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. 2020 Mar 27;11:489. doi: 10.3389/fmicb.2020.00489

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Copyright © 2020 Hernández-Cabanyero, Sanjuán, Fouz, Pajuelo, Vallejos-Vidal, Reyes-López and Amaro.

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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Life cycle of the zoonotic pathogen V. vulnificus: role of iron and temperature. This figure summarizes the role of iron levels and temperature in the surrounding environment in determining the life strategy of V. vulnificus. The main steps and processes as well as some genes involved are shown. (1) Resuscitation and induction of the viable but non-culturable state (VBNC). As a free living form, the pathogen swifts between a VBNC and a vegetative state depending on nutrient availability as well as on water temperature and salinity. (2) Capsule and flagellum production in the environment. Vegetative bacteria produce a capsule and a polar flagellum when iron, and probably other nutrients, are available. The flagellum production is also controlled by temperature. (3) Host colonization. Motile/unmotile bacteria could be attracted by blood/mucus (chemotaxis) from their susceptible hosts (eels and humans with high iron-levels in the blood) and colonize a wound or fish mucus. Alternatively, bacteria can be uptaken by filtering organisms and infect humans by ingestion and colonize the intestine or can infect humans by diseased fish handling. (4) Septicemia. From the wound or mucosal tissue, the pathogen arrives to the bloodstream; in case of humans with high iron levels, the pathogen produces a capsule, multiplies and secretes the toxins VvhA and RtxA1 that cause the death by a toxic sepsis; in case of an eel, only the cells with the plasmid produce two iron-regulated outer membrane proteins, Fpcrp (fish phagocytosis complement resistance protein) and Ftbp (fish transferrin binding protein) that protect against innate immunity (in addition to an envelope enriched in O-antigen), multiply and secrete VvhA, which lyses erythrocytes, increases iron levels and, indirectly, actives the production of RtxA1, which causes the death of the fish by a toxic sepsis. (5) Shedding bacteria to water. Diseased fish liberate bacteria to water. If water is rich in iron, bacteria can infect humans (zoonosis). (6) Biofilm formation and dispersion. Bacteria could be attached to surfaces (including fish mucosae) and to form biofilms under iron restriction. Under iron excess, bacteria will be dispersed from the biofilms as capsulated motile bacteria. Figure modified from Pajuelo et al. (2016).