Disease Association

Chronic gastritis Strong causal association

Peptic ulcer disease Strong causal association

Gastric carcinoma Strong causal association

Gastric MALT lymphoma * Definitive etiologic role

* MALT, mucosa-associated lymphoid tissue

areas where infection is endemic, the organism seems to be acquired in childhood and persists for decades. The mode of transmission of H. pylori has not been well defined, although oraloral

transmission, fecal-oral transmission, and environmental spread are among the possible routes. Most infected persons also have the associated gastritis but are asymptomatic.

Nevertheless, infected persons are at increased risk for the development of peptic ulcer disease and possibly gastric cancer.

H. pylori is a nonsporing, curvilinear gram-negative rod measuring approximately 3.5 × 0.5 μm. H. pylori is part of a genus of bacteria that have adapted to the ecologic niche provided by

gastric mucus, which is lethal to most bacteria. The specialized traits that allow it to flourish include:

• Motility (via flagella), allowing it to swim through viscous mucus

• Elaboration of a urease, which produces ammonia and carbon dioxide from endogenous urea, thereby buffering gastric acid in the immediate vicinity of the organism

• Expression of bacterial adhesins, such as BabA, which binds to the fucosylated Lewis B blood-group antigens, enhances binding to blood group O antigen bearing cells.[23]

• Expression of bacterial toxins, such as cytotoxin association gene A (CagA) and vacuolating cytotoxin gene A (VacA).[24] These are discussed later under "Peptic Ulcer."

The H. pylori genome is 1.65 million base pairs and encodes approximately 1500 proteins. Extensive molecular studies suggest that the bacteria cause gastritis by stimulating production of

pro-inflammatory cytokines and by directly injuring epithelial cells (discussed later).

After initial exposure to H. pylori, gastritis occurs in two patterns: a predominantly antral-type gastritis with high acid production and elevated risk for duodenal ulcer, and a pangastritis

that is followed by multifocal atrophy (multifocal atrophic gastritis) with lower gastric acid secretion and higher risk for adenocarcinoma. The underlying mechanisms contributing to this

difference are not completely clear, but host-microorganism interplay appears to be critical. IL-1b is a potent pro-inflammatory cytokine and a powerful gastric acid inhibitor. Patients who

have higher IL-1b production in response to H. pylori infection tend to develop pangastritis, while patients who have lower IL-1b production exhibit antral-type gastritis. [25]

A number of diagnostic tests have been developed for the detection of H. pylori. Noninvasive tests include a serologic test for antibodies, fecal bacterial detection, and a urea breath test.

The breath test is based on the generation of ammonia by bacterial urease. Invasive tests are based on the identification of H. pylori in gastric biopsy tissue. Detection methods in gastric

tissue include visualization of the bacteria in histologic sections, bacterial culture, a rapid urease test, and bacterial DNA detection by the polymerase chain reaction.

Patients with chronic gastritis and H. pylori usually improve when treated with antibiotics. Relapses are associated with reappearance of the organism. The current treatment regimens

include antibiotics and hydrogen pump inhibitors.[22] Prophylactic and therapeutic vaccine development is still in the early research stage, but it holds the promise to eradicate or at least

greatly reduce the worldwide prevalence of H. pylori infection.

In addition to H. pylori, humans can also be infected by Helicobacter heilmannii, a spiral bacterium found in dogs, cats, and nonhuman primates.[26] This bacterium causes a relatively mild

gastritis.

Date: 2016-04-22; view: 665