H. pylori is an organism that is uniquely equipped to deal with the harsh environment of the stomach. H. pylori has very strong urease activity, which allows it to adjust the acidity of its microenvironment.

The fecal-oral route of transmission is the most well documented method of transmission but there are reports of gastric-oral and oral-oral infection [5]. Children have been shown to transmit the infection by emesis in day care settings and H. pylori has been shown to exist in dental plaque. The risk of acquiring H. pylori is increased by the presence of infected parents and siblings [6]. Crowded living conditions, poor sanitation, and poor hygiene are risk factors for transmission.

Infection with H. pylori causes a transient acute gastritis after which the infection may resolve or may go on to become chronic. Acute gastritis is associated with a neutrophilic infiltrate and a transient hypochlorhydria [2]. If the organism colonizes the stomach successfully, an antrum-predominant gastritis develops (Figs. 27.1, 27.2). This form of gastritis is associated with reduced somatostatin production, enhanced gastrin production, and increased gastric acid secretion. The increased acid is delivered into the proximal duodenum and can cause ulcers in some cases. As the infection proceeds progressive inflammation causes a loss of gastrin producing cells and acid production falls. This is accompanied by changes of atrophy on biopsy and intestinal metaplasia develops in some cases. As the environment becomes more alkaline, the infection moves into the corpus of the stomach where continuing inflammation causes a loss of gastric glands and further decreases in acid secretion. Gastric cancer is associated with extensive corpus gastritis, atrophy, and extensive intestinal metaplasia [2] (Fig. 27.4).

Gastritis may be asymptomatic or may be associated with mild dyspeptic symptoms. In other patients, symptoms resembling peptic ulcer disease may be present, including epigastric burning pain and postprandial distress. None of these symptoms is diagnostic of the pathological condition of gastritis but clinicians often use the term gastritis to describe this constellation of symptoms although this use of the term has no specific pathological correlation.

Several tests are available to check for H. pylori infection, including noninvasive and invasive approaches. Endoscopy with biopsy is the only way to demonstrate gastritis but the presence of infection can be determined by noninvasive tests.

Anti-microbial therapy is required to eradicate H. pylori and this results in a gradual improvement in gastritis. Eradication of H. pylori reduces recurrences of peptic ulcer disease and can be curative of early MALT lymphoma and prevent recurrent gastric cancers in patients who have a resection of an early gastric cancer. The recently published guidelines of the Maastricht IV consensus suggest that standard triple therapy may be used in parts of the world where clarithromycin resistance is less than 15% [12]. Doses and durations are listed in Fig. 27.2. In patients with amoxicillin resistance, metronidazole may be substituted. Bismuth-based quadruple therapy is recommended in areas with high clarithromycin resistance. Second-line therapy recommended by the Maastricht group is levofloxacin-based triple therapy [12]. If second-line therapy fails, culture and sensitivity testing are recommended if available. High dose PPI therapy with amoxicillin and rifabutin triple therapy are alternatives when culture and sensitivity testing is not available.