ECU Libraries Catalog

The glutamate decarboxylase genes, gadBC, are not required for brucella abortus resistance to low pH or virulence in the mouse model / by Tim D. Brown.

Author/creator Brown, Tim D. author.
Other author/creatorKalmus, Gerhard W., degree supervisor.
Other author/creatorEast Carolina University. Department of Biology.
Format Theses and dissertations and Archival & Manuscript Material
Production Info 2007.
Description68 leaves : illustrations (some color) ; 28 cm
Supplemental Content Access via ScholarShip
Subject(s)
Summary Brucella abortus is a Gram-negative, facultative bacterium, which is an extremely successful pathogen of humans and domesticated animals. The ability of Brucella to cause disease is directly related to the organism's ability to survive and persist in host phagocytes. In order to maintain residence in macrophages the brucellae require a low pH environment, which triggers gene expression that allows for replication and alteration of the host cell's endosomal maturation pathway. It is clear that the brucellae must have a mechanism to withstand low pH, however, this mechanism is currently unknown. The gadBC gene products play a role in low pH resistance in Escherichia coli and the Brucella spp. have putative homologs with 79.2% and 29.2% identity at the amino acid level. Mutants in the Brucella abortus 2308 gadBC genes were constructed and characterized for acid resistance and virulence in the mouse model. Surprisingly, the mutants were no more sensitive than the parent to low pH, and were able to establish and maintain a chronic spleen infection in mice.
General notePresented to the faculty of the Department of Biology.
General noteAdvisor: Gerhard Kalmus
Dissertation noteM.S. East Carolina University 2007
Bibliography noteIncludes bibliographical references (leaves 53-64).
Genre/formAcademic theses.
Genre/formAcademic theses.
Genre/formThèses et écrits académiques.

Available Items

Library Location Call Number Status Item Actions
University Archives ASK AT SPECIAL COLLECTIONS DESK ✔ Available Request Material
Electronic Resources Access Content Online ✔ Available