Biological characteristics [3]
Hp is a unipolar, flagellated, obtuse-circular, spirally curved bacterium with 1 ~ 2 tiny bends, 2 ~ 4 microns long, 0.5 ~ 1.0 microns wide, and only one circular chromosome. At the end of 1997, the complete sequence of Hp genome has been determined. About 2/3 genes can be found in the gene database, and their possible biological functions can be inferred. The function of 1/5 gene is unknown, and 1/4 gene is unique to Hp. Gram staining is negative. Under the electron microscope, a bacterium is often arranged in an S-shape or a seagull shape.
There are many crusted flagella at one or both ends, which are active and usually unevenly distributed in groups under the mucosa, on the surface of mucosal epithelium, in the gastric pits and in the glandular cavities. Micro-aerobic, carbon dioxide is needed for growth, and the nutritional requirements are high. Culture requires animal serum or blood. The optimum growth temperature is 37℃, and the optimum PH value is 6 ~ 8. In addition, a certain humidity (98% relative humidity) is needed. After 3 ~ 6 days of culture, needle-like colorless transparent colonies can be seen. After subculture, it can become rod-shaped or spherical. Biochemical reaction is inactive, and sugar is decomposed. Catalase and oxidase are positive, and urease is rich, which can quickly decompose urea and release ammonia, which is one of the main basis for identifying the strain. In addition, alkaline phosphatase, deoxyribonuclease and leucylpeptidase can also be distinguished from other campylobacter. 2
Pathogenic mechanism
The infection rate of Helicobacter pylori is different among different people. The diversity of clinical outcome after Hp infection shows the complexity of its pathogenic mechanism, including colonization of Hp, gastric mucosal damage caused by toxin, gastric mucosal damage mediated by host immune response and different gastric acid secretion caused by imbalance of gastrin and somatostatin regulation after Hp infection.
Author: Institute of Pathogenic Biological Detection, Tianjin Center for Disease Control and Prevention, Tianjin 3000 1 1 About the author: Yu Lingqi (1962-), female, deputy chief technician, engaged in medical microbiology research.
Chang et al [4], involving inflammation, immunity, acid secretion, oxidation and other aspects, toxic factors, cytokines, free radicals, virulence genes and other Hp pathogenic factors are involved [5]. The toxicity of Hp is due to flagellar motility, adhesin, superadhesive factors and lipids, mainly urease,
Catalase and phospholipase A of polysaccharide [6]. The role of these virulence factors cannot explain why Hp infected people have different clinical manifestations. Recent studies have found that there are many strains of Helicobacter pylori, which determine the virulence and pathogenicity of bacteria. It is also found that Hp virulence factors can produce local pathogenic effects related to the occurrence of diseases.
8]
The difference of pathogenicity of Hp strains is mainly related to the polymorphism of their virulence genotypes [7, they
As well as cytotoxic genes (CagA group includes vacuolar cytotoxin gene (VacA gene)) and toxicity-related gene proteins. Recent studies believe that the diversity between strains and hosts is due to the infection of multiple strains rather than the genetic diversity of hosts caused by a single strain [9]. In recent years, the difference of protein expression level and activity caused by gene polymorphism at the same site has gradually become a new explanation for the clinical outcome of Hp infected hosts. With the detection of disease-related genes and gene expression level differences, combined with the method of gene mutation, the function of protein encoded by related genes was further clarified, and a series of new pathogenic genes (BabA, SabA, OipA, DupA, etc. ) has been gradually discovered, which is helpful to clarify the pathogenesis of Hp and predict the prognosis of Hp infection. 3 epidemiological characteristics
The transmission routes of Hp are feces-mouth, mouth-mouth, close contact and animal origin [10], and the infection of Hp infected people has family aggregation. Drinking polluted water,
Close contact, eating, contact between children and students in kindergartens and schools, and eating unclean food on the roadside can all cause the spread of Hp. After being infected by Hp, bacteria will lurk in the stomach for a long time without any symptoms, and some patients will have recurrent abdominal pain, vomiting, iron deficiency anemia, chronic gastritis and duodenal ulcer [1 1]. It has been reported that the hospital was infected with Helicobacter pylori due to contaminated endoscope [12]. Helicobacter pylori can be transmitted by iatrogenic route, and the iatrogenic transmission of Helicobacter pylori caused by gastroscopy is an important route. After the examination of Hp positive patients, PCR found that the surface and internal channels of 6 1% gastroscope were contaminated by Hp, and the biopsy forceps were more polluted. It was confirmed by DNA fingerprinting that HP was infected by gastroscope pollution [13]. The infection rate of HP in developed countries is different, ranging from 70% to 80% in developing countries. Among that develope China countries in China,
In fact, it is a child infection; The infection rate of children in developed countries is very low, but they are over 40 years old.