H Pylori Microbiology

[Otilia Mojarro]

Helicobacterpylori (H. pylori) infection occurs when Helicobacter pylori (H. pylori) bacteria infect your stomach. This usually happens during childhood. A common cause of stomach ulcers (peptic ulcers), H. pylori infection may be present in more than half the people in the world.

Most people don't realize they have H. pylori infection because they never get sick from it. If you develop signs and symptoms of a peptic ulcer, your health care provider will probably test you for H. pylori infection. A peptic ulcer is a sore on the lining of the stomach (gastric ulcer) or the first part of the small intestine (duodenal ulcer).

Most people with H. pylori infection will never have any signs or symptoms. It's not clear why many people don't have symptoms. But some people may be born with more resistance to the harmful effects of H. pylori.

H. pylori infection occurs when H. pylori bacteria infect your stomach. H. pylori bacteria are usually passed from person to person through direct contact with saliva, vomit or stool. H. pylori may also be spread through contaminated food or water. The exact way H. pylori bacteria causes gastritis or a peptic ulcer in some people is still unknown.

In areas of the world where H. pylori infection and its complications are common, health care providers sometimes test healthy people for H. pylori. Whether there is a benefit to testing for H. pylori infection when you have no signs or symptoms of infection is controversial among experts.

If you're concerned about H. pylori infection or you think you may have a high risk of stomach cancer, talk to your health care provider. Together you can decide whether you may benefit from H. pylori testing.

Helicobacter pylori, previously known as Campylobacter pylori, is a gram-negative, flagellated, helical bacterium. Mutants can have a rod or curved rod shape, and these are less effective.[1][2] Its helical body (from which the genus name, Helicobacter, derives) is thought to have evolved in order to penetrate the mucous lining of the stomach, helped by its flagella, and thereby establish infection.[3][2] The bacterium was first identified as the causal agent of gastric ulcers in 1983 by the Australian doctors Barry Marshall and Robin Warren, who obtained the Nobel prize in Medicine for this discovery.[4][5]

Infection of the stomach with H. pylori is not the cause of illness itself; over half of the global population is infected but most are asymptomatic.[6][7] Persistent colonization with more virulent strains can induce a number of gastric and extragastric disorders.[8] Gastric disorders due to infection begin with gastritis, inflammation of the stomach lining.[9] When infection is persistent the prolonged inflammation will become chronic gastritis. Initially this will be non-atrophic gastritis, but damage caused to the stomach lining can bring about the change to atrophic gastritis, and the development of ulcers both within the stomach itself or in the duodenum, the nearest part of the intestine.[9] At this stage the risk of developing gastric cancer is high.[10] However, the development of a duodenal ulcer has a lower risk of cancer.[11]Helicobacter pylori is a class 1 carcinogen, and potential cancers include gastric mucosa-associated lymphoid tissue (MALT) lymphomas and gastric cancer.[9][10] Infection with H. pylori is responsible for around 89 per cent of all gastric cancers, and is linked to the development of 5.5 per cent of all cases of cancer worldwide.[12][13] H. pylori is the only bacterium known to cause cancer.[14]

Extragastric complications that have been linked to H. pylori include anemia due either to iron-deficiency or vitamin B12 deficiency, diabetes mellitus, cardiovascular, and certain neurological disorders.[15] An inverse link has also been claimed with H. pylori having a positive protective effect on many disorders including asthma, esophageal cancer, IBD (including GERD and Crohn's disease) and other disorders.[15]

Some studies suggest that H. pylori plays an important role in the natural stomach ecology by influencing the type of bacteria that colonize the gastrointestinal tract.[16][17] Other studies suggest that non-pathogenic strains of H. pylori may beneficially normalize stomach acid secretion, and regulate appetite.[18]

In 2023, it was estimated that about two-thirds of the world's population were infected with H. pylori, being more common in developing countries.[19] The prevalence has declined in many countries due to eradication treatments with antibiotics and proton-pump inhibitors, and with increased standards of living.[20][21]

H. pylori can be demonstrated in tissue by Gram stain, Giemsa stain, H&E stain, Warthin-Starry silver stain, acridine orange stain, and phase-contrast microscopy. It is capable of forming biofilms. Biofilms help to hinder the action of antibiotics and can contribute to treatment failure.[29][30]

To successfully colonize its host, H. pylori uses many different virulence factors including oxidase, catalase, and urease.[31] Urease is the most abundant protein, its expression representing about 10% of the total protein weight.[32]

