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Approximately one-half of the world’s population is estimated to be infected with Helicobacter pylori, a gram-negative, curved bacterial rod, which has been associated with symptoms ranging from peptic ulcer disease and dyspepsia to gastric adenocarcinoma and mucosa-associated lymphoid tissue (MALT) lymphoma. The currently available diagnostic assays for detection of H pylori can be classified as either invasive, requiring gastric endoscopy and tissue biopsy, or noninvasive, requiring readily available specimen types (ie, serum, breath, and stool samples). Following recovery of 1 or more gastric tissue biopsies, evaluation for the presence of H pylori can be accomplished by 1 of 4 methods—culture, rapid urease tests, histopathology, or molecular testing (Table). Isolation of H pylori by culture of a biopsy specimen is definitive evidence of active infection and isolates can subsequently be tested for susceptibility to various antimicrobial agents (Figure 1). Rapid urease tests (RUTs) are based on a pH color indicator system and are designed to detect the presence of urease, an enzyme produced by H pylori that metabolizes urea to ammonia and carbon dioxide.
Similar to culture, the detection of H pylori in gastric biopsies by histopathologic evaluation is considered diagnostic for active infection (Figure 2). Finally, molecular evaluation of biopsy specimens for the presence of H pylori DNA by real-time polymerase chain reaction (RT-PCR) is promising and numerous studies have found increased sensitivity and specificity of this method compared to culture, RUTs, and histopathology. Similar to the RUT, the principle behind the urea breath test (UBT) is based on production of urease by H pylori and a positive result is indicative of active infection. The clinical sensitivity and specificity of the UBT to detect active H pylori infection exceeds 93% in most studies, though a few reports indicate potential cross-reactivity with other gastric urease-producing organisms.3-6 A distinct advantage of this assay is that it can also be used to determine treatment efficacy.
Despite the excellent performance characteristics, the utility of the UBT is limited by a number of factors. The stool antigen test (SAT) is an enzyme immunoassay (EIA) designed to detect H pylori in fecal specimens by measuring H pylori antigen released from organisms lining the stomach wall (Figure 4). Despite these advantages, serologic testing for antibodies to H pylori should be ordered and results should be considered with significant caution. To minimize improper diagnosis and unnecessary treatment regimens, providers are strongly encouraged to amend their testing strategies by replacing serologic evaluation of patients with suspected H pylori infection, with either the UBT or the SAT assay. To conform to current H pylori testing guidelines and to improve patient management, leadership from Mayo Clinic’s divisions of Clinical Microbiology and Gastroenterology worked together to update our algorithm to detect H pylori infection. In conclusion, this article outlines the advantages and limitations of the available invasive and noninvasive testing methods to diagnose H pylori infection.
Brandi G, Biavati B, Calabrese C, et al: Urease-positive bacteria other than Helicobacter pylori in human gastric juice and mucosa. Chey WD, Metz DC, Shaw S, et al: Appropriate timing of the 14C-urea breath test to establish eradication of Helicobacter pylori infection. Chey WD, Wong BC: American College of Gastroenterology guideline on the management of Helicobacter pylori infection.
Loy CT, Irwig LM, Katelaris PH, Talley NJ: Do commercial serological kits for Helicobacter pylori infection differ in accuracy? Helicobacter pylori, previously Campylobacter pylori, is a gram-negative, microaerophilic bacterium found usually in the stomach.
Another such adhesion, SabA, binds to increased levels of sialyl-Lewis x antigen expressed on gastric mucosa.
Ulcers in the stomach and duodenum result when the consequences of inflammation allow stomach acid and the digestive enzyme pepsin to overwhelm the mechanisms that protect the stomach and duodenal mucous membranes. The type-IV secretion apparatus also injects the cag PAI-encoded protein CagA into the stomach's epithelial cells, where it disrupts the cytoskeleton, adherence to adjacent cells, intracellular signaling, cell polarity, and other cellular activities. Vulnerability to oxidative stress and oxidative DNA damage occurs commonly in many studied bacterial pathogens, including Neisseria gonorrhoeae, Hemophilus influenzae, Streptococcus pneumoniae, S. Transformation (the transfer of DNA from one bacterial cell to another through the intervening medium) appears to be part of an adaptation for DNA repair. An increasing number of infected individuals are found to harbor antibiotic-resistant bacteria. American Journal of Clinical Nutrition found evidence that " -->Ingesting lactic acid bacteria exerts a suppressive effect on H. The substance sulforaphane, which occurs in broccoli and cauliflower, has been proposed as a treatment.
