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. 2019 Feb 1;10:123. doi: 10.3389/fmicb.2019.00123

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Copyright © 2019 Yamazaki, Kashimoto, Morita, Kado, Matsuda, Yamasaki and Ueno.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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STM screening reveals the essential factors whereby V. vulnificus invades, spreads, proliferates, and causes wound infection. (A) V. vulnificus adheres to cells located at the local wound infection site via the pilus. Biofilm formation and CPS contribute to resistance against immune cells. (B) V. vulnificus spreads in soft-tissues by flagellar based motility based on chemotaxis. (C) Two different sizes of chromosomes enable rapid chromosome replication leading to rapid cell division and proliferation. Iron, which is an essential element in bacterial metabolic and informational cellular pathways, is acquired via a siderophore-mediated system. (D) CPS and LPS induce inflammation-associated cytokines leading to septic shock.