Mycoplasma
⭐ The definition ★★★
Mycoplasmas are the smallest, cell-wall-free prokaryotes that can live freely in nature and on artificial medium. They are pleomorphic and can pass through bacterial filters.
Every clause of that sentence is a mark, and each is a discriminating point:
• Smallest — 0.1–0.3 µm.
• Cell-wall-free, and therefore resistant to penicillin and all β-lactams, which act on the wall.
• Free-living on artificial medium — this is what separates them from the Rickettsia and Chlamydia of the next two units, which are obligate intracellular parasites.
• Pleomorphic and filter-passing — no wall to hold a shape.
If you have room, add the membrane: a triple-layered membrane containing sterols (~36%), unique among prokaryotes and the reason they resist osmotic lysis without a wall.
This is the only term the examiners have set in both modern papers. Learn it verbatim.
| Rank | Name |
|---|---|
| Class | Mollicutes — mollis soft, cutis skin |
| Order | Mycoplasmatales |
| Family | Mycoplasmataceae |
| Genus | Mycoplasma and Ureaplasma |
About 20 species come from the human body, as pathogens and opportunistic pathogens: M. pneumoniae (Mpn) · M. genitalium (Mg) · M. hominis (Mh) · M. fermentans (Mf) · M. penetrans (Mpe) · M. pirum (Mpi) · U. urealyticum (Uu).
- Define Mycoplasma. → The smallest, cell-wall-free prokaryotes able to live freely in nature and on artificial medium; pleomorphic, and able to pass through bacterial filters
- Give the class name and its meaning. → Mollicutes — mollis (soft) + cutis (skin)
- Name the two genera. → Mycoplasma and Ureaplasma
Biological properties ★★★
| Property | Detail |
|---|---|
| Size and shape | 0.1–0.3 µm; deformable and highly pleomorphic — coccoid, bacillary, pear-shaped and filamentous; pass through 0.2 µm filters |
| Structure | Lack a cell wall. A triple-layered cell membrane: outer and inner layers of protein, intermediate layer with a high content of sterols (~36%), which prevent osmotic lysis. May have a capsule. Non-motile. A tip structure (attachment organelle) — e.g. P1 adhesin in M. pneumoniae, a specialised terminal protein attachment factor |
| Growth | Grow in cell-free artificial medium with 10–20% human or animal serum (supplying fatty acids and cholesterol). Facultative anaerobes — EXCEPT M. pneumoniae, a strict aerobe. 35–37 °C; binary fission; slow, fastidious growth; generation time 1–6 hours or more |
| Colony | Very small — 10–600 µm — with a FRIED-EGG appearance. T strains (tiny strains) = Ureaplasma |
| Growth times | Species |
|---|---|
| 5–14 days — very slow, particularly on primary isolation | M. pneumoniae |
| 2–4 days | M. hominis |
| 24–28 hours — but grows very poorly in vitro | U. urealyticum |
They are the common cause of contamination of cell culture in the laboratory.
⭐ Resistance
| Detail | |
|---|---|
| Physical and chemical agents | More susceptible than ordinary bacteria — e.g. to lipid solvents |
| Resistant to | Penicillin, cephalosporin, vancomycin (all wall-active) · also alkali and crystal violet |
| Sensitive to | Erythromycin, tetracycline, streptomycin |
Every property in the table above follows from one absence.
No wall means no shape — hence pleomorphic, hence passing through a 0.2 µm filter that stops other bacteria.
No wall means no penicillin target — the summary slide's clinical warning: Mycoplasma and Ureaplasma infections do not respond to β-lactam antibiotics; tetracyclines, macrolides and quinolones are the agents of choice. Treat an atypical pneumonia with amoxicillin and nothing happens.
But no wall should also mean bursting under osmotic pressure — Unit 7 §7's second function. It does not, and the reason is the 36% sterol content of the membrane, which stiffens it enough to resist. That is unique among prokaryotes; it is why the medium needs 10–20% serum (to supply cholesterol they cannot make), and it is the single feature that most cleanly separates Mycoplasma from an L form in §3.
It also explains their vulnerability to lipid solvents: a membrane is all they have.
- How big are they, and what shapes? → 0.1–0.3 µm; coccoid, bacillary, pear-shaped, filamentous — highly pleomorphic
- Describe the membrane. → Triple-layered: protein outer and inner layers, an intermediate layer with ~36% sterols preventing osmotic lysis
- What is P1 adhesin? → The tip attachment organelle of M. pneumoniae
- What does the medium need, and why? → 10–20% human or animal serum, for fatty acids and cholesterol
- Which species is a strict aerobe? → M. pneumoniae — the others are facultative anaerobes
- Describe the colony. → Very small (10–600 µm) with a fried-egg appearance; T strains are Ureaplasma
- Which antibiotics fail, and which work? → Fail: penicillin, cephalosporin, vancomycin (wall-active). Work: erythromycin, tetracycline, streptomycin, quinolones
⭐ Mycoplasma versus L-form bacteria ★★★
“List the similarities and differences between mycoplasmas and L-form bacteria” is question 3 on the TMU homework list, and the deck devotes two slides to it. Unit 2 §6 defined the L form; here is the comparison in full.
