Members of the genus Helicobacter are curved or spiral organisms (Figure 1). They have a rapid, corkscrew motility resulting from multiple polar flagella. Helicobacter pylori, the species of human significance, is microaerophilic, and produces urease. It causes acute gastritis and duodenal and gastric ulcers. H. pylori (and several other Helicobacter species) are unusual in their ability to colonize the stomach, where low pH normally protects against bacterial infection. H. pylori infections are relatively common and worldwide in distribution.

fig1. Helicobacter pylori in a gastric pit.

A. Pathogenesis

 Transmission of H. pylori is thought to be from person to person, because the organism has not been isolated from food or water. Untreated, infections tend to be chronic, even lifelong. H. pylori colonizes gastric mucosal (epithelial) cells in the stomach and metaplastic gastric epithelium in the duodenum or esophagus but does not colonize the rest of the intestinal epithelium. The organism survives in the mucus layer that coats the epithelium and causes chronic inflammation of the mucosa (Figure 2). Although the organism is noninvasive, it recruits and activates inflammatory cells. Urease released by H. pylori produces ammonia ions that neutralize stomach acid in the vicinity of the organism, favoring bacterial multiplication. Ammonia may also both cause injury and potentiate the effects of a cytotoxin produced by H. pylori.

fig2. Helicobacter pylori infection, resulting in ulceration of the stomach.

B. Clinical significance

 Initial infection with H. pylori causes acute gastritis, sometimes with diarrhea that lasts about 1 week. The infection usually becomes chronic, with diffuse, superficial gastritis that may be associated with epigastric discomfort. Both duodenal ulcers and gastric ulcers are closely correlated with infection by H. pylori. [Note: H. pylori infection is found in more than 95 percent of duodenal ulcer patients and in nearly all patients with gastric ulcers who do not use aspirin or other nonsteroidal anti-inflammatory drugs, both risk factors for gastric ulcers.] H. pylori infection appears to be a risk factor for development of gastric carcinoma and gastric B-cell lymphoma (mucosa associated lymphoid tumors, or MALTomas).

C. Laboratory identification

 Noninvasive diagnostic tests include serologic tests (enzyme-linked immunosorbent assay, commonly known as ELISA, for serum anti bodies to H. pylori,  and breath tests for urease. [Note: Breath tests involve administering radioactively labeled urea by mouth. If H. pylori are present in the patient's stomach, the urease produced by the organism will split the urea to CO2 (radioactively labeled and exhaled) and NH3.] Invasive tests involve gastric biopsy specimens obtained by endoscopy. H. pylori can be detected in such specimens histologically, by culture, or by a test for urease.

D. Treatment and prevention

 Elimination of H. pylori requires combination therapy with two or more antibiotics. Although H. pylori is innately sensitive to many antibiotics, resistance readily develops. A typical regimen includes amoxicillin plus clarithromycin plus a proton pump inhibitor such as omeprazole (Figure 3).

fig3. Summary of Helicobacter disease. 1 Indicates first-line drugs.