At least half the world's population is infected by the bacterium, making it the most widespread infection in the world.
Before the research of Marshall and Warren, German scientists found spiral-shaped bacteria in the lining of the human stomach in 1875, but they were unable to culture them, and the results were eventually forgotten. Interest in understanding the role of bacteria in stomach diseases was rekindled in the 1970s, with the visualization of bacteria in the stomachs of people with gastric ulcers. Some skepticism was expressed initially, but within a few years multiple research groups had verified the association of H. In October 1987, a group of experts met in Copenhagen to found the European Helicobacter Study Group (EHSG), an international multidisciplinary research group and the only institution focused on H. Due to the potentially severe consequences of infection, accurate diagnosis and prompt initiation of therapy are important for successful disease resolution.
The specific indications for endoscopy will not be discussed in this article, although, in general, clinicians may wish to rule out malignancies or other noninfectious causes of the patient’s symptoms.
However, the sensitivity of this method is limited by a number of factors, including 1) the site of biopsy and the quantity of viable organisms, 2) ability to maintain viability of this fastidious bacterium during transport to the laboratory (<3 hours from collection to culture), and 3) unique culture conditions that are not routinely available in all clinical laboratories. For this assay, biopsy samples are submerged into the RUT solution, and if ammonia is produced, the pH will increase, leading to a color change that indirectly indicates the presence of H pylori. However, the sensitivity of this method is likewise limited by the site of biopsy and a lack of specificity as other nonpathogenic, curved bacteria may reside in the gastric mucosa. However, RT-PCR is not widely available in the clinical setting and is currently restricted to research laboratories. Of the 3 assays, the urea breath test (UBT) and the stool antigen test (SAT) are preferred over serologic evaluation to identify active disease. For the UBT, the patient is asked to ingest a preparation containing 13C-labeled urea—a nonradioactive carbon isotope.
Most notable is the decreased sensitivity of this assay in patients who have taken proton pump inhibitors (PPIs), bismuth-containing products, or antibiotics within 14 days prior to testing.
Additionally, unlike other noninvasive methods (ie, UBT and SAT), serologic profiles are not affected by prior use of PPIs, bismuth-containing compounds, or antibiotics, making serology an increasingly attractive method for immediate patient evaluation.

As a result of this meeting, Mayo Clinic providers will now order either the UBT or the SAT for patients with suspected H pylori infection. Implementation of this practice change will lead to more accurate diagnosis of active H pylori infection and is expected to decrease the number of prescriptions for unnecessary antimicrobial agents. It was identified in 1982 by Australian scientists Barry Marshall and Robin Warren, who found that it was present in a person with chronic gastritis and gastric ulcers, conditions not previously believed to have a microbial cause. Once inside the cell, the CagA protein is phosphorylated on tyrosine residues by a host cell membrane-associated tyrosine kinase (TK). This results in initial treatment failure and requires additional rounds of antibiotic therapy or alternative strategies, such as a quadruple therapy, which adds a bismuth colloid, such as bismuth subsalicylate. Periodontal therapy or scaling and root planing has also been suggested as an additional treatment.
Actual infection rates vary from nation to nation; the developing world has much higher infection rates than the West (Western Europe, North America, Australasia), where rates are estimated to be around 25%. Consistent with these transmission routes, the bacteria have been isolated from feces, saliva, and dental plaque of some infected people. The Italian researcher Giulio Bizzozero described similarly shaped bacteria living in the acidic environment of the stomach of dogs in 1893. The bacteria had also been observed in 1979, by Robin Warren, who researched it further with Barry Marshall from 1981. Multiple different testing methodologies are available commercially to detect H pylori infection. When symptoms are considered typical of H pylori disease, noninvasive testing for that infection will be initially performed.
Due to the rigorous transport conditions, Mayo Medical Laboratories will currently only perform antimicrobial susceptibility testing on specimens submitted as H pylori isolates.
