Chlamydia
Definition and common properties ★★★
A prokaryote that is an obligate intracellular parasite of eukaryotic cells, has a unique developmental cycle, and can pass through bacterial filters.
Common properties
- Small; obligate intracellular parasites
- Cell wall similar to Gram-negative bacteria, but LACKING a peptidoglycan layer
- No capsule and no flagella
- Contain DNA, RNA and ribosomes
- Have a unique developmental cycle
- Reproduce by binary fission
- Susceptible to certain antibiotics
The deck's key-points slide adds: chlamydiae are small organisms that multiply in the cytoplasm of their host cells using a unique biphasic developmental cycle, and diagnosis is made serologically; doxycycline is used for treatment.
Module C now has three organisms that are all “not quite bacteria”. Fix the discriminator for each and no exam question can confuse them.
Mycoplasma — NO cell wall at all, and it grows freely on artificial medium.
Rickettsia — has a wall, obligate intracellular, and is transmitted by an arthropod vector.
Chlamydia — has a wall but no peptidoglycan in it, is obligate intracellular, has no vector, and is the only one with a two-form developmental cycle.
Note the practical consequence of that second row: no peptidoglycan means penicillin does not work — the deck says so explicitly. Chlamydia reaches the same clinical conclusion as Mycoplasma by a different route: one has no wall, the other has a wall without the layer penicillin attacks.
- Define Chlamydia. → A prokaryote that is an obligate intracellular parasite of eukaryotic cells, with a unique developmental cycle, able to pass through bacterial filters
- List its common properties. → Small, obligate intracellular · G−-like wall but NO peptidoglycan · no capsule or flagella · DNA, RNA and ribosomes · unique developmental cycle · binary fission · susceptible to certain antibiotics
- Why does penicillin fail? → The wall contains no peptidoglycan layer
- How does it differ from Mycoplasma and Rickettsia? → Mycoplasma has no wall and grows on artificial medium; Rickettsia is intracellular with an arthropod vector; Chlamydia is intracellular with no vector and a unique two-form cycle
⭐ The developmental cycle — EB and RB ★★★
| Elementary body (EB) | Reticulate body (RB) / initial body | |
|---|---|---|
| Location | Extracellular | Intracytoplasmic |
| Role | The INFECTIOUS form | The REPRODUCTIVE form |
| Size | Small — 0.2–0.4 µm | Larger — 0.5–1.2 µm |
| Replication | Binds to receptors on host cells, but CANNOT replicate | Replicates by binary fission within host cells |
| Infectivity | Infectious | Non-infectious |
| Membrane | Rigid outer membrane — resistant to a harsh environment | Fragile membrane |
The cycle — 48–72 hours
- The EB binds receptors on the host cell and enters by endocytosis
- Within 8–12 hours it reorganises into the RB inside a membrane-bound vacuole
- The RB divides by binary fission — 24–36 hours — forming an inclusion body
- From 30–45 hours the RBs condense back into EBs
- At 48–72 hours the cell releases infectious EBs
A cytoplasmic body containing RBs and EBs at different developmental stages. In C. trachomatis the inclusions are glycogen-rich and stain dark brown with iodine, or bright yellow-green with a fluorescein-labelled antibody.
Ask why an organism would need two bodies rather than one, and the design becomes obvious.
An obligate intracellular parasite must do two things that cannot be done by the same structure. It must survive outside a cell long enough to reach the next one — which demands a tough, rigid, metabolically quiet particle. And it must multiply rapidly inside — which demands a large, fragile, metabolically active one.
So EB = the travelling form: small, rigid, environmentally stable, infectious, and unable to divide. RB = the working form: larger, fragile, dividing, and useless outside the cell.
A spore-forming bacterium solves the same problem the same way. And a virus solves it with a capsid — which is why chlamydia was mistaken for a virus for years, and why its culture, as §3 says, resembles viral cultivation.
If a question asks which form is infectious, the answer is always EB.
