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Find PatientPrintBacteriology and epidemiology of Helicobacter pylori infectionBacteriology and epidemiology of Helicobacter pylori infectionAuthorSheila E Crowe, MD, FRCPC, FACP, FACG, AGAFSection EditorMark Feldman, MD, MACP, AGAF, FACG

Deputy EditorShilpa Grover, MD, MPHDisclosures: Sheila E Crowe, MD, FRCPC, FACP, FACG, AGAF Nothing to disclose. Mark Feldman, MD, MACP, AGAF, FACG Nothing to disclose. Shilpa Grover, MD, MPHEmployee of UpToDate, Inc.

Contributor disclosures are reviewed for conflicts of interest by the editorial group. When found, these are addressed by vetting through a multi-level review process, and through requirements for references to be provided to support the content. Appropriately referenced content is required of all authors and must conform to UpToDate standards of evidence.

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All topics are updated as new evidence becomes available and our peer review process is complete.Literature review current through: Feb 2015. | This topic last updated: Nov 22, 2013.

INTRODUCTION — Gastric organisms were first observed more than 100 years ago and

their association with gastritis has been recognized since the 1970s [1]. The true implication of these microbes was not fully realized, however, until 1982 when Marshall and Warren identified and subsequently cultured the gastric bacterium, Campylobacter pyloridis, later reclassified as Helicobacter pylori (H. pylori) [2]. This organism is now known to cause chronic gastritis, most peptic ulcers, and gastric adenocarcinoma and lymphoma. (See appropriate topic reviews.)

The bacteriology and epidemiology of H. pylori will be reviewed here. Understanding its bacteriology and the unique features that enable it to survive in an environment as hostile as the stomach are important in appreciating how H. pylori causes tissue injury and clinical disease. (See "Pathophysiology of and immune response to Helicobacter pylori infection".) The epidemiology of this infection sheds light on the geographic, ethnic, and racial differences in prevalence of H. pylori-associated diseases and the changing incidence of these conditions throughout the world.

BACTERIOLOGY

Microbiology — H. pylori is a spiral shaped, microaerophilic, gram negative bacterium measuring approximately 3.5 microns in length and 0.5 microns in width (picture 1). In vitro, it is a slow growing organism that can be cultured on blood agar or selective media such as Skirrow's media incubated at 37ºC in a 5 percent oxygen atmosphere for three to seven days [3]. Small, uniformly sized, translucent bacterial colonies form and the organisms can be morphologically characterized by Gram stain and their typical spiral or rod shaped appearance. High power microscopy reveals that the organism has two to seven unipolar sheathed flagella which enhance its mobility through viscous solutions.

If the growth environment is less than ideal, coccoid forms of H. pylori can occasionally be seen in culture [3]. These coccoid forms are thought to represent an adaptation to hostile surroundings; they appear to be more resistant and may enable the organism to survive for periods of time outside the human host in feces or in drinking water.

In addition to morphologic characterization, the organism can be biochemically characterized as catalase, oxidase, and urease positive. Urease appears to be vital for its survival and colonization; it is produced in abundance, making up more than 5 percent of the organism's total protein weight. Bacterial urease activity is clinically important because it forms the basis for several invasive and noninvasive tests to diagnose infection (see "Indications and diagnostic tests for Helicobacter pylori infection").

Gastric adaptation of H. pylori — The organism's urease, motility, and ability to adhere to gastric epithelium are factors that allow it to survive and proliferate in the gastric milieu [4]. Disruption of urease activity, bacterial mobility, or attachment prevents H. pylori colonization [5]. The interactions of H. pylori proteins underlying these activities are rapidly being uncovered [6,7].

Bacterial urease hydrolyzes gastric luminal urea to form ammonia that helps neutralize gastric acid and form a

protective cloud around the organism, enabling it to penetrate the gastric mucus layer [8]. A specific gene (ureI) exists within H. pylori's urease gene cluster that encodes for a pH dependent urea channel [9]. As the pH outside the organism drops, the urea channel permits internal movement of urea to maintain a favorable intracellular pH, allowing the bacterium to survive in an acid milieu.

