viii, 164, xvi leaves : ill., plates (part col.) ; 25 cm. / Title page, contents and abstract only. The complete thesis in print form is available from the University Library. / Thesis (Ph.D.) from the Dept. of Plant Pathology, University of Adelaide, 1974

Thesis (M.S.P.H.)--University of Michigan, 1940.

Thesis (M.S.P.H.)--University of Michigan, 1940.

Thesis (M.S.)--University of Wisconsin--Madison, 1967. / eContent provider-neutral record in process. Description based on print version record. Includes bibliographical references.

Thesis (M.S.)--University of Wisconsin--Madison, 1966. / eContent provider-neutral record in process. Description based on print version record. Bibliography: l. 92-102.

Thesis (M.S.)--University of Wisconsin--Madison, 1968. / eContent provider-neutral record in process. Description based on print version record. Includes bibliographical references.

Thesis (M.S.)--University of Wisconsin--Madison, 1968. / eContent provider-neutral record in process. Description based on print version record. Includes bibliographical references.

Thesis (Ph. D.)--University of Wisconsin--Madison, 1971. / Typescript. Vita. eContent provider-neutral record in process. Description based on print version record. Includes bibliographical references.

Members of the Staphylococcus genus are found as a part of normal microflora in humans and can commonly be found on the skin or in the nasal cavity. However, these microorganisms can cause serious and life-threatening opportunistic infections when there is a break in the physical barrier of skin. These infections have become difficult to treat as resistant strains emerge, particularly Methicillin Resistant Staphylococcus aureus (MRSA). MRSA has become a commonly acquired nosocomial infection which is difficult to treat with conventional antibiotics of the blactam class. Even Vancomycin, a last resort antibiotic, has been ineffective on some infections. Furthermore, S. aureus readily forms biofilms on implanted medical devices which establishes a hardy and difficult to treat infection. These biofilms serve as a point of infection to the bloodstream. Research involving polymicrobial interactions and the inhibitory effects of bacterial-bacterial interactions could be a starting point for the discovery of a new therapeutic treatment for infections. It has been shown in our lab that Alcaligenes faecalishas inhibitory effects on Staphylococcus aureusplanktonic growth. Therefore, in this study, we wanted to examine 1) The mechanism by which A. faecalisinhibitsS. aureus growth and 2) how A. faecalisimpacts the various phases of S. aureusbiofilm growth. It was found that A. faecalislikely inhibits S. aureususing a physical mechanism that requires close contact, rather than using a secreted molecule. However, a Type VI secretion system could also produce similar results. Further research involving the formation of mutants to find the gene allowing A. faecalisto inhibit S. aureuswas started, but no viable mutants were created during the course of this research. A. faecaliswas found to inhibit the formation of S. aureus biofilm growth, but when added to a mature S. aureusbiofilm, the slow growth rate of A. faecaliscould not overtake the quickly replicating S. aureus. Further research in the polymicrobial interactions between S. aureus and A. faecaliscould lead to a finding of a new therapeutic target for antibiotics or the use of A. faecalisin infections.

No description available.