- Define the elementary body. → The extracellular, infectious form: small (0.2–0.4 µm), rigid outer membrane, environmentally resistant, binds host-cell receptors but cannot replicate
- Define the reticulate body. → The intracytoplasmic, reproductive form: larger (0.5–1.2 µm), fragile membrane, non-infectious, replicating by binary fission inside the host cell
- How long is the cycle? → 48–72 hours
- Describe the cycle. → EB binds and enters by endocytosis → becomes RB at 8–12 h → RB divides by binary fission (24–36 h) forming an inclusion body → condenses back to EB (30–45 h) → release at 48–72 h
- What is an inclusion body? → A cytoplasmic body containing RBs and EBs at different stages; in C. trachomatis it is glycogen-rich and stains brown with iodine
Culture and resistance ★★
| Detail | |
|---|---|
| Culture | Similar to viral cultivation — embryonated egg, cell culture, animals |
| Resistance | Weak |
| Sensitive to | Heat — killed after 10 min at 60 °C · 0.1% formalin, ether · antibiotics: erythromycin, doxycycline, sulfanilamide, tetracycline |
| ⚠️ Not effective | Penicillin |
- How is Chlamydia cultured? → Like a virus — in embryonated eggs, cell culture or animals
- What is it sensitive to? → Heat (60 °C for 10 min), 0.1% formalin, ether; erythromycin, doxycycline, sulfanilamide, tetracycline
- Which antibiotic is ineffective? → Penicillin
Chlamydia trachomatis ★★★
Two genera are medically important — Chlamydia and Chlamydophila. C. trachomatis has 3 biological variants and 18 serotypes: biovar trachoma with 14 serotypes (A, B, Ba, C, D, Da, E, F, G, H, I, Ia, J, K); biovar lymphogranuloma venereum (LGV) with 4 serotypes (L1, L2, L2a, L3); and biovar mouse.
⭐ The serotypes determine the clinical manifestation
| Serotypes | Diseases |
|---|---|
| A, B, Ba, C | Trachoma |
| B – K | Inclusion conjunctivitis — newborns: neonatal purulent conjunctivitis; adults: acute follicular conjunctivitis |
| D – K | Nongonococcal urethritis (NGU) — males: NGU, dysuria, epididymitis; females: NGU, cervicitis, salpingitis and PID. Also infant pneumonia |
| L1, L2, L2a, L3 | Lymphogranuloma venereum (LGV) |
Trachoma
- Limited to humans
- The greatest single cause of blindness; prominent in areas with poor sanitation
- Direct contact: eye–hand–eye. Indirect contact: sharing a basin, towel or toys
- Symptoms: tears, mucosal congestion, increasing purulent discharge
- Chronic infection and reinfection are common
- Results in conjunctival scarring — then trachomatous trichiasis (ingrowing eyelash) and corneal opacity
C. trachomatis appears twice in the eye table, and the difference matters.
Trachoma (A, B, Ba, C) is not a single infection but chronic infection and repeated reinfection over years, in conditions of poor sanitation, passed eye–hand–eye and on shared towels. The blindness comes not from the organism destroying the eye but from scarring: the conjunctiva contracts, the lid turns inward, the lashes scrape the cornea (trichiasis), and the cornea opacifies. Immunological damage over decades — the same theme as Unit 13's granuloma.
Inclusion conjunctivitis (D–K) is a genital-tract organism reaching the eye. In the newborn it arrives during delivery — vertical transmission, as with the gonococcus in Unit 9 §7. The distinction is timing: gonococcal ophthalmia neonatorum appears in the first days and threatens the cornea immediately; chlamydial conjunctivitis appears at one to two weeks and is milder. Both are prevented by treating the mother.
And the same D–K serotypes cause the infant pneumonia in the table — acquired by the same route, appearing weeks later.
