Helicobacter pylori bacterium (formerly known as Campylobacter pylori or pyloridis) is a gram-negative bacterium that is usually found in the stomach and is considered to cause gastritis and gastric ulcers.
The Helicobacter pylori bacterium is a small, coma- or S-shaped, non-sporing, gram-negative organism with a width of approximately 0.5 to 1.0 μm and length of about 2.5 to 4.0 μm, aditionally the bacteriu, is highly motile with a rapid corkscrew-like motion. It thrives within the mucous membrane of the stomach and the duodenum thanks to their ability to live in the environment with low oxygen concentrations and their high urease production – this substance neutralizes stomach acid and protects the bacteria. The urease production is especially relevant for the physicians, as some diagnostic tools used to detect H. pylori are based on the presence of urease.
Helicobacter pylori bacterium spreads via oral-to-oral, fecal-to-oral contact, contaminated food or water and is typically acquired during childhood. Sometimes the bacterium may be transmitted via improperly cleaned endoscopes.
Helicobacter pylori bacterium attaches to the mucus cells of the stomach, causing the production of proinflammatory substances and infiltration of the mucus membrane with the leukocytes, namely, causing gastric inflammation. The chronic inflammatory reaction may in the future result in the stomach mucous membrane apples and lead to the development of gastric or duodenal cancer.
Approximately 50% of humans were reported to be infected with Helicobacter pylori, which is known as the main risk factor for the development of antral gastritis, peptic ulcer, stomach cancer (adenocarcinoma) and mucosa-associated lymphoid tissue (MALT) lymphoma. At the same time Helicobacter pylori is considered to have protective properties against gastroesophageal reflux disease and esophageal cancer.
Signs or symptoms of H. pylori infection may include:
An ache or burning pain in the abdomen;
Abdominal discomfort or pain that worsens when the stomach is empty;
Foul breath (halitosis);
Loss of appetite (anorexia);
Unintentional and unexplained weight loss;
Bloody or black-colored feces (so called tar-like stools) or vomit due to the bleeding of the ulcer;
To detect the presence of H. pylori several tests may be performed:
Stool test: H. pylori fecal antigen test;
Carbon 13 or carbon 14 urea breath test – a person is drinking urea (usually with a beverage) labeled with a carbon isotope (carbon 13 or carbon 14). After some time the concentration of the carbon is measured in the breath;
Helicobacter pylori serologic assays – detection of immunoglobulin G antibodies against H. pylori;
Antibioticogram to evaluate the susceptibility of the bacterium to the antibiotics;
Other tests include:
Esophagogastroduodenoscopy with biopsy of the stomach lining and biopsy-based urease test;
There are several regimens that may be used to eradicate Helicobacter pylori infection.
Triple therapy (Proton pump inhibitor (PPI such asomeprazole, pantoprazole etc.) plus clarithromycin 500 mg BID or metronidazole 500 mg BID plus amoxicillin 1000 mg BID or metronidazole) is an option for first-line therapy in areas of low clarithromycin resistance.
Nonbismuth quadruple therapy may be given sequentially or concomitantly. Sequential therapy requires a 14-day intake of medications (PPI plus amoxicillin for 5-7 days, then PPI plus 2 other antibiotics (usually clarythromycin and metronidazole) for the next 5-7 days).
Bismuth-based therapy is an alternative first-line therapy (in areas with high clarithromycin and metronidazole resistance) or second-line therapy. It lasts for 10-14 days and includes intake of PPI or H2 receptor antagonist plus bismuth subsalicylate 525 mg QID plus metronidazole 250 mg QID plus tetracycline 500 mg QID.
DISCLAIMER: This information should not substitute for seeking responsible, professional medical care.