Many of the high-virulence strains of the marine fish pathogen Vibrio anguillarum isolated from epizootics of the widespread fish disease vibriosis, harbour a specific plamid class which is absent from low-virulence strains. Curing experiments have confirmed a link between this specific plasmic class and the ability of V. anguillarum to establish infections. In general, all bacterial virulence factors promote growth in the antagonistic environment of the host defence mechanisms. One line of defence is provided by the proteins transferrin and lactoferrin, which bind iron, rendering it unavailable to pathogens. A mechanism whereby invading bacteria may successfully compete for the otherwise unavailable iron could therefore become crucial in enabling them to proliferate in body fluids and tissues. I report here evidence which shows that the V. anguillarum virulence plasmid specifies a very efficient iron-sequestering system enabling bacteria to survive in conditions of limited iron availability.