outline how penicillin acts on bacteria and why antibiotics do not affect viruses

Resources → Subject Notes → Biology → Lesson Plan

Antibiotics – Penicillin, Other Antibiotic Classes & Why Antibiotics Do Not Affect Viruses

Learning Objective (AO1)

Outline how penicillin acts on bacteria, describe the main groups of antibiotics and their targets, and explain why antibacterial agents have no effect on viruses.

Link to Cambridge International AS & A Level Biology (9700) Syllabus

  • Topic 10 – Infectious diseases: bacterial pathogens, mechanisms of control (antibiotics), resistance.
  • Topic 11 – Immunity: vaccination and the role of antibiotics in preventing secondary bacterial infection.
  • Assessment Objectives:
    • AO1 – recall of definitions, mechanisms, spectrum, and resistance.
    • AO2 – application of knowledge to data (e.g., zone‑of‑inhibition results) and evaluation of resistance strategies.
    • AO3 – design, conduct and critical evaluation of a practical investigation.

1. Penicillin – Mechanism of Action (AO1)

Penicillin belongs to the β‑lactam class of antibiotics. Its bactericidal activity results from inhibition of cell‑wall synthesis.

  1. Target enzymes – Penicillin‑Binding Proteins (PBPs)
    • PBPs are transpeptidases (and sometimes carboxypeptidases) that catalyse the cross‑linking of peptidoglycan strands during cell‑wall construction.
    • Two functional groups are relevant in clinical practice:
      • High‑affinity PBPs – normally inhibited by penicillin, causing rapid lysis.
      • Low‑affinity PBPs – altered forms that reduce drug binding and contribute to resistance.
  2. Binding mechanism
    • The β‑lactam ring mimics the D‑alanine‑D‑alanine terminus of the peptidoglycan precursor.
    • It forms a covalent acyl‑enzyme complex with the active‑site serine of PBPs, permanently inactivating the enzyme.
  3. Cell‑wall consequences
    • Inhibition of peptidoglycan cross‑linking → weakened wall.
    • During active growth, osmotic pressure causes the bacterium to burst (lysis).

Clinical relevance – Common resistance mechanisms (AO2)

Resistance mechanism How it works Typical counter‑measure
β‑lactamase production Enzyme hydrolyses the β‑lactam ring, destroying activity. Co‑administration of β‑lactamase inhibitors (e.g., clavulanic acid, sulbactam).
Altered PBPs (low‑affinity) Mutations change the binding site, reducing affinity for penicillin. Use of newer β‑lactams (e.g., cephalosporins) or non‑β‑lactam antibiotics.
Reduced permeability (Gram‑negative outer membrane) Loss or modification of porin channels limits drug entry. Combination therapy with agents that increase membrane permeability.

Spectrum of activity (AO1)

Bacterial group Cell‑wall features Penicillin effectiveness
Gram‑positive cocci (e.g., Streptococcus, Staphylococcus aureus) Thick peptidoglycan layer, no outer membrane. Highly susceptible – drug reaches PBPs easily.
Gram‑negative rods (e.g., Escherichia coli) Thin peptidoglycan + outer lipopolysaccharide membrane. Less susceptible; many produce β‑lactamases and limit drug entry.

Pharmacokinetics – ADME (AO2)

  • Absorption: Good oral absorption for penicillin V; penicillin G given intramuscularly or intravenously.
  • Distribution: Widely distributed in body fluids; poor penetration of the blood‑brain barrier unless meningitis is present.
  • Metabolism: Minimal hepatic metabolism; most drug is excreted unchanged.
  • Excretion: Renal elimination; dose adjustment required in renal impairment.

2. Other Major Antibiotic Classes (AO1)

The Cambridge syllabus expects knowledge of the main groups of antibacterial agents, their primary targets and typical spectra.

Class Primary bacterial target Representative drug(s) Typical spectrum Common resistance mechanisms
β‑lactams (penicillins, cephalosporins, carbapenems, monobactams) PBPs – cell‑wall synthesis Penicillin G, Ceftriaxone, Imipenem Gram‑positive; some Gram‑negative (especially later‑generation cephalosporins) β‑lactamases, altered PBPs, reduced permeability
Aminoglycosides 30 S ribosomal subunit – protein synthesis (mis‑reading of mRNA) Gentamicin, Amikacin Obligate aerobic Gram‑negative rods Enzymatic modification, reduced uptake, methylation of ribosomal binding site
Tetracyclines 30 S ribosomal subunit – block attachment of tRNA Doxycycline, Tetracycline Broad‑spectrum (Gram‑+, Gram‑‑, intracellular) Efflux pumps, ribosomal protection proteins
Quinolones (fluoroquinolones) DNA gyrase / topoisomerase IV – DNA replication Ciprofloxacin, Levofloxacin Gram‑negative (especially urinary pathogens); some Gram‑positive Mutations in gyrA/gyrB, efflux, plasmid‑mediated protection
Sulfonamides (often combined with trimethoprim) Folate synthesis – inhibition of dihydropteroate synthase (DHPS) Trimethoprim‑sulfamethoxazole Broad‑spectrum (bacteriostatic) Overproduction of PABA, mutated DHPS

3. Why Antibiotics Do Not Affect Viruses (AO1)

Antibiotics target structures or metabolic pathways that are unique to bacteria. Viruses lack these features, so antibacterial agents are ineffective.

