Helicobacter species were known for long as a causative agent of gastritis. H. pylori associated gastritis is characterized by the presence of acute and chronic inflammation. Previously, it was believed that in H. pylori gastritis, fundic inflammation was less important than that of the antral mucosa. However, H. pylori and gastroesophageal reflux disease create, or arise concurrently, may also be caused by the anatomical role of the inflammatory cell infiltrate. The source of H. pylori is mostly unknown. H. pylori has a small host range and is present in people and some non-human primates nearly exclusively. In rare cases, the presence of pets may be a concern for H. pylori infection; hence, pets should be isolated. There is also no definitive proof for zoonotic H. pylori transmission. The direct transmission from person to person, either oral or fecal-oral route or both, is expected to lead to new infections. H. pylori colonization is not an infection itself, but it impacts the relative likelihood that multiple pathological conditions of the upper gastrointestinal tract and even the hepatobiliary tract will grow. Therefore, H. pylori examination alone is not relevant but can be done in order to ascertain the cause of a basic disorder, such as peptic ulcer disease or to avoid disease, for example in subjects with family gastric carcinoma. A positive test result will validate the procedure, and a negative test result can suggest that other etiological causes or prevention steps needs to be examined. Gastritis is divided into acute and chronic. Several virulence factors play a role in the disease such as cag PAI (Pathogenicity Island) and VacA vacuolating cytotoxin. Different adhesins and their receptors aid in H. pylori colonization and invasion. Based on analogy with other mucosal infections, it was initially assumed that a protective immune response against H. pylori would predominantly be mediated by antibodies. Subsequent experiments have indicated that the relevance of the humoral system for protective immunity is only marginal. Antibodies can effectively prevent infection and reduce colonization in animal models.
Part of the book: Esophagitis and Gastritis