Phenotypic and molecular antimicrobial susceptibility of Helicobacter pylori

Derrick Chen, Scott A. Cunningham, Nicolynn C. Cole, Peggy C. Kohner, Jayawant Mandrekar, Robin Patel

Research output: Contribution to journalArticle

9 Citations (Scopus)

Abstract

Failure to eradicate Helicobacter pylori infection 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 in H. pylori isolates 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 413 H. pylori isolates 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 archived H. pylori isolates 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. Clinical H. pylori isolates 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-resistant H. pylori was similar to that reported from other parts of the world; these mutations predict phenotypic resistance to clarithromycin.

Original languageEnglish (US)
Article numbere02530
JournalAntimicrobial Agents and Chemotherapy
Volume61
Issue number4
DOIs
StatePublished - Apr 1 2017

Fingerprint

Clarithromycin
Helicobacter pylori
rRNA Genes
Point Mutation
Mutation
Metronidazole
Ciprofloxacin
Helicobacter Infections
Agar
Genotype
Phenotype

Keywords

  • 23S rRNA
  • Antibiotic resistance
  • Helicobacter pylori
  • Macrolide resistance

ASJC Scopus subject areas

  • Pharmacology
  • Pharmacology (medical)
  • Infectious Diseases

Cite this

Phenotypic and molecular antimicrobial susceptibility of Helicobacter pylori. / Chen, Derrick; Cunningham, Scott A.; Cole, Nicolynn C.; Kohner, Peggy C.; Mandrekar, Jayawant; Patel, Robin.

In: Antimicrobial Agents and Chemotherapy, Vol. 61, No. 4, e02530, 01.04.2017.

Research output: Contribution to journalArticle

Chen, Derrick ; Cunningham, Scott A. ; Cole, Nicolynn C. ; Kohner, Peggy C. ; Mandrekar, Jayawant ; Patel, Robin. / Phenotypic and molecular antimicrobial susceptibility of Helicobacter pylori. In: Antimicrobial Agents and Chemotherapy. 2017 ; Vol. 61, No. 4.
@article{bf47c09bb186423a82b396050440dcb5,
title = "Phenotypic and molecular antimicrobial susceptibility of Helicobacter pylori",
abstract = "Failure to eradicate Helicobacter pylori infection 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 in H. pylori isolates 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 413 H. pylori isolates 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 archived H. pylori isolates 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. Clinical H. pylori isolates 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-resistant H. pylori was similar to that reported from other parts of the world; these mutations predict phenotypic resistance to clarithromycin.",
keywords = "23S rRNA, Antibiotic resistance, Helicobacter pylori, Macrolide resistance",
author = "Derrick Chen and Cunningham, {Scott A.} and Cole, {Nicolynn C.} and Kohner, {Peggy C.} and Jayawant Mandrekar and Robin Patel",
year = "2017",
month = "4",
day = "1",
doi = "10.1128/AAC.02530-16",
language = "English (US)",
volume = "61",
journal = "Antimicrobial Agents and Chemotherapy",
issn = "0066-4804",
publisher = "American Society for Microbiology",
number = "4",

}

TY - JOUR

T1 - Phenotypic and molecular antimicrobial susceptibility of Helicobacter pylori

AU - Chen, Derrick

AU - Cunningham, Scott A.

AU - Cole, Nicolynn C.

AU - Kohner, Peggy C.

AU - Mandrekar, Jayawant

AU - Patel, Robin

PY - 2017/4/1

Y1 - 2017/4/1

N2 - Failure to eradicate Helicobacter pylori infection 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 in H. pylori isolates 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 413 H. pylori isolates 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 archived H. pylori isolates 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. Clinical H. pylori isolates 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-resistant H. pylori was similar to that reported from other parts of the world; these mutations predict phenotypic resistance to clarithromycin.

AB - Failure to eradicate Helicobacter pylori infection 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 in H. pylori isolates 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 413 H. pylori isolates 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 archived H. pylori isolates 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. Clinical H. pylori isolates 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-resistant H. pylori was similar to that reported from other parts of the world; these mutations predict phenotypic resistance to clarithromycin.

KW - 23S rRNA

KW - Antibiotic resistance

KW - Helicobacter pylori

KW - Macrolide resistance

UR - http://www.scopus.com/inward/record.url?scp=85017001158&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=85017001158&partnerID=8YFLogxK

U2 - 10.1128/AAC.02530-16

DO - 10.1128/AAC.02530-16

M3 - Article

C2 - 28167563

AN - SCOPUS:85017001158

VL - 61

JO - Antimicrobial Agents and Chemotherapy

JF - Antimicrobial Agents and Chemotherapy

SN - 0066-4804

IS - 4

M1 - e02530

ER -