| Accession | ARO:3000010 |
| CARD Short Name | vanA |
| Definition | VanA is a D-Ala-D-Ala ligase homolog that synthesizes D-Ala-D-Lac, an alternative substrate for peptidoglycan synthesis that reduces vancomycin binding affinity. It has been isolated from VREs. It is associated with both vancomycin and teicoplanin resistance. |
| AMR Gene Family | glycopeptide resistance gene cluster, Van ligase |
| Drug Class | glycopeptide antibiotic |
| Resistance Mechanism | antibiotic target alteration |
| Resistomes with Perfect Matches | Enterococcus faecalisp+wgs, Enterococcus faeciump+wgs, Klebsiella pneumoniaewgs, Staphylococcus aureusp+wgs, Streptococcus gallolyticuswgs |
| Resistomes with Sequence Variants | Brevibacillus laterosporuswgs, Enterococcus aviump, Enterococcus faecalisp+wgs, Enterococcus faeciumg+p+wgs, Klebsiella pneumoniaewgs, Staphylococcus aureusg+p+wgs, Streptococcus gallolyticuswgs |
| Classification | 14 ontology terms | Show + process or component of antibiotic biology or chemistry + mechanism of antibiotic resistance + antibiotic target alteration [Resistance Mechanism] + restructuring of bacterial cell wall conferring antibiotic resistance + determinant of antibiotic resistance + antibiotic molecule + protein(s) conferring antibiotic resistance via molecular bypass + glycopeptide antibiotic [Drug Class] + gene(s) or protein(s) associated with a glycopeptide resistance cluster + antibiotic resistance gene cluster, cassette, or operon + glycopeptide resistance gene cluster [AMR Gene Family] + Van ligase [AMR Gene Family] + vancomycin [Antibiotic] + teicoplanin [Antibiotic] |
| Parent Term(s) | 2 ontology terms | Show |
| Publications | Marshall CG, et al. 1997. Proc Natl Acad Sci U S A 94(12): 6480-6483. D-Ala-D-Ala ligases from glycopeptide antibiotic-producing organisms are highly homologous to the enterococcal vancomycin-resistance ligases VanA and VanB. (PMID 9177243) |
Prevalence of vanA among the sequenced genomes, plasmids, and whole-genome shotgun assemblies available at NCBI or IslandViewer for 413 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).
| Species | NCBI Chromosome | NCBI Plasmid | NCBI WGS | NCBI GI |
|---|---|---|---|---|
| Brevibacillus laterosporus | 0% | 0% | 11.76% | 0% |
| Enterococcus avium | 0% | 33.33% | 0% | 0% |
| Enterococcus faecalis | 0% | 2.71% | 6.24% | 0% |
| Enterococcus faecium | 0.96% | 10.75% | 28.71% | 0% |
| Klebsiella pneumoniae | 0% | 0% | 0.01% | 0% |
| Staphylococcus aureus | 0.7% | 0.19% | 0.1% | 0% |
| Streptococcus gallolyticus | 0% | 0% | 2.27% | 0% |
Model Type: protein homolog model
Model Definition: Protein Homolog Models (PHM) detect protein sequences based on their similarity to a curated reference sequence, using curated BLASTP bitscore cut-offs. Protein Homolog Models apply to all genes that confer resistance through their presence in an organism, such as the presence of a beta-lactamase gene on a plasmid. PHMs include a reference sequence and a bitscore cut-off for detection using BLASTP. A Perfect RGI match is 100% identical to the reference protein sequence along its entire length, a Strict RGI match is not identical but the bit-score of the matched sequence is greater than the curated BLASTP bit-score cutoff, Loose RGI matches have a bit-score less than the curated BLASTP bit-score cut-off.
Bit-score Cut-off (blastP): 350
