Helicobacter pylori (bacteria that cause stomach ulcers)

2021-08-19 05:53 PM

H. pylori is very mobile, penetrating through the mucus layer and invading the gastric epithelium, especially the intercellular space

From 1900 to 1980, the presence of a spiral-shaped bacterium was occasionally reported in the gastric mucosa. But those findings did not get enough attention, because, until the end of the 20th century, it was largely assumed that the stomach was a bacteria-free environment due to its acidic pH. It wasn't until 1979 that Warren theorized that it was bacteria that caused inflammation and ulcers in the stomach and duodenum. In 1981, Marshall began to find a method to isolate this bacterium, in 1982 he successfully cultured and found this bacterium to be similar to Campylobacter jejuni, in 1983 he officially published this bacterium in the Lancet ( Paris) as Campylobacter pyloridis, later known as Campylobacter pylori. 1989,

Biological characteristics

These are small bacteria when isolated from the gastric mucosa biopsies, are curved, or S-shaped, standing in clusters. If transplanted many times, there is a rod shape. Gram-negative bacteria, very mobile thanks to 2 - 6 hairs on one end. Bacteria do not produce spores.

Bacteria require microaerobic conditions. High nutritional requirements, culture medium requires animal blood or serum. Bacteria grow slowly, on Colombia blood agar or tryptose blood agar after 3 days of incubation at 37 0 C, small, colorless colonies with sharp peaks can be seen.

Bacteria do not ferment sugars, have oxidase and catalase, and strongly positive urease. Strong positive urease is the property used to distinguish H. pylori from other curvilinear bacteria such as Campylobacter...

Immune

Local immune response

At the site of entry of H. pylori, a large concentration of neutrophils and lymphocytes occurs. Lymphocytes and leukocytes release interleukins and oxidative free radicals, but this local inflammatory response is not capable of eliminating H. pylori.

Humoral immune response

When studying antibodies in the blood of patients with peptic ulcer disease in the presence of H. pylori, an increase in IgG, IgA, and especially IgM antibodies was found. These antibodies decreased significantly after the eradication of H. pylori. This problem has been applied in serological diagnosis and monitoring of treatment results.

Possibility to cause disease in humans

Possibility to cause disease

Since Marshall successfully isolated this bacterium, many studies on the pathogenic role of H. pylori have been carried out. People have also conducted research on volunteers, who do not have inflammatory syndromes, stomach ulcers; they were given H. pylori. After a while, they developed gastritis; After that, people used measures to kill H. pylori, then these people got rid of gastritis. Recently, many authors commented that almost all cases of peptic ulcer disease are related to H. pylori infection; especially in atrophic form, a type that is very likely to lead to stomach cancer, but this bacterium is always present.

Disease mechanisms

H. pylori is very mobile, penetrating through the mucus layer and invading the gastric epithelium, especially the intercellular space. Bacteria are very strong urease producers; this enzyme is active in breaking down urea into ammonia. Urea is a metabolic product of tissue cells, they enter the blood partly and are eliminated through the kidneys. Some of the urea from the blood passes through the stomach lining into the gastric juice. Ammonia has an alkaline reaction that temporarily raises the local pH to about 6.5 and allows bacteria to survive in the very acidic environment of the stomach. In addition, ammonia is also directly toxic to gastric mucosal cells. H.pylori also reduces the mucus that protects the stomach wall, so gastric acid directly affects the stomach wall. The combination of many factors above causes inflammation, gastric ulcer. In patients with gastritis - duodenal ulcers can be isolated H.pylori in 80%-90% of cases.

Epidemiology

Socioeconomic status has a great influence on H. pylori infection. Even in the US, the rate of H. pylori infection in blacks is also higher than in whites, because it is related to spiritual, material, and environmental life.

The source of infection is humans, which can be seen in monkeys but is not significant. The main route of transmission is person-to-person. The mode of transmission is the fecal-oral route and the oral-oral route, in which the fecal-oral route plays a major role.

Microbiological diagnosis

Direct diagnosis

Bacterial isolation from specimens, the most common specimen is gastric mucosal biopsy during endoscopy, or possibly gastric juice. Culture on suitable media such as Colombia blood agar, incubate at 37oC under microaerobic conditions, after 3 days, if suspicious colonies are found, then separate and then Gram stain (need to replace Safranin red with Fuchsin red to make the red color clear. than due to small bacteria), testing for biochemistry properties to identify bacteria.

Rapid diagnosis by urease test

Put the biopsy sample in the Urea-Christensen medium, if there is H.pylorium in the sample, they will decompose the urea into ammonium and carbon dioxide, making the pH of the environment alkaline and changing the color of the indicator phenol red from pink. lotus petals red.

Test to measure carbon content of radioisotope C13 in breath

According to the principle, the CO2 formed after the urea decomposition reaction will follow the blood to the lungs and exhale with the breath. Put into the patient's body with C13-bound urea, measure the amount of C13 released by the breath to determine whether or not H.pylori is infected.

Look for antibodies against H.pylori

Find anti-H.pylori antibodies in serum, saliva or gastric juice by ELISA test. Commonly used in the epidemiological investigation of H.pylori infection.

Gene amplification (PCR)

PCR technique can detect H.pylori-specific gene fragments in gastric biopsy fragments, gastric juice, saliva, and stool of the patient.

Prevention and treatment

Prevention

General prevention: gastroduodenal disease depends very much on socio-economic conditions. Improving people's lives is very necessary, in which environmental sanitation also plays an important role because the disease is mainly transmitted through the fecal-oral route.

Specific prevention: effective prevention and, ideally, vaccination. Currently, a vaccine against peptic ulcer disease is being interested and experimented with by researchers around the world, hoping in the near future there will be a vaccine to prevent this disease.

Treatment

Currently, in the treatment of gastric and duodenal ulcers, in addition to using antisecretory drugs, people also use antibiotics to destroy the root cause of H. pylori bacteria, often using two antibiotics in combination such as Metronidazole or Tinidazole with Amoxicillin or Clarithromycin, the effect is better than using one.