Commonly prescribed antibiotics used to treat H. pylori infection include amoxicillin (Amoxil, Trimox), clarithromycin (Biaxin), metronidazole (Flagyl), and tetracycline (Sumycin). To work with the antibiotics, physicians often prescribe one or more of the following: Proton pump inhibitors (PPIs) prevent the stomach from producing acid.
Full Answer
What is the role of cytotoxins in Helicobacter pylori colonization?
Vacuolating cytotoxin of Helicobacter pylori plays a role during colonization in a mouse model of infection. Infect. Immun. 69:730-736.
What is the main component of H pylori acid resistance?
The main component of H. pylori acid resistance is the urease enzyme, which converts urea into ammonia and carbamate, which spontaneously decomposes into another ammonia molecule and carbon dioxide ( 70 ).
What is the role of Helicobacter pylori in the inflammatory response?
H. pylori is thought to downregulate inflammation and control the host's immune response through a wide range of virulence factors that are involved in both provoking and maintaining a proinflammatory immune response.
What is the pathophysiology of H pylori colonization of the murine stomach?
Colonization of the murine stomach by H. pylori and H. felis results in the development of lymphocytic gastritis, but it does not progress to peptic ulcer or gastric adenocarcinoma.
How is H. pylori treated?
How is H.pylori infection treated? If H. pylori is found, it can be treated using eradication therapy , which usually consists of two antibiotics and another type of medicine called proton pump inhibitor (PPI).
Where is H. pylori most common?
H. pylori is more common in countries or areas that lack clean water or are without a good sewerage system. You can easily pick up the bacteria from food, water, utensils, or through contact with the saliva or other body fluids of infected people. There is a greater risk of spreading the infection in overcrowded living areas.
How to tell if you have H pylori?
The symptoms of H. pylori reflect those of dyspepsia (indigestion) or an ulcer and may include: 1 A dull or burning pain in your stomach that is worse if you haven't eaten 2 Bloating 3 Indigestion or heartburn 4 Nausea 5 Low appetite 6 Frequent burping 7 Acid burps 8 Weight loss.
What is the name of the bacteria that can infect the stomach?
Helicobacter pylori ( H.pylori) is a type of bacteria that can infect your stomach and digestive tract. Infection is common, and more than two-thirds of the world’s population is infected, although the rate of infection is declining as more people get access to clean water and sanitation.
What are the symptoms of H. pylori?
The symptoms of H. pylori reflect those of dyspepsia (indigestion) or an ulcer and may include: A dull or burning pain in your stomach that is worse if you haven't eaten. Bloating. Indigestion or heartburn. Nausea.
What test detects H pylori in the stomach?
An urea breath test. This detects H. pylori in the stomach. An upper gastrointestinal endoscopy to look into your stomach and small intestine and to collect a sample which can be tested for the presence of bacteria. An X-ray.
Can a doctor look for H pylori?
Doctors do not usually go looking for H. pylori unless you develop ongoing or frequent dyspepsia (indigestion) or gastric ulcers. Your doctor will ask you about your medical history, any symptoms, and what medications you take.
What is the role of acid secretion in H. pylori?
Acid secretion and the associated pattern of gastritis play an important role in disease outcome in H. pylori infection. The figure displays the correlations between the pattern of H. pylori colonization, inflammation, acid secretion, gastric and duodenal histology, and clinical outcome.
What is the first result of H. pylori colonization?
Colonization of the gastric mucosa by H. pylori first results in the induction of an inflammatory response, predominantly of the Th1 type. The initial acute gastritis is followed by active chronic gastritis, which lasts for life if the infection is not treated ( 340 ).
What is the interaction between H. pylori and gastric antrum?
pylori infection. In subjects with intact acid secretion, H. pylori in particular colonizes the gastric antrum, where few acid-secretory parietal cells are present. This colonization pattern is associated with an antrum-predominant gastritis.
What is the pathogen of cheetahs?