Similarities — five
- Cell wall deficient
- Not sensitive to penicillin
- Pleomorphic
- Pass through filters
- Fried-egg-shaped colony
⭐ Differences — five
| Mycoplasma | L-form bacteria | |
|---|---|---|
| Relationship to bacteria | No genetic relationship with bacteria | Related to their parental bacteria; sometimes revert to the walled parental form |
| Membrane | Cholesterol in the cell membrane | No cholesterol in the cell membrane |
| Medium | Stable in ordinary medium | Need hypertonic medium |
| Colony | Grow slowly; small colony, Ø 0.01–0.6 mm | Larger colony, Ø 0.5–1.0 mm |
| Liquid medium | Low turbidity | High turbidity; may adhere to the wall or bottom of the tube |
Learn the table if you must, but it collapses to two ideas.
Origin. An L form was a walled bacterium and can become one again — it has a parent. A Mycoplasma has no genetic relationship with bacteria; this is what it has always been, and it never reverts. That single fact is the discriminating answer if only one is wanted.
Cholesterol. Mycoplasma puts sterols in its membrane and is therefore stable in ordinary medium. The L form has none, so it needs hypertonic medium to keep from bursting — exactly what Unit 2 §6 said when it required solidified medium with agar and proper osmotic strength.
The colony size and turbidity rows are just observations that follow.
And the similarities are all downstream of the missing wall — no wall, so no shape, no filter retention, no penicillin target, and a colony that spreads flat into the agar with a dense centre: the fried egg.
- Name five similarities. → Cell wall deficient · not sensitive to penicillin · pleomorphic · pass through filters · fried-egg colony
- Name five differences. → Genetic relationship to bacteria and reversion · cholesterol in the membrane · ordinary vs hypertonic medium · small vs larger colony · low vs high turbidity in liquid medium
- If only one difference is wanted, which? → The L form derives from a walled bacterium and can revert; Mycoplasma has no genetic relationship with bacteria and never reverts
Pathogenesis ★★★
| Transmission route | Example |
|---|---|
| Respiratory tract — droplets | M. pneumoniae |
| Sexual contact | U. urealyticum |
The three mechanisms
| Mechanism | Detail |
|---|---|
| 1 · Close adherence and absorption of nutrition | Specific binding — e.g. P1 adhesin of M. pneumoniae |
| 2 · Toxic metabolites | H₂O₂ and O₂⁻ → oxidative damage |
| 3 · Hypersensitivity | Serological cross-reaction between M. pneumoniae and brain and lung antigens → extrapulmonary manifestations: arthritis, rashes, cardiovascular or neurological problems. Autoantibody — e.g. cold agglutinin (IgM) |
- Name the two transmission routes with examples. → Respiratory droplets (M. pneumoniae) and sexual contact (U. urealyticum)
- Name the three pathogenic mechanisms. → Close adherence and nutrient absorption via specific adhesins · toxic metabolites H₂O₂ and O₂⁻ causing oxidative damage · hypersensitivity from cross-reaction with brain and lung antigens
- Which autoantibody is characteristic? → Cold agglutinin, an IgM
The organisms and their diseases ★★★
| Organism | Diseases |
|---|---|
| M. pneumoniae | Pharyngitis · tracheobronchitis · pneumonia (primary atypical pneumonia) |
| M. hominis — commonly an inhabitant of the urogenital tract, e.g. the healthy female vagina | Female: pelvic inflammatory disease (PID), pyelonephritis, postpartum fever, stillbirth, spontaneous abortion. Male: epididymitis. Newborn: pneumonia, encephalitis, brain abscess |
| M. genitalium | Nongonococcal urethritis (NGU), cervicitis, endometritis, PID, infertility |
| U. urealyticum | Nongonococcal urethritis (NGU) · habitual spontaneous abortion · low-weight infants; also PID, postpartum fever, stillbirth and acute urethral syndrome, and it induces infertility |
⭐ Mycoplasma pneumoniae — primary atypical pneumonia
| Detail | |
|---|---|
| Also called | Mycoplasmal pneumonia, interstitial pneumonia |
| Burden | Responsible for 15–50% of all pneumonias |
| Transmission | Droplets; epidemics from late autumn to early spring |
| Incubation | 2–3 weeks |
| Course | Initial symptoms mild and self-limited → malaise, fever, headache → a dry, non-productive cough lasting 2–3 weeks. 3–10% of cases develop pneumonia. More severe in adults than in children |
| Complications | Immunopathologic mechanisms → extrapulmonary manifestations: arthritis, rashes, cardiovascular or neurological problems, haemolytic anaemia |
M. fermentans, M. penetrans and M. pirum are isolated in AIDS and immunocompromised patients and act as co-factors in AIDS development.
The word is not a vague adjective — it names a specific clinical mismatch, and it is worth a mark.
A typical pneumonia — the lobar pneumonia of S. pneumoniae in Unit 9 §6 — is abrupt, with a productive cough, consolidation of a lobe, and a very sick patient.
