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Research ArticleOpen Access

Helicobacter Pylori and Antibiotic Resistance Volume 56- Issue 1

Jonatan Vukovic1,2 and Pavle Vrebalov Cindro1*

  • 1Clinical Psychology, Senior Lecturer in Mental Health, MOI University, Kenya
  • 2Clinical Psychology, Student in Mental Health, Eldoret, Kenya

Received: April 10, 2024; Published: April 17, 2024

*Corresponding author: Pavle Vrebalov Cindro, Department of Gastroenterology, University Hospital of Split, 21000 Split, Croatia

DOI: 10.26717/BJSTR.2024.56.008809

Abstract PDF


H. pylori (H. pylori) is a global health problem and it is important to inform the general population with the aspects of this infection. Helicobacter pylori eradication is becoming increasingly difficult. High prevalence of H. pylori infection, the complexity of its treatment, poor patient adherence to the treatment may contribute to antibiotic resistance and healthcare costs.

Keywords: Helicobacter Pylori; Antibiotic Resistance

Abbreviations: MALT Lymphoma: Extranodal Marginal Zone Lymphoma of Mucosa-Associated Lymphoid Tissue; 23S rRNA: Component of the Large Subunit (50S) of the Bacterial/Archean Ribosome


Helicobacter pylori (H. pylori) has been established as the most prevalent chronic infection globally, that, has affected more than a half of the world population [1]. Helicobacter pylori is a Gram-negative bacterium that has been classified within the Epsilonproteobacteria class, under the order Campylobacterales, within the Helicobacteraceae family, and is part of the Helicobacter genus. To date, more than 40 species within the Helicobacter genus have been identified and categorized, capable of colonizing the stomach (e.g., H. pylori) or intestines (e.g., H. cinaedi and H. fennelliae) [2]. Humans are the primary hosts for H. pylori, with evidence suggesting that the bacterium is transmitted through oral or fecal-oral pathways [3,4]. This bacterium predominantly colonizes the gastric mucosa, though it has also been detected in dental plaque and saliva of infected individuals. The International Agency for Research on Cancer and the World Health Organization (WHO) have also classified H. pylori as a first category carcinogen, due to its significant role in the etiology of stomach cancer, highlighting the potential for cancer prevention through early eradication of the bacterium [5]. Infection with H. pylori poses a substantial clinical challenge, as it is associated with conditions such as gastritis, gastric and duodenal ulcers, MALT lymphoma, and stomach cancer [6-9].

Importantly, treating H. pylori infection in populations at high risk has been shown to decrease the incidence of stomach cancer among asymptomatic individuals [10]. The standard treatment regimen for H. pylori infection combines antibiotics, antisecretory agents, and proton pump inhibitors [11]. Initially, therapy often involves a combination of clarithromycin, amoxicillin, metronidazole, and proton pump inhibitors, with clarithromycin serving as a primary treatment option due to its effectiveness against the infection [12]. Should initial treatment fail, secondary therapies, such as triple therapy with levofloxacin (comprising levofloxacin, amoxicillin, and a proton pump inhibitor), are considered [13]. However, the global increase in H. pylori resistance to antibiotics presents a significant challenge [14]. Resistance rates exceed 15% for clarithromycin, range between 45% to 55% for metronidazole, and between 14% to 20% for levofloxacin [15]. Resistance to clarithromycin and levofloxacin primarily arises from point mutations in the bacterium's genetic material, which alter the antibiotics' target sites and interfere with drug activity [16]. In Croatia, a rise in primary resistance to these antibiotics in H. pylori has been noted, with mutations identified in the 23S rRNA, gyrA, and gyrB genes affecting clarithromycin and levofloxacin resistance by modifying target sites or protein structures, thereby diminishing treatment efficacy [17].


Molecular docking analyses have shown that H. pylori strains harboring resistance-related mutations exhibit reduced susceptibility to clarithromycin and levofloxacin compared to wild-type strains, due to altered non-covalent interactions (e.g., hydrogen bonds, ionic interactions) that weaken antibiotic-protein binding, leading to antibiotic resistance. The occurrence of dual resistance to clarithromycin and levofloxacin highlights the bacterium's evolving resistance to different antimicrobials, posing an increased health risk. Research of Samanic et al. into H. pylori's antibiotic resistance represents a crucial step towards a more comprehensive understanding of this issue, suggesting that a broader research approach could shed light on the intricate interplay between patient characteristics, H. pylori genetics, and antibiotic resistance at a molecular level [17]. Further studies, including molecular dynamics, could reveal the dynamic nature of antibiotic-target site interactions in the bacterium, offering insights into antibiotic resistance mechanisms at an atomic level. Such in-depth research is vital for advancing H. pylori treatment strategies, contributing to the development of targeted therapies, and addressing the challenge of antibiotic-resistant strains.

