Microbiology · MU Sofia

74. Genus Clostridium - C. tetani.

Covers Clostridium tetani, starting with the genus overview and a table linking Clostridium species to their diseases, then the spore-forming, anaerobic bacterium's characteristics and its toxin-mediated pathogenesis. Also describes clinical features including neonatal tetanus, laboratory diagnosis, treatment for mild and severe cases, and vaccination-based prevention.

Inside: 9 sections · 6 labelled pictures · 2 tables · 16 flashcards · 3 min

Topic 74 of 113 in the MU Sofia syllabus for Microbiology (Dental Medicine, Year 2). The free AceMed note covers it in 9 sections, about 365 words (3 min of reading), with 16 flashcards.

In this note

  1. Genus Clostridium – C. tetani
  2. Overview of Genus Clostridium
  3. General Characteristics
  4. Virulence Factors
  5. Pathogenesis of Tetanus
  6. Clinical Features
  7. Laboratory Diagnosis
  8. Treatment
  9. Prevention

Overview of Genus Clostridium

  • Gram-positive, spore-forming rods
  • Strict anaerobes
  • Found in soil, decaying vegetation, and the intestinal tract of animals/humans
  • All Clostridium species produce exotoxins, many of which are neurotoxins or cytotoxins

General Characteristics

  • Gram-positive bacilli with terminal round spores
  • Characteristic “drumstick” appearance
  • Motile — has peritrichous flagella
  • Strict anaerobe
  • Found in soil, dust, animal feces, and contaminated objects like cotton, wool, and surgical instruments
  • Spores are extremely resistant and survive in harsh environments

Virulence Factors

  • Tetanospasmin is antigenic and can be neutralized by antitoxin.
  • All serotypes produce the same toxin, though they differ in surface antigens.

Pathogenesis of Tetanus

  1. 1. Spores enter via wound (deep puncture wounds, unsterile instruments, umbilical stump, injections, etc.)
  2. 2. Anaerobic conditions allow spores to germinate
  3. 3. Vegetative bacteria release tetanospasmin
  4. 4. Toxin binds to motor nerve endings, travels retrograde to CNS
  5. 5. Inhibits release of GABA & glycine → uncontrolled muscle contraction
  6. 6. Results in spastic paralysis, starting with lockjaw (trismus)

No tissue invasion or inflammation by the bacteria; disease is entirely toxin-mediated.

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