M. pneumoniae is the opposite of every one of those. The onset is insidious over two to three weeks; the cough is dry and non-productive; the pathology is interstitial rather than alveolar, so the chest film looks far worse than the patient does — the classic “walking pneumonia”.
Three practical consequences: no organism on Gram stain (no wall to take up the stain), no response to penicillin (no wall to attack), and diagnosis made clinically and confirmed by serology — a fourfold rise in IgG or IgM — because culture takes 5–14 days and is useless in real time.
And the haemolytic anaemia in the complication list is the cold agglutinin of §6 acting in vivo — the same autoantibody the laboratory measures.
- Which diseases does M. pneumoniae cause? → Pharyngitis, tracheobronchitis, and primary atypical pneumonia
- Give its epidemiology and course. → 15–50% of all pneumonias; droplet spread, epidemic from late autumn to early spring; incubation 2–3 weeks; malaise, fever, headache and a dry cough for 2–3 weeks; 3–10% develop pneumonia; more severe in adults
- Name the extrapulmonary complications. → Arthritis, rashes, cardiovascular or neurological problems, haemolytic anaemia
- Which organisms cause nongonococcal urethritis? → M. genitalium and U. urealyticum
- Which mycoplasmas are linked with AIDS? → M. fermentans, M. penetrans, M. pirum
Diagnosis and treatment ★★★
Isolation and cultivation are not commonly used. Diagnosis rests on serological and molecular methods: the complement fixation test (CF), the cold agglutinin test (for M. pneumoniae), ELISA and PCR.
A NON-SPECIFIC test performed to detect the presence of cold-reacting antibody that causes type O human red blood cells to clump at 4 °C and unclump at 37 °C. The cold agglutinin itself is an autoantibody (IgM).
| Positive in | Frequency |
|---|---|
| Patients with M. pneumoniae infection | 50–65% |
| Also positive in | Infectious mononucleosis, influenza, mumps, measles, scarlet fever, some parasitic infections, liver cirrhosis, leukaemia — hence not specific |
Treatment: tetracycline, erythromycin, quinolones. There are no vaccines.
- Define the cold agglutinin test. → A non-specific test detecting cold-reacting antibody that makes type O human RBCs clump at 4 °C and unclump at 37 °C
- How often is it positive in M. pneumoniae, and why is it non-specific? → 50–65%; it is also positive in infectious mononucleosis, influenza, mumps, measles, scarlet fever, parasitic infections, cirrhosis and leukaemia
- How is mycoplasmal infection treated? → Tetracycline, erythromycin, quinolones — never β-lactams; there is no vaccine
Revision
The deck's summary slide and its multiple-choice
The slide names definitions: mycoplasma, T strains, the cold agglutinin test; then the biological properties, the pathogenesis, diagnosis and treatment. Its multiple-choice — “The reason why mycoplasma differs from ordinary bacteria is…” — has the answer A. No cell wall. (B, C and D are true of ordinary bacteria too; E is true of mycoplasma but is not what distinguishes it from bacteria — it is what distinguishes it from Rickettsia and Chlamydia.)
The whole unit on one screen
| Question | Answer |
|---|---|
| ⭐ Definition? | Smallest, cell-wall-free prokaryotes, free-living in nature and on artificial medium; pleomorphic; pass bacterial filters |
| Size? | 0.1–0.3 µm; pass a 0.2 µm filter |
| Membrane? | Triple-layered, ~36% sterols, preventing osmotic lysis |
| Colony? | Fried-egg, 10–600 µm; T strains = Ureaplasma |
| Adhesin? | P1 in M. pneumoniae |
| Antibiotics? | Resistant to penicillin, cephalosporin, vancomycin; sensitive to erythromycin, tetracycline, streptomycin, quinolones |
| ⭐ vs L-form? | No genetic relation to bacteria; never reverts; has cholesterol; stable in ordinary medium; smaller colony; low turbidity |
| Pathogenesis? | Adherence · H₂O₂ and O₂⁻ · hypersensitivity and autoantibody |
| M. pneumoniae? | Primary atypical pneumonia — 15–50% of pneumonias, dry cough, interstitial |
| Cold agglutinin test? | Non-specific; type O RBCs clump at 4 °C, unclump at 37 °C; positive in 50–65% |
- Define Mycoplasma for 4 marks. → The smallest cell-wall-free prokaryotes able to live freely in nature and on artificial medium; pleomorphic, passing bacterial filters; sterol-containing triple-layered membrane; resistant to all β-lactams
- List the similarities and differences with L forms. → Similar: wall-deficient, penicillin-resistant, pleomorphic, filter-passing, fried-egg colony. Different: no genetic relation to bacteria and no reversion · cholesterol present · ordinary medium · smaller colony · low turbidity
- Why do β-lactams fail? → There is no cell wall for them to act on
- Define the cold agglutinin test and state its limitation. → A non-specific test for cold-reacting antibody clumping type O RBCs at 4 °C and unclumping at 37 °C; positive in only 50–65% of M. pneumoniae and in many other conditions
- Which mycoplasmas cause urogenital disease? → M. hominis (PID, pyelonephritis, postpartum fever), M. genitalium and U. urealyticum (NGU)