An H. pylori infection is a bacterial infection of the stomach lining caused by Helicobacter pylori, a spiral-shaped bacterium that has evolved to survive in the harsh acid environment of the human stomach. It is remarkably common: roughly 44% of adults worldwide carry the infection. Most people with H. pylori never feel a thing, but in 10 to 20% of cases, the infection causes ulcers, chronic stomach inflammation, or raises the risk of stomach cancer.
How H. pylori Survives in Your Stomach
Your stomach produces hydrochloric acid strong enough to break down food, which would kill most bacteria on contact. H. pylori gets around this by producing large amounts of an enzyme called urease, which breaks down urea (a natural compound present in the stomach) into ammonia and carbon dioxide. The ammonia neutralizes the acid in the bacterium’s immediate surroundings, creating a thin bubble of neutral pH that keeps it alive.
This acid-neutralizing trick does something else: it changes the consistency of the protective mucus layer that coats your stomach wall. Normally, stomach mucus is a thick gel. When H. pylori raises the local pH, the mucus becomes thinner and more liquid, allowing the bacterium to swim freely through it and burrow toward the stomach lining. Once nestled against the lining, the bacteria trigger chronic inflammation that can persist for decades if untreated.
How the Infection Spreads
H. pylori passes from person to person, most commonly through fecal-oral, oral-oral, or gastric-oral routes. In practical terms, this means contact with contaminated food, water, saliva, or vomit. The bacterium has been most reliably recovered from vomit and from stool during episodes of rapid intestinal transit like diarrhea.
Household transmission is a major pathway. A CDC-supported study found that exposure to vomit from an infected household member explained over 50% of new infections in a household. Living with someone who had a stomach illness and vomited carried a sixfold increase in the odds of picking up H. pylori, compared to households without that exposure. Crowded living conditions and poor sanitation are the strongest environmental risk factors, which is why infection rates are substantially higher in lower-income regions.
Most people acquire the infection during childhood. About 35% of children and adolescents worldwide already carry H. pylori.
Symptoms and Who Gets Sick
The defining feature of H. pylori infection is how often it causes no symptoms at all. An estimated 80 to 90% of infected people remain completely asymptomatic throughout their lives. The remaining 10 to 20% develop problems that range from mild to serious.
When symptoms do appear, they typically reflect gastritis (inflammation of the stomach lining) or peptic ulcers. Common complaints include:
- Burning or gnawing pain in the upper abdomen, often worse on an empty stomach
- Bloating and frequent burping
- Nausea, sometimes with vomiting
- Loss of appetite and unintended weight loss
- Feeling full quickly after eating small amounts
More alarming signs, like vomiting blood, black or tarry stools, or severe abdominal pain, can indicate a bleeding ulcer and need immediate medical attention.
Long-Term Risks: Ulcers and Cancer
Left untreated for years or decades, chronic H. pylori infection can do real damage. The persistent inflammation it causes is the leading cause of peptic ulcers, both in the stomach and in the duodenum (the first section of the small intestine).
The cancer connection is well established. People with chronic infections face an increased risk of gastric adenocarcinoma, the most common form of stomach cancer. This risk applies to cancer in the main body of the stomach and, in regions where stomach cancer is already common (particularly parts of Asia), to cancer near the junction of the stomach and esophagus as well. H. pylori is also strongly linked to a type of stomach lymphoma called MALT lymphoma. Nearly all patients diagnosed with gastric MALT lymphoma show signs of H. pylori infection.
It’s worth keeping perspective: although H. pylori raises cancer risk, only a small fraction of infected people ever develop stomach cancer. But because the infection is so widespread globally, it remains one of the most significant preventable causes of gastric malignancy.
How It’s Diagnosed
Several reliable tests can detect H. pylori, and they fall into two categories: those that require an endoscopy (a camera passed into the stomach) and those that don’t.
Non-Invasive Tests
The urea breath test is the most commonly used non-invasive option. You swallow a small amount of specially labeled urea. If H. pylori is present, the bacterium’s urease enzyme breaks down the urea, and the labeled carbon dioxide shows up in your breath. Sensitivity and specificity both exceed 95% with modern versions of the test, making it highly accurate.
Stool antigen tests detect H. pylori proteins in a stool sample, with accuracy above 90%. These are particularly useful for children or when a breath test isn’t available.
Endoscopy-Based Tests
When an endoscopy is performed for other reasons (investigating an ulcer, for instance), a small tissue sample can be tested on the spot using a rapid urease test, which has roughly 90% sensitivity and 95 to 100% specificity. The sample can also be examined under a microscope, though accuracy varies depending on the staining technique used.
Treatment: Why the Standard Approach Has Changed
For years, the go-to treatment was “triple therapy,” a combination of an acid-reducing medication and two antibiotics, one of which was clarithromycin. That regimen is now falling out of favor because H. pylori has developed widespread resistance to clarithromycin. Resistance rates exceed 15% in most countries surveyed, and in parts of Asia they range as high as 92%. The American College of Gastroenterology now specifically recommends against using clarithromycin-based triple therapy unless lab testing has confirmed the bacteria are still sensitive to it.
The current first-line recommendation is a 14-day course of bismuth-based quadruple therapy. This involves four medications taken together: an acid reducer, bismuth (the active ingredient in Pepto-Bismol), and two different antibiotics. Real-world data from Europe show this regimen clears the infection in over 90% of patients, even when one of the antibiotics faces resistance, because the bismuth helps overcome it.
Alternative regimens exist for people who can’t tolerate the standard approach or who have already failed a first round of treatment. The key takeaway is that treatment has become more aggressive and longer (14 days instead of the older 7 to 10 day courses) specifically because the bacterium has gotten harder to kill.
Confirming the Infection Is Gone
Finishing the antibiotics isn’t the end of the process. Follow-up testing is recommended at least four weeks after completing treatment to confirm the bacteria have been eradicated. The same tests used for diagnosis, typically a breath test or stool antigen test, work for this purpose.
Timing matters for accuracy. If your treatment included bismuth or acid-reducing medications like proton pump inhibitors, you may need to stop those drugs up to two weeks before the follow-up test, because they can interfere with results and produce a false negative. Your provider will give you specific instructions on when to pause which medications. Skipping this confirmation step is a common mistake: without it, you won’t know if a resistant strain survived and the infection is still active.