Date of Award

Fall 2024

Project Type

Thesis

Program or Major

Microbiology

Degree Name

Master of Science

First Advisor

Stephen H Jones

Second Advisor

Loren Launen

Abstract

Over the past 12 years, infections from the ubiquitous coastal bacterium and human pathogen V. parahaemolyticus have increased in the Northeast USA. The majority of the infections here are caused by the hypervirulent ST36 which originated in the Pacific Northwest USA where it caused only sporadic infections. This sequence type seems to have found its niche in the Northwest Atlantic where climate events likely created environmental conditions allowing ST36 strains or strains carrying one of the unique virulence factors on the VPaIγ, associated with this sequence type, to maintain and spread up the coast of New England. In the Great Bay estuary (GBE), NH there has only been rare infection caused by V. parahaemolyticus but detection of the T3SS2β, a virulence factor critical for human infection and present on the mobile pathogenicity island, VPaIγ, is increasing. One theory on why these genes are maintained in Northeastern USA water is that they could help confer resistance to native planktonic predation. The relationship between Vibrio spp. and plankton is well documented and important, and plankton are the highest consumers of bacteria in the environment. I hypothesized that when pathogenic strains of V. parahaemolyticus can secrete toxins from the T3SS2β in the presence of GBE native plankton they will survive better than those that do not have the ability to secrete toxins. Using GBE microcosms and inoculation of ST36 pathogenic strains of V. parahaemolyticus with and without the ability to secrete toxins from the T3SS2β I found that in certain circumstances V. parahaemolyticus survives better without the selective removal of protozoan predators and it is possible that when the ability to secret toxins is retained, zooplankton populations are negatively impacted. Additionally, V. parahaemolyticus survives significantly better in the GBE without protozoa, bacterial competitors, or particles.

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