Variability of the tdh-related hemolysin (trh) gene of Vibrio parahaemolyticus of Pacific Northwest isolates: implications for detection and potential virulence of trh+ strains.
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- Terrestrial and Aquatic Ecology
Vibrio parahaemolyticus (Vp) is the most common cause of illness related to the consumption of raw or undercooked seafood. Globally, the O3:K6 serotype comprises the majority of clinical strains and is often referenced as a “pandemic complex.” Strains belonging to this complex encode the thermostable direct hemolysin (tdh), which is widely considered a reliable virulence marker. In the Pacific Northwest (PNW), the pandemic complex is abundant in the estuarine environment; however, no clinical cases have been associated the O3:K6 serotype in this region. Clinical cases in the PNW are largely associated with the geographically isolated O4:K12 serotype, which carries the similar but phylogenetically distinct tdh-related hemolysin (trh). We have recently shown that trh may be a more accurate marker of virulence in the PNW. Further, recent O4:K12 outbreaks in New York and Spain suggest that trh could become a globally important marker for virulence. Unfortunately, sequence variability in the trh gene is an obstacle to the development of reliable detection methods. Therefore, to identify suitable conserved regions for primer development, we evaluated trh sequence variability in over 50 trh+ Vp isolates. Preliminary results show the trh gene exhibits significant interstrain variation and is likely too variable for accurate detection. We propose the less variable urease R gene (ureR), which is genetically linked to trh, could serve as a useful proxy for the detection of trh+ strains. Current efforts are focused on the validation of ureR as a marker of virulent strains. Additionally, we are conducting an evolutionary analysis of the trh gene to identify the mechanisms responsible for the observed sequence variability. We hypothesize that the recent positive selection is shaping the evolution of this gene and we discuss how key nonsynonymous mutations may affect TRH functionality.