A bacterium called Helicobacter pylori (H. pylori) is the primary bacterial cause of stomach and duodenal ulcers. For most of the 20th century, doctors blamed ulcers on stress and spicy food, but in 1982 two Australian researchers proved that this spiral-shaped bacterium living in the stomach lining was the real culprit. H. pylori is estimated to infect roughly half the world’s population, though most carriers never develop symptoms.
How H. pylori Survives in Stomach Acid
Your stomach produces hydrochloric acid strong enough to dissolve metal, yet H. pylori thrives there. The bacterium produces an enzyme called urease that breaks down urea into ammonia, creating a small alkaline cloud around itself that neutralizes the surrounding acid. This chemical shield lets H. pylori burrow into the mucus layer that protects your stomach wall.
Once embedded, the bacterium goes to work on your defenses. It depletes glutathione, a molecule your cells rely on to protect themselves from damage and regulate immune responses. H. pylori also manipulates the cells that control acid production: it suppresses the cells that put the brakes on acid output while stimulating the cells that ramp it up. The result is more acid hitting a weakened lining.
Two proteins do much of the direct damage. One, called Vac-A, is a toxin that punches holes in stomach lining cells by forming large vacuoles inside them. The other, Cag-A, triggers your immune system to send inflammatory cells flooding into the area. That inflammation, sustained over months or years, erodes the protective mucus barrier until acid eats through to the tissue underneath, forming an ulcer.
H. pylori Is Not the Only Cause
While H. pylori gets the most attention, the landscape of ulcer causes has shifted. In a study of 389 patients with peptic ulcer disease, 57% were using nonsteroidal anti-inflammatory drugs (NSAIDs like ibuprofen, aspirin, or naproxen) and only 41% tested positive for H. pylori. About 22% of ulcer patients had neither an H. pylori infection nor NSAID use, pointing to less common causes like excessive alcohol, smoking, or rare conditions where the stomach overproduces acid.
NSAIDs cause ulcers through a completely different mechanism. They block enzymes that help maintain the stomach’s protective mucus layer, leaving the lining vulnerable to acid. If you take NSAIDs regularly and also carry H. pylori, the two risks compound each other significantly.
How H. pylori Spreads
H. pylori passes from person to person, most commonly within households. Research from the CDC found that exposure to vomit from an infected person accounted for more than half of all new infections tracked in homes, and over 70% of confirmed new cases. The bacterium can also spread through the fecal-oral route, meaning contaminated water or food, or close personal contact in crowded living conditions.
Most people who carry H. pylori were infected during childhood. Rates are higher in developing countries where sanitation infrastructure is limited, and infection tends to cluster in families. You can carry the bacterium for decades without knowing it.
Symptoms That Point to an Ulcer
The hallmark symptom is a burning or gnawing pain in the upper abdomen, often between meals or in the early morning when the stomach is empty. Eating or taking antacids may temporarily relieve it. Other common signs include bloating, nausea, loss of appetite, and unintentional weight loss.
More serious warning signs include vomiting blood (which may look like coffee grounds), dark or tarry stools indicating bleeding in the digestive tract, sudden sharp abdominal pain that doesn’t let up, and feeling faint or lightheaded. These suggest a bleeding or perforated ulcer and need immediate medical attention.
Testing for H. pylori
Several reliable tests can detect H. pylori without any invasive procedure. The urea breath test has you swallow a small capsule containing a harmless labeled compound. If H. pylori is present, its urease enzyme breaks down the compound, and the byproduct shows up in your breath. This test is highly accurate, with sensitivity around 96% and specificity around 93% for the most commonly used version.
A stool antigen test, which detects H. pylori proteins in a stool sample, offers accuracy above 90% and is particularly useful for confirming the infection has cleared after treatment. Blood antibody tests exist but are less helpful because antibodies can linger for months after the bacteria are gone, making it impossible to distinguish a past infection from a current one.
If you’re having an endoscopy (where a thin camera is passed into your stomach), your doctor can take a small tissue sample and run a rapid urease test on it. This delivers results in hours with over 90% sensitivity and near-perfect specificity. The tissue can also be examined under a microscope or cultured in a lab, which is the gold standard for identifying exactly which antibiotics the bacteria will respond to.
How H. pylori Infections Are Treated
Treating H. pylori requires a combination of medications taken together, typically for 10 to 14 days. The current recommended first-line approach is bismuth quadruple therapy: a proton pump inhibitor (a strong acid-suppressing medication), bismuth (similar to what’s in Pepto-Bismol), tetracycline, and metronidazole. The acid suppressor lets the stomach lining heal while the antibiotics and bismuth attack the bacteria from different angles.
This multi-drug approach exists because H. pylori is notoriously difficult to kill with a single antibiotic. The bacterium hides within the stomach’s mucus layer, and the acidic environment reduces the effectiveness of many drugs. Taking all medications exactly as prescribed for the full course is critical, because incomplete treatment is one of the main drivers of antibiotic resistance.
Growing Antibiotic Resistance
H. pylori is becoming harder to treat worldwide. Resistance to clarithromycin, once a cornerstone of ulcer therapy, now exceeds 15% in the majority of countries studied. In parts of Asia, clarithromycin resistance ranges from 7% to over 92%. European rates run between 12% and 22%. Resistance to levofloxacin, another commonly used antibiotic, reaches as high as 65% in parts of Africa and Asia.
Amoxicillin remains effective in most of the world, with resistance under 2% in the majority of countries, though parts of Africa have reported resistance above 90%. Tetracycline resistance stays below 1% globally, making it a reliable backbone for treatment regimens. These patterns explain why doctors increasingly favor bismuth quadruple therapy over older clarithromycin-based regimens, and why antibiotic susceptibility testing before treatment is becoming more common.
The Link to Stomach Cancer
Chronic H. pylori infection does more than cause ulcers. The National Cancer Institute notes that the majority of gastric adenocarcinoma cases, the most common form of stomach cancer, are attributed to H. pylori infection. The bacterium is also responsible for most cases of gastric MALT lymphoma, a cancer of the immune tissue in the stomach wall.
The risk is highest for cancer in the main body of the stomach, and in regions where stomach cancer is common (particularly East Asia), the risk extends to cancer near the junction of the stomach and esophagus. The progression from infection to cancer takes decades and moves through a predictable sequence: chronic inflammation, thinning of the stomach lining, abnormal cell changes, and eventually malignant growth. Eradicating the infection, especially earlier in this chain, significantly reduces the cancer risk.