Many individuals infected with H. pylori are asymptomatic and may not develop any complications. 

About 10–20% ultimately develop ulcers. The pain characteristically occurs on an empty stomach or between meals, and in the early hours of the morning. Other symptoms may include nausea, vomiting, and loss of appetite. 

Gastrointestinal bleeding can also occur; leading to anaemia, fatigue and even syncope. If bleeding is uncontrolled and rapid, patients may present with the following symptoms such as melena (black tarry stool) or hematemesis (vomiting blood).

H. pylori infection is associated with a 1–2% lifetime risk of gastric cancer and <1% risk of gastric MALT lymphoma.

You should consider testing for H. pylori infection if you have chronic gastric symptoms such as gastric pain, bloating and nausea. 

Individuals diagnosed with peptic ulcer disease, low-grade gastric MALT lymphoma or early gastric cancer should also get tested.

Screening for H. pylori may be considered for healthy individuals who are asymptomatic with a first-degree family history of gastric cancer.

H. pylori enters the body through the mouth, moves through the digestive system, and infects the stomach. Unlike other bacteria, H. pylori bacteria can survive in a harsh acidic environment such as in the stomach, as it can produce a substance that neutralises stomach acid. H. pylori is a classic symbiote in that it can persist in an individual’s stomach for decades. It induces inflammation (gastritis) of the gastric mucosa (lining).

H. pylori is contagious, although the exact route of transmission is not known. Transmission between people probably occurs through either oral–oral or faecal-oral routes. In line with this, H. pylori can isolate from faeces, saliva, and dental plaques of infected individuals. 

Transmission occurs most commonly within family groups in developed nations, but can also be acquired from the community in the developing world via a combination of untreated water, crowded conditions, and poor hygiene. 

The majority of infections occur in early childhood in all countries, but the overall rates of infection increases with age. The age of initial infection appears to be associated with the potential outcome of infection. People infected at an earlier age are likely to develop more extensive inflammation, gastric atrophy and a higher risk of gastric ulcers and cancer.

Noninvasive tests for ongoing H. pylori infection include stool antigen tests or the 14C or 13C labelled carbon urea breath test. 

Biopsies performed during upper GI endoscopy can also diagnose H. pylori infection. The most accurate method for detecting H. pylori infection is through a histological examination of the gastric mucosa obtained from two separate sites, combined with either a rapid urease test or microbial culture.

Extensive research has shown that the treatment of H. pylori reduces the risk of gastric cancer in previously infected individuals, suggesting the continued presence of H. pylori is a risk factor in 65% of gastric cancers. 

The standard first-line therapy is 14 days of “triple therapy”. Triple therapy consists of proton pump inhibitors (PPIs) such as omeprazole and a combination of antibiotics clarithromycin and amoxicillin.

An increasing number of infected individuals (up to 15% to 20% in some countries) are found to harbour antibiotic-resistant bacteria. This resistance can be towards clarithromycin and metronidazole. Hence, first-line treatment regimes often result in treatment failure and requires additional rounds of antibiotic therapy or alternative strategies, such as a quadruple therapy, which adds bismuth subsalicylate. 

Lactic acid bacteria are proven to exert a suppressive effect on H. pylori infection in both animals and humans. Therefore, the doctor may prescribe a course of probiotics together with the antibiotics to facilitate successful eradication.