Bacterial Cell Structure
Shape, size and how we see them ★★
Bacteria are measured in micrometres (µm), and the size varies with the kind. Three basic shapes account for nearly all of them.
| Shape | Description and size | Example |
|---|---|---|
| Cocci | Sphere, 1 µm | Staphylococcus aureus · Neisseria gonorrhoeae |
| Bacilli | Rods, 0.5–1 µm wide × 3 µm long | Bacillus anthracis · E. coli |
| Spiral bacteria | 0.3–0.6 µm wide × 1–3 µm long | Vibrio cholerae |
Two families of technique make them visible. Optical methods — light, electron, darkfield, fluorescence and confocal microscopy. And staining methods: simple staining; differential staining — the Gram stain and the acid-fast stain; and special staining — negative, spore and flagella stains.
The Gram stain was first published by Christian Gram in 1884. It is still the single most useful test in bacteriology, and §4 explains why.
- Name the three basic shapes and their sizes. → Cocci (sphere, 1 µm); bacilli (rods, 0.5–1 × 3 µm); spiral (0.3–0.6 × 1–3 µm)
- Name the two differential stains. → Gram stain and acid-fast stain
- Who published the Gram stain, and when? → Christian Gram, 1884
- Name the three special stains. → Negative, spore and flagella stains
Essential and particular structures ★★★
The lecture divides bacterial structures in two, and the division is examinable because it distinguishes what every bacterium has from what only some have.
| Essential structures — all bacteria | Particular structures — some bacteria |
|---|---|
| Cell wall | Capsule |
| Cell membrane | Flagella |
| Cytoplasm | Pili |
| Nuclear material (nucleoid) | Spore |
That right-hand column is not a list of optional extras — it is very nearly a list of reasons a bacterium is dangerous.
A capsule resists phagocytosis. Flagella provide motility, letting an organism reach tissue it could not otherwise. Pili provide adhesion — and, in one form, gene transfer. Spores allow survival of heat, drying and disinfectant for years.
So when a later unit asks for the virulence factors of a named organism — as the 2019 paper does for Staphylococcus aureus — the particular structures are where the answer starts.
- Name the four essential structures. → Cell wall, cell membrane, cytoplasm, nuclear material (nucleoid)
- Name the four particular structures. → Capsule, flagella, pili, spore
- Why do the particular structures matter clinically? → They are largely the virulence factors — resisting phagocytosis, motility, adhesion, survival
Peptidoglycan — the common layer ★★★
The cell wall is the outermost portion of the bacterium, 15–30 nm thick and 10–25% of the dry weight. Every bacterial wall is built on the same polymer, and the differences between Gram-positive and Gram-negative are differences in what is added to it.
| Component of peptidoglycan | Present in |
|---|---|
| A backbone of N-acetylglucosamine and N-acetylmuramic acid | Both Gram-positive and Gram-negative |
| A set of identical tetrapeptide side chains attached to N-acetylmuramic acid | Both — but with different components and binding modes in Gram+ and Gram− |
| A set of identical peptide cross-bridges | Gram-positive only |
The lecture flags two agents against this structure, and they attack different things.
Penicillin blocks the formation of the cross-links, so newly made wall cannot be stitched together — the bacterium builds a defective wall and bursts under its own osmotic pressure. Note that this only harms a growing organism, since it prevents construction rather than destroying what exists.
Lysozyme — in your tears, saliva and nasal secretions — instead hydrolyses the β1→4 linkage of the backbone itself, cutting the existing polymer.
One prevents building, the other demolishes. Both leave the organism in the state §6 calls wall-less.
- What is the peptidoglycan backbone made of? → N-acetylglucosamine and N-acetylmuramic acid
- Which component is Gram-positive only? → The peptide cross-bridges
- What does penicillin block? → Cross-link formation in the wall
- What does lysozyme cleave? → The β1→4 linkage of the backbone
- How thick is the cell wall, and what fraction of dry weight? → 15–30 nm; 10–25%
⭐ Gram-positive versus Gram-negative ★★★
This is a 7-mark brief-answer question from the 2019 paper, and it is the single most reusable comparison in bacteriology. The difference is entirely in what is added to the shared peptidoglycan.
