Conditions are described for the production, in high titers, of heat-labile, antigenic, extracellular toxin(s) by Vibrio vulnificus, a recently recognized human pathogen. Bacteriologically sterile culture filtrate preparations obtained from mid-logarithmic-phase cultures of the bacterium possessed cytolytic activity against mammalian erythrocytes, cytotoxic activity for Chinese hamster ovary cells, vascular permeability factor activity in guinea pig skin, and lethal activity for mice. The specific activity of toxin preparations from cultures of a virulent strain of the bacterium was ca. 25-fold more than that of toxin preparations obtained from cultures of a weakly virulent strain. The four toxic activities were inseparable by gel filtration with Sephadex G-100; however, two components, which had markedly different elution behavior but which possessed the four activities mentioned above, were obtained. The major (ca. 88% of recovered activity) and minor components had apparent molecular weights of ca. 38,500 and >150,000, respectively. Vibrio vulnificus, also called "lactose-positive Vibrio species" and Beneckea uulnifica (2, 9), is a halophilic bacterium which has been erroneously identified as V. parahaemolyticus, "unnamed marine vibrio," and "halophilic, noncholera vibrio" (4, 10, 22-25), but is now known to be a distinct etiological agent of wound infections, septicemia, meningitis, pneumonia, and keratitis (4, 6, 7, 10, 11, 13, 16, 18-20). Published data concerning the pathogenesis of disease caused by V. vulnificus, presented in the papers cited above and summarized in a recent review article (5), consist of information concerning the portals of entry of the bacterium, the host factors which predispose to disease, and the pathological features of naturally occurring disease in humans and of experimentally induced disease in mice. However, previous publications have not dealt with the possible role(s) of bacterial products in causing the extensive tissue damage and the often rapidly fatal outcome characteristic of V. vulnificus-induced disease. In this