Question
Helicobacter pylori.
Answer
Helicobacter pylori is a Gram-negative, spiral/curved, microaerophilic bacterium that colonizes the gastric mucosa (mainly the antrum), and is the major recognized cause of chronic gastritis, peptic ulcer disease, and a Group I (definite) carcinogen for gastric adenocarcinoma and gastric MALT lymphoma.
Key virulence features and pathogenesis: multiple polar flagella provide motility to burrow through the protective gastric mucus layer and reach the less acidic environment near the epithelial surface; produces abundant urease, which hydrolyses urea to ammonia and CO2, locally neutralizing gastric acid and creating a favourable microenvironment around the organism (this property is also exploited diagnostically); the CagA and VacA virulence factors (present in more pathogenic strains) directly damage epithelial cells and provoke a chronic inflammatory response, contributing to mucosal injury, ulceration, and the stepwise progression toward malignancy in long-standing infection.
Laboratory diagnosis:
- Invasive (endoscopy-based): rapid urease test (CLO test) on a biopsy sample — a rapid, low-cost presumptive test exploiting the organism’s urease activity; histopathology (biopsy with special stains, e.g., Giemsa, showing curved organisms in the mucus layer); culture (technically demanding, microaerophilic conditions required, but allows antibiotic susceptibility testing).
- Non-invasive: urea breath test — patient ingests radiolabelled/isotope-labelled urea, and labelled CO2 in exhaled breath (produced by bacterial urease) confirms infection, also useful to confirm eradication after treatment; stool antigen test; serology (detects past or current exposure, cannot distinguish active from past infection, so not useful to confirm cure).
Treatment: triple/quadruple therapy combining a proton-pump inhibitor with two antibiotics (commonly amoxicillin, clarithromycin, or metronidazole, ± bismuth), for 10–14 days, to eradicate the organism and allow ulcer healing.