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Background and objectives: Peptic ulcer disease, chronic gastritis, and stomach cancer are all caused by H. pylori. The most notable drug for the treatment is the antibiotic clarithromycin, which is currently the drug of choice. H. pylori clarithromycin resistance has been associated with point mutations in 23srRNA, the most prominent of which are A2143 and A2144G. In H. pylori bacteria, methylase synthesis, macrolide-inactivating enzyme activity, and active efflux have all been found to be resistance mechanisms. The goal of the study is to determine how resistant H. pylori is to clarithromycin and what the minimum inhibitory concentration is for various antimicrobials. Furthermore, gastro-endoscopy will be performed on Iraqi patients to detect the presence of A2143G and A2144G point mutations in Helicobacter pylori infections, as diagnosed from the pyloric region and other anatomical regions. Methods: One hundred fifteen samples were collected from patients strongly suspected of H. pylori infection presented for upper gastrointestinal endoscopy at Ramadi Teaching Hospitals and Private Clinics for the period from January 2020 until February 2021. Specimens were cultured on brain heart infusion agar containing various antibiotics and were incubated at 37
C under microaerophilic conditions. For identification of H. pylori, isolates of the biochemical tests and RT-PCR assay were applied. The Epsilometer test was used in the antibiotic susceptibility testing as dependent on the CLSI standard. The Restriction Fragment Length Polymorphism technique was used to determine point mutations. Results: In total, 55 (47.8%) Helicobacter pylori isolates were cultured from the 115 biopsy specimens, among which 16 (29.1%), 38 (69.1%), 20 (36.4%), and 40 (72.7%) revealed some degree of resistance to levofloxacin, clarithromycin, ciprofloxacin, and metronidazole, respectively. The frequency of A2144G and A2143 point mutations were 23 (60.5%) and 19 (50%), respectively. Conclusions: According to our results, Helicobacter pylori showed high resistance to clarithromycin. Our results demonstrate the requirement for antibiotic susceptibility testing and molecular methods in selecting drug regimens.

n total, 115 patients who submitted for routine upper gastrointestinal endoscopy at Ramadi Teaching Hospitals during the period from January 2020 until February 2021 constituted the sample. The patients included 80 (69.6%) males and 35 (30.4%) females with ages ranging from 17 to 69 years. The clinical diagnoses based on endoscopy included antral gastritis (n = 53), combined gastritis and duodenitis (n = 2), duodenitis (n = 7), gastric tumour, and adenocarcinoma (n = 1), hiatus hernia (n = 4), combined gastric and duodenal ulcers (n = 19), esophagitis (n = 1), and patients with dyspepsia (n = 28) (Table 1). The exclusion criteria were applied to patients who had received H2 receptor blockers, antimicrobial therapy, PPI, and/or non-steroid anti-inflammatory drugs one month pre-endoscopy. Subjects with the following clinical conditions were also excluded from the study: cirrhosis, nephropathy in critical stages, and pregnancy. Information about demographic and socioeconomic factors, and the personal treatment histories of the included patients was already reported in a questionnaire. The gastric biopsy samples obtained from the antrum and corpus of the stomach during routine endoscopy by an expert clinician (gastroenterologist) were placed in sterile tubes containing brain heart infusion broth medium and 5% of foetal bovine serum for transportation. Further, the results of an invasive rapid urease test (RUT) were found using a urea agar slant tube, RT-PCR amplification of 16srRNA using the thermal cycler (Sacace - Italy) with a RT-PCR kit for qualitative detection of H. pylori ((Sacace- Italy), UBT using a HUBT-20p H. pylori detector (HEADWAY, China) using14 a C-urea, 99-atom%14 C-labelled urea capsule. SAT was performed using the H. pylori Ag Rapid Test CE (CTK - Biotech, USA), whilst cagA-IgG was performed using a commercial Human H. Pylori Cytotoxin-Associated Gene A Protein IgG (HP-CagA-IgG) ELISA Kit (CUSABIO, USA) by ELISA system (Human, Germany) (Hussein et al., 2021)

