Helicobacter pylori colonizes the stomach in ~50% of the world’s human population, essentially for life unless eradicated by antibiotic treatment. Colonization with this organism is the main risk factor for peptic ulceration (Chap. 348) as well as for gastric adenocarcinoma and gastric mucosa-associated lymphoid tissue (MALT) lymphoma (Chap. 109). Treatment for H. pylori has revolutionized the management of peptic ulcer disease, providing a permanent cure in most cases. Such treatment also represents first-line therapy for patients with low-grade gastric MALT lymphoma. Treatment of H. pylori is of no benefit in the treatment of gastric adenocarcinoma, but prevention of H. pylori colonization could potentially prevent gastric malignancy and peptic ulceration. In contrast, increasing evidence indicates that lifelong H. pylori colonization may offer some protection against complications of gastroesophageal reflux disease (GERD), including esophageal adenocarcinoma. Recent research has focused on whether H. pylori colonization is also a risk factor for some extragastric diseases and whether it is protective against some recently emergent medical problems, such as childhood-onset asthma and obesity.
H. pylori is a gram-negative bacillus that has naturally colonized humans for at least 100,000 years, and probably throughout human evolution. It lives in gastric mucus, with a small proportion of the bacteria adherent to the mucosa and possibly a very small number of the organisms entering cells or penetrating the mucosa; the organism’s distribution is never systemic. Its spiral shape and flagella render H. pylori motile in the mucus environment. The organism has several acid-resistance mechanisms, most notably a highly expressed urease that catalyzes urea hydrolysis to produce buffering ammonia. H. pylori is microaerophilic (i.e., requires low levels of oxygen), is slow-growing, and requires complex growth media in vitro.
Other Helicobacter Species
A very small proportion of gastric Helico-bacter infections are due to species other than H. pylori, possibly acquired as zoonoses. These non-pylori gastric helicobacters are associated with low-level inflammation and occasionally with disease. In immunocompromised hosts, several nongastric (intestinal) Helicobacter species can cause disease with clinical features resembling those of Campylobacter infections; these species are covered in Chap. 192.
Prevalence and Risk Factors
The prevalence of H. pylori among adults is <30% in most parts of the United States and in other developed countries as opposed to >80% in most developing countries. In the United States, prevalence varies with age: up to 50% of 60-year-old persons, ~20% of 30-year-old persons, and fewer than 10% of children are colonized. H. pylori is usually acquired in childhood. The age association is due mostly to a birth-cohort effect whereby current 60-year-olds were more commonly colonized as children than are current children. Spontaneous acquisition or loss of H. pylori in adulthood is uncommon. Childhood acquisition explains why the main risk factors for infection are markers of crowding and social deprivation in childhood.