Helicobacter pylori infection

Introduction to Helicobacter pylori infection Helicobacter pylori is a helical, gram-negative, microaerophilic bacterium. Almost half of the population is infected for life, and the infection is mainly in the stomach and the duodenal bulb. It is known that the incidence of Helicobacter pylori infection is closely related to socioeconomic level, population intensity, public health conditions and water supply. Helicobacter pylori infection is now mainly treated with anti-Helicobacter pylori drugs. basic knowledge The proportion of sickness: 9.7% Susceptible people: no special people Infection method: pathogen infection Complications: stomach cancer

Cause of Helicobacter pylori infection

(1) Causes of the disease

Hp Gram stain negative, often S-shaped or curved, with 1 to 3 spirals, 2.5-4.0 m long, 0.5-1.0 m wide, prolonged culture time or after drug treatment, often spherical, two bacteria The ends are obtuse, and there are 2 to 6 sheathed flagella at one or both ends of the cells. The flagella is about 1.0 to 1.5 times longer than the cells, and the thickness is about 30 nm. Each has a hair point and the hair spots are not invaginated. The tip of the flagella is round or oval, and the cell wall is smooth, closely adhering to the epithelial cell membrane. There is a distinct electron density reduction zone at the cytoplasmic end of the inner side of the flagellar root, which may be related to the energy storage of flagellar movement. Helicobacter Felis, Hf) and Helicobacter helimannii (Hh) are 3 to 12 tight helices, which are easily distinguishable from Hp. Hp strains isolated from human gastric biopsy specimens have diverse gene phenotypes.

There are at least two types: type I with cytotoxin associated gene A (Cag A), CagA protein and vacuolar toxin (Vac A); type II without Cag A, both Does not express Cag A protein, nor does it express Vac A. Hp is an obligate microaerophilic bacteria whose stable growth depends on 5% to 8% oxygen in the growing microenvironment, in the atmosphere and absolute anaerobic environment. Can not grow in the middle, Hp growth is slow, usually takes 3 to 5 days to form a needle-shaped small colony (0.5 ~ 1.0mm), can produce urease, catalase, lipase, phospholipase and protease, bacteria external environment The resistance is not strong, sensitive to both drying and heat, and it is easy to kill a variety of commonly used disinfectants.

(two) pathogenesis

Hp enters the low pH environment of human stomach, can grow and multiply, and cause tissue damage. Its pathogenic effect is mainly as follows: the setting of bacteria on the gastric mucosa, the invasion of the host's immune defense system, the direct action of toxins and induction. Inflammatory response and immune response.

1. The local colonization site of Hp is located in the surface of gastric mucosa and the bottom of gastric mucus. It is distributed in a dot-like manner. The number of gastric antrum is large, and the corpus and stomach are less. Hp can also be colonized in the duodenum. Gastric mucosal metaplasia, Barrett's esophagus and Meckel's diverticulum, etc., in the ectopic gastric mucosa, Hp enters the stomach to reach the mucosal surface and mucus bottom colonization, in addition to resisting the killing effect of gastric acid and other unfavorable factors, but also rely on The dynamic penetrating mucus layer, its spiral cells provide the basis for Hp movement in viscous gastric mucus; while the swing of flagella provides sufficient power for Hp movement, urease produced by Hp can decompose urea For ammonia and carbon dioxide, ammonia forms an "ammonia cloud" around Hp, neutralizing gastric acid to protect Hp, and the resulting superoxide dismutase (SOD) and catalase can protect it from neutrophils. In addition, It also produces a variety of adhesion factors that allow it to adhere tightly to the surface of the gastric epithelium.

2. Toxins that damage the stomach and duodenal mucosa Hp and toxic enzymes and Hp-induced mucosal inflammation can cause damage to the gastric and duodenal mucosal barrier.

(1) Hp toxin: about 60% Hp strain can produce active vacuolating toxin (Vac A, 87kda), which can cause vacuolar degeneration of epithelial cells, expression of Vac A and toxicity and Vac A genotype and cells The toxic-related gene protein (Cag A, 128kda) is related to the pathogenicity difference of Hp strain. The Vac A s1/m1 genotype toxin has the strongest activity, and the Vac s2/m2 genotype has no toxin activity.

(2) Cag pathogenicity island: In 1996, Censini et al found that Hp strain contains a special gene fragment of about 40 kb, which is present in pathogenic strains and has typical structural features of bacteria to diseased islands. In diseased islands, studies have shown that Cag pathogenicity islands and Vac A are produced, and that Hp binds to Leb antigen receptors on the surface of gastric epithelial cells and is involved in actin involved in cytoskeletal rearrangement.

(3) Urease: In addition to protecting Hp itself, urease can also cause damage to the gastric mucosal barrier. First, urease can decompose urea to produce direct cytotoxicity of ammonia. Second, urease can induce gastric epithelial cells and Neutrophils express and secrete interleukin-6 (IL-6), tumor necrosis factor- (TNT-) and other inflammatory mediators.

(4) Hp protease, lipase and phospholipid: can destroy the integrity of gastric mucus layer, increase the solubility of mucus and reduce its hydrophobicity, thereby reducing the protective effect of mucus on epithelial cells.