| Gram-positive | Gram-negative | |
|---|---|---|
| Peptidoglycan | Thick, with peptide cross-bridges | Thin, no cross-bridges |
| Special component | Teichoic acid — 50% of the cell wall's dry weight. Wall teichoic acid (WTA) and membrane teichoic acid = lipoteichoic acid (LTA) | Outer membrane — lipoprotein · lipid bilayer · lipopolysaccharide (LPS) |
| Outer membrane | Absent | Present |
| Endotoxin | None | Lipid A of the LPS |
The three parts of LPS — each with a different job
| Part of LPS | Property |
|---|---|
| O polysaccharide (O antigen) | Species specificity |
| Core polysaccharide | Genus specificity |
| Lipid A | Endotoxic properties |
Those three rows answer three different exam questions at once.
The O antigen is why organisms are typed as E. coli O157 — the serotyping used throughout the Enterobacteriaceae unit is reading this molecule. It varies between species, so it identifies.
The core varies between genera — one level up.
Lipid A is the endotoxin, and it is structurally conserved. That is exactly why Gram-negative sepsis looks the same whichever organism causes it: fever, hypotension, shock. The clinical syndrome is a response to the lipid, not to the species — and it explains why killing the bacteria with antibiotics can transiently make a septic patient worse, as lysis releases more of it.
One molecule: the identifier is on the outside, the poison is on the inside.
Seven rows for seven marks. If there is room, add the consequences: Gram-positives are more susceptible to penicillin and lysozyme, Gram-negatives produce endotoxic shock.
- Which special component is Gram-positive? → Teichoic acid — 50% of cell wall dry weight, as WTA and LTA
- Which is Gram-negative? → The outer membrane: lipoprotein, lipid bilayer and LPS
- Name the three parts of LPS and their properties. → O polysaccharide (species specificity), core polysaccharide (genus specificity), lipid A (endotoxic)
- Which part is the endotoxin? → Lipid A
- Which wall has peptide cross-bridges? → Gram-positive only
The acid-fast cell wall ★★★
A third wall type exists, and “Acid-fast” was set as a Section I term in 2019 (4 marks). It belongs to Mycobacterium tuberculosis and its relatives.
| Layer | Content |
|---|---|
| Peptidoglycan | Present, as in all bacteria |
| An external asymmetric lipid bilayer | Inner leaflet: mycolic acid and wax Outer leaflet: other extractable lipids |
The consequence is stated plainly: this wall is resistant to many harsh chemicals, including detergents and strong acids. The acid-fast stain uses carbol fuchsin, then acid alcohol as the decolouriser, then methylene blue as counterstain. An organism that keeps the red carbol fuchsin despite the acid alcohol is acid-fast positive.
Ask why a stain would be designed around resistance to acid, and the clinical picture falls out of it.
Mycolic acid makes the wall a waxy, near-impermeable barrier. In the laboratory that means the organism holds its stain against acid alcohol — hence acid-fast.
In the patient it means far more. The same barrier lets the organism survive inside a macrophage that has just tried to digest it — which is why tuberculosis is an intracellular, chronic, granulomatous disease rather than an acute one. It is also why antituberculous drugs must be given for months rather than days, and why the organism resists ordinary disinfectants.
The property that makes it stainable is the property that makes it dangerous.
- What makes a wall acid-fast? → An external asymmetric lipid bilayer, with mycolic acid and wax in the inner leaflet
- Which organism? → Mycobacterium tuberculosis
- Name the three acid-fast stain reagents. → Carbol fuchsin, acid alcohol, methylene blue
- What is the wall resistant to? → Many harsh chemicals, including detergents and strong acids
- How does this explain the disease? → The waxy barrier lets it survive inside macrophages — chronic, granulomatous infection needing months of therapy
Wall-less forms ★★★
“L-form” was a Section I term in 2020, worth 4 marks. It arises when the wall is removed — and the lecture is precise about the naming.
Bacteria lose their wall when treated with enzymes lytic for the cell wall, such as lysozyme, or with antibiotics that interfere with peptidoglycan biosynthesis. What you then call the result depends on what remains:
| Form | Definition |
|---|---|
| Spheroplast | When an outer membrane is present |
| Protoplast | When an outer membrane is not present |
| L-form | When the wall-less bacteria are able to grow and divide |
| L-form property | Detail |
|---|---|
| Culture | Difficult — requires solidified medium with agar and proper osmotic strength |
| Reversion | Can revert to the original bacterial shape |
| Clinical | Chronic infection |
This is the discriminating point, and the lecture places the two side by side deliberately.
