Abstract. The purpose of this study, initiated in 1964 and concluded in 1967, was to define the distribution of Pseudomonas (now Burkholderia) pseudomallei in Thailand, to evaluate its importance as an etiologic agent, and to survey the presence of antibody in people that might indicate prior infection and/or contact with the microorganism.
Summary
Procholeragen A, a choleragenic moiety elaborated by Vibrio cholerae 569 B Inaba, has been concentrated and partially purified by gel filtration with Sephadex G-200. Purified Procholeragen A, which is essentially free of cholera endotoxin but still not pure, gives a single zone of precipitation with rabbit anti-choleragen antibody adsorbed with live vibrios and causes experimental cholera when amounts as little as 6.0-µg are administered, with Procholeragen B, per os in infant rabbits. When inoculated intradermally in adult rabbits in 0.1 to 0.2-µg amounts, it causes a delayed but sustained local erythematous edematous induration which fixes intravenous Evans blue dye. Procholeragen B, which was formerly considered to be essential for the activity of Procholeragen A, simply serves to protect the latter against destruction under acid conditions in the stomach and can be replaced by a variety of buffers. Procholeragen A causes experimental cholera when inoculated, by itself, into the small bowel of infant rabbits. On the basis of the experimental observations, it is suggested, as an operational concept, that an increase of villus capillary permeability, as a consequence of the direct action of a Procholeragen A-like factor elaborated by cholera vibrios in the small intestines, is a major factor in the pathogenesis of cholera.
Summary
Choleragen, an antigenic, choleragenic moiety elaborated by some cholera vibrio strains in vitro, has been identified by disc immunoelectrophoresis as a protein migrating in a manner similar to human 7 S γ-globulin. Although preparations of choleragen have mucinolytic activity which is neutralized by antiserum against choleragen, the mucinase has been proven to be a separate entity which is not involved in the production of the diarrhea of experimental cholera. Similarly, it is choleragen, and not mucinase, which causes an increase of vascular permeability characterized by a delayed but sustained erythematous, edematous induration. Choleragen elaborated in vitro by an Ogawa serotype El Tor vibrio was serologically identical to that produced by the routinely used Inaba serotype classical cholera vibrio strain.
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