Helicobacter pylori Infection, Clinical Features and Nutritional Aspects: Comparison
Please note this is a comparison between Version 4 by Birsen Yılmaz and Version 3 by Amina Yu.

Helicobacter pylori (H. pylori) is a 0.5–1 µm wide, 2–4 µm long, short helical, S-shaped Gram-negative microorganism. It is mostly found in the pyloric region of the stomach and causes chronic gastric infection. It is estimated that these bacteria infect more than half of the world’s population. The mode of transmission and infection of H. pylori is still not known exactly, but the faecal–oral and oral–oral routes via water or food consumption are thought to be a very common cause.

  • H. pylori
  • nutrition
  • infection
  • diet
  • clinical treatment

1. H. pylori Infection Epidemiology

There are many about the prevalence of H. pylori, and its risk factors and pathways [1][2][3]. It is claimed that half of the world’s population is infected with H. pylori, but it is clear that more evidence-based research is still needed. The incidence of this infection is higher in low socioeconomic status groups and developing countries [4]. Vilaichone et al. found that the prevalence of H. pylori varies not only from country to country but also in different regions of the same country [5]. Its prevalence is significantly difficult to determine, as no health system compiles registry-based results of the prevalence of H. pylori in developing countries [6].
According to the regional prevalence estimates, there are approximately 4.4 billion H. pylori-infected people worldwide [7]. The countries with the highest H. pylori burden compared with the general population were found to be Nigeria, Portugal, Estonia, Kazakhstan, and Pakistan, and the lowest burden was in Switzerland [6]. Mezmale et al. (2020), a high prevalence of H. pylori infection was determined in Russia, Jordan, Iran, China, Canada, and Latin American countries [8].
Studies conducted in Turkey show that the rate of H. pylori infection is high. For example, Uyanıkoğlu et al. in 2010, 918 of 1298 patients who had antrum biopsy were positive for H. pylori. The prevalence of H. pylori infection is similar in males and females, and the incidence of H. pylori infection is 73.2% between the ages of 14 and 30, 71.5% between the ages of 31 and 45, 68.6% between the ages of 46 and 60, and 70.4% between the ages of 61 and 88 [9].  Özen et al. in 2011, 161 of 473 children studying in four different primary and secondary schools in Istanbul were found to be H. pylori-positive [10]. Similarly, Özaydın et al. screened 4622 people for H. pylori infection in 55 cities using the C-urea breath test in 2013, and 3852 people (2075 females and 1777 males) were found to be positive for H. pylori [11]. In the review by Hooi et al., it was reported that in Turkey up to 2015, the total number of participants was 6036, and the prevalence was 77.2% [6]. Soylu et al. in 2019, the number of H. pylori-positive patients was found to be 46 (21 females and 25 males) in biopsy samples taken from 88 patients (53 females and 35 males) aged 18–77 years with dyspeptic complaints. Compared with the total number of participants, male patients were found to be more H. pylori-positive [12]. In Nepal, it was reported that 18.2% of 6- to 59-month-old children, 14% of boys and 16% of girls aged 10–19 years, and 40% of non-pregnant women aged 20–49 years were infected with H. pylori [13].

2. H. pylori Transmission

Although the mode of transmission of H. pylori is not known exactly, it is thought that it can be transmitted directly from one person to another or indirectly from the environment to people [14]. Person-to-person transmission is thought to be the primary mode of transmission, especially in developed countries. Food- and waterborne transmission are more likely in developing countries and H. pylori spreads more rapidly in areas with poor hygienic conditions [15][16].
The prevalence of H. pylori infection in the rural community, Goodman et al. reported that people who are consumers of raw vegetables are more likely to be infected. Moreover, swimming in streams and rivers and using streams as drinking water may increase infection because of contamination by irrigation water or unpurified water [17]. Although some suggested that the transmission of H. pylori is from environmental contamination to food products, there is insufficient evidence to confirm this information [15][18]. It is accepted that interpersonal transmission routes are more frequent than environmental exposures. However, special attention should be paid to the sources of contamination (unhygienic water) that may lead to contamination through food [14].
Person-to-person transmission is thought to occur through the oral–oral, faecal–oral, gastric–oral, or sexual routes [14]. The literature indicates that H. pylori is present in the dental plaque and saliva of infected individuals [19][20][21], which shows that H. pylori infection spreads at a much higher rate than expected and, especially, transmission between family members is very frequent [22].