Conflict of Interest

Authors have no conflict of interests associated with this article.


  1. McNicholl AG, O'Morain CA, Megraud F, Gisbert JP (2019) Protocol of the European Registry on the management of Helicobacter pylori infection (Hp-EuReg). Helicobacter 24(5): e12630.
  2. Murray PR, Rosenthal K, Pfaller MA (2021) Medical Microbiology, (9th)., Elsevier: Houston, TX, USA, pp. 872.
  3. Baj J, Forma A, Flieger W, Morawska I, Michalski A, et al. (2021) Helicobacter pylori Infection and Extragastric Diseases-A Focus on the Central Nervous System. Cells 10(9): 2191.
  4. Baj J, Forma A, Sitarz M, Portincasa P, Garruti G, et al. (2020) Helicobacter pylori Virulence Factors-Mechanisms of Bacterial Pathogenicity in the Gastric Microenvironment. Cells 10(1): 27.
  5. Tacconelli E, Carrara E, Savoldi A, Harbarth S, Mendelson M, et al. (2018) Discovery, research, and development of new antibiotics: the WHO priority list of antibiotic-resistant bacteria and tuberculosis. Lancet Infect Dis 18(3): 318-327.
  6. Chey WD, Leontiadis GI, Howden CW, Moss SF (2017) ACG Clinical Guideline: Treatment of Helicobacter pylori Infection. Am J Gastroenterol 112(2): 212-239.
  7. Malfertheiner P, Megraud F, O'Morain CA, Gisbert JP, Kuipers EJ, et al. (2017) Management of Helicobacter pylori infection-the Maastricht V/Florence Consensus Report. Gut 66(1): 6-30.
  8. Plummer M, Franceschi S, Vignat J, Forman D, de Martel C (2015) Global burden of gastric cancer attributable to Helicobacter pylori. Int J Cancer 136(2): 487-490.
  9. Fock KM, Graham DY, Malfertheiner P (2013) Helicobacter pylori research: historical insights and future directions. Nat Rev Gastroenterol Hepatol 10(8): 495-500.
  10. Mommersteeg MC, Yu J, Peppelenbosch MP, Fuhler GM (2018) Genetic host factors in Helicobacter pylori-induced carcinogenesis: Emerging new paradigms. Biochim Biophys Acta Rev Cancer 1869(1): 42-52.
  11. Oztekin M, Yilmaz B, Agagunduz D, Capasso R (2021) Overview of Helicobacter pylori Infection: Clinical Features, Treatment, and Nutritional Aspects. Diseases 9(4): 66.
  12. Sugano K, Tack J, Kuipers EJ, Graham DY, El-Omar EM, et al. (2015) Kyoto global consensus report on Helicobacter pylori gastritis. Gut 64(9): 1353-1367.
  13. Bennett JE, Dolin, R, Blaser MJ (2015) Principles and Practice of Infectious Diseases (8th)., In: John, E., Bennett, R.D., Blaser, M.J., (Eds.)., Elsevier/Saunders: Philadelphia PA, 1: 3577.
  14. Morehead MS, Scarbrough C (2018) Emergence of Global Antibiotic Resistance. Prim Care 45(3): 467-484.
  15. Megraud F, Bruyndonckx R, Coenen S, Wittkop L, Huang TD, et al. (2021) Helicobacter pylori resistance to antibiotics in Europe in 2018 and its relationship to antibiotic consumption in the community. Gut 70(10): 1815-1822.
  16. Tshibangu-Kabamba E, Yamaoka Y (2021) Helicobacter pylori infection and antibiotic resistance - from biology to clinical implications. Nat Rev Gastroenterol Hepatol 18(9): 613-629.
  17. Samanic I, Dadic B, Sanader Marsic Z, Dzelalija M, Maravic A, et al. (2023) Molecular Characterization and Mutational Analysis of Clarithromycin- and Levofloxacin-Resistance Genes in Helicobacter pylori from Gastric Biopsies in Southern Croatia. Int J Mol Sci 24(19): 14560.