Helicobacter pylori 16S rRNA mutation conferring resistance to tetracycline

Accession ARO:3003510
CARD Short NameHpyl_16S_TET
DefinitionTetracycline binds tightly to the helix 34 domain in 16S rRNA, where it interferes sterically with the binding of aminoacyl-tRNA to the ribosome A site to block protein synthesis. Mutations in the nucleotide sequence in this domain of Helicobacter pylori can result in resistance against tetracycline.
AMR Gene Family16S rRNA with mutation conferring resistance to tetracycline derivatives
Drug Classtetracycline antibiotic
Resistance Mechanismantibiotic target alteration
Classification10 ontology terms | Show
Parent Term(s)2 ontology terms | Show
+ confers_resistance_to_antibiotic tetracycline [Antibiotic]
+ 16S rRNA with mutation conferring resistance to tetracycline derivatives [AMR Gene Family]
Publications

Dailidiene D, et al. 2002. Antimicrob Agents Chemother 46(12): 3940-3946. Emergence of tetracycline resistance in Helicobacter pylori: multiple mutational changes in 16S ribosomal DNA and other genetic loci. (PMID 12435699)

Trieber CA, et al. 2002. J Bacteriol 184(8): 2131-2140. Mutations in the 16S rRNA genes of Helicobacter pylori mediate resistance to tetracycline. (PMID 11914344)

Gerrits MM, et al. 2002. Antimicrob Agents Chemother 46(9):2996-3000 16S rRNA mutation-mediated tetracycline resistance in Helicobacter pylori. (PMID 12183259)

Toledo H, et al. 2010. J Antimicrob Chemother 65(3):470-3 Tetracycline resistance in Chilean clinical isolates of Helicobacter pylori. (PMID 20035020)

Resistomes

Prevalence of Helicobacter pylori 16S rRNA mutation conferring resistance to tetracycline among the sequenced genomes, plasmids, and whole-genome shotgun assemblies available at NCBI or IslandViewer for 414 important pathogens (see methodological details and complete list of analyzed pathogens). Values reflect percentage of genomes, plasmids, genome islands, or whole-genome shotgun assemblies that have at least one hit to the AMR detection model. Default view includes percentages calculated based on Perfect plus Strict RGI hits. Select the checkbox to view percentages based on only Perfect matches to AMR reference sequences curated in CARD (note: this excludes resistance via mutation as references in protein variant models are often wild-type, sensitive sequences).

Prevalence: rRNA gene variant model

SpeciesNCBI ChromosomeNCBI PlasmidNCBI WGSNCBI GIGRDI-AMR2
No prevalence data


Detection Models

Model Type: rRNA gene variant model

Model Definition: Ribosomal RNA (rRNA) Gene Variant Models (RVM) are similar to Protein Variant Models (PVM), i.e. detect sequences based on their similarity to a curated reference sequence and secondarily screen query sequences for curated sets of mutations to differentiate them from antibiotic susceptible wild-type alleles, except RVMs are designed to detect AMR acquired via mutation of genes encoding ribosomal RNAs (rRNA). RVMs include a rRNA reference sequence (often from antibiotic susceptible wild-type alleles), a curated bit-score cut-off, and mapped resistance variants. Mapped resistance variants may include any or all of single point mutations, insertions, or deletions curated from the scientific literature. A Strict RGI match has a BLASTN bit-score above the curated BLASTN cutoff value and contains at least one curated mutation from amongst the mapped resistance variants, while a Loose RGI match has a bit-score less than the curated BLASTN bit-score cut-off but still contains at least one curated mutation from amongst the mapped resistance variants.

Bit-score Cut-off (blastN): 2700

PubMed: mutation data hand curated from the scientific literature, evaluated as conferring resistance (R). CRyPTIC: mutation data acquired from the CRyPTIC catalog, evaluated as resistant (R), susceptible (S), or undetermined (U). ReSeqTB: mutation data acquired from the ReSeqTB catalog, evaluated as conferring resistance (Minimal, Moderate, High), not conferring resistance (None), or Indeterminate. WHO: mutation data acquired from the WHO 2023 catalog, evaluated as resistant (R), susceptible (S), or undetermined (U).

