What exactly is Helicobacter Pylori and can someone die from it? I was wondering if anyone knew someone suffering from this and how I can help my mom. She can't eat and hasnt done so for a whole week. Please post links, if you have on medicine. First of all, please do not freak out. H. Pylori is much more common than most people realize. Most of the time a doctor will recommend a combination of a proton pump inhibitor (this med blocks the acid production of the stomach) such as Prilosec and an antibiotic such as Clarithromycin. Rarely, only an antibiotic is prescribed. Actually, in my experience with patients with this bacterium, doctors use a combination of medications. The chance of your mom dying from H. Pylori alone is extremely rare. It is actually easily treatable with early diagnoses. Just make sure she sees a doctor and follows the medication regiment to the letter. Since you know that she has this, she should be on a treatment plan already. Best of luck to you and your mom :-) She need antibiotics to get rid of this infection. H-Pylori bacteria is what is causing her stomach ulcer so she needs antibiotics to get rid of this infection and things like tagement or maalox etc to help with the pain in her abdomin. If she is not on antibiotics for this then be sure she sees a doc and gets this treated. Hi i had this about 8 years ago and the doc put me on an antibiotic with 3 other pills and it took it away but i couldn't eat anything either because your stomach hurts all the time, im sorry i don't know what the pills are called it has been so long ago, sounds like she went to the doc , did he put her on meds for this? It is painful and I'm pretty sure it is an infection in the stomach, i heard if it isn't treated things can happen, but if your mom went to the doc and he gave her the meds there really shouldn't be anything to worry about. But of course we all worry about our parents. Well i hope this helped a little and i hope your mom feels better soon. Helicobacter pylori is a bacteria that has been associated with the development of stomach ulcers. It can be treated using antibiotics along with antacids for the ulcer. Treatment may take as long as 4-6 weeks. Infection is not fatal except if there is a chronic untreated ulcer and it bleeds or perforates the stomach. Get treatment and try not to worry Hi there , First of all if the diagnosis is confirmed , then the doctor must have prescribed a triple or quadruple therapy of drugs which should be taken for 1 0r 2 weeks and after that a post H pylori test is done to confirm the eradication of that bacteria , ie urea breathe test and the treatment is based on the follow up . There is nothing to worry about . Helicobacter pylori is the bacteria that causes stomach ulcers. A course of antibiotics and some antacids should do the trick. Helicobacter pylori
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Helicobacter pylori
Scientific classification
Kingdom: Bacteria
Phylum: Proteobacteria
Class: Epsilon Proteobacteria
Order: Campylobacterales
Family: Helicobacteraceae
Genus: Helicobacter
Species: H. pylori
Binomial name
Helicobacter pylori
((Marshall et al. 1985) Goodwin et al. 1989)
Helicobacter pylori is a helical shaped Gram-negative bacterium that infects various areas of the stomach and duodenum. Many cases of peptic ulcers, gastritis, duodenitis, and perhaps some cancer are caused by H. pylori infection. However, many who are infected do not show any symptoms of disease. Helicobacter spp. are the only known microorganisms that can thrive in the highly acidic environment of the stomach. Its helical shape (from which the genus name is derived) is thought to have evolved to penetrate and favor its motility in the mucus gel layer.[1]
Contents [hide]
1 History
2 Structure
3 Colonization
4 Diagnosis of infection
5 Treatment of infection
6 Helicobacter and cancer
7 Genome studies of different strains
8 See also
9 Notes
10 References
11 External links
[edit] History
See also: Timeline of peptic ulcer disease and Helicobacter pylori
In 1875, German scientists found helical shaped bacteria in the lining of the human stomach. The bacteria could not be grown in culture and the results were eventually forgotten.[2]
In 1893, the Italian researcher Giulio Bizzozero described helical shaped bacteria living in the acidic environment of the stomach of dogs.