Helicobacter pylori

Creative Commons Attribution 4.0 International

Background and objectives: Peptic ulcer disease, chronic gastritis, and stomach cancer are all caused by H. pylori. The most notable drug for the treatment is the antibiotic clarithromycin, which is currently the drug of choice. H. pylori clarithromycin resistance has been associated with point mutations in 23srRNA, the most prominent of which are A2143 and A2144G. In H. pylori bacteria, methylase synthesis, macrolide-inactivating enzyme activity, and active efflux have all been found to be resistance mechanisms. The goal of the study is to determine how resistant H. pylori is to clarithromycin and what the minimum inhibitory concentration is for various antimicrobials. Furthermore, gastro-endoscopy will be performed on Iraqi patients to detect the presence of A2143G and A2144G point mutations in Helicobacter pylori infections, as diagnosed from the pyloric region and other anatomical regions. Methods: One hundred fifteen samples were collected from patients strongly suspected of H. pylori infection presented for upper gastrointestinal endoscopy at Ramadi Teaching Hospitals and Private Clinics for the period from January 2020 until February 2021. Specimens were cultured on brain heart infusion agar containing various antibiotics and were incubated at 37
C under microaerophilic conditions. For identification of H. pylori, isolates of the biochemical tests and RT-PCR assay were applied. The Epsilometer test was used in the antibiotic susceptibility testing as dependent on the CLSI standard. The Restriction Fragment Length Polymorphism technique was used to determine point mutations. Results: In total, 55 (47.8%) Helicobacter pylori isolates were cultured from the 115 biopsy specimens, among which 16 (29.1%), 38 (69.1%), 20 (36.4%), and 40 (72.7%) revealed some degree of resistance to levofloxacin, clarithromycin, ciprofloxacin, and metronidazole, respectively. The frequency of A2144G and A2143 point mutations were 23 (60.5%) and 19 (50%), respectively. Conclusions: According to our results, Helicobacter pylori showed high resistance to clarithromycin. Our results demonstrate the requirement for antibiotic susceptibility testing and molecular methods in selecting drug regimens.

n total, 115 patients who submitted for routine upper gastrointestinal endoscopy at Ramadi Teaching Hospitals during the period from January 2020 until February 2021 constituted the sample. The patients included 80 (69.6%) males and 35 (30.4%) females with ages ranging from 17 to 69 years. The clinical diagnoses based on endoscopy included antral gastritis (n = 53), combined gastritis and duodenitis (n = 2), duodenitis (n = 7), gastric tumour, and adenocarcinoma (n = 1), hiatus hernia (n = 4), combined gastric and duodenal ulcers (n = 19), esophagitis (n = 1), and patients with dyspepsia (n = 28) (Table 1). The exclusion criteria were applied to patients who had received H2 receptor blockers, antimicrobial therapy, PPI, and/or non-steroid anti-inflammatory drugs one month pre-endoscopy. Subjects with the following clinical conditions were also excluded from the study: cirrhosis, nephropathy in critical stages, and pregnancy. Information about demographic and socioeconomic factors, and the personal treatment histories of the included patients was already reported in a questionnaire. The gastric biopsy samples obtained from the antrum and corpus of the stomach during routine endoscopy by an expert clinician (gastroenterologist) were placed in sterile tubes containing brain heart infusion broth medium and 5% of foetal bovine serum for transportation. Further, the results of an invasive rapid urease test (RUT) were found using a urea agar slant tube, RT-PCR amplification of 16srRNA using the thermal cycler (Sacace - Italy) with a RT-PCR kit for qualitative detection of H. pylori ((Sacace- Italy), UBT using a HUBT-20p H. pylori detector (HEADWAY, China) using14 a C-urea, 99-atom%14 C-labelled urea capsule. SAT was performed using the H. pylori Ag Rapid Test CE (CTK - Biotech, USA), whilst cagA-IgG was performed using a commercial Human H. Pylori Cytotoxin-Associated Gene A Protein IgG (HP-CagA-IgG) ELISA Kit (CUSABIO, USA) by ELISA system (Human, Germany) (Hussein et al., 2021)

Helicobacter pylori

Creative Commons Attribution 4.0 International