Immunohistochemical stains have been developed to improve specificity, though cross-reactivity has been seen with other Helicobacter species (ie, Helicobacter heilmannii). If H pylori urease is present in the stomach, the urea is degraded to ammonia and labeled carbon dioxide (13CO2). Additionally, the performance characteristics of these assays are poor, with clinical sensitivity and specificity parameters ranging from 76% to 85% and 79% to 90%, respectively.8,11 Finally, as antibodies to H pylori often remain for years following resolution of infection, serologic testing cannot be used to distinguish active from past infection or to document eradication of the organism following successful treatment. Infection is more prevalent in developing countries, and incidence is decreasing in Western countries. Acute infection may appear as an acute gastritis with abdominal pain (stomach ache) or nausea. Inflammation of the pyloric antrum is more likely to lead to duodenal ulcers, while inflammation of the corpus (body of the stomach) is more likely to lead to gastric ulcers and gastric carcinoma. It is microaerophilic; that is, it requires oxygen, but at lower concentration than is found in the atmosphere. The characteristic sheathed flagellar filaments of Helicobacter are composed of two copolymerized flagellins, FlaA and FlaB. The genome of the strain "26695" consists of about 1.7 million base pairs, with some 1,576 genes.
It adheres to the epithelial cells by producing adhesins, which bind to lipids and carbohydrates in the epithelial cell membrane. The ammonia produced to regulate pH is toxic to epithelial cells, as are biochemicals produced by H. Helicobacter cysteine-rich proteins (Hcp), particularly HcpA (hp0211), are known to trigger an immune response, causing inflammation. Gastrin stimulates the parietal cells to secrete more acid into the stomach lumen, and over time increases the number of parietal cells, as well. Rising antibiotic resistance increases the need to search for new therapeutic strategies; this might include prevention in form of vaccination.
The standard first-line therapy is a one-week "triple therapy" consisting of proton pump inhibitors such as omeprazole and the antibiotics clarithromycin and amoxicillin. The incidence of acid reflux disease, Barrett's esophagus, and esophageal cancer have been rising dramatically at the same time as H. The lower rate of infection in the West is largely attributed to higher hygiene standards and widespread use of antibiotics.
Using the genetic diversity data, researchers have created simulations that indicate the bacteria seem to have spread from East Africa around 58,000 years ago. Professor Walery Jaworski of the Jagiellonian University in Krakow investigated sediments of gastric washings obtained by lavage from humans in 1899. After unsuccessful attempts at culturing the bacteria from the stomach, they finally succeeded in visualizing colonies in 1982, when they unintentionally left their Petri dishes incubating for five days over the Easter weekend. The Group is involved with the Annual International Workshop on Helicobacter and Related Bacteria, the Maastricht Consensus Reports (European Consensus on the management of H. Serologic evaluation for the presence of antibodies to H pylori is the most commonly ordered assay. The advantages and limitations of the various testing methodologies will be reviewed within this article. The labeled 13CO2 is exhaled through normal respiration and collected in a specialized bag. For individuals <18 years, Mayo Medical Laboratories recommends that the stool antigen test (SAT) be offered instead. However, over 80% of individuals infected with the bacterium are asymptomatic, and it may play an important role in the natural stomach ecology.
Where this develops into chronic gastritis, the symptoms, if present, are often those of non-ulcer dyspepsia: stomach pains, nausea, bloating, belching, and sometimes vomiting or black stool.
It contains a hydrogenase which can be used to obtain energy by oxidizing molecular hydrogen (H2) produced by intestinal bacteria. The two sequenced strains show large genetic differences, with up to 6% of the nucleotides differing.
One such adhesion, BabA, binds to the Lewis b antigen displayed on the surface of stomach epithelial cells.

The increased acid load damages the duodenum, which may eventually result in ulcers forming in the duodenum. Western people infected with strains carrying the cag PAI have a stronger inflammatory response in the stomach and are at a greater risk of developing peptic ulcers or stomach cancer than those infected with strains lacking the island. While many organisms are competent only under certain environmental conditions, such as starvation, H. Much work has been done on developing viable vaccines aimed at providing an alternative strategy to control H. Variations of the triple therapy have been developed over the years, such as using a different proton pump inhibitor, as with pantoprazole or rabeprazole, or replacing amoxicillin with metronidazole for people who are allergic to penicillin. Symbiotic butyrate-producing bacteria which are normally present in the intestine are sometimes used as probiotics to help suppress H. At the time, the conventional thinking was that no bacterium could live in the acid environment of the human stomach.
