Helicobacter pylori is the normal commensal bacteria which is present in the stomach. It has the capability to invades the lining of the stomach and can cause serious complications
Helicobacter pylori pathogenesis and disease outcomes are mediated by the complex interaction between the bacteria and virulence factors, host and environmental factors. After the H. pylori enters the stomach of the host the following four steps are very much important for the bacteria to establish the successful colonization, persistent infection, and disease pathogenesis.
The first mechanism is that the bacteria is capable of surviving in the stomach
Since the bacteria possess the flagella which helps them in the motility of the bacteria towards the surface lining the stomach.
Attachment to host cells by adhesins/receptors interaction
Causing tissue damage by toxin release.
The virulence nature possessed by the bacteria includes bacterial adhesins , cag pathogenicity and vacuolating cytotoxins. The screening methods including the proteomic and transcriptomic tools has been used to determine the complex gene regulatory networks in H.pylori.
In the acidic environment of the stomach lumen the bacteria uses the flagella to burrow into the mucus lining of the stomach to reach the epithelial cells underneath, where it is less acidic when compared to the external surface of the lumen. H. pylori is capable of sensing the pH gradient in the mucosal cells and move towards the less acidic region which is called as chemotaxis. This aids the bacteria from being swept away into the lumen with the bacteria’s mucus environment which is constantly moving from the site of creation at the epithelium to its dissolution at the lumen interface.
H. pylori is found in the mucus, on the inner surface of the epithelium. The bacteria produces adhesins which helps the bacteria to bind to the lipids and carbohydrates of the epithelial cell membrane. The adhesin which is termed as the BabA binds to the Lewis b antigen displayed on the surface of the stomach epithelial cells. H. pylori adherence via BabA is acid sensitive and it can be reversed by decreased pH. This adhesin BabA’s acid response enables adherence and also helps the bacteria to escape from the acidic environment present in the stomach and favours the growth of the bacteria to adapt itself in this environment. Another such adhesin, SabA binds to increased levels of sialyl – Lewis x antigen expressed on gastric mucosa. In addition to using chemotaxis to restrict the areas of low pH, H.pylori also neutralizes the acid in the environment by producing the large amounts of the urease which breaksdown the urea present in the stomach to carbon di oxide and ammonia. These reaction with the strong acids in the environment produces a neutralized area around H. pylori. Urease mutants are incapable of colonization. The urease expression is not only required for the initial colonization but it is also required for the sustaining the chronic infection.
This urease enzyme produced by the bacteria leads to the formation of the ammonia and helps the bacteria to survive in the acidic environment. Arginase secreated by the bacterium in human stomach a member of the ureohydrolase family, catalyzes the conversion of L – arginine to L – ornithine and urea where thr ornithine is converted into polyamines which plays a major role in various metabolic process.
The above mechanism elicited by the bacteria provides the acid resistance and it is the important for colonization of the bacterium in the gastric epithelial cells. This reduces the synthesis of NO which plays an important role in the innate immunity and an effective antimicrobial agent that is able to kill the invading the pathogens. The changes in the availability of L arginine and its metabolism into polyamines results in deteriorated activity of the host innate immune mechanism
A number of other symptoms may be associated with H. pylori infection, including:
Excessive belching or eractation
Feeling bloated
Nausea
Heartburn
Fever
Lack of appetite
Flatulence
Anorexia
Unexplained weight loss
Difficulty in swallowing
Anaemia
Blood in the stool
Digestive problems
Sometimes regurgitation of the foods might occur
Endoscopy:
The thin tube is inserted into the esophagus to view the internal structure of the stomach. The endoscopy is a invasive procedure through which the biopsies can be obtained.
Urea breath test:
The urea in the bacteria detects the presence of the bacteria in the breath. In H.pylori infected patients hydrolyzation of the bacteria results in the production of the carbon di oxide . Then this CO2 gets trapped in the lungs and it gets exhaled in the breath.
Stool antigen test:
This method provides greater help when there is the absence of the urease breath test. But the factors such as the upper GIT bleeding, antibiotic consumption and proton pump inhibitors and bowel movement provides false negative.
Serological test:
Development of the specific type of the antibodies to the antigens is useful in detecting the bacteria.
The different bacterial components include whole cell lysate, specific outer membrane proteins, LPS, heat shock protein (HSP), catalase, and cagA protein and many of the adhesions were applied to induce specific antibodies in the host for facilitating the serological assay.
Histology:
Warthin starry silver stain produces the different colonies of the bacterium. The other dyes such as toludine blue, Romanowski, giemenez and giemsa stain can also be used in the detection of the virus.
Rapid urease test:
It is the inexpensive method of diagnosing the infection. It reveals the presence of the chronic infection.
PCR:
This is the specific test for the diagnosing the H pylori infection. It uses amplification of the bacterial DNA for the detection of the bacteria.
the prognosis is excellent on taking proper antibiotics and antacids. treatment should be cotinued till the test shows the absence of bacteria.
Maintain healthy lifestyle
Avoid spicy food
Proper washing of the hand
