Detection of Cytotoxin-Associated and Vacuolating Cytotoxin Genotypes of Helicobacter pylori in Patients with Peptic Inflammatory/Ulcerative Disorders

Mohammad Mostafa Alkherkhisy1, Mohammad Mostafa Alsaadawy,1 Mohammad Samy Alhakim2, Almahdy Mohammad Alatrouny1, Ali Monis Yasin3

Detection of Cytotoxin-Associated and Vacuolating Cytotoxin Genotypes of Helicobacter pylori in Patients with Peptic Inflammatory/Ulcerative Disorders

Document Type : Original Article

Author

Mohammad Mostafa Alsaadawy,1 Mohammad Samy Alhakim2, Almahdy Mohammad Alatrouny1, Ali Monis Yasin3 Mohammad Mostafa Alkherkhisy1

1Department of Microbiology and Immunology, Faculty of Medicine, Al-Azhar University, 2Department of Pathology, Faculty of Medicine, Al-Azhar University and 3Department of Internal Medicine, Faculty of Medicine, Ain Shams University

Abstract

Background: Helicobacter pylori is a Gram negative, spiral, rod-shaped, and flagellated bacteria that colonizes the human gastric mucosa and can cause a strong inflammatory state and lesions. However, genomic and phenotypic features of different strains allow the expression of virulence factors which enable some strains, rather than others, to cause disease. Aims: The aim of the present study was to evaluate the role of the cytotoxicity genes, CagA and VacA, of H. pylori in patients with peptic inflammatory/ulcerative disorders and correlate between different genotypes and peptic lesions. Patients and methods: Upper gastrointestinal endoscopy and histopathological examination of gastric biopsy samples were done for 112 patients complaining of upper gastrointestinal symptoms and clinically suspected to have H. Pylori infection. CagA and VacA genotyping by PCR were done for 50 H. pylori +ve patients (diagnosed by histopathology). Results: CagA gene and VacA gene were detected in 42.0% and 70% of H. pylori +ve patients respectively. There was a significant positive correlation between CagA and duodenal erosion and ulceration visualized by endoscopy. There was also a positive correlation between CagA and gastric erosion and ulceration visualized by endoscopy, but it didn`t reach a significant level. There was also a significant positive correlation between the VacA m1s1 subtype and duodenal erosion and ulceration detected by endoscopy. VacA m2s2 was correlated to presence of both gastric erosions and ulcerations and presence of metaplasia and atrophy. There was only one H. pylori +ve patient with gastric cancer. This patient was positive for both CagA and VacA m2s2. Conclusions: The CagA gene is associated with severe forms of gastric pathology (peptic ulcer disease "PUD" and precancerous gastric lesions) and the VacA m2s2 subtype is associated with variable forms of gastric pathology rather than other VacA gene subtypes. Recommendations: Genotyping for VacA and CagA of H. pylori infected patients is helpful to determine the patients at more risk. Further studies are needed to evaluate the virulence factors in H. pylori with emphasis on role of CagA and VacA m2s2 both in vivo and in vitro.

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