outline how bacteria become resistant to antibiotics as an example of natural selection

Natural and Artificial Selection (Cambridge A‑Level Biology – Topic 17)

Learning Objective

Outline how bacteria become resistant to antibiotics as an example of natural selection.

1. Natural Selection – Core Concepts

  • Variation – Individuals in a population differ in heritable traits.
  • Differential survival & reproduction – In a given environment some variants leave more offspring than others.
  • Inheritance – The advantageous traits are passed to the next generation.
  • Change in population over time – The frequency of the advantageous trait increases.

2. Sources of Genetic Variation

  • Spontaneous mutation – Errors in DNA replication (e.g., point mutations, insertions, deletions).
  • Sexual recombination (in eukaryotes) – Crossing‑over and independent assortment during meiosis generate new allele combinations.
  • Gene flow – Movement of individuals (or their gametes/plasmids) between populations introduces new alleles.
  • Horizontal gene transfer (HGT) in bacteria

    • Conjugation – plasmid transfer via a pilus.
    • Transformation – uptake of free DNA from the environment.
    • Transduction – bacteriophage‑mediated DNA transfer.

3. Fitness and Selective Pressure

  • Relative fitness (w) – Reproductive success of a genotype relative to the most successful genotype (set as w = 1).
  • Selective pressure – Any environmental factor that influences survival. In the antibiotic‑resistance example the drug is a strong selective pressure favouring resistant cells.

4. Simple Population‑Genetics Idea (Cambridge‑level)

When a genotype has a lower fitness, its frequency falls each generation. For a resistant allele (frequency 

) and a susceptible allele (frequency  caused by selection can be expressed as:

\[

\Delta p = \frac{s\,p\,q}{1 - s\,q}

\]

  • p – frequency of the resistant allele.
  • q – frequency of the susceptible allele.
  • s – selection coefficient (0 ≤ s ≤ 1); the proportion by which the fitness of susceptible bacteria is reduced.

Only a short worked example is needed to illustrate that even a small initial p can rise rapidly under strong selection.

5. Types of Natural Selection (with familiar examples)

  • Directional selection – favours one extreme (e.g., larger beak size in finches during drought; antibiotic resistance in bacteria).
  • Stabilising selection – favours intermediate phenotypes (e.g., human birth weight).
  • Disruptive selection – favours both extremes over the intermediate form (e.g., colour morphs in peppered moths).

6. Natural Selection in Bacteria – The Antibiotic‑Resistance Cycle

  1. Generation of variation – Random mutations or acquisition of resistance genes by HGT create a few resistant cells.
  2. Application of selective pressure – The patient receives an antibiotic; the drug kills susceptible cells.
  3. Differential survival & reproduction – Resistant cells survive, continue to divide and out‑compete the killed cells.
  4. Increase in allele frequency – The resistant genotype becomes more common; the population shifts toward resistance.

7. Main Mechanisms of Antibiotic Resistance

MechanismTypical Genetic BasisEffect on the Antibiotic
Enzymatic degradationPlasmid‑encoded β‑lactamase genesDrug is chemically destroyed before reaching its target.
Altered target sitePoint mutations in ribosomal RNA, DNA gyrase, or penicillin‑binding proteinsBinding affinity of the drug is reduced or abolished.
Efflux pumpsChromosomal or plasmid genes encoding membrane transport proteins (e.g., AcrAB‑TolC)Drug is actively expelled, lowering intracellular concentration.
Reduced permeabilityMutations in outer‑membrane porin proteinsFewer drug molecules enter the cell.

8. Links to Other Syllabus Topics

  • Topic 6 – Nucleic acids & protein synthesis: Mutations that confer resistance are changes in DNA; altered target sites often involve ribosomal proteins.
  • Topic 10 – Infectious disease: Resistant bacteria affect treatment strategies, vaccine design and public‑health policies.
  • Topic 12 – Genetics: Inheritance of resistance genes follows Mendelian patterns (dominant/recessive) and can be transferred via plasmids (non‑Mendelian).

9. Artificial Selection – Human‑Driven Antibiotic Use

Although natural selection occurs without intent, our actions can create powerful artificial selective pressures:

  • Over‑prescribing antibiotics in medicine and agriculture.
  • Patients not completing a prescribed course.
  • Using sub‑therapeutic doses as growth promoters in livestock.

These practices accelerate the spread of resistance, effectively “directing” evolution.

10. Health Implications & Mitigation Strategies

  • Prudent prescribing – Use the narrow‑spectrum drug at the correct dose and duration.
  • Combination therapy – Reduces the chance that a single mutation confers resistance to all drugs.
  • Adjuvant drugs – β‑lactamase inhibitors, efflux‑pump blockers, or agents that increase membrane permeability.
  • Infection‑control measures – Hygiene, vaccination, surveillance and isolation of resistant strains.

11. Long‑Term Evolutionary Consequences

Prolonged directional selection can cause sub‑populations to diverge. In bacteria this may lead to distinct lineages that are reproductively isolated by incompatibility of plasmids or by occupation of different ecological niches – an early step toward speciation. Similar processes are seen in multicellular organisms (e.g., cichlid fish radiations).

12. Summary

Antibiotic resistance provides a clear, syllabus‑relevant example of natural selection. Random genetic variation (mutation or HGT) creates a few resistant cells. The antibiotic acts as a selective pressure, giving those cells a higher relative fitness. As they reproduce, the resistance allele frequency rises, shifting the whole population toward resistance. Understanding this cycle connects directly to DNA structure, genetics, disease control and highlights the impact of human behaviour on evolutionary change.

Suggested diagram: Flowchart – (1) Mutation/HGT → (2) Antibiotic exposure → (3) Survival of resistant cells → (4) Increase in resistant allele frequency → (5) Spread of resistance within the patient and the community.