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      Helicobacter pylori vacA, cagA and iceA genotypes in dyspeptic patients from southwestern region, Saudi Arabia: distribution and association with clinical outcomes and histopathological changes

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          Abstract

          Background

          The aim of this study was to identify the common H. pylori virulence genes among dyspeptic Southwestern Saudi patients and their association with clinical outcomes and histopathological findings to help practitioners and researchers in the region for better management of infections caused by such bacteria.

          Methods

          Four hundred two gastric biopsy specimens were analyzed using histopathological examination and real time-PCR. The positive 187 specimens by RT-PCR were genotyped using PCR targeting cagA, vacA and iceA genes.

          Results

          One hundred twenty-eight gastric biopsy specimens were positive in genotyping PCRs. The cagA, vacA, iceA1 and iceA2 genes were detected in rates of 49.2% (63/128), 100%(128/128), 42.2% (54/128), 32.8% (42/128), respectively. The vacA s1as1bm2 subtype was the highest 23.4% (30/128), followed by m2 and s1a1b subtypes which were equally detected [16.4% (21/128) for each]. The iceA genes were significantly associated with gastritis and gastric ulcer. Overall, vacA genotypes were significantly associated with gastritis, gastric and duodenal ulcers. The vacA subtypes: s1as1bm2, s1a1b and s2 m2 showed chronic active gastritis in percentages of 90.0, 81, and 84.2%, respectively. All vacA mixed genotypes showed chronic active gastritis.

          Conclusions

          H. pylori virulence genes are highly prevalent and diverse among patients with dyspepsia in Southwestern region of Saudi Arabia. The iceA genes and the different vacA subtypes are significantly associated with the clinical outcomes and histopathological changes especially chronic active gastritis.

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          Most cited references44

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          Classification and grading of gastritis. The updated Sydney System. International Workshop on the Histopathology of Gastritis, Houston 1994.

          M F Dixon, R M Genta, J Yardley … (1996)
          The Sydney System for the classification of gastritis emphasized the importance of combining topographical, morphological, and etiological information into a schema that would help to generate reproducible and clinically useful diagnoses. To reappraise the Sydney System 4 years after its introduction, a group of gastrointestinal pathologists from various parts of the world met in Houston, Texas, in September 1994. The aims of the workshop were (a) to establish an agreed terminology of gastritis; (b) to identify, define, and attempt to resolve some of the problems associated with the Sydney System. This article introduces the Sydney System as it was revised at the Houston Gastritis Workshop and represents the consensus of the participants. Overall, the principles and grading of the Sydney System were only slightly modified, the grading being aided by the provision of a visual analogue scale. The terminology of the final classification has been improved to emphasize the distinction between the atrophic and nonatrophic stomach; the names used for each entity were selected because they are generally acceptable to both pathologists and gastroenterologists. In addition to the main categories and atrophic and nonatrophic gastritis, the special or distinctive forms are described and their respective diagnostic criteria are provided. The article includes practical guidelines for optimal biopsy sampling of the stomach, for the use of the visual analogue scales for grading the histopathologic features, and for the formulation of a comprehensive standardized diagnosis. A glossary of gastritis-related terms as used in this article is provided.
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            Mosaicism in vacuolating cytotoxin alleles of Helicobacter pylori. Association of specific vacA types with cytotoxin production and peptic ulceration.

            J Atherton, P. Cao, R M Peek … (1995)
            Approximately 50% of Helicobacter pylori strains produce a cytotoxin, encoded by vacA, that induces vacuolation of eukaryotic cells. Analysis of a clinically isolated tox- strain (Tx30a) indicated secretion of a 93-kDa product from a 3933-base pair vacA open reading frame. Characterization of 59 different H. pylori isolates indicated the existence of three different families of vacA signal sequences (s1a, s1b, and s2) and two different families of middle-region alleles (m1 and m2). All possible combinations of these vacA regions were identified, with the exception of s2/m1 (p < 0.001); this mosaic organization implies that recombination has occurred in vivo between vacA alleles. Type s1/m1 strains produced a higher level of cytotoxin activity in vitro than type s1/m2 strains; none of 19 type s2/m2 strains produced detectable cytotoxin activity. The presence of cagA (cytotoxin-associated gene A) was closely associated with the presence of vacA signal sequence type s1 (p < 0.001). Among patients with past or present peptic ulceration, 21 (91%) of 23 harbored type s1 strains compared with 16 (48%) of 33 patients without peptic ulcers; only 2 (10%) of 19 subjects harboring type s2 strains had past or present peptic ulcers (p < 0.005). Thus, specific vacA genotypes of H. pylori strains are associated with the level of in vitro cytotoxin activity as well as clinical consequences.
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              Host-bacterial interactions in Helicobacter pylori infection.