An L-form is a normally-walled bacterium that has lost its wall — and it can revert. A Mycoplasma is a bacterium that lacks a cell wall and contains no peptidoglycan as its natural state, and never reverts to the walled state.
The clinical consequence of the L-form is the reason it is examinable. Give penicillin, which works by blocking wall synthesis, and any organism surviving as an L-form is immune to it — there is no wall to attack. It persists through the course of treatment, then reverts when the drug is withdrawn. That is a mechanism of chronic and relapsing infection which no culture will show, because L-forms grow only on special osmotically-balanced medium.
- Define an L-form. → A wall-less bacterium that is still able to grow and divide
- What causes wall loss? → Lytic enzymes such as lysozyme, or antibiotics blocking peptidoglycan synthesis
- Spheroplast vs protoplast? → Spheroplast retains an outer membrane; protoplast does not
- How does an L-form differ from Mycoplasma? → The L-form has lost its wall and can revert; Mycoplasma naturally lacks one and never reverts
- Why do L-forms cause chronic infection? → With no wall, penicillin cannot act; they persist and revert after treatment stops
Functions of the cell wall ★★
- Maintaining the cell's characteristic shape — the rigid wall compensates for the flexibility of the phospholipid membrane and stops the cell becoming spherical
- Countering the effects of osmotic pressure
- Providing attachment sites for bacteriophages
- Providing a rigid platform for surface appendages — flagella and pili emanate from the wall and extend beyond it
- Playing an essential role in cell division
Function 2 is the one that kills. A bacterium in a dilute environment is under constant osmotic pressure; the wall is what contains it. Remove the wall — with penicillin or lysozyme — and unless the medium is osmotically balanced, as §6 requires for L-forms, the cell simply bursts.
- Name five functions of the cell wall. → Maintain shape · counter osmotic pressure · provide phage attachment sites · platform for flagella and pili · essential role in cell division
- Which function explains why penicillin kills? → Countering osmotic pressure — without a wall the cell bursts
Revision
The exam map for this unit
| Paper | Item | From |
|---|---|---|
| 2019 Section III | ⭐ Gram-positive vs Gram-negative cell wall (7 marks) | §4 |
| 2019 Section I | Acid-fast (4 marks) | §5 |
| 2020 Section I | L-form (4 marks) | §6 |
The whole unit on one screen
| Question | Answer |
|---|---|
| Three basic shapes? | Cocci (1 µm) · bacilli (0.5–1 × 3 µm) · spiral (0.3–0.6 × 1–3 µm) |
| Essential structures? | Cell wall · membrane · cytoplasm · nucleoid |
| Particular structures? | Capsule · flagella · pili · spore |
| Peptidoglycan backbone? | N-acetylglucosamine + N-acetylmuramic acid |
| Cross-bridges? | Gram-positive only |
| Gram+ special component? | Teichoic acid — 50% of wall dry weight (WTA, LTA) |
| Gram− special component? | Outer membrane — lipoprotein, lipid bilayer, LPS |
| Three parts of LPS? | O polysaccharide (species) · core (genus) · lipid A (endotoxin) |
| Acid-fast wall? | Peptidoglycan + external lipid bilayer with mycolic acid |
| Acid-fast stain? | Carbol fuchsin → acid alcohol → methylene blue |
| L-form? | Wall-less bacterium still able to grow and divide; can revert |
| Mycoplasma vs L-form? | Mycoplasma never had a wall and never reverts |
| Penicillin vs lysozyme? | Penicillin blocks cross-linking; lysozyme cleaves the β1→4 backbone |
- Give five differences between Gram+ and Gram− cell walls. → Peptidoglycan thickness · cross-bridges · teichoic acid · outer membrane · LPS/endotoxin
- Which LPS component is the endotoxin? → Lipid A
- Define acid-fast. → A wall with an external lipid bilayer containing mycolic acid, resisting decolourisation by acid alcohol
- Define L-form. → A wall-less bacterium still able to grow and divide, which can revert to the walled form
- Why do L-forms matter clinically? → They resist penicillin, persist through treatment, and cause chronic relapsing infection