Inhibiting Bacterial Biofilm Formation on Stainless Steel 316L Using Self-Assembled Monolayers

Defense Date

10-8-2012

Graduation Date

Fall 1-1-2012

Availability

Immediate Access

Submission Type

dissertation

Degree Name

PhD

Department

Chemistry and Biochemistry

Committee Chair

Ellen Gawalt

Committee Member

Rita Mihailescu

Committee Member

Jeffry Madura

Committee Member

Luanne Hall-Stoodley

Committee Member

Ralph Wheeler

Committee Member

David Seybert

Keywords

Biofilms, Orthopedic implants, Self-assembled monolayers

Abstract

Stainless steel 316L (SS316L) is commonly used to construct orthopedic implants, which can fail due to bacterial biofilm infection. Since infection typically occurs around the time of implant surgery, it is important to reduce bacterial adhesion early on during the wound healing process. Two approaches were utilized to combat the problem of bacterial adhesion using self-assembled monolayers (SAMs) as the basis for the surface modification. In a passive approach, SAMs with long alkyl chains presenting hydrophobic (-CH3) or hydrophilic (tri- and penta-ethylene glycol) tail groups were used. In an orthogonal approach, active antimicrobial coatings were formed by using SAMs to immobilize the antibiotics gentamicin or vancomycin individually and in combination.

Modified surfaces were characterized using diffuse reflectance infrared Fourier transform (DRIFT) spectroscopy, matrix assisted laser desorption ionization time of flight (MALDI-TOF) mass spectrometry, atomic force microscopy (AFM), and contact angle analysis. Staphylococcus aureus biofilm growth on modified surfaces was monitored using confocal laser scanning microscopy (CLSM), scanning electron microscopy (SEM), and colony forming unit (CFU) analysis. Neither hydrophobic nor hydrophilic SAMs inhibited biofilm development. However, antibiotic-linked films significantly reduced biofilm growth by 99 % up to 48 hours. Gentamicin-linked films were shown to be effective from 2-24 hours while vancomycin-linked films significantly inhibited biofilm growth at longer time points (6-48 hours). Combining the antibiotics limited biofilm development from 2-24 hours. This is significant because reducing initial bacterial adhesion at early time points is critical to limiting biofilm infection and implant failure. Further, this approach would deliver active antibiotic molecules directly to the implant site and improve upon current treatment strategies which rely on high doses of intravenous antibiotics that can contribute to antibiotic resistance and increasingly virulent strains of bacteria.

Format

PDF

Language

English

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