Thesis (Ph. D.)--University of Pennsylvania, 1936. / "Reprint from the American review of tuberculosis, vol. xxxv, no. 6." Bibliography: p. 831-832.

Proefschrift--Utrecht. / "Summary and conclusions": p. 131-135. "Litteratuur": p. 142-157.

Thesis (M.S.)--University of Wisconsin--Madison, 1965. / eContent provider-neutral record in process. Description based on print version record. Bibliography: l. 44.

Thesis (M.S.)--University of Wisconsin--Madison, 1969. / eContent provider-neutral record in process. Description based on print version record. Includes bibliographical references.

Thesis (Ph. D.)--University of Wisconsin--Madison, 1968. / Typescript. Vita. eContent provider-neutral record in process. Description based on print version record. Includes bibliography.

Thesis (M.S.)--University of Wisconsin--Madison, 1963. / Typescript. eContent provider-neutral record in process. Description based on print version record. Includes bibliographical references (leaves 52-55).

Thesis (M.S. in electrical engineering)--Washington State University, May 2007. / Includes bibliographical references (p. 17-18).

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The fish pathogenic bacterium Aeromonas salmonicida is the causative agent of furunculosis in salmonids, a systemic disease that causes important economic losses in salmon aquaculture. Since the paracrystalline S-layer of Aeromonas salmonicida, known as the A-layer, is essential for virulence, the virulence mechanisms associated with this structure were studied. Structural studies demonstrated that the A-layer is flexible and plastic, being capable of acquiring different conformations and/or structural patterns, in which divalent cations play an important role. It was rigorously demonstrated that the A-layer acts as an adhesin, promoting adherence to macrophages, and fish cell lines. Since the macrophage is a professional phagocyte involved in ingesting and destroying bacteria, the ability of A. salmonicida to replicate inside macrophages was examined. A. salmonicida replicated inside macrophages and eventually destroyed them. This characteristic, together with the fact that A. salmonicida also penetrated epithelial fish cells, make it a facultatively intracellular, invasive pathogen. The A-layer provided an initial protection against oxidative agents, increasing the opportunities for A. salmonicida cells to induce an A-layer-independent mechanism involved in high resistance to oxidative agents, and thereby increase survival inside macrophages. Studies with in vivo grown. A. salmonicida provided further insight into the pathogenic process of furunculosis, and suggested that the A-layer plays a crucial role in colonization and penetration of the host, as well as survival inside the host (early events of the infectious process). However, it was found that in vivo grown A. salmonicida is capable of expressing a slime layer that shields its entire surface and provides full protection against complement-mediated killing an phagocytosis, thus relegating the A-layer to a secondary or minor role in the later stages of infection. The results presented have contributed significantly to our knowledge of the virulence factors of A. salmonicida, and could by used practically in the prevention of furunculosis in the salmon aquacultural industry. / Graduate