Abstract
Pathogenicity islands (PAIs) are large genomic regions that contain virulence genes, which aid pathogens in establishing infections. While PAIs in clinical strains (strains isolated from a human infection) are well-studied, less is known about the occurrence of PAIs in strains isolated from the environment. In this study we describe three PAIs found in environmental Vibrio vulnificus and Vibrio parahaemolyticus strains, as well as a genomic fitness island found in a Vibrio diabolicus strain. All four islands had markedly different GC profiles than the rest of the genome, indicating that all of these islands were acquired via lateral gene transfer. Genes on the PAIs and fitness island were characterized. The PAI found in V. parahaemolyticus contained the tdh gene, a collagenase gene, and genes involved in the type 3 secretion system II (T3SS2). A V. vulnificus environmental strain contained two PAIs, a small 25 kbp PAI and a larger 143 kbp PAI. Both PAIs contained virulence genes. Toxin–antitoxin (TA) genes were found in all three species: on the V. diabolicus fitness island, and on the V. parahaemolyticus and V. vulnificus PAIs.
Highlights
Vibrio parahaemolyticus and Vibrio vulnificus can cause illnesses in humans, with an estimated 80,000 cases occurring annually in the United States (Scallan et al 2011; CDC 2017)
V. parahaemolyticus island Vibrio parahaemolyticus strain TS-8-11-4 was isolated from salt marsh sediments (Gutierrez West et al 2013; Klein et al 2014) at the pristine North Inlet estuary in South Carolina, USA
The virulence factor genes that were found on this island included the thermostable direct hemolysin gene, genes involved in the type three secretion system II (T3SS2), a collagenase gene, as well as capsule production genes
Summary
Vibrio parahaemolyticus and Vibrio vulnificus can cause illnesses in humans, with an estimated 80,000 cases occurring annually in the United States (Scallan et al 2011; CDC 2017). The hospitalization and mortality rates of V. parahaemolyticus gastroenteritis are 22% and 1%, respectively (Scallan et al 2011). The majority of reported V. vulnificus cases are from wound infections (45%) and septicemia (43%); only 5% are gastroenteritis (Scallan et al 2011). The mortality rate of V. vulnificus when it invades the bloodstream (sepsis) increases to 60%. Pathogenesis of both species is complex, and while some virulence factor genes have been implicated, the mechanisms underlying V. vulnificus and V. parahaemolyticus virulence are not well understood (Broberg et al 2011; Lovell 2017; Klein and Lovell 2016)
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