Feature Bacteria Viruses Relevance to antibiotics
Cellular organization Prokaryotic cell with membrane, cytoplasm, ribosomes, and cell wall. Acellular particle consisting of nucleic acid + protein coat (± lipid envelope). Antibiotics act on cell‑wall synthesis, bacterial ribosomes, or bacterial enzymes – none exist in viruses.
Genetic material Single circular DNA chromosome (or linear in some). DNA or RNA (single‑ or double‑stranded) packaged in a capsid. Drugs that inhibit bacterial DNA gyrase or DHPS have no viral target.
Metabolism Independent metabolism; synthesises proteins, nucleotides, lipids. Metabolically inert; relies entirely on host cell machinery. Metabolic inhibitors (e.g., sulfonamides) cannot act on a virus.
Reproduction Binary fission requiring cell‑wall synthesis. Replication inside a host cell using host enzymes. Agents that disrupt bacterial cell division (penicillin, vancomycin) are irrelevant to viruses.

Key point (AO1)

  • Antibiotics act on structures or processes **unique to bacteria** (cell wall, bacterial ribosomes, bacterial enzymes).
  • Viruses lack these structures and instead hijack the host cell’s machinery; therefore antibacterial agents have no effect.

What effective antivirals target (AO2)

  • Viral entry (e.g., fusion inhibitors for HIV, attachment blockers for influenza).
  • Viral nucleic‑acid polymerases (e.g., acyclovir for HSV, remdesivir for SARS‑CoV‑2).
  • Viral proteases (e.g., protease inhibitors for HIV and HCV).
  • Release of mature virions (e.g., neuraminidase inhibitors for influenza).

4. Practical Activity – Zone‑of‑Inhibition Assay (AO3)

Objective: Demonstrate the bactericidal effect of penicillin and relate the results to bacterial cell‑wall structure.

  1. Materials
    • Mueller‑Hinton agar plates
    • Sterile cotton swabs
    • Penicillin‑impregnated discs (10 U)
    • Control discs (no active drug)
    • Two bacterial cultures: Streptococcus pyogenes (Gram‑positive) and Escherichia coli (Gram‑negative)
    • Ruler, permanent marker, incubator (37 °C, 18‑24 h)
  2. Method
    • Label each plate quadrant for the organism to be tested.
    • Using a sterile swab, spread a uniform lawn of the first organism; repeat on a second plate for the second organism.
    • Place one penicillin disc and one control disc on each lawn, keeping discs ≥25 mm apart.
    • Incubate plates inverted for 18‑24 h.
  3. Data recording
    OrganismZone diameter (mm)Interpretation
    Streptococcus pyogenes
    Escherichia coli
  4. Evaluation (AO3)
    • Explain why the Gram‑positive organism typically shows a larger clear zone (no outer membrane, easier drug access).
    • Discuss limitations: diffusion differences, inoculum density, presence of β‑lactamases, agar thickness.
    • Suggested improvements: use a standard 0.5 McFarland inoculum, include a β‑lactamase inhibitor disc, and repeat with a range of penicillin concentrations.

5. Summary (AO1)

  • Penicillin’s β‑lactam ring binds irreversibly to PBPs, halting peptidoglycan cross‑linking and causing osmotic lysis of actively dividing bacteria.
  • Other major antibiotic classes act on bacterial ribosomes, DNA‑gyrase, or folate synthesis; each class has a characteristic spectrum and typical resistance mechanisms.
  • Resistance can arise through enzymatic drug destruction, target modification, or reduced drug entry; clinicians counteract these by using inhibitors, newer drug generations, or combination therapy.
  • Viruses lack cell walls, bacterial ribosomes, and independent metabolism, so antibacterial agents have no target. Antiviral drugs therefore focus on virus‑specific proteins or steps in the viral life cycle.

6. Quick Reference Table – Antibiotic Classes (AO1)

Class Primary target Example(s) Typical spectrum
β‑lactams (penicillins, cephalosporins, carbapenems) PBPs – cell‑wall synthesis Penicillin G, Ceftriaxone, Imipenem Gram‑positive; some Gram‑negative (esp. later‑generation cephalosporins)
Aminoglycosides 30 S ribosomal subunit – protein synthesis Gentamicin, Amikacin Obligate aerobic Gram‑negative rods
Tetracyclines 30 S ribosomal subunit – block tRNA attachment Doxycycline, Tetracycline Broad‑spectrum (Gram‑+, Gram‑‑, intracellular)
Quinolones (fluoroquinolones) DNA gyrase / topoisomerase IV – DNA replication Ciprofloxacin, Levofloxacin Gram‑negative urinary pathogens; some Gram‑positive
Sulfonamides (often with trimethoprim) Folate synthesis – DHPS inhibition Trimethoprim‑sulfamethoxazole Broad‑spectrum (bacteriostatic)

7. Links to Assessment Objectives

  • AO1 – Knowledge: Definitions, mechanisms of action, spectra, resistance, and why antibiotics do not affect viruses.
  • AO2 – Application: Interpreting zone‑of‑inhibition data, relating bacterial cell‑wall structure to drug efficacy, evaluating resistance strategies, and describing antiviral targets.
  • AO3 – Practical skills & evaluation: Designing the assay, recording measurements, critiquing methodology, and suggesting improvements.

Create an account or Login to take a Quiz

90 views
0 improvement suggestions

Log in to suggest improvements to this note.