MutationMutation typePubMed
a926gsingle resistance variantPMID:20035020
a926g,g927g,a928cmultiple resistance variantsPMID:20035020
a926t,g927t,a928cmultiple resistance variantsPMID:12183259
a928csingle resistance variantPMID:20035020
a965t,g966t,a967cmultiple resistance variantsPMID:11914344
a965gsingle resistance variantPMID:12435699
a965g,a967cmultiple resistance variantsPMID:12435699
a965g,g966tmultiple resistance variantsPMID:12435699
a967csingle resistance variantPMID:12435699


>gb|CP003904.1|-|1511157-1512657|Helicobacter pylori 16S rRNA mutation conferring resistance to tetracycline [Helicobacter pylori 26695]
AGGAGGTGATCCAACCGCAGGTTCACTACGGTTACCTTGTTACGACTTCACCCCAGTCGCTGTGTGTGCCGTGGGCAGTAGCCAATTTAG
CATCCTGACTTAAGGCAAACACAACTCCCATGGTGTGACGGGCGGTGAGTACAAGACCCGGGAACGTATTCACCGCAACATGGCTGATTT
GCGATTACTAGCGATTCCAGCTTCATGCAGGCGAGTTGCAGCCTACAATCCGAACTGAGAGGTGTTTTGAAGATTGGCTCCATTCGCAGT
ATTGCTTCTCTTTGTGCACCCCATTGTAGCACGTGTGTAGCCCTAGGCGTAAGGGCCATGATGACTTGACGTCGTCCCCACCTTCCTNCC
CTTACGGAGGCAGTATCCTTAGAGTTCTCAGCATAACCTGTTAGCAACTAAGAAAAGGGGTTGCGCTCGTTGCGGGACTTAACCCAACAT
CTCACGACACGAGCTGACGACAGCCGTGCAGCACCTGTTTTCAAGGTCTGGCAAGCCAGACACTCCACTATTTCTAGCGGATTCTCTCAA
TGTCAAGCCTAGGTAAGGTTCTTCGTGTATCTTCGAATTAAACCACATGCTCCACCGCTTGTGCGGGTCCCCGTCTATTCCTTTGAGTTT
TAATCTTGCGACCGTACTCCCCAGGCGGGATGCTTAATGCGTTAGCTGCATTACTGGAGAGACTAAGCCCTCCAACAACTAGCATCCATC
GTTTAGGGCGTGGACTACCAGGGTATCTAATCCTGTTTGCTCCCCAACMGCTTTCGCGCAATCAGCGTCAGTAATGTTCCAGCAGGTCGC
CTTCGCAATGAGTATTCCTCTTGATCTCTACGGATTTTACCCCTACACCAAGAATTCCACCTACCTCTCCCACACTCTAGAATAGTAGTT
TCAAATGCAGTTCTATGGTTAAGCCATAGGATTTCACACCTGACTGACTATCCCGCCTACGCGCTCTTTACGCCCAGTGATTCCGAGTAA
CGCTTGCACCCTCCGTATTACCGCGGCTGCTGGCACGGAGTTAGCCGGTGCTTATTCGTTAGATACCGTCATTATCTTCTCTAACAAAAG
GAGTTTACAATCCTAAAACCTTCATCCTCCACGCGGCGTTGCTGCTTCAGGGTTTCCCCCATTGAGCAATATTCCCTACTGCTGCCTCCC
GTAGGAGTCTGGACCGTGTCTCAGTTCCAGTGTGTCCGTTCACCCTCTCAGGCCGGATACCCGTCATAGCCTTGGTAAGCCATTACCTTA
CCAACAAGCTGATAGGACATAGGCTGATCTCTTAGCGATAAATCTTTCCCCCGTAGGAGTATCTGGTATTAATCATCGTTTCCAATGGCT
ATCCCAAACTAAGAGGCACATAACCTATGCGTTACTCACCCGTGCGCCACTAATCAGCACTCTAGCAAGCTAGAAGCTTCATCGTTCGAC
TTGCATGTATTAGGCACGCCGCCAGCGTTCACTCTGAGCCAGGATCAAACTCTCCATAAAA

Curator Acknowledgements
Curator Description Most Recent Edit