3. H. pylori Diagnosis

Each of the diagnostic tests used to detect the presence of H. pylori has advantages, disadvantages, and limitations, and the necessity of endoscopy is taken into account when classifying the methods. Histological evaluations using gastric biopsy specimens include rapid urease testing, culture, and polymerase chain reaction (PCR) [23]. Where invasive methods are time-consuming and not cost-effective, non-invasive diagnostic methods are used. Non-invasive tests include serological evaluation, stool antigen analyses, and the commonly used urea breath tests [24]. On the other hand, there is also non-Helicobacter pylori helicobacter (NHPH), which does not have a spiral morphology in the stomach [25]. Neither is the gold standard due to poor sensitivity or specificity. Combinations of more than one test give more reliable results [26].

4. H. pylori Pathogenesis

H. pylori is easily killed in hydrochloric acid solutions with a pH below 4.0. It is quite paradoxical for a microorganism whose primary site is the stomach. H. pylori continues to live in the lower part of the stomach by penetrating the mucus layer of the stomach through the contribution of its spiral shape and flagella [27]. To neutralise the acidic pH-related bactericidal activity against H. pylori, which can colonise the gastric epithelial surface, H. pylori hydrolyses urea to ammonia and carbon dioxide with the urease enzyme it produces [28]. In addition to its toxic effects on gastric mucosal epithelial cells, the ammonia formed increases the mucosal pH [29]. By damaging the protective mucus layer, which is rich in phospholipid and lipase, with the bacterial protease enzyme, it also delays the diffusion ability of H ions and increases its damaging effect [30].
It is known that H. pylori secretes a vacuole-forming cytotoxin (VacA) that adheres to the surface epithelium with adhesin proteins and causes vacuolization. The vacuole-forming cytotoxin induces host cell death through pore formation and apoptosis in mitochondrial membranes [31]. In addition to VacA, cytotoxin-associated antigen (CagA), known as an oncoprotein, is delivered into gastric epithelial cells and disrupts vesicular trafficking and autophagy pathways. It has been shown that cytotoxin-associated antigens affect the cell shape of bacterial proteins, disrupt cell assembly activity, increase cell motility, and are responsible for gastric ulcers and cancers [32][33][34].
Lipopolysaccharide (LPS), found in the outer membrane of H. pylori, is an effective immunomodulator in the human body and causes chronic inflammation by triggering the immune system. LPSs of H. pylori can mimic Lewis blood group antigens and, during infection, LPS can produce pathogenic anti-Lewis antibodies [35]. Lewis blood group antigens in the glycoprotein structure found on gastric epithelial surfaces mediate the binding of BabA, known as an adhesin, which binds to blood group antigens on the outer membrane of H. pylori, to surface mucosal cells and the gastric pit, and causes tissue destruction [36].

5. Conclusions

H. pylori is estimated to infect half of the world’s population and causes permanent infections as well as many health issues such as gastritis and MALT lymphoma, as well as peptic ulcer and gastric cancer. In H. pylori infection, there are some treatment limitations due to its ability to create resistance to antibiotic treatments in treatment strategies. Therefore, it has become necessary to seek alternatives to fight against H. pylori infection. Especially in the last few years, research has clearly shown the pathogenicity, microbial activity, and genetic predisposition to help understand the severity of gastric atrophy and gastric cancer caused by H. pylori. This situation is expected to affect the treatment process positively. Combination treatments, including with phytochemicals and probiotics found in natural products, seem to have beneficial effects in the eradication of H. pylori.
Due to the effects of hormones such as ghrelin and leptin, which control both growth and appetite, and the formation of malabsorption of various nutrients such as vitamin C, iron, cobalamin, and vitamin E in H. pylori-infected individuals, detailed nutritional information should be provided during and after treatment. It is important to provide optimal nutrition through the determination of strategies and the application of a suitable diet for the person by authorised dietitians. Besides, there have been some promising effects for probiotics added to treatment strategies; however, detailed research is needed. Most importantly, a diet rich in fruits and vegetables and reduced in salt and processed meat products has good prophylactic potential, especially against cancer in the eradication of H. pylori.


