Date of Award

Winter 2019

Project Type


Program or Major


Degree Name

Master of Science

First Advisor

Cheryl Whistler

Second Advisor

Stephen Jones

Third Advisor

Loren Launen


Vibrio parahaemolyticus a ubiquitous coastal inhabitant, is the leading cause of bacterial seafood-borne illnesses in the United States. An increasing number of reported cases and rapid expansion into new areas has led to the classification of V. parahaemolyticus as an emergent pathogen. Most strains of V. parahaemolyticus are not virulent; however, the spread of virulent lineages from their native ranges to new locations has contributed drastically to the increase in vibriosis attributed to V. parahaemolyticus in recent years. In the United States (US), sequence type (ST) 36, a virulent strain endemic to the Pacific Northwest (PNW), spread from its native range up and down both coasts of North America even crossed the Atlantic to cause an outbreak in Spain in 2012, Specifically, the North Atlantic coast of the US traditionally did not have a major disease burden due to V. parahaemolyticus; however, the introduction of ST36 and the evolution of local pathogenic lineages have led to a sharp increase in the number of cases traced to product from this region.

Here we use genomics and phylogeographic analysis to examine the dynamics of the expansion of ST36 and its subsequent establishment in Northeast coastal waters. The impact of basal acquisition of two unique filamentous bacteriophages by distinct clonal clades within the Northeastern ST36 populations is also explored. We propose that the acquisition of these bacteriophages influenced the fitness of their hosts and enabled the establishment of robust local populations of pathogenic V. parahaemolyticus, contributing greatly to the disease burden in the Northeast. Filamentous bacteriophages are distributed throughout many V. parahaemolyticus populations and may be important drivers of evolution amongst these strains. In direct competition under laboratory conditions, the bacteriophage associated with the Gulf of Maine clonal population, Vipa26, does not impact growth of persistently infected isolates and protects them from superinfection by similar phages. Upon new infection, the growth of susceptible isolates slows dramatically before the integration and down regulation of phage production. qPCR assays for integrated and replicative form of phage elucidate this dynamic during infection. This implicates Vipa26 as a potential sword and shield for this strain, possibly aiding the progenitor of the Gulf of Maine population of ST36 in its subsequent global expansion. Impact of phage on biofilm formation, resistance to predatory grazing and competitive fitness in natural seawater microcosms were also investigated. These studies indicate that phage integration is linked to environmental fitness of ST36 and further investigation into the phage-host relationship is warranted to shed light onto the dynamics of the establishment of novel V. parahaemolyticus populations.