Among some rod-like bacteria, he also found bacteria with a characteristic spiral shape, which he called Vibrio rugula. In their original paper, Warren and Marshall contended that most stomach ulcers and gastritis were caused by bacterial infection and not by stress or spicy food, as had been assumed before. The sample is subsequently analyzed on a spectrophotometer, which determines the level of 13CO2 present.
Finally, the performance of this assay requires prolonged patient preparation (approximately 1 hour) and careful sample collection, which may be challenging if the collecting laboratory is unfamiliar with this test. More importantly, this study identified a total of 1,907 transcriptional start sites, 337 primary operons, and 126 additional suboperons, and 66 monocistrons. The cag pathogenicity island (PAI) has about 30 genes, part of which code for a complex type IV secretion system. Cytotoxin associated gene CagA can also cause inflammation and is potentially a carcinogen.
These proteins are directly toxic to cells lining the stomach and signal strongly to the immune system that an invasion is underway. This oxidative stress response induces potentially lethal and mutagenic oxidative DNA adducts in the H. Such a therapy has revolutionized the treatment of peptic ulcers and has made a cure to the disease possible. In recognition of their discovery, Marshall and Warren were awarded the 2005 Nobel Prize in Physiology or Medicine. He was the first to suggest a possible role of this organism in the pathogenesis of gastric diseases.
This value is compared to a breath sample taken prior to ingestion of the labeled urea and a final result of positive or negative is determined (Figure 3). It is capable of forming biofilms and can convert from spiral to a possibly viable but nonculturable coccoid form, both likely to favor its survival and be factors in the epidemiology of the bacterium. The low GC-content of the cag PAI relative to the rest of the Helicobacter genome suggests the island was acquired by horizontal transfer from another bacterial species. As a result of the bacterial presence, neutrophils and macrophages set up residence in the tissue to fight the bacteria assault.
All organisms encode genetic programs for response to stressful conditions including those that cause DNA damage. Researchers are studying different adjuvants, antigens, and routes of immunization to ascertain the most appropriate system of immune protection; however, most of the research only recently moved from animal to human trials. Previously, the only option was symptom control using antacids, H2-antagonists or proton pump inhibitors alone. His work was included in the Handbook of Gastric Diseases, but it had little impact, as it was written in Polish. Several small studies conducted in the early 20th century demonstrated the presence of curved rods in the stomachs of many people with peptic ulcers and stomach cancers. A C-terminal region of the CagA protein (amino acids 873–1002) has also been suggested to be able to regulate host cell gene transcription, independent of protein tyrosine phosphorylation. Its subsequent evolution created seven prototypes—Europe (isolated from Europe, the Middle East, India, and Iran), NE Africa (from northeast Africa), Africa1 (from countries in Western Africa and South Africa), Africa2 (from South Africa), Asia2 (from Northern India and among isolates from Bangladesh, Thailand, and Malaysia), Sahul (from Australian Aboriginals and Papua New Guineans) and East Asia with the subpopulations E Asia (from East Asians), Maori (from Taiwanese Aboriginals, Melanesians and Polynesians) and Amerind (Native Americans). Interest in the bacteria waned, however, when an American study published in 1954 failed to observe the bacteria in 1180 stomach biopsies. This also keeps the bacteria from being swept away into the lumen with the bacteria’s mucus environment, which is constantly moving from its site of creation at the epithelium to its dissolution at the lumen interface. The precursors of these prototypes have been named ancestral Europe1, ancestral Europe2, ancestral East Asia, ancestral Africa1, ancestral Africa2, and ancestral Sahul.
At least one antisense TSS is associated with about 46% of all open reading frames, including many housekeeping genes. European and African strains were introduced into the Americas along with its colonisation—both thousands of years ago and more recently in the slave trade.
Marshall and Warren went on to demonstrate antibiotics are effective in the treatment of many cases of gastritis.
According to the proposed perigenetic mechanism, inflammation-associated signaling molecules, such as TNF-?, can alter gastric epithelial cell adhesion and lead to the dispersion and migration of mutated epithelial cells without the need for additional mutations in tumor suppressor genes, such as genes that code for cell adhesion proteins. In 1987, the Sydney gastroenterologist Thomas Borody invented the first triple therapy for the treatment of duodenal ulcers. In 1994, the National Institutes of Health stated most recurrent duodenal and gastric ulcers were caused by H.

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