©2019 by VanEpps Research Laboratory

Healthcare associated infections are a leading cause of morbidity and mortality in the U.S., with over 60% associated with implanted medical devices.  Despite engineering advances in materials and healthcare process improvements, infections rates remain unacceptably high.  As new devices are developed, indications for use are expanded, and the immunocompromised population continues to climb, this trend is likely to continue or worsen in the future.  The fundamental pathogenic issue is the adhesion and subsequent colonization of implanted materials with bacterial biofilms.  Biofilms on implanted devices confer significant protection from host immune response and antibiotics.  Ultimately, life-sustaining devices such as dialysis catheters, pacemakers, or heart valves must be surgically removed, adding to morbidity, mortality, and cost.  Our group has been focused on developing in situ treatment strategies for device salvage as an alternative to surgical removal and replacement.


Understanding biofilm development as the consequence of adsorption, growth and detachment with each effect governed by self-assembly, fluid mechanics, and transport phenomena, we are exposing biofilms to external stimuli which we believe will manipulate the rheological characteristics of the bacterial communities, thereby preventing or remediating biofilm growth.  A key feature of this work is the development of biofilm experimental models that more closely resemble human biofilm-associated infections. 


Although most experimental models of biofilm infection draw upon isolated bacterial biofilms, in fact there is no infection without host protein contribution.  Therefore, we have developed a new model for medical device infection – that of an infected fibrin clot – and show that the common blood borne pathogen Staphylococcus epidermidis influences this in vitro model of a blood clot mechanically and structurally on both microscopic and macroscopic scales. We have also developed an in vitro biofilm reactor system with precise control over flow rate and temperature to mimic the physiologic conditions surrounding a dialysis catheter.  This model allows us to evaluate biofilm growth, maturation and response to thermal, chemical, and mechanical treatments.  Indeed, in this system, modest increases in temperature and shear stress can decrease bioburden and cell viability and alter biofilm morphology.  Finally, we have a well-established animal model of catheter associated bloodstream infection (CLABSI) for pre-clinical evaluation of the most promising therapies. 

Background: ​ Scanning electron microscope sample for the inside of a bacterial infected catheter 

Biofilm Biomechanics