A helical, Gram-negative bacterium that colonizes the human stomach and duodenum, causing chronic gastritis and playing a causal role in peptic ulcer disease and gastric cancer.
Explanation
Helicobacter pylori is a curved or spiral-shaped bacterium that thrives in the harsh environment of the stomach. It is microaerophilic and Gram‑negative, with multiple polar flagella that enable it to penetrate mucus and adhere to the gastric epithelium. The organism produces large amounts of urease, which hydrolyses urea to ammonia and carbon dioxide. The resulting alkaline microenvironment helps neutralize gastric acid and allows the bacterium to survive. H. pylori was first isolated in 1982 by Barry Marshall and Robin Warren, who showed its association with chronic gastritis and peptic ulcer disease. Subsequent research established it as an important factor in the development of duodenal and gastric ulcers and as a risk factor for gastric adenocarcinoma and mucosa‑associated lymphoid tissue (MALT) lymphoma. In 1994 the International Agency for Research on Cancer classified H. pylori as a Group 1 carcinogen.
Infection is usually acquired during childhood and may persist for decades if untreated. Host factors, bacterial virulence factors such as the cytotoxin‑associated gene A (CagA) and vacuolating cytotoxin A (VacA), and environmental influences determine clinical outcomes. Diagnosis can be made by non‑invasive tests such as the urea breath test, stool antigen detection and serologic assays, or by endoscopy with gastric biopsy for histology, culture and rapid urease testing. Standard treatment consists of combinations of acid suppression and antibiotics, often a proton pump inhibitor plus clarithromycin and amoxicillin or metronidazole; however, increasing antibiotic resistance has led to use of bismuth quadruple therapy and other regimens. Eradication of H. pylori heals most ulcers and reduces the risk of gastric cancer, but some studies suggest the bacterium may have protective effects against conditions like gastroesophageal reflux disease and asthma.
Colonization and Clinical Significance
H. pylori colonizes the gastric antrum and corpus by moving through mucus, attaching to epithelial cells and evading immune responses. The bacteria induce inflammation via secretion of virulence factors, leading to mucosal damage and, over time, atrophic gastritis and intestinal metaplasia. While most infected individuals remain asymptomatic, about 10–15 % develop peptic ulcers and a smaller proportion develop gastric cancer. Geographic variation in prevalence and disease outcomes reflects differences in strains, host genetics and socioeconomic factors. Public health strategies include improving sanitation to reduce transmission and using test‑and‑treat approaches in populations at high risk for gastric cancer.
Understanding H. pylori has transformed management of peptic ulcer disease. Identification and eradication of the bacterium have reduced ulcer recurrence and clarified the link between chronic infection and gastric cancer. Ongoing surveillance of resistance patterns and improved vaccines or alternative therapies remain important goals.
Related Terms: Gastritis, Peptic ulcer, Urease, Microaerophilic, Gastric cancer