Overview
Vancomycin is a glycopeptide antibiotic targeting Gram-positive bacteria by binding D-Ala-D-Ala of peptidoglycan precursors. It is the last-resort treatment for MRSA and oral vancomycin is first-line for severe clostridioides difficile infection. In the WikiBiome framework, vancomycin exemplifies the antibiotic-microbiome paradox: it treats C. difficile but causes profound dysbiosis that increases future C. difficile recurrence risk.
Microbiome Impact
- Vancomycin dramatically reduces Gram-positive commensals (Firmicutes, especially lachnospiraceae, ruminococcaceae) while sparing Gram-negatives → Proteobacteria bloom.
- Early-life vancomycin exposure alters gut microbiome development and increases autoimmune diabetes risk in NOD mice candon 2015 antibiotics early life gut microbiome autoimmune diabetes nod.
- Destroys colonization resistance → enables secondary infections bing 2019 antibiotic induced dysbiosis gut microbiota.
VRE and Metal Co-Selection
Vancomycin-resistant enterococcus (VRE) is a critical AMR threat. The vanA resistance gene co-locates with mercury and arsenic resistance genes on the same mobile genetic elements — meaning environmental metal exposure selects for vancomycin resistance without antibiotic exposure rebelo 2021 enterococcus metal antibiotic resistance. This is the paradigm case for co selection.
Cross-References
- clostridioides difficile — vancomycin as first-line treatment
- enterococcus — VRE as AMR threat
- co selection — vanA + metal resistance on shared plasmids
- colonization resistance — vancomycin destroys it
- antimicrobial resistance — VRE as critical priority pathogen