H. acinonychis, a pathogen of cheetahs and other big cats (formerly named Helicobacter acinonyx [ 145 ]), is currently the closest known relative to H. pylori ( 242) and has been suggested to have diverged from its last common ancestor ( H. pylori) only relatively recently ( 241 ). The presence of H. acinonychis is associated with chronic gastritis and ulceration, a frequent cause of death of cheetahs in captivity ( 444 ). Furthermore, eradication treatment of H. acinonychis led to the resolution of gastric lesions in tigers ( 77 ), similar to the effect of antibiotic treatment of H. pylori infection ( 228 ). H. acinonychis is susceptible to antibiotic therapy, as used for H. pylori infection, and utilizes similar mechanisms for antimicrobial resistance ( 509 ).
What animal is used for H pylori?
The mouse is the most widely used animal host for investigations of the pathogenicity of H. pylori and other bacteria. The murine immune response has been well documented, and many different knockout mice that lack specific components of the immune system are available. In addition, mice are readily available and their housing is relatively cheap. However, the mouse model has distinct limitations (reviewed in references 318, 477, and 512 ). H. pylori infection of many commonly used mouse strains results mostly in lymphocytic gastritis without progression to H. pylori -associated pathology, such as peptic ulcers or gastric cancer ( 318, 477, 512 ). Also, the architecture of the murine stomach is distinct from that of the human stomach and may lack components involved in the development of gastric pathology. Finally, the murine stomach is not sterile, in contrast to the healthy human stomach, and so other bacteria may influence the outcome of H. pylori infection ( 318, 477, 512 ). Therefore, the use of the mouse model is mostly restricted to testing the colonization properties of distinct H. pylori mutants.
How prevalent is H. pylori?
In various developing countries, more than 80% of the population is H. pylori positive, even at young ages ( 500 ). The prevalence of H. pylori in industrialized countries generally remains under 40% and is considerably lower in children and adolescents than in adults and elderly people ( 510 ). Within geographical areas, the prevalence of H. pylori inversely correlates with socioeconomic status, in particular in relation to living conditions during childhood ( 389 ). In Western countries, the prevalence of this bacterium is often considerably higher among first- and second-generation immigrants from the developing world ( 499, 635 ). While the prevalence of H. pylori infection in developing countries remains relatively constant, it is rapidly declining in the industrialized world ( 220 ). The latter is thought to be caused by the reduced chances of childhood infection due to improved hygiene and sanitation and the active elimination of carriership via antimicrobial treatment. In developing countries, H. pylori infection rates rise rapidly in the first 5 years of life and remain constantly high thereafter, indicating that H. pylori is acquired early in childhood ( 184 ). However, in industrialized countries the prevalence of H. pylori infection is low early in childhood and slowly rises with increasing age. This increase results only to a small extent from H. pylori acquisition at later age. The incidence of new H. pylori infections among adults in the Western world is less than 0.5% per year; the higher prevalence of infection among the elderly thus reflects a birth cohort effect with higher infection rates in the past ( 336, 488 ). The active elimination of H. pylori from the population and improved hygiene and housing conditions have resulted in a lower infection rate in children, which is reflected in the age distribution of this lifelong-colonizing bacterium ( 322, 524, 531 ). Overall, new infection more commonly occurs in childhood and lasts for life unless specifically treated.
Why do we need an animal model for H. pylori?
pylori and acute gastritis via the infamous self-infection experiment ( 398, 401, 684 ), it was apparent that an animal model was required to allow elucidation of the mechanisms governing disease development and the pathogenic properties of H. pylori, as well as for testing the effects of treatment and vaccination on the pathogenesis of H. pylori infection. However, the choice of the most appropriate animal model has proven to be quite difficult, as all of the models used so far have deficiencies that may prevent translation to the human situation. As each model has its pros and cons, the choice of the most appropriate model is dependent on the hypothesis that is being tested. Here we briefly discuss the most commonly used animal models for H. pylori.