Abstract
Vibrio vulnificus can cause severe necrotic lesions within a short time. Recently, it has been reported that the numbers of wound infection cases in healthy hosts are increasing, for which surgical procedures are essential in many instances to eliminate the pathogen owing to its rapid proliferation. However, the mechanisms by which V. vulnificus can achieve wound infection in healthy hosts have not been elucidated. Here, we advance a systematic understanding of V. vulnificus wound infection through genome-wide identification of the relevant genes. Signature-tagged mutagenesis (STM) has been developed to identify functions required for the establishment of infection including colonization, rapid proliferation, and pathogenicity. Previously, STM had been regarded to be unsuitable for negative selection to detect the virulence genes of V. vulnificus owing to the low colonization and proliferation ability of this pathogen in the intestinal tract and systemic circulation. Alternatively, we successfully identified the virulence genes by applying STM to a murine model of wound infection. We examined a total of 5418 independent transposon insertion mutants by signature-tagged transposon mutagenesis and detected 71 clones as attenuated mutants consequent to disruption of genes by the insertion of a transposon. This is the first report demonstrating that the pathogenicity of V. vulnificus during wound infection is highly dependent on its characteristics: flagellar-based motility, siderophore-mediated iron acquisition system, capsular polysaccharide, lipopolysaccharide, and rapid chromosome partitioning. In particular, these functions during the wound infection process and are indispensable for proliferation in healthy hosts. Our results may thus allow the potential development of new strategies and reagents to control the proliferation of V. vulnificus and prevent human infections.
Highlights
Vibrio vulnificus is a Gram-negative halophilic bacterium and opportunistic human pathogen that causes primary septicemia and wound infections (Oliver, 2005, 2015; Menon et al, 2014)
In vivo expression technology (IVET), in vivoinduced antigen technology (IVIAT), and signature-tagged mutagenesis (STM) have been used to identify virulence factors of V. vulnificus that are functionally expressed in vivo, focusing on primary septicemia (Kim et al, 2003; Lee et al, 2007; Yamamoto et al, 2015)
We could show that a sufficient number of bacteria required for the STM can be collected from a murine model of wound infection and that the lethal outcomes cannot be prevented if allowing sufficient proliferation by V. vulnificus in muscle tissue (Yamazaki et al, 2017)
Summary
Vibrio vulnificus is a Gram-negative halophilic bacterium and opportunistic human pathogen that causes primary septicemia and wound infections (Oliver, 2005, 2015; Menon et al, 2014). These findings encourage the hypothesis that V. vulnificus carries mechanisms for immune evasion, colonization, and rapid proliferation especially in wound infection These processes would be mediated by factors that are constitutively expressed and preemptively function in early stages of infection, underlying its pathogenic ability to establish wound infection within a short time. To test this hypothesis, we applied STM to a murine model of wound infection, which was expected to resolve the problems of low-efficiencies in harvesting the pathogen from systemically infected animals, and identified the genes and functions required by V. vulnificus for efficient proliferation in wound infection
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