Its spiral shape, flagella, and the mucolytic enzymes which it produces facilitate its passage through the mucus layer to the gastric surface epithelium [3]. On the other hand, gastric mucin appears to serve as a natural antibiotic, protecting the host against H. pylori infection [10].

H. pylori then attaches to gastric epithelial cells by means of specific receptor-mediated adhesion (picture 2A-B) [5,11]. Although attachment is dependent upon binding of bacterial surface adhesins to specific epithelial cell receptors, host factors can modulate this process. As an example, certain individuals may express

specific surface receptors or greater numbers of receptors, making them more susceptible to H. pylori attachment and colonization [12].

EPIDEMIOLOGY — H. pylori is the most common chronic bacterial infection in humans [13,14]. Studies involving genetic sequence analysis suggest that humans have been infected with H. pylori since they first migrated from Africa around 58,000 years ago [15]. H. pylori has been demonstrated worldwide and in individuals of all ages. Conservative estimates suggest that 50 percent of the world's population is affected. Infection is more frequent and acquired at an earlier age in developing countries compared with industrialized nations [14]. Once acquired, infection persists and may or may not produce gastroduodenal disease.

In developing nations, where the majority of children are infected before the age of 10, the prevalence in adults peaks at more than 80 percent before age 50 [14,16]. In developed countries, such as the United States, evidence

of infection in children is unusual but becomes more common during adulthood. Serologic evidence of H. pylori is rarely found before age 10 but increases to 10 percent in those between 18 and 30 years of age and to 50 percent in those older than age 60 [14]. Within any age group, infection appears to be more common in blacks and Hispanics compared to the white population; these differences are probably in part related to socioeconomic factors [17,18].

The increased prevalence of infection with age was initially thought to represent a continuing rate of bacterial acquisition throughout one's lifetime. However, epidemiologic evidence now indicates most infections are acquired during childhood even in developed countries [14,19]. Most infections were acquired before five years of age with a declining incidence thereafter in one report from Ireland [20]. Thus, the frequency of H. pylori infection for any age group in any locality reflects that particular cohort's rate of bacterial acquisition during childhood years [19]. The organisms can be cultured from vomitus or diarrheal stools

suggesting the potential for transmission among family members during periods of illness [21,22].

The risk of acquiring H. pylori infection is related to socioeconomic status and living conditions early in life. Factors such as density of housing, overcrowding, number of siblings, sharing a bed, and lack of running water have all been linked to a higher acquisition rate of H. pylori infection [23-25]. More recent studies continue to show that in developing countries such as Iran, childhood hygiene practices and family education determine the prevalence of H. pylori infection [26]. The association of H. pylori infection with level of education, income, and race/ethnicity is not unique to H. pylori since similar associations have been described with other chronic infections including cytomegalovirus, herpes simplex virus-1 and hepatitis B [27]. Within a particular country, a decline in prevalence of H. pylori appears to parallel economic improvement. In Japan, for example, 70 to 80 percent of adults born before 1950, 45 percent of those born between 1950 and 1960, and 25 percent of those born

between 1960 and 1970 are infected [28]. This rapid decline of infection has been attributed to Japan's post-war economic progress and improvement in sanitation.

The consumption of salted food appears to increase the possibility of persistent infection with H. pylori infection [29,30]. In addition, a synergistic interaction between H. pylori infection and salted food intake to increase the risk of gastric cancer has also been reported in case-control studies [31,32]. (See "Risk factors for gastric cancer".)

Possible hereditary susceptibility — Hereditary susceptibility to H. pylori infection has not been proven. However, studies do suggest that members of certain ethnic and racial groups including Hispanics and African-Americans have a higher rate of infection than Caucasians. These differences are not entirely explained by differences in socioeconomic status [33].

Twin studies also support genetic susceptibility to infection [34,35]. Monozygotic twins raised in different households have a greater

concordance of H. pyloriinfection than do dizygotic twins raised apart. However, twins raised together have a higher concordance of H. pylori status than twins raised separately, emphasizing the role of childhood environment in H. pylori acquisition.

