Bruna Maria Roesler

Additional information is available at the end of the chapter Bruna Maria RoeslerAdditional information is available at the end of the chapter

http://dx.doi.org/10.5772/intechopen.88806

#### **1. Introduction**

The human stomach is an unfriendly place for most infective bacteria probably due to the very low pH found in this place. However, the first isolation of a spiral-shaped, Gram-negative and microaerophilic bacterium in 1982 by Warren and Marshall [1] significantly changed the concepts of gastric microbiology.

Initially, this bacterium was named *Campylobacter pyloridis*, but analysis of nucleic acid sequence and ultrastructural studies besides the helical shape allowed differentiation of this genus to *Helicobacter*. Finally, the species was named *pylori* because it can be found most often in the antral mucosa, near the pylorus [2].

*Helicobacter pylori* (*H. pylori*) organisms are 2.5–5.0 μm long and 0.5–1.0 μm wide, with two to six unipolar-sheathed flagella, which are essential for bacterial motility [3]. It has been described that bacteria can exist in three different morphologic forms: the viable and culturable spiral form, the viable but nonculturable (VBNC) coccoid form which are less virulent, and the nonviable degenerative *H. pylori* form [4].

Colonization with *H. pylori* is commonly acquired during childhood and induces chronic gastritis in all infected individuals unless specific treatment is given [5, 6]. While over 80% of infected subjects remain asymptomatic [7], *H. pylori* chronic infection has been associated with the development of various clinical disorders of the upper gastrointestinal tract, such as chronic gastritis, peptic ulcer disease, mucosa-associated lymphoid tissue (MALT) lymphoma, and gastric adenocarcinoma [8]. In fact, *H. pylori* infection is a significant risk factor for the development of gastric cancer, and bacterium is classified as a group I carcinogen by the World Health Organization [9].

© 2016 The Author(s). Licensee InTech. This chapter is distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. © 2019 The Author(s). Licensee IntechOpen. This chapter is distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Although *H. pylori* is primarily responsible for the upper gastrointestinal diseases, only 10% of people colonized with this bacterium portray disease symptoms. It suggests that host and bacterial factors also contributed to differences in *H. pylori* pathogenicity [10, 11]. For instance, the risk of developing gastric cancer is also related to genetic characteristics of the host and environmental factors, which, associated with specific bacterial strain characteristics, influence the severity of the chronic inflammatory response [12, 13].

patters of *H. pylori* have been shown to be extremely diverse, and gastric mucosa may be colonized by strains with small differences in the genomic patterns suggesting subtype varia-

Introductory Chapter: *Helicobacter pylori* - An Overview of an Old Human Microorganism

http://dx.doi.org/10.5772/intechopen.88806

The prevalence of *H. pylori* infection varies widely by geographic area, age, race, and socioeconomic status. While the infection is on a fast decline in the most of the Western countries, mainly due to the success of therapeutic regimens and improved personal and community hygiene that prevents reinfection, in developing countries, the prevalence rates can reach 90% and is higher among individuals belonging to low socioeconomic status group [28, 29]. It occurs especially due to failure of treatment and emergence of drug resis-

Most studies suggest that males and females are infected at approximately the same rates [31–33]. In spite of it, a meta-analysis population-based study reported a male predominance

The infection probably occurs in the childhood, and children are often infected by a strain with a genetic fingerprint identical to that of their parents [35]. Besides, local prevalence of *H. pylori* within a country also should be considered, and there are estimates that infection is

Moreover, differences by ethnic and racial groups are evident [31, 32, 37]. In addition, the main risk factors of *H. pylori* infection, especially if present during childhood, have been associated with socioeconomic status. Malaty and Graham [38] demonstrated that there is probably an inverse correlation between prevalence and socioeconomic status. It has also been reported that overcrowding, such as living in a crowded environment, sibship size, number of persons or children in the home, number of persons per room, crowding index, and living in an institutionalized population, is a situation consistently related to *H. pylori*

Finally, it is important to consider that the pathogenetic role of *H. pylori* in gastroduodenal pathologies has been elucidated and confirmed in the past 30 years [43] redirecting the scientific and medical understanding of great part of gastrointestinal diseases. The development of effective therapies against *H. pylori* infection has progressed, and its successful eradication leads to healing of chronic active gastritis and reverses inflammation of the mucosa. In spite of it, the challenge nowadays is gastric cancer and the understanding of gastric carcinogenesis,

Although the natural niche for *H. pylori* is the human stomach, some questions about other possible reservoirs for bacterium have been appearing in the last years. Nevertheless, most part of the questions about the transmission of *H. pylori* remains unclear, and, because of it, the possible modes of transmission are still unknown. Consequently, the routes of transmis-

of *H. pylori*-related diseases in adults but not in children [34].

almost always associated with *H. pylori* long-term infection [44].

sion of *H. pylori* are supposed to occur via an array of different pathways.

more common in rural developing areas than in urban developed ones [36].

tion [27].

tance [25, 30].

positivity [39–42].

**3. Transmission pathways**

*H. pylori* is perhaps the most ubiquitous and successful human pathogen, since it colonizes the stomach of more than 50% of the world population [14, 15]. It has been demonstrated that *H. pylori* has a long period of coevolution with humans, going back at least since human migration out of Africa about 60,000 years ago [16, 17]. There are very well-characterized mechanisms of adaptation which was developed by ancestral *H. pylori* over the time. Through selection and coevolution, this bacterium established measures which actively and passively avoid the human immune response [18].

*H. pylori* infection results in recruitment of neutrophils, lymphocytes, and macrophages into the gastric mucosa through the induction of several cytokines such as TNF-α, IL-6, and IL-8 [19, 20]. It is believed that the immune response during infection plays an important role in the pathogenesis. *H. pylori* successfully establishes a chronic infection by achieving a delicate balance between inducing immune response and surviving in the inflammatory milieu by using an array of important virulence factors [15].

*H. pylori* presents important virulence factors which are essential both for bacterium colonization and maintenance in the human stomach (such as urease and flagella) and for the interaction with the gastric epithelial cells, the bacterial adhesins (blood group antigen-binding adhesion (BabA), sialic acid-binding adhesion (SabA), AlpA and AlpB, HopZ, and OipA). Besides, virulence factors involved in gastric inflammation are important for the development of chronic infection and clinical symptoms of gastrointestinal diseases (the principal are cytotoxin-associated gene-pathogenicity island (cagPAI), vacuolating cytotoxin A (VacA), and duodenal ulcer promoting gene (dupA)).
