Abstract
Vibrio vulnificus causes rapid septicemia in susceptible individuals who have ingested contaminated foods or have open wounds exposed to seawater contaminated with the bacteria. Despite antibiotic therapy and aggressive debridement, mortality from septicemia is high. In this study, we showed that MukB mutation (mukB::Tn) affected the proliferation of V. vulnificus in the systemic circulation but not at the inoculation site in the wound infection model. A comparison of mukB::Tn with WT and a mukB complement strain (mukB::Tn/pmukB) on the bacterial burden in the muscle at the infection site showed that spreading and proliferation of the mukB::Tn strain was similar to those of the other strains. However, the bacterial burden of mukB::Tn in the spleen was reduced compared to that of the WT strain in the wound infection model. In a competition experiment, we found a lower bacterial burden of mukB::Tn in the spleen than that of the WT strain infecting the systemic circulation. Here, we report on a gene required for the rapid proliferation of V. vulnificus only in the systemic circulation and potentially required for its survival. Our finding may provide a novel therapeutic target for V. vulnificus septicemia.
Highlights
Our results showed that MukB is one of the necessary genes for rapid proliferation of V. vulnificus in the systemic circulation but not at the inoculation site in the wound infection model
Using signature-tagged mutagenesis (STM), we identified two mutant clones of MukB that contained a transposon at different positions into the MukB open reading frame
By using a local alignment search tool, we found the amino acids sequences aligned between MukB in E. coli K12 (1486 a.a.) and MukB in V. vulnificus
Summary
Vibrio vulnificus is a Gram-negative bacterium that can cause severe septicemia [1,2,3]. Even after treatment with antibiotics, aggressive surgery, or both, Vibrio vulnificus rapidly proliferates in some patients [5]. It is essential to identify virulence factors necessary for the rapid proliferation of V. vulnificus after its invasion into the systemic circulation. These factors could be targeted to develop effective treatments for septicemia. In a murine infection model, several factors have already been reported: a capsular polysaccharide, lipopolysaccharide, repeats-in- toxins, an iron acquisition system, and chemotactic ability [6,7,8,9]. The mechanisms causing severe and rapid septicemia resulting from V. vulnificus infection have not been fully understood
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