H. pylori transmission — The route by which infection occurs remains unknown [13,36]. Person-to-person transmission of H. pylori through either fecal/oral ororal/oral exposure seems most likely [22,36]. Humans appear to be the major reservoir of infection; however, H. pylori has been isolated from primates in captivity and from domestic cats [37]. It is unclear how these animals originally acquired H. pylori infection. However, at least in the case of cats, isolation of viable organisms from saliva and gastric juice samples suggests that transmission to humans might occur [38]. One report described the identification of H. pylori in milk and gastric tissue of sheep suggesting that sheep may be a natural host for the organism [39]. This may explain the higher

infection rate that has been observed among shepherds compared to their siblings [40].

Fecal/oral transmission of bacteria is also possible. Contaminated water supplies in developing countries may serve as an environmental source of bacteria. The organism remains viable in water for several days and, using polymerase chain reaction techniques, evidence of H. pylori can be found in most samples of municipal water from endemic areas of infection [41-43]. Children who regularly swim in rivers, streams, pools, drink stream water, or eat uncooked vegetables are more likely to be infected [44]. H. pylori has been cultured from diarrheal stools of children in The Gambia, West Africa where almost all inhabitants are infected by five years of age [45].

Intrafamilial clustering of infection further supports person-to-person transmission. Infected individuals are more likely to have infected spouses and children than uninfected individuals [25,46]. A study of children in Colombia found that the risk of infection correlated directly with the number of children

aged two to nine in the household while younger children were more likely to be infected if older siblings were also infected [47]. Isolation of genetically identical strains ofH. pylori from multiple family members [48] as well as custodial patients in the same institution [49] further supports transmission among persons sharing the same living environment. In addition to the familial type of transmission that occurs in developed and other nations, horizontal transmission between persons who do not belong to a core family also appears to take place in countries where the prevalence of infection is high [50].

Oral/oral transmission of bacteria has yet to be confirmed. Organisms have been identified in dental plaque [51], but the prevalence can be quite low [52] so it is not known if this location can serve as a source or reservoir. Dentists and oral hygienists who have continual occupational exposure to dental plaque do not have a higher prevalence of H. pylori [53]. On the other hand, infected gastric secretions can serve as a source of bacterial transmission [54,55].

Iatrogenic infection has been documented following the use of a variety of inadequately disinfected gastric devices, endoscopes, and endoscopic accessories [55]. In addition, gastroenterologists and nurses appear to be at increased risk for acquiring H. pylori; this is presumably due to occupational exposure to infected gastric secretions [23]. Mandated universal precautions, standardized equipment disinfection, and use of video-endoscopes which remove the instrument channel away from the mouth should reduce occupational and iatrogenic H. pylori transmission [55].

Reinfection — Reinfection with H. pylori following successful bacterial cure is unusual. Recurrence of infection most commonly represents recrudescence of the original bacterial strain. In adults, reacquisition of bacteria occurs in less than 2 percent of persons per year [56,57], a rate that is similar to primary adult acquisition of infection [19]. The low reinfection rate in adults supports the lower risk for infection during adulthood, although acquired immunity conferred by primary infection may also be important.

It has been hypothesized that the reinfection rates may be higher in children, in developing countries, and in those from low socioeconomic status. However, a study from China found that the reinfection rates were comparable to reports from the west (annual recurrence rate of 1 percent) [58]. Similarly, another report found a low annual reinfection rate (2 percent) in children older than five, regardless of socioeconomic status [59].

INFORMATION FOR PATIENTS — UpToDate offers two types of patient education materials, "The Basics" and "Beyond the Basics." The Basics patient education pieces are written in plain language, at the 5th to 6th grade reading level, and they answer the four or five key questions a patient might have about a given condition. These articles are best for patients who want a general overview and who prefer short, easy-to-read materials. Beyond the Basics patient education pieces are longer, more sophisticated, and more detailed. These articles are written at the 10th to 12th grade reading level and are best for patients who want

in-depth information and are comfortable with some medical jargon.

Here are the patient education articles that are relevant to this topic. We encourage you to print or e-mail these topics to your patients. (You can also locate patient education articles on a variety of subjects by searching on "patient info" and the keyword(s) of interest.)

Basics topics (see "Patient information: H. pylori infection (The Basics)")

Beyond the Basics topics (see "Patient information: Helicobacter pylori infection and treatment (Beyond the Basics)")

SUMMARY