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Helicobacter pylori is the cause of one of the most common human infections worldwide. Patients colonized with this gram-negative bacterium can be asymptomatic, or they may experience such significant GI manifestations as chronic gastritis, peptic ulcer disease (PUD) and gastric malignancy.

Diagnostic testing and treatment are readily available, but increasing antibiotic resistance has made H. pylori difficult to treat. Primary-care providers need a solid understanding of the bacterium, including prevalence, mode of transmission, diagnostic testing and effective treatment toward eradication. 

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In 1893, Polish scientist Walery Jarowski first reported
observation of a spiral bacterium that he called Vibrio rugula.1 Later researchers called the organism Campylobacter pyloridis. Eventually, the name was changed to H. pylori because of the organism’s helical shape.

In 1982, Marshall and Warren confirmed the presence of H. pylori in patients with chronic gastritis and gastric ulcers. At the time, ulcer treatment was focused on chronic reduction of gastric acid. The identification of H. pylori and what it meant for the possible eradication of PUD was significant. The researchers won a Nobel Prize in 2005 for this finding.2


The prevalence of H. pylori infection increases with age and is highest in immigrants and low socioeconomic groups. In the United States, more than 50% of asymptomatic persons older than age 60 years show evidence of active or past H. pylori infection.3

Worldwide, at least 30% to 50% of the population is colonized by this bacterium, but the rate is declining. For instance, the infection rate in Poland had reached a high of 58.29% of the population. During the past 10 years, widespread application of a test-and-treat strategy has lowered the Polish H. pylori infection rate to 30%. Blaser, who attributes the worldwide decline in H. pylori prevalence to improved standards of living, notes that the reduction has been accompanied by an increase in the occurrence of gastroesophageal reflux disease, Barrett’s esophagus, and esophageal carcinoma.4

Mode of transmission

The exact mode of H. pylori transmission is still unknown. Transmission has been proposed to occur via contaminated groundwater, food and human saliva (e.g., from kissing or sharing water bottles).5 The organism has also been found on unsterilized endoscopy equipment. Periodontal disease has recently been associated with H. pylori. Numerous studies have confirmed a correlation between gastric infection and the presence of H. pylori in the mouth. Dental plaque has been reported to be a reservoir for H. pylori.6 Some authors have found H. pylori to be part of the normal flora in the mouth,7 while others feel more studies are needed to confirm this finding.8


The stomach is a remarkable organ. It secretes juices that aid in food digestion, but it does not digest itself. Food entering the stomach initiates a chain of highly complex actions. The secretion of gastrin, production of hydrochloric acid and conversion of pepsinogen to pepsin are all interconnected.

During digestion, the gastric mucosa is injured frequently, but a rapid process called gastric cytoprotection provides repair and multiple layers of defense to prevent any significant disruption of function. The stomach’s protective mechanisms include a well-defined mucus layer that covers the lining; alkaline bicarbonate secretion under the mucus layer; a continuous, insoluble mucus epithelial layer that creates a buffer zone; and a rich blood supply that maintains epithelial integrity. The stomach also contains cytoprotective substances, such as prostaglandins, which provide protection by suppressing gastric acid. The only condition that puts our gastric defenses at risk is inflammation. 

Colonization of the stomach by H. pylori can cause chronic gastritis, or inflammation of the stomach lining, as the gram-negative, flagellated and motile H. pylori organisms interact with a gastric host (Figure 1).

Specific factors of the susceptible host may influence the manner in which H. pylori will affect it; the precise nature of these factors is presently unknown. Similar to other gram-negative bacteria, H. pylori possesses a lipopolysaccharide that acts to disrupt mucosal integrity.9 Once H. pylori invades the host, numerous toxins, enzymes and/or pathogenic proteins are released, which also disturb the integrity of the gastric layer. One example of a pathologic protein is CagA protein, which is produced by cytotoxic-associated gene A and predisposes the host to more aggressive clinical syndromes, such as PUD, duodenal ulcer, and gastric carcinoma.10