Browsing by Author "Brindle, Eric R."

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An experimentally validated immersed boundary model of fluid-biofilm interaction
(2010-06) Vo, Garret D.; Brindle, Eric R.; Heys, Jeffrey J.
Biofilms are colonies of microorganisms that live on wetted surfaces in a matrix consisting of polysaccharides, proteins, and nucleic acids. According to the National Institute of Health (NIH), biofilms play a role in over 80 percent of microbial infections in the body and these infections are remarkably difficult to treat with antimicrobial compounds. The objective here is to understand and predict the physical interaction between a biofilm and the surrounding fluid flow.We have developed a biofilm-fluid interaction model, based on the Immersed Boundary Method, to simulate the interaction between the biofilm and a moving fluid. The model predictions of biofilm deformation quantitatively agree with experimental measurements for a range a biofilms using a simple immersed elastic solid to model the biofilm matrix. An immersed viscoelastic solid model is also developed and compared with experimental measurements. The results show that the viscoelastic behavior inherent to the immersed boundary method (even when using a simple immersed elastic solid) is sufficient for some biofilms, but a slightly viscoelastic solid gives more general agreement with experimental measurements.
Hydrodynamic deformation and removal of Staphylococcus epidermidis biofilms treated with urea, chlorhexidine, iron chloride, or DispersinB
(2011-07) Brindle, Eric R.; Miller, David A.; Stewart, Philip S.
The force-deflection and removal characteristics of bacterial biofilm were measured by two different techniques before and after chemical, or enzymatic, treatment. The first technique involved time lapse imaging of a biofilm grown in a capillary flow cell and subjected to a brief shear stress challenge imparted through increased fluid flow. Biofilm removal was determined by calculating the reduction in biofilm area from quantitative analysis of transmission images. The second technique was based on microindentation using an atomic force microscope. In both cases, biofilms formed by Staphylococcus epidermidis were exposed to buffer (untreated control), urea, chlorhexidine, iron chloride, or DispersinB.In control experiments, the biofilm exhibited force-deflection responses that were similar before and after the same treatment. The biofilm structure was stable during the post-treatment shear challenge (1% loss). Biofilms treated with chlorhexidine became less deformable after treatment and no increase in biomass removal was seen during the post-treatment shear challenge (2% loss). In contrast, biofilms treated with urea or DispersinB became more deformable and exhibited significant biofilm loss during the post-treatment flow challenge (71% and 40%, respectively). During the treatment soak phase, biofilms exposed to urea swelled. Biofilms exposed to iron chloride showed little difference from the control other than slight contraction during the treatment soak. These observations suggest the following interpretations: (1) chemical or enzymatic treatments, including those that are not frankly antimicrobial, can alter the cohesion of bacterial biofilm; (2) biocidal treatments (e.g., chlorhexidine) do not necessarily weaken the biofilm; and (3) biofilm removal following treatment with agents that make the biofilm more deformable (e.g., urea, DispersinB) depend on interaction between the moving fluid and the biofilm structure. Measurements such as those reported here open the door to development of new technologies for controlling detrimental biofilms by targeting biofilm cohesion rather than killing microorganisms.