Bacterial infections can include mutant cells called persisters that are dormant, metabolically inactive, and thus antibiotic tolerant. These persisters hide within a protective shield of biofilm, which is difficult to penetrate with antibiotics. Persisters remain unaffected by antibiotics when the original infection is treated, and can rise out of dormancy and cause recurring infections. These are often worse than the original. MRSA persisters and biofilm are associated with recurrence. Very little is known about the genetic control of the persister phenotype, but kinases are known to invariably control cellular functions across most living organisms. We hypothesized that a MRSA kinase must control persister formation. We tested MRSA gene knockout strains in hopes of observing a reduction in persisters. Bacterial biofilm was grown, and the medium was removed. The biofilm was then exposed to excess antibiotics to kill metabolically active cells. At the desired time points, the antibiotic was removed, biofilm was disrupted, and CFU counts were performed to enumerate the live cells. This experiment was performed for Nebraska Transposon Mutant Library (NTML) strains lacking prominent histidine kinases and the isogenic wild-type parent strain; The CFU counts were similar for all strains, demonstrating these genes are unrelated to persister formation. Eventually, we will identify genes that control this phenotype.

Finding drug targets for control of persisters in MRSA biofilm

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