H. pylori possesses five major outer membrane protein families.[31] The largest family includes known and putative adhesins. The other four families are porins, iron transporters, flagellum-associated proteins, and proteins of unknown function. Like other typical gram-negative bacteria, the outer membrane of H. pylori consists of phospholipids and lipopolysaccharide (LPS). The O-antigen of LPS may be fucosylated and mimic Lewis blood group antigens found on the gastric epithelium.[31]

Helicobacter pylori consists of a large diversity of strains, and hundreds of genomes have been completely sequenced.[33][34][35] The genome of the strain 26695 consists of about 1.7 million base pairs, with some 1,576 genes.[36][37] The pan-genome, that is the combined set of 30 sequenced strains, encodes 2,239 protein families (orthologous groups OGs).[38] Among them, 1,248 OGs are conserved in all the 30 strains, and represent the universal core. The remaining 991 OGs correspond to the accessory genome in which 277 OGs are unique to one strain.[39]

The proteome of H. pylori has been systematically analyzed and more than 70% of its proteins have been detected by mass spectrometry, and other methods. About 50% of the proteome has been quantified, informing of the number of protein copies in a typical cell.[41]

An infection with Helicobacter pylori can either have no symptoms even when lasting a lifetime, or can harm the stomach and duodenal linings by inflammatory responses induced by several mechanisms associated with a number of virulence factors. Colonization can initially cause H. pylori induced gastritis, an inflammation of the stomach lining that became a listed disease in ICD11.[43][44][45] This will progress to chronic gastritis if left untreated. Chronic gastritis may lead to atrophy of the stomach lining, and the development of peptic ulcers (gastric or duodenal). These changes may be seen as stages in the development of gastric cancer, known as Correa's cascade.[46][47] Extragastric complications that have been linked to H. pylori include anemia due either to iron-deficiency or vitamin B12 deficiency, diabetes mellitus, cardiovascular, and certain neurological disorders.[15]

Peptic ulcers are a consequence of inflammation that allows stomach acid and the digestive enzyme pepsin to overwhelm the protective mechanisms of the mucous membranes. The location of colonization of H. pylori, which affects the location of the ulcer, depends on the acidity of the stomach.[48] In people producing large amounts of acid, H. pylori colonizes near the pyloric antrum (exit to the duodenum) to avoid the acid-secreting parietal cells at the fundus (near the entrance to the stomach).[31] G cells express relatively high levels of PD-L1 that protects these cells from H. pylori-induced immune destruction.[49] In people producing normal or reduced amounts of acid, H. pylori can also colonize the rest of the stomach.

The inflammatory response caused by bacteria colonizing near the pyloric antrum induces G cells in the antrum to secrete the hormone gastrin, which travels through the bloodstream to parietal cells in the fundus.[50] Gastrin stimulates the parietal cells to secrete more acid into the stomach lumen, and over time increases the number of parietal cells, as well.[51] The increased acid load damages the duodenum, which may eventually lead to the formation of ulcers.

Helicobacter pylori is a class I carcinogen, and potential cancers include gastric mucosa-associated lymphoid tissue (MALT) lymphomas and gastric cancer.[9][10][52] Less commonly, diffuse large B-cell lymphoma of the stomach is a risk.[53] Infection with H. pylori is responsible for around 89 per cent of all gastric cancers, and is linked to the development of 5.5 per cent of all cases of cancer worldwide.[12][13] Although the data varies between different countries, overall about 1% to 3% of people infected with Helicobacter pylori develop gastric cancer in their lifetime compared to 0.13% of individuals who have had no H. pylori infection.[54][31] H. pylori-induced gastric cancer is the third highest cause of worldwide cancer mortality as of 2018.[55] Because of the usual lack of symptoms, when gastric cancer is finally diagnosed it is often fairly advanced. More than half of gastric cancer patients have lymph node metastasis when they are initially diagnosed.[56]

Chronic inflammation that is a feature of cancer development is characterized by infiltration of neutrophils and macrophages to the gastric epithelium, which favors the accumulation of pro-inflammatory cytokines, reactive oxygen species (ROS) and reactive nitrogen species (RNS) that cause DNA damage.[57] The oxidative DNA damage and levels of oxidative stress can be indicated by a biomarker, 8-oxo-dG.[57][58] Other damage to DNA includes double-strand breaks.[59]

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