Shanti Pandey
Chronic staphylococcal infections are primarily caused by the persister cells; a phenotypic variant that shows extreme tolerance to antibiotics resulting in treatment failure. While this phenomenon has posed a great threat in public health, mechanism underlying their formation in Staphylococcus aureus remains largely unknown. Mounting evidences of causal link between persister cells and recalcitrant infections underscore the great urgency to unravel the mechanism by which these cells are formed and survived. We characterized msaABCR operon that regulates virulence, biofilm development and antibiotic resistance in S. aureus.
Transcriptome of the operon deletion mutant shows differential expression of genes involved in various metabolic pathways including down-regulation of more than 10 genes involved in oxidative stress that led us to hypothesize that the operon play role in persister formation against antibiotics as well as oxidative stress leading to intracellular persister formation. In this study, we examined the persister cell formation in wild type S. aureus (USA300 LAC), isogenic msaABCR deletion mutant and complemented mutant strains against clinically relevant bactericidal antibiotics Rifampicin, Vancomycin, Daptomycin, Gentamicin and Linezolid. The persister ratio was measured at different time points after adding antibiotics.
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