Phenotypic and Molecular Antimicrobial Susceptibility of Helicobacter pylori.
Failure to eradicateHelicobacter pyloriinfection is often a result of antimicrobial resistance, which for clarithromycin is typically mediated by specific point mutations in the 23S rRNA gene. The purpose of this study was to define current patterns of antimicrobial susceptibility inH. pyloriisolates derived primarily from the United States and to survey them for the presence of point mutations in the 23S rRNA gene and assess the ability of these mutations to predict phenotypic clarithromycin susceptibility. Antimicrobial susceptibility testing was performed using agar dilution on 413H. pyloriisolates submitted to Mayo Medical Laboratories for susceptibility testing. For a subset of these isolates, a 150-bp segment of the 23S rRNA gene was sequenced. A total of 1,970 MICs were reported over the 4-year study period. The rate of clarithromycin resistance was high (70.4%), and elevated MICs were frequently observed for metronidazole (82.4% of isolates had an MIC of >8 μg/ml) and ciprofloxacin (53.5% of isolates had an MIC of >1 μg/ml). A total of 111 archivedH. pyloriisolates underwent 23S rRNA gene sequencing; we found 95% concordance between genotypes and phenotypes (P= 0.9802). Resistance to clarithromycin was most commonly due to an A2143G mutation (82%), followed by A2142G (14%) and A2142C (4%) mutations. ClinicalH. pyloriisolates derived primarily from the United States demonstrated a high rate of clarithromycin resistance and elevated metronidazole and ciprofloxacin MICs. The relative distribution of point mutations at positions 2143 and 2142 in the 23S rRNA gene in clarithromycin-resistantH. pyloriwas similar to that reported from other parts of the world; these mutations predict phenotypic resistance to clarithromycin.
Department of Pathology and Laboratory Medicine, University of Wisconsin, Madison, Wisconsin, USA.|Division of Clinical Microbiology, Mayo Clinic, Rochester, Minnesota, USA.
Derrick
D
Chen
Division of Clinical Microbiology, Mayo Clinic, Rochester, Minnesota, USA.
Scott A
SA
Cunningham
Division of Clinical Microbiology, Mayo Clinic, Rochester, Minnesota, USA.
Nicolynn C
NC
Cole
Division of Clinical Microbiology, Mayo Clinic, Rochester, Minnesota, USA.
Peggy C
PC
Kohner
Division of Biomedical Statistics and Informatics, Mayo Clinic, Rochester, Minnesota, USA.
Jayawant N
JN
Mandrekar
Division of Clinical Microbiology, Mayo Clinic, Rochester, Minnesota, USA patel.robin@mayo.edu.|Division of Infectious Diseases, Mayo Clinic, Rochester, Minnesota, USA.
Robin
0000-0001-6344-4141
R
Patel
D000890:Anti-Infective Agents / Q000494:pharmacology*; D017291:Clarithromycin / Q000494:pharmacology; D024881:Drug Resistance, Bacterial / Q000235:genetics; D016480:Helicobacter pylori / Q000187:drug effects* / Q000235:genetics; D018942:Macrolides / Q000494:pharmacology; D008826:Microbial Sensitivity Tests; D009154:Mutation; D012338:RNA, Ribosomal, 23S / Q000235:genetics
D000890:Anti-Infective Agents; D018942:Macrolides; D012338:RNA, Ribosomal, 23S; D017291:Clarithromycin
23S rRNA; Helicobacter pylori; antibiotic resistance; macrolide resistance