Microbiology · MU Sofia

84. Genus Rickettsia, Genus Caxiella.

Covers the two genera together, starting with Rickettsia: general features as obligate intracellular bacteria, the spotted fever and typhus groups, endothelial tropism, and arthropod transmission. It then reviews clinical syndromes such as Rocky Mountain spotted fever and epidemic typhus in a comparison table, plus diagnosis, doxycycline-based treatment and prevention. The Coxiella section follows, covering the spore-like, highly infectious Coxiella burnetii, its zoonotic spread, acute and chronic Q fever, and treatment durations.

Inside: 18 sections · 8 labelled pictures · 3 tables · 16 flashcards · 4 min

Topic 84 of 113 in the MU Sofia syllabus for Microbiology (Dental Medicine, Year 2). The free AceMed note covers it in 11 sections, about 445 words (4 min of reading), with 16 flashcards.

In this note

  1. Genus Rickettsia, Genus Caxiella.
  2. I. General Characteristics
  3. II. Morphology & Life Cycle
  4. III. Virulence Factors
  5. IV. Epidemiology
  6. V. Clinical Manifestations
  7. VI. Diagnosis
  8. VII. Treatment
  9. VIII. Prevention
  10. Genus Coxiella
  11. II. Morphology and Pathogenesis

I. General Characteristics

  • Obligate intracellular Gram-negative rods.
  • Poor Gram stain visibility; better seen with Giemsa or Gimenez stain.
  • Non-motile, non-spore-forming, pleomorphic.
  • Aerobic, requires host ATP → "energy parasite".
  • Infects endothelial cells, leading to vasculitis and increased vascular permeability.
  • Arthropod-borne (ticks, lice, fleas, mites) – key to transmission.
  • Divided into groups:
  • Spotted fever group: e.g., R. rickettsii, R. conorii.
  • Typhus group: e.g., R. prowazekii, R. typhi.

II. Morphology & Life Cycle

  • Requires cell culture, embryonated eggs, or tissue for growth.
  • Uses actin polymerization to move within and between host cells.

III. Virulence Factors

  • Phospholipase D and membrane peroxidation: help escape phagosome.
  • Endothelial cell infection → vascular damage → rash, edema, organ ischemia.
  • Induce host cytokines → inflammatory response.

IV. Epidemiology

  • Reservoirs: Wild rodents, humans (for epidemic typhus), small mammals.
  • Vectors:
  • R. rickettsii – ticks (Dermacentor)
  • R. prowazekii – body louse
  • R. typhi – fleas
  • Worldwide distribution; endemic areas depend on vector presence.

VI. Diagnosis

  • Clinical suspicion (fever + rash + vector exposure).
  • Serology (Weil-Felix test) – obsolete, low specificity.
  • Immunofluorescence antibody (IFA) – gold standard.
  • PCR – detects rickettsial DNA in blood or tissue biopsy.
  • Skin biopsy: shows vasculitis with intracellular bacteria.

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