The ability of a bacterium to infect depends on immunity
In our country, 37,000 new cases of stomach cancer are still registered annually, which ranks 4th in the structure of oncological morbidity and 2nd in the structure of mortality in oncological diseases. Many are infected with HP, but not everyone will get cancer. The bacterium increases the risk of peptic ulcer cancer in susceptible individuals.
Once in the stomach, HP quickly moves with the help of flagella, overcomes the protective layer of mucus and populates the mucosa. Further, the bacterium begins to produce urease, which breaks down urea, due to which the concentration of ammonia increases near the growing colony and the pH rises (the environment becomes alkaline), such an environment for HP is as comfortable as possible. In response to this, the cells of the stomach with a vengeance do everything to increase acidity (normally, the stomach is acidic).
In addition, HP produces enzymes (mucinase, protease, lipase) that destroy the protective mucus of the stomach, as a result of which hydrochloric acid gains direct access to the exposed gastric mucosa and begins to corrode it, causing a chemical burn, inflammation and ulceration of the mucous membrane. As a result of inflammation in the gastric mucosa, certain types of cells grow, the so-called gastric cell hyperplasia.
HP also produces toxins that cause damage and cell death. BUT! The ability of HP to damage the mucosa depends on the state of immunity of the host organism, the characteristics of a particular strain of bacteria.
Where is Helicobacter pylori located?
Helicobacter most of all “loves” the output (pyloric) section of the stomach and the initial section (bulb) of the duodenum. It is there that the ulcer most often occurs. At this stage, the secretory function is preserved or even increased, since the main secretory cells of the stomach are not in the antrum, but in the body and bottom of the stomach. The main manifestation of helicobacteriosis is the development of gastritis, which develops chronically in absolutely everyone. It is necessary to know the ways of transmission of HP in order to carry out the prevention of infection. The only proven reservoir (place where the bacterium breeds) of HP is the human stomach.
The main source of HP is man. HP has been detected in cats, dogs, sheep, pigs, and macaques, but it is not known whether they can transmit the infection to humans. In some studies, different strains of HP have been identified in humans and domestic animals. Slaughterhouse workers have a higher rate of HP infection than office workers. But this is probably due to socio-economic conditions, and not to contact with animals. In vegetarians and meat eaters, the incidence of HP is comparable. Probably, animals do not make a significant contribution to the spread of HP.
HP lives at a temperature of 37-42 °C, dies at 15-20 °C. Under unfavorable conditions, HP forms coccal forms, which are likely to exist outside the body.
How does infection usually occur?
There are 2 ways of infection:
• vertical (more often in developed countries) – from parents to children (in the family);
• horizontal (more often in developing countries) – from person to person outside the family. Most often, HP is acquired at preschool age, without treatment it persists for life.
There are several hypotheses of the ways of infection with the most common infection on Earth. The fecal-oral route is currently considered one of the most likely to transmit HP, especially in close contact and poor hygiene settings. It is most common in developing countries and also among children.
The oral-oral (gastro-oral) route is from mouth to mouth. HP is detected in saliva, plaque, tonsil tissue, and on the tongue. It is assumed that HP does not live, but survives in the mouth. Waiting for better times, then to get into the stomach. Thus, gastro-oral transmission is possible through close contact, for example, in families, groups of children. According to a meta-analysis of 16 studies (2009), it is shown that in groups of children (in kindergarten) the risks are not so high.
The best prevention is hygiene
And the most “dangerous” for children are mothers and grandmothers. Chewing food, sharing spoons, nipples, toothbrushes by infected family members increases the risk of infection of the child. Genetic factors also play a role in the family. However, the frequent identification of different strains of HP in mother and child, as well as in spouses, suggests that oral transmission is not the main route of HP infection in adults.
Compliance with the rules of hygiene from childhood is the most important means in the prevention of HP. For the first time in your life, any method will do for diagnosis.
The main methods are as follows:
• Breath test with urea labeled with C-13.
• HP antigen in feces.
• Quick helix breath test.
• Gastroscopy with biopsy from two sections of the stomach by bacteriological, morphological methods.
• Gastroscopy with rapid urease test to obtain a biopsy of the antrum and body of the stomach.
• Determination of HP antibodies in the blood.
Who is eligible for treatment
If you are shown a gastroscopy, then it should be carried out immediately with a biopsy for Helicobacter pylori from two departments. If there is no need for endoscopic examination of the stomach, then a breath test with urea labeled with C-13, or the determination of HP antigen in feces, is preferable. After a course of anti-Helicobacter therapy, it is necessary to check its effectiveness, but not earlier than 6 weeks after treatment.
To control treatment, only a breath test with urea labeled with C-13, or HP antigen in feces, is suitable, subject to all the rules for preparing for research. If nothing bothers you, you can not look for HP. If, nevertheless, a Helicobacter pylori infection is detected, you will be offered eradication (treatment aimed at destroying the bacterium). Treatment should be discussed with the attending physician in order to select an effective treatment regimen.
Patients who have:
• peptic ulcer of the stomach and duodenum;
• chronic gastritis, especially with atrophy;
• MALT-lymphoma of the stomach;
• gastropathy caused by taking NSAIDs, or if long-term use of aspirin and other NSAIDs is planned;
• a close relative with stomach cancer;
• functional dyspepsia.
As well as patients with GERD who plan to take long-term PPIs (as this leads to the spread of infection throughout the stomach). In addition, the wishes of the patient are taken into account.