Helicobacter pylori

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Microbiology - Stomach's Spiral Squatter

Helicobacter pylori attaching to stomach lining

  • Gram-negative, spiral-shaped rod colonizing the gastric antrum.
  • Highly motile via flagella; catalase, oxidase, and urease-positive.
    • Urease neutralizes stomach acid, enabling survival.
  • Causes chronic gastritis, peptic ulcers (duodenal > gastric), and is a major risk factor for gastric adenocarcinoma and MALT lymphoma.
  • Diagnosis: Urea breath test, stool antigen.
  • Treatment: 📌 Triple therapy (Clarithromycin, Amoxicillin, PPI).

H. pylori is the first formally recognized bacterial carcinogen.

Pathogenesis & Virulence - Acid-Proofing Antics

  • Primary Challenge: Survives in the highly acidic (pH 1-2) stomach lumen.
  • Key Enzyme: Urease
    • Abundantly produced, found on the bacterial surface and cytoplasm.
    • Catalyzes urea hydrolysis: $Urea + H_2O \rightarrow 2NH_3 + CO_2$.
    • Ammonia ($NH_3$) buffers gastric acid ($HCl$), creating a neutral pH microenvironment.
    • This allows the bacterium to burrow into the protective mucus layer.

H. pylori pathogenesis and immune response

CagA (Cytotoxin-associated gene A): An injected oncoprotein delivered by a type IV secretion system. It disrupts the cytoskeleton, increases cell proliferation, and is strongly associated with gastric adenocarcinoma.

Clinical Presentation - Belly's Burning Burden

  • Gastritis & Peptic Ulcers: Chronic, gnawing epigastric pain.
    • Duodenal Ulcer (>90% assoc.): Pain improves with meals. More common.
    • Gastric Ulcer (70% assoc.): Pain worsens with meals.
  • Increased Cancer Risk:
    • MALT Lymphoma (can regress with H. pylori treatment).
    • Gastric Adenocarcinoma.

⭐ The majority of duodenal ulcers are caused by H. pylori, whereas the association is strong but less frequent for gastric ulcers. This is a classic exam distinction.

Diagnosis - Finding the Fiend

  • Non-Invasive Tests (Initial Dx & Eradication Check)

    • Urea Breath Test: High sensitivity & specificity. Detects active infection.
    • Stool Antigen Assay: Good for initial diagnosis & post-treatment confirmation.
    • Serology (IgG): Shows exposure, not active infection; less useful.
  • Invasive Tests (Endoscopy with Biopsy - Gold Standard)

    • Rapid Urease Test (RUT): Quick, presumptive ID on biopsy sample.
    • Histology: Warthin-Starry silver stain reveals spiral-shaped organisms.
    • Culture: For antibiotic susceptibility testing, especially in treatment failure.

⭐ The Urea Breath Test relies on H. pylori’s urease splitting labeled urea into ammonia and labeled $CO_2$, which is detected in exhaled breath.

H. pylori in gastric biopsy (Warthin-Starry stain)

Treatment - Eviction Notice Protocol

  • Primary Goal: Eradicate H. pylori to prevent recurrence of peptic ulcers and reduce gastric cancer risk.
  • Standard First-Line Therapy (Triple):
    • Proton Pump Inhibitor (PPI)
    • Clarithromycin
    • Amoxicillin (or Metronidazole if penicillin allergic)
  • **Quadruple Therapy (First-line in high resistance areas >15% or salvage):
    • PPI
    • Bismuth subsalicylate
    • Metronidazole
    • Tetracycline

⭐ For treatment failure, salvage therapy should avoid antibiotics used in the initial regimen. If triple therapy fails, switch to quadruple therapy or a levofloxacin-based regimen.

📌 Mnemonic (Quad Therapy): Please Make Tummy Better (PPI, Metronidazole, Tetracycline, Bismuth).

  • H. pylori is a Gram-negative, spiral-shaped bacterium strongly linked to peptic ulcer disease (especially duodenal ulcers), gastric adenocarcinoma, and MALT lymphoma.
  • Its key virulence factor is urease, which hydrolyzes urea into ammonia, neutralizing gastric acid and allowing survival in the stomach.
  • The urea breath test is a common non-invasive diagnostic method.
  • Standard treatment is triple therapy: a proton pump inhibitor (PPI) plus two antibiotics, typically clarithromycin and amoxicillin.

Practice Questions: Helicobacter pylori

Test your understanding with these related questions

A 45-year-old woman has a history of mild epigastric pain, which seems to have gotten worse over the last month. Her pain is most severe several hours after a meal and is somewhat relieved with over-the-counter antacids. The patient denies abnormal tastes in her mouth or radiating pain. She does not take any other over-the-counter medications. She denies bleeding, anemia, or unexplained weight loss, and denies a family history of gastrointestinal malignancy. Which of the following is the best next step in the management of this patient?

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Flashcards: Helicobacter pylori

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Which of the common gram-negative nosocomial infections(Klebsiella, Serratia, Enterobacter)is urease-positive?_____

TAP TO REVEAL ANSWER

Which of the common gram-negative nosocomial infections(Klebsiella, Serratia, Enterobacter)is urease-positive?_____

Klebsiella

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