Detection of  Helicobacter pylori  and its virulence genes ( cag A , dup A ,  and  vac A) among patients with gastroduodenal diseases in Chris Hani Baragwanath Academic Hospital, South Africa

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Abstract

Background

The global prevalence of H. pylori approaches 50%, with prevalence rates between 20 and 40% in developed countries and up to 90% in Africa and other developing nations of the world. Development of H. pylori-associated diseases is determined by a number of virulence factors. This study aimed at determining the prevalence of H. pylori infections and virulence genes ( cagA , dupA , and vacA); the relationship between virulence factors and gastroduodenal diseases among patients.

Methods

Gastric biopsies were obtained from patients and cultured, DNA was extracted from cultured isolates and biopsies for PCR assay after which samples were investigated using standard laboratory procedures. Data of associated risk factors were obtained with the aid of questionnaires.

Results

Of the 444 participants, H. pylori was detected in 115 (25.9%) from culture analysis and 217 (48.9%) by direct PCR method. Ninety-eight (85.2%) of the culture-positive patients were also detected by PCR giving an overall prevalence of 52.7% (234/444). The highest number of H. pylori isolates 76.9% (180/234) was obtained from patients suffering from pangastritis. The CagA virulence gene was found in 62% (145/234), dupA in 53.4% (125/234) and vacA in 90.6% (212/234). VacA genotype s1 m1 was the most prevalent [56.4% (132)] followed by s2 m2 [11.5% (27)], s2 m1 [10.3% (24)] and [s1 m2 9.4% (22)]. There was a significant association observed in vacA s1 and peptic ulcer disease, as well as vacA s1/m2 and gastric erosion ( P < 0.05).

Conclusion

The study revealed a significant association between virulence genes and the development of certain forms of gastric infections while the variations in H. pylori detection and the associated risk factors investigated in the study were not significantly related.

Electronic supplementary material

The online version of this article (10.1186/s12876-019-0986-0) contains supplementary material, which is available to authorized users.

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Most cited references 50

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Pathobiology of Helicobacter pylori-Induced Gastric Cancer.

Manuel Ricardo Amieva, Richard Peek (2016)

Colonization of the human stomach by Helicobacter pylori and its role in causing gastric cancer is one of the richest examples of a complex relationship among human cells, microbes, and their environment. It is also a puzzle of enormous medical importance given the incidence and lethality of gastric cancer worldwide. We review recent findings that have changed how we view these relationships and affected the direction of gastric cancer research. For example, recent data have indicated that subtle mismatches between host and microbe genetic traits greatly affect the risk of gastric cancer. The ability of H pylori and its oncoprotein CagA to reprogram epithelial cells and activate properties of stemness show the sophisticated relationship between H pylori and progenitor cells in the gastric mucosa. The observation that cell-associated H pylori can colonize the gastric glands and directly affect precursor and stem cells supports these observations. The ability to mimic these interactions in human gastric organoid cultures as well as animal models will allow investigators to more fully unravel the extent of H pylori control on the renewing gastric epithelium. Finally, our realization that external environmental factors, such as dietary components and essential micronutrients, as well as the gastrointestinal microbiota, can change the balance between H pylori's activity as a commensal or a pathogen has provided direction to studies aimed at defining the full carcinogenic potential of this organism.

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Helicobacter pylori: epidemiology and routes of transmission.

Andrew M Brown (1999)

H. pylori is a common bacterium, and approximately 50 percent of the world's population has been estimated to be infected (198). Humans are the principal reservoir. The prevalence of H. pylori infection varies widely by geographic area, age, race, ethnicity, and SES. Rates appear to be higher in developing than in developed countries, with most of the infections occurring during childhood, and they seem to be decreasing with improvements in hygiene practices. H. pylori causes chronic gastritis and has been associated with several serious diseases of the gastrointestinal tract, including duodenal ulcer and gastric cancer. Since its "discovery" in 1982 by Warren and Marshall (1), H. pylori has been the topic of extensive research. A number of studies have used questionnaire components to investigate factors possibly related to the etiology of H. pylori infection. The majority of recent studies have not found tobacco use or alcohol consumption to be risk factors for H. pylori infection. Adequate nutritional status, especially frequent consumption of fruits and vegetables and of vitamin C, appears to protect against infection with H. pylori. In contrast, food prepared under less than ideal conditions or exposed to contaminated water or soil may increase the risk. Overall, inadequate sanitation practices, low social class, and crowded or high-density living conditions seem to be related to a higher prevalence of H. pylori infection. This finding suggests that poor hygiene and crowded conditions may facilitate transmission of infection among family members and is consistent with data on intrafamilial and institutional clustering of H. pylori infection. Understanding the route of H. pylori transmission is important if public health measures to prevent its spread are to be implemented. Iatrogenic transmission of H. pylori following endoscopy is the only proven mode. For the general population, the most likely mode of transmission is from person to person, by either the oral-oral route (through vomitus or possibly saliva) or perhaps the fecal-oral route. The person-to-person mode of transmission is supported by the higher incidence of infection among institutionalized children and adults and the clustering of H. pylori infection within families. Also lending support to this concept is the detection of H. pylori DNA in vomitus, saliva, dental plaque, gastric juice, and feces. Waterborne transmission, probably due to fecal contamination, may be an important source of infection, especially in parts of the world in which untreated water is common. Recent studies in the United States have linked clinical H. pylori infection with consumption of H. pylori-contaminated well water. This area of research is worthy of further investigation. Although H. pylori has been isolated in domestic cats, additional research has suggested that H. pylori is probably uncommon in domestic cats and thus is probably not a major concern for cat owners. Several studies have suggested sheep as a possible source of H. pylori transmission, a hypothesis that deserves additional investigation. The most recent reservoir suggested for H. pylori transmission is the housefly. However, evidence is lacking that H. pylori can be transmitted to humans from flies that have been in contact with H. pylori-infected feces. Nevertheless, the hypothesis is appealing since flies are known to carry many other infectious diseases. Knowledge of the epidemiology and mode of transmission of H. pylori is important to prevent its spread and may be useful in identifying high-risk populations, especially in areas that have high rates of gastric lymphoma, gastric cancer, and gastric ulcer.

