Microbiology · MU Sofia

83. Genus Chlamydia

Covers the genus Chlamydia as obligate intracellular Gram-negative bacteria, starting with general features such as the lack of peptidoglycan and the biphasic elementary and reticulate body life cycle. It then moves through virulence factors, epidemiology and the diseases caused by C. trachomatis, C. pneumoniae and C. psittaci, presented in a serovar-group table. Diagnostic tests and treatment choices are summarised in tables, followed by prevention measures.

Inside: 9 sections · 6 labelled pictures · 4 tables · 15 flashcards · 3 min

Topic 83 of 113 in the MU Sofia syllabus for Microbiology (Dental Medicine, Year 2). The free AceMed note covers it in 9 sections, about 335 words (3 min of reading), with 15 flashcards.

In this note

  1. Genus Chlamydia
  2. I. General Characteristics
  3. II. Morphology and Life Cycle
  4. III. Virulence Factors
  5. IV. Epidemiology
  6. V. Clinical Manifestations
  7. VI. Laboratory Diagnosis
  8. VII. Treatment
  9. VIII. Prevention

I. General Characteristics

  • Obligate intracellular Gram-negative bacteria — cannot synthesize their own ATP (“energy parasites”).
  • Lack peptidoglycan in their cell wall despite having a Gram-negative structure.
  • Not visible on Gram stain; best visualized using Giemsa stain or immunofluorescence.
  • Possess a unique biphasic life cycle involving:
  • Elementary body (EB): infectious, extracellular, metabolically inactive.
  • Reticulate body (RB): non-infectious, intracellular, metabolically active replicating form.
  • Sensitive to tetracyclines and macrolides (e.g., azithromycin).
  • Species of clinical importance:
  • Chlamydia trachomatis
  • Chlamydophila pneumoniae
  • Chlamydophila psittaci

II. Morphology and Life Cycle

  • Life cycle (approx. 48–72 hours):
  1. 1. EB attaches to host cell and enters via endocytosis.
  2. 2. EB transforms into RB inside a membrane-bound vacuole (inclusion).
  3. 3. RB replicates by binary fission.
  4. 4. RBs transform back into EBs.
  5. 5. Cell lysis or extrusion releases new EBs to infect other cells.

III. Virulence Factors

  • Intracellular lifestyle: avoids host immune detection.
  • Prevention of phagosome-lysosome fusion.
  • LPS: weak endotoxin effect.
  • Heat shock proteins (Hsp60): chronic inflammation → scarring in persistent infections.
  • Antigenic variation of outer membrane proteins (esp. MOMP – major outer membrane protein).
  • Cytokine stimulation → recruitment of inflammatory cells → tissue damage.

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