Professor Walery Jaworski of the Jagiellonian University in Krak贸w investigated sediments of gastric washings obtained from humans in 1899. Among some rod-like bacteria, he also found bacteria with a characteristic helical shape, which he called Vibrio rugula. He was the first to suggest a possible role of this organism in the pathogeny of gastric diseases. This work was included in the "Handbook of Gastric Diseases" but it did not have much impact as it was written in Polish.[3]
The bacterium was rediscovered in 1979 by Australian pathologist Robin Warren, who did further research on it with Barry Marshall beginning in 1981; they isolated the organisms from mucosal specimens from human stomachs and were the first to successfully culture them.[4] In their original paper,[5] Warren and Marshall contended that most stomach ulcers and gastritis were caused by infection by this bacterium and not by stress or spicy food as had been assumed before.[6]
The medical community was slow to recognize the role of this bacterium in stomach ulcers and gastritis, believing that no microorganism could survive for long in the acidic environment of the stomach. The community began to come around after further studies were done, including one in which Marshall drank a Petri dish of H. pylori, developed gastritis, and the bacteria were recovered from his stomach lining, thereby satisfying three out of the four Koch's postulates. The fourth was satisfied after a second endoscopy ten days after inoculation revealed signs of gastritis and the presence of "H. pylori". Marshall was then able to treat himself using a fourteen day dual therapy with bismuth salts and metronidazole. Marshall and Warren went on to show that antibiotics are effective in the treatment of many cases of gastritis. In 1994, the National Institutes of Health (USA) published an opinion stating that most recurrent gastric ulcers were caused by H. pylori, and recommended that antibiotics be included in the treatment regimen.[7] Evidence has been accumulating to suggest that duodenal ulcers are also associated with H. pylori infection.[8][9] In 2005, Warren and Marshall were awarded the Nobel Prize in Medicine for their work on H. pylori.[10]
Before the appreciation of the bacterium's role, stomach ulcers were typically treated with medicines that neutralize gastric acid or decrease its production. While this worked well, the ulcers very often reappeared. A very often used medication against gastritis and peptic ulcers was bismuth subsalicylate. It was often effective, but fell out of use, since its mechanism of action was a mystery. Nowadays it is quite clear that it is due to the bismuth salt acting as an antibiotic. Today, many stomach ulcers are treated with antibiotics effective against H. pylori.
The bacterium was initially named Campylobacter pyloridis, then C. pylori (after a correction to the Latin grammar) and in 1989, after DNA sequencing and other data showed that the bacterium did not belong in the Campylobacter genus, it was placed in its own genus, Helicobacter. The name pyl艒ri means "of the pylorus" or pyloric valve (the circular opening leading from the stomach into the duodenum), from the Greek word 蟺蠀位蠅蟻蠈蟼, which means gatekeeper.
While H. pylori remains the most medically important bacterial inhabitant of the human stomach, other species of the Helicobacter genus have been identified in other mammals and some birds, and some of these can infect humans.[citation needed] Helicobacter species have also been found to infect the livers of certain mammals and to cause liver disease.[11]
[edit] Structure
H. pylori is a helical shaped Gram-negative bacterium, about 3 micrometres long with a diameter of about 0.5 micrometre. It has 4鈥? flagella. It is microaerophilic, i.e. it requires oxygen but at lower levels than those contained in the atmosphere. It contains a hydrogenase which can be used to obtain energy by oxidizing molecular hydrogen (H2) that is produced by other intestinal bacteria.[12] It tests positive for oxidase, catalase, and urease. It is capable of forming biofilms[13] and conversion from helical to coccoid form[14], both likely to favor its survival and be factors in the epidemiology of the bacterium. The coccoid form of the organism has not been cultured, but has been found in the water supply in the US. This form has also been found to be able to adhere to gastric epithelial cells in vitro.
Molecular model of H. pylori urease enzyme
[edit] Colonization
With its flagella, the bacterium moves through the stomach lumen and drills into the mucus gel layer of the stomach. It then finds ways to live in various areas of the stomach. The known areas include: inside the mucus gel layer (with a preference for the superficial area), above epithelial cells, and inside vacuoles formed by H. pylori in epithelial cells. It produces adhesins which bind to membrane-associated lipids and carbohydrates and help its adhesion to epithelial cells. It produces large amounts of urease enzymes which are localized inside and outside of the bacterium. Urease metabolizes urea (which is normally secreted into the stomach) to carbon dioxide and ammonia which neutralizes gastric acid. The survival of H. pylori in the acidic stomach is dependant on urease, and it would eventually die without it. The ammonia that is produced is toxic to the epithelial cells, and with other products of H. pylori, including protease, catalase, and phospholipases, causes damage to those cells.
