Helicobacter pylori

Helicobacter pylori is a curved or spiral gram-negative rod with multiple flagella that let it burrow through gastric mucus. Its signature laboratory feature is being urease positive: the organism splits urea into ammonia and carbon dioxide, and the resulting ammonia neutralizes acid in its immediate surroundings, allowing survival in a stomach environment that kills most bacteria. It is also oxidase and catalase positive and grows best in a microaerophilic atmosphere.

Colonization triggers chronic inflammation of the gastric mucosa. Infection of the antrum increases gastrin release and acid output, which favors duodenal ulcers; infection spreading to the gastric body causes atrophy and reduced acid, which favors gastric ulcers and, over time, intestinal metaplasia. H. pylori is responsible for the large majority of duodenal ulcers and most gastric ulcers not attributable to NSAIDs. Long-standing infection is associated with gastric adenocarcinoma and with MALT lymphoma, which can regress after the organism is eradicated.

Diagnosis uses noninvasive tests — the urea breath test and stool antigen assay — or endoscopic biopsy with histology and a rapid urease test. Because acid suppression and antibiotics reduce bacterial load, those medications are held before testing to avoid false negatives. Treatment combines a proton pump inhibitor with two or more antibiotics, and eradication is confirmed after therapy.

USMLE Step 1 microbiology asks about the urease mechanism, the gram stain and morphology, and the link to ulcers and gastric malignancy. CCMA candidates meet H. pylori in gastroenterology content as the principal infectious cause of peptic ulcer disease, along with the specimen handling and patient preparation involved in breath and stool testing.