" in your answer.
  5. MRSA is described as a "superbug" in the media. Explain what makes MRSA difficult to treat and suggest one measure hospitals can take to reduce its spread.

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TLDR

This guide breaks down everything the IGCSE Biology syllabus requires on drugs, antibiotics, antibiotic resistance and MRSA, with comparison tables, the natural selection mechanism behind resistance, common exam traps and self-check questions.