Date on Master's Thesis/Doctoral Dissertation


Document Type

Doctoral Dissertation

Degree Name

Ph. D.



Degree Program

Biology, PhD

Committee Chair

Yoder-Himes, Deborah

Committee Co-Chair (if applicable)

Perlin, Michael

Committee Member

Perlin, Michael

Committee Member

Rabin, Shira

Committee Member

Lai, Alexander

Committee Member

Remold, Susana

Author's Keywords

Pathogen evolution; Pseudomonas aeruginosa; Acanthamoeba castellanii; virulence factors


Understanding how innocuous organisms can evolve to be pathogenic to humans is of increasing global concern. Further, understanding how existing pathogens may evolved to be more virulent is also vital to our ability to provide healthcare to people afflicted with diseases that promote chronic bacterial infections, such as cystic fibrosis. With the rise of antibiotic resistance in both bacteria and fungi it is paramount that new therapeutics are identified. Understanding what mutations occur that result in increased virulence in microbes can potentially provide new targets for antimicrobial drugs to combat antibiotic resistance. The Coincidental Evolution Hypothesis is a fundamental hypothesis in the field of pathogen evolution. It states that virulence factors in human bacterial pathogens are a serendipitous byproduct of anti-predation adaptations accrued over a long co-evolutionary history with predators in their natural environment, such as amoebae. This hypothesis has theoretical support but has heretofore not been directly tested experimentally. The goal of my graduate research was to directly test the Coincidental Evolution Hypothesis by performing an experimental evolution by competing the opportunistic human pathogen Pseudomonas aeruginosa against its natural predator Acanthamoeba castellanii. Then I assessed if evolved lineages of P. aeruginosa exhibited increased virulence against novel host organisms. Along the way I also identified biotic and abiotic factors that would allow for the successful long-term co-culture of these two species (Chapter II). I also identified the phenotypic changes that occur in P. aeruginosa in response to long-term culture in low nutrients at ambient temperature under static culture conditions (Chapter III). Finally, I identified that co-evolution with A. castellanii resulted in evolved P. aeruginosa lineages that were more virulent against novel predators than their ancestors thus providing direct experimental evidence for the Coincidental Evolution Hypothesis (Chapter IV). However, I also demonstrate that these results are strain dependent and may be linked to the life history of the P. aeruginosa strains tested. Furthermore, I also identified that abiotic factors, rather than just predation pressure, also play a key role in the evolution of virulence factors in this species. Taken together, the data I have collected largely supports the Coincidental Evolution Hypothesis.