Gram-negativeBacilliCurved / comma-shaped

Helicobacter pylori

Gram-negative, microaerophilic, spiral-shaped bacillus that colonizes the gastric mucosa, causing chronic gastritis, peptic ulcer disease, and predisposing to gastric adenocarcinoma and MALT lymphoma.

Organism Card

DomainMust know
Identity
  • G−ve spiral/curved rod (coccobacillus), unipolar flagella [1][2]
  • Microaerophilic; formerly classified as Campylobacter [2]
  • Strong urease activity — key survival mechanism in acidic stomach [1][2]
Lab discriminator
  • Urease +++ (basis of CLO test & urea breath test) [1][2]
  • Oxidase +, catalase +
  • vs Campylobacter: H. pylori is urease + and grows at 37°C (not 42°C); spiral not comma-shaped
  • Culture: microaerophilic, slow growth on selective media (Skirrow's); low yield clinically [2]
Reservoir / transmission
  • Human-only reservoir; no environmental source [2]
  • Oral–oral (main) and faecal–oral transmission [3][4]
  • Infection mostly acquired in childhood (age ≤ 5, gastric acid not yet potent) [2]
  • ~50% adults in HK / China; developing countries 50–80%, developed 10–30% [2][3]
  • Risk factors: low socioeconomic status, overcrowding, poor hygiene [2][3]
Key virulence
  • Urease → hydrolyses urea to NH₃ + HCO₃⁻ → neutralises gastric acid → survival [1][2]
  • Flagella + mucolytic enzymes → penetrate mucus layer to gastric epithelium [4]
  • CagA (cytotoxin-associated gene A) → ↑inflammation, ↑gastric cancer risk
  • VacA (vacuolating cytotoxin) → epithelial cell vacuolation and apoptosis
  • Adhesins (BabA, SabA) → bind gastric epithelial cells
Clinical syndromes
  • Chronic gastritis (antral-predominant) [2]
  • Peptic ulcer disease: DU (>90% a/w H. pylori) & GU [2][5]
  • Gastric adenocarcinoma (intestinal type): chronic atrophic gastritis → intestinal metaplasia → dysplasia → carcinoma [6]
  • Gastric MALT lymphoma (WHO Class I carcinogen)
  • Functional dyspepsia: H. pylori eradication may relieve symptoms in a subgroup [7]
  • Hyperplastic gastric polyps: a/w H. pylori; treat if +ve [6]
Diagnosis
  • Invasive (requires OGD + antral biopsy): [1][2][4]
  • Rapid urease test (CLO test) — biopsy in urea medium, colour change yellow → pink; FN if recent PPI/antibiotics or active bleeding [2][8]
  • Histology — H&E ± special stains (Warthin-Starry silver, modified Giemsa, Genta) [2]
  • Culture with antibiotic sensitivity — only for refractory cases [1][4]
  • Non-invasive: [1][3]
  • Urea breath test (¹³C or ¹⁴C-labelled urea) — best for confirming eradication [4]
  • Stool antigen ELISA — also good for post-treatment monitoring [1]
  • Serology (antibody ELISA)CANNOT distinguish active vs past infection; NOT for eradication monitoring [3][8]
  • PPIs & antibiotics must be stopped ≥ 2–4 weeks before testing (except serology) to avoid FN [3][8]
  • H2RA and antacids do NOT affect test results [3]
Treatment
  • Standard (clarithromycin-based) triple therapy: PPI + amoxicillin + clarithromycin × 14 days [5][9]
  • Bismuth quadruple therapy (for clarithromycin resistance or failed triple therapy): PPI + bismuth subsalicylate + tetracycline + metronidazole [8][9]
  • Post-treatment testing ≥ 4 weeks after stopping all drugs; use UBT or stool antigen (NOT serology) [3][8]
  • Recurrence ~90% without eradication; eradication → long-term remission of PUD [2]
  • 14-day regimen now preferred over 7-day [8]
Prevention
  • No vaccine currently available
  • Improved sanitation, hygiene, and clean water supply
  • Not a notifiable disease in Hong Kong
  • Test all PUD patients for H. pylori and eradicate if positive [4]
Classic traps
  • Serology trap: antibody titres remain elevated 6–12 months post-eradication → do NOT use for confirming cure [3]
  • CLO test FN: recent PPI/antibiotics suppress organisms below threshold; also FN with active bleeding in ulcer bed [2][8]
  • H. pylori + functional dyspepsia: coexistence possible; eradication may help but does not exclude FD [7]
  • Zollinger-Ellison syndrome: recurrent PUD despite adequate treatment + H. pylori −ve + no NSAIDs → suspect gastrinoma [4]
  • NSAIDs are the most common cause of PUD apart from H. pylori [5][9]

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