Helicobacter pylori is a Gram-negative, microaerophilic bacterium that can inhabit various areas of the stomach, particularly the antrum. It causes low-level inflammation of the stomach lining and is linked to gastric ulcers and stomach cancer. Out of those infected, 80%, are asymptomatic.
It was initially named Campyloacter pyloridis and then renamed C. pylori to correct the Latin grammar error. It was later placed in the genus, Helicobacter. Over 50% of the population has H. pylori in their gastrointestinal tract. It is more prevalent in developing countries. Infection results in a stomach ache, abdominal pain, acid reflux, regurgitation, vomiting, belching, flatulence, and nausea.
Untreated, the infection may be related to several serious illnesses. It possesses five major outer membrane protein families. The outer membrane of H. pylori consists of phospholipids and lipopolysaccharide.
There is a large diversity of strains and three of the genomes have been completely sequenced. Studies of H. Pylori genome is generally attempted to understand pathogenesis which is the ability of this organism to cause disease. The cagA gene code is associated with an ability to cause ulcers.
H. pylori must survive the acidic pH of the lumen in order to colonize in the stomach. The bacterium’s flagella move through the stomach lumen and drill into the mucoid lining of the stomach. A lot of bacteria can be found deep in the mucus that is being continually secreted. It can also be found on the inner surface of the stomach epithelial cells. It produces large amounts of urease, molecules which are localized inside and outside of the bacterium. The urease breaks down urea into carbon dioxide and ammonia. The survival of H. pylori is dependent on the urease in the stomach.
When H. pylori colonizes the stomach it results in chronic gastritis. Many times the inflammation can lead to stomach ulcers. The type of ulcer depends on the location of chronic gastritis. Chronic inflammation can eventually lead to atrophy of the stomach lining. Western patients with the cag PAI have a stronger inflammatory response in the stomach and are at a greater risk of developing peptic ulcers or stomach cancer.
It is possible that H. pylori can promote cancer through enhanced production of free radicals near H. pylori and an increased rate of host cell mutation. It could also promote cancer through enhancement of the transformed host cell phenotype by means of alterations in cell proteins.
Diagnosis is done through dyspeptic symptoms and tests that can indicate H. pylori infection. Doctors use blood antibody tests, stool antigen tests, and carbon urea breath tests to detect infection. The most reliable test is a biopsy check during endoscopy with a rapid urease test, histological examination, and microbial culture. None of these methods are completely failsafe. Some studies have researched how diet factors into the disease.