Scholarship & Research
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Item A three-dimensional computer model of four hypothetical mechanisms protecting biofilms from antimicrobials(2006-03) Chambless, Jason Daniel; Hunt, Stephen Michael; Stewart, Philip S.Four hypothetical mechanisms for protection of biofilms against antimicrobials were incorporated into a three-dimensional model of biofilm growth and development. The model integrated processes of substrate utilization, diffusion, growth, cell migration, death, and detachment in a cellular automaton framework. Compared to simulations of unprotected biofilms, each of the protective mechanisms provided some tolerance to antimicrobial action. When the mechanisms were compared to each other, the behaviors of the four protective mechanisms produced distinct shapes of killing curves, non-uniform spatial patterns of survival and cell type distribution, and anticipated susceptibility patterns for dispersed biofilm cells. The differences between the protective mechanisms predicted in these simulations could guide the design of experiments to discriminate antimicrobial tolerance mechanisms in biofilms. Each of the mechanisms could be a plausible avenue of biofilm protection.Item A 3D computer model investigation of biofilm detachment and protection mechanisms(Montana State University - Bozeman, College of Engineering, 2008) Chambless, Jason Daniel; Chairperson, Graduate Committee: Philip S. Stewart.A biofilm is a dense aggregation of microorganisms attached to each other and a supporting surface. Biofilms are ubiquitous in industrial environments and are also frequently recognized as the source of persistent infections. Biofilm invasions and biofilm-induced infections are often difficult or impossible to remedy. This dissertation presents the results of a 3D hybrid computer model, BacLAB, which was used to simulate detachment and protection mechanisms of biofilms in a cellular automata framework. Protection against antimicrobials afforded by each of four hypothesized protective mechanisms was investigated in order to examine population survival versus antimicrobial exposure time, and the spatial patterns of chemical species and cell types. When compared to each other, the behaviors of the slow penetration, adaptive stress response, substrate limitation, and persister mechanisms produced distinct shapes of killing curves, non-uniform spatial patterns of survival and cell type distribution, and anticipated susceptibility patterns of dispersed biofilm cells.