Thesis (Ph. D.)--University of Texas at Austin, 1999. / Vita. Includes bibliographical references (leaves 93-99). Available also in a digital version from Dissertation Abstracts.

Reproduction de : Thèse doctorat : Génie informatique, automatique et traitement du signal : Reims : 2004. / Titre provenant de l'écran titre. Bibliogr. f.121-126.

Reproduction de : Thèse doctorat : Traitement des images et du signal : Cergy-Pontoise : 2007. / Bibliogr. p. 169-175.

Aachen, Techn. Hochsch., Thesis (doctoral), 2001.

Thesis (Ph. D.)--University of Washington, 2004. / Vita. Includes bibliographical references (leaves 131-147).

Thesis (Ph. D.)--Electrical and Computer Engineering, Georgia Institute of Technology, 2004. / Dr. Bonnie S. Heck, Committee Chair; David G. Taylor, Committee Member; Thomas. G. Habetler, Committee Member; Linda M. Wills, Committee Member; Eric Johnson, Committee Member. Includes bibliography.

Thesis--M.D., University of Hong Kong, 1983. / Vol. 2: Appendix.

Thesis (M. Phil.)--University of Hong Kong, 1978.

Thesis (Ph. D.)--University of Queensland, 2002. / Includes bibliographical references.

Most Salmonella enterica serovars are believed to have a cyclical lifestyle involving both host-associated and environment-associated, persistent phases. Their ability to persist in the environment increases the probability that they will be transmitted. Our hypothesis is that the genetic factors required for cellular aggregation and biofilm formation are important for host-to-host transmission. A link between biofilm formation, environmental persistence and transmissibility has not been observed, due to the lack of an appropriate model. We developed a murine model of Salmonella transmission allowing us to study the genetic factors involved in the transmission process. To test the role of aggregation and biofilm formation we used the ∆csgD mutant, which is deficient in both processes. We also engineered luciferase reporter strains of Salmonella enterica serovar Typhimurium (Salmonella Typhimurium) to track infection within a mouse population before the onset of clinical signs using bioluminescent imaging. We determined that mice shed high levels of Salmonella Typhimurium in their feces when pre-treated with streptomycin. To observe the transmission efficiency of Salmonella, we tracked their spread from infected mice to naive mice, and determined that Salmonella could be transmitted only after pre-treatment with streptomycin. We compared the shedding potential and colonization levels of mice challenged with either wild-type Salmonella Typhimurium or the ∆csgD mutant and determined them to be statistically similar when challenged separately. We found that wild-type Salmonella Typhimurium persisted in fecal pellets at higher levels than the ∆csgD mutant. We compared both the short- and long- transmission potential of the ∆csgD mutant to wild type Salmonella Typhimurium, and found that the mutant did not have a defect in either process. Though not observed in our model, we believe that environmental persistence and biofilm formation are important for the transmission of Salmonella due to its cyclical lifestyle. The model we generated remains useful to test the role of other genes in transmission. It can be further refined to more accurately mimic environmental transmission of Salmonella. Further understanding of the transition of Salmonella from infected hosts to the environment and back into new hosts will aid in reducing its environmental persistence and transmission.