Title of Dissertation / Thesis : INTERACTIONS OF VIBRIO CHOLERAE SEROGROUPS O 1 AND O 139

Title of Dissertation / Thesis: INTERACTIONS OF VIBRIO CHOLERAE SEROGROUPS O1 AND O139 AND COPEPODS Tonya Kafí Rawlings, Doctor of Philosophy, 2005 Dissertation / Thesis Directed By: Dr. Rita R. Colwell, Department of Cell Biology and Molecular Genetics Vibrio cholerae O1 El Tor and O139 Bengal have caused cholera epidemics throughout Bangladesh and elsewhere in the world with a seasonal regularity. This has raised questions about whether clinical presentations of cholera caused by these two epidemic serogroups of V. cholerae reflect similar responses to their aquatic habitat. The association of V. cholerae with plankton has been suggested to be an important factor in transmission of the disease. In this study, differences in resource utilization of copepods and chitin by V. cholerae O1 and O139 were analyzed using laboratory microcosm experiments. When occurring separately, V. cholerae O1 and O139 were able to colonize copepods, including Acartia tonsa and Eurytemora affinis. However, V. cholerae O1 had a higher affinity for colonizing adults of both copepod species, as well as the multiple life stages of E. affinis, than V. cholerae O139. In sympatry, colonization of copepods by V. cholerae O1 and O139 did not result in specific exclusion of one serogroup by the other. Results of this study indicate that cells that are already established may facilitate attachment through new biofilm formation, notably by V. cholerae O139. Soluble chitin, employed as a nutrient source, supported growth of V. cholerae O1 and O139. Growth of both serogroups with the addition of chitin was significantly greater than in river water alone. In competition assays, V. cholerae O139 had a deleterious effect on V. cholerae O1 growth, but not vice versa. Together, these data indicate that V. cholerae O1 and O139 respond differently to copepods as habitat, as well as nutrient resources. Such differences may play a role in cholera epidemics. The spatiotemporal dynamics of V. cholerae in the environment is complex, and understanding what drives cholera outbreaks requires explicit consideration of population responses and interactions of multiple