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Last reviewed: 19.11.2021

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Helicobacter pylori was discovered in 1982 by B. Marshall and R. Warren in the study of biopsies of the gastric mucosa. To the genus Helicobacter, there are now more than 10 species, some of which were previously included in the genus Campylobacter.

trusted-source[1], [2], [3], [4], [5], [6], [7], [8], [9], [10], [11], [12], [13], [14]

Morphology of Helicobacter

H. Pylori is somewhat larger than other species (0.5-1.0 x 2.5-5 μm) and has the shape of a stick, a spiral or an "arc of the ox". Lofotrich (up to 5 flagella) or monotrich, sometimes in the population there are both forms. On agar media not moving or immovable. It grows on media for campylobacteria, but it grows better on "chocolate" agar, forming on it after 2-7 days. Colonies 0.5-1.0 mm in diameter. On a 10% blood agar, a weak hemolysis is noted. For growth, microaerophilic conditions or an atmosphere enriched in CO2 are required. In aerobic or anaerobic conditions, bacteria do not grow.

Biochemical properties of Helicobacter

H. Pylori is oxidase- and catalase-positive; hydrogen sulphide does not form, hippurate does not hydrolyze, has high urease activity. It is resistant to chloride of triphenyltetrazolium in a concentration of 0.4-1.0 mg / ml; resistant to a 0.1% solution of sodium selenite, to a lesser extent - to 1% glycine.

trusted-source[15], [16], [17], [18], [19], [20]

Pathogenicity factors of Helicobacter pylori

The virulence factors of N. Pylori are mobility; urease (neutralizes HC1 and damages epithelial cells); protein cytotoxin, which causes vacuolization of epithelial cells and damages intercellular bridges; lipopolysaccharide; proteinase; lipase; catalase, hemolysin, etc.

Epidemiology of Helicobacteriosis

Infection of people, most likely, occurs on the fecal-oral mechanism. The causative agent, penetrating mucin into the submucosal stomach, colonizes epithelial cells, often penetrating into them. Progressing focal inflammation leads to the development of gastritis, peptic ulcers of the stomach and duodenum. Later, adenocarcinoma or gastric lymphoma may develop (Mucosa Associated Lymphoid Tissue Lymphoma).

trusted-source[21], [22], [23], [24], [25], [26], [27], [28], [29], [30]

Treatment of Helicobacteriosis

The most effective drug for the treatment of chronic gastritis and peptic ulcer of the stomach or duodenum is DeNol (colloidal bismuth sub-citrate), which acts selectively only on H. Pylori, which is combined with trichopole (metronidazole) and amoxicillin (or clarithromycin) to enhance the therapeutic effect.

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