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      Antibacterial Activity of Ciprofloxacin-incorporated Central Venous Catheters and its Mechanism Against Planktonic Bacterial Cells

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      https://www.riss.kr/link?id=A76358049

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      Bloodstream infections (BSI) are caused by planktonic microorganisms, sometimes leading to serious infections such as bacteremia and sepsis. BSI occurs more frequently to the patients wearing the central venous catheter (CVC). The ciprofloxacin-incorporated CVC (CFX-CVC) has been reported previously to possess antimicrobial activity. In this study, the antibacterial activity of CFX-CVC and its mechanism against planktonic BSI cells were explored by using the shake flask test and by examining the release rate of 260 nm-absorbing substances from the bacterial cells indicative of the membrane damage of the bacterial cells. CFX-CVC reduced more than 99.9% of the viable planktonic BSI cells demonstrating its potent antibacterial activity. It provoked bacteriolysis causing leakage of a large amount of 260 nmabsorbing materials from the planktonic bacterial cells like S. aureus and E. coli. These results provide evidence that the antibacterial activity of CFX-CVC came from the inhibition of the stability of the planktonic bacterial cells.
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      Bloodstream infections (BSI) are caused by planktonic microorganisms, sometimes leading to serious infections such as bacteremia and sepsis. BSI occurs more frequently to the patients wearing the central venous catheter (CVC). The ciprofloxacin-incorp...

      Bloodstream infections (BSI) are caused by planktonic microorganisms, sometimes leading to serious infections such as bacteremia and sepsis. BSI occurs more frequently to the patients wearing the central venous catheter (CVC). The ciprofloxacin-incorporated CVC (CFX-CVC) has been reported previously to possess antimicrobial activity. In this study, the antibacterial activity of CFX-CVC and its mechanism against planktonic BSI cells were explored by using the shake flask test and by examining the release rate of 260 nm-absorbing substances from the bacterial cells indicative of the membrane damage of the bacterial cells. CFX-CVC reduced more than 99.9% of the viable planktonic BSI cells demonstrating its potent antibacterial activity. It provoked bacteriolysis causing leakage of a large amount of 260 nmabsorbing materials from the planktonic bacterial cells like S. aureus and E. coli. These results provide evidence that the antibacterial activity of CFX-CVC came from the inhibition of the stability of the planktonic bacterial cells.

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