Microbiology · MU Sofia

81. Genus Helicobacter

Covers the genus Helicobacter, centred on H. pylori: its spiral, microaerophilic, urease-positive features and sheathed polar flagella, then its virulence factors such as urease, adhesins, VacA and CagA. It also outlines epidemiology, clinical disease from chronic gastritis to gastric cancer and MALT lymphoma, laboratory diagnosis by breath, stool, biopsy and serological tests, treatment regimens, and prevention. Tables summarise morphology and diagnostic tests.

Inside: 9 sections · 4 labelled pictures · 2 tables · 14 flashcards · 4 min

Topic 81 of 113 in the MU Sofia syllabus for Microbiology (Dental Medicine, Year 2). The free AceMed note covers it in 9 sections, about 342 words (4 min of reading), with 14 flashcards.

In this note

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

I. General Characteristics

  • Gram-negative, helical/spiral-shaped rods.
  • Motile with multiple polar flagella (sheathed) → corkscrew motility.
  • Microaerophilic: requires 5–10% O₂ and 5–12% CO₂ for growth.
  • Catalase-positive, oxidase-positive, and urease-positive (key feature).
  • Best known species: Helicobacter pylori, the causative agent of chronic gastritis, peptic ulcers, and a risk factor for gastric carcinoma.
  • Other species (e.g., H. hepaticus, H. cinaedi) cause extra-gastric diseases, particularly in immunocompromised hosts.

III. Virulence Factors

  • Urease: Produces ammonia → neutralizes gastric acid → protects the bacteria.
  • Flagella: Enables penetration through gastric mucus.
  • Adhesins (BabA, SabA): Bind to Lewis blood group antigens on gastric epithelium.
  • VacA (vacuolating cytotoxin A): Induces vacuole formation in epithelial cells → apoptosis.
  • CagA (cytotoxin-associated gene A):
  • Delivered into host cells via type IV secretion system.
  • Alters cell signaling → inflammation, loss of cell polarity → carcinogenesis.
  • LPS: Less immunogenic than enterobacterial LPS → aids immune evasion.
  • Immune modulation: Disrupts T cell response, promoting chronic infection.

IV. Epidemiology

  • Reservoir: Human stomach — natural host.
  • Transmission:
  • Fecal-oral, oral-oral, and gastric-oral routes suspected.
  • Acquired primarily during childhood.
  • Global prevalence: Very high; up to 80% in developing countries.
  • Associated with lower socioeconomic status, crowded living, and poor sanitation.

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