9477 / 2027

Lesson 3 of 5 / Infection, vaccination and disease spread

Antibiotics target bacterial processes

Why can penicillin affect growing bacteria without treating a virus?

I can explain antibiotic modes of action, including inhibition of wall synthesis.

  • I can explain antibiotic action, including penicillin.Syllabus

    Syllabus 9477, Extension A(i). Explain antibiotic action, including penicillin.

About 6 min

Make a guess. You are not marked.

Penicillin kills growing bacteria but barely affects bacteria that are not dividing. Why?

  1. Penicillin only enters cells that are dividing.
  2. It blocks building new cell wall.
  3. Dormant bacteria have no cell wall.
Show the answer

It blocks building new cell wall.

Penicillin inhibits transpeptidase cross-linking. A growing cell with a weak new wall bursts by osmosis.

The key idea

Selective toxicity exploits bacterial structures or processes; viruses lack the bacterial targets of antibiotics.

Connect cause and consequence

Is the drug target present?

Newly assembled wall regionCell membrane below the wall

Peptidoglycan cross-linking helps the wall resist osmotic stress. This model assumes a susceptible, growing bacterium.

Green lines = peptidoglycan chains; brown connectors = cross-links; blue double line = membrane. Other antibiotics target other bacterial processes, such as protein synthesis. This is a mechanism lesson, not a treatment recommendation.

Explanation

Antibiotics act on susceptible bacteria by interfering with essential processes. Different classes can inhibit cell-wall synthesis, bacterial protein synthesis, nucleic-acid processes or particular metabolic pathways. The target and susceptibility matter; no single antibiotic is effective against every bacterium.

Penicillin-type beta-lactams interfere with enzymes that cross-link peptidoglycan during wall formation. A weakened wall may fail to withstand osmotic pressure, especially in growing cells. The target is wall synthesis, not direct destruction of every DNA molecule.

Human cells lack peptidoglycan walls, providing a basis for selective toxicity. Other antibiotics exploit differences between bacterial 70S and eukaryotic cytosolic 80S ribosomes. Selectivity is not identical to absence of all side effects, and susceptibility must not be inferred from a simple classroom drawing.

Viruses lack peptidoglycan walls and their own bacterial ribosomes, so antibacterial drugs do not directly treat viral replication through these targets. Resistance mechanisms, such as drug inactivation or target alteration, can reduce effectiveness; selection changes resistant-lineage frequencies rather than teaching bacteria to need a mutation.

Write the penicillin answer as a full chain, because each link is a marking point. (1) Peptidoglycan chains in the bacterial wall are joined by cross-links made by the enzyme transpeptidase. (2) Penicillin has a shape similar to the part of the peptide that transpeptidase normally binds, so it binds to the active site of transpeptidase, competing with the normal substrate, and stays bound. (3) Fewer cross-links form, so new wall made by a growing bacterium is weak. (4) The cytoplasm has a lower water potential than the surroundings, so water enters the bacterium by osmosis. (5) The weakened wall cannot resist the pressure, and the cell bursts. This is osmotic lysis.

Because the chain depends on wall being built, penicillin acts mainly on bacteria that are growing and dividing. Human cells have no peptidoglycan and no transpeptidase, which is why penicillin is selectively toxic to bacteria.

Step by step
  1. 1

    Name the target

    Wall, ribosome or another bacterial process.

  2. 2

    Explain the failure

    Connect inhibited synthesis to cell survival or growth.

  3. 3

    Check organism identity

    A virus does not supply a bacterial wall target.

Worked example

Work through the evidence

Why can a wall-synthesis inhibitor have a stronger effect on actively growing bacteria than on non-growing cells?

One way to explain it

Growing cells need ongoing peptidoglycan construction and remodelling, so blocking that process more directly compromises wall integrity during growth.

Why this answer works
  • The effect depends on an active target process.
  • This is a mechanism explanation, not a drug-selection recommendation.

Watch out for this

A student says: "An antibiotic works on any infectious agent because infection is one process." What is wrong with this?

Show the answer

Bacteria, viruses and other pathogens have different targets; the agent and mechanism must match.

Check your understanding

Which explains penicillin's bacterial selectivity?

  1. It inhibits cellulose cross-linking in bacterial walls.
  2. Its wall-synthesis target is present in susceptible bacteria but absent from human cells.
  3. It digests the existing peptidoglycan of every bacterium, whether growing or not.
  4. It attacks a structure shared equally by human and bacterial cells.
Show the answer

Its wall-synthesis target is present in susceptible bacteria but absent from human cells.

Target differences provide selective toxicity.

Exam-style questions

Check your understanding

Which is NOT a reason penicillin is selectively toxic to bacteria?

  1. Human cells have no transpeptidase
  2. Penicillin cannot enter human cells at all
  3. Human cells have no peptidoglycan wall
  4. Only bacteria build cross-linked walls
Show the answer

Penicillin cannot enter human cells at all

Selectivity comes from the target: transpeptidase and peptidoglycan exist only in bacteria. Entry into human cells is not the reason.

Quick recall

Card 1 of 3. Answer in your head, then check.

Why can penicillin affect growing bacteria without treating a virus?

You can return to this lesson any time.