The small intestine is prone to infections by bacteria that can adhere to the surface wall. We wish to better understand an infection of the small intestine caused by enteropathogenic Escherichia coli (EPEC) and to achieve this objective we present three models: a chemostat and two mechanistic spatial models in 1-D and 2-D. The chemostat model is a dynamic model where four biologically significant steady states of the infection were observed: washout, persistence, threshold, and blowup. These results concur with previous work done in this field; however in this instance our model is far less complex. The 2-D mechanistic spatial model suggests that bacteria that adhere to the intestinal wall cause the infection to persist. The 2-D model also suggests that the radial gradients of EPEC are less important than the longitudinal gradients, allowing us to proceed with a 1-D analysis. The 1-D model permits an in-depth realization of the infection process, including bacterial growth and microvilli growth kinetics. This paper will discuss how our 3 models merge EPEC pathogenesis mechanisms with current-day CSTR and PFR colonization models.
Identifer | oai:union.ndltd.org:NCSU/oai:NCSU:etd-06062007-130811 |
Date | 11 July 2007 |
Creators | Smith, Althea |
Contributors | Dr. Sharon Lubkin, Dr. Fred Breidt, Dr. Alun Lloyd, Dr. Mette Olufson |
Publisher | NCSU |
Source Sets | North Carolina State University |
Language | English |
Detected Language | English |
Type | text |
Format | application/pdf |
Source | http://www.lib.ncsu.edu/theses/available/etd-06062007-130811/ |
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