Exploring Alternative Treatment Choices for Multidrug-Resistant Clinical Strains of Helicobacter pylori in Mongolia

Author:

Khangai Ayush12,Saruuljavkhlan Batsaikhan13ORCID,Azzaya Dashdorj4,Gantuya Boldbaatar3,Oyuntsetseg Khasag3,Akada Junko1ORCID,Matsumoto Takashi1,Yamaoka Yoshio1567ORCID

Affiliation:

1. Department of Environmental and Preventive Medicine, Oita University Faculty of Medicine, Yufu 879-5593, Japan

2. The Gastroenterology Center, The First Central Hospital of Mongolia, Ulaanbaatar 14210, Mongolia

3. Endoscopy Unit, Department of Gastroenterology, Mongolia Japan Hospital of Mongolian National University of Medical Sciences, Ulaanbaatar 14210, Mongolia

4. Department of Gastroenterology, Mongolian National University of Medical Sciences, Ulaanbaatar 14210, Mongolia

5. Division of Gastroentero-Hepatology, Department of Internal Medicine, Faculty of Medicine-Dr. Soetomo Teaching Hospital, Universitas Airlangga, Surabaya 60115, Indonesia

6. Research Center for GLOBAL and LOCAL Infectious Diseases, Oita University, Yufu 879-5593, Japan

7. Department of Medicine-Gastroenterology, Baylor College of Medicine, Houston, TX 77030, USA

Abstract

Helicobacter pylori is a pathogen related to severe diseases such as gastric cancer; because of rising antimicrobial-resistant strains, failure to eradicate H. pylori with antibiotics has increased worldwide. Multidrug-resistant H. pylori and gastric cancer is common in Mongolia; therefore, we aimed to explore alternative antimicrobial treatments and the genomes of resistant strains in this country. A total of 361 H. pylori strains isolated from patients in Mongolia were considered. Minimal inhibitory concentrations for two fluoroquinolones (ciprofloxacin and moxifloxacin), rifabutin, and furazolidone were determined via two-fold agar dilution. Genomic mutations in antibiotic-resistant strains were identified by next-generation sequencing using the Illumina Miseq platform and compared with genes from a reference H. pylori strain (26695). The resistance rate of H. pylori strains to quinolones was high (44% to ciprofloxacin and 42% to moxifloxacin), and resistance to rifabutin was low (0.5%); none were resistant to furazolidone. Most quinolone-resistant strains possessed gyrA gene mutations causing amino acid changes (e.g., N87K, A88P, and D91G/Y/N). While one rifabutin-resistant strain had amino acid-substituting mutations in rpoB (D530N and R701C), the other had three novel rpoB mutations; both rifabutin-resistant strains were sensitive to furazolidone. Overall, our findings suggest that rifabutin and/or furazolidone may be an alternative, effective H. pylori treatment in patients who have failed to respond to other treatment regimens.

Publisher

MDPI AG

Subject

Virology,Microbiology (medical),Microbiology

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