- How many biovars and serotypes has C. trachomatis? → Three biovars, 18 serotypes — trachoma (14), LGV (4), and biovar mouse
- Which serotypes cause which diseases? → A, B, Ba, C — trachoma · B–K — inclusion conjunctivitis · D–K — NGU and infant pneumonia · L1, L2, L2a, L3 — LGV
- Describe trachoma. → Limited to humans; the greatest single cause of blindness; spread eye–hand–eye and by shared basins, towels and toys; tears, congestion and purulent discharge; chronic reinfection leading to conjunctival scarring, trichiasis and corneal opacity
- What does C. trachomatis cause in men and women? → Men: NGU, dysuria, epididymitis. Women: NGU, cervicitis, salpingitis, PID
C. pneumoniae and C. psittaci ★★★
| C. pneumoniae | Detail |
|---|---|
| Serotype | A single serotype: TWAR — Taiwan Acute Respiratory strain |
| Disease | A cause of atypical pneumonia; pharyngitis is common |
| Transmission | Person to person by droplets |
| Symptoms | Asymptomatic in most cases. Symptomatic: sore throat, hoarseness, fever, headache, persistent cough |
| Extrapulmonary link | Myocarditis, pericarditis, endocarditis, coronary heart disease, atherosclerosis |
| C. psittaci | Detail |
|---|---|
| Disease | Psittacosis — parrot fever |
| Natural hosts | Avian and non-primate animals; the natural reservoir is ANY species of bird — parrots, pigeons, domestic poultry |
| Spread to humans | Respiratory tract — exposure to the infected animal, or inhalation of dust containing dry bird excrement. Person-to-person transmission is rare |
| Disease range | From subclinical to fatal pneumonia; most are atypical pneumonia — fever, chills, dry cough, headache, sore throat, nausea, vomiting |
Treatment: erythromycin, tetracycline, quinolone. For trachoma, long-term therapy is necessary.
- What is TWAR? → The single serotype of C. pneumoniae — Taiwan Acute Respiratory strain
- What does C. pneumoniae cause? → Atypical pneumonia and pharyngitis, spread person to person by droplets; most cases asymptomatic; linked to myocarditis, endocarditis, coronary heart disease and atherosclerosis
- What is psittacosis, and how is it acquired? → Parrot fever from C. psittaci; from any species of bird, by exposure to the animal or inhalation of dust from dry excrement; person-to-person spread is rare
- How are chlamydial infections treated? → Erythromycin, tetracycline, quinolone — long-term for trachoma
Revision
The deck's multiple-choice
“Each of the following statements concerning Chlamydia trachomatis is correct EXCEPT…” — the answer is C. it is an important cause of subacute bacterial endocarditis. SBE is caused by Streptococcus viridans — Unit 9 §5. A, B and D are all true of C. trachomatis.
The whole unit on one screen
| Question | Answer |
|---|---|
| Definition? | Prokaryote, obligate intracellular parasite, unique developmental cycle, passes bacterial filters |
| Cell wall? | Like G− but NO peptidoglycan → penicillin ineffective |
| ⭐ EB? | Extracellular, INFECTIOUS, 0.2–0.4 µm, rigid, cannot replicate |
| ⭐ RB? | Intracytoplasmic, REPRODUCTIVE, 0.5–1.2 µm, fragile, non-infectious, binary fission |
| Cycle length? | 48–72 hours |
| Trachoma serotypes? | A, B, Ba, C — the greatest single cause of blindness |
| Genital serotypes? | D–K — NGU, cervicitis, PID, infant pneumonia, inclusion conjunctivitis |
| LGV serotypes? | L1, L2, L2a, L3 |
| C. pneumoniae? | TWAR — atypical pneumonia, droplet spread |
| C. psittaci? | Psittacosis from birds, by inhalation of dry excrement |
| Treatment? | Erythromycin, tetracycline, doxycycline, quinolone — never penicillin |
- Define Chlamydia, EB and RB. → An obligate intracellular prokaryotic parasite with a unique developmental cycle, passing bacterial filters. EB: extracellular, infectious, rigid, non-replicating. RB: intracytoplasmic, reproductive, fragile, non-infectious
- Describe the developmental cycle. → EB attaches and enters by endocytosis → converts to RB at 8–12 h → RB divides by binary fission forming an inclusion body → condenses to EB from 30–45 h → released at 48–72 h
- Match serotypes to disease. → A, B, Ba, C trachoma · B–K inclusion conjunctivitis · D–K NGU and infant pneumonia · L1–L3 LGV
- Why is penicillin useless against Chlamydia? → Its wall lacks a peptidoglycan layer
- Compare the three atypical organisms. → Mycoplasma: no wall, grows on artificial medium. Rickettsia: intracellular, arthropod vector. Chlamydia: intracellular, no vector, unique EB/RB cycle