Two Forms of Existence
Chlamydia exhibit marked polymorphism. During their development, the microorganism exists in two radically different forms.
| Feature | Elementary Bodies (EB) | Reticulate Bodies (RB) |
|---|---|---|
| Function | Infectious form (transmission/infection) | Vegetative form (growth and division) |
| Localization | Extracellular | Intracellular (typically near the nucleus) |
| Morphology | Small (0.2–0.3 µm), spherical | Large (up to 1.2 µm), ovoid |
| Staining (Giemsa) | Red | Blue or purple |
| Structural features | Thick envelope (inner and outer membranes), lacks N-acetylmuramic acid | Metabolically active, capable of binary fission |
Elementary bodies are highly resilient in the external environment: they withstand freezing down to –70 °C and prolonged drying, but are rapidly inactivated by heat and disinfectants.
Chlamydial Life Cycle
The reproductive process occurs intracellularly, predominantly in epithelial tissues, and includes strictly sequential stages:
- Adsorption and penetration. The elementary body attaches to the target cell and enters via endocytosis, ending up in a phagosome.
- Defense against lysis. This is a critical survival moment: chlamydial proteins block the fusion of the phagosome with cellular lysosomes, avoiding contact with destructive enzymes.
- Transformation and division. Inside the vacuole, the EB transforms into a metabolically active reticulate body. RBs begin repeated binary fission, forming intracellular inclusions.
- Maturation and release. Reticulate bodies condense, undergoing reverse differentiation back into elementary bodies. Finally, the membranes of the vacuole and the host cell rupture (lysis), and new infectious forms are released.
Classification and Clinical Significance
The family Chlamydiaceae includes human pathogens in the genera Chlamydia and Chlamydophila. Species differ by antigenic structure (serovars) and the pathologies they cause:
- Chlamydia trachomatis (anthroponosis, 20 serovars). Serovars A–C cause trachoma (a severe eye infection leading to blindness due to corneal scarring). Serovars D–K are responsible for urogenital chlamydiasis, which can lead to adhesions, infertility, and ectopic pregnancy; in newborns, they cause pneumonia and conjunctivitis. Serovars L1–L3 are the causative agents of lymphogranuloma venereum.
- Chlamydophila psittaci (zoonosis, 10 serovars). Causes psittacosis (ornithosis), a severe lung infection. Interestingly, humans are a "dead-end" host for this infection (person-to-person transmission does not occur).
- Chlamydophila pneumoniae (anthroponosis, 1 serovar). Provokes acute respiratory infections (bronchitis, pneumonia, pharyngitis). Chronic persistence is associated with the development of atherosclerosis, bronchial asthma, and sarcoidosis.
Metabolism and Pathogenicity Factors
Chlamydia occupy a unique position between viruses and classical bacteria. They possess their own ribosomes and protein synthesis systems, and they can ferment pyruvic acid. However, they entirely lack oxidative phosphorylation systems and do not synthesize high-energy compounds. Consequently, they are forced to use host cell ATP, earning them the designation of "energy parasites".
Key pathogenicity factors include:
- Adhesins — outer membrane proteins of elementary bodies.
- Endotoxin — genus-specific lipopolysaccharide (LPS) of the cell wall.
- Antiphagocytic proteins — prevent digestion within macrophages.
- Heat shock proteins (HSPs) — capable of triggering autoimmune reactions. A prime example is Reiter's syndrome, which develops in men following urogenital chlamydial infection.