Examination of the biological activities of the two known toxins of Clostridium difficile revealed that one of the toxins (toxin A) elicited a hemorrhagic fluid response in rabbit intestinal loops and a positive fluid response in infant mice. The other toxin (toxin B) did not produce a significant fluid response in either model, although the toxin was more lethal in infant mice. Both toxins elicited erythematous and hemorrhagic skin reactions and increased vascular permeability in rabbit skin.

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

The results of studies with cell-free extracts and culture supernatant fluids of Vibrio fluvialis (a recently recognized, potential enteric pathogen for humans) grown in the absence and presence of lincomycin indicated that the bacterium could produce (i) a factor which causes CHO cell elongation (CEF) similar to that elicited by V. cholerae enterotoxin and by the heat-labile enterotoxin of Escherichia coli, (ii) cytolysin(s) active against erythrocytes, (iii) nonhemolytic, CHO cell-killing factor(s), and (iv) protease(s) active against azocasein. The CEF was heat labile and ammonium sulfate precipitable, and it had an isoelectric point (estimated by sucrose density gradient electrofocusing) and molecular weight (estimated by gel filtration) of about 5.1 and 135,000, respectively.

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