Some strains of the bacteria have a particular mechanism for "injecting" the inflammatory inducing agent peptidoglycan from their own cell wall into epithelial stomach cells. (See below for "cagA pathogenicity island" in the section Genome studies of different strains) This factor may play a role in allowing certain strains to invade host tissue.[15]
[edit] Diagnosis of infection
Immunohistochemical staining of H. pylori from a gastric biopsy.Diagnosis of infection is usually made by checking for dyspepetic symptoms and then doing tests which can suggest H. pylori infection. One can test noninvasively for H. pylori infection with a blood antibody test, stool antigen test, or with the carbon urea breath test (in which the patient drinks 14C- or 13C-labelled urea, which the bacterium metabolizes producing labelled carbon dioxide that can be detected in the breath). However, the most reliable method for detecting H .pylori infection is a biopsy check during endoscopy with a rapid urease test, histological examination, and microbial culture. Except for the biopsy check, none of the test methods are completely failsafe. Blood antibody tests, for example, range from 76% to 84% sensitivity. Some drugs can affect H. pylori urease activity and give "false negatives" with the urea-based tests.
Infection may be symptomatic or asymptomatic (without perceptible ill effects). It is estimated that up to 70% of infection is asymptomatic and that about 2/3 of the world population are infected by the bacterium, making it the most widespread infection in the world. Actual infection rates vary from nation to nation - the West (Western Europe, North America, Australasia) having rates around 25% and much higher in the Third World. In the latter, it is common, probably due to poor sanitary conditions, to find infections in children. In the United States, infection is primarily in the older generations (about 50% for those over the age of 60 compared with 20% under 40 years) and the poorest.
This is largely attributed to higher hygiene standards and widespread use of antibiotics. However, antibiotic resistance is appearing in H. pylori.[16] There are already many metronidazole resistant strains in Europe, the United States, and developing countries.
The bacteria have been isolated from feces, saliva and dental plaque of infected patients, which suggests gastro-oral or fecal-oral as possible transmission routes.
It is widely believed that in the absence of treatment, H. pylori infection鈥攐nce established in its gastric niche鈥攑ersists for life. In the elderly, however, it is likely infection can disappear as the stomach's mucosa becomes increasingly atrophic and inhospitable to colonization. The proportion of acute infections that persist is not known, but several studies that followed the natural history in populations have reported apparent spontaneous elimination.[17][18]
[edit] Treatment of infection
H. pylori colonized on the surface of regenerative epithelium (Warthin-Starry's silver)In peptic ulcer patients where infection is detected, the normal procedure is eradicating H. pylori to allow the ulcer to heal. The standard first-line therapy is a one week triple therapy. The Sydney gastroenterolgist Thomas Borody invented the first triple therapy in 1987.[19] Today, the standard triple therapy is amoxicillin, clarithromycin and a proton pump inhibitor such as omeprazole.[20] Variations of the triple therapy have been developed over the years, such as using a different proton pump inhibitor, as in PantoPac, or using metronidazole instead of amoxicillin in those allergic to penicillin.[21] Such a therapy has revolutionised the treatment of peptic ulcers and has made a cure to the disease possible, where previously symptom control using antacids, H2-antagonists or proton pump inhibitors alone was the only option.[22][23]
A meta-analysis of randomized controlled trials suggests that supplementation with probiotics can improve eradication rates and reduce adverse events.[24]
Unfortunately, an increasing number of infected individuals are found to harbour antibiotic-resistant bacteria. This results in initial treatment failure and requires additional rounds of antibiotic therapy or alternative strategies such as a quadruple therapy. Bismuth compounds are also effective in combination with the above drugs. For the treatment of clarithromycin-resistant strains of H. pylori the use of levofloxacin as part of the therapy has been suggested.
Some studies show that consumption of broccoli sprouts can be effective at inhibiting H. pylori growth[25] with sulforaphane being at least one of the active agents[26].
Some studies show that mastic gum can destroy H. pylori in vitro, but studies done in vivo have shown it to be ineffective.[27]
A study done on Mongolian gerbils indicates that green tea extract can suppress H. pylori growth.[28] Another study done in South Korea suggests that an acidic polysaccharide found in green tea is significantly effective in preventing adhesion of H. pylori to human cultures of epithelial cells.[29]
As explained below, some authors suggest that some strains of H. pylori may be protective against certain diseases of the esophagus and cardia. Therefore, a more cautious approach than complete eradication may be necessary in some cases. |
