Helicobacter pylori
Helicobacter pylori, or H. pylori for short, is a bacterium found in the stomach of over half of the world’s population.
In some individuals it can cause inflammation of the stomach lining; and can result in peptic ulcers. In fact, complications from H.
pylori ulcers is thought to have been the cause of the death for the famous writer, James Joyce. H.
pylori is a gram-negative bacteria that’s shaped like a curved rod and it has 2 to 6 flagella, kind of like multiple tails, all at one end which it uses for movement.
It’s positive for urease, oxidase and catalase; and is a microaerophile, so that means it needs oxygen to survive, but requires less than the levels typically found in the atmosphere.
Now in the stomach, there are four regions - the cardia, the fundus, the body, and the pylorus. And the pylorus itself is made up two main parts: the antrum; and the pyloric canal, which connects to the first section of the small intestines called the duodenum.
Ok, now normally, the inner wall of the entire gastrointestinal tract is lined with mucosa, which consists of three cell layers.
The innermost layer is the epithelial layer and it absorbs and secretes mucus and digestive enzymes. The middle layer is the lamina propria and it has blood and lymph vessels.
The outermost layer of the mucosa is the muscularis mucosa, and it’s a layer of smooth muscle that contracts and helps with the break down food.
The epithelial layer dips down below the surface of the stomach lining to form gastric pits. And these pits are contiguous with gastric glands below which contain various epithelial cell types - each secreting a variety of substances.
So for example, foveolar cells, or surface mucus cells, secrete mucus, which is a mix of water and glycoproteins that coats the stomach epithelial cells.
With all of these digestive enzymes and hydrochloric acid floating around, the stomach and duodenal mucosa would get digested if not for this mucus which coats and protects the epithelial cells.
Within the glands, particularly in the body and fundus of the stomach, are parietal cells, which secrete hydrochloric acid to help maintain an acidic pH in the stomach.
There are also chief cells that secrete pepsinogen to digest proteins. And then there are G cells which secrete gastrin, which has a number of effects, including stimulation of parietal cells.
An H. pylori infection is thought to spread through fecal-oral, gastro-oral, and perhaps oral-oral transmission, from one infected individual to another.
That is - through contamination of food and water or even directly, with fecal matter, vomitus, or saliva. However it makes its way into the body - once it arrives within the stomach, H.
pylori uses its flagella to propel toward the stomach lining. Typically, it will migrate to regions where pH is less acidic - like the antrum, which has fewer parietal cells.
It then uses adhesin proteins to stick to the surface of foveolar cells where it can release a number of virulence factors which help it both survive and thrive, and cause damage to the mucosa.
One of the most important enzymes for their survival is urease because it converts urea in the gastric juices to carbon dioxide and ammonia.
Ammonia, which is basic, locally neutralizes the acid gastric environment and protects H. pylori from the harsh, acidic environment of the stomach.
While H. pylori itself does not typically go inside the epithelial cells, some of the virulence factors it releases do - and they cause extensive damage to epithelial cells.
For example, some strains of H. pylori produce cytotoxin-associated gene A, or cagA, which interferes with the attachments between epithelial cells that normally help protect the underlying mucosal layers.
That induces an inflammatory immune response within the gastric lining, called gastritis, as mononuclear immune cells become attracted to the infection site.
In chronic infections, cagA has been linked to the development of two gastric cancers: mucosa-associated lymphoid tissue or MALT lymphoma, which involves B cells; and adenocarcinoma, which involves cells within the gastric glands.
Some strains of H. pylori produce exotoxin vacuolating cytotoxin A, or vacA, which causes epithelial cell death and exposes the underlying mucosal layers to gastric acid.
As more and more cell layers die, deep holes through the mucosa form - called ulcers. Now, inflammation also stimulates the G cells to secrete gastrin, which in turn stimulates parietal cells to produce even more hydrochloric acid.
And all this excess acid can spur the formation of both gastric ulcers and duodenal ulcers - the main distinction being the exact location of the gastritis.
Antral gastritis leads to duodenal ulcers whereas corpus gastritis leads to gastric ulcers. Very deep ulcers can erode underlying blood vessels and may even erode all the way through the wall of the stomach, or duodenum in particular, causing a perforation.
Finally, and very rarely, long-standing duodenal ulcers in the pyloric canal, can sometimes have so much edema or scarring that they obstruct the normal passage of gastric contents into the duodenum.
The majority of individuals with H. pylori don’t have any symptoms, and it may play an important role in the natural stomach ecology.
But in some individuals there can be a chronic infection, particularly with strains that have cagA and vacA. That can cause symptoms like heartburn, shortness of breath, and loss of appetite with or without weight-loss, and pain in the abdomen just above the stomach that worsens a few hours after eating.
If a perforation occurs, air can collected under the diaphragm, irritating the phrenic nerve, and sending referred pain up to the shoulder.
Finally, a chronic infection can also lead to iron-deficiency anemia - it’s thought that the bacteria sequester dietary iron - literally eating it before you can get to it!
There are a few ways to diagnosis an H. pylori infection.
Lastly, upper gastrointestinal endoscopy can be used to get a gastric biopsy. Finally, a diagnosis can be made by culturing H.
pylori from a gastric biopsy. Without the presence of clinical symptoms, H.
pylori is not typically treated. But if it’s detected in a person with a family history of gastrointestinal cancers; or when clinical symptoms are present - triple therapy is effective and consists of two antibiotics, typically amoxicillin and clarithromycin, and a proton pump inhibitor.
So, to recap: Helicobacter pylori is a gram-negative, microaerophilic bacterium commonly found in the stomach. The majority of individuals infected with the bacterium are asymptomatic, and it may play an important role in the natural stomach ecology.It’s linked to the development of gastric and duodenal ulcers, MALT lymphomas, and gastric cancer.
Acute infection may appear as an acute gastritis with abdominal pain or nausea. Treatment includes antibiotics and a proton pump inhibitor.
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