  1. Brown, L.M. Helicobacter pylori: Epidemiology and routes of transmission. Epidemiol. Rev. 2000, 22, 283–297.
  2. Mégraud, F.; Broutet, N. Epidemiology, acquisition and transmission of Helicobacter pylori. Rev. Prat. 2000, 50, 1414–1417.
  3. Tursi, A.; Cammarota, G.; Papa, A.; Cuoco, L.; Gentiloni, N.; Fedeli, P.; Fedeli, G.; Gasbarrini, G. The modes of transmission of Helicobacter pylori infection. Recenti. Prog. Med. 1997, 88, 232–236.
  4. Lehours, P. Actual diagnosis of Helicobacter pylori infection. Minerva Gastroenterol. Dietol. 2018, 64, 267–279.
  5. Vilaichone, R.-k.; Mahachai, V.; Shiota, S.; Uchida, T.; Ratanachu-ek, T.; Tshering, L.; Tung, N.L.; Fujioka, T.; Moriyama, M.; Yamaoka, Y. Extremely high prevalence of Helicobacter pylori infection in Bhutan. World J. Gastroenterol. 2013, 19, 2806–2810.
  6. Hooi, J.K.Y.; Lai, W.Y.; Ng, W.K.; Suen, M.M.Y.; Underwood, F.E.; Tanyingoh, D.; Malfertheiner, P.; Graham, D.Y.; Wong, V.W.S.; Wu, J.C.Y.; et al. Global prevalence of Helicobacter pylori ınfection: Systematic review and meta-analysis. Gastroenterology 2017, 153, 420–429.
  7. Khoder, G.; Muhammad, J.S.; Mahmoud, I.; Soliman, S.S.M.; Burucoa, C. Prevalence of Helicobacter pylori and ıts associated factors among healthy asymptomatic residents in the United Arab Emirates. Pathogens 2019, 8, 44.
  8. Mezmale, L.; Coelho, L.G.; Bordin, D.; Leja, M. Review: Epidemiology of Helicobacter pylori. Helicobacter 2020, 25 Suppl 1, e12734.
  9. Uyanıkoğlu, A.; Coşkun, M.; Binici, D.N.; Uçar, Ş.; Kibar, Y.İ.; Tay, A.; Öztürk, Y. Frequency of Helicobacter pylori in patients underwent endoscopy. Dicle Tıp Derg. 2012, 39, 197–200.
  10. Ozen, A.; Furman, A.; Berber, M.; Karatepe, H.O.; Mutlu, N.; Sarıçoban, H.E.; Büyükgebiz, B. The effect of Helicobacter pylori and economic status on growth parameters and leptin, ghrelin, and insulin-like growth factor (IGF)-I concentrations in children. Helicobacter 2011, 16, 55–65.
  11. Ozaydin, N.; Turkyilmaz, S.A.; Cali, S. Prevalence and risk factors of Helicobacter pylori in Turkey: A nationally-representative, cross-sectional, screening with the ¹3C-Urea breath test. BMC Public Health 2013, 13, 1215.
  12. Soylu, A.; Peker, K.D.; Yırgın, H.; Polat Sarı, S.; Akgül, Ö.; Sapmaz, B.; Adaş, G.T.; Öner, Y.A.; Kayacan, Z.Ç.; Çalışkan, R. Dispepsili hastalarda, H. pylori ve histopatolojik bulguların değerlendirilmesi. Tıp Fakültesi Klin. Derg. 2019, 2, 139–141.
  13. Mehata, S.; Parajuli, K.R.; Pant, N.D.; Rayamajhee, B.; Yadav, U.N.; Mehta, R.K.; Jha, P.; Mehta, N.; Dhimal, M.; Singh, D.R. Prevalence and correlates of Helicobacter pylori infection among under-five children, adolescent and non-pregnant women in Nepal: Further analysis of Nepal national micronutrient status survey 2016. PLoS Negl. Trop. Dis. 2021, 15, e0009510.
  14. Zamani, M.; Vahedi, A.; Maghdouri, Z.; shokri-shirvani, J. Role of food in environmental transmission of Helicobacter pylori. Casp. J. Intern. Med. 2017, 8, 146–152.
  15. Vale, F.F.; Vítor, J.M.B. Transmission pathway of Helicobacter pylori: Does food play a role in rural and urban areas? Int. J. Food Microbiol. 2010, 138, 1–12.
  16. Zhang, Y.Y.; Xia, H.H.; Zhuang, Z.H.; Zhong, J. Review article: ’True’ re-infection of Helicobacter pylori after successful eradication--worldwide annual rates, risk factors and clinical implications. Aliment. Pharmacol. Ther. 2009, 29, 145–160.
  17. Goodman, K.J.; Correa, P.; Tenganá Aux, H.J.; Ramírez, H.; DeLany, J.P.; Guerrero Pepinosa, O.; López Quiñones, M.; Collazos Parra, T. Helicobacter pylori infection in the Colombian Andes: A population-based study of transmission pathways. Am. J. Epidemiol. 1996, 144, 290–299.
  18. Quaglia, N.C.; Dambrosio, A. Helicobacter pylori: A foodborne pathogen? World J. Gastroenterol. 2018, 24, 3472–3487.