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Helicobacter pylori evolution and phenotypic diversification in a changing host.

Christine Josenhans, Sebastian Suerbaum (2007)

Helicobacter pylori colonizes the stomachs of more than 50% of the world's population, making it one of the most successful of all human pathogens. One striking characteristic of H. pylori biology is its remarkable allelic diversity and genetic variability. Not only does almost every infected person harbour their own individual H. pylori strain, but strains can undergo genetic alteration in vivo, driven by an elevated mutation rate and frequent intraspecific recombination. This genetic variability, which affects both housekeeping and virulence genes, has long been thought to contribute to host adaptation, and several recently published studies support this concept. We review the available knowledge relating to the genetic variation of H. pylori, with special emphasis on the changes that occur during chronic colonization, and argue that H. pylori uses mutation and recombination processes to adapt to its individual host by modifying molecules that interact with the host. Finally, we put forward the hypothesis that the lack of opportunity for intraspecies recombination as a result of the decreasing prevalence of H. pylori could accelerate its disappearance from Western populations.

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Author and article information

Contributors

Ayodeji Idowu:

ORCID: http://orcid.org/0000-0003-2497-4662

+27 630 110 478 , dejimicro@yahoo.com

Asisipho Mzukwa: amzukwa32@gmail.com

Ute Harrison: ute.harrison@gmx.de

Pia Palamides: palamides@mvp.lmu.de

Rainer Haas: haas@mvp.lmu.de

Melvin Mbao: melmbao@gmail.com

Razinah Mamdoo: razinahmamdoo@gmail.com

Jonathan Bolon: jgbolon@gmail.com

Tolulope Jolaiya: oshuntee@gmail.com

Stella Smith: stellaismith@yahoo.com

Reidwaan Ally: aiddgit@mweb.co.za

Anna Clarke: aclarke@ufh.ac.za

Henry Njom: njomhenry@yahoo.com

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): 14 May 2019

Publication date PMC-release: 14 May 2019

Publication date Collection: 2019

Volume: 19

Electronic Location Identifier: 73

Affiliations

[1 ]ISNI 0000 0001 2152 8048, GRID grid.413110.6, Department of Biochemistry and Microbiology, , University of Fort Hare, ; Alice, Eastern Cape 5700 South Africa

[2 ]ISNI 0000 0004 1936 973X, GRID grid.5252.0, Chair of Medical Microbiology and Hospital Epidemiology, Max von Pettenkofer-Institute, Faculty of Medicine, , LMU Munich, ; Munich, Germany

[3 ]ISNI 0000 0004 0367 6954, GRID grid.414240.7, Division of Gastroenterology, , Chris Hani Baragwanath Academic Hospital (CHBAH), ; Soweto, Johannesburg, 2013 South Africa

[4 ]ISNI 0000 0004 1803 1817, GRID grid.411782.9, Department of Microbiology, , University of Lagos, ; Akoka, Yaba Lagos Nigeria

[5 ]ISNI 0000 0001 0247 1197, GRID grid.416197.c, Molecular Biology Department, , Nigerian Institute of Medical Research, ; Yaba, Lagos, Nigeria

Author information

Ayodeji Idowu http://orcid.org/0000-0003-2497-4662

Article

Publisher ID: 986

DOI: 10.1186/s12876-019-0986-0

PMC ID: 6518451

PubMed ID: 31088381

SO-VID: 8b022e3a-91b8-4b18-81ef-d9f0997b063f

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 : 1 October 2018

Date accepted : 11 April 2019

Funding

Funded by: FundRef http://dx.doi.org/10.13039/501100001659, Deutsche Forschungsgemeinschaft;

Award ID: HA2697/18-1

Award Recipient : Rainer Haas

Custom metadata

ScienceOpen disciplines: Gastroenterology & Hepatology

Keywords: h. pylori,peptic ulcer,pcr assay,virulence genes,caga,dupa,and vaca,patients

Data availability:

ScienceOpen disciplines: Gastroenterology & Hepatology

Keywords: h. pylori, peptic ulcer, pcr assay, virulence genes, caga, dupa, and vaca, patients

Detection of Helicobacter pylori and its virulence genes ( cagA , dupA , and vacA) among patients with gastroduodenal diseases in Chris Hani Baragwanath Academic Hospital, South Africa

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Abstract

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Conclusion

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Most cited references 50

Pathobiology of Helicobacter pylori-Induced Gastric Cancer.

Helicobacter pylori: epidemiology and routes of transmission.

Helicobacter pylori evolution and phenotypic diversification in a changing host.

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