Helicobacter pylori is a pathogen that thrives in an individual’s stomach. It is spiral in shape and is classified as a unipolar, microaerophilic, gram-negative bacterium. This bacterium was discovered to be the cause of more than eighty percent of all peptic ulcers2. H. Pylori have four to six flagella that help with its motility1. Its flagella also enable it to move into and take up residence in the thick mucus layer of the stomach3. This part of the stomach protects the bacterium from highly acidic contents. H. pylori’s genome was found to be one-third the size of E-coli’s genome2. This indicates that there are possibly many specializations or variation involved with H. pylori.
It is characterized that this organism produces the enzymes catalase and urease. Both catalase and urease helps with the bacterium’s pathogenicity. Urease enzyme is considered the main virulence factor of H. pylori. It breaks down urea, which then produces ammonia that protects the bacterium from the acid in the stomach3. Ammonia presents as a buffer that neutralizes stomach acid, helping H. pylori to thrive2. As well, catalase enhances its ability to overcome the white blood cells that tries to kill the bacteria1. H. pylori produces two more enzymes right after it colonizes the stomach. Protease and phospholipase are enzymes that act on gastric epithelium to destroy the mucus layer of the stomach1. Surrounding H. pylori, there is a structure called adhesins that enable it to bind to the host cell. H. pylori’s adhesins are also virulent factors since its adherence to the gastric mucosa protects it from the acidic pH. The most notable adhesin of this bacterium is a protein called “BabA” or blood group antigen binding adhesion2. When BabA bind to gastric epithelial cells, it creates inflammatory responses to the stomach. H. pylori is also persistent due to the mechanism of cag pathogenicity island which delivers proteins to the host cell4. These proteins are considered toxic, which results in the killing or altering of the host cell.
H. pylori is often found within the antrum of the stomach. In the antrum, there is no acid-producing parietal cells and therefore protects this region from acidic contents3. H. pylori then digs deep down the epithelium with the aid of its flagella. During this process, it also releases its enzymes (protease and phospholipase) that destroy the epithelium’s structure. H. pylori then weakens the gastric mucosa by disrupting the tight junctions between the cells3. As a result, the gastric mucosa will become leakier than normal. Acid and pepsin will diffuse into the mucosa leading to ulcer in the stomach wall3.
Ulcers can have serious consequences. Hemorrhage resulting from damage to submucosal capillaries may occur2. The stomach wall can also perforate, leading to the leakage of gastric contents into the abdominal cavity. This will then result in extreme pain of the stomach. Common symptoms that occur may include weight loss, nausea...