Tigecycline resistance can occur independently of the ramA gene in Klebsiella pneumoniae.
Tigecycline resistance in Klebsiella pneumoniae results from ramA upregulation that causes the overexpression of the efflux pump, AcrAB-TolC. Tigecycline mutants, derived from Ecl8ΔramA, can exhibit a multidrug resistance phenotype due to increased transcription of the marA, rarA, acrAB, and oqxAB genes. These findings support the idea that tigecycline or multidrug resistance in K. pneumoniae, first, is not solely dependent on the ramA gene, and second, can arise via alternative regulatory pathways in K. pneumoniae.
Centre for Infection and Immunity, Queen's University Belfast, Medical Biology Centre, Belfast, United Kingdom.
Mark
M
Veleba
Thamarai
T
Schneiders
D000900:Anti-Bacterial Agents / Q000494:pharmacology*; D001426:Bacterial Proteins / Q000235:genetics*; D024901:Drug Resistance, Multiple, Bacterial / Q000235:genetics; D005798:Genes, Bacterial; D007711:Klebsiella pneumoniae / Q000187:drug effects* / Q000235:genetics* / Q000378:metabolism; D026901:Membrane Transport Proteins / Q000096:biosynthesis* / Q000235:genetics / Q000378:metabolism; D008826:Microbial Sensitivity Tests; D008911:Minocycline / Q000031:analogs & derivatives* / Q000494:pharmacology; D000078304:Tigecycline; D015854:Up-Regulation
D000900:Anti-Bacterial Agents; D001426:Bacterial Proteins; D026901:Membrane Transport Proteins; C095947:RamA protein, Klebsiella; D000078304:Tigecycline; D008911:Minocycline