(5) Proinflammatory factors: Hp surface and secreted soluble components and chemotactic proteins can chemotaxis of neutrophils, monocytes and macrophages, producing TNF-, leukotrienes, IL-1 and IL- 2, and further strengthen the activation response of IL-8, promote inflammation of the mucosa.

(6) Gastrointestinal hormones: Most literatures have confirmed that the release of somatostatin is decreased in Hp-infected patients, and the release of gastrin is increased, resulting in high gastric acid secretion, aggravating gastric mucosal acid load; gastrin promotes mucosal cell proliferation, May be related to tumor formation.

(7) Immune response: Hp infection induces specific cellular and humoral immunity, and induces the body's autoimmune response, which damages the gastrointestinal mucosa. After mucosal injury, the process from inflammation to cancer may be: chronic gastritis atrophic gastritis Intestinal metaplasia dysplasia carcinogenesis, recent studies suggest that eradication of Hp can prevent the development of this process.

Helicobacter pylori infection prevention

In view of the fact that the source of infection and the route of transmission of Hp infection are not well understood, it has brought difficulties in preventing Hp infection. Since the 1990s, the research on Hp vaccine has made great progress, and it is expected that in the near future, the vaccine will be adopted. Prevention and treatment of Hp infection will become a reality, and may also be an important measure for the prevention and treatment of Hp-related diseases in the future.

Helicobacter pylori infection complications Complications

Stomach hemorrhage: mucosal atrophy and thinning, vascular exposure, rough food smashing, mucous membrane smashing bleeding, with black stool as the main performance, if the amount of bleeding can suddenly vomit blood, severe dizziness, palpitation, black sleep, sweat, and even Shock and so on.

Helicobacter pylori infection symptoms common symptoms high gastrinemia abdominal pain bloating nausea edema peptic ulcer hernia congestion

Most patients with Hp infection are occult, no systemic symptoms of bacterial infection, and often no acute symptoms of gastritis. Clinically, patients often present with chronic gastritis, peptic ulcer, etc., from the results of volunteers who have swallowed live bacteria, Infection first causes acute gastritis, untreated or not completely treated, and develops into chronic gastritis. The incubation period of acute infection is 2 to 7 days. The endoscopy is characterized by acute congestion and erosion of gastric antrum. Histological examination of mucosal layer is hyperemia, edema and neutrophil. Cell infiltration, symptoms can be expressed as abdominal pain, abdominal distension, morning nausea, acid reflux, suffocation, hunger, severe vomiting, there is enough evidence to show that Hp is the main cause of chronic gastritis, chronic gastritis Hp detection rate 54% to 100%, the detection rate of Hp in chronic active gastritis is more than 90%, which not only causes antral sinusitis, but also causes dermatitis.

Helicobacter pylori infection check

1. Bacterial culture The gastric mucosa specimens are directly seeded onto a solid medium or the gastric mucosa specimens are ground into a homogenate and inoculated. Under micro-oxygen conditions, the relative humidity is above 90%, and the results are observed after incubation at 37 ° C for 48-72 hours. At least according to smear staining microscopy, urease, catalase and oxidase identification.

2. Gastric biopsy mucosa smear Apply the biopsy mucosal surface directly to the clean glass slide, and dry it after Gram stain or red staining, and observe with oil lens.

3. Tissue section stained gastric mucosal biopsy specimens (multiple points should be taken) vertically embedded sections, using Warthin-Starry and Centa silver staining or HE staining, Giem sa staining, fluorescein acridine orange staining, mipirin staining and no labeling Antibody PAP staining and the like were observed under an oil microscope or a fluorescence microscope.

4. Urease test Hp has high urease activity, can decompose urea to produce NH+4, and indirectly judge whether there is Hp infection by measuring the presence or absence of NH+4, there are pH indicator method, analytical chemical method and isotope-labeled urea test. And other methods.

5.14C urea breath test to patients with oral 14C urea, if there is Hp infection, after 20min, the patient exhaled gas has 14CO2, no Hp infection, no 14CO2 exhalation, this test is safe, accurate, reproducible, but due to equipment and other reasons It is not easy to promote the application.

6. Serological examination ELISA was used to detect anti-Hp IgG or anti-Hp IgA in serum or saliva as specificity and sensitivity indicators.

7. Polymerase chain reaction (PCR) technology can detect gastric juice, gastric mucosa, saliva Hp, the positive rate is higher than the urease method.

8. In situ identification Monoclonal antibodies can be used for immunohistochemical detection, Hp specific probes or primers for in situ hybridization and PCR detection.

Tissue section staining: gastric mucosal biopsy specimens (multiple points should be taken) vertically embedded sections, using Warthin-Starry and centa silver staining or HE staining, Giemsa staining, fluorescein acridine orange staining, mipirin staining and label-free antibody PAP Dyeing and the like are observed under an oil microscope or a fluorescence microscope.

Diagnosis and diagnosis of Helicobacter pylori infection

Bacteriological examinations need to be differentiated from other bacteria present in the gastric mucosa, such as human gastric Helicobacter pylori and curved bacteria-II.

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