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J Med Microbiol. 2011 Jul;60(Pt 7):950-60. doi: 10.1099/jmm.0.026013-0. Epub 2011 Mar 17.

Evidence for persisters in Staphylococcus epidermidis RP62a planktonic cultures and biofilms.

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Department of Microbiology and Immunology, Kirksville College of Osteopathic Medicine, A. T. Still University of Health Sciences, Kirksville, MO 63501, USA.


The pathogenesis of Staphylococcus epidermidis in foreign device-related infections is attributed primarily to its ability to form biofilms on a polymer surface. One mechanism proposed for the survival of organisms in a biofilm is the presence of persister cells. Persister cells survive antibiotic treatment without acquiring heritable antibiotic resistance. This study was conducted to determine if S. epidermidis RP62a growing in planktonic cultures and biofilms could survive as persister cells following treatment with levofloxacin and vancomycin. S. epidermidis RP62a produced a small percentage of persisters (levofloxacin, 3.09×10⁻⁷%; vancomycin, 8.21×10⁻⁵ %) when grown to exponential phase, whereas biofilms contained 28 and 94 % persisters, following exposure to levofloxacin and vancomycin, respectively. The highest percentages of persisters were obtained during stationary phase in planktonic cultures and the lowest percentages of persisters were obtained during mid-exponential phase. An increase in persister number was not due to activation of quorum-sensing regulons. Confocal laser scanning microscopy images of biofilms exposed to levofloxacin demonstrated that the antibiotic was able to kill bacteria throughout the biofilm. Our results suggest that antibiotic tolerance in biofilms and in planktonic cultures of S. epidermidis RP62a is due in part to the presence of persister cells.

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