Gut decolonization of CRE/MDRO carriage
Carbapenem-resistant Klebsiella gut carriage is a major reservoir; phages offer strain-specific, microbiome-sparing decolonization. This overview is realistic length for the page and explains the clinical problem briefly.
How phages act here
Mechanism
Phages target Klebsiella capsule and LPS receptors; capsule loss attenuates virulence.
Where it stands
Current evidence
Mostly preclinical mouse data; first human trial NCT07525089 launched 2026.
Evidence confidence: medium
The data
Key studies & trials
- Rotman E, et al. Rapid design of bacteriophage cocktails to suppress gut-resident carbapenem-resistant Klebsiella pneumoniae. Cell Host and Microbe. 2024. PMID 39368473. ↗
- Fang Q, et al. Safety and efficacy of phage application in bacterial decolonisation: a systematic review. Lancet Microbe. 2024. PMID 38452780. ↗
- Tan D, et al. Decolonization of carbapenem-resistant Klebsiella pneumoniae from intestinal microbiota of mice by phages targeting two surface structures. Front Microbiol. 2022;13:877074. ↗
- Decolonization Efficacy of BM111 Against CRE and VRE. BioMe Inc. NCT07525089, 2026. ↗
Who is working on it
Programs & centers
The possibility
Picture a CRE-positive transplant or ICU patient swallowing an isolate-matched phage cocktail that clears resistant Klebsiella from the gut over days, with no broad-spectrum collateral damage and no new resistance debt, converting a high-risk carrier into a non-carrier before surgery. Because phages exploit the very capsule that makes Klebsiella infectious and transmissible, the bacterium either dies or disarms itself by shedding the capsule and becomes easy prey for the immune system. If early trials hold up, PhageBank matching plus engineered host-range expansion could make gut decolonization a routine, microbiome-sparing infection-control tool.