  19. Nisha, K.J.; Nandakumar, K.; Shenoy, K.T.; Janam, P. Periodontal disease and Helicobacter pylori infection: A community-based study using serology and rapid urease test. J. Investig. Clin. Dent. 2016, 7, 37–45.
  20. Aksit Bıcak, D.; Akyuz, S.; Kıratlı, B.; Usta, M.; Urganci, N.; Alev, B.; Yarat, A.; Sahin, F. The investigation of Helicobacter pylori in the dental biofilm and saliva samples of children with dyspeptic complaints. BMC Oral. Health 2017, 17, 67.
  21. Silva, D.G.; Stevens, R.H.; Macedo, J.M.; Albano, R.M.; Falabella, M.E.; Fischer, R.G.; Veerman, E.C.; Tinoco, E.M. Presence of Helicobacter pylori in supragingival dental plaque of individuals with periodontal disease and upper gastric diseases. Arch. Oral. Biol. 2010, 55, 896–901.
  22. Goh, K.L.; Chan, W.K.; Shiota, S.; Yamaoka, Y. Epidemiology of Helicobacter pylori infection and public health implications. Helicobacter 2011, 16, 1–9.
  23. Garza-González, E.; Perez-Perez, G.I.; Maldonado-Garza, H.J.; Bosques-Padilla, F.J. A review of Helicobacter pylori diagnosis, treatment, and methods to detect eradication. World J. Gastroenterol. 2014, 20, 1438–1449.
  24. Pohl, D.; Keller, P.M.; Bordier, V.; Wagner, K. Review of current diagnostic methods and advances in Helicobacter pylori diagnostics in the era of next generation sequencing. World J. Gastroenterol. 2019, 25, 4629–4660.
  25. Baele, M.; Pasmans, F.; Flahou, B.; Chiers, K.; Ducatelle, R.; Haesebrouck, F. Non-Helicobacter pylori helicobacters detected in the stomach of humans comprise several naturally occurring Helicobacter species in animals. FEMS Immunol. Med. Microbiol. 2009, 55, 306–313.
  26. Patel, S.K.; Pratap, C.B.; Jain, A.K.; Gulati, A.K.; Nath, G. Diagnosis of Helicobacter pylori: What should be the gold standard? World J. Gastroenterol. 2014, 20, 12847–12859.
  27. Baron, S.; Fons, M.; Albrecht, T. Viral pathogenesis. In Medical Microbiology; Baron, S., Ed.; The University of Texas Medical Branch at Galveston: Galveston, TX, USA, 1996.
  28. Ansari, S.; Yamaoka, Y. Survival of Helicobacter pylori in gastric acidic territory. Helicobacter 2017, 22, e12386.
  29. Usta, Y.; Özen, H. Helicobacter pylori enfeksiyonu. Çocuk Sağlığı Hast. Derg. 2007, 50, 136–145.
  30. Uzunismail, H. Helicobacter pylori ve Eradikasyon. Gastrointest. Sist. Hast. Sempozyumu 2001, 19–26.
  31. Amieva, M.R.; El-Omar, E.M. Host-bacterial interactions in Helicobacter pylori infection. Gastroenterology 2008, 134, 306–323.
  32. Buti, L.; Spooner, E.; Van der Veen, A.G.; Rappuoli, R.; Covacci, A.; Ploegh, H.L. Helicobacter pylori cytotoxin-associated gene A (CagA) subverts the apoptosis-stimulating protein of p53 (ASPP2) tumor suppressor pathway of the host. Proc. Natl. Acad. Sci. USA 2011, 108, 9238–9243.
  33. Alzahrani, S.; Lina, T.T.; Gonzalez, J.; Pinchuk, I.V.; Beswick, E.J.; Reyes, V.E. Effect of Helicobacter pylori on gastric epithelial cells. World J. Gastroenterol. 2014, 20, 12767–12780.
  34. Lee, I.O.; Kim, J.H.; Choi, Y.J.; Pillinger, M.H.; Kim, S.Y.; Blaser, M.J.; Lee, Y.C. Helicobacter pylori CagA phosphorylation status determines the gp130-activated SHP2/ERK and JAK/STAT signal transduction pathways in gastric epithelial cells. J. Biol. Chem. 2010, 285, 16042–16050.
  35. Chmiela, M.; Gonciarz, W. Molecular mimicry in Helicobacter pylori infections. World J. Gastroenterol. 2017, 23, 3964–3977.
  36. Gerhard, M.; Lehn, N.; Neumayer, N.; Borén, T.; Rad, R.; Schepp, W.; Miehlke, S.; Classen, M.; Prinz, C. Clinical relevance of the Helicobacter pylori gene for blood-group antigen-binding adhesin. In Proceedings of the National Academy of Sciences; 1999; Volume 96, pp. 12778–12783.
Video Production Service