              E Omar, Manuel R. Amieva (2007)
              Helicobacter pylori are spiral-shaped gram-negative bacteria with polar flagella that live near the surface of the human gastric mucosa. They have evolved intricate mechanisms to avoid the bactericidal acid in the gastric lumen and to survive near, to attach to, and to communicate with the human gastric epithelium and host immune system. This interaction sometimes results in severe gastric pathology. H pylori infection is the strongest known risk factor for the development of gastroduodenal ulcers, with infection being present in 60%-80% of gastric and 95% of duodenal ulcers.(1)H pylori is also the first bacterium to be classified as a definite carcinogen by the World Health Organization's International Agency for Research on Cancer because of its epidemiologic relationship to gastric adenocarcinoma and gastric mucosa-associated lymphoid tissue lymphoma.(2) In the last 25 years, since H pylori was first described and cultured, a complete paradigm shift has occurred in our clinical approach to these gastric diseases, and more than 20,000 scientific publications have appeared on the subject. From the medical point of view, H pylori is a formidable pathogen responsible for much morbidity and mortality worldwide. However, H pylori infection occurs in approximately half of the world population, with disease being an exception rather than the rule. Understanding how this organism interacts with its host is essential for formulating an intelligent strategy for dealing with its most important clinical consequences. This review offers an insight into H pylori host-bacterial interactions.
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                Author and article information

                Contributors
                Mohammed Akeel:
                ORCID: http://orcid.org/0000-0002-2573-9309
                00966-561120210 , m.akeel@jazanu.edu.sa
                Atef Shehata: mycology_atef@yahoo.com
                Ahmed Elhafey: elhafeya@yahoo.com
                Erwa Elmakki: erwamakki@gmail.com
                Thanaa Aboshouk: thanaa84@yahoo.com
                Hussein Ageely: hageely@jazanu.edu.sa
                Mohammed Mahfouz: mmahfouz@jazanu.edu.sa
                Journal
                Journal ID (nlm-ta): BMC Gastroenterol
                Journal ID (iso-abbrev): BMC Gastroenterol
                Title: BMC Gastroenterology
                Publisher: BioMed Central (London )
                ISSN (Electronic): 1471-230X
                Publication date (Electronic): 25 January 2019
                Publication date PMC-release: 25 January 2019
                Publication date Collection: 2019
                Volume: 19
                Electronic Location Identifier: 16
                Affiliations
                [1 ]ISNI 0000 0004 0398 1027, GRID grid.411831.e, Department of Anatomy, Faculty of Medicine, , Jazan University, ; Jazan, Kingdom of Saudi Arabia
                [2 ]ISNI 0000 0004 0398 1027, GRID grid.411831.e, Department of Microbiology and Immunology, Faculty of Medicine, , Jazan University, ; Jazan, Kingdom of Saudi Arabia
                [3 ]ISNI 0000 0004 0398 1027, GRID grid.411831.e, Department of Pathology, Faculty of Medicine, , Jazan University, ; Jazan, Kingdom of Saudi Arabia
                [4 ]ISNI 0000 0004 0398 1027, GRID grid.411831.e, Department of Internal Medicine, , Faculty of Medicine, Jazan University, ; Jazan, Kingdom of Saudi Arabia
                [5 ]ISNI 0000 0004 0398 1027, GRID grid.411831.e, Department of Biochemistry, Faculty of Medicine, , Jazan University, ; Jazan, Kingdom of Saudi Arabia
                [6 ]ISNI 0000 0004 0398 1027, GRID grid.411831.e, Department of Family and Community Medicine, Faculty of Medicine, , Jazan University, ; Jazan, Kingdom of Saudi Arabia
                [7 ]ISNI 0000 0000 9889 5690, GRID grid.33003.33, Department of Microbiology and Immunology, Faculty of Medicine, , Suez Canal University, ; Ismailia, Egypt
                [8 ]ISNI 0000 0001 2155 6022, GRID grid.411303.4, Department of Pathology, Faculty of Medicine, , Al-Azhar University, ; Cairo, Egypt
                Author information
                http://orcid.org/0000-0002-2573-9309
                Article
                Publisher ID: 934
                DOI: 10.1186/s12876-019-0934-z
                PMC ID: 6346553
                PubMed ID: 30683054
                SO-VID: 98d0ba3f-a51a-43eb-83e9-b9a852179f59
                Copyright © © The Author(s). 2019
                License:

                Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License ( http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver ( http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

                History
                Date received : 20 July 2018
                Date accepted : 16 January 2019
                Funding
                Funded by: King Abdulaziz City for Science and Technology (SA)
                Award ID: ARP-47-32
                Categories
                Subject: Research Article
                Custom metadata
                issue-copyright-statement © The Author(s) 2019

                ScienceOpen disciplines: Gastroenterology & Hepatology
                Keywords: h. pylori,pcr,virulence genes,genotype,gastritis,gastric ulcer
                Data availability:
                ScienceOpen disciplines: Gastroenterology & Hepatology
                Keywords: h. pylori, pcr, virulence genes, genotype, gastritis, gastric ulcer

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