The coincidental evolution hypothesis: examining the factors that affect virulence in an opportunistic pathogen

UNCG Author/Contributor (non-UNCG co-authors, if there are any, appear on document)
Heather A. Hopkins (Creator)
Institution
The University of North Carolina at Greensboro (UNCG )
Web Site: http://library.uncg.edu/
Advisor
Kasie Raymann

Abstract: The coincidental evolution hypothesis proposes that virulence in an opportunistic bacterial pathogen arises in response to selection from predators in the outside host environment. Opportunistic pathogens, unlike obligate pathogens, do not need a host for survival, and exist in multiple environments where they face selective pressure from eukaryotic predators. This results in a population of bacteria with the best defenses against predation—mechanisms which “coincidentally” cause harm during host infection. Few studies have examined the coincidental evolution hypothesis, and those that have present conflicting results. Here, we investigated the validity of the coincidental evolution hypothesis by subjecting the opportunistic pathogen Serratia marcescens to three different scenarios: (1) co-culture with the ciliate predator Tetrahymena thermophila, (2) growth in the absence of predators alone in media, and (3) growth within the guts of germ-free honey bees. We hypothesized that strains evolved in the presence of a predator would display increased virulence and strains evolved in the absence of predators or within a host would exhibit decreased virulence. Our study revealed that evolution in the presence of a predator resulted in increased virulence of S. marcescens. When compared to the media-evolved isolate, all predator-evolved lines exhibited increased pathogenicity in honey bees. However, when investigating how within-host evolution impacts virulence, we observed little to no change in virulence in host-evolved lines. We hypothesize that the lack of attenuated virulence in within-host-evolved strains is due to lack of selective pressure due to S. marcescens already being found at low levels in the bee gut. Overall, our findings indicate that predation plays a role in the evolution of virulence in opportunistic pathogens and thus support the coincidental evolution hypothesis. We were also able to identify mutations and genes potentially associated with virulence. This study sheds light of the factors that impact virulence and drive the evolution of opportunistic pathogens.

Additional Information

Publication
Thesis
Language: English
Date: 2021
Keywords
Coincidental evolution hypothesis, Opportunistic pathogens, Serratia marcescens
Subjects
Serratia marcescens
Pathogenic microorganisms

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