Abstract
Gastric infections caused by the environmentally transmitted pathogen, Vibrio parahaemolyticus, have increased over the last two decades, including in many parts of the United States (US). However, until recently, infections linked to shellfish from the cool northeastern US waters were rare. Cases have risen in the Northeast, consistent with changes in local V. parahaemolyticus populations toward greater abundance or a shift in constituent pathogens. We examined 94 clinical isolates from a period of increasing disease in the region and compared them to 200 environmental counterparts to identify resident and non-indigenous lineages and to gain insight into the emergence of pathogenic types. Genotyping and multi-locus sequence analysis (MLSA) of clinical isolates collected from 2010 to 2013 in Massachusetts, New Hampshire, and Maine revealed their polyphyletic nature. Although 80% of the clinical isolates harbored the trh hemolysin either alone or with tdh, and were urease positive, 14% harbored neither hemolysin exposing a limitation for these traits in pathogen detection. Resident sequence type (ST) 631 strains caused seven infections, and show a relatively recent history of recombination with other clinical and environmental lineages present in the region. ST34 and ST674 strains were each linked to a single infection and these strain types were also identified from the environment as isolates harboring hemolysin genes. Forty-two ST36 isolates were identified from the clinical collection, consistent with reports that this strain type caused a rise in regional infections starting in 2012. Whole-genome phylogenies that included three ST36 outbreak isolates traced to at least two local sources demonstrated that the US Atlantic coastal population of this strain type was indeed derived from the Pacific population. This study lays the foundation for understanding dynamics within natural populations associated with emergence and invasion of pathogenic strain types in the region.
Highlights
Rare pathogenic variants of Vibrio parahaemolyticus, a ubiquitous yet typically harmless estuarine bacterium, can cause human gastric infections most often from the consumption of raw or improperly handled seafood, and wound infections from recreational aquatic activities (Daniels et al, 2000; Scallan et al, 2011)
Genetic Diversity Among Clinical Isolates and Distribution of tdh, trh, and Urease Activity In light of the recent rise of V. parahaemolyticus infections in the northeastern United States (US), clinical isolates from infections reported in MA, New Hampshire (NH), and ME were obtained to identify pathogenic strain types, and determine whether they belong to resident or invasive lineages (See Table 1)
Even though clinical isolates were not archived from every infection, and information was incomplete, this collection provides an extensive survey of regional infections (Table 1)
Summary
Rare pathogenic variants of Vibrio parahaemolyticus, a ubiquitous yet typically harmless estuarine bacterium, can cause human gastric infections most often from the consumption of raw or improperly handled seafood, and wound infections from recreational aquatic activities (Daniels et al, 2000; Scallan et al, 2011). Recurrent infections and outbreaks have occurred in cooler waters of the Pacific Northwest (PNW) for decades where pathogens reemerge each year from among diverse residential populations (Altekruse et al, 2000; Johnson et al, 2010; Paranjpye et al, 2012; Turner et al, 2013; Banerjee et al, 2014). In the last several years, reported cases have been increasing in the Northeast, with outbreaks in NY in 2012, and in NY, CT, and Massachusetts (MA) in 2013 (Newton et al, 2014) (Figure 1) This abrupt increase in cases coincided with both warmer than usual ocean temperatures in the region (Figure 1) and the probable Atlantic ecological invasion of a lineage of ST36 strains, which are indigenous to the cooler waters of the PNW (Martinez-Urtaza et al, 2013; Newton et al, 2014). Characterizing clinical strains from the region and relating them to native nonpathogens during this period of increased disease incidence could provide insight into how changes in the bacterial population have led to increased disease
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