Helicobacter pylori

Last updated: November 01, 2022

Helicobacter pylori

Spring 21 Unit 7

Spring 21 Unit 7

Brain herniation
Diabetic nephropathy
Supraventricular arrhythmias: Pathology review
Ventricular arrhythmias: Pathology review
Myocardial infarction
ECG cardiac infarction and ischemia
DALY and QALY
Atherosclerosis and arteriosclerosis: Pathology review
Insulins
Miscellaneous hypoglycemics
Diabetes mellitus
Diabetes mellitus: Pathology review
Diabetes insipidus
Diabetes mellitus: Clinical
Diabetic retinopathy
Urinary incontinence
Plasma anion gap
Hypoglycemics: Insulin secretagogues
Coagulation (secondary hemostasis)
Role of Vitamin K in coagulation
Anticoagulants: Direct factor inhibitors
Anticoagulants: Warfarin
Clot retraction and fibrinolysis
Anticoagulants: Heparin
Thrombolytics
Antiplatelet medications
Ischemic stroke
Dizziness and vertigo: Clinical
Stroke: Clinical
Cerebellum
Vertigo
Zollinger-Ellison syndrome
MEN syndromes: Clinical
Multiple endocrine neoplasia: Pathology review
GERD, peptic ulcers, gastritis, and stomach cancer: Pathology review
Acid reducing medications
Pancreatic neuroendocrine neoplasms
Peptic ulcer
Peptic ulcers and stomach cancer: Clinical
Ulcerative colitis
Helicobacter pylori
Coronary artery disease: Pathology review
Heart blocks: Pathology review
Peripheral artery disease: Pathology review
Ventricular fibrillation
Wolff-Parkinson-White syndrome
Inflammation
Lupus nephritis
Systemic lupus erythematosus
Systemic lupus erythematosus (SLE): Pathology review
Systemic lupus erythematosus (SLE): Clinical
Antiphospholipid syndrome
Raynaud phenomenon
Sjogren syndrome: Clinical
Sjogren syndrome
Scleroderma
Limited systemic sclerosis (CREST syndrome)
Cervical cancer
Cervical cancer: Pathology review
Class I antiarrhythmics: Sodium channel blockers
Class II antiarrhythmics: Beta blockers
Class III antiarrhythmics: Potassium channel blockers
Class IV antiarrhythmics: Calcium channel blockers and others
Long QT syndrome and Torsade de pointes
Calcium channel blockers
Cranial nerves
Introduction to the cranial nerves
Treponema pallidum (Syphilis)
Rheumatoid arthritis
Rheumatoid arthritis: Clinical
Aortic dissection
Measles virus
Mumps virus
Rubella virus

Transcript

Watch video only

Content Reviewers

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 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 of 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 aurease 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.