HELICOBACTER PYLORI

HELICOBACTER PYLORI

• definition – Helicobacter pylori is a Gram‑negative, microaerophilic, helical bacterium that colonises the gastric mucosa

• transmission / causes – fecal‑oral, oral‑oral, contaminated water/food, close person‑to‑person contact; usually acquired in childhood

• important strains – CagA‑positive (high virulence), VacA toxin variants, BabA, OipA adhesins

• morphology – spiral/curved rod 0.5‑1 µm wide, 2‑5 µm long, 4‑6 unipolar flagella, urease +, catalase +, oxidase +; Gram‑negative cell wall

• pathogenesis (step‑wise)

  1. ingestion → stomach
  2. urease hydrolyses urea → NH₃ + CO₂ → neutralises gastric acid → creates a protective niche
  3. flagella provide motility → bacteria swim through mucus layer
  4. adhesins (BabA, SabA) bind Lewis b antigens on epithelial cells → close attachment
  5. type IV secretion system injects CagA → disrupts signalling, ↑ IL‑8, chronic inflammation
  6. VacA forms pores → mitochondrial damage, apoptosis, further inflammation
  7. persistent inflammation → chronic gastritis → atrophy/metaplasia → ulceration or carcinoma

• clinical features

  • chronic gastritis: epigastric pain, nausea, early satiety
  • peptic ulcer disease: duodenal > gastric ulcer, burning pain, relief with food/antacids
  • dyspepsia, weight loss, iron‑deficiency anemia
  • extra‑gastric associations: MALT lymphoma, gastric adenocarcinoma

• complications

  • gastric or duodenal ulcer perforation, bleeding
  • atrophic gastritis → intestinal metaplasia → gastric cancer
  • mucosa‑associated lymphoid tissue (MALT) lymphoma

• laboratory diagnosis (point‑wise)

  1. invasive (endoscopic biopsy)
     • rapid urease test (RUT) → colour change (yellow) if urease present
     • histopathology (Warthin‑Starry, Giemsa, immunohistochemistry) → curved bacilli on gastric mucosa
     • culture on selective media (Campylobacter agar, microaerophilic, 5‑7 days) → definitive identification
     • PCR for CagA/VacA genes → strain typing
  2. non‑invasive
     • urea breath test (13C/14C) → labelled CO₂ in exhaled breath indicates active infection
     • stool antigen ELISA (monoclonal) → detects current infection
     • serology (IgG ELISA) → indicates exposure, not useful for cure monitoring

• management (first‑line triple therapy)

  • proton‑pump inhibitor (e.g., omeprazole 20 mg bid) + clarithromycin 500 mg bid + amoxicillin 1 g bid for 14 days
  • alternative quadruple regimen (if clarithromycin resistance) – PPI + bismuth subcitrate + tetracycline + metronidazole for 10‑14 days
  • test‑of‑cure 4 weeks after therapy (UBT or stool antigen)

• prevention

  • safe drinking water, proper sanitation, hand‑washing
  • avoid sharing utensils, cook food thoroughly

• memory trick (rhyming) for pathogenesis
  “Urease makes the pH rise, flagella cut the mucus ties, adhesins stick, CagA tricks, VacA pores, inflammation roars